Obstructive sleep apnea (OSA) is a respiratory disorder that negatively interferes with the phases of sleep, completely, partially, or intermittently interrupting the eupneic act. OSA can have central or peripheral origins. Injuries to the central nervous system can cause a functional limitation of the respiratory drive, with a total or partial decrease in diaphragmatic movement; peripheral obstructions may lead to the collapse of the pharyngeal airway, reducing the amount of inhaled air into the lungs [1]. A study that examined.1,520 asymptomatic adults in the United States found a percentage of peripheral OSA in about 15% in men and about 5% in women [2]. A recent study performed in Europe, with 1288 participants, found a peripheral OSA finding rate of about 30% in men and about 13% in women [3]. In the pediatric population, the finding of OSA is approximately 2-4% [4]. There are multiple risk factors for developing peripheral OSA. The presence of asthma and asthma medications can increase or develop collapsibility, or narrowing of the upper airways [5]. Asthma can lead to obesity and gastroesophageal reflux, the latter two being factors risk for the evolution of OSA [6]. A retrospective study has shown that the coexistence of asthma and OSA increases the rate of hospitalization for the acute exacerbation of asthma, compared to the co-presence of other diseases [7]. Increased bronchial hyperresponsiveness and the presence of systemic inflammation could be the most relevant causes of exacerbation in the presence of OSA and asthma [8]. Gastroesophageal reflux disease (GERD) can cause laryngeal dysfunction, leading to peripheral OSA, although the precise causes are elusive [9,10]. GERD does not exacerbate OSA and is not correlated with the severity of respiratory indices [11]. Obesity predisposes the onset of OSA (and obesity-hypoventilation syndrome), altering the muscular anatomy of the upper respiratory tract with greater nocturnal collapse; the systemic inflammatory environment related to obesity is linked as one of the leading causes of asthma and GERD, creating a vicious circle [6,12,13]. Most patients diagnosed with OSA are overweight (BMI 25.0-29.9) or obese (BMI>30) (approximately '80%) [14]. The systemic inflammation found in allergic rhinitis and chronic sinusitis triggers the same upper respiratory tract dysfunction mechanisms present in asthma, predisposing the onset of OSA [13]. Other causes can induce the presence of peripheral OSA. An observational study has highlighted that bilateral mandibular fracture can lead to the development of OSA while surgery to improve the orthopedic picture of the bone is able to induce the disappearance of OSA, probably due to purely mechanical factors [15]. We know that morphological and functional craniofacial alterations can predispose to the onset of peripheral OSA. Hypomobility or retrusion of the mandible, a structural alteration of the maxillary bone (hypoplasia), a non-physiological (lower) position of the hyoid bone, and an extended postural attitude of the cervico-occipital tract create the conditions for the finding of OSA. Through cephalometric measurements, it has been shown that patients with OSA have a higher vertical measurement in the facial area (tendentially), compared to people without OSA [16]. OSA can induce the onset of various co-morbidities with an increase in the mortality rate. Sleep apnea causes sleep fragmentation and chronic intermittent hypoxia; the frequency and severity of apneas/hypopneas are measured with the apnea-hypopnea index (AHI) while the level of desaturation is measured with the oxygen desaturation index (ODI) [17,18]. The presence of OSA with a high AHI and a severe ODI induces a decline in testosterone levels (particularly in middle-aged men), an altered pituitary-gonadal axis, with evidence of sexual dysfunction [19]. Hypogonadism may be associated with the presence of obesity in patients with OSA [20]. Regardless of hypogonadism, OSA can induce metabolic syndrome, diabetes, and obesity. OSA can activate a non-physiological metabolic environment, leading to a metabolic syndrome with diabetes mellitus, insulin resistance with pancreatic beta cell dysfunction, hypertension and dyslipidemia, cardiovascular disease, and obesity. Approximately 40% of patients with obesity develop peripheral OSA while approximately 70% of patients with OSA are obese. Metabolic syndrome can develop regardless of body mass index (BMI) and obesity [21]. There are several factors proposed to explain the onset and connection with OSA and the resultant metabolic and cardiovascular diseases (heart attack, atherosclerosis, atrial fibrillation, heart failure) in patients. OSA can induce an increase in the activity of the sympathetic system, create a systemic inflammatory environment (elevation of inflammatory cytokines and leptin), a higher generation of cellular oxidation; increases the activity of the renin-angiotensin system [22-24]. OSA increases the risk of long-term all-cause mortality, compared to the absence of OSA, by approximately 46%-54% more and approximately 1.9 times in patients with severe OSA [25]. OSA increases the finding of pulmonary hypertension (from 17% to 53%), probably, due to hemodynamic changes related to sleep apnea (pulmonary vasoconstriction and endothelial dysfunction) [22]. OSA can exacerbate acute episodes in patients with co-presence of chronic obstructive disease (COPD); the finding of OSA and COPD is referred to as overlapping syndrome and affects 1.0%-3.6% of the general population [26]. Acute exacerbation of OSA-COPD can involve about 61.4% of affected patients, with an increased mortality rate on first admission [26]. The cardiovascular and metabolic problems deriving from the presence of OSA are also reflected in the brain. There is a reduction in the thickness of the gray matter at the cortical level (paracentral and precentral anterior lobule) [27]. There is a cognitive decline, neuropsychological alterations, anxiety, and depression; such events are probably related to hypoxia with a decrease in glucose synthesis, an increase in deposits of beta-amyloid peptides (β-amyloid or Aβ), and a decline in cleansing by the glymphatic system [21]. The repeated desaturation of oxyhemoglobin during sleep apnea leads to a greater onset of stroke and cerebrovascular damage (optic and otological neuropathy) for about 61.9% of patients [22]. The anatomical areas on which the clinician's attention focuses in the presence of OSA are the upper airways, in particular, the lingual complex [28-30]. An anatomical area that very often does not attract the clinician's attention is the diaphragm muscle, despite the eupneic act involving multiple anatomical areas (from the nose to the pelvic floor) through a common central pattern generator (CPG) [31,32]. The article reviews the functional anatomy and adaptation in patients with OSA of the respiration muscles of the upper airways, and the functional anatomy and adaptations caused by sleep apnea in the diaphragm muscle, trying to emphasize the importance of the latter, in order to obtain a clinical picture that is as complete as possible.

Functional anatomy and adaptation of the upper respiratory tract with OSA

All respiratory, secondary, and accessory muscles are managed by a central pattern generator (CPG), consisting of a neural network between the brain stem and the spinal cord where, in particular, we find important areas, such as the pre-Bötzinger complex, nucleus tractus solitarius (or nucleus of the solitary tract), ambiguous nucleus, parabrachial/Kölliker-Fuse complex, raphe-pontomedullary network, medullary division of the lateral tegmental field, and nucleus subcoeruleus [31]. Several other neurological areas intervene to coordinate the final act of breathing such as the cranial and spinal nerves, cerebellum, cortical and subcortical centers, and midbrain [31]. CPG controls 700 breaths per hour in a state of rest in a healthy person. We can divide the eupneic act into three distinct phases: preinspiratory, inspiratory, and expiratory. To the latter, two other phases are added, such as the post-inspiratory phase (extending the inspiratory phase) and the active expiratory phase [31]. The alae nasi or dilator naris is an extradiaphragmatic inspiratory muscle innervated by the facial nerve, which affects nasal airflow by opening the nasal passages and decreasing airflow resistance (stiffening the airways and preventing collapse) [32,33]. The airflow passes from the nasopharynx (or rhino-pharynx) to the oropharynx and then to the hypopharynx; these latter anatomical areas may become obstructed in patients with peripheral OSA [34]. The posterior area of the nasopharynx consists of loose connective tissue, in which area we can find some important structures such as the Eustachian tube, the pharyngeal bursa, and the Rosenmüller fossa (or lateral pharyngeal recess) [35]. Alae nasi is activated with the same timing activation of the genioglossus muscle and always before the diaphragm muscle in healthy subjects [36,37]. With OSA patients, electromyographic values increase, reducing latency; muscle contraction increases with increasing apnea episodes with a minor contractile pause between contractions, until awakening [38]. The dilator muscles of the airways in OSA patients, such as the alae nasi, are more active during wakefulness than in healthy subjects [39]. Dysfunction of this muscle can alter negative air pressure flows to the pharyngeal compartment, stimulating airway collapse [39]. We do not know how alae nasi fits metabolically and phenotypically in the presence of constant apneas. The nasopharynx area can undergo stenosis due to the increase of fibrotic tissue due to iatrogenic causes, in particular, due to previous surgery (and radiotherapy) at this site, causing the appearance of OSA over time (Figure 1) [40]. The resolution is surgical. In patients with OSA, it is possible to find a restriction of this area for various pathogenic causes, without reaching complete stenosis [41].

The nasopharynx is located between the pharyngeal vault (non-muscular non-collapsing upper end of the nasopharynx) and the upper face of the soft palate, putting the nasal cavities in continuity with the oropharynx [35]. The soft palate is made up of five muscles covered by mucus membranes: tensor veli palatini (TVP), levator veli palatini (LVP); musculus uvulae or uvular muscle (UM); palatoglossus (PG), and palatopharyngeus (PP) [42,43]. The flow of air entering the nasopharynx is affected by TVP; the latter merges its aponeurosis with the uvula, the PP, and the PG and has rhythmic activation with the phases of the breath. In the animal model, TVP is able to influence the pharyngeal lumen at the level of the soft palate, but in the human model, we do not have a definitive result [42]. The innervation of the TVP derives from the maxillary branch of the trigeminal nerve [44]. LVP comprises about 40% of the length of the soft palate and is located between the hard palate and the uvula [42]. This muscle is longer in men than in women, but the action remains the same: raise and pull the soft palate, closing the wall pharyngeal posteriorly [42]. The activation of the LVP facilitates the work of the genioglossus muscle during respiratory acts, in synchrony with the alae nasi and palatoglossus [36]. Motor branches for LVP arise from the lesser palatine nerve (trigeminal nerve), and from the pharyngeal plexus [44]. We do not know the specific adaptation of this muscle in the presence of OSA. The contraction of UM allows to shorten the uvula, creating a convex shape to the velum, giving rigidity and extending the same velum toward the posteriority; UM is innervated by the lesser palatine nerve [44,45]. UM crosses and interconnects dorsally with the LVP and may consist of a single muscle medially or of bundles of muscles placed in parallel [45]. UM is capable of increasing its contractile capacity if the LVP undergoes a functional decrease, thus preserving the velopharyngeal closure [45]. In patients with OSA, UM undergoes non-physiological adaptations, altering its correct functionality. Cytoskeletal proteins, such as desmin (intermediate filament) and dystrophin (sub-sarcolemmal protein) undergo a reduction in their presence, negatively contributing to the contractile capacity of the muscle, compared to healthy subjects [46]. Muscle fibers change morphology, with a not as homogeneous form, with an increase in the connective tissue between the fibers; neurotrophin levels increase, such as brain-derived neurotrophic factor (BDNF), whose values indicate neuromotor remodeling processes in the presence of constant lesion [47]. UM undergoes a decrease in the capillary network and in the number of mitochondria, with decreased oxidative capacity; these adaptations lead to faster fatigue [48]. Muscle fibers exhibit an inflammatory environment in individuals with OSA, with increased levels of tumor necrosis factor (TNF)-alpha [49]. PG constitutes the soft palate below and is an integral part of the extrinsic muscles of the tongue, influencing its complex function and shape; it is founded on some intrinsic muscles of the tongue (superior longitudinalis and transversalis muscles) [50]. The contraction of the PG muscle allows bringing the soft palate toward the lingual complex (downward), in order to pass the food bolus correctly, reducing the measure of the oropharyngeal isthmus [50]. It constitutes the palatoglossal arches in the lateral pharyngeal area, preventing saliva from entering the oropharyngeal region (coming from the vestibular area) [50]. PG intervenes in the pronunciation of some phonemes through the deformation of the veil and the tongue [51]. It works with PP to create a sling effect during phronesis so that the oropharyngeal isthmus behaves like a sphincter [52]. PG would act as an antagonist to LVP [50]. Innervation is uncertain; depending on the literature, it could derive from the glossopharyngeal nerve, vagus nerve, or hypoglossal nerve [39,42,44]. During inspiration, it is activated in myoelectric coordination with the alae nasi, LVP, tongue, and diaphragm [36]. In patients with OSA, PG has a reduced myofibrillar diameter size and reduced capillary and mitochondrial density; fibrotic and heavy chain myosin fibers with non-specific type isoform are found [48]. These adaptations mirror a muscle that undergoes continuous remodeling in the presence of neuromuscular lesions, such as in dystrophies [48]. PG appears to undergo a more non-physiological adaptation. This is important as compared to UM [48]. Generally, in healthy subjects, PG and TVP have a balance in the distribution of oxidative and glycolytic fibers while there is a predominance of white fibers for MU and PP; LVP is rich in red fibers [53]. If this phenotypic physiological distribution in the muscles of the soft palate is altered, the function assigned to each district and the functions expressed in a group context will inevitably change. No muscle ever acts alone [44]. PP is a broad and flat muscle below the PG muscle, which connects the pharyngeal area with the soft palate; it coordinates with the LVP and the superior constrictor muscle of the pharynx (SCP) [42]. Together with the SCP, PP forms Passavant's ridge during the phase of velopharyngeal closure (during swallowing and phronesis) [54]. There is fusion in the lower portion of the salpingopharyngeal and PP muscle, and with the stylopharyngeal muscle at the level of the thyroid cartilage [55]. It is composed of a longitudinal bundle (ventral and dorsal) and a transverse bundle; during swallowing it contracts to shorten and medialize the pharynx, while during breathing it depresses the soft palate modulating the closure of the velopharyngeal, and acts as a sphincter for the nasopharynx area (separating the nasopharynx from the oropharynx) (Figure 2) [42,56,57]. PP is innervated by the lesser palatine nerve and the pharyngeal plexus [44]. In patients with OSA, the PP muscle fibers undergo a decline in their volume (atrophy), with increases in connective tissue (fibrosis); the muscle loses its contractile capacity [58]. As in other areas, there is a decrease in the oxidative capacity and in the number of capillaries of the contractile fibers [48].

The hypopharynx or laryngopharynx (below the oropharynx and behind the larynx) extends from the epiglottis to the lower limit of the cricoid; it is responsible for the passage of food to the passage of air and is a site of possible obstruction in patients with OSA [59]. This area could collapse due to various causes, such as the presence of macroglossia, decreased muscle tone, and hypertrophic lingual tonsils. The hypopharynx includes the posterior pharyngeal wall, pyriform sinuses, and the post-cricoid portion of the pharynx [59]. Below the hypopharynx, we can find the upper esophageal sphincter (UES) and the upper portion of the esophagus or the cervical esophagus [60]. The pharyngeal muscles include complex circular striated muscles of the outer layer: upper, middle, and lower pharyngeal constrictor. A fourth cricothyropharyngeus muscle arises from the cricoid arch until it crosses the inferior constrictor muscle, in particular, the cricolaryngeal portion; with loose connective bundles, it attaches to the lower horn of the thyroid gland and to the cricothyroid joint [61]. The external pharyngeal longitudinal muscles include the stylopharyngeal, salpingopharyngeal, and palatopharyngeal (previously described) [61]. The pharyngeal constricting muscles (PC), as regards the passage of air, are activated to increase the pharyngeal tone in the presence of negative pressure, avoiding the collapsibility of the pharyngeal tube: they manage the lumen of the pharynx [61]. The lower PCs are able to pull the hyoid bone posteriorly [39]. The transition area of the superior constrictor and the PP, at the level of the posterior-lateral area of the isthmus, is called Passavant's ridge; the latter is formed when the veil is closed during swallowing or phronesis [54]. The longitudinal muscles elevate and shorten the pharynx, fundamental actions in the swallowing process [62,63]. The actions of the longitudinal muscles can vary from subject to subject, according to their insertion, which can give a different vector force; in some people, these muscles can help the arytenoid muscle (vocal cords) during phronesis [64]. The pharyngeal and esophageal longitudinal muscles are in close anatomical communication, as is the coordination of the constricting and longitudinal pharyngeal muscles [55,65]. The superior constrictor merges with the buccinator and mylohyoid muscle through some fascicles and the lingual complex; the middle constrictor, in some subjects, shares an insertional portion on the hyoid bone with the mylohyoid muscle [42,66,67]. The pharyngeal muscles are innervated by the pharyngeal plexus via the vagus nerve and the glossopharyngeal nerve [39,44,62]. Neuromuscular incoordination is present in patients with OSA, and this involves the creation of a very complex clinical picture to visualize, without taking into account all the anatomical and functional relationships of the muscles mentioned. The space of the musculomembranous pharyngeal tube is reduced in OSA, compared to healthy subjects, for several reasons, including the posture of the occipitocervical area in extension and a more caudal position of the hyoid bone [16]. During sleep, the pharyngeal area is more prone to collapse, despite the possible electromyographic increase in the lingual complex; There is a lack of correct neurocoordination between the lingual complex and the peri-pharyngeal muscles, which are activated at lower electrical frequencies during the rest phase [68]. This is not a question of muscle fatigue but of a neuromotor dissociation between the tongue and peri-pharyngeal during sleep [69]. The collapse of the pharyngeal area may be more likely to occur during the last phase of exhalation [70]. The constricting muscles show structural protein and mitochondrial alterations and an increase in intramyocellular lipid droplets; there is an increase in apnea indices and an increase in such muscular dysfunctions [71]. In particular, in the upper constricting muscles, there is an increase in connective tissue (fibrosis), which increases contractile dysfunction; in the medium constricting muscles, there is a myopathy, typical of continuous remodeling from chronic injury, and an increase in anaerobic metabolism [72,73]. We do not know the specific adaptations of the lower constricting muscles. To the knowledge of the authors, we do not know in detail how the structure of the stylopharyngeal muscle and salpingopharyngeal muscle fits in patients with peripheral OSA. The laryngeal area can be a site of obstruction in patients with OSA due to a lack of coordination of the muscles that manage movement, and/or a decreased tone of the epiglottis (lax or ptotic), which can occlude the larynx. The thyroarytenoid, lateral cricoarytenoid, and interarytenoid muscles are able to close the glottis, through an adduction action; the posterior cricoarytenoid muscle (PCA) opens the glottis with an abduction action [74]. During the inhalation, the posterior cricoarytenoid raises the epiglottis (opens the glottis), reducing the resistance of the airflow; while, with the exhalation, the other three muscles contract to lower the epiglottis (closing of the glottis) [74]. With a deep inhalation, a fifth intrinsic laryngeal muscle contracts, the cricoarytenoid (CT) muscle; the latter stretches the vocal cords with minimal electrical activity in the phases of quiet breathing, but intervenes for deep inspiratory acts, allowing the anteroposterior laryngeal diameter to increase [74]. In this way, it increases the glottal area. CT is considered an accessory respiratory muscle and is activated in the presence of insufficient lung inflation and hypercapnia; CT is able to work in synergy with PCA to widen the glottal space to the maximum [75]. Cricothyropharyngeus muscle (CTP) during breathing helps the cricoid cartilage slide (forward and backward) and rotate, increasing the range of motion of the larynx and improving the movement of air flows [76]. The laryngeal and CTP muscles are innervated by the pharyngeal plexus [76]. Depending on the studies carried out on laryngeal obstruction, the percentages can range from about 12% to 23% of patients with OSA; the epiglottis would be longer in patients with glottal obstruction [77-80]. The collapse of the epiglottis can be classified as primary if the cause is the muscle itself, or secondary if the posterior tongue portion compresses the epiglottis and obstructs the larynx (Figure 3) [77].

Functional anatomy and adaptation of the lingual complex with OSA

The tongue is a finely coordinated muscular structure made up of intrinsic and extrinsic muscles. The intrinsic contractile districts (4 pairs) are transversalis, verticalis, inferior longitudinalis, and superior longitudinalis [81]. The extrinsic muscles (4 pairs) are genioglossus (GG), styloglossus (SG), hyoglossus (HG), and palatoglossus (PG) [81]. In the literature, it is possible to find two other muscles, such as the glossopharyngeus and chondroglossus, which are considered part of the extrinsic muscles [81]. The glossopharyngeus is a set of contractile fiber bundles deriving from the superior pharyngeal constrictor muscle; the chondroglossus derives from the hyoglossus muscle [81]. In the animal model, the superior and inferior longitudinal intrinsic muscles (and the genioglossus) are capable of producing a higher isometric force than the other lingual muscles; the intrinsic muscles are rich in glycolytic fibers and, in particular, in the anterior portion of the tongue, with a progressive decrease going towards the posterior [82,83]. As for size, the fibers of the intrinsic muscles possess a greater volume in the posterior portion, compared to the anterior of the tongue [83]. This organization could reveal different functions based on the organizational topography; finer and faster movements at the tip of the tongue and coarser and slower actions posteriorly [83]. In the aging process, it appears that the intrinsic muscles are spared from major phenotypic and morphological changes [83]. The superior longitudinal muscle (SL) in an animal model is active during inspiration while the posterior transverse muscle seems to play a role in maintaining the passage of airflow [83]. SL interdigitates with PG and with the outermost fibers of the HG; their connection allows for lateral lingual movement and retrusion [84]. The contraction of the SL allows the tongue to manage length during different actions [85]. The inferior longitudinal muscle (IL) has a close relationship with the lateral portion of the HG; both are coordinated by a dorsiflexion movement while, if IL is specifically activated, it is able to pull the lingual apex toward the posteriority and inferiority [84]. The fibers of the transversalis muscle (TV) control the thickness of the tongue and, in coordination with HG and PG, are activated by lateral retraction of the tongue [84,85]. The fibers of the verticalis muscle (V) are able to flatten the tongue laterally, to the right or to the left, and control the height of the tongue [84,85]. The tongue is considered a muscular hydrostat, that is, it not only keeps the volume constant, but the different movements carried out in the different functions are the result of the intervention of all the muscles that make up the tongue, in a percentage that is not synchronous [86]. It becomes almost impossible to distinguish specific activation in vivo of different lingual fibers and vectors [86]. Intrinsic muscles are active in maintaining the tonic for opening the upper airway in the presence of hypoxia (animal model) [87]. Currently, we do not know, specifically, the adaptations of intrinsic muscles in the presence of OSA. GG is the most studied muscle in the literature with OSA. GG is made up of type I and IIa fibers, which are interconnected on the horizontal (posterior area) and oblique (anterior area) planes, with an increase in volume going toward the posteriority; this arrangement allows the muscle to diversify the activation of the anatomical areas based on the action performed [82,88,89]. We must remember that the movement of the lingual complex is allowed due to all the muscles adjacent to the same tongue and not only to the GG [89]. GG is the most voluminous extrinsic muscle of the tongue; its fibers interconnect with all intrinsic muscles [89]. The actions of the GG are to protrude the tongue, depress the lingual body, perform retrusion of the apical portion of the tongue and ventroflexion, and stimulate the back of the tongue to form a convexity (useful for swallowing and phronesis) [89]. During the inhalation, GG pushes the hyoid bone forward to dilate the airways, with posterior-dorsal caudal traction and a subjective sensation of lingual retrusion [31]. GG activates approximately 250 milliseconds before it enters the airflow and before the movement of the diaphragm muscle, with a movement of about 2 millimeters in the inhale [90]. SG is the most lateral muscle of the lingual complex; with the posterior portion, it interdigitates with HG while with the anterior (wider), it connects with GG, HG, and IL [89]. When contracting, it allows the tongue to retrude and elevate the lingual lateral margin [89]. There does not seem to be a prevalence of a type of fiber (red or white), however, with advancing age, an increase in oxidative fibers may occur as compared to glycolytic ones [91]. HG appears to have a prevalence of glycolytic fibers, which decline with advancing age [91]. HG is activated in the phases of inspiration (animal model) [92]. In coordination with SG, it retracts the tongue, while activated alone and to the side, it depresses the lateral lingual portion [85,89]. The HG muscle is a thin district but interdigitates with all the muscles of the tongue [89]. PG shows a phenotypic balance of muscle fibers and a close relationship with the intrinsic muscle TV [53.89]. PG plays a role in the correct stimulation of lingual protrusion, improving the retropalatal opening [93]. Chondroglossus derives from the lesser cornu of the hyoid bone and is interdigitated with the intrinsic muscles of the tongue (in particular with IL) and merges with GG; working synergistically with and as HG [89,94]. The innervation of the tongue muscles is complex, and it is not always possible to have a clear distinction as to which nerve ending involves a specific contractile district. Each lingual muscle is made up of neuromuscular compartments (groups of fibers), which ensure different functions for the same muscle [95]. We must remember that the muscle complex of the tongue is made up of efferent and afferent fibers; the set of such neural information allows communication between the peripheral and central nervous systems. An important motor role is played by the hypoglossal cranial nerve (XII) while the sensory innervation is given by the glossopharyngeal nerve (IX), the lingual nerve (branch of the trigeminal nerve or V), the vagus nerve (X), part of the facial nerve (VII) and sympathetic branches from the superior cervical ganglion [39,95,96]. In patients with OSA, the lingual complex is enlarged and more voluminous, increasing resistance during inhalation; stiffness decreases or increases, depending on the study performed and with respect to non-OSA subjects [97]. These dimensional parameters do not seem to vary with the severity of the disease. The increase in volumes reflects the increase in adipose tissue within the muscles of the tongue, in particular, at the base [97]. The tongue suffers from apraxia and decreased stereognosis in patients with OSA, with an expressed strength that is less (measured by Iowa Oral Performance Instrument - IOPI) as compared to healthy subjects [98]. As mentioned, the GG is the most cited lingual district in research, as it plays an important role in the pharyngeal opening during inspiration, through lingual protrusion [99]. GG presents altered electromyographic responses, where it can be seen that in OSA, the muscle is less likely to mirror the presence of negative pressures (reflex for inspiration), both during sleep and during wakefulness [68,70]. There is a GG response latency, with a time of about 32 milliseconds, compared to healthy subjects with a latency time of about 24-26 milliseconds [70]. Despite the latency, the electrical spectrum of GG at rest and when awake is more active than in healthy subjects; the lack of ability of the muscle to dilate the upper airways correctly could depend on the incoordination between GG and the other contractile districts (electro-mechanical dissociation) [68]. The deformation of GG (movement) is less in patients than in subjects without OSA (less than about 1 millimeter on average); this reflects the presence of hypotonia (fibrosis, hypotrophy, phenotypic alteration, and myopathy), and the direct relationship between GG dysfunction and higher critical pressure (Pcrit) values [100,101]. In an animal model fed with many lipids, GG resulted in a numerical reduction of contractile fibers, a phenotypic imbalance (more white fibers), a reduction in mitochondrial function, and the presence of oxidation and apoptosis [102]. With OSA and advancing age, GG shows a lower myocellular repair capacity and more pronounced frailty in the face of hypoxia [103]. In obese patients and with OSA, GG is less prone to glucose uptake, with an altered metabolic environment (fewer resources for regeneration) and values of greater fatigue than in healthy subjects [104,105]. We have no specific data on other lingual intrinsic and extrinsic muscles in the presence of OSA. There is probably an electrical reduction in patients compared to non-OSA subjects [106]. Another muscle that attracts attention to obtaining a complete view of the muscles that allow correct breathing is the geniohyoid. The latter is not part of the lingual muscles; we find it below the GG, between the mandible and the hyoid bone [107]. The muscle is innervated by the hypoglossal nerve, probably via the anterolateral cervical atlanto-occipital plexus [108]. In patients with OSA, it may have an altered (dysfunctional) stiffness and a slowing down of electrical activity [99,106]. During the eupneic act (inhale), this muscle is active, albeit slightly, moving the hyoid bone forward, and is supposed to be useful for dilating the upper airways (Figure 4[109].

Functional anatomy and adaptation of the diaphragm muscle with OSA

The diaphragm muscle (DM) is the muscular boundary between the lower portion of the mediastinum and the upper portion of the abdomen. DM is the main muscle that allows eupneic acts while the other contractile districts are not directly able to guide the air inside the lung area but can facilitate or slow down its transit [39,110]. DM is asymmetrical, with a thickness and a vertical fiber position greater posteriorly, and thinner, with more horizontal contractile fibers anteriorly, with an average thickness of about 2-4 millimeters; this topographical disparity of the contractile fibers will affect the expression of movement [31]. DM remembers a mantle as morphology, with one side on the right raised by about 2 centimeters compared to the side on the left [31]. DM is crossed by multiple structures of the nervous, vascular, and muscular types: the sympathetic nervous system and vagus nerve; aorta and vena cava, superior epigastric vessels, thoracic duct, azygos and hemiazygos veins, lumbar venous plexus; and esophagus [31]. The portions of the DM involve the sternal area (xiphoid process), the vertebral area (from the thoracic vertebra 11 to the lumbar vertebra 4) through the pillars, and the costal area (the last 6 ribs) [31]. The main innervation comes from the phrenic nerve while the crural portion, where the esophageal hiatus resides, is innervated by the vagus nerve [31]. Before the DM, the dilator muscles of the upper respiratory tract are activated, thanks to the control of the CPG, allowing the entry of airflow. DM is rich in aerobic fibers, about 55% of which will be involved during a calm breath; the inspiration will determine the descent of the DM from a minimum of 2 centimeters to a maximum of approximately 10 centimeters [31]. The motion vectors during the inspiration will be caudal and oblique-anterior; specifically, the posterolateral area will move with greater emphasis (40% more than the anterolateral area), with an inclination of approximately 23.80° [31]. The anterolateral portion will have a movement with caudal and dorsoventrally direction; the right hemidiaphragm will have a smaller and slower range of motion than the left hemidiaphragm due to the presence of the liver (Figure 5) [31].

The vagus nerve manages the contraction of the esophageal hiatus so that during the actions of the rest of the DM's body, there is no antagonism for the passage of air and food [31]. One of the factors that determine the caliber of the airways is lung capacity and how they are filled (inflation) with the negative pressures created by the DM; if the DM is in dysfunction, the vital capacity decreases with an increase in the tendency of the dilator muscles not to intervene correctly, with a finding of the collapse of the upper airways. If intrapleural pressures are not present effectively (with a decrease in pulmonary inflation), the C-type lung afferent fibers send inhibitory information to the hypoglossal nerve; this mechanism will slow down the intervention of the lingual musculature, compared to the activation of the diaphragm, with the possible collapse of the airways [111,112]. If the relationship between DM and pulmonary inflation is not effective, there will be an increase in the finding of OSA [113]. Pressure intrathoracic is not directly related to AHI values, and airflow limitation is seen in many patients during daylight hours, to a greater extent than polysomnography evaluation alone [114]. Remember the importance of DM in patients with OSA could make a difference in the clinical setting. What do we know about the adaptation of the DM with OSA? DM appears to have a greater thickness in patients, through ultrasound measurements, but we do not know if this increase in size is related to hypertrophy (overcoming constant air resistance) or fibrosis (constant inflammation) [115,116]. An increase in thickness could be the result of greater constant contraction of the muscle due to constant obstructions of the upper airways. The literature is not always unique in indicating a decline in strength expressed by the DM; we do not know if there is actually fatigue of the central type (less neuromotor activation), or of the peripheral type (muscle metabolic alteration), or both. We know that there is a decline in the strength and endurance of DM in patients with OSA; probably, this condition could be linked to an inability to exhaustively recruit the motor units responsible for breathing [117-120]. We know that OSA is a systemic and not just a local disease, as demonstrated in the non-physiological adaptations of some peripheral muscles (anterior tibialis and quadriceps), where these muscles exhibit phenotypic, morphological, electrical, and metabolic alterations [117,121]. Stimulating DM with respiratory physiotherapy aimed at improving inspiratory musculature, decreases some parameters related to the diagnosis of OSA (AHI, Epworth sleepiness scale), making lung improvements recorded instrumentally (spirometry - forced vital capacity) [122,123]. DM is not only closely coordinated with the dilating muscles, during sleep and during wakefulness, but by stimulating the intervention (respiratory rehabilitation), it improves the symptomatological picture of the patient with OSA [58,123,124]. Another aspect that is hardly taken into consideration in the clinical setting related to DM and OSA is the vagus nerve, which innervates the diaphragmatic muscle area where the esophagus passes; the literature shows a reduction of the parasympathetic system in OSA [125]. This reduction is one of the causes that trigger cardiovascular disease and systemic inflammation [126]. We know that patients with OSA can suffer from nocturnal reflux and dysphagia, alterations attributable to a loss of synergy between the nerve phrenic and vagus nerve [127-129]. Stimulating the DM with breathing exercises improves the symptomatological picture related to gastric reflux and swallowing difficulties [130,131]. We do not know if exercises that stimulate DM are able to improve some symptomatic aspects, such as reflux and dysphagia, and the systemic response to inflammation. Evaluating how the DM behaves could be useful to indirectly understand the behavior of the CPG, and to highlight the neural dyssynergy of the respiratory muscles of the upper airways [132]. From the activity of the extra-diaphragmatic muscles (such as the alae nasi and GG), we cannot draw useful parameters to understand how the DM behaves; on the contrary, by examining the DM, we have useful clues to understand how the extra-diaphragmatic musculature is activated [132,133]. Considering that the DM is the main engine that allows the creation of negative pressures in the thoracic cavity and the entry of air into the lungs, allowing to obtain the mechanical and biochemical reflexes for the optimal management of the upper airway muscles, DM should have increased space of interest in the clinic with OSA patients. Many aspects of the pathology of OSA are not taken into consideration with respect to DM, both as an adaptation and as a rehabilitation. Further clinical and research efforts should be made to improve patient care management.

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Most body parts or organs in your body react to injury or infection by swelling. This indicates something is wrong in that particular area. This is no different when it comes to your legs. Port Saint Lucie leg swelling is a typical problem affecting many people. However, this issue can be ignored as it is common and happens all the time due to the constant movement of your legs and feet. This issue ignored can lead to further problems that may result in the loss of part of your leg. More about leg swelling and all it involves is highlighted in detail below.

What is Leg Swelling?

This happens on any leg part, including the ankles, feet, thighs, and calves. It can come from inflammation or fluid buildup in diseased or injured joints or tissues. Most causes of leg swelling like sitting or standing for long periods or even injury are not typically concerning. The leg swelling in certain instances however, may indicate a more severe issue like a blood clot or heart disease.

If your legs swell up and are painful or are accompanied by chest pain or breathing difficulties, seek immediate medical attention as it may indicate a heart condition or a blood clot in the lungs.

Many issues can make legs swell, all ranging in severity, including:

Fluid Buildup

Fluid can be retained in tissues of the leg, causing a swelling condition called peripheral edema. This can be due to an issue with the venous circulation system, the kidneys, or the lymphatic system.

Swelling of the leg is not always an indication of a circulation or heart issue. Fluid buildup may cause swelling due to being inactive, overweight, wearing tight jeans or stockings, or standing or sitting for extended periods. Factors associated with fluid buildup include:

·         Cardiomyopathy

·         Acute kidney failure

·         Chronic kidney disease

·         Chemotherapy

·         Deep vein thrombosis

·         Liver cirrhosis

·         Hormone therapy

·         Heart failure

·         Nephrotic syndrome

·         Blockage in the lymph system

·         Pain relievers like naproxen or ibuprofen

·         Obesity

·         Pregnancy

·         Inflammation of the tissue around the heart

·         Pulmonary hypertension

·         Prescription drugs such as those for high blood pressure or diabetes

·         Standing for a long time

·         Sitting for a long time 

·         Venous insufficiency or leg veins having problems getting blood to the heart

·         Blood clot in your leg


Inflammation in leg tissues or joints can be due to inflammatory conditions like rheumatoid arthritis or a normal response to an ailment or injury. Inflammatory disorders are usually accompanied by pain in the affected areas. Some conditions that can lead to inflammation in your leg include:

·         Tearing of the anterior cruciate ligament of your knee

·         Achilles tendon rupture

·         Broken ankle

·         Baker’s cyst

·         Broken leg

·         Broken foot

·         Skin infections like cellulitis

·         Burns

·         Osteoarthritis

·         Knee bursitis

·         Sprained ankle

·         Inflammatory joint diseases like rheumatoid arthritis

A severe heart condition or a blood clot in your lungs can be indicated by swelling of your legs and comes with breathing difficulties, chest pain, or dizziness. Swelling of the leg that is not going away after some time should also be checked out. For more inquiries on leg swelling, check our website, or call our offices in Port Saint Lucie, FL.

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We report a female infant who was born at 41+6 weeks of gestation to a consanguineous parent, and the initial newborn examination was within normal. At 12 hours of age, she developed tachypnea; with desaturation, she had continuous thick whitish oral secretion. Admitted to the neonatal intensive care unit (NICU) for further management, her initial blood investigation, including blood gas and chest X-ray, was normal. Due to the persistent unexplained respiratory distress with a normal chest X-ray, we obtained a further history from parents with three siblings with respiratory symptoms but no definitive diagnosis. The genetic testing of whole-exome sequences (WES) confirmed a homozygous variant c.804_806del, p.(Lys268del) in the RSPH9 gene that causes primary ciliary dyskinesia (PCD). Her three siblings were tested and found to have the same genetic mutation.


Primary ciliary dyskinesia (PCD) is a rare autosomal recessive genetic disorder that causes defects in the function and/or structure of the cilia lining the respiratory tract, fallopian tube, and flagellum of sperm cells [1]. PCD is often underdiagnosed, and it is estimated to occur in 1/15,000-20,000 individuals [2-3]. Moreover, due to the high consanguinity rates, PCD is more common in Arab societies, although little is known about its actual prevalence and characteristics [4]. Patients with PCD may present with neonatal respiratory distress and/or laterality defects in about half of the cases. Studies have shown that more than 80% of neonate patients present with respiratory distress symptoms within the first 1-2 days of life, with most cases appearing 12 hours after birth [3]. In this article, we report an unusual case of respiratory distress in a full-term female infant. The diagnosis of primary ciliary dyskinesia was confirmed by genetic testing, which led to the same diagnosis in three siblings at different ages. 

Case Presentation

A female infant was born at 41+6 weeks of gestation via an emergency Cesarean section due to abnormal fetal heart rhythm. The infant's mother was diabetic. The parent is a first-degree cousin. She had three siblings diagnosed with bronchial asthma and chronic otitis media. Antenatal ultrasounds were unremarkable, and the maternal laboratory findings are as follows: hepatitis B was negative; group B Streptococcus was positive. Her appearance, pulse, grimace, activity, and respiration (APGAR) scores were nine and nine at one and five minutes, respectively, and her weight was 4 kg. Her vital signs were stable (temperature of 36.9ºC; heart rate of 150 beats/min; respiratory rate of 55 breaths/min; blood pressure of 66/40 mmHg; oxygen saturation of 96%), and the initial newborn examination presented normal results. At 12 hours of age, the baby started to be tachypneic; with desaturation in room air, she had continuous thick whitish oral secretions. A full sepsis workup was done. Complete blood cell count revealed a white blood cell count of 6,000/mL with a normal differential, hemoglobin of 15.8 g/dL, and platelet count of 250×103/μL. Her initial blood gas and chest X-ray were normal (Figure 1). 

An echocardiogram showed normal structure and function of the heart with no evidence of pulmonary hypertension. Initially, she was on a high-flow nasal cannula (HFNC) of eight liters per minute with a fraction of inspired oxygen (FiO2) of 35%. She was treated for clinical sepsis with five days of antibiotics. Her respiratory distress improved with respiratory support. She needed oxygen for a total period of 14 days, and then she was observed for two days without supplemental oxygen before being discharged. The genetic testing was requested based on unexplained respiratory distress with normal chest X-ray and normal echocardiography. The whole-exome sequences (WES) confirmed a homozygous variant c.804 to 806del, p.(Lys268del) in the RSPH9 gene (OMIM: 612648) that causes PCD. Her three siblings were tested for the same gene and confirmed the same genetic mutation.

Four months later, the patient was admitted to another hospital with fever and respiratory symptoms for two days. After a month, she presented to the emergency department with fever and increased work of breathing; pneumonia was confirmed and treated with HFNC 14 L/min with FiO2 of 25%. Intravenous antibiotics were continued for ten days, bronchodilators and a 3% normal saline nebulizer with chest physiotherapy were provided. Chest X-ray showed that the right upper lobe had collapsed (Figure 2). The respiratory culture isolated Streptococcus pneumonia, and the respiratory multiplex was positive for rhino/enterovirus. After completing the antibiotic course, the baby was discharged home. Since then, the baby has done well; she only had to continue chest physiotherapy and hypertonic nebulizer 3%. All her siblings have started to follow up with the pulmonologist after confirming their diagnosis.


Although infants with PCD are often diagnosed with transient tachypnea of the newborn (TTN), the clinical presentation in PCD is different with later onset of respiratory distress, longer duration of oxygen therapy use, and higher frequency of atelectasis and/or lobar collapse upon chest imaging [1].

There is no single gold standard diagnostic test for PCD; the current diagnosis requires a combination of investigations that may not be feasible in all hospitals. Those tests include nasal nitric oxide, high-speed video microscopy analysis, transmission electron microscopy, high-resolution immunofluorescence analysis, and genetic testing [5].

The current therapies for PCD are extrapolated from cystic fibrosis (CF) and patients with non-CF bronchiectasis and lack validation for PCD-specific use [1-6]. The main goal of the treatment is to manage the condition symptomatically, clear the trapped mucus from the airways, and treat the respiratory infection using antibiotics. PCD patients need regular follow-up visits with pediatric pulmonology, otolaryngology, and respiratory therapists. The progression of lung disease varies and is affected by the time of diagnosis, the ability of medical treatment to control symptoms, and the prevention of complications that affect the quality of life [7].

In this case, we reported a full-term neonate with unexplained respiratory distress who needed oxygen therapy for 14 days. Later, her genetic testing was positive for a mutation in the RSPH9 gene, causing PCD. Our patient did not have a laterality defect on chest X-ray and abdominal ultrasound, which made the diagnosis challenging. However, careful history taking of the older siblings, who also had unexplained neonatal respiratory distress and her needing oxygen for a period after birth as well as having chronic wet cough, increased our suspicion about the diagnosis. 

Casey et al. reported similar cases of a family with three individuals who had respiratory distress symptoms as well as PCD, confirmed with genetic testing, associated with laterality defects, which is considered to be due to a homozygous missense variant in CCDC103 on chromosome 17 according to exome sequencing [8]. Another study presented a group of term neonates who had PCD and a history of neonatal respiratory distress [9]. The study showed that cases with PCD required more oxygen therapy for a longer duration and had a later onset of neonatal respiratory distress and a higher frequency of lobar collapse and situs inversus.

It was suggested that when encountering term neonates with unexplained respiratory distress, PCD should be considered in those with lobar collapse, situs inversus, and/or prolonged oxygen therapy (>2 days); moreover, treatment should be initiated immediately to reduce the risk of complications [9]


Primary ciliary dyskinesia (PCD) is a rare autosomal recessive disorder that can present with respiratory distress at birth or in the first few days after birth. Unexplained respiratory distress with the presence of a family history of undiagnosed respiratory symptoms should prompt further investigation for a genetic disease. Whole-exome sequences are the modality of choice for the diagnosis of PCD. The main goal of the treatment is to manage the condition symptomatically, control infections, and clear the trapped mucus from the airways, which can slow the progression of the disease. Careful history taking is vital; in this case, the diagnosis of PCD in three siblings at different ages shows us how PCD is still underdiagnosed and can be easily missed for many years.

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Jul. 30—GENEVA — University Hospitals Geneva Medical Center recently opened a new pulmonary rehabilitation center, and is now seeing patients.

People who suffer with lung diseases can live and breathe easier by working with a team of specialists in a variety of supervised medical programs.

"Chronic lung disease is an ongoing problem and can take a toll on a person's quality of life by making everyday activities they're used to participating in much more difficult," said Kimberly Smith, RRT, Respiratory Therapy Supervisor at UH Conneaut, Geneva and Geauga Medical Centers. "We are happy to be able to expand our available respiratory services to our local community in the Geneva area."

The medically supervised programs help those with chronic pulmonary diseases, such as asthma, emphysema, chronic bronchitis and COPD.

Programs are also available for those with restrictive lung disease such as pulmonary fibrosis and sarcoidosis, and lung conditions such as lung cancer, primary pulmonary hypertension and obesity-related respiratory disease.

The center also sees patients who have neuromuscular disorders, and those who are working through long-haul COVID-19 symptoms.

At the UH Geneva Pulmonary Rehabilitation Center, patients can:

—Learn more about their condition, symptoms, medications and oxygen.

—Participate in supervised exercise classes and instruction.

—Learn breathing techniques.

—Take part in nutritional counseling.

—Join the Pulmonary Support Group, in conjunction with the American Lung Association Better Breathers Club.

—Take smoking cessation classes or one-on-one smoking cessation sessions.

"Patients receive a number of positive benefits from participating in the pulmonary rehabilitation program at UH Geneva," said Smith. "Managing and relieving shortness of breath and fatigue; reducing anxiety; increasing exercise capacity and daily stamina; and enhancing quality of life, just to name a few. Our patients also have access to a number of specialists in one location, including registered respiratory therapists, nurses, exercise physiologists, registered dietitians, pharmacists, pulmonologists and other experts as they may need them."

To learn more about respiratory therapy services offered at UH, please visit: UHhospitals.org. To make an appointment at the UH Geneva Pulmonary Rehabilitation Center, call 440-415-0297.

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Diastolic dysfunction is a condition that leads to diastolic heart failure, also known as heart failure with preserved ejection fraction (HFpEF). People may not experience symptoms in the early stages of diastolic dysfunction, but diagnosis and treatment are key to improved outcomes.

On the other hand, some people with diastolic heart failure symptoms such as difficulty breathing may have "normal" findings on diagnostic tests, such as an echocardiogram (echo). A range of tests for diagnostic dysfunction, alongside symptoms and overall health history, are needed.

This article explains the tests used to arrive at a diagnosis and begin appropriate diastolic dysfunction treatment. It also explains complications that may arise, including diastolic heart failure.

Symptoms and Complications of Heart Failure

Who Is at Risk for Diastolic Dysfunction

Certain factors contribute to the risk of developing diastolic dysfunction. Some studies indicate that these risk factors are different for biological males and females. They include:

Diastolic Heart Failure Stages

There are four stages of heart failure (lowest stage A through highest stage D) in the 2022 guidelines of the American College of Cardiology, the American Heart Association, and the Heart Failure Society of America. Certain people with HFpEF are considered class C. In the United States, 121.5 million people with high blood pressure and 28 million people with diabetes can be considered stage A.


There's no home test for diastolic dysfunction. Diastolic dysfunction tends to develop gradually, and some people may begin to experience classic symptoms of heart failure as it progresses.

Symptoms of diastolic dysfunction include:

  • Dyspnea (shortness of breath)
  • Labored breathing during exercise that gets progressively worse
  • Difficulty breathing while lying down
  • Difficulty breathing while sleeping
  • A chronic cough
  • Excessive fatigue
  • Unusual weight gain
  • Edema (swelling) of the legs and ankles
  • Fast or irregular heartbeat (arrhythmia)

You can experience any combination of these symptoms with diastolic dysfunction, and some may affect you more than others.

Systolic vs. Diastolic Heart Failure

Diastolic heart failure, also called heart failure with preserved ejection fraction (HFpEF), occurs when the heart's chambers no longer fill with blood correctly. This is due to diastolic dysfunction that causes stiffening, rather than the weakened heart muscle that is the typical cause of systolic heart failure.

B-Type Natriuretic Peptide (BNP) Blood Test

B-type natriuretic peptide (BNP), which is measured with a blood test, can be elevated in association with diastolic dysfunction.

BNP is a molecule released into the blood by heart cells in response to elevated pressure within the heart. It causes the kidneys to excrete sodium and water, which serves to lower the pressure in the blood vessels and the heart.

There is a large gray zone between what is considered a normal level of BNP and what is not, and so this test cannot be a reliable indicator of heart failure on its own. Sometimes, a BNP blood test is used in conjunction with other tests to support a diagnosis of diastolic dysfunction.

Laura Porter / Verywell

Imaging Tests

Imaging tests are useful in diagnosing diastolic dysfunction and for assessing the severity of the condition.

Echocardiogram (Echo)

This specialized non-invasive ultrasound provides views of the heart as it is moving. The echocardiogram can give an indication of how well the heart muscle and valves are functioning. It also can be used to assess diastolic relaxation and the degree of left ventricular stiffness.

An echocardiogram can also sometimes reveal conditions that may be the cause of diastolic dysfunction:

Left Ventricular Ejection Fraction (LVEF)

An echocardiogram also can measure left ventricular ejection fraction (LVEF). This is the percentage of blood the left ventricle of the heart is able to pump out with each beat.

A normal LVEF is greater than 50%, which means the left ventricle is able to pump out more than half of the blood that's inside it.

Usually, heart failure is associated with a low LVEF, which is a reflection of systolic function (the heart's ability to eject blood with a strong pumping action). But some people with diastolic heart failure have a normal systolic function and a normal left ventricular ejection fraction.

Electrocardiogram (ECG, EKG)

An electrocardiogram (ECG) is a noninvasive test that evaluates the electrical system of the heart. During this test, electrodes (flat metal discs) are placed in certain positions on a person's chest, arms, and legs.

The electrodes are attached to a machine that reads the electrical charges generated by each heartbeat. The test takes about five minutes and the information is graphed as wave patterns.

Cardiac magnetic resonance imaging (MRI, CMR)

Cardiac MRI uses a powerful magnetic field, radio waves, and a computer to produce detailed pictures of the structures within and around the heart. It requires that you remain completely still while lying inside an MRI scanner—a tube large enough to surround the entire body.

A cardiac MRI can tell a doctor a lot about how much strain the heart is undergoing and can assess deformation, left atrial size, and trans-mitral blood flow.

This test yields high contrast and high-resolution images by mapping radio wave signals absorbed and emitted by hydrogen nuclei (protons) in a powerful magnetic field. Because it's costly, it is not widely used.

Nuclear imaging

Imaging tests such as the positron emission test (PET) and the single-photon emission computerized tomography (SPECT) sometimes are used to identify diastolic dysfunction before symptoms begin.

These tests involve the injection of radioactive dyes known as radiotracers. The heart's absorption of the tracers depends on how it's functioning. The resulting color changes indicate whether certain muscles of the heart are not able to pump as they normally would.

Cardiac Stress Test

A cardiac stress test (also known as a cardiac exercise test) measures the heart's response to physical exertion in a controlled setting. It involves walking on a treadmill or pedaling a stationary bike for approximately 20 minutes during which your blood oxygen level, heart rhythm, pulse, and blood pressure are simultaneously monitored.

There are several types of stress tests, any of which might be used to help diagnose diastolic dysfunction and heart failure:

  • Electrocardiogram stress test: Electrode patches attached to the chest measure electrical signals triggered by the heart during exercise.
  • Echocardiogram stress tests (or echo or cardio ultrasound): Sound waves create a moving picture of how the chambers and valves of the heart function while under stress. It can reveal areas of diminished blood flow, dead muscle tissue, and areas of the heart muscle wall that aren’t contracting well or may not be getting enough blood.
  • Nuclear stress tests: Radioactive dye is injected into the bloodstream to highlight blood flow. Images created by the test show how much dye has reached various parts of the heart during exercise and at rest.
  • Multiple gated acquisition (MUGA) scan: Uses radionuclide ventriculography (RVG) or radionuclide angiography (RNA) to produce a computerized image of the beating heart and the pumping function of the left and right ventricles. It is particularly useful for reading the overall pumping ability of the heart.
  • Chemical stress tests: A medication such as regadenoson, dobutamine, or adenosine, is injected into the bloodstream to stress the heart.

Other Tests

A few other tests may be used to diagnose diastolic dysfunction, focusing on the performance of the heart and lungs.

Cardiac Catheterization

Cardiac catheterization is an invasive procedure in which a long, thin, flexible tube is inserted into the arm or groin and guided to blood vessels in the heart. Dye is injected into blood vessels so they can be observed with an X-ray or ultrasound.

Cardiac catheterization can reveal if there are problems with how the heart relaxes and if the ventricles are not relaxing and filling normally.

Testing for inflammatory biomarkers called cytokines, when done in conjunction with cardiac catheterization, also may help to diagnose certain types of diastolic dysfunction and predict a progression to diastolic heart failure.

For example, one study has found that high levels of interleukin-17 and interleukin-6 biomarkers correlated with poorer survival rates and life expectancy with diastolic heart failure.


A spirometry test measures lung function, which is frequently impaired in association with heart failure. It involves breathing into a tube attached to a spirometer device that can measure how forcefully a person is able to push air out of their lungs.

Chest X-ray

A chest X-ray can show if the heart is enlarged or if there are signs of congestion in the lungs.

Diastolic Dysfunction Complications

Complications of diastolic dysfunction include its progression into diastolic heart failure. Other complications of diastolic dysfunction include:

  • Pulmonary hypertension, a serious and chronic lung condition
  • Sudden cardiac death due to lethal arrhythmias
  • Worsening renal (kidney) failure in those with chronic kidney disease

What Can Be Done for Diastolic Heart Failure?

Diastolic dysfunction and diastolic heart failure do not go away, and there currently is no cure. However, lifestyle changes and the treatment of diastolic dysfunction can slow its progress. This may include changes in diet, smoking habits, and medication to treat diabetes and other underlying causes.

A Word From Verywell

Although diastolic dysfunction is common, many people with this disease may never experience symptoms. Those who do may dismiss their symptoms as just normal aging. It's important to know what the symptoms are and take them seriously if you begin to experience them. Getting an early diagnosis may prevent you from suffering the serious consequences of heart failure.

Frequently Asked Questions

  • What is the number one cause of diastolic dysfunction?

    High blood pressure is a leading cause of diastolic dysfunction. Other factors that contribute to your risk include diabetes, obesity, and sleep apnea. People who experience high blood pressure during pregnancy, including preeclampsia, also are at risk for diastolic dysfunction.

  • What is the difference between congestive heart failure and diastolic heart failure?

    Diastolic heart failure, also called heart failure with preserved ejection fraction (HFpEF), is a progressive condition that affects the heart's filling capacity. It accounts for half of all heart failure cases. Congestive heart failure (CHF) involves the heart's ability to pump blood, and is diagnosed and treated differently.

  • Is diastolic dysfunction heart failure serious?

    Yes, it's a chronic condition that requires lifelong treatment and lifestyle changes. There's a higher risk of related death, but many people manage their disease and live well with it. The prognosis is less favorable for older people, those with a previous heart attack, and people living with conditions including COPD and diabetes.

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Coughing up blood — a symptom known as hemoptysis — can be a sign of several different conditions. Many of these conditions can be serious, and some even life threatening.

One of the conditions in which hemoptysis may appear is a pulmonary embolism, a blood clot in your lung. When these two occur together, it can be a challenge for doctors. The standard treatments for each condition can actually cause the other condition to worsen.

This article will highlight how hemoptysis happens in pulmonary embolism and how doctors treat the two conditions.

A pulmonary embolism (PE) is essentially a blood clot that becomes lodged somewhere in the lungs. These clots usually come from somewhere else (often your leg) and travel to the lungs.

Once lodged in place, these clots can cut off blood flow in your lungs, causing blood to back up behind the clot. The backup results in increased pressure in the vessels on one side of the clot, and a lack of blood flow and oxygen on the other side.

PE can lead to further blood clots, obstructions, and smaller infarcts — or areas where tissue has died from a lack of oxygen. The increased pressure or lack of oxygen can damage your lung tissue, causing bleeding. This can appear as blood in your sputum.

A PE that can cause such high blood pressure in the lungs would need to be very large and high risk (massive). You would likely experience other serious symptoms and could even become unconscious.

There are different degrees of hemoptysis. Mild hemoptysis is when you cough up less than 100 milliliters of blood in 24 hours. Mild hemoptysis goes away on its own in 9 out of 10 cases.

Massive hemoptysis is when you cough up greater than 100 milliliters of blood in 24 hours. This is when the condition is potentially life threatening. In 90% of cases, massive hemoptysis is due to injury or damage to the bronchial artery.

A 2015 case study suggests that people with chronic PE should seek treatment for even mild hemoptysis.

Since there can be several possible causes of your hemoptysis, your doctor will first need to determine the location of the bleeding. Pinpointing a location can help identify a cause.

Your doctor will usually use imaging like a chest X-ray or computed tomography (CT) scan. With these scans, they should be able to determine the location and severity of the problem.

In addition to diagnostic imaging, your doctor may run other tests to determine the effect of hemoptysis on your overall health. Possible tests include:

Once your doctor has determined the cause and extent of your hemoptysis, they will begin to develop a treatment plan. In the case of PE, treatment options can be more complicated. How doctors treat PE depends on:

  • where the clot is
  • how large the clot is
  • how much damage the clot has already caused

Regardless of the extent or location of the blood clot, immediate medical treatment for PE is critical. The goal of treatment is to either dissolve the clots and keep new ones from forming, or to physically remove or break up the clot and restore blood flow.

The standard treatment for PE is anticoagulation. But when hemoptysis is present, doctors face a dilemma. Anticoagulation can increase your risk of bleeding.

Vena cava filter

In this case, your doctor may opt for a vena cava filter. Your doctor will place this filter in your inferior vena cava, a large blood vessel. Doctors only use a vena cava filter for patients who can’t take anticoagulants.

A vena cava filter won’t treat the clot in your lungs, but it can prevent new clots from traveling to your lungs.

Tranexamic acid

But doctors still need to stop the bleeding. They’ll often use tranexamic acid (TXA) to relieve hemoptysis. In case studies from 2017 and 2021 of patients with both hemoptysis and PE, doctors administered TXA by IV.

Previous studies have raised concerns about TXA leading to blood clots and PE. But a large 2019 Japanese study and a 2021 review found it safe.

Bronchial artery embolization

Doctors may also use bronchial angiography to both locate the source of the bleeding and treat it. This minimally invasive procedure allows them to first view the source, and then treat it using a process called trans-catheter bronchial artery embolization (BAE).

In trans-catheter BAE, doctors thread a small tube through your thigh up to your bronchial artery. Doctors then inject tiny particles through the catheter that clot the vessel to stop the bleeding.

BAE is usually very effective, with studies finding its initial success rate to be between 70% and 99%. But there is a chance that hemoptysis may reoccur. Studies found the recurrence rate to be between 10% and 57%.

Several case studies report successful use of BAE to manage hemoptysis with PE. But some older studies saw mixed results.

A 2019 study found that BAE was a safe and effective way to treat hemoptysis in people with chronic thromboembolic pulmonary hypertension (CTEPH), a complication of PE. But the study was small, and researchers stressed the need for more studies.

Coughing up blood isn’t necessarily a sign of PE, but it can happen. More common signs of PE that could suggest a problem include:

Your recovery from PE will depend almost entirely on the size and location of the clot and how quickly you get medical attention.

Without treatment, about 30% of people who develop PE die, according to 2013 research. About 10% of people who develop severe and sudden PE die almost immediately. However, with proper diagnosis and treatment, the mortality rate for PE drops to about 8%.

According to a 2021 review, the mortality rate for hemoptysis is between 9% and 38%. But the same review found that treatment with tranexamic acid reduced mortality rate, bleeding time, and duration of hospital stay.

A 2017 study looking into symptoms of PE found that hemoptysis was usually linked to massive (high-risk) PE. This means that the presence of hemoptysis indicates that your PE is more severe. According to a landmark study, massive PE has a mortality rate of up to 65%.

Early diagnosis and treatment are key to achieving the best possible outlook.

Coughing or spitting up blood can be a sign of several conditions. It doesn’t always appear with pulmonary embolism. But if PE is the cause of this symptom, you need to get medical attention right away.

Immediate and accurate diagnosis and treatment of PE can significantly improve your chances of survival.

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    Systemic hypertension is high blood pressure in the arteries that carry blood from your heart to your body’s tissues. The term is sometimes used interchangeably with high blood pressure.

    Systemic hypertension is measured with a pressure cuff around your upper arm. The cuff is connected to a blood pressure monitor. The numbers on the monitor can reveal whether your blood pressure is high.

    High blood pressure usually has no symptoms, unless the levels are high enough to cause a hypertensive emergency. It can develop due to a range of medical conditions and lifestyle behaviors.

    The potential health complications of hypertension can be severe. But you can often prevent or manage high blood pressure by addressing potential underlying causes and maintaining a healthy lifestyle.

    This article will take a closer look at the causes and treatment of systemic hypertension, as well as the steps you can take to help prevent it.

    Systemic hypertension happens when the blood pressure in the arteries that send blood from your heart to the rest of your body — except your lungs — is higher than it should be. High blood pressure in the arteries that carry blood from the right side of your heart to your lungs is called pulmonary hypertension.

    Blood pressure is often expressed as a fraction with two numbers. The top number is the systolic pressure and the bottom number is the diastolic pressure.

    Systolic pressure is the force of blood against the inner wall of the arteries and is measured while your heart is contracting. Diastolic pressure. This is the force of blood against the artery walls when your heart is resting between beats.

    The readings are measured in millimeters of mercury (mm Hg). Typical blood pressure is defined by the American Heart Association as a systolic pressure of less than 120 mm Hg and a diastolic pressure of less than 80 mm Hg.

    You may hear a healthcare professional refer to this as “120 over 80,” and they may use similar phrasing to tell you what your own blood pressure reading is.

    For most adults, blood pressure readings are categorized as follows:

    Systemic hypertension usually has no symptoms. It’s why the condition is sometimes called the silent killer. The only way to know that you have hypertension is by having your blood pressure checked.

    If hypertension reaches the level of a hypertensive emergency — systolic pressure of 180 mm Hg or higher or a diastolic pressure of 120 mm Hg or higher — the following symptoms may be present:

    Some people experience high blood pressure only at a doctor’s appointment but not at other times. This is known as white coat syndrome or white coat hypertension. For these individuals, regular home monitoring of blood pressure is recommended.

    Home monitoring is also a good idea for anyone at risk of systemic hypertension, including people with the following risk factors:

    Systemic hypertension has many potential causes, including underlying health conditions and environmental or lifestyle factors. Health conditions that may increase the risk of systemic hypertension include:

    When an underlying medical condition causes an increase in blood pressure, it’s known as secondary hypertension. Pregnancy can also trigger the onset of high blood pressure, but this usually resolves once the baby is born.

    Some of the more common lifestyle and environmental factors that may increase the risk of systemic hypertension include:

    • a high sodium diet
    • alcohol and drug use
    • lack of physical activity
    • smoking
    • insufficient sleep

    The Centers for Disease Control and Prevention (CDC) reports that Black individuals, particularly males, face a higher risk of hypertension than many other groups of people. This may be due to factors like racism, methods for coping with racism, misinformation about hypertension, limited access to care, socioeconomic status, location, and underlying health concerns.

    A diagnosis of hypertension may result in a treatment plan that involves lifestyle changes and medications. If you receive a diagnosis of hypertension, your healthcare professional may suggest lifestyle changes that focus on:

    • a heart-healthy diet, such as the Mediterranean diet, the DASH diet, or a whole-food plant-based diet
    • limiting or cutting out foods that are high in salt (sodium)
    • getting at least 30 minutes of exercise 5 or more days per week
    • losing weight if you’re considered overweight
    • quitting smoking if you smoke
    • limiting alcohol consumption if you drink alcohol
    • getting at least 7 hours of sleep each night

    If lifestyle changes don’t reduce your blood pressure enough, your doctor may recommend medication.

    A 2019 study suggests that antihypertensive medications are both safe and effective for lowering blood pressure in most people. The primary first-line medications for systemic hypertension include:

    According to a 2018 report, treatment decisions for high blood pressure should be based on an individual’s cardiovascular risk profile and personal preferences.

    For example, aggressive treatment with medications may cause some unwanted side effects. If this is the case, you may prefer medications with fewer side effects, or you may opt to focus more on exercising or other lifestyle changes.

    Because hypertension affects the health and function of your arteries, all the organs and tissues in your body are at risk of complications from poorly controlled high blood pressure.

    Hypertension can cause your arteries to become stiffer, weaker, and less effective at handling blood flow properly. Some of the many health complications that can stem from hypertension include:

    When should you see a doctor?

    Keeping up with your annual checkups is one way to keep track of changes in your blood pressure. But you should also make a point to have your blood pressure checked if you have other conditions, such as high cholesterol or diabetes.

    You likely won’t notice symptoms of hypertension. Having other risk factors for high blood pressure should prompt a visit to the doctor and a professional check on your blood pressure.

    Can you prevent hypertension?

    Hypertension can’t always be prevented, but there are some established strategies to help keep your blood pressure at healthy levels. This include:

    Is systemic hypertension hereditary?

    Hypertension is a condition that can run in families, meaning that people who live a heart-healthy lifestyle are still at a higher risk for high blood pressure if their parents had hypertension.

    However, a 2017 study suggests that modifying certain lifestyle behaviors and other environmental factors (such as secondhand smoke exposure) may reduce the effects of inherited high blood pressure in some people.

    Can lifestyle changes cure hypertension?

    There is no actual cure for hypertension. Health experts instead use terms such as “manage” or “control” to describe ways of keeping blood pressure in a healthy range.

    For some people, healthy lifestyle changes can be enough to lower high blood pressure and keep it in a standard range. As with taking medications to control hypertension, you have to stick with those healthy lifestyle behaviors for them to have a positive effect on your blood pressure. Otherwise, you can expect your blood pressure to rise.

    Systemic hypertension is another way to describe high blood pressure, a condition that can develop as the result of an underlying health condition or due to lifestyle choices. You can also genetically inherit high blood pressure.

    Focusing on a heart-healthy lifestyle that includes regular exercise and a low sodium diet may help reduce your risk of developing systemic hypertension. Specific types of medications can also help control systemic hypertension and manage the risks of complications.

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    Pulmonary embolism (PE) is a common and potentially life threatening condition that doctors categorize as acute, subacute, or chronic. Deep vein thrombosis can increase a person’s risk of any type of PE.

    This article discusses the definition and types of PE, the tests doctors use to diagnose it, and available treatments. It also looks into life expectancy for those with PE and how a person can reduce their risk.

    The National Cancer Institute (NCI) describes PE as a blockage of an artery in the lungs. This can occur when a blood clot called a thrombus — usually in the leg or pelvis — breaks loose and travels into the lung. Doctors call these blood clots deep vein thrombosis (DVT).

    A PE can be life threatening, especially if there are many blood clots or the blockage is large.

    PE can lead to:

    Half of those who have PE do not experience any symptoms. However, symptoms can include:

    There are three types of PE: acute, subacute, and chronic. Below is a deeper look into each of these types.


    The National Center for Biotechnology Information (NCBI) states that acute PE is a common condition that can be difficult to diagnose. This is because symptoms can vary between individuals.

    The most common symptoms include:

    Risk factors for acute PE include gene mutations, protein S and protein C deficiency, and other factors such as prolonged periods of rest or inactivity, orthopedic surgery, obesity, pregnancy, and taking the contraceptive pill.

    The NCBI further splits acute PE into two categories. The first — hemodynamically unstable — is a high risk form of PE that results in a significant change in blood pressure. This increases the chance of obstructive shock, which stops blood and oxygen from getting to the organs. It also has a higher mortality rate.

    The second category is hemodynamically stable, an acute form of PE that can result in mild hypertension and present an intermediate risk. However, it is stable and may respond to fluid therapy.


    According to a 2020 article, subacute PE can develop gradually and is difficult to diagnose. This can mean there can be delays in treatment, resulting in poorer outcomes. People with subacute PE have a higher mortality rate than those with acute PE.

    Symptoms can develop over 2–12 weeks. The most common symptoms can include:

    • progressive dyspnea
    • pleuritic chest pain
    • coughing up blood

    The authors of the 2020 study write that people with subacute PE have a higher risk of hypertension due to thromboembolism in comparison with those with acute PE.


    A 2018 report states that in chronic PE, residual blood clots can remain attached to the walls of the pulmonary vessels after treatment.

    This can cause chronic thromboembolic pulmonary hypertension (CTEPH). According to a 2022 overview of acute PE, up to 5% of people with PE will develop CTEPH.

    The most common cause of PE is DVT.

    Conditions or events that can increase a person’s risk of DVT, and in turn, PE, include:

    • Factor V Leiden mutation: This is a genetic mutation that increases a person’s risk of blood clots. Although the most common complications of Factor V Leiden mutation include DVT and PE, many people with this mutation will not develop a blood clot.
    • Prothrombin gene mutation: An inherited genetic condition that increases a person’s risk of DVT.
    • Protein C deficiency: A deficiency in protein C can increase a person’s risk of DVT. This condition can be mild or severe. And while some people will never develop blood clots, protein C deficiency can be life threatening in some infants. It can cause blockages in blood flow and body tissue death.
    • Cancer: People with these conditions have the highest risk of developing a blood clot in their veins:
    • Large bone fractures: The United Kingdom National Health Service (NHS) states that if a person fractures a large bone, such as the thigh bone, fat particles from inside the bone can release into the bloodstream. A fat embolism can go away on its own, but it can cause potentially life threatening complications, such as organ dysfunction.
    • Prolonged inactivity: Bed rest for longer than 3 days and traveling by bus, car, train, or plane for over 4 hours can increase a person’s risk of PE. This is because sitting for long periods can slow the blood flow in the veins in the legs. Individuals can reduce their risk of DVT while traveling by walking around every 2–3 hours, exercising their calf muscles while sitting down, stretching their legs, and wearing compression stockings.
    • Pregnancy and childbirth: A person is at the highest risk of PE for 6 weeks after giving birth. During pregnancy, a person’s body changes so that it forms blood clots more easily, lessening the risk of blood loss during labor and delivery. Additionally, the fetus can restrict blood flow to the lower legs because it can press on the blood vessels around the pelvis.

    According to health experts, PE can be difficult to diagnose, as half of the people with the condition have no symptoms.

    Diagnosing any type of PE includes reviewing a person’s medical history and carrying out a physical exam at a doctor’s office.

    Running certain tests can effectively help a doctor or healthcare professional identify any blood clots and pinpoint the risk and severity of PE.

    Some of these tests include:

    • Arterial blood gas analysis (ABG): An ABG can help determine whether a person has PE. In uncommon cases, the analysis shows lower than expected levels of oxygen in the arteries, which could be a sign of shock and respiratory arrest.
    • D-dimer: A common test that physicians use in combination with clinical assessment, probability, and other tests to determine whether an individual has PE. The D-dimer test looks for a small protein fragment that the body produces to break down blood clots. If a person has elevated D-dimer levels, this may suggest that their body is working to break down a blood clot.
    • EKG: A standard EKG can help pinpoint tachycardia and irregular heartbeat patterns, such as straining in the right ventricular pathway of the heart and lung. These have links to PE, but not everyone with tachycardia or other irregularities will have PE, as many conditions can affect how the heart beats.
    • CT pulmonary angiography: This is the diagnostic test of choice for people with a high risk of PE. It allows specialists to see the pulmonary arteries and visualize any pressure in the bloodstream.
    • Ultrasound: An ultrasound scan of the lower extremities is the most accurate noninvasive test to diagnose DVT. It allows doctors to see a person’s veins and identify blood clots.

    In large hospitals or cases involving a higher risk of PE in an individual, doctors have to follow test protocols by carrying out some of the above tests to rule out or confirm the condition.

    However, smaller clinics may not have all the equipment to run various tests. As someone can stay asymptomatic for a long time and PE symptoms can vary, health departments have devised criteria for ruling out a PE.

    The following criteria suggest that a person does not have a PE:

    • they are younger than 50 years old
    • their heart rate is lower than 100 beats per minute
    • blood oxygen is higher than 94%
    • no hemoptysis
    • no estrogen use
    • no prior PE or DVT
    • no unilateral leg swelling
    • no surgery or trauma with hospitalization in the past 4 weeks

    Conversely, other criteria exist to determine the likelihood of PE. This can help doctors and specialists make recommendations for specific tests to confirm or rule out the condition. These depend on rules that doctors determine according to the individual’s medical history.

    Examples of risk factors include:

    • having active cancer
    • being older than 65 years
    • having had surgery or a fracture in the past month
    • having lower-limb pain
    • having a previous PE or DVT

    A person should seek medical advice if they have any symptoms of a PE, as early treatment improves the outcome.

    Treatment of PE can vary depending on the severity, hemodynamic stability, and type of PE a person has.

    According to this 2022 article, treatment for acute PE can take the form of:

    • supplemental oxygen
    • vasopressors
    • anticoagulant medication
    • vitamin K antagonists to help reduce the action of vitamin K that can cause blood clotting
    • thrombolysis, involving medication or a catheter to dissolve clots
    • vena cava filters, which block the path of blood clots, stopping them from entering the lungs

    These treatments can be similar for subacute cases. In fact, a 2020 paper reports the case of a man who had subacute PE. He achieved clinical recovery after going through thrombolysis with streptokinase.

    Additionally, a 2018 article states that in the case of chronic PE, pulmonary endarterectomy, which removes clotted blood from the pulmonary arteries, and balloon pulmonary angioplasty can cure CTEPH.

    The Centers for Disease Control and Prevention (CDC) state that:

    • 25% of people with PE have sudden death
    • up to 30% die within 1 month of diagnosis
    • up to 50% of individuals who had a DVT can have long-term complications
    • up to 33% of people with DVT or PE have a recurrence within 10 years

    It is extremely important for those at risk of PE to try and minimize their risk of developing or recurring PE.

    A person can achieve this by:

    • going for regular checkups for early diagnosis
    • continuing the use of blood thinners after PE or DVT
    • making lifestyle changes, such as eating a balanced diet and exercising regularly
    • avoiding smoking, if applicable
    • moving around regularly, especially after long periods of rest

    Anyone can get a PE, which can be life threatening. Doctors split PE into three categories: acute, subacute, and chronic PE. The most common cause of PE is DVT, but genetic mutations and lifestyle factors, such as pregnancy, can also play a role in a person’s risk.

    Someone with a PE may not develop any symptoms, but those who do may experience shortness of breath and coughing up blood.

    There is a wide range of diagnostic tests, medicines, and procedures that can help identify and treat PE.

    People with PE should regularly consult a doctor for checkups, continue their medication, and work to decrease their risk of complications by eating a balanced diet and exercising regularly.

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    If you have a snoring problem, you are hardly alone. It’s estimated that nearly half of the people in United States snore at some point. One in four does it regularly.

    Much of the time, snoring is little more than an unwanted sleep disruption for those around you. But for 25 percent of men and 10 percent of women, it’s the most visible -- vocal -- symptom of sleep apnea, a disorder that prevents you from getting a good night’s rest. Worse, it can contribute to a wide range of serious health problems, including heart attacks.

    Sleep apneas fall into two categories:

    Obstructive sleep apnea: This is when the airway at the back of the throat becomes blocked, causing temporary pauses in breathing.

    Central sleep apnea: This is related to a problem in the brain system that controls the muscles used for respiration, causing slow and shallow breathing.

    Sleep Apnea Symptoms

    Sleep apnea is typically thought of as a male disease in this country. But there doesn’t appear to be any reason for that to be the case. It’s far more likely that the condition is significantly underdiagnosed in women. This could be because women don’t like to admit that they snore or aren’t being told about their snoring.

    As a result, women often don’t realize they have the condition until accompanying a partner to a doctor’s visit, where they realize they share some of the same symptoms. Those include:

    • Snoring: This is the most common symptom, though not everyone who snores has sleep apnea. Snoring can come and go throughout the night and often is loud enough to disturb the sleep of others.
    • Daytime sleepiness: This may be particularly noticeable while driving.
    • Breathing pauses while sleeping: After the pause, you may wake up abruptly, gasping and choking.
    • Difficulty concentrating
    • Moodiness
    • Morning headaches
    • Dry mouth
    • Chronic fatigue

    Is Sleep Apnea Dangerous?

    Sleep apnea can be a significant contributor to a range of silent conditions – those that may not be noticed until they reach a life-threatening level.

    The biggest dangers are to the cardiovascular and neurovascular systems, increasing the risk for a variety of health problems, including:

    • Heart attack
    • Heart arrhythmia
    • Abnormal heartbeat
    • High blood pressure
    • Stroke
    • Pulmonary hypertension

    While these are some of the more dangerous conditions impacted by sleep apnea, there is growing evidence about the effect of the condition on our overall health. For example, there also appears to be a link between sleep apnea and post-traumatic stress disorder, general anxiety and depression. A possible explanation is that sleep deprivation makes symptoms worse and recovery slower.

    Diagnosing Sleep Apnea

    Sleep apnea is diagnosed through one of two types of sleep study. The simplest is a kit that you can use at home. You hook yourself to it at night during sleep and then send it back for analysis. It collects a variety of information, including heart rate, blood oxygen level and breathing patterns.

    For more complicated cases – including those that might involve more than one sleep disorder – diagnosis takes place in a lab sleep study. You will travel to a sleep center and stay overnight while sleep specialists monitor you.

    How Is Sleep Apnea Treated?

    The gold standard for treatment is the continuous positive airway pressure (CPAP) machine. It's been around for ages, and it's highly successful. It's the starting point for patients with moderate to severe sleep apnea. The machine delivers air pressure through a mask while you sleep. It keeps the upper airway passages open to prevent apnea and snoring.

    There are, however, cases where CPAP doesn’t work. This could be for a variety of reasons,  including patients who can’t find a good fit with a mask or who simply cannot sleep while wearing one.

    A newer surgical option involves the insertion of a nerve stimulator under your chin and a monitor in your chest – both done during outpatient surgery. While you sleep, the device monitors your breathing and uses pulses to force your tongue forward in your mouth, clearing the airway.

    In general, treatment is guided by the severity of the disorder, though some treatments are better for some people, based on their unique characteristics.  These options could include treating nasal congestion, tonsil removal and custom-fitted oral appliances that help keep your throat open while sleeping.

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    A pulmonary embolism (PE) is a medical emergency. One of the arteries (large blood vessels) in the lungs becomes blocked by a blood clot that travels from the leg or another part of the body.

    While this condition is most common among adults ages 40 and above, it can also occur in babies, children, and teens.

    Here’s how to spot the symptoms of pulmonary embolism in kids, how doctors diagnose this condition, and what the outcome may be after treatment.

    Any situation that allows a blood clot to form in the body may lead to pulmonary embolism. Clots most commonly form in the legs, which is called deep vein thrombosis (DVT).

    They can also form elsewhere, including the veins in the abdomen, arms, pelvis, or even in the brain. With time, the clot may travel to the lungs, fully or partially blocking off the blood supply.

    While uncommon in kids, there are some situations where a child may develop a pulmonary embolism. For example, children with congenital heart disease, infection, or a central venous line (CVL) for cancer treatment may be at particularly high risk.

    Other conditions that put kids at risk include:

    Age and race may play a role as well. A 2017 review suggests infants, toddlers, and adolescents are more likely to develop PE than kids of other ages. The study also suggests that Black children are more likely to develop PE than white children.

    A 2021 study notes that disparities in healthcare access and quality can influence PE severity and mortality in Black populations.

    If your child has risk factors and is also having issues with breathing or complaining of chest pain, be sure to pay close attention.

    Symptoms of PE may include:

    That said, experts share that children may not always show these classic signs. Instead, they may be asymptomatic, or their symptoms may be nonspecific.

    As a result, doctors may not always come to a diagnosis quickly. They may misdiagnose it as pneumonia or heart failure.

    Seek emergency care

    A pulmonary embolism is a medical emergency. Call emergency services or seek immediate medical attention if your child develops any symptoms associated with PE.

    Diagnosing PE in children involves first discussing your child’s medical history and risk factors.

    A physical exam may help assess issues with breathing, pain, or related symptoms. But signs of PE can mimic other illnesses, so some tests can aid your doctor with making a specific diagnosis.

    Imaging via CT scans or MRI scans is considered to be the most useful diagnostic tool available today. These scans are also noninvasive and relatively safe. MRIs are especially safe as they do not expose children to high doses of radiation.

    A ventilation/perfusion (VQ) scan is another option your doctor may suggest. This diagnostic tool can measure:

    • how air is flowing through the lungs
    • how and where blood is flowing
    • where blood flow is blocked

    The problem with diagnosis is that many kids have few to no symptoms. As a result, some studies have shown that a diagnosis of PE in children may take as long as 7 days.

    Treatment for PE generally involves medications to thin the blood, like:

    Also known as anticoagulation therapy, blood-thinning medications help prevent clots from growing and slow new clots from forming.

    Other treatment options include:

    • Thrombolysis. Also called fibrinolytic therapy, this method involves using medication to break up existing blood clots.
    • Thrombectomy. This minimally invasive surgical procedure physically removes clots from the arteries or veins.
    • Inferior vena cava (IVC) filter. This device can keep clots from reaching the lungs. It’s generally only used with children who weigh more than 22 pounds.

    Pediatric patients receive treatment similar to adults with PE. Still, your individual child’s treatment will vary depending on factors, including age, health history, hospital practices, and how he or she responds to each treatment.

    Again, since PE is less common in kids and may not produce notable symptoms, some doctors may overlook it as a diagnosis.

    In a 2020 case study, 50 percent of children who experienced a PE had signs of the condition, but only a third received a correct initial diagnosis.

    With the delay in diagnosis, the mortality rate of pulmonary embolism is somewhere around 10 percent in children. When kids get prompt diagnosis and medical care, on the other hand, their outlook is good.

    Follow-up is critically important after treatment. Experts share that tracking the resolution, progression, or chance of recurrence is key. At least one study shows that Black and Hispanic children may be at the highest risk of recurrence.

    Your child’s pediatrician will also use follow-up appointments to monitor for any long-term issues that may arise, like pulmonary hypertension or chronic PE.

    While PE is rare in children, some kids may be at higher risk, either due to existing health conditions, age, or race.

    Classic symptoms may include trouble breathing or chest pain. But many kids show no symptoms or nonspecific symptoms, making diagnosis difficult.

    Fortunately, doctors are becoming more aware of the risks for PE in children so that diagnosis can be quicker and treatment can start sooner, leading to better outcomes.

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    For the most up-to-date news and information about the coronavirus pandemic, visit the WHO and CDC websites.

    Smartwatches can measure everything from heart rate to sleep quality, but one health metric has become particularly relevant over the past two years: blood oxygen saturation. Two of the world's biggest smartwatch makers, Apple and Samsung, added blood oxygen monitoring to their wearables in 2020. The COVID-19 pandemic also made measuring vitals from home more desirable. 

    But the arrival of blood oxygen monitoring in smartwatches also raised questions about how useful this information is without the context of a medical professional. In CNET's review of the Apple Watch Series 6, Vanessa Hand Orellana said she wished the Apple Watch could provide more guidance to accompany blood oxygen readings. (When her levels dropped to 92% overnight, she didn't know whether to be concerned.) Most smartwatches also aren't cleared by the US Food and Drug Administration for blood oxygen measurements and can't be used for medical purposes, making it difficult to understand how these metrics should be interpreted. 

    Roughly two years later, are blood oxygen readings any more useful than they were in 2020? The answer isn't that simple. Medical experts say measuring blood oxygen throughout the day and under different conditions could unlock insights you won't get with a traditional pulse oximeter. Plus, having more access to health data from home is also usually a good thing. 

    But these sensors still have shortcomings that can limit usefulness. And smartwatch makers are still figuring out the best ways to incorporate blood oxygen measurements into broader features that give users a complete picture of their overall health. 

    "We know the science behind them is still not as accurate as the ones that are hospital grade with regard to the way the oxygen is determined," said Dr. Albert Rizzo, chief medical officer at the American Lung Association. "But having said that, they've become useful from the standpoint of patients, or not even people who are medically ill, even well persons, to be able to track another vital sign."

    Blood oxygen monitoring's breakthrough


    The Apple Watch Series 6 was the company's first app to measure blood oxygen levels. 

    Screenshot by Sarah Mitroff/CNET

    To understand whether measuring blood oxygen levels from your smartwatch is useful, it's crucial to know what this metric means and how it's implemented in today's wearables first. Your blood oxygen level, also known as SpO2, refers to how much oxygen your red blood cells carry. It's considered an important indicator of respiratory health since it signals how well your body is able to absorb oxygen. 

    Blood oxygen saturation is typically measured through a pulse oximeter that clips onto your finger. Smartwatches like the Apple Watch measure this by shining a light through your wrist and measuring the light reflected. 

    If your current smartwatch or fitness tracker can't measure your blood oxygen levels, chances are the next one you buy will. The technology has become a staple in today's wearables and can be found in products from Apple, Samsung, Fitbit, Garmin and Withings, among others. 

    The Apple Watch Series 6 and Series 7 both measure blood oxygen levels, as do the Samsung Galaxy Watch 3 and Watch 4. Fitbit devices such as its Sense, Ionic and Versa smartwatches and the Charge 4, Charge 5 and Luxe fitness bands can also measure blood oxygen levels overnight during sleep. 

    But most companies haven't received FDA clearance for their blood oxygen measuring technology. Withings is the exception; the blood oxygen monitor in its ScanWatch and ScanWatch Horizon are both FDA-cleared. Maxime Dumont, Withings' product manager for smartwatches, says the FDA clearance should make its data more trustworthy to doctors.

    "We will never replace a doctor, and we are not intended to make any diagnosis with a watch," he said. "But the watch results are reliable for a physician."

    Read more: Fitbit and Apple Know Their Smartwatches Aren't Medical Devices. But Do You?

    Even though it was possible to take blood oxygen readings from a smartwatch before 2020, the technology had a breakout moment two years ago. As the pandemic overwhelmed hospitals and the healthcare system, there's been more interest in researching how wearables can monitor bodily changes at home. 

    Devices from Apple, Fitbit, Garmin and Oura have all been used in research examining whether wearable devices can predict disease early by measuring changes in bodily signals like heart rate and temperature. A 2021 study published in Scientific Reports from researchers at the University of Sao Paolo and Centro Universitário FMABC also found the Apple Watch Series 6 to be reliable at gathering SpO2 and heart rate data in patients with lung disease in a controlled environment.

    "The massive number of people that the health system had to deal with made it a little easy for health systems to experiment with these non clinical-grade oxygen sensors," said Dr. Nauman Mushtaq, medical director of cardiology at Northwestern Medicine Central DuPage and Delnor hospitals. 

    How useful are these sensors in smartwatches?

    Withings ScanWatch Horizon

    The Withings ScanWatch Horizon is FDA-cleared for blood oxygen monitoring. 

    Lisa Eadicicco/CNET

    While health sensors in smartwatches show promise in research, some experts are unsure how often these sensors are being used in everyday circumstances. "I have had a few patients who have used Apple Watches or similar devices to monitor their blood oxygen levels," said Dr. Ashraf Fawzy, a pulmonologist and critical care physician and Assistant Professor of Medicine at Johns Hopkins University. "But it hasn't been as common as I would have thought." 

    Regarding regular use, Dr. Mushtaq sees blood oxygen sensors in devices like the Apple Watch as most useful for adding more context regarding overall wellness. In most cases, the average healthy person would experience physical warning signs before experiencing hypoxemia, or low blood oxygen, he said.

    "I don't think it, to be honest, does anything that is clinically meaningful for an average person," he said. 

    That doesn't mean medical experts don't see potential. Smartwatches have a big advantage over traditional pulse oximeters: their position on your wrist all day. Many smartwatches can take background blood oxygen measurements in addition to providing spot checks, meaning they can gather data at different times during the day. 

    Read more: Apple Watch Series 8 Rumors: More Health Features, New Rugged Version

    Fitbit, Samsung, Garmin and Apple devices can monitor blood oxygen levels passively during sleep, unlike a traditional pulse oximeter which is used for taking on-demand measurements. Both Apple and Garmin can also sample blood oxygen levels periodically throughout the day.

    But smartwatches are only good at checking SpO2 levels at rest, even when taking scans in the background. (Apple says its background measurements happen when the wearer isn't moving, and Garmin says it takes readings less often if it detects high movement). 

    Measuring blood oxygen levels during strenuous activities would make these devices more useful since it could help doctors know whether to adjust the amount of oxygen a patient is being prescribed, according to Dr. Fawzy. Dr. Mushtaq also said patients with heart failure or pulmonary hypertension could benefit from seeing whether their blood oxygen levels drop during exercise. 

    "That can certainly help," said Dr. Fawzy. "Because for some people, their oxygen levels only drop when they're being active and will be normal when they're sitting quietly."

    Health metrics are most useful when put in context, whether it be blood oxygen levels or how many steps you've taken. The numbers and charts only matter when you know how to put them to good use.

    "Ultimately, consumers aren't buying sensors," Julie Ask, vice president and principal analyst at research firm Forrester, said in a previous interview with CNET. "They're not buying data. Consumers are buying what they hope is help achieving an outcome."


    Samsung's Galaxy Watch 4 measures blood oxygen levels overnight.

    Scott Stein/CNET

    So what kind of context do smartwatches need to provide to make blood oxygen readings more useful? Some companies are trying to answer that question by weaving SpO2 results into other features and in-app wellness reports to better understand your overall health. Samsung, for example, incorporates SpO2 measurements into its sleep coaching feature on the Galaxy Watch 4 to help you make sense of your sleep patterns, according to a Samsung representative. Withings uses blood oxygen levels as one of the metrics it analyzes when determining breathing disturbances, along with heart rate and motion. 

    Phil McClendon, the manager of Garmin's wellness product management team, couldn't comment on future plans when asked whether SpO2 measurements would be factored into other health insights. But he pointed to Garmin's Health Snapshot as an example of the company's approach to making health data more meaningful. 

    Read more: How WatchOS 9 Is Paving the Way for the Apple Watch's Future

    Health Snapshot compiles various metrics (including heart rate, blood oxygen, heart rate variability, respiration and stress) to provide a high-level view of your cardiovascular status. McClendon said the feature helps people quantify changes that may be happening in their bodies during abnormal events.

    "So maybe they're having a panic attack, and they're like 'I want to record this thing and export the PDF to take to my healthcare provider," he said as an example. 

    Right now, the biggest benefit of measuring blood oxygen levels from your smartwatch is learning what's considered normal for your body. Even though smartwatches aren't meant for medical diagnosis, it's another signal you can take to your doctor if you're not feeling well or notice a bodily change.

    "Whatever device you're using, compare it to your baseline, use it as a trend monitor so that you know that you're off from your baseline," said the American Lung Association's Dr. Rizzo. "It may allow you to change what you're doing or seek help sooner than you otherwise would." 

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    Ryan Haumschild, PharmD, MS, MBA: We’ve talked about the clinical burden, we’ve talked about the difficulty in terms of managing and diagnosing these patients, but how do these diseases impact patients with ILD [interstitial lung disease] in terms of their morbidity and mortality? When we think of interstitial lung disease, I know from my perspective, when I’m managing cost and covered lives, we also think about patient quality of life. That’s something else that employers are concerned about within this patient population. I don’t know if you could talk to us a little about how does this disease impact morbidity and mortality and lastly, what is the impact you see it make on patients’ quality of life?

    Kristin Highland, MD: Interstitial lung disease is frequently progressive, and it’s the leading cause of morbidity and mortality in scleroderma. It’s the second leading cause of death in rheumatoid arthritis. IPF [idiopathic pulmonary fibrosis] is relentlessly progressive, with patients having an average survival of 3 to 5 years. They get on the internet, Dr Google, and the first thing they read is the mortality associated with IPF, no matter what kind of interstitial lung disease they have. So they come to us anxious, scared, depressed, but they’re also short of breath. Often they don’t even know how short of breath they are because the body often naturally, subconsciously, slows down. Often patients show up to my office because they’ve gone on vacation and they’ve done something out of the ordinary, and they all of a sudden discovered how limited they are. With time, they’re able to do less and less. They become deconditioned. That decreases their ability to be independent. As Dr Noble stated, patients desaturate, and so now they have to wear supplemental oxygen. They can no longer hide their disease. Wearing oxygen affects their vanity. It’s very difficult to maneuver these oxygen tanks. Payers do not want to pay for portable concentrators, and so patients are tied to their house. They don’t have the flexibility to leave their house without bringing multiple tanks, and many of our patients are quite frail. The burden of having to wear oxygen is very real and needs to be solved.

    In addition, patients often have a nonproductive cough, which can be quite debilitating, quite embarrassing, patients are afraid to leave the home because people think they have some kind of infection, especially during the COVID-19 pandemic. People are afraid that they’re going to be accused of having COVID-19 and spreading the virus just because they have this unrelenting cough. I think we should not underestimate the effect of interstitial lung disease on the caregiver. Not only is the patient burdened by their disease, but the caregiver has a significant amount of issues with lost work, with anxiety and depression over this illness as well. There is a huge clinical burden with the diagnosis of interstitial lung disease.

    Ryan Haumschild, PharmD, MS, MBA: I appreciate that overview because you know these patients better than anybody. I think there is a lot of societal concern when patients don’t feel like they can leave the house, whether that be based on their pulmonary function or other people are going to think they have COVID-19, and I think those are things we need to be more aware of. It’s interesting too because as patients have this, and you mentioned depression and some of these comorbidities that are associated with the disease, it tends to impact treatment. What I mean by that is there’s also the economic burden, [and] as you eloquently put it, the clinical burden. When we look at the economic burden, I think that’s also something that comes to the top when we’re looking at interstitial lung disease. Speaking from that payer management side, we always look at the medical costs that are associated with this disease. I think as Dr Noble and Dr Culver spoke about, if we don’t have early diagnosis, these patients have high utilization of seeking out practitioners’ primary care. However, they don’t really see disease control until they get in front of that pulmonologist, get the proper diagnosis, and then proper control, either therapeutically or medically. I think that’s one of the biggest things that we look at as the annual medical costs continue to increase. I think as you start to look at more data around progressing patients, where I think the future of data is coming out, you see even higher medical expenses.

    When you look at some of these claims, you can see it typically run about $15,000 higher per year in medical expense for payers if these patients aren’t being managed appropriately. I think that pulls into a lot of what we’re hearing about, having that right specialist manage the patient means less ED [emergency department] utilization, less outpatient utilization, and better quality of life. When we look at some of these health care utilizations and some of the related costs, we see that cost increase over time. They can increase over time because patients may not have great adherence to therapies, they may not feel like their condition is controlled, or they may have other disease manifestations that occur in terms of being a rheumatological patient, but also being managed by their pulmonary [physician], and how often are those providers really communicating in more of the community setting? I think that’s what payers are looking for too. How do we manage that? How do we get in front of that so that we have better large-scale management of these patients, more timely management, and therefore not duplicating some of the services that are provided?

    Before we move on, I just want to hit on a few last comments around the economic burden because I think it’s such an important consideration as payers are managing these diseases, making sure patients get access to these right medications in the upfront setting. I know we sometimes use a lot of step therapies and go through those prior authorizations, which are important, but we know that patients who have comorbid disease, whether it be COPD [chronic obstructive pulmonary disease], pulmonary hypertension, whatever you want to talk about, you see higher ILD-related treatment costs along with those other disease-related expenses. I think that’s something also really important; patients don’t usually just have 1 disease on their own. They can have depression, they can have anxiety based on their pulmonary function, and that leads into other treatments and management that the payer has to consider.

    As we look at lastly, real-world data, there are a couple of articles published in Advances in Therapy that showed a correlation between an increased frequency of pulmonology visits and an increased frequency of utilization. When they actually saw the specialist, you saw the utilization of provider visits go down a little, but you had longer management of disease. I think [it is important for] patients to truly understand the benefit of staying compliant with their treatment and also being checked on whenever some of these manifestations occur, or if another provider’s looking to change therapies, to also reduce any drug-drug interactions. With that being said, I feel like that’s really the economic burden, it’s the care of the patient, but also the management of comorbidities, especially when a lot of patients present with both.

    Lastly, I want to hit on one more main takeaway before we move on to the rest of our discussion. It’s creating the awareness of interstitial lung disease among payers, health plans, and employer groups because at the end of the day a lot of these employers are the ones that are paying the insurance companies to manage their benefit. What we’ve realized is there’s not a lot of awareness in terms of interstitial lung disease. There’s a lot of awareness of how we manage medical expense, but as you mentioned, Dr Highland, there’s a lot in terms of quality of life. If you have patients working for you who are actively working, if they have interstitial lung disease, there’s a high chance that they could have high absenteeism.

    We’ve actually seen that, in the Annals of American Thoracic Society, that some of these patients with more progressive interstitial lung disease, about 50% of them have said that they’ve missed work directly related to their disease. This is related to they weren’t having a great day or they felt like they weren’t being managed and couldn’t perform the function, which leads to higher absenteeism. When I think about that and we think about this as integrated delivery networks, we know right now staffing is one of the most difficult things for us to manage. We have a lot of expenses across our different health systems and provider clinics, but if we can get in front of having better presenteeism, reduce absenteeism by better management of disease, and having that pulmonary or lung doctor managing the total treatment, I think that’s going to improve quality of life for the patient and the caregiver. At the end of the day, it’s going to save these employer groups when you’re looking at filling those shifts or coming up with better staffing plans.

    Kristin Highland, MD: I’d like to add that management of these patients includes not just drugs, but also includes oxygen and having the availability of portable concentrators, but also access to pulmonary rehabilitation, and often repeat courses of pulmonary rehabilitation, because that can improve exercise tolerance, quality of life, independence of the patient, and less reliance on the caregiver. As we think about treating our patients comprehensively, thinking about these ancillary ways to improve the quality of life of our patients and improve their functionality, it’s important to consider in addition to the medications.

    Daniel Culver, DO: I’d like to chime in too, Kristin, one more point to that. The thing we never want to have to do, but we do have to in this specialty, is also deal with the severe patient and the patient who’s going to die from their interstitial lung disease, and perhaps the patient who’s not a candidate for lung transplantation. A very important part of what we do is manage those patients with palliative medicine, with hospice. My goal for patients with advanced interstitial lung disease is to keep them out of the hospital. I think one of the worst ways to die with interstitial lung disease is in the hospital on a ventilator. That’s the right thing to do for the patient, but it’s also economically a prudent thing to do, to support patients as they approach the end of their life and the end of their journey in ILD with a way to keep them at home, to keep them comfortable, and to focus on quality of life rather than repeated emergency department visits, admissions to the ICU [intensive care unit] and LTAC [long-term acute care], and all of the other things that come from that.

    This transcript has been edited for clarity.

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    Aside from the unrelenting pregnancy sickness, Talisa Young-Tisdale’s first pregnancy was relatively uneventful. She didn’t know she had what she calls “stroke level” blood pressure until she was diagnosed with preeclampsia at a routine prenatal visit.

    Although delivery is often the best treatment for preeclampsia, this wasn’t a viable option for Talisa, who was only 22 weeks pregnant. Her baby girl needed more time to grow and develop – her survival depended on it.

    Talisa was immediately admitted to Atrium Health’s Carolinas Medical Center, where her care team worked to keep her baby and blood pressure as stable as possible, for as long as possible. “I was basically trying to wait it out for as long as I could,” Talisa recalls.

    Talisa always knew she’d deliver at Atrium Health’s Carolinas Medical Center – it’s where her Atrium Health Women’s Care OB/GYN delivers, after all. She just didn’t expect it to be this early, while she was still in her second trimester. Fortunately, it was the best place for both Talisa and her newborn. In addition to offering the full spectrum of care, Carolinas Medical Center is connected to Atrium Health’s Levine Children’s Hospital and the region’s most advanced NICU.

    It was exactly where baby Tuli needed to be when she was born by emergency C-section at 26 weeks gestation.

    Though she’d gained four lifesaving weeks in her mother’s womb, Tuli was still born prematurely, with underdeveloped lungs. “She had a combination of severe bronchopulmonary dysplasia and pulmonary hypertension,” says Ashley Chadha, MD, Tuli’s pulmonologist at Atrium Health Levine Children’s. The conditions together resulted in damaged lungs and constricted airways, making it impossible for Tuli to breathe on her own.

    Tuli’s pulmonologists tried a variety of treatments, like intubation, steroids and oxygen, and just as she’d seem to be getting better, her health would decline or her oxygen would dip. As days turned to weeks and weeks turned to months, it became clear that Tuli needed a different approach. That’s because her condition was so severe, it would require more than therapies and expertise to heal – it would require time.

    Though Tuli had a long road ahead of her, her family and care team turned their focus to a new strategy: helping Tuli heal at home.

    The turning point

    Sending a baby home in Tuli’s condition isn’t easy. It demands advanced treatment, a leading-edge team of specialists and a failproof plan of care. Fortunately, Levine Children’s Hospital had all three. It’s even home to one of the nation’s best pediatric pulmonology programs and is the Charlotte region’s only children’s hospital recognized by U.S. News & World Report.

    Dr. Chadha and the pulmonology team determined mechanical ventilation via a tracheostomy tube would be the safest way to get Tuli home. “The severity of Tuli’s illness warranted long-term ventilation to allow her to outgrow her premature lung disease,” he explains.

    In the procedure, an opening was made in Tuli’s windpipe, where the tracheostomy tube – or trach – was inserted. Then, a machine called a mechanical ventilator was connected to the tube to keep Tuli’s breathing under control.  

    Although Tuli’s parents had been anxious about the procedure – and the equipment that came with it – they quickly said it was “the best thing we did.” Before the trach, their daughter’s energy levels had been low. Within a week, she was playful, laughing and showing off the bubbly personality her parents had long waited to see.

    “That was the turning point,” says Talisa. And it was also the solution that got Tuli home for the very first time.

    Learning to breathe

    On April 27, 2021 – 225 days after her birth – Tuli went home. Though the Young-Tisdales had the house prepared for a newborn, they never imagined they’d bring home machinery and medical equipment, too. “You prepare your baby’s nursery and have no idea this will happen to you. But after a few months, it started to feel more normal,” says Talisa.

    For families like Tuli’s, Atrium Health Levine Children’s offers special pulmonology programs to help with the transition home. This includes a tracheostomy navigator program, which consists of a full-service team of respiratory therapists and nurses who support families and walk them through how to use the machines. “Everyone really cares about Tuli,” says Talisa. “They’re really invested in our journey, and we never feel alone.”

    Since coming home, Tuli has only continued to thrive. She’s crawling, standing and even taking steps – a triumph for an 18-month-old who was once told she might not walk until 2 or 3. And that’s not even her biggest achievement. Today, Tuli is off the oxygen and ventilator, and she’s learning to breathe through her nose and mouth.

    “She’s had a tough go of it in the first phase of her life,” says Templeton, Tuli’s dad. “But one thing she’s shown us is that doesn’t stop you from living.”

    As Tuli’s lungs keep getting stronger, the next step will be to remove the trach. But Talisa and Templeton are in no rush. They know Tuli will do it all in her own time – and crush everything that comes her way.

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    Rudy Lucero, 55, recovers from double lung transplant surgery in an apartment in Aurora, Colorado. The surgery became necessary after a COVID infection last year seriously scarred his lungs, impeding his ability to breathe. (Courtesy Deborah Lucero)

    Copyright © 2022 Albuquerque Journal

    Rudy Lucero believes in miracles. He sees one each time he looks in the mirror.

    The Albuquerque resident is recovering in a Colorado hospital after having a May 2 double lung transplant, made necessary after a COVID infection scarred his lungs and made breathing nearly impossible.

    He expects that he and his wife, Deborah, will have to remain in Colorado another 2-3 months as he continues to get stronger and more independent.

    Colorado is a good place to be, considering where Rudy was heading.

    “I’m really close to the way I felt before I got sick, but I’ve lost a lot of weight and my muscles are weak,” Rudy said. “I’ve been going to pulmonary rehab, just trying to get stronger.”

    All he knows of his organ donor is that the lungs came from a 33-year-old male. The hospital, he said, would not release any additional information.

    On New Year’s Day, 2021, Rudy and his then longtime girlfriend, Deborah Ortiz, both tested positive for COVID. Vaccines had just started to become available and the couple did not yet have access to them. Over the next five days, as Deborah got better, Rudy, who also has diabetes, experienced a profound deterioration in his ability to breathe. He wound up being rushed by ambulance to a hospital.

    Rudy, 55, and Deborah, 53, had each been married before. They had known one another for more than 15 years and had plans to get married and have a honeymoon in Hawaii. Rudy had even traveled to Los Angeles to purchase a zoot suit for the occasion.

    COVID put the kibosh on that.

    As Rudy lingered in a bed at Lovelace Medical Center, he realized he faced an uncertain future and suggested that he and Deborah get married right away. So on Feb. 7, 2021, Super Bowl Sunday, they exchanged vows – Rudy still in his hospital bed, and Deborah in the parking lot below, holding a cellphone with an audio-video connection and surrounded by about 100 mask-wearing friends and a procession of classic cars.

    Rudy Lucero leaves Lovelace Medical Center in June 2021, accompanied by his wife, Deborah, left. Lucero had been hospitalized going on six months because of COVID. (Roberto E. Rosales/Albuquerque Journal)

    On June 23, closing in on a six-month hospitalization, Deborah was finally able to take Rudy home, but life was not easy for him. Rudy, who owned a plumbing company for 30 years, had to sell his business. Deborah, formerly a cosmetologist, became Rudy’s primary caregiver. More than 70% of his lungs were scarred, causing a permanent condition called pulmonary fibrosis, which would require him to be on oxygen for the rest of his life, his doctors informed him.

    In October, Rudy experienced another setback. He was hospitalized with pulmonary hypertension, which causes the heart to work at a dangerously high rate to pump blood through the lungs. It was at that point, Deborah said, “that we started talking about a double lung transplant,” a discussion they had hoped to put off as long as possible.

    In March, the couple went to the University of Colorado Anschutz Medical Center in Aurora, which has a lung transplant program. With his oxygen levels still falling, Rudy was placed on the transplant list and eight pairs of donor lungs were considered before an acceptable pair was located. The surgery took more than eight hours, Rudy said.

    “There’s a small window where someone can be not yet sick enough to have the transplant, but then there’s also a line where a person can be too sick to have the transplant,” Deborah said. “Rudy was close to being too sick.”

    When he finally awoke 24 hours after the surgery, it was a revelation, Rudy said. “I was breathing normal. It was crazy. The way I was living before, there was no quality of life. I couldn’t get up and go to the bathroom without gasping for air, so this was amazing. I’m still on a little bit of oxygen, but eventually I won’t need it at all.”

    He will, however, have to take anti-rejection medication for the rest of his life, an assortment of 15 to 20 pills daily.

    “It’s not a possibility of rejection, he will definitely have rejection at one point or another, if not multiple times,” Deborah said. “But as long as we keep on top of it, and when we see signs – a common cold, fatigue, fever – we can let the doctors know immediately and they can test him quickly and give him antibiotics or whatever he’s going to need. But it’s not a matter of if, it’s a matter of when.”

    Rudy and Deborah Lucero visit the Mother Cabrini Shrine in the foothills of the Rocky Mountains, west of Aurora, Colorado, on Sunday, their first outing since Rudy’s double lung transplant surgery. (Courtesy Deborah Lucero)

    For the next couple of months or so, the couple is living close to the medical center in housing subsidized by Brent’s Place, a nonprofit that helps people like the Luceros. Rudy goes to pulmonary rehab three times a week and visits his doctor once a week.

    Deborah, in the meantime, is planning their return to Albuquerque and the more elaborate wedding that they missed out on earlier, including the procession of classic cars adorned with a thousand tissue paper flowers that have been waiting in storage.

    “We had a really, really rough year and a half, and if it has anything to do with the marriage vows about ‘in sickness and in health,’ well, we’ve already done the sickness part, so it’s time to do the healthy part and be happy,” Deborah said.

    Rudy knows how lucky he is to have survived the medical crisis. “I would never have made it without Deborah,” he said.

    And every day he gets up and looks in the mirror he recognizes that his second chance at life “is nothing short of a miracle.”

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    Source: Pixaby.com

    Have ever experienced dizziness, light-headedness, shortness of breath, or nausea in the mountains? You may have had a case of what is referred to as altitude sickness or acute mountain sickness (AMS). Altitude sickness can occur at altitudes above 6500 ft (2000 m) and a more extreme and severe case of altitude sickness is High-altitude pulmonary edema (HAPE) which is induced by hypoxia and can be life-threatening if not treated promptly. HAPE occurs when blood vessels in the lungs constrict, increasing pressure and causing fluid to leak from the blood vessels into the lung tissue and eventually into the air sacs


    HAPE is most commonly seen in people who travel to elevations higher than 8,200 ft (2500 m) over a short period of time. Even folks who are acclimatized or live at high altitudes can experience what is referred to as ‘Re-entry HAPE’ after returning from a visit to lower altitudes. 

    Free photos of Snow

    Source: Pixaby.com

    What Causes HAPE?

    There are many factors that can make a difference and may increase a person’s susceptibility to developing HAPE. These include genetic make-up, the rate of ascent, the elevation and time spent at that elevation, how many days (if any) the person has been able to acclimatize to the higher elevation, cold exposure, as well as the extent and rigor of physical activity at high altitude. 

    HAPE generally occurs 2-4 days after rapid ascent to altitudes in excess of 8000ft. Young people and people previously acclimatized who briefly visit a lower elevation and then go back up to a higher elevation seem to be more predisposed to HAPE. 

    People with pre-existing heart & lung (cardiopulmonary) conditions such as coronary heart disease or pulmonary hypertension are also more susceptible to HAPE and it is recommended to consult a physician prior to a trip to high elevation.

    What are the telltale signs of HAPE and how can it be treated?

    If at least 2 of the following symptoms or signs are present, there is a very high likelihood of the onset of HAPE: Shortness of breath, rapid breathing, rapid heart rate, crackling or wheezing while breathing, chest tightness or congestion, coughing, skin turning blue, weakness or decreased physical performance.

    If left untreated HAPE can have serious long-term effects and can even be fatal. The first thing to do with the onset of HAPE is to stop any further ascent. Resting, administering oxygen, and descending as quickly as feasible are the best steps to combatting HAPE. It can also be treated medically with drugs like Acetazolamide, Diamox, or Nifedipine, which can also be administered as a preventative medication to those with pre-existing cardiopulmonary conditions or those who are susceptible to HAPE.

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    Asthma is a lung condition in which the airways become inflamed and narrowed. This narrowing restricts the amount of air that can move through the bronchioles and usually causes distinct breathing sounds such as wheezing and coughing.

    In silent asthma, no wheezing or coughing is present. This may be a variation in asthma symptoms, or it could be a phenomenon that healthcare providers sometimes refer to as the "silent chest." Silent chest can be associated with severe forms of asthma, including status asthmaticus and fatal asthma.

    This article discusses the causes of silent asthma as well as symptoms, diagnosis, treatment, and prevention.

    Karl Tapales / Getty Images

    Silent Asthma Symptoms

    Silent asthma symptoms are similar to those of regular asthma, with the absence of coughing or wheezing. Symptoms may include:

    • Distress, anxiety, or restlessness
    • Fatigue
    • Chest tightness
    • Feeling short of breath
    • Difficulty speaking

    Severe symptoms that require immediate medical attention may include:

    • Breathing retractions that look like an area of sinking or sucking in that occurs when breathing muscles are working hard (retractions may be most noticeable between the ribs or at the base of the neck)
    • Rapid breathing
    • Inability to talk due to difficulty breathing
    • Cyanosis (bluish color around the lips or beds of the fingernails, which indicates poor oxygenation)
    • Dizziness or passing out


    A specific cause of asthma cannot always be identified. However, there are some known risk factors for the development of asthma:

    • Genetics
    • Allergies
    • Environmental factors, such as exposure to pollution
    • Respiratory infections
    • Obesity

    It's worth noting that the term "silent asthma" is not well-defined or researched. If you have been told that you have silent asthma by a healthcare provider, it could simply mean that you are have mild or moderate symptoms of asthma without wheezing or coughing.

    However, at some point, almost everyone with asthma will experience wheezing and coughing, even if you don't experience the more audible symptoms all the time.

    One reason you may not have wheezing or coughing is that your airways have not tightened so much as to restrict air movement through your bronchioles, or at least not enough to produce these characteristic breathing noises.

    It's also possible that you are wheezing, but it is so faint that it's difficult to hear. Not everyone with asthma experiences the same symptoms, and your symptoms may vary depending on the day and circumstance.

    Status Asthmaticus and Silent Chest

    Status asthmaticus is a severe form of asthma that doesn't respond well to typical treatments. An individual with status asthmaticus can experience such a severe asthma attack that it leads to silent chest. Silent chest is the absence of wheezing and coughing due to fatigue and inability to move any air through severely constricted bronchioles. Silent chest usually precedes respiratory failure and is a life-threatening medical emergency.


    If your healthcare provider suspects asthma based on your symptoms, physical examination, and medical history, they might order one or more of the following tests to confirm the diagnosis:


    There are several differ treatment options for asthma, including medication, procedures, and avoiding triggers.


    Triggers are anything that brings on asthma symptoms. Identifying and avoiding asthma triggers can be an important part of your treatment plan.

    Potential asthma triggers include:

    • Allergens (i.e., mold, pollen, pet dander)
    • Air pollution
    • Chemicals or toxins (i.e., tobacco smoke, cleaning supplies, paint fumes)
    • Exercise


    Long-acting or maintenance medications for asthma work to prevent asthma attacks. These include:

    Short-acting or rescue medications for asthma relieve the symptoms of an acute asthma attack. They include:


    Bronchothermoplasty is a procedure used to treat severe asthma that cannot be controlled with other treatments. It involves using a bronchoscope to apply heat to the muscles of the bronchioles, which thins and weakens the muscles, making it more difficult for them to constrict during an asthma attack.

    Asthma Action Plan

    Another name for your treatment regimen is an asthma action plan. An asthma action plan is a plan you develop with your healthcare provider that outlines how to prevent and treat asthma symptoms. It should clearly define what medications you should use and when, as well as when you need to seek professional medical help, including when to call 911.

    Preventing Asthma Attacks

    The best way to prevent asthma attacks is to stick to your asthma action plan. In particular, make sure to use your long-acting asthma medications on time and as prescribed, and identify and avoid triggers.


    While wheezing and coughing are classic symptoms of asthma, it is possible to have asthma without experiencing these symptoms. This is known as silent asthma. This form of asthma can include a mild to moderate variation of symptoms. However, if it occurs after a prolonged asthma attack or is accompanied by serious symptoms, such as cyanosis or loss of consciousness, it could be a life-threatening condition called silent chest.

    If you suspect silent chest, call 911 or go to your nearest emergency room.

    A Word From Verywell

    Silent asthma can be a particularly frightening condition because the lack of obvious symptoms makes it more difficult to diagnose. While there is no cure for asthma, symptoms can be managed once a diagnosis is made. The best way to manage the condition is to create an asthma action plan with a qualified healthcare provider and stick to it.

    Frequently Asked Questions

    • Can you have asthma without knowing?

      Yes, it is possible to have asthma without knowing it, especially if your symptoms are mild or atypical. If you suspect asthma or any kind of respiratory condition, you should consult a healthcare provider for a proper diagnosis.

    • What can be mistaken for asthma?

      The symptoms of asthma can mimic many other health conditions including COPD, GERD, respiratory infections, sarcoidosis, pulmonary hypertension, pulmonary embolism, bronchiectasis, eosinophilic bronchitis, and allergic rhinitis to name a few.

    • What does silent asthma feel like?

      Silent asthma may feel like a tightening of your chest, shortness of breath, and difficulty speaking. You may also feel anxious and unable to hold still.

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    Approximately 7–8% of adults in the United States (US) currently identify as Veterans of the Armed Forces; of these, approximately 42–49% are recipients of Veteran Affairs (VA) benefits, which include services such as healthcare, disability compensation or pension, loan and insurance programs, and burial services.1,2 In general, Veterans who complete a minimum 24 months of service with an honorable discharge are eligible for healthcare through the Veterans Health Administration (VHA), one of the largest nationally integrated systems. Although VA benefits are available to most Veterans, due to priority assignments for enrollment (based on service connection, disability, and income) and copays, the approximately 9 million Veterans who currently utilize VA healthcare and participate in VA-sponsored research represent a unique subset of the Veteran population.1,2

    Recipients of VA healthcare are typically older than the general population (median age 64 versus 38 years, respectively) and are predominantly (91%) male, although enrollment of female Veterans is rising.1,2 The proportion of Veterans who utilize VA with an annual household income less than $35,000 is higher than that of the general US population (43% versus 26%)1,3 as is the prevalence of ever-smoking (60% versus 35–40%).1,2,4 Economic disadvantage and increased rates of smoking, coupled with service-related and occupational exposures, have likely contributed to the high prevalence and rising incidence of chronic respiratory diseases, including chronic obstructive pulmonary disease (COPD), among Veterans.5,6

    COPD is not objectively different in terms of disease manifestation in Veterans compared to civilians.7 However, the prevalence of COPD among Veterans, which is currently estimated to be between 8% and 19%,6,8 is higher than among the general population (6%).9 Importantly, COPD is likely underdiagnosed among Veterans, with only a minority of individuals with objective airflow limitation on lung function testing reporting a clinical diagnosis of COPD.10 Veterans with COPD have increased all-cause and respiratory-related health-care utilization as well as higher rates of comorbid conditions relative to Veterans without COPD.6 Moreover, the prevalence of mental health conditions, particularly alcohol and substance abuse, is higher in Veterans compared to civilians.11 Comorbid mental health conditions commonly serve as a barrier to utilization and/or responsiveness to evidence-based care, such as self-management interventions.12 Given the prevalence and significant burden of COPD within the VHA, substantial resources have been applied towards both clinical and research initiatives to improve outcomes for Veterans with COPD.

    The VHA provides evidence-based treatment to Veterans with COPD in order to optimize physiological, physical, and psychological health. These treatments and interventions are comprehensively described in the Global Initiative for Obstructive Lung Disease (GOLD) guidelines.13 Notably, Veterans with COPD and VHA researchers have contributed to early research examining such treatments and interventions to improve COPD outcomes. The objective of this paper is to provide a narrative review of interventions for key physiological, physical, and psychological health outcomes in US Veterans. Articles were identified if they were conducted with US Veterans and broadly addressed interventions for physiological, physical, or psychological outcomes.

    Physiological Outcomes and Interventions to Optimize Them in Veterans with COPD

    Due to the high burden of COPD within the VA, Veterans and VHA investigators have been involved in studies which have contributed to the collective knowledge on COPD physiology. Physiological and clinical outcomes which have been examined among Veterans with COPD have included lung function, hypoxemia, and systemic effects associated with disease, such as alterations in body composition and bone mineral density. These studies support current evidence-based guidelines which include both pharmacological and non-pharmacological management of both stable COPD and acute exacerbations of COPD. Key studies examining these physiological and clinical outcomes are summarized below.

    Longitudinal studies based within the VHA, such as the Normative Aging Study (NAS), have resulted in an improved understanding of and delineation between healthy aging and disease processes such as COPD.14,15 Comprised of over 2000 participants who were first enrolled in 1963 who have triennial follow-up data,16 the NAS represents a rich source of multi-dimensional information contributing to studies which have identified environmental (eg, smoking, air pollution)17,18 as well as genetic, epigenetic, and genomic risk factors that affect lung function and COPD susceptibility.14,15,17,19

    Oxygen Supplementation

    VHA research was a key stakeholder in establishing the detrimental effects of hypoxemia on not only end organ function but also reactive vasoconstriction in the pulmonary vasculature leading to pulmonary hypertension and cor pulmonale. Sentinel publications supported by the VHA include a brief report by Renzetti et al20 in 1968 which established the associations between COPD and mortality, spirometric lung function, and hypoxemia. Findings from this observational report gave rise to numerous subsequent studies, both within and outside of the VHA, which established the safety and benefit of supplemental oxygen on exercise tolerance and dyspnea,21 cardiovascular parameters,21 and survival22 among COPD patients with significant hypoxemia. As research practices evolved over the decades from single-site studies to multi-center collaborative initiatives, VA investigators continued to contribute to research on the management of hypoxemia in COPD patients. Multiple VA facilities served as research study sites for the Long-Term Oxygen Treatment Trial (LOTT) which examined oxygen supplementation for COPD patients with moderate resting or exercise-induced hypoxemia.23 While the benefits of oxygen supplementation in COPD patients with severe resting hypoxemia (defined as an oxygen saturation (SpO2) <89% or an arterial oxygen tension, PaO2 ≤55 mmHg, or PaO2≤59 or SpO2≤89% with signs of cor pulmonale) had been previously established,24,25 LOTT demonstrated that routine supplementation in moderate resting (SpO2 89–93%) or exercise-induced hypoxemia (SpO2 80–90%) was not associated with improved all-cause mortality or time to first hospitalization,23 leading to a significant revision of management guidelines issued by the VHA, professional societies, and the GOLD recommendations.13 Current guidelines on the initiation of oxygen supplementation (as outlined above) as well as the titration of supplemental oxygen to a goal SpO2 >90–92% represent the integrated results of trials conducted both within and outside the VHA.

    Pharmacological Management

    Veterans and VHA investigators have contributed substantially to studies of medications, such as bronchodilators, that improve symptoms through improvements in lung function by increasing airway diameter and decreasing air trapping and hyperinflation. Early trials examined systemic bronchodilators, such as theophylline26 and metaproterenol,27,28 and were later supplanted by studies of inhaled beta-agonists and antimuscarinic agents,29 the two dominant classes of bronchodilators in use today. Use of long-acting inhaled beta-agonists and antimuscarinic agents is currently recommended as first-line, evidence-based maintenance therapies for COPD.13 Additional studies of pharmacological agents have included investigations of the effect of morphine on dyspnea,30 an important strategy for the palliative care of Veterans with advanced chronic lung disease associated with air hunger.

    Significant morbidity is attributed to acute exacerbations of COPD and investigations into pharmacological strategies to treat and prevent these events have also involved Veteran populations. In a multi-center, randomized controlled trial (RCT) sponsored by the VA Cooperative Studies Program (CSP), systemic corticosteroids for Veterans hospitalized with acute exacerbations of COPD were found to reduce the incidence of a combined endpoint of all-cause mortality, mechanical ventilation, readmission for COPD, or escalation of therapy relative to placebo.31 Systemic corticosteroids are now considered the standard of care for management of acute exacerbations of COPD,13 although the optimal doses and duration of therapy remain active areas of investigation.

    Significant resources have also been allocated to preventing acute exacerbations among COPD patients. Multiple VA medical centers served as research study sites for a RCT of chronic macrolide therapy using azithromycin to target chronic airways inflammation and prevent acute exacerbations of COPD.32 Findings from the study, which examined daily azithromycin taken for a year in addition to usual therapy, were notable for decreased COPD exacerbations and improved health-related quality of life (HRQoL), but also increased risk for hearing loss. Chronic suppressive macrolide therapy is now endorsed by the GOLD guidelines as an adjunctive maintenance medication for exacerbation-prone individuals.13

    The performance of roflumilast, another pharmacological agent for the prevention of exacerbations, was examined relative to chronic suppressive azithromycin use among Veterans. In this observational study, the unified medical records system within the VHA, known as the Corporate Data Warehouse, was examined along with Medicare usage data for 3875 Veterans. Results showed that roflumilast, an oral selective phosphodiesterase-4 inhibitor, was associated with increased all-cause mortality and COPD-related hospitalizations relative to chronic suppressive macrolide therapy.33 The findings from this study supported the need for head-to-head studies of chronic macrolide therapy relative to roflumilast which are currently being investigated through an ongoing RCT (clinicaltrials.gov NCT04069312).

    Systemic Effects of COPD

    Although airflow obstruction is the defining feature of COPD, there is increasing appreciation of the extra-pulmonary and systemic consequences of COPD. Due to the higher rates of and cumulative exposure to smoking, as well as intermittent use of systemic corticosteroids, COPD has been identified as an independent risk factor for osteoporosis among Veterans.34 The clinical consequences of the increased prevalence of osteoporosis were subsequently confirmed in a study of 87,360 Veterans aged >50 years with newly diagnosed COPD between 1999 and 2003, where high rates of hip and wrist fragility fractures were observed.35 Additional findings from this study included low rates of bone mineral density testing and anti-resorptive treatment (eg, bisphosphonates)35 and identified a crucial need for screening for bone health among Veterans with COPD.

    In addition to bone health, there has been increasing attention given to the impact of differences in body mass and body composition among Veterans with COPD. Body-mass index (BMI), a widely used metric of the weight-to-height relationship, is an integral component of the BMI, obstruction, dyspnea, and exercise limitation (BODE) index, which correlates with mortality and exacerbation frequency in COPD and has been validated in Veterans.36 In addition to body mass, the role of fat-free mass, a proxy measure for muscle mass, and its relationship with functional outcomes and exercise tolerance in Veterans with COPD represent important future areas of research.37

    Care Coordination Interventions

    Other work in Veterans to improve physical outcomes in COPD has focused less on the individual patient, and more on the quality and type of care the patient receives. Although the majority of COPD-related care is managed by primary care providers, Veteran access to specialty care and referrals patterns to pulmonologists for COPD are comparable to those in the general community.38 A significant proportion of the morbidity and direct costs associated with COPD within the VHA arise from hospitalizations due to acute exacerbations of COPD.8 In an effort to develop and introduce programs to reduce COPD hospitalizations, the VHA sponsored a multicenter RCT examining the efficacy of a multidisciplinary comprehensive care management plan comprised patient and primary care provider education, the development of an action plan for exacerbation management, and proactive case management relative to usual care.39 Unfortunately, the study was terminated prematurely in 2012 due to increased rates of COPD-related hospitalizations and excess all-cause mortality in the intervention (comprehensive care) arm.39 Notably, similar results for comprehensive care programs at non-VHA hospitals have subsequently been reported,40 supporting that additional research and alternative strategies for preventing COPD hospitalizations are needed.

    While effective strategies to prevent COPD hospitalizations remain an active field of investigation, programs to reduce the length of stay and prevent re-admissions have also received priority within the VHA. VHA-wide initiatives to reduce hospital utilization through expanded outpatient care resulted in a 51% reduction in length of stay for COPD exacerbations over 1994–1998, notably without increased mortality or non-VA hospital use.41 Additionally, individual programs focused on coordinated transitional care, a nurse-driven, telephone-based program targeting high-risk patients with comorbid COPD and congestive heart failure prior to discharge to home at an urban VA medical center resulted in a 54% reduction in 30-day re-hospitalization risk and was shown to be cost-effective.42 Moreover, one study examined the association of using non-VA outpatient care (both VA and non-VA care [ie, dual-care], and non-VA care only) and VA-only care with 30-day re-admission among Veterans. Overall, compared to Veterans who received VA-only care, Veterans who received dual-care and non-VA care only were 20% more likely to be readmitted for a COPD-specific exacerbation.43 These initiatives likely explain the recent finding of lower rates for 30-day re-admissions following hospitalizations for COPD at VA relative to non-VA hospitals.44

    Physical Outcomes and Interventions to Improve Them in Veterans with COPD

    An overarching goal in the treatment of Veterans with COPD is to maximize physical function. However, the clinical course of COPD can contribute to a vicious cycle of reduced function. Patients who experience dyspnea, a major symptom of COPD, tend to avoid physical activities that worsen dyspnea, causing further muscle deconditioning and reductions in exercise capacity.45 Pain is another common symptom of COPD, which can also contribute to lower physical function.46 Physical outcomes, such as dyspnea, exercise capacity, physical activity (PA), and pain, reflect potentially modifiable risk factors of all-cause and respiratory-related mortality.47 As such, there has been great interest within VHA to develop effective interventions to improve physical outcomes in Veterans with COPD. The following sections detail several of these interventions, and highlight the impact of these interventions on dyspnea, PA, exercise capacity, pain, and risk for acute COPD exacerbations.

    Pulmonary Rehabilitation

    Pulmonary rehabilitation (PR) is a well-established treatment of COPD, effectively improving exercise capacity, dyspnea, and HRQoL.48 PR is a comprehensive intervention that focuses on exercise training and self-management education. It typically occurs 2–3 times a week across 8–12 weeks. Access to traditional, in-person PR can be difficult. In the VA with regional medical centers, distance is a significant barrier. In the National Emphysema Treatment Trial, participants who lived greater than 36 miles from the treatment facility were 51% less likely to complete PR compared to those who lived less than 6 miles away.49 In one urban VA medical center, 25% of initially evaluated Veterans never started PR, 29% dropped-out, while only 46% completed a full course of 18 sessions.50 Some Veterans who would benefit from PR decline participation due to access-related barriers, such as time and distance to travel to the program.50,51 Earlier work within VA compared outcomes in Veterans who completed PR to Veterans who were referred to PR but declined.52 Overall, Veterans with COPD who completed PR significantly improved exercise capacity, as measured with the 6-minute walk test (6MWT) by an average of 75 m and reported a decrease in dyspnea on the UCSD Shortness of Breath Questionnaire by 7.3 points.52 Additionally, COPD-related acute emergency visits and hospitalizations declined post-PR.52 More recently, predictors of Veterans’ PR engagement were examined through a retrospective study of Veterans who attended their initial PR intake session between 2010 and 2018.50 Participants who dropped out of PR (ie, dropped out before session 18) compared to completers (ie, Veterans who completed all 18 session) had worse dyspnea, as measured by the Chronic Respiratory Questionnaire-Self-Reported (CRQ-SR) at baseline, and were more likely to be current smokers and have a history of alcohol use disorder. No differences emerged between those who never started and those who dropped out.50 Thus, while PR is unequivocally effective for improving physical outcomes, it is important that future work continue to address ongoing access barriers to PR.

    Physical Activity and Exercise Interventions

    Patients with COPD tend to engage in significantly less daily PA compared to healthy-matched controls.53 Physical activity as an outcome is important in COPD, as it is directly associated with poor health outcomes such as increased risk of acute exacerbations and increased mortality, independent of lung function.54 Many factors can contribute to lower levels of PA, including physiologic, behavioral, and environmental factors.55 As such, there has been a substantial amount of work within VA to develop effective interventions that promote and sustain PA and exercise.

    There have been several related RCTs examining the effectiveness of a web-mediated, pedometer-based PA intervention in Veterans with COPD (Taking Healthy Steps,56 Every Step Counts,57 and Walking and Education to Breathe58). This web intervention provides Veterans with COPD personalized daily step count goals, iterative feedback, disease-specific education, motivational tips, and an online community forum. Taking Healthy Steps was a RCT conducted virtually in a national sample of Veterans with COPD identified by diagnosis code. Compared to those who were randomly assigned to use a pedometer alone, those who were assigned to the website walked on average 779 more steps per day at 4 months.56 Every Step Counts used a more well-characterized cohort (ie, COPD diagnosis validated via spirometry). Compared to the pedometer-only control group, Veterans assigned to the website significantly increased their daily step count by 804 steps at 3 months.57 Those assigned to the intervention also demonstrated a significant reduced risk of experiencing a COPD acute exacerbation across a 12-month follow-up.59 Walking and Education to Breathe, the most recent RCT, evaluated the effectiveness of the intervention across two VA sites to include a more heterogeneous sample, and examined if lengthening the duration of the intervention period to 6 months would translate into improvements in exercise capacity. At 6 months, participants who were assigned to the web-based intervention walked on average 1312 more steps per day compared to those who were assigned to usual care.58 Across these three studies, despite the significant improvements in daily step count (779–1312), there were no significant differences between the intervention and control groups in changes with respect to exercise capacity (6MWT distance) or dyspnea (mMRC).56–58

    Additionally, a priority in PR is to facilitate behavior change so patients will sustain engagement in long-term exercise. However, it remains difficult to maintain improvements in exercise after PR. Coultas et al tested the efficacy of a 20-week, telephone-based lifestyle PA intervention compared to usual care in COPD patients eligible for PR. They did not find significant differences for their primary outcome of 6MWT distance; however, subgroup analysis found that among Veterans with moderate COPD, the intervention resulted in stability of 6MWT distance at 18 months compared to participants who received usual care.60

    In addition to daily walking, the effectiveness of alternative exercise forms, such as Tai Chi and yoga, has been explored in Veterans with COPD. Tai Chi may be a promising intervention to support physical outcomes. Compared to a mind-body breathing intervention, a Tai Chi intervention resulted in more substantial improvements in exercise capacity (6MWT distance) among persons with COPD.61 Similarly, a recent pilot RCT found that Tai Chi after completion of PR may support maintaining exercise capacity (6MWT distance) compared to usual care in persons with COPD after completing PR.62 Results from another RCT suggest that Tai Chi over 6 months may help to maintain exercise capacity.63 However, participants in the RCT reported barriers to attending the Tai Chi program similar to those reported for center-based PR (ie, distance, time).63 One recent pilot examined the effect of yoga training on inspiratory muscle performance.64 Inspiratory muscle strength is impaired in patients with COPD and leads to debilitating dyspnea and poor functional performance.65 Veterans were assigned to a 6-week yoga training program that included poses (asana) and controlled breathing (pranayama). Inspiratory muscle performance (measured via the Test of Incremental Respiratory Endurance) significantly improved from baseline, although no significant improvements were seen in exercise capacity (6MWT distance).64

    In many patients with COPD, dynamic hyperinflation of the lungs during exercise is a major contributor to decreased exercise capacity.66 A recent study in Veterans examined if breathing retraining coupled with exercise training, a cornerstone of PR,48 would improve exercise capacity more than exercise training alone.67 Exercise training occurred via treadmill and took place three times every week for 12 weeks. The researchers used a metronome to provide acoustic feedback to train participants to achieve a slower respiratory rate and prolonged exhalation. Overall, despite achieving changes in breathing pattern with breathing retraining, improvements in exercise duration and dynamic hyperinflation were not significantly different with exercise training plus breathing retraining versus with exercise training alone.68

    Psychological Outcomes and Interventions to Optimize Them in Veterans with COPD

    Depressive disorders are by far the most studied psychological disorder among Veterans with COPD. Rates of depressive disorder diagnosed by structured clinical interview range from 38% to 86% based on the study sample.69,70 Rates of diagnosed anxiety disorders range from 23% to 61%.69,70 Despite the high prevalence of depression and anxiety in Veterans with COPD, only a third receive any mental health treatment.69 In cross-sectional studies of Veterans, clinically significant depression symptoms were associated with low PA levels,71 worse self-reported functional impairment,72–74 greater dyspnea,72 and worse HRQoL.72,73 Moreover, epidemiological studies in large samples of Veterans with COPD have shown that depression is associated with 1.53 times higher 30-day mortality compared to Veterans without depression.75 Depression was also associated with 1.36 times increased risk of 30-day hospital readmission for COPD acute exacerbation.75 Clinically significant anxiety among Veterans with COPD shows similar associations to health and functional outcomes such as depression. Anxiety symptoms are associated with greater self-reported functional impairment and worse HRQoL. One study found a significant association between clinically significant anxiety and greater daily PA,71 a finding that requires replication in prospective studies. Anxiety is associated with 1.72 times higher 30-day mortality compared to Veterans without anxiety and 1.22 times increased risk of 30-day hospital readmission for COPD acute exacerbation.75

    Insomnia is an independent psychological disorder characterized by difficulty initiating or maintaining sleep, or early morning awakenings that cause significant distress and occur outside the diagnosis of another mental health condition.76 Research on insomnia in Veterans remains scarce. In one study, insomnia was found to occur in 27% (50 of 183) of Veterans with COPD. A much larger percentage of Veterans reported sleep complaints with 50% of the sample reporting at least one or more sleep complaint more than three times per week.77

    A key outcome in Veterans with COPD, HRQoL reflects an individual’s perception of their quality of life when they consider their overall health (eg, 36-Item Short Form Survey (SF-36))78 or in reference to their COPD diagnosis (eg, The Chronic Respiratory Questionnaire).79 Illness intrusiveness, a psychological construct, describes the extent to which an individual perceives their illness to impede in their daily life and valued activities and can be assessed with self-report measures. It is a meaningful treatment outcome for Veterans with COPD who prioritize daily functioning. The VHA has prioritized intervention development to improve psychological outcomes in Veterans with COPD. The following sections describe several of these interventions and their impact on psychological outcomes.

    Cognitive Behavioral Therapy (CBT)

    CBT is a time-limited, collaborative, present-focused, skills-based intervention that focuses on behavioral and cognitive change to treat psychological disorders. CBT is transdiagnostic, thus applicable in the treatment of the most common psychological disorders in COPD. Fundamental to CBT is that suffering is not directly caused by events themselves, but is a result of clients’ interpretation, appraisal, meaning, and behavioral response attached to events. Thus, treatment focuses on addressing the connection between events, thoughts, emotions, and behaviors while challenging and modifying unhelpful patterns.80

    While CBT has been studied by several research groups in civilian samples with COPD, only one research group in the US accounts for almost all empirical research on the efficacy of CBT in Veterans with COPD. Cully et al81 conducted an RCT comparing brief cognitive behavioral therapy (bCBT) to enhanced usual care (EUC) in 302 Veterans with either heart failure (HF) or COPD and clinically significant depression and/or anxiety symptoms. The primary outcomes were depression and anxiety symptoms measured by validated self-report measures. HRQoL was the secondary outcome.

    bCBT was delivered in six sessions either in-person or by telephone based on patient preference with two booster sessions provided over four months. Each session focused on a particular skill and the number of sessions varied based on patient preference and discussion with their therapist. Skill sessions focused on modification of unhelpful thinking patterns, behavioral activation, relaxation, and chronic disease self-management. Content was adapted to focus on the intersection between physical symptoms and mental health. Like traditional CBT, bCBT addressed topics such as usual and past coping styles and strengths and resources in the patient’s life. Skills were taught alongside practice assignments focused on goal setting and modifying behavior and thinking patterns. Therapists for the study ranged from psychology and social work trainees to staff psychologists and physician assistants. The EUC group received assessment of mental health symptoms and a note in their chart for their primary care provider to address these concerns. Outcomes were assessed at baseline and 4 (post-intervention), 8, and 12 months.

    At 4 months, there were meaningful improvements in depression and anxiety symptoms in patients with COPD or HF. Veterans with COPD showed significant improvement in all domains of HRQoL. At 12 months, differences were maintained between the treatment and control group, but there was no further improvement in symptoms.81

    Stemming from this parent study, secondary analyses were conducted in several separate articles and provide important insights into the optimization of psychological health in Veterans with COPD. First, the impact of bCBT on illness intrusiveness was examined among Veterans with COPD in the parent study.82 Illness intrusiveness was measured with the Illness Intrusiveness Rating Scale (IIRS) which provides a total score, as well as three validated subscales: Relationships (eg, family, civil engagement), Intimacy (eg, sexual functioning, relationship with spouse), and Instrumental (eg, health, work, active recreation). bCBT significantly improved IIRS total score at four months compared to EUC. At the subscale level, differences were found for Intimacy and Instrumental but not Relationships.

    Second, in a separate study,83 bCBT was found to result in a significant reduction of high-frequency suicidal ideation (SI) in the bCBT group compared to the EUC at 4- and 8-month time points after controlling for baseline SI but the treatment effect was not sustained at 12 months. Specifically, at 4 and 8 months, respectively, participants who received bCBT compared to EUC had 72% and 68% lower likelihood of reporting high-frequency SI.

    Third, predictors of treatment response to bCBT were explored in secondary analysis.84 Multivariate regression models examined whether hypothesized baseline variables including baseline depression or anxiety symptoms, functional limitations, self-efficacy for disease management, adaptive coping, maladaptive coping, number of sessions attended, and working alliance (ie, relationship between therapist and client) predicted improvement in primary outcomes of depression symptoms or anxiety symptoms. The same predictors emerged for both improvement in depression and anxiety symptoms. Participants with greater physical functioning impairment and lower self-efficacy showed less improvement in anxiety and depression symptoms. Those with greater baseline depression or anxiety showed greater improvement in symptoms.

    The fourth and final study stemming from the parent study describes a utilization analysis of the content delivered in bCBT.85 They found that participants who received the “physical health” and “thoughts” modules earlier in treatment had a greater likelihood of remaining in treatment. Results have important clinical implications suggesting that early psychoeducation and skill building should focus on the intersection between physical and mental health, as well as dysfunctional or unhelpful thought patterns to optimize treatment completion rates. Together, these studies offer important data on the efficacy of bCBT, as well as treatment predictors.

    Pulmonary Rehabilitation and Physical Activity

    As described in the physical outcomes section, PR is the standard of care for Veterans with COPD targeting exercise capacity and physical functioning. However, PR also improves many psychological outcomes, but studies with Veteran samples are limited. In a retrospective study, Veterans with COPD who participated in twice weekly outpatient PR for 18 weeks demonstrated significant improvement in depression symptoms over the course of PR. Greater reduction in depression over the course of treatment was significantly associated with greater improvement in CRQ-SR total score and the following subscales: fatigue, mastery, and emotional function.86 Similar findings were documented in a prior study examining the relation between change in depression symptoms and change in CRQ-SR subscales. In a sample of 81 Veterans enrolled in 8 weeks of biweekly PR, significant improvements were found for depression symptoms but not anxiety symptoms. Moreover, change in depression symptoms, but not anxiety symptoms, was associated with change in CRQ-SR domains of fatigue, emotion, and mastery.87 PR, a core treatment for Veterans with COPD and significant depression symptoms, improves physical functioning and psychological outcomes. However, depression and anxiety symptoms, particularly in Veterans with more than one mental health diagnosis and/or lifetime/chronic course of psychological disorders may require more intensive outpatient therapy specifically for mental health following PR or concurrently. Re-assessment of depression and anxiety symptoms is important at the end of PR to determine treatment needs.

    Other work within VA has examined the effect of PR on insomnia. A recent retrospective study examined subjective and objective sleep changes after eight weeks of conventional, in-person, structured PR and 12 months of an unstructured exercise program.88 Despite sustained improvements in exercise capacity (measured via the 6MWT distance; mean improvement 68.8 m) and dyspnea (measured via the mMRC; mean difference −0.4 points), neither subjective sleep (measured via the Pittsburgh Sleep Quality Index) nor objective sleep (measured via actigraphy) improved.88

    Surprisingly, research testing PA interventions in Veterans with COPD has not found significant improvements in depression or anxiety symptoms. One VA-based study compared the effects of a 4-month pedometer plus internet-mediated intervention to waitlist control (pedometer) on HRQoL in Veterans with COPD measured at 4 and 12 months.56,89,90 While HRQoL improved in the intervention group compared to the control group at 4 months, there was no difference at 12 months. Moreover, no change in depression scores was observed at either 4 or 12 months. However, these results are confounded by the fact that the treatment of anxiety and depression was not the main focus nor well characterized in the sample. For example, participants were not recruited based on significant levels of depression and anxiety nor was the intervention personalized in any way to participants based on their depression and/or anxiety levels.


    Research on pharmacotherapy to improve psychological outcomes in individuals with COPD is limited in both civilian and Veterans samples. Drawing from the general literature, a Cochrane review published in 2018 found insufficient evidence for pharmacotherapy for the treatment of depression in individuals with COPD.91 In their review of the literature on anti-depressants for depression in COPD, no recommendation was made for any anti-depressant type. Rather, non-pharmacological treatments, such as collaborative care models and CBT, were encouraged as first-line therapy.92

    Future Directions to Advance COPD Research and Clinical Care in Veterans with COPD

    Advances in Physiological Outcomes

    Pharmacological treatment of COPD is focused on maximizing lung function, reducing risk for acute exacerbations, and symptoms management, namely the reduction of dyspnea.93 More recently, advances in COPD treatment have utilized precision medicine to target COPD in its early stages or before disease onset.94 However, to our knowledge, there are few funded research studies in the VHA focused on early COPD or prevention efforts. This is notable given that Veterans of the Iraq and Afghanistan conflicts will be entering midlife and have already been identified to be at greater risk for respiratory diseases given environmental exposures.95 Prior studies in civilians have begun to characterize those who may have “early” COPD targeting adults <50 years of age with ≥10 pack-years of smoking history with evidence of lung function abnormality by CT or spirometry that do not meet criteria for COPD.96 Improved understanding of Preserved Ratio Impaired Spirometry, a classification of individuals who have proportional reductions in FEV1 and FVC but preserved ratio, provides a group of individuals at higher risk for transitioning to COPD and may particularly benefit from early intervention.97 Advances in imaging technology can help identify those who may be at-risk for COPD.98 At least one funded study within the VHA is exploring the application of computation imaging technology (CT) using Quantitative Imaging Analysis (QIA) to identify structural defects in the lungs before disease onset. By targeting individuals in the early COPD stage, effective clinical management can be offered and presents a vital area for future research in Veterans.

    Similarly, identification of predictive biomarkers within COPD remains an active area of research with many unanswered questions.94 While review of the research on biomarkers of COPD is beyond the scope of this paper, more research is needed exploring COPD biomarkers in Veterans with careful delineation of endotypes connected to the proposed biomarker and clinical manifestation of disease activity.99 For example, past research in civilians established an association between epigenetic changes and inflammatory-response cytokines in COPD patients undergoing a prolonged, 24-session exercise training regimen.100 Early changes were observed in DNA methylation between baseline and after the first session but no changes were observed in H4 acetylation status at any point during the intervention. Inflammatory markers changed in response to the exercise intervention with an increase in interleukin-6 (IL-6) and a decrease in growth factor-beta after session 24.

    In Veteran samples using a cross-sectional design, greater daily step count and higher 6MWT distance were associated with lower systematic inflammation, as measured by CRP and IL-6.101 After controlling for age, FEV1% predicted, pack-years smoked, cardiac disease, current statin use, history of acute exacerbations, and season, each 1000-step increase in daily step count was significantly associated with 0.94 mg/L and 0.96 pg/mL decrease in CRP level. Similarly, for every 30-m increase in 6MWT distance, there was a 0.94 pg/mL decrease in CRP and 0.96 pg/mL decrease in IL-6 level. While not causal, these studies point to potential epigenetic changes associated with exercise-induced inflammatory biomarkers in COPD.

    Research with Veteran samples has established correlations between epigenetic markers of biological age and functioning in COPD.102 At baseline, epigenetic age and age acceleration, measures that capture the difference between biological and chronological age, were inversely associated with 6MWT distance and PA after adjusting for chronological age, sex, race, smoking status, pack-years, BMI, cohort, and estimated cell counts. Importantly, longitudinal change in one of the measures of epigenetic age was inversely associated with change in 6MWT distance at 12 weeks, suggesting that epigenetic age may represent a potentially modifiable molecular signature of exercise capacity.102 Potential applications of epigenetics and biomarkers for the prediction of clinical outcomes, such as COPD acute exacerbations or response to exercise training programs such as pulmonary rehabilitation, represent active areas of investigation.

    Advances in Physical Functioning

    While PA promotion interventions show promising short- and some long-term benefit in terms of increasing daily PA and reducing COPD acute exacerbation risk, improvements in exercise capacity have not been observed.58 In the next decade, RCTs are needed to test the dose of PA promotion (ie, duration, intensity) required to sustain functional improvements. Long-term trials testing beyond 12 months are necessary. Moreover, development and testing of novel interventions that leverage varying levels of Veteran engagement, such as hybrid approaches that combine self-guided and in-person/provider-delivered components are needed to examine the impact of frequency of promotional and supportive messages and check-ins from staff.58 Additionally, little is known about the social context and its association with short- and long-term adoption of PA. Studies exploring the role caregivers, family members, and friends in the adoption and maintenance of PA in COPD are needed, particularly given that social context has proved important for the success of COPD self-management efforts.103,104 Finally, it is important to consider the effects of the COVID-19 pandemic on habitual PA and exercise patterns.105,106 Indoor walking and exercise in malls, gyms, and senior centers have been reduced and alternatives are not always available. As such, innovative research is needed to better understand how patients with COPD prefer to engage in PA in their current environments and preferences for in-home exercises.

    Notably, the VHA is a leader in telemedicine and prioritized access to care well before the COVID-19 pandemic107 which only expanded over the last two years.108 The VHA system provides iPad, with built in internet access, at no cost to Veterans without a personal device and/or internet access. Moreover, the VA has an established Care Coordination/Home Telehealth (CCHT)109 for chronic diseases including COPD, which provides home equipment for daily monitoring and disease management by a nurse care coordinator. In 2017, from funding through the VA’s Office of Rural Health, home-based PR was offered across 13 VA medical centers. While several studies in civilians have established the efficacy of home-based PR,110,111 until 2017 only hospital-based PR was offered in the VHA system. Based on home-based cardiac rehabilitation provided in the VA,112 home-based PR involves an initial in-person evaluation, followed by 11 weekly telephone or video appointments, an in-person evaluation at week 12, and follow-up phone/video calls at 3 and 6 months. A final in-person evaluation occurs at 12 months from the start of the program.112 However, the extent to virtual only rehabilitation and exercise programs are available to Veterans varies by VA. Future research is needed to demonstrate implementation of existing evidence-based PR programs delivered virtually in the VHA as part of routine clinical care.

    Advances in Psychological Functioning

    There is extensive evidence documenting increased inflammatory markers in psychological disorders and, in particular, major depressive disorder. Increases in pro-inflammatory markers including peripheral blood IL-1β, IL-6, Tumor Necrosis Factor (TNF) and C-reactive protein (CRP) are well documented.113 Yet, the role of inflammation and shared pathways between depression and COPD remain inconclusive. Limited cross-sectional research on civilians with COPD has found that greater depression symptoms are associated with higher TNF-α and sTNFR after adjusting for possible confounders.114,115 However, one prospective study did not find a significant association between depression and inflammatory markers in individuals with stable COPD.116 Janssen et al116 measured several inflammatory markers (white blood cell, hsCRP, IL6, fibrinogen) in COPD patients at baseline and 36-month follow-up. They classified individuals as having persistent systemic inflammation if they had 2 or more markers elevated in the upper quartile at baseline and follow-up or no inflammation corresponding to no elevation in inflammation at either time point. They found no association between baseline depression scores and inflammation group after adjusting for confounders, and no differences were found either in change in depression scores or mean levels at follow-up between inflammation groups. Nonetheless, given the notable role of inflammation in both COPD and depression, as well as the heterogeneity of both diseases, future research examining the association between inflammation and depression in COPD utilizing prospective designs is needed. Furthermore, reduction in inflammatory markers reflects a meaningful marker of treatment response in COPD100,101 and depression,117 thus it is plausible that targeting both COPD symptoms and depression concurrently could result in greater reduction in inflammatory markers corresponding to treatment response compared standalone therapies that separately target physical functioning and psychological symptoms.

    In order to advance interventions for psychological outcomes in COPD, it is critical that researchers begin dually targeting both physical functioning and psychological outcomes. For example, past research with patients with diabetes and HF found that combining a physical intervention (ie, exercise) with psychotherapy (ie, CBT) produced superior outcomes in both functioning and mental health symptoms.118,119 Yet, up to this point, two independent bodies of literature have focused on separately addressing physical functioning via pulmonary rehabilitation and exercise, and mental health through psychotherapy/behavioral interventions. One funded study in the VHA is testing the integration of a pedometer-based walking intervention with CBT in a 12-week virtual intervention with Veterans with COPD, low PA levels, and clinically significant depression and/or anxiety symptoms (NCT04953806). The intervention will target daily step count and self-reported physical disability, as well as depression and anxiety symptoms.

    Future Areas for Clinical Improvement

    While research establishing the efficacy of treatments for COPD has been fruitful, implementation of guideline-based care remains fraught with health-care inequities. Women Veterans hospitalized for COPD are less likely to have received inhaler therapies prior to admission compared to men.43 In addition, women are less likely during the course of a COPD hospitalization to receive appropriate inhaler combinations and more likely to receive inappropriate inhaler combinations.43 Moreover, women, racial and ethnic minorities, and individuals with drug and alcohol use disorders are less likely to have pulmonary function tests performed, possibly leading to delays in diagnosis and under-treatment.120 In considering optimizing outcomes, it is imperative to consider and equally target health-care inequities that serve as barriers to guideline-based care. Similarly, enhanced recruitment of underserved groups (ie, lower socioeconomic status, racial and ethnic minorities) in COPD research studies is needed. Research and quality improvement projects are important to examine system and individual-level approaches to ensure equity in guideline-based care for all Veterans with COPD. Funding for COPD research that include focus on minority healthcare is needed.


    The coming decade will see an increase in COPD prevalence in US Veterans as Vietnam era Veterans fully reach older adulthood and Iraq and Afghanistan conflict Veterans enter midlife. A multi-pronged agenda targeting system-level factors that increase access and improve care delivery, as well as bench and clinical research will be needed to advance our understanding, treatment, and management of COPD in Veterans. Partnerships with all stakeholders including patients, university-affiliated hospitals, industry, and the international research community will be critical to accelerate the development and implementation of novel treatments to improve physiological, physical, and psychological health outcomes for this heterogenous disease.


    This work was supported, in part, by the following grants from the US Department of Veterans Affairs Rehabilitation Research and Development Service: Merit Award I01 RX001150 (M.L.M.); Career Development Award-2 (CDA2) Award 1IK2RX003527-01A2 (P.M.B.); and CDA2 Award IK2RX002165 (E.S.W.).


    The authors report no conflicts of interest in this work.


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    Persistent pulmonary hypertension of the newborn is a serious disorder that occurs when a baby fails to adapt to the circulatory transition as they breathe through their lungs after birth.

    Circulatory adaptation occurs minutes after birth as the baby transitions from receiving oxygen from the placenta through the umbilical cord to breathing independently.

    When this does not happen, the blood flow from the heart to the lungs becomes insufficient. In turn, not enough oxygen reaches the bloodstream to supply the brain and the rest of the body.

    This article discusses pulmonary hypertension in newborns, its signs and symptoms, risks, and complications.

    Persistent pulmonary hypertension of the newborn (PPHN) occurs when conditions like low oxygen levels or breathing problems prevent natural circulatory changes.

    During pregnancy, babies get their oxygen from the placenta, an organ in the womb supplying oxygen and nutrients from the mother’s blood to the baby through the umbilical cord.

    Upon taking their first breath, the blood vessels of the newborn’s lungs widen or dilate. This dilation should cause a rapid increase in blood flow to the lungs, closing the fetal pathway and causing circulation changes. This process causes blood to travel through the lungs to get oxygen before it flows to the rest of the body.

    In PPHN, pulmonary arteries do not widen enough, limiting the blood flow to the lungs and causing the pressure in the lungs’ blood vessels to build up. This condition also results in the persistence of the old blood pathway where blood flows from the right to the left atrium, which bypasses the lungs.

    How common is it?

    PPHN happens in 2 in every 1,000 live births. It occurs more in full-term babies, those born past their due dates, and those born after 42 weeks. Doctors are also diagnosing PPHH increasingly more in premature babies.

    Despite advances in care, it is still one of the leading causes of morbidity and death among babies, reaching a 4–33% mortality rate.

    Doctors can identify symptoms of PHNN at birth or within the first hours of birth. These include:

    • rapid breathing and shortness of breath
    • respiratory distress, including nose-flaring, grunting, or moaning
    • retractions or pulling in of the skin under the ribs when breathing hard and fast
    • cyanosis or pale blue color of the skin, lips, skin, hands, and feet
    • low blood oxygen levels, even when doctors provide 100% oxygen
    • hands and feet are cool to the touch
    • low blood pressure
    • low APGAR scores
    • heart murmur, or the presence of an extra or an abnormal heartbeat
    • weak pulses

    Meanwhile, 1 in 4 babies who survive will have some impairment because of PPHN.

    Lack of oxygen to the brain may cause long-term health problems, including:

    • developmental delays
    • hearing problems such as deafness
    • functional disabilities, or decreased ability to perform physical activities

    PPHN occurs when the blood vessels in the lungs fail to dilate. Conditions that prevent the vessels from dilating include:

    Risk factors

    Babies are at a higher risk of PPHN if they have:

    A pediatrician will check for the baby’s health status and delivery history. They will then do the following tests to determine if the newborn has PPHN:

    • Monitoring oxygen saturation levels: This measures the oxygen saturation level in different body parts to see whether the newborn’s tissues are receiving enough oxygen.
    • Echocardiogram: This test sends sound waves to generate an image of the heart and blood vessels. It is the most reliable test to establish a diagnosis of PPHN and look for structural heart diseases.
    • X-ray: Checks for underlying lung or heart disease, including meconium aspiration syndrome and pneumonia. It also identifies whether the heart is too large.
    • Blood tests:
      • glucose and serum electrolyte levels

    The treatment of PPHN depends on the underlying cause, severity, symptoms, and general health. The main goals of treatment are to:

    • increase the oxygen levels in the newborn’s blood
    • maintain appropriate blood pressure
    • open the blood vessels in the lungs to improve blood flow

    Respiratory support

    Doctors will supply newborns with oxygen through various means:

    • Supplemental oxygen: Medical professionals send oxygen through a small tube with prongs placed in the nostrils, a plastic hood, or a mask.
    • Endotracheal tube: Doctors place a tube through the windpipe, known as the trachea, to provide oxygen.
    • Ventilator or mechanical breathing machine: A breathing tube connected to a ventilator passes through the windpipe. The machine breathes for the newborn until they can do it by themselves.
    • Continuous positive air pressure: This is a noninvasive machine that gently delivers oxygen into the lungs
    • High-frequency oscillation ventilation: This machine rapidly delivers very short bursts of oxygen through a breathing tube. This machine aims to improve oxygen levels when others are not effective.

    Nitric oxide

    Nitric oxide is the only drug approved for widening or dilating the pulmonary blood vessels used specifically for the treatment of PPHN. Doctors administer nitric oxide through the breathing machine to reach the lungs directly.


    Different medications can help treat PPHN, depending on the underlying cause and related symptoms. Doctors usually administer these medications through an IV line directly into the vein. These may include:

    • Blood pressure medication: These keep the newborn’s blood pressure stable.
    • Sedatives: These drugs help keep the baby calm and help the machines that give them oxygen work better.
    • Surfactants: Surfactants help the lungs work better, allowing them to use oxygen and remove carbon dioxide. Doctors give these through a breathing tube to premature infants and full-term babies with parenchymal lung disease.
    • Antibiotics: Doctors prescribe these to treat infections.
    • Inotropes: These medicines go directly into the bloodstream to keep the newborn’s blood pressure high, inducing the heart to pump more blood into the lungs.

    Supportive care

    Doctors will also check the following for a newborn:

    • maintain body temperature
    • check glucose and electrolyte levels
    • correct metabolic imbalances and blood abnormalities
    • provide nutritional support
    • assess blood pressure
    • monitor oxygen levels

    Extracorporeal membrane oxygenation (ECMO)

    Doctors use ECMO when all the other approaches fail to increase the newborn’s oxygen saturation levels. It takes over the functions of the lungs and the heart.

    They drain blood from the newborn into an artificial lung, which places oxygen and removes carbon dioxide from the newborn’s blood. Doctors then pump the blood back to the newborn.

    PPHN is a severe condition. It occurs when the newborn fails to transition from fetal circulation to the expected circulation, which involves the heart pumping blood to the lungs.

    Different factors may cause this, but it often occurs in babies with a difficult birth and full-term and babies born past their due dates.

    The goal of treatment is to increase the oxygen levels in the blood. Long-term health problems and complications can occur if the baby does not get enough oxygen delivered to the brain and other organs.

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    A pulmonary embolism (PE) happens when a blood clot disrupts blood flow in your lungs. While its exact prevalence is unknown, studies estimate that PE impacts 39 to 115 per 100,000 people each year.

    Pulmonary embolisms are categorized based on risk. A submassive PE is at an intermediate risk level.

    It’s difficult to define exactly what a submassive PE is because doctors must consider many factors when assessing risk. Groups like the American Heart Association, American College of Chest Physicians, and European Society of Cardiology all have different definitions and guidelines.

    Below, we’ll detail submassive (intermediate risk) PEs, what causes them, and how doctors diagnose and treat them.

    A submassive PE is an intermediate risk type of PE. Let’s explore what that means.

    Hemodynamic stability

    A submassive PE is hemodynamically stable. This means that a person’s heart rate and blood pressure remain steady.

    More severe PEs are characterized by hemodynamic instability. In those situations, a person’s heartbeat can be irregular, and their blood pressure decreases.

    Right ventricular dysfunction

    Another feature of submassive PE is right ventricular dysfunction (RVD). The right ventricle is the chamber of the heart that sends blood with low oxygen into the lungs to receive fresh oxygen.

    While the right ventricle can accommodate large amounts of blood, it’s not built to deal with high levels of pressure. When a PE disrupts blood flow in the lungs, it can lead to an increase in pressure.

    When this happens, the right ventricle has to work harder to pump blood into the lungs. This can lead to the right ventricle not functioning as it should, causing serious problems for the heart and its ability to pump blood.

    High troponins

    Elevated troponin levels are another potential finding in submassive PE. Troponins are proteins that are released when damage to the heart has occurred.

    Comparison chart

    The table below compares the characteristics of each type of PE.

    *According to the American Heart Association’s definition, in addition to being hemodynamically stable, a submassive PE has either RVD or high troponin levels. It’s also possible for both of these findings to be present.

    A PE happens when a blood clot disrupts blood flow in your lungs. Clots typically form in response to an injury, although other risk factors play an important role.

    Most PEs develop from a blood clot that forms in the deep veins, typically in the leg. In some cases, part of this clot can break off and travel to the lungs, where it ends up blocking an artery.

    The symptoms of a submassive PE may include:

    Seek emergency care

    All PEs are medical emergencies that require prompt treatment. Call emergency services or go to the emergency room if you have unexplained shortness of breath or sudden chest pain.

    In addition to getting your medical history and doing a physical examination, your doctor can use the following tests to help make a diagnosis of submassive PE:

    • Chest X-ray. Your doctor may initially take a chest X-ray to look at your heart and lungs to see if there are any obvious explanations for your symptoms. However, with PE, most chest X-rays appear typical.
    • Electrocardiogram (EKG). An EKG measures the electrical activity in your heart. Certain EKG changes can show how much strain a PE is putting on your heart. It can also help your doctor rule out other conditions that can cause chest pain.
    • D-dimer test. The D-dimer test looks for a protein that’s made when a blood clot dissolves in your body. High levels can indicate a problem with blood clots.
    • Troponin test. The troponin test looks for increased troponin levels in a sample of blood.
    • Arterial blood gas (ABG). The ABG test uses a blood sample from an artery. It measures oxygen and carbon dioxide levels in the blood to give your doctor an idea of how well your lungs are working.
    • CT angiography. CT angiography uses a special dye and CT scan technology to generate pictures of the blood vessels in your chest. This can help your doctor see if a blood clot is present.
    • Ventilation-perfusion (VQ) scan. A VQ scan uses radioactive material to assess both the airflow and blood flow in your lungs.
    • Echocardiogram. An echocardiogram uses ultrasound technology to visualize the chambers of your heart. Your doctor can use it to check for signs of RVD.

    There are a few different treatment options available for submassive PE. The type of treatment you receive can depend on the severity of your PE.

    PE severity is usually estimated using the Pulmonary Embolism Severity Index (PESI). This is a points-based system in which a higher score suggests a higher PE severity and less favorable outlook. It takes the following factors into account:

    Now let’s look at treatment options for submassive PE.


    One of the main treatments for submassive PE is anticoagulant therapy. Anticoagulant drugs are also called blood thinners.

    These drugs interfere with proteins that are important for clotting. Heparin is an example of an anticoagulant drug that doctors may use to treat submassive PE.

    Systemic thrombolytic therapy

    Another potential treatment option is systemic thrombolytic therapy. Thrombolytic drugs work to dissolve clots quickly. However, their use with submassive PE is controversial, according to a 2019 consensus paper.

    A 2014 study investigated systemic thrombolytic therapy in submassive PE. Overall, it found that while systemic thrombolytic therapy helped keep participants’ conditions from worsening, it also increased the risk of serious bleeding and stroke.

    As such, a doctor must carefully weigh the risks and benefits of systemic thrombolytic therapy for submassive PE.

    Generally, doctors may consider low dose thrombolytic therapy for people with submassive PE who are at low risk of bleeding and whose condition is worsening.

    Catheter-directed thrombolysis

    A catheter is a thin, flexible tube inserted into blood vessels. In catheter-directed thrombolysis, doctors use a catheter to deliver low doses of thrombolytic drugs at the location of the PE.


    An embolectomy involves removing the blood clot from the body. Doctors can do this either using a catheter or through a surgical procedure.

    In addition to being a life threatening condition, submassive PE can lead to a variety of complications:

    • Repeat events. If you’ve had a PE, you may be at risk of another serious blood clot event. In fact, 1 in 3 people with PE or deep vein thrombosis (DVT) has a repeat event within the next 10 years.
    • Post-PE syndrome. Post-PE syndrome refers to persistent symptoms like shortness of breath, difficulty exercising, and reduced quality of life after PE.
    • Pulmonary hypertension. Your pulmonary arteries lead from your heart to your lungs. Pulmonary hypertension is when the blood pressure in your pulmonary arteries is too high. It can lead to heart failure.
    • Chronic thromboembolic pulmonary hypertension (CTEPH). CTEPH is a specific type of pulmonary hypertension. It happens when the blood pressure in your pulmonary arteries is too high due to the presence of blood clots.

    As you recover from a submassive PE, your doctor will want to regularly monitor your condition. This can help prevent a repeat event and detect and address other complications, like pulmonary hypertension.

    The overall mortality rate for PE can be up to 30 percent if it’s left untreated. However, with timely medical treatment, the mortality rate drops to 8 percent. The exact mortality rate for submassive PE is still unclear.

    A 2016 study divided people with PE into four risk categories:

    • high
    • intermediate-high
    • intermediate-low
    • low

    The researchers found that the mortality rate for intermediate-high and intermediate-low PE was 7.7 and 6.0 percent, respectively.

    Both RVD and troponin levels can contribute to the outlook for submassive PE. Worsening RVD, high troponin levels, or both generally point toward a less favorable outlook.

    Studies have also looked into the rate of complications after a submassive PE. For example, a 2017 study looked at the long-term outlook in people with submassive PE treated with systemic thrombolytic therapy.

    The researchers found that 36 percent of the participants had persistent symptoms like shortness of breath. CTEPH was also seen, but only in 2.1 percent of participants.

    Several things can increase your risk of PE. These include:

    Remember that having risk factors for submassive PE doesn’t mean that you’ll experience one in the future. It just means that you’re at an increased risk compared with people without any risk factors.

    There are things you can do to help lower your risk of experiencing a PE:

    • Move around. Try to avoid being immobile for long periods of time. For example:
      • Be as active as is appropriate following a period of bed rest, such as after an injury, surgery, or illness.
      • Stop and walk around every couple of hours when you’re on a long trip.
      • If you’re sitting for a long period of time and cannot get up, exercise your legs by tightening and relaxing your leg muscles or raising and lowering your heels off the floor.
    • Make health-promoting lifestyle choices. Aiming to live a balanced lifestyle can reduce your risk of blood clots and other health conditions. Try to:
      • Eat a balanced, nutritious diet.
      • Reduce your stress levels, when possible.
      • Get enough sleep each night.
      • Quit smoking, if you smoke.
    • Manage other health conditions. If you have health conditions, such as obesity or heart disease, that increase your risk of blood clots, make sure you’re taking steps to manage them.
    • Ask a doctor about preventive measures. If you’re at a higher risk of blood clots, talk with a doctor about preventive options like compression stockings or blood-thinning medications.

    A submassive PE is an intermediate risk PE. People with this type of PE have stable blood pressure and heart rate but have RVD, high troponin levels, or both.

    Any type of PE is a medical emergency, and outlook greatly improves with timely treatment. Seek care immediately if you have unexplained shortness of breath or chest pain that comes on suddenly.

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