The Detroit Pistons, and Ausar Thompson, received a shock this week when the rookie forward was diagnosed with a season-ending blood clot on Wednesday. 

The 2023 No. 5 overall pick had already missed five games prior to the announcement with what was initially characterized as “asthma.” Despite the gravity of the diagnosis, Thompson has already been cleared for conditioning work and is expected to return to non-contact basketball activities after the season’s conclusion on April 14. 

The Free Press spoke with Dr. Geoffrey Barnes, cardiologist and vascular medicine specialist at the University of Michigan Health Frankel Cardiovascular Center, about blood clots and how they impact professional athletes. Barnes is not involved in Thompson’s medical care, and the Pistons didn’t provide details on the exact nature of his clot. 

Most commonly, a blood clot diagnosis references a clot in the veins of the legs (a deep vein thrombosis, or DVT), or a blood clot that has broken free from the veins, traveled up through the body and lodged itself into the lungs (a pulmonary embolism, or PE). 

HIGH HOPES: Why Pistons are optimistic after Ausar Thompson's scary blood clot diagnosis

The former is often accompanied with pain or swelling in one leg. Pulmonary embolisms impact the upper body — chest discomfort, shortness of breath, a sped-up heartbeat and potential lightheadedness and dizziness if it becomes more severe. 

“That’s usually what people mean when they say ‘Oh, they have blood clots,’" Barnes said. “It’s something in the vein system, starts in the legs, can break free and travel to the lungs. It’s incredibly common, over a million people every year in America get these. 

“They tend to happen most commonly in folks as they age, so it’s much more common in people over the age of 60 or 65 than in younger folks. They can happen for a wide range of reasons. But oftentimes they just come out of the blue and we can never figure out exactly why somebody developed their blood clot.” 

The severity of the symptoms, coupled with diagnostic testing, allows doctors to determine the severity of the clot, Barnes said. A small clot in the leg may be accompanied by mild swelling and soreness, and can be treated with blood thinners without the need for a hospital stay. 

On the extreme end, a large clot lodged into the lung could block blood flow and strain the heart — leading to a quickened heart rate and fast breathing due to a lack of oxygen. 

“That’s when people are in the hospital, we often have to do surgery or procedure to try and remove the blood clot and figure out ways to really support them through it,” he said. “It’s a really wide-ranging condition. Thankfully, the vast majority of people do very well and have more minor blood clots, the forms in the legs or a small one in the lungs that aren’t life-threatening.”

Outcomes have varied for NBA players recently diagnosed with blood clots. The most notable example is Hall of Famer Chris Bosh, whose career was ended prematurely by clots. He was ruled out for the remainder of the 2014-15 season in late February after a clot was discovered in one of his lungs. 

Bosh, a two-time NBA champ with the Miami Heat, reportedly felt pain in his back and side for several days before getting his symptoms checked out. He returned for Miami’s season opener in 2015-16, but a blood clot in his leg shut him down for the final time the following February. The NBA eventually ruled continued clotting issues were a career-ending illness. 

Other players, such as New Orleans Pelicans forward Brandon Ingram, have been able to resume their careers without further issues. 

The good news, Barnes said, is that most professional athletes are low-risk due to their age. But there are factors, such as dehydration and longer-distance flights, that can increase the risk for athletes.

The main treatment for everyone who has a clot, regardless of athletic status, is to be put on a blood thinner. The medicine prevents new clots from forming, but also comes with an increased risk for bleeding. It’s often why athletes can’t play while they’re on thinners, he said. 

When athletes develop PEs, they work with doctors to make sure their heart and lungs sufficiently heal afterward. Symptoms such as chest discomfort and lightheadedness while walking are tracked. Physical activity can ramp up from there, starting with climbing stairs or going for a bike ride or jog. For DVTs, doctors check to see if pain and swelling have resolved. 

With that, athletes also go through cardiopulmonary exercise testing that allows them to measure heart and lung function. Recovery is quick for some — weeks to a couple of months. But it can take six months or more in extreme cases. In the worst cases, long term or permanent damage can prevent athletes from getting back to their prior status. It largely has to do with the size of the clot. 

Once a first clot happens, the risk of having a second one increases, Barnes said. But with minimized risk factors, many people are able to live the rest of their lives without a second complication. 

“The highest-risk people maybe have a genetic disorder that puts them at risk for blood clots,” he said. “Maybe they have cancer or another condition. Those are people who I get really concerned about. Some people have one blood clot and never have anything again the rest of their life, and don’t have other significant risk factors. 

“As you think about an athlete, it really depends on what kind of athlete and what kinds of activities that they’re doing. You could imagine that maybe a golfer or a billiard player, somebody who is a high-level athlete but doesn’t necessarily have that same level of cardiovascular strain might not be at quite as high a risk as somebody who, say, is a soccer player who’s having to run 10 miles every game and is having issues with dehydration and is flying all over the world. It depends on the situation for each athlete.”

Contact Omari Sankofa II at [email protected]. Follow him @omarisankofa.



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Introduction

The coronavirus disease of 2019 (COVID-19) is defined as an illness caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Most people infected with the virus will experience mild to moderate respiratory symptoms and recover without needing treatment.1 Fever, sore throat, cough, shortness of breath, diarrhoea, and widespread weariness are the most prevalent symptoms. Acute respiratory distress syndrome, myocarditis, heart failure, renal failure, and recurrent pulmonary embolism are all complications of COVID-19.2

The most frequent neurological symptoms of COVID-19 infection are anosmia, ageusia, and headache. However, case series and observational studies show data on a large number of patients who develop cerebrovascular accidents (CVD), Guillain-Barré syndrome (G.B.S.), de novo status epilepticus and encephalopathy.3 In clinical terms, lower motor neuron lesion facial palsy is called Bell’s palsy. Bell’s palsy is usually idiopathic unilateral, acute weakness of the face and may be partial or complete, occurring with equal frequency on either side of the face.4 Additionally, tumours, trauma, infection, autoimmune illnesses, vasculitis, pregnancy and medicines can also cause Bell’s palsy.

After the COVID-19 pandemic, there was a documented link between COVID-19 and Bell’s palsy.5 Although, there was no clear explanation at the time; possible explanations include it could be caused by the direct action of the virus, an autoimmune response, or the recurrence of a coexisting herpes zoster infection.5 Additionally, in numerous countries, including the United States, a relationship between COVID-19 vaccines and lower motor neuron lesion facial palsy has been observed, although the causative link has yet to be proven.6 Although the precise mechanism of the neurological difficulties induced by COVID-19 vaccines is unknown, numerous theories have been proposed to classify these neurological disorders, including vascular, immunological, infectious, and functional causes.7

Cases’ Presentation

Case 1

A 65-year-old Sudanese woman was admitted to Omdurman Teaching Hospital with a high-grade fever and dry irritating cough. Clinical examination indicated a feverish patient with a pulse rate of 100 beats per minute and blood pressure of 100/70 mm Hg. Apart from the previous findings, clinical examination of the respiratory, cardiovascular, neurological and abdominal systems were normal. Her COVID-19 real-time polymerase chain reaction (RT-PCR) test was positive.

Three days after admission she complained of incomplete left eye closure and right-sided mouth deviation. A lower motor neuron injury affecting the facial nerve was discovered during cranial nerves and higher functions examination (facial nerve palsy). (Figure 1) Other cranial nerves were found to be normal. She did not experience skin eruptions, parotid enlargement, or tongue fissures. Upper and lower limb examinations were performed and found to be normal. She has no truncal or neck weakness and no area of hypoesthesia. Complete blood count (C.B.C), blood urea, serum creatinine, chest X-ray, and CT-brain were among the tests performed. All the tests were within normal limits. Following her COVID-19 infection, a diagnosis of Bell’s palsy was made. She was treated with prednisolone 60 mg daily for five days, then reduced by 10 mg daily. After ten days of corticosteroids, she exhibited significant improvement. No antiviral therapy nor physiotherapy was used for her condition.

Figure 1 An incomplete left eye closure and a right-sided mouth deviation (Bell’s palsy) following COVID-19 infection.

Case 2

A 45-year-old Sudanese man with no history of diabetes or hypertension presented to our private neurology clinic with an inability to close his right eye. On neurological examination, facial paralysis on the right side and a leftward displacement of the mouth were found. (Figure 2) All other neurological studies were within the normal range (muscle tone, reflexes).

Figure 2 Facial paralysis on the right side, inability to close the right eye and leftward displacement of the mouth following AstraZeneca vaccine administration.

The findings appeared three days after receiving the AZD1222 Vaxzervria (AstraZeneca) COVID-19 vaccination. Facial damage, ear pain and ear skin eruption did not precede the paralysis. His sense of taste was intact, and no transitory neurological symptoms preceded the event he described. He appeared ill, pale, and anxious during the assessment. His pulse rate was 87 beats per minute and his blood pressure was 130/75 mm Hg. There were no abnormalities found on systemic evaluation. He was diagnosed with a right-sided lower motor neuron lesion of the seventh cranial nerve, and the abnormalities were confined to the peripheral nervous system. Blood urea, serum creatinine, urine analysis, and a brain MRI were all performed and the results came back normal. Due to the absence of any apparent symptoms or signs that could specify the cause, a diagnosis of right-sided lower motor neuron lesion facial nerve palsy caused by the COVID-19 AZD1222 Vaxzervria (AstraZeneca) vaccine was made. He was treated with prednisolone 60 mg daily for five days, then reduced by 10 mg daily. After ten days of corticosteroids, he exhibited significant improvement. No antiviral therapy nor physiotherapy was used for his condition.

Discussion

COVID-19 is predominantly a respiratory illness, but it can cause multiple neurological symptoms such as headache, Guillain-Barre syndrome, transverse myelitis, epilepsy, and cranial nerve palsies.8 Bell’s palsy is an idiopathic, acute peripheral-nerve palsy involving the facial nerve, which supplies all the muscles of facial expression. The annual incidence of Bell’s palsy is 15 to 30 per 100,000 persons, with equal numbers of men and women affected. There is no preference for either side of the face. Bell’s palsy has been described in patients of all ages, with a peak incidence in the 40s.9

In this report, we documented two cases of Bell’s palsy, one after exposure to COVID-19 infection and the other after administration of COVID-19 AZD1222 Vaxzervria (AstraZeneca) Vaccine. Bell’s palsy is usually idiopathic; however, hypertension, diabetes, obesity, pregnancy, preeclampsia, trauma, tumours, infections, autoimmune illnesses and vasculitis have all been linked. According to the Clinical Practice Guidelines, which have identified Bell’s palsy as a diagnosis of exclusion, we considered all related causes of Bell’s palsy in our report.10 Other possible causes of Bell’s palsy such as trauma, malignancy, congenital causes, post-surgical and infectious etiologies were all negative after clinical evaluation. Thus, the diagnosis of Bell’s palsy for our two cases due to COVID-19 infection and COVID-19 AZD1222 Vaxzervria (AstraZeneca) vaccine was confirmed. The aetiology of Bell’s palsy following exposure to COVID-19 infection or vaccination requires further analysis, but it could be due to direct facial nerve inflammation and nerve compression inside the facial nerve canal. Another observed cause was immune-mediated damage to the facial nerve.7 Bell’s palsy is a severe unusual side effect of messenger R.N.A. (mRNA) COVID-19 vaccines. It is believed to be immune-mediated possibly via vaccine antigens mimicking host molecules or by activating autoreactive dormant T-cells, with a prevalence after mRNA-1273 (Moderna) vaccine not higher than the standard viral immunizations.11 According to a study by Wan et al in Hong Kong on the relationship between Bell’s palsy and the mRNA-based BNT162 b2 vaccine, patients who received the COVID-19 vaccine have a higher risk of getting Bell’s palsy than those who were not vaccinated.5 According to the US Food and Drug Administration and the UK Medicine and Healthcare Regulatory Agency, the observed prevalence of Bell’s palsy among vaccinated persons was no more significant than the expected background rate.12

Most of Bell’s palsy cases improved independently over time. Clinically important improvement occurs within 3 weeks in 85% of people and 3 to 5 months in the remaining 15%; however, some cases remain with residual facial weakness.4 Both patients in this report showed significant improvement after 10-day courses of corticosteroids.

Conclusion

COVID-19 infections have various clinical presentations including Bell’s palsy, a relatively rare symptom following COVID-19 infection as well as vaccination. This case report presented 2 cases of Bell’s palsy following COVID-19 infection and Vaccination. Nevertheless, the benefits of immunization outweigh the low reported incidence of similar vaccine’s adverse effects.

Data Sharing Statement

The data used in this report is available from the corresponding author upon reasonable request.

Consent for Publication

Both patients provided written informed consent for their case details and images to be published.

No institutional approval was required to publish this case report.

Acknowledgment

We acknowledge that this manuscript was released as a preprint in Authorea under the DOI: doi.org/10.22541/au.164787778.85729887/v1.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

The authors themselves funded the study, and no funds were granted.

Disclosure

The authors declare that there is no conflict of interest in this work.

References

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    The National Blood Clot Alliance Volunteer President Leslie Lake called upon Congress to protect the American public from blood clots by supporting the bipartisan Charles Rochester Blood Clot Prevention and Treatment Act (HR 5699) during a press conference hosted by Rep. Lisa Blunt Rochester (D-Del.) Wednesday.

    “As the nation’s leading patient advocacy organization focused on the prevention, early diagnosis, and treatment of life-threatening blood clots, NBCA unequivocally supports the passage of the Charles Rochester Blood Clot Prevention and Treatment Act and we urge Congress to do the same,” Lake said.

    Named after Blunt Rochester’s husband, Charles, who died of a pulmonary embolism in 2014, the Charles Rochester Blood Clot Prevention and Treatment Act’s goals are to raise awareness, establish an advisory committee, and enhance data collection around blood clots. Blunt Rochester introduced the bill in September 2023.

    To align with her work on the bill, Blunt Rochester on Wednesday unveiled a comprehensive toolkit, “Blood Clot Awareness Action, and Advocacy: The Toolkit,” containing information on blood clots, Blunt Rochester’s bipartisan work in Congress to spread awareness of blood clots, and ways the public can advocate for themselves and others at the doctor’s office.

    “This toolkit is intended to help individuals recognize the signs and symptoms of blood clots and inspire action and advocacy,” she said. “Blood clots are treatable when caught, but too often there is a lack of information on how to properly get treatment – this is especially true for patients of color, seniors, and cancer survivors. I will continue my bipartisan efforts in Congress to get the Charles Rochester Blood Clot Prevention and Treatment Act over the finish line so we can strengthen awareness on this issue and save lives.”

    Paul Tonko (D-NY), a co-sponsor of the Charles Rochester Blood Clot Prevention and Treatment Act, said he became aware of the danger of blood clots from the family of Jennifer Luft, a constituent who died in 2022 due to a blood clot being misdiagnosed.

    “These deadly but preventable blood clots take lives every day, but raising awareness about the signs can make all the difference,” Tonko said. “I’m proud to join my friend and colleague, Congresswoman Blunt Rochester, in supporting this legislation that honors the memory of her late husband and will save lives.”

    Dr. Deron Burton, director of the Division of Blood Disorders and Public Health Genomics, Centers for Disease Control and Prevention (CDC), pointed out that blood clots can affect anyone, but they are preventable and can be treated if discovered early.

    “It’s important that Americans know how to protect themselves from blood clots, and how to recognize the signs and symptoms of blood clots so they know when to seek care,” Burton said.

    The toolkit is available here.



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    As an attending physician in Ottawa, I often treat women who are recently diagnosed with a blood clot. My female patients are of all ages — from young women to the elderly — but they often have one thing in common: They never expected to get a blood clot.

    Indeed, many female patients have no idea about the possible risk factors they face as women. While blood clots affect up to 900,000 people each year in the United States, women face unique risk factors, in particular if they use estrogen-containing oral contraceptives, are pregnant, or are in the period up to three months postpartum, according to the Centers for Disease Control and Prevention (CDC).

    In recognition of Blood Clot Awareness Month throughout March, we should take time to understand women’s blood clot risks, signs, symptoms and prevention strategies.

    Risks of Estrogen-Containing Birth Control

    Several factors increase a woman's risk of developing blood clots. Estrogen-containing combined hormonal oral contraceptives (birth control) can elevate the chance of a blood clot, which affects about 10 in 10,000 individuals on estrogen-containing birth control per year, per the CDC.



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    Medical life-saving techniques include mechanical ventilation. During the COVID-19 epidemic, the lack of inexpensive, precise, and accessible mechanical ventilation equipment was the biggest challenge. The global need exploded, especially in developing nations. Global researchers and engineers are developing inexpensive, portable medical ventilators. A simpler mechanical ventilator system with a realistic lungs model is simulated in this work. A systematic ventilation study is done using the dynamic simulation of the model. Simulation findings of various medical disorders are compared to standard data. The maximum lung pressure (Pmax) was 15.78 cmH2O for healthy lungs, 17.72 for cardiogenic pulmonary edema, 16.05 for pneumonia, 19.74 for acute respiratory distress syndrome (ARDS), 17.1 for AECOPD, 19.64 for asthma, and 15.09 for acute intracranial illnesses and head traumas. All were below 30 cmH2O, the average maximum pressure. The computed maximum tidal volume (TDVmax) is 0.5849 l, substantially lower than that of the healthy lungs (0.700 l). The pneumonia measurement was 0.4256 l, substantially lower than the typical 0.798 l. TDVmax was 0.3333 l for ARDS, lower than the usual 0.497 l. The computed TDVmax for AECOPD was 0.6084 l, lower than the normal 0.700 l. Asthma had a TDVmax of 0.4729 l, lower than the typical 0.798 l. In individuals with acute cerebral diseases and head traumas, TDVmax is 0.3511 l, lower than the typical 0.700 l. The results show the viability of the model as it performs accurately to the presented medical condition parameters. Further clinical trials are needed to assess the safety and reliability of the simulation model.

    Patients who are diagnosed with COVID-19 suffer from a major drop in blood oxygen saturation and face difficulty breathing. Mechanical ventilation is a crucial procedure for providing respiratory support to individuals facing inconveniences in breathing by assisting the breathing or controlling the respiration.1 In severe COVID-19 individuals, thromboembolic consequences, such as deep venous thrombosis, pulmonary embolism (PE), and acute mesenteric ischemia (AMI), have been observed. Lung illness can cause respiratory failure in many ways. Depending on immunity, COVID-19 might induce mild to severe breathing issues. The virus enters the human body through the nose, mouth, and eyes. COVID-19 causes bilateral pneumonia. Fluid in the lungs limits oxygen intake and causes shortness of breath, which can lead to acute respiratory distress syndrome (ARDS) and sepsis. Mechanical ventilation can help with breathing problems.2 

    Modern hospital ventilators are highly functional and technologically advanced, but in resource-limited health systems, they are very expensive.3 Severe Acute Respiratory Syndrome (SARS) caused by microcirculation thrombotic events promotes severe hypoxemia and multiple-organ dysfunction in patients with this disease.4 Mechanical ventilators are life support devices for patients in intensive care units (ICUs) who need assistance with ventilation diseases, trauma, congenital malformations, drug interactions, or surgical emergencies. However, the current need for respiratory mechanical ventilation due to COVID-19 outweighs the ability of health systems worldwide to obtain and deliver mechanical ventilators.5 

    Mechanical ventilation through modern mechanical ventilators is carried out in different modes. Modes of mechanical ventilation are widely discussed in Refs. 6 and 7. The present study is mainly focused on controlled modes, which can be divided into VCV (volume-controlled ventilation) and PCV (pressure-controlled ventilation). The most important advantage of minute-based ventilation is that it keeps the waveforms stable. VCV mode requires setting tidal volume, minute respiratory rate, inspiration-to-expiration (I/E) ratio, positive end-expiratory pressure (PEEP), and FiO2. PCV mode requires setting PiO2, minute respiratory rate, I/E ratio, PEEP, and FiO2. A VCV breath is a tidal volume delivered to the lungs. After a set tidal volume, the ventilator cycles. Flow rate determines inspiratory time. Lung pressures—peak inspiratory pressures (PIPs) and end-inspiratory alveolar pressures—depend on respiratory system resistance, compliance, and tidal volume. Controlling tidal volume and minute ventilation is the main benefit of VC, but in cases of impaired respiratory system compliance, it may cause dangerously high airway pressures and barotrauma. PCV uses airway pressure to expand the lungs for a set time. The clinician sets the inspiratory pressure, while dynamic lung compliance and airway resistance determine the delivered tidal volume and flow rate. After an inspiratory time, the ventilator stops delivering pressure. Controlling lung pressure prevents barotrauma. In intubated patients with high respiratory drive, PCV may improve ventilator synchrony because inspiratory flow is not fixed. PCV’s inability to guarantee or limit tidal volume due to acute lung compliance changes is a major drawback.8 

    In this uncertain situation, many researchers and engineers are actively participating to design a ventilator that can be produced by any suitable manufacturing facility. A plastic air tank, two wooden or plastic circles, a bendable wire, two check valves, a DC motor, and a guide cylinder were used in El Majid et al.’s9 design. The motor bends the wire and pulls the bottom circle up, squeezing the tank’s air. Through the check valve, the compressed air enters pipes. This is the inspiration stage of breathing. Since the patient’s lungs have a higher pressure than the air tank, the device will draw air from them. This is the expiration state. Low-cost embedded boards, such as Arduinos or ESP32s, will control the components. Although still in development, this concept offers a promising and affordable alternative to mechanical ventilation.

    The RapidVent group and Northwell Health have figured out a way to transform a non-invasive BiPAP machine into an invasive ventilator for COVID patients.10 The researchers also invented a low-cost Brazilian emergency mechanical ventilator called 10D-EMV.11 The simulation model in this study was inspired by “Manshema,” a doctor-scientist-developed emergency ventilation machine. The model was based on MathWorks® “Medical Ventilator with Lung Model” and altered to classify the mechanical ventilator design, control method, and autonomously breathing patients. The Manshema Ventilator helps autonomously breathing patients maintain PEEP and blood oxygen saturation.12 A compact mechanical ventilator was created by automating bag-valve-mask (BVM) ventilation. Those projects used cam mechanisms, mechanical arms, and servo motors to move the BVM. Barotrauma from this cheap and easy design may damage the patient’s lungs. Robotic mechanisms squeeze and release the Ambu bag, but they cannot accurately control inspiration pressure.13,14

    Researchers attempted cost savings in similar ways. Modifying the bag-valve-mask (BVM) with a ventilation rate alarm system and comparing it to conventional BVMs maximized minute ventilation volume delivery.15 In a simulation model, Culbreth and Gardenhire examined RT manual ventilation performance. Ninety-eight respiratory therapists were taught to ventilate a BVM manikin for 18 breaths. Therapists with more confidence provided higher peak pressures and flow rates. Thus, BVM ventilation may injure the patient’s lungs, emphasizing the need for an intervention to just provide safe and effective manual ventilation.16 Many emergency mechanical ventilator designs were also proposed based on mechanism, shape, cost, accessibility, novel sensors, and actuators.17–20 Complex ventilator designs were also manufactured by some researchers using 3-D printing technology.21,22

    Guler et al. created a closed-loop intelligent mechanical ventilator using LabVIEW® to monitor and maintain respiratory variables to reduce clinician’s burden. The performance of device was tested with eight female Wistar albino rats using pressure-controlled ventilation.23,24 The present study standardized the mechanical ventilator design using these studies.23,24 To improve student learning, Guler and Ata created an instructional mechanical ventilator set. The training dataset controls inspiration and expiration valves and evaluates pressure sensors.25 Kato et al. studied trait–respiratory variable relationships. They examined silent breathing patterns.26 

    In volume control ventilation, preliminary ventilator configurations involve tidal volume, method of ventilation, plateau pressure, peak inspiratory pressure, and set inspiratory pressure. In pressure control ventilation, input parameters include set respiration rate, actual respirations, PEEP, and FiO2.27 Volume-targeted ventilation and pressure-targeted ventilation are used for patients on volume control and pressure-release volume control.

    A recent article reviewed gas exchange monitoring during artificial ventilation.28 Avoiding volutrauma and barotrauma from uncorrected ventilation is crucial. Thus, flow meters are essential for accurately measuring patient gas exchange volumes. Accurate monitoring of flow rate and volume exchanges is also essential to minimize ventilator-induced lung injury (VILI). Mechanical ventilators use flowmeters to estimate patient gas delivery using the flow signal as input to adjust gas delivery. Flow meters must meet strict static or dynamic criteria because of their importance.29 Thus, mechanical ventilators use linear pneumotachographs, variable and fixed cost orifice meters, hot wire anemometers, and ultrasonic flow meters. Micromachined and fiber optic flow meter research is growing.30 Some studies have shown that flowmeters with high sensitivity, low pneumatic resistance, compact size, bi-directional features, and immunity from electromagnetic interference can give more accurate results and lead to concise choices.31 

    Mechanical ventilation requires many simultaneous operations and is delicate. Proper planning and monitoring of all operating parameters is essential. Mechanical ventilator mismanagement during initial ventilation can also harm patients. Tidal volume, ventilation rate, IE ratio, and PEEP are simultaneously adjusted to manage oxygenation. VILI occurs in 2.9% of artificially ventilated patients and usually causes pneumonia, lifelong lung bruising, and organ failure.32 To decrease VILI risk and ensure arterial oxygen supply and acid–base balance, these ventilator settings must be optimized.33 Mathematical simulation can help us understand organ and organism-level procedures and translate scattered knowledge into medically applicable effective treatments.

    Mechanical ventilation in ARDS patients is risky. A poorly set mechanical breath can worsen ARDS-related lung injury, causing supplementary ventilator-induced lung injury. Mechanical ventilation reduces VILI and ARDS mortality.34 PEEP could be adapted to physiologic variables, usually oxygenation. Dead space, lung stress, lung compliance, and strain; ventilation trends using Computed Tomography (CT) or Electrical impedance tomography (EIT); inflection marks on the pressure/volume curve (P/V); and the expiratory flow curve slope utilizing airway pressure release ventilation (APRV) have, indeed, been tested to personalize PEEP.35 Personalizing PEEP helps ventilator settings match lungs’ pathophysiology. Novel PEEP personalization uses the expiratory flow trend during APRV.36 Expiratory duration adjusts with acute lung injury. Intrinsic PEEP stabilizes the lungs during short expiration.37 

    Guideline-based ventilator weaning reduces ventilator-associated pneumonia (VAP) and ICU length of stay. VAP is usually diagnosed by infection control specialists. Guideline-based weaning lessens mechanical ventilation and VAP risk. Complications drop significantly in wounded and general surgical patients, but ICU length depends on medical system resources. Because of the prolonged respiratory care, ICU discharge of the patient was often delayed. VAP and impromptu reintubation are reduced along with mechanical ventilation use. Injury and general surgery patients benefit the most from the implementation of this procedure.38,39 Mechanical ventilator simulation and mathematical modeling research by Refs. 40–42 was also perceived.

    Using MATLAB®, SimscapeTM, and Simulink® tools, this study attempts to develop a physiological simulation model that describes the allocation of airflow and oxygenation in the lungs of healthy individuals and medically ill patients with ventilation issues. A simple clinical ventilator system with a real-world lungs model and patient–ventilator synchronization is simulated in this study. Mathematical modeling is used to present a system using just a mathematical concept. Computational software packages, such as MATLAB, Simscape, and LabVIEW, make it easy to study mathematical models and simulate them under varying conditions.

    Biomedical engineering relies on modeling and simulation, especially respiratory system models, which save lives. This study successfully simulated a pressure-controlled ventilator. The simulations were carried out for different test cases, which include healthy human lungs (normal lungs model); hypoxemic respiratory failure, including cardiogenic pulmonary edema (CPE), pneumonia (without ARDS), and ARDS; hypercapnic respiratory failure for obstructive lung disease, including acute exacerbation of COPD (AECOPD) and asthma; and hypercapnic respiratory failure for acute intracranial disorders and head injuries with elevated intracranial pressure (ICP). The process for creating the mechanical ventilation model is covered in detail in Sec. II, Methodology. In Sec. III, results and discussion, the simulation parameter settings, model output for various test cases, and correlation with standard data are reviewed. A computational model of a medical ventilator and a patient's respiratory system is used in Sec. IV, or the conclusion, to demonstrate the importance of mathematical modeling in biomedical research.

    In the present study, MathWorks MATLAB and Simulink Simscape are used to create the simulation model for the mechanical ventilator. The software aids in developing a system-design platform to predict the outcome of the project with a better visualization and accuracy without bringing the prototype into actual existence and helps in avoiding the risk of a patient’s life for experimental purposes. Simulink has a vast collection of tools on Simscape to create the simulation model in domains such as electrical, gas, hydraulics, and moist air. This model is created in the moist air domain. A reservoir block is used as a source of oxygen and air. A pulse generator block is used for performing the breathing cycles. To monitor the system, sensor blocks, such as volumetric flow rate sensors, pressure and temperature sensors, and ideal translational motion sensors, are used. The scope block is used to plot the data measured by sensors. Furthermore, to control pressure, volume, flow, etc., tools such as controlled pressure sources, controlled volumetric flow rate sources, and local restrictions are used.

    Figure 2 shows the Simulink model of a mechanical ventilator in Pressure Controlled Ventilation (PCV) mode. It is based on the schematic diagram shown in Fig. 1. The model comprises a lungs model, which is a replication of the actual lungs of the patient. The model of the lungs is created in the mechanical domain to make the system more realistic. A translational mechanical converter, spring, damper, and force source model the lungs. The force source simulates muscle-induced pressure,43 and the spring and damper model the lungs’ mechanical compliance and resistance.44 Fresnel et al.43 described exponential functions for muscle contraction and relaxation pressure, Pmuscle,

    Pmuscle=Pmax1etτc,0tTtot,Pmaxetτr,T1tTtot,

    where T1 is the muscle contraction time and Ttot is the breathing cycle length. Pmax is the maximum muscle-induced pressure, and τc and τr are the contraction and relaxation time constants.

    FIG. 2.

    Simulink model of mechanical ventilator.

    Simulink model of mechanical ventilator.

    FIG. 2.

    Simulink model of mechanical ventilator.

    Simulink model of mechanical ventilator.

    Close modal

    While developing the MathWorks MATLAB and Simulink Simscape mechanical ventilation simulation model, several assumptions and limitations were taken into account. The first assumption was that all the sensors, actuators, and controllers are ideal components in MATLAB. However, in real, these components are not ideal and possess some degree of error or limitation. The second supposition is that the Simulink model might take steady-state circumstances for granted and ignore the transient effects that occur when the mechanical ventilation system starts and stops. This may have an effect on how well the ventilation system operates. In addition, the model may disregard the real-time variation of temperature, humidity, and density in the atmosphere by assuming that these parameters are constant. Whenever there is a relationship between the environment and the ventilation model components, this was mostly taken into consideration when constructing the model. The model may also imply that, unlike other electrical systems, it functions as an isolated system and does not interact with external disturbances.

    The simulation model for the mechanical ventilation system will have certain limitations because it is based on assumptions. There may be differences between the system conditions that are modeled and the actual system conditions since the correctness of the model is dependent on the underlying mathematical equations and assumptions. In addition, the model will fall short in capturing the nonlinearities and delays that are inherent in the response of sensors and actuators. The performance and response time of the system may be impacted by this. Model simplification is frequently done to increase computational efficiency, but it can have an adverse effect on accuracy by leaving out important aspects of the physical phenomenon. In certain instances, it is possible that the model oversimplified control methods rather than accurately capturing the intricacies of actual control systems. It is possible that any parameter variability was omitted, which could have an impact on the model’s performance. Although all safety precautions were taken, such as fail-safe valves and real-time gas exit to the atmosphere or reservoir, the model may not fully account for all real-world scenarios that could arise during actual operation. Therefore, additional testing of the model in real-world scenarios is necessary to avoid these limitations and close any gaps.

    For simulation purposes, the predicted body weight (PBW) and tidal volume of the patient are taken from the NHLBI ARDS Network (available at www.ardsnet.org/). The PBW is taken as 70 kg, and the corresponding tidal volumes are referred to for the validation of the model.

    ARDS is a serious lung injury with several causes. It is commonly linked to sepsis and multi-organ failure, and it is associated with increased mortality. ARDS induces diffuse alveolar injury, pulmonary micro-vascular thrombus formation, inflammatory cell collation, and blood flow stagnation. Hypoxemia and increased respiratory work typify ARDS. PEEP, high FiO2, and lowered breathing work alter hypoxemia. Often, these ARDS issues require MV. MV has been detrimental for five decades. Ventilators were adjusted to stabilize blood gas values in the late 1960s. Healthcare professionals used a TDV of 12–15 ml/kg of body weight.60 In serious ARDS, 90% of deaths occurred from pneumothorax, pneumomediastinum, and pneumoperitoneum.61 Amato and colleagues62 and the ARDSNet (Acute Respiratory Distress Syndrome Network)63 trial conducted in the year 2000 indicated that low TDV ventilation [4–6 ml/kg Ideal Body Weight (IBW)] seemed to be better than higher TDV ventilation (10–12 ml/kg IBW). IBW anticipates lung capacity better than weight. Recent progress in the VILI investigation has rekindled interest in lung protective ventilation strategies (LPVS).64 Recent evidence indicates that reducing the tidal volume in patients without ARDS could be beneficial.65–68 

    Four main theories describe ventilator-induced lung injury: barotrauma, volutrauma, atelectrauma, and biotrauma.65 High airway pressure causes lung barotrauma (i.e., pneumothorax or pneumomediastinum). High-TV-induced volutrauma produces alveoli overdistribution. Atelectrauma is caused by shear and strain of retractable lung units opening and closing, and biotrauma is caused by proinflammatory cytokines and immune-mediated damage from unphysiologic stress or strain.64 LPVS focus on limiting tidal volume, end-inspiratory plateau pressure (Pplat), PEEP, and FiO2.68 MV patients without ARDS have no optimal TDV.68–70 Mammalian TDV is 6.3 ml/kg.71 ARDSNet63 and other trials65–67 imply that TDV exceeding 10 ml/kg IBW is injurious. In cardiac surgery patients, a TDV less than 10 ml/kg IBW reduced organ failure and ICU length of stay (LOS), according to Lellouche and colleagues.65 A reduced intra-operative TDV (6–8 ml/kg IBW) after abdominal surgery lowered postoperative ventilatory support, pneumonia, and hospital LOS in the IMPROVE66 study group. LPVS and low TDV require high RR to retain Vm. By taking the above data into account, the input parameters provided to the model are listed in Table VII. The output obtained from the model simulation is listed in Table VIII.

    TABLE VII.

    Input parameters for the model.

    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypoxemic respiratory failure  ARDS  27  4.5  12  15 
    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypoxemic respiratory failure  ARDS  27  4.5  12  15 

    TABLE VIII.

    Output parameters obtained from the model.

    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypoxemic respiratory failure  ARDS  19.74  3.995  32.21  0.3333 
    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypoxemic respiratory failure  ARDS  19.74  3.995  32.21  0.3333 

    LPVS limit airway pressure to avoid barotrauma. Pplat estimates alveolar pressure throughout inspiration. Preventing airflow after inspiration achieves this. No Pplat is safe. Pplat must be under 30 cmH2O in ARDS. Hager and colleagues72 found that lower Pplat values improved ARDSNet outcomes. PEEP configuration and selection methods are debated.73,74 The validated and easy-to-use ARDSNet PEEP table75 is recommended for ED management.73 So, PEEP and FiO2 are provided to the model according to these data. An Fmax of 32.21 l/min is obtained during the simulation, which can be observed in Fig. 15. The pressure variation is shown in Fig. 16, where a Pmax of 19.74 cmH2O is obtained, which is less than the Pplat pressure limit for an ARDS patient. From Fig. 17, a TDVmax of 0.3333 l is obtained, which is a low tidal volume and specifically suitable for ARDS patients.

    FIG. 15.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    FIG. 15.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    Close modal

    FIG. 16.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    FIG. 16.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    Close modal

    FIG. 17.

    Tidal volume (l) vs time (s).

    Tidal volume (l) vs time (s).

    In Fig. 18, the variation of the overall flow rate, lung pressure, and lung volume during the total simulation time is presented. A gradual increase in pressure and variation of the built-up volume as per the flow rate can be predominantly observed in the figure.

    FIG. 18.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    FIG. 18.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Close modal

    COPD patients’ airway function and respiratory symptoms worsen suddenly during acute exacerbations (AECOPD). Such exacerbations could, indeed, range from self-limiting diseases to florid respiratory failure, mandating mechanical ventilation. The average COPD patient has two such episodes per year, which use a myriad of medical resources.76 Viral diseases and environmental factors can also cause AECOPD. AECOPD episodes can be sparked or complicated by other comorbid conditions, such as cardiovascular disease, other lung diseases (e.g., pulmonary emboli, aspiration, pneumothorax), or systemic processes. In most patients, antibiotics, corticosteroids, and bronchodilators are prescribed. Certain patients may benefit from oxygen, physical therapy, mucolytics, and airway clearance devices.77 

    Non-invasive positive pressure ventilation may delay endotracheal intubation in hypercapnic respiratory failure. Invasive mechanical ventilation should avoid ventilator-induced lung injury and reduce inherent positive end-expiratory pressure. For these instances, restrict breathing by limiting the ventilation and allow hypercapnia. Mild AECOPD is usually reversible, but serious breathing failure is linked to high mortality and long-term impairment.78 PCV or VCV can be used. Setting rate and inspiratory time makes PCV better than pressure support ventilation (PSV). PCV’s patient-demand-driven flow is an advantage. PCV reduces tidal volume with increased auto-PEEP. With VCV, tidal volume does not decrease with increased auto-PEEP, but there is a risk of increased plateau pressure and overdistention. By taking the above data into consideration, the input parameters for the model are derived and tabulated in Table IX. The resulting output from the model is listed in Table X.

    TABLE IX.

    Input parameters for the model.

    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypercapnic  Obstructive lung disease  12  4.1  14.3 
    respiratory failure  (acute exacerbation of COPD) 
    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypercapnic  Obstructive lung disease  12  4.1  14.3 
    respiratory failure  (acute exacerbation of COPD) 

    TABLE X.

    Output parameters obtained from the model.

    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypercapnic respiratory  Obstructive lung disease  17.1  3.841  32.11  0.6084 
    failure  (acute exacerbation of COPD) 
    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypercapnic respiratory  Obstructive lung disease  17.1  3.841  32.11  0.6084 
    failure  (acute exacerbation of COPD) 

    From Fig. 19, it is observed that the flow rate particularly drops when the outlet valve opens and rises at the start of the inhalation process. From Fig. 20, a lung peak pressure, Pmax, of 17.1 cmH2O is observed, which is particularly safe as it is less than the safe limit of ≤30 cmH2O.79 A TDVmax value of 0.6084 l is obtained from the model as shown in Fig. 21. By making the PEEP higher, the tidal volume can be cut down even more.

    FIG. 19.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    FIG. 19.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    Close modal

    FIG. 20.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    FIG. 20.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    Close modal

    FIG. 21.

    Tidal volume (l) vs time (s).

    Tidal volume (l) vs time (s).

    The variation of the overall flow rate, lung pressure, and lung volume during the total simulation time is presented in Fig. 22. A gradual increase in pressure and variation of the built-up volume as per the flow rate can be predominantly observed in the figure.

    FIG. 22.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    FIG. 22.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Close modal

    A person is said to have hypercapnic respiratory failure if their PaCO2 is higher than 45 mmHg and their PaO2 is lower than 60 mmHg. With asthma, it can be hard to tell when regular treatment has not worked and extra help with breathing is needed. Many people with severe asthma are young and fit otherwise, and they can still breathe even though they have to work much harder to do so.80–82 These people can keep their PaCO2 below or equal to 40 mmHg until they have been completely worn out. When CO2 is kept inside the body, serious hypercapnia and acidosis can happen quickly. So, mechanical ventilation can be used when PaCO2 is higher than 40 mmHg, or sooner if the patient shows signs of being tired. At this point, the patient is growing tired, and waiting longer to start ventilation causes even less air to get into the lungs.82 Auto-positive end-expiratory pressure and air trapping happen in individuals with serious acute asthma (auto-PEEP). The air gets stuck because bronchospasm, inflammation, and secretions make the airways less flexible. The large changes in intrathoracic pressure during the breathing cycle are caused by the auto-PEEP and the increased resistive load. This is called pulsus paradoxus. Either VCV or PCV can be used, but at the start of respiratory support, VCV is often needed. Due to the high resistance in the airways, people with very acute asthma need a high driving pressure to get the tidal volume.83,84

    Once the asthma severity improves, the patient can be transitioned to PCV per the clinician’s bias. With PCV, changes in the delivered tidal volume at a fixed pressure are a reflection of changes in resistance and air trapping. As the severity of the asthma improves, the delivery of TDV with PCV increases. To minimize the development of auto-PEEP, a small TDV (4–6 ml/kg) should be used. The tidal volume must be selected so that the pressure at the plateau is less than 30 cmH2O. The threshold of pulmonary congestion and auto-PEEP should be used to decide how fast a person should breathe. In theory, a lower rate makes air trapping less likely. However, in some asthma patients, the rate can be raised to 15–20 breaths per min without the need for a big change in auto-PEEP. CO2 stays in the body when the tidal volume is low and the rate is slow. Most of the time, it is enough to keep the pH at 7.20 or higher. Even a lower pH may be fine for young asthmatics who are otherwise healthy. Most of the time, the risk of auto-PEEP, lung damage, and low blood pressure is higher than the risk of acidosis.84 Whether or not PEEP should be used to treat asthma is a point of debate. In asthma, auto-PEEP is not usually caused by a lack of airflow as it is in COPD. If flow is not limited, adding PEEP may not be able to counterbalance auto-PEEP, but it may instead raise alveolar pressure.85 In addition, the advantage of PEEP in the case of auto-PEEP might be brought into question if the patient is getting full ventilation and is not trying to wake up the machine. When PEEP is used, lung units that do not make their own auto-PEEP may be recruited and stabilized, which could make the way air moves through the body better. Patients with acute asthma should not be given PEEP if it leads to a rise in plateau pressure and total PEEP.86 If PEEP is used in this situation, gas exchange, auto-PEEP, plateau pressure, and the way the heart works must be watched. Taking the above things into consideration, the input parameters for simulating the model are presented in Table XI. The output from the simulation model is shown in Table XII.

    TABLE XI.

    Input parameters for the model.

    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypercapnic respiratory  Obstructive lung  17  4.8  11  14.3 
    failure  disease (asthma) 
    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Hypercapnic respiratory  Obstructive lung  17  4.8  11  14.3 
    failure  disease (asthma) 

    TABLE XII.

    Output parameters obtained from the model.

    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypercapnic respiratory  Obstructive lung disease  19.64  4.051  32.52  0.4729 
    failure  (asthma)         
    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Hypercapnic respiratory  Obstructive lung disease  19.64  4.051  32.52  0.4729 
    failure  (asthma)         

    The flow rate variation is shown in Fig. 23. From the figure, it is observed that the flow rate is low as per the respiratory rate of the patient and is suitable for the said respiratory condition, as discussed previously. From Fig. 24, a Pmax of 19.64 cmH2O is observed, which is sufficiently less than the recommended safe pressure for acute asthmatic patients. The plateau pressure is also within the safe ≤30 cmH2O limit.86 The PCV mode is utilized here to simulate the model. The tidal volume variation obtained from the model, as shown in Fig. 25, can be utilized by the clinician as one of the parameters for determining the severity of the patient. A TDVmax of 0.4729 l is obtained, which is suitable as per the input parameters provided to the patient.86 

    FIG. 23.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    FIG. 23.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    Close modal

    FIG. 24.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    FIG. 24.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    Close modal

    FIG. 25.

    Tidal volume (l) vs time (s).

    Tidal volume (l) vs time (s).

    In Fig. 26, the variation of the overall flow rate, lung pressure, and lung volume during the total simulation time is presented. A gradual increase in pressure and variation of the built-up volume as per the flow rate can be predominantly observed in the figure.

    FIG. 26.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    FIG. 26.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Close modal

    Most of the time, central respiratory depression causes people with head injuries to need mechanical ventilation. ICP goes up when the amount of fluid in the brain goes up because the skull is rigid. Even though a slight increase in the intracranial volume does not cause ICP to rise, ICP goes up a lot when the intracranial volume goes up a lot. This rise in ICP cuts off blood flow to the brain, which leads to a lack of oxygen in the brain. When the ICP goes up a lot, the brain starts to swell and pushes through the tentorium. This puts pressure on the brain stem. Controlling ICP is a big part of how head injuries are treated. The difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP) is called the cerebral perfusion pressure (CPP): CPP = MAP − ICP.

    The normal CPP is greater than 80 mmHg because ICP is less than 10 mmHg and MAP is equal to 90 mmHg. The goal CPP is between 50 and 70 mmHg. CPP should not be less than 50 mm Hg. When someone has a head injury, the ICP is often measured. Either a drop in MAP or a rise in ICP will cause CPP to go down. Because of the higher intrathoracic pressure that comes with mechanical ventilation, ICP can go up and CPP can go down. PEEP could cause MAP and venous return to go down. When venous return goes down, ICP goes up, and when MAP goes down, CPP goes down. Acute head injuries need both blood flow management and breathing management. Caution shall be exercised to avoid a high MAP, which can hurt CPP by lowering venous return (which causes ICP to rise) and lowering cardiac output (resulting in a decrease in MAP). When a patient has an ICP that is too high, the goal of ventilation is to get their oxygen levels and acid–base balance back to normal. When the pressure in the lungs goes up, the veins do not get as much blood back and the heart does not pump as much blood out.87 

    Most of the time, such patients need to be ventilated because the primary injury has caused their central breathing to slow down. In these cases, the lung function could be close to normal, and it is easy to use mechanical ventilation. When a person has a traumatic injury, they might have injuries to their chest, abdomen, or spine, meaning that they require mechanical ventilation. Because of neurogenic pulmonary edema, it may also be necessary to use positive pressure ventilation. Finally, some treatments for a severe head injury, such as barbiturates, sedation, and paralysis, slow down the central respiratory system. This makes mechanical ventilation necessary.88, Table XIII shows recommendations for the first settings of the ventilator for patients with head injuries. Oxygenation is probably not necessary for people with head injuries since their lungs usually work pretty well. At first, 100% oxygen is given to these patients, but pulse oximetry makes it easy to reduce the amount of oxygen quickly. Most of the time, a PEEP level of 5 cmH2O is a good starting point. Even though there are worries about how PEEP affects ICP, it usually does not hurt ICP at levels less than or equal to 10 cmH2O. Oxygenation is treated the same way for neurogenic pulmonary edema as for other types of ARDS, but caution must be exercised to prevent the effects of a high MAP on ICP. When a patient needs high levels of PEEP, the head of the bed must be lifted to lessen the effects of the enhanced intrathoracic pressure, and ICP should be watched carefully.89,90

    TABLE XIII.

    Input parameters for the model.

    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Permissive  Acute intracranial disorders  18  12 
    hypercapnia  and head injuries 
    Ventilation strategies Disease/condition RR P01 PEEP IPAP EPAP
        Breaths/min  cmH2 cmH2 cmH2 cmH2
    Permissive  Acute intracranial disorders  18  12 
    hypercapnia  and head injuries 

    The clinician’s personal preference determines whether volume-controlled ventilation or pressure-controlled ventilation is used. If the plateau pressure is kept below 30 cmH2O, a tidal volume of 6–8 ml/kg of ideal body weight can be used. Most of the time, this is not an issue since these patients have almost normal lung and chest wall compliance. If the patient has both short-term and long-term respiratory problems, the tidal volume is set lower. The right breathing rate must be selected to keep the acid–base balance in the body normal. Most of the time, this can be done by taking 15–25 breaths per min. The input parameters presented to the model based on the above data and the output from the model are listed in Tables XIII and XIV, respectively.

    TABLE XIV.

    Output parameters obtained from the model.

    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Permissive  Acute intracranial disorders  15.09  3.533  32.12  0.3511 
    hypercapnia  and head injuries 
    Ventilation strategies Disease/condition Pmax Vmax Fmax TDVmax
        cmH2 l/min 
    Permissive  Acute intracranial disorders  15.09  3.533  32.12  0.3511 
    hypercapnia  and head injuries 

    The flow rate during the inhalation and exhalation processes of the patient is shown in Fig. 27. From the figure, it is observed that the flow rate is accurately following the breathing pattern of the patient. As recommended from the previous studies, the plateau pressure should be maintained below 30 cmH2O. Here, from Fig. 28, a maximum lung pressure (Pmax) of 15.09 cmH2O is observed, and the plateau pressure is well within the limit.91 

    FIG. 27.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    FIG. 27.

    Flow of outlet and lungs (l/min) vs time (s).

    Flow of outlet and lungs (l/min) vs time (s).

    Close modal

    FIG. 28.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    FIG. 28.

    Valve and lung pressure (cmH2O) vs time (s).

    Valve and lung pressure (cmH2O) vs time (s).

    Close modal

    The maximum tidal volume (TDVmax) from Fig. 29 is observed to be 0.3511 l, which is considered a low tidal volume and generally recommended for elevated ICP patients. The tidal volume curve shows no significant deflection from the ideal TDV curve.

    FIG. 29.

    Tidal volume (l) vs time (s).

    Tidal volume (l) vs time (s).

    In Fig. 30, the variation of the overall flow rate, lung pressure, and lung volume during the total simulation time is shown. As visible from the figure, at the onset of breathing, the solenoid valve opens, and due to the high flow rate, a corresponding pressure drop and an increase in volume are observed.

    FIG. 30.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    FIG. 30.

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Flow (l/min), pressure (cmH2O), and volume (l) vs simulation time (s).

    Close modal

    In the present study, a simulation model is presented for the bulk of the individually built ventilators developed globally in response to the COVID‐19 issue. MATLAB/Simulink, a program for computational modeling, is used to develop a simulation model of mechanical ventilation systems. An examination of the operation of a mechanical ventilator can be conducted using the suggested simulation model. Through the Simulink interface, all model parameters can be monitored, and the data plots may be utilized to examine appropriate ventilation details. The model is used to test various medical conditions that require mechanical ventilation, such as hypoxemic respiratory failures, including cardiogenic pulmonary edema (CPE), pneumonia (without ARDS), and ARDS; hypercapnic respiratory failure due to obstructive lung diseases, including acute exacerbation of COPD (AECOPD) and asthma; and hypercapnic respiratory failure for acute intracranial disorders and head injuries with elevated intracranial pressure (ICP), and the simulation results showed a high degree of agreement with the commonly accessible data. Pmax was calculated to be 15.78 cmH2O for the healthy lungs case, which is much lower than the standard maximum value of 30 cmH2O. TDVmax was calculated to be 0.5849 l, which is much lower than the typical value of 0.700 l. In the case of cardiogenic pulmonary edema (CPE), a maximum pressure of 17.72 cmH2O is measured, which is lower than the typical maximum pressure of 30 cmH2O. The TDVmax of 0.5053 l is lower than the average TDVmax, which is 0.798 l. In the case of pneumonia, Pmax is calculated to be 16.05 cmH2O, which is significantly lower than the Pmax that is typical, which is 30 cmH2O. TDVmax was calculated to be 0.4256 l, which is much lower than the usual value of 0.798 l. The Pmax for the case of ARDS was determined to be 19.74 cmH2O, which is lower than the usual Pmax of 30 cmH2O. The value of 0.3333 l that was achieved for TDVmax is lower than the value of 0.497 l that is typically used for TDVmax. In the case of AECOPD, the maximum pressure measured was 17.1 cmH2O, which is lower than the typical maximum pressure of 30 cmH2O. In addition, the TDVmax that was calculated came out to be 0.6084 l, which is lower than the usual TDVmax value of 0.700 l. In the case of asthma, the maximum pressure measured was 19.64 cmH2O, which is lower than the typical maximum pressure of 30 cmH2O. In addition, the TDVmax that was calculated came out to be 0.4729 l, which is lower than the usual value of 0.798 l. The Pmax that was measured in patients with acute intracranial disorders and head injuries was 15.09 cmH2O, which is lower than the Pmax that is typically measured, which is 30 cmH2O. In addition, the TDVmax is lower than the normal value of 0.700 l, coming in at 0.3511 l. This validates the accuracy of the simulation model. Through the use of a realistic lung model and human response comparison, the simulation model provides an opportunity to assess the level of quality between the developed devices and the digital twin model. By better visualizing and accurately forecasting the results, this simulation model can aid in the prototype building of the real mechanical ventilator.

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    STARVING for air sounds like something from a horror film.

    But "air hunger" is a real condition that leaves sufferers feeling like they can't take a full breath. Sound familiar?

    1

    Credit: Getty

    Up to one in ten Brits will experience dyspnea - as it's medically known - at some point in their lives,

    "It happens when your brain detects low levels of oxygen," Dr Sarah Jarvis, a GP and clinical consultant to Patient.info, told the Sun.

    "It’s common in lung problems like asthma and chronic obstructive pulmonary disease (COPD) when not enough air gets to the lungs.

    "It can also be caused by heart problems, where the heart isn’t pumping out efficiently and isn’t getting oxygen-rich blood to the organs," she added.

    Heart conditions such as angina, heart attacks, heart failure and some abnormal heart rhythms like atrial fibrillation can all cause shortness of breath, according to the NHS.

    The terrifying feeling can also be a sign of anxiety, explained psychologist Dr Kirren Schnack, from Oxford.

    "One of the physical changes anxiety causes in your body is the redirection of oxygen to large muscle groups," she said in a video posted on TikTok.

    It’s like there’s no oxygen in the air

    Dr Kwan Kin

    "This means the demand for oxygen increases, so you try to inhale more and more air to meet that demand," she added.

    "You then feel short of breath, which triggers more anxiety about your breathing and that feeling of air hunger."

    The term has gone viral on social media after Dr Kwan Kin Pang, a US-based board-certified chiropractor specialising in functional neurology, posted a video about it.

    “You try to breathe, but your breath doesn’t feel like its enough," Dr Kwan said when explaining the condition.

    "You force a yawn but still can’t get the air to fill your lungs. It’s like there’s no oxygen in the air or like your lungs are too weak."

    The video has been viewed over 18.2million times, and thousands of people turned to the comments, thanking the expert for finally placing a name to the sneaky symptom.

    "I’ve been trying to explain this feeling for so long thank you for this," a user named @catcudmoree wrote.

    Another, called @jaclynamber, added: "This happens to me a lot, it makes me start to panic when I can’t get my lungs to feel satisfied."

    "Finally found the suitable description of what I feel," a user called @hulyalala said.

    How can I fix it?

    In a follow-up video, Dr Kirren demonstrated an exercise that can help stabilise breathing.

    "Instead of taking short, shallow breaths from your chest, you need to breathe from your stomach," she said.

    She started by placing her hands below her ribcage and breathing in through her nose.

    As you do this you should feel your diaphragm (a dome-shaped muscle that sits below your lungs and heart) move down towards your stomach, she said.

    "Now, hold your breath for about five seconds before you breathe out from a pouted mouth," she added.

    Make sure you try and get "every last bit of air out" while doing this, she said.

    "The feeling of air hunger will stop once you are breathing at a normal rate and the balance of gasses in your brain and blood go back to normal."

    When to get help

    Shortness of breath might not be anything to worry about, but sometimes it can be serious and you'll need to get medical help.

    You should seen your GP if your shortness of breath gets worse when you've been doing your normal activities, or when you lie down, accoridng to the NHS.

    But if you have severe difficulty breathing difficulties and are not able to get any words out, you should call 999.

    Full list of condions that cause 'air hunger'

    HEART or lung disease and other conditions can cause shortness of breath.

    Lung and airway conditions

    • Asthma
    • Allergies
    • Chronic obstructive pulmonary disease (COPD)
    • Respiratory illness (like bronchitis, Covid-19, the flu or other viral or bacterial infections)
    • Pneumonia
    • Inflammation (pleurisy) or fluid (pleural effusion) around your lungs
    • Fluid (pulmonary oedema) or scarring (fibrosis) inside your lungs.
    • Lung cancer or pleural mesothelioma
    • High blood pressure in your lungs (pulmonary hypertension)
    • Sarcoidosis
    • Tuberculosis
    • Partial or complete collapsed lung (pneumothorax or atelectasis)
    • Blood clot (pulmonary embolism)
    • Choking

    Heart and blood conditions

    • Anemia
    • Heart failure
    • Conditions that affect your heart muscle (cardiomyopathy)
    • Abnormal heart rhythm (arrhythmia)
    • Inflammation in or around your heart (endocarditis, pericarditis or myocarditis)

    Other conditions

    • Anxiety
    • Injury that makes breathing difficult (like a broken rib)
    • Medication: Statins (cholesterol-lowering drugs) and beta-blockers (used to treat high blood pressure) are two types of medications that can cause dyspnea
    • Extreme temperatures (being very hot or very cold)
    • Body mass index (BMI) over 30
    • Lack of exercise (muscle deconditioning)
    • Sleep apnea can cause paroxysmal nocturnal dyspnea (PND)

    Source: Cleveland Clinic

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    It is no news that popular Nollywood comic actor, John Okafor, also known as Mr Ibu lost battle to Blood clots disease last week.

    These are what you need to know about the killer disease and how it ended Mr Ibu’s life.

    See signs, symptoms and cure of Blood clots disease.

    Understanding Blood Clots:

    Blood clots, or thrombi, are clusters of blood that transform a liquid to a gel-like state. This coagulation process is a natural response to prevent blood vessels from leaking on the skin’s surface or within the body. Platelets and clotting factors, proteins in the blood, collaborate to form clots, halting bleeding.

    Typically, blood clots dissolve when no longer needed. However, in some instances, clots may obstruct blood vessels or migrate to different body parts, called emboli. These situations can lead to various medical issues requiring immediate attention:

    1. Arterial embolism: A clot travels through an artery, disrupting blood supply to an organ or body part.
    2. Deep vein thrombosis (DVT): A clot forms in veins, usually in the legs or arms.
    3. Heart attack: A clot develops to repair a damaged vessel near the heart, blocking blood supply.
    4. Pulmonary embolism (PE): A clot travels from a vein into the heart, potentially blocking blood supply to the lungs.
    5. Stroke: A blood clot moves into an artery supplying the brain, halting blood flow.
    6. Thrombophlebitis: Swelling occurs from a clot obstructing a vein.

    Several factors, including medical conditions, medications, and habits, can heighten the risk of these complications. Conditions such as atrial fibrillation, cancer, diabetes, and lifestyle factors like inactivity or smoking contribute to the potential development of blood clots.

    Causes of Blood Clots:

    Blood clots naturally form as part of the body’s healing response to injuries, surgeries, or other medical procedures. They can also result from damage to arteries known as atherosclerosis. Some individuals may experience abnormal clotting due to age, genetics, or specific medical conditions.

    Risk factors for blood clots include age (especially over 60), blood clotting disorders, certain medical conditions, hormonal influences like estrogen, inactivity, pregnancy, and smoking.

    Symptoms of Blood Clots:

    Symptoms of blood clots vary based on their location. Common signs include pain or tenderness, swelling, warmth, trouble speaking, vision changes, sudden headaches, chest pain, breathing difficulties, and coughing up blood.

    Diagnosis of Blood Clots:

    Doctors employ various methods to diagnose suspected blood clots, including physical exams, discussions about medical history and risk factors, blood tests to evaluate clotting factors, and imaging techniques like ultrasound and computed tomography (CT).

    Blood Clot Treatment:

    Treatment depends on the clot’s location, severity, and urgency. Urgent cases may involve thrombolytic drugs or medical procedures for clot removal. Less urgent situations may be addressed with blood thinners (anticoagulants or antiplatelets), and additional measures to mitigate future risks may be discussed.

    A multidisciplinary team, including cardiologists, hematologists, interventional pulmonologists, interventional radiologists, neurologists, or vascular surgeons, may collaborate to provide comprehensive care. Specific blood clot treatments can be explored further through consultation with medical professionals.

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    By Charles Awuzie

    I still have a clot in my left leg. 200,000 Nigerians die of Blood Clot annually. Please know the symptoms. I almost died if not for medical intervention.

    This was 3 years ago…

    I lived with undiagnosed DVT for several months…

    Then it dislodged and traveled to my lungs, causing Pulmonary Embolism…

    I almost died…

    Breathing was like stabbing myself with every draw of air…

    Already walking was almost impossible…

    At one point, I couldn’t get out of bed because of the pain…

    Doctors couldn’t find what was wrong…

    Blood tests and X-ray couldn’t find anything…

    This is where many Africans become superstitious and conclude that they are being ‘pursued by village people’….

    I was undiagnosed until the day I almost stopped breathing…

    I remember walking into my GP’s room that morning…

    Immediately he saw me, he ordered a D-Dimer blood test…

    This is a test that checks for blood clotting problems by measuring the amount of the D-dimer level in your body.

    My result came out positive and he ordered an ambulance to take me straight to hospital… according to him, I could drop dead any moment from then if I wasn’t admitted in hospital…

    I told him I needed to see my family and kiss them goodbye before being taken to hospital…

    I drove myself back to the house, packed my laptop and few clothes, said my goodbyes to the family and drove myself to the hospital…

    It was during COVID so hospitals were filled with COVID patients and it took longer to get me admitted…

    Once fully admitted, they injected me with CLEXANE…

    My oxygen level was dropping…

    I was taken in for a CT scan and boom, it was confirmed that I had clots in my lungs. I was diagnosed of Bilateral Massive Pulmonary Embolism. The size of the blood that clotted in my lungs is what was described as massive.

    It was then that my physician told me I would have died in 2 days if I didn’t make it to hospital…

    At that point, everything lost value…

    I knew I could die any moment…

    I called a few friends and prepared them for my potential exit…

    I contacted business partners and shared every necessary information they need for continuity…

    I blocked my mind from thinking about my son as the thought of him in this world without me was killing me faster than the massive clot in my lungs…

    But I had faith in medical science…

    I trusted the process…

    I surrounded myself with friends in the medical field – from Dr. Idee in the UK who first mentioned i should be checked for DVT/PE, sister Joy in the US, Dr. Adetola in the US and others.

    On ground, I had the best specialists monitoring me closely.

    After 10 days of fighting for my life in hospital, my physician discharged me and said I cheated death.

    According to him, blood clots kills faster yet few people are aware of it.

    I knew at that point that the universe wanted me to use my story to raise awareness about this killer but unpopular medical condition…

    If you sit long hours in flights or at work, you are at a risk of developing a blood clot.

    If you have high blood pressure, cancer or on cancer therapy, your risk of clotting is high.

    If you have a sibling or relative who suffered blood clot, please investigate the possibility of a genetic clotting disorder.

    And finally, if you’re sick and multiple blood tests do not show what’s wrong with you, do not conclude that the condition is spiritual. You just haven’t been tested correctly. Some laboratory tests or radiological scans may also not be available in your city. A lot of Nigerians die because they mistook a medical condition for a spiritual problem.


    My name is Charles Awuzie and I just wanted to raise awareness about blood clots especially after learning that Mr. Ibu died of clot related complications.

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    The term “medical miracle” is sometimes used to describe any situation in which the patient’s outcome defies the odds. But 42-year-old Aaron Cengiz and the medical staff at UChicago Medicine AdventHealth Bolingbrook believe that he is alive today because of a real miracle.

    In late June 2022, Cengiz, a father of six and an avid runner, was on a run with his dog when he rolled his ankle badly. A few weeks later, he thought he might have COVID-19 because of his incessant cough. He also began experiencing severe pain in the back of his knee. He made an appointment to take a COVID-19 test, but when he went to get tested, he felt dizzy and light-headed, and had difficulty breathing. He called his wife, Tami, but his breathing worsened. Then he called 911 and started to pray.  

    After he was admitted to the hospital, Cengiz’s oxygen level was determined to be dangerously low at 79 percent despite being at 100 percent oxygen.   

    “My breathing got worse, and I actually thought: This is it. I am going to die here,” Cengiz said. At that point, the staff sedated him and that is all he remembers for a long time. 

    “Miracle Patient” Aaron Cengiz is back to running and cycling after suffering a pulmonary embolism that caused his heart to stop multiple times in July 2022. 
    “Miracle Patient” Aaron Cengiz is back to running and cycling after suffering a pulmonary embolism that caused his heart to stop multiple times in July 2022. 

    Cengiz’s lungs were full of clots that had developed after his ankle injury, and the clots were causing a massive pulmonary embolism. He was taken to the Interventional Radiology Lab where doctors used the Inari device, which removes clots from the bloodstream and then filters the blood and returns it to the patient. The device successfully removed the clots, but Cengiz’s heart stopped twice during the procedure. “There was significant improvement with no more clots present. But his heart had just had enough,” said Elizabeth Kraft, RN, manager of Cardiac Services at the hospital. 

    After the procedure, Cengiz was moved to the Intensive Care Unit (ICU) for monitoring.  The doctors talked to Tami and explained to her that Cengiz’s heart was failing and even if he survived, he might suffer permanent brain damage because his brain had been deprived of oxygen. “We were not hopeful he was going to recover,” said Dr. Ali Bawamia, who noted that Cengiz nearly died again in the ICU.  

    When the medical staffers who had worked with him on Friday night checked on him Saturday morning, they feared the worst. But the staff found that not only had Cengiz survived, but he had improved considerably. 

    “We became hopeful,” Bawamia said. “I was very emotional. It is one of those cases I cannot forget. As human beings we do the best we can. But sometimes it takes intervention from above.” 

    Aaron Cengiz (left) and Elizabeth Kraft, RN, (right) walked together in the 2023 American Heart Association Heart Walk at the DuPage County Fairgrounds in Wheaton, Illinois. 
    Aaron Cengiz (left) and Elizabeth Kraft, RN, (right) walked together in the 2023 American Heart Association Heart Walk at the DuPage County Fairgrounds in Wheaton, Illinois. 

    Cengiz’s progress continued. He woke up fully on Sunday evening, and by Monday morning he was off the ventilator. Amazingly, the medical team could not identify any lingering issues from his near-death experience. A week later, he was home.   

    “Sometimes in health care, we need a miracle to keep us going, to remind us why we do what we do,” Kraft said. “This man walked out of the building because of our amazing work as a team and by the grace of God!” 

    Cengiz also believes his recovery was miraculous. “I felt like God had used these professionals as instruments in His hands to perform this miracle,” he said.  


    Julie Busch, associate vice president, marketing and communications for UChicago Medicine AdventHealth 

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    In 2003, while covering the war in Iraq for NBC News, journalist David Bloom died of a blood clot that formed in his leg and traveled to his lungs.

    In memory of Bloom, a U.S. Senate bill in 2005, sponsored by Arlen Specter (R-PA), declared March Deep Vein Thrombosis Awareness Month.

    In 2009, Representatives Lois Capps (D-CA) and Cathy McMorris Rodgers (R-WA) came together in an bipartisan effort to reinforce March as a time to focus on blood clots. Capps’ husband Walter died of a pulmonary embolism (PE) in 2006, and a friend and mentor of McMorris Rodgers, Rep. Jennifer Dunn, died of a PE in 2007.



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    March is Blood Clot Awareness Month (BCAM), a time dedicated to spreading the word about blood clots and their potentially fatal complication, pulmonary embolism.  

    Throughout the month, NBCA’s  awareness campaign, “Recognize the Signs, Save Lives,” promotes learning the signs and symptoms of blood clots. This is because knowing the signs and symptoms and acting quickly can be the difference between life and death.

    What will be happening during Blood Clot Awareness Month?

    • NBCA is working to raise $100,000 and reach 100,000 people in honor of the 100,000 who die each year from preventable blood clots through the 100,000 Reasons Challenge.
    • To honor the 100,000 people who die every year as a result of a blood clot, NBCA is asking their loved ones to share their stories. These stories will be shared during March on our website and social platforms.
    • To build awareness of the signs and symptoms of blood clots, NBCA is asking blood clot survivors to create short videos describing the signs and symptoms they experienced, tagging @stoptheclot, and posting it to their social media platforms. NBCA will reshare this content throughout the month.
    • NBCA staff and volunteers are gathering in Washington, DC to meet with members of Congress to urge them to increase funding for blood clot education and awareness.

    Why is it important to raise blood clot awareness?

    • Less than 6% of Americans know what blood clots are and how to prevent them, yet they affect as many as 900,000 Americans every year.
    • Every six minutes in the U.S., someone dies of a blood clot.
    • The overall incidence of venous blood clots is 30-60% higher in Black patients compared to white patients.
    • 274 people die every day in the U.S. from blood clots.
    • A blood clot in the lung is one of the most common causes of pregnancy-related death in the U.S.
    • Blood clots are the second leading cause of death in cancer patients, aside from cancer itself.

    How can you get involved?

    • Sign up for the 100,000 Reasons Challenge. Ride, run, walk, or move your body during this 31-day virtual challenge in March. Help us raise $100,000 and reach 100,000 people in honor of the 100,000 who die each year from preventable blood clots.
    • Use our BCAM Social Media Toolkit and Action Guide to share resources about blood clots to your social platforms and learn about other ways to get involved.
    • Urge Congress to expand funding for blood clot awareness and education by sending a message to your representatives.
    • If you’ve experienced deep vein thrombosis or pulmonary embolism, post a short video on social media describing your blood clot signs and symptoms and use the hashtags #BCAM2024, #BCAM and #StopTheClot. Make sure to tag @StopTheClot.
    • If you’ve lost a loved one to a blood clot, we urge you to share their story. Doing so is a meaningful action you can take to help raise awareness, educate others about signs and symptoms, promote prevention, and foster a supportive community. We will share these stories on our website and social media platforms throughout the month.

    Learn more about Blood Clot Awareness Month 2024.

     

     



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    Michelle Lyons, a 33-year-old social studies teacher, recalls the first time she noticed something was wrong. As she played with her 3-year-old daughter, she struggled to catch her breath. Since RSV and flu were going around, she thought it might be the beginning of a respiratory illness. By the evening, she felt better and went to sleep.

    But the breathless feeling continued, so Michelle sought care at the Emergency Department at Atrium Health Wake Forest Baptist Medical Center, where test results revealed she had a large blood clot, known as a pulmonary embolism, in her lung. In addition, she had two blood clots in her heart. Dr. Bart Imielski, cardiothoracic surgeon and professor of surgical sciences with Atrium Health Wake Forest Baptist, evaluated her in light of this potentially life-threatening condition.

    As her condition stabilized, Imielski recommended initial medical management and prescribed anticlotting medication to dissolve the clots. At that point, surgery would be a last resort. Performing a thrombectomy to remove some of the lung clot carried the risk of showering small emboli (portions of the blood clot) further into her lung. 

    After six months on the medication, Michelle still didn’t feel well. She couldn’t pick up her daughter without feeling out of breath, and a follow-up CT scan showed the blood clots were still in her lung and heart. Imielski diagnosed Michelle with chronic thromboembolism pulmonary hypertension, meaning the blood clot in her lung was stuck in her pulmonary artery.

    “As the embolism grows, it creates a lot of resistance to blood flow in the lungs,” explains Imielski. “It's a serious problem because it can eventually cause heart failure.”

    About 5% of patients with pulmonary embolisms will not reabsorb or dissolve them. While it's a relatively small patient population, it can be very debilitating, especially for young patients with busy schedules. Since Michelle’s quality of life continued to be affected, Imielski recommended surgery to remove the clots.

    Open-heart surgery

    Imielski’s team scheduled Michelle’s surgery during her summer break. Using open-heart surgery, he performed a pulmonary thromboembolectomy to remove the blood clots.

    “It's a complex procedure that requires periodically stopping the patient’s blood flow throughout the body,” Imielski explains. “We put the patient on cardiopulmonary bypass, which is a machine that takes over the patient’s breathing and blood circulation. This allows us to access the area where the pulmonary arteries are located and cut them open.”

    When Imielski entered Michelle’s chest and saw the lung clot, he noticed that it had grown into the wall of the pulmonary artery. He had to surgically remove the clot from the lung artery. While peeling it away, Imielski got to a point within the dependent portion of the pulmonary artery where the blood was pulling and there was still some clot remaining. The only way he could go deeper to finish removing the clot was by shutting off the bypass machine. This allows the team to work through the surgery without blood.

    Imielski’s surgical team cooled Michelle’s body to 18 degrees Celsius for about 15 minutes and then turned off the pump. Cooling the patient’s body allows the brain to survive brief periods without blood flow. Once the surgical team gets as far down into the pulmonary arteries as possible, they turn the bypass pump back on. After the remaining portions of the clot were removed, they warmed Michelle’s body back to normal.

    Once the clot in the lung was removed, Imielski removed the clots in Michelle’s heart.

    Unique surgical program

    According to Imielski, pulmonary thromboembolectomy is an established procedure. However, only about 12 centers in the U.S. perform the surgery.

    “Most medical programs don't train surgeons on this procedure,” notes Imielski. “Most surgeons in the U.S. who do this procedure were trained directly or indirectly through Dr. Michael Madani, cardiothoracic surgeon with the University of California San Diego. I was lucky enough that one of my mentors at Northwestern University trained with him, so I was able to learn his technique.”

    In addition, there are few programs established to evaluate patients with chronic thromboembolism pulmonary hypertension. Most primary care doctors are unfamiliar with the condition and its treatment.

    A chronic thromboembolism pulmonary hypertension program requires close collaboration between experts in CT surgery and pulmonary medicine. Additionally, the surgery can only be performed at experienced centers with advanced technologies, such as extracorporeal membrane oxygenation (ECMO), which are needed to manage rare but potentially known complications of the procedure. Wake Forest Baptist offers the collaboration and supportive technologies required to provide safe, effective cardiothoracic surgery.

    Confidence in care

    “I went to the right hospital at the right time,” says Michelle. “They knew what it was and came up with a plan of action immediately. I’m thankful this great hospital is located just five minutes from home and in the same city as my family.”

    Michelle also felt confident in Imielski’s ability to deliver a positive outcome.

    “He made me feel very comfortable with the procedure,” Michelle says. “He explained his background and training and helped me understand everything involved.”

    Michelle says the nurses, especially those in the ICU, were fantastic.

    “It’s a lot to process and go through,” Michelle says, “They were kind, understanding and supportive. They were willing to sit and listen to me express my feelings.”

    Results and recovery

    Following surgery, Michelle’s pulmonary artery pressure dropped by half and back into the normal range, leaving her feeling great from the moment she woke up. Her shortness of breath was gone. She just needed time to recover from open-heart surgery.

    Michelle spent about five days in the hospital, followed by continued rest at home. Imielski encouraged her to walk every day to foster healing. She was unable to do any heavy lifting or driving for the first month of her recovery. During the second month, she was allowed to slowly resume her normal activities.

    Back to normal and breathing easy

    Nine months after surgery, Michelle’s life has returned to normal. She’s able to walk around and teach in the classroom with ease. She can keep up with her young daughter without struggling to breathe.

    Michelle takes a low-dose blood thinner to maintain her health. Her care team is trying to figure out why she developed the blood clots. Her pregnancy in 2020, case of COVID-19 in 2021 and years of taking the birth control pill may have created the “perfect storm” for forming blood clots.

    Michelle is looking forward to supporting her family’s fundraiser for the American Lung Association’s Fight For Air Climb in the spring. This event promotes lung disease awareness and involves climbing stairs with friends and family in a fun, positive atmosphere.

    “When you do the stair climb, you support people with lung disease who are fighting for every breath,” says Michelle. “I know firsthand what it’s like to struggle to breathe, so I’m glad I feel well enough to support those still struggling.” 

    Learn more about cardiothoracic surgery at Wake Forest Baptist.

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    The SARS-CoV-2 virus has caused long-term health problems in those who recover from COVID-19, including pulmonary embolism, myocarditis, acute coronary events, and lung scarring.1 While successive SARS-COV-2 variants have demonstrated increased transmissibility, there is no evidence to date that the variants have become more virulent. The severity of the latest COVID-19 infections has been attenuated by widespread prior infection and vaccination.2

    For athletes who have contracted COVID-19, there is a need for more research on the appropriate timing of resumption of physical activity. Two clinical vignettes are presented to explore this issue.

    Case 1

    A 27-year-old college basketball player was diagnosed with mild symptoms of COVID-19 in June of 2022, including fever and cough, and recovered after resting and isolating for 7 days. The patient is healthy, with no previous medical history or surgeries, and does not take medications other than over-the-counter multivitamins. The patient confirmed receiving the COVID-19 vaccine along with one booster shot. The patient stated this was his first time testing positive for COVID-19. After testing negative for COVID-19, the patient was medically assessed to evaluate if he is able to return to physical activity. A scan of the patient’s lungs showed mild lung damage and the patient is being monitored. The patient is advised to start with light activity and slowly progress, increasing the intensity and duration of his workouts. 

    Case 2

    A 32-year-old professional runner tested positive for COVID-19 in March of 2021 and experienced severe symptoms, including shortness of breath, chest pain, and fever. She was hospitalized for 7 days. The patient has no previous medical history or history of surgeries, and takes multivitamins, vitamin B12, and loratadine, as needed, for allergies. The patient denied receiving the COVID-19 vaccine. The patient stated this was her first time testing positive for COVID-19. After testing negative for COVID-19, she was re-evaluated and additional scans were obtained. The scans show myocarditis and the patient is advised to rest for 3 months. After resting, the patient is reassessed for myocarditis before returning to physical activity. The patient is able to go back to training but her progress is slow; the patient requires rehabilitation and additional monitoring. 

    Athletes who partake in exercise during the acute phase of viral myocarditis have increased risk of developing myocardial injury and triggering fatal ventricular arrhythmias.

    Return to Physical Activity After COVID-19

    When to return to competitive physical activity after COVID-19 is a difficult question to answer as each case is unique. The medical literature has published a number of case reports early in the pandemic that try to address this question. Santos-Silva et al considered the case of a soccer player who developed a pulmonary embolism after being infected with COVID-19.3 The soccer player had a computed tomography (CT) of the chest while he was ill, which did not show a pulmonary embolism. After quarantining for 14 days, the player resumed physical activity. On day 10 of training, he started complaining of shortness of breath and weakness. A computed tomography angiogram (CTA) showed the athlete had a pulmonary embolism. This study showed that although the player did not have any history of medical problems when he was ill with COVID-19, the virus can have residual effects. Caution and reassessment are advised before releasing athletes back to training.3

    Metzl et al discussed considerations regarding the length of time athletes should be monitored prior to resuming training. Every COVID-19 case is unique and should be treated individually, based on the athlete’s symptoms and the time it takes them to recover. The authors recommended that the athlete’s activity should progress slowly and that exercise should be withheld if the athlete is still experiencing cough, chest pain, palpitations, fever, or shortness of breath at rest.4

    All athletes should be monitored closely during the first 3 to 6 months of activity post COVID-19 infection, and athletes should be educated on notifying physicians of any new symptoms such as chest pain, shortness of breath, or palpitations. Athletes with prior cardiovascular or pulmonary disease should follow up with a physician prior to resuming physical activity. Assessments should include physical examination, testing of lung and cardiac function, and blood work such as cardiac enzymes, blood gases, clotting factors, and complete blood count. These tests are important in monitoring the athletes to ensure that they can safely return to physical activity. 

    Slowly Initiate Physical Activity

    Athletes who were diagnosed with COVID-19 should not initiate physical activity until they no longer experience viral symptoms and should slowly ease back into physical activity. This means that they should not resume their pre-COVID-19 training regimen immediately. Metzl et al4 recommend educating patients on slowly initiating activity by using the 50/30/20/10 rule created by the National Strength and Conditioning Association (NSCA) and Collegiate Strength and Condition Coaches Association (CSCCA) Joint Committee (Table).5 This rule advises that volume of conditioning for the first week should be reduced by at least 50% of the normal exercise load, followed by 30%, 20%, and 10% in the subsequent 3 weeks, if the athlete is comfortable at the end of each week. 

    The application of this guideline is dependent on the severity of symptoms. Athletes who experienced mild COVID-19 symptoms can use this rule over a 4-week period. Those who experienced more severe symptoms should use this rule over 3 to 6 months, depending on the rehabilitation improvement of the patient. As always, athletes should be educated to monitor themselves for any signs of shortness of breath, chest pain, or fatigue. Patients who are diagnosed with myocarditis should return to exercise with caution, as myocarditis accounts for 7% to 20% of sudden cardiac deaths in young athletes.6

    Persistent Symptoms

    A study by Petek et al assessed the prevalence of persistent or exertional cardiopulmonary symptoms in competitive athletes following COVID-19 infection.7 The study included 3598 athletes, of whom 1.2% reported persistent symptoms after 3 weeks of infection, and 0.06% reported symptoms lasting longer than 12 weeks. Exertional cardiopulmonary symptoms were present in 4.0% of athletes. Athletes who had chest pain when returning to physical activity underwent a cardiac magnetic resonance imaging (cMRI), where 5 out of 24 athletes (20.8%) had cardiac involvement.7 Athletes who partook in exercise during the acute phase of viral myocarditis had increased risk of developing myocardial injury and triggering fatal ventricular arrhythmias.8 

    A screening protocol for potential cardiac involvement in competitive athletes recovering from COVID-19 was outlined by Phelan et al in October 2020, during the height of the pandemic and before vaccines were made available.9 In their paper they acknowledge that screening recommendations will continue to evolve. “The evaluation of athletes with persistent symptoms after recovery from acute COVID-19 will be guided by the nature of the symptoms, whereas the evaluation of the asymptomatic athlete will be oriented around screening for subclinical pathology,” they wrote.

    Phelan et al recommend a 12-lead electrocardiogram (ECG) for all athletes prior to initiating a training routine.  This test will pick up abnormal ventricular beats and arrhythmias. After COVID-19, the authors recommend a high-sensitivity troponin (hs-cTn) test to detect subclinical myocardial injury in athletes.9 If an athlete has a normal ECG and hs-cTn they can be allowed a graded return to play. For patients with positive tests or ongoing clinical concerns, a cMRI is recommended. As noted, cMRI will pick up myocarditis and pericarditis, including pericardial effusion. After cMRI, secondary imaging is directed by clinical suspicion and includes computed tomography (CT) angiography, stress ECG/cardiopulmonary exercise testing (PET), and nuclear PET.9

    Conclusion

    The prevalence of cardiac problems in athletes related to COVID-19 is difficult to establish due to very limited data. Athletes preparing to return to strenuous exercise after a diagnosis of COVID-19 present a challenge for clinicians caring for these patients. Athletes who contract COVID-19 should not return to physical activity until they have fully recovered from the virus and have undergone a medical evaluation and are approved to return to physical exercise.

    There have been reports of pulmonary embolism and myocarditis among athletes recovering from COVID-19 diagnosed via cMRI.2,7-9 Clinicians should treat these athletes individually and screen them based on their symptoms. With proper care and attention, athletes can safely return to physical activity after recovering from COVID-19 and continue to pursue their athletic goals.  

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    It was a normal day for Gary Morgan. The grandfather of three has lived in Gastonia his whole life and during a walk with his miniature schnauzer, Pepper, became unusually short of breath. While the sensation was uncomfortable, he did not think much of it at first. But soon, the shortness of breath turned into an uncomfortable inability to breathe accompanied by an impending sense of dread. Aided by a neighbor and Gaston County Emergency Medical Services (GEMS), Morgan was rushed to the emergency room at CaroMont Regional Medical Center. 

    “I wasn’t just hard to breathe, although I could not catch my breath,” remembers Mr. Morgan. “But I felt sure I was going to die in the ambulance. I had an overwhelming sense of doom. It was not peaceful at all; it was frightening.” 


    Gary Morgan, Gastonia native is passionate about living a healthy life after a recent medical crisis.

    Recognizing the danger of Mr. Morgan’s symptoms, medical professionals, including Dr. John Schindler, Interventional Cardiologist with CaroMont Heart and Vascular, got to work. Mr. Morgan was suffering from a saddle pulmonary embolism, or blood clots blocking both sides of his lungs. Imaging revealed the clots were extensive, preventing his flow of oxygen. Pulmonary embolisms affect over 900,000 individuals a year in the United States, but the severity of Mr. Morgan’s condition caused alarm. 

    “A saddle pulmonary embolism results in death for about 40% of those who develop it,” said Dr. Schindler who specializes in structural cardiology. “Mr. Morgan had a spectrum of clots when he came in through the emergency department and his entire blood flow to the lungs was impaired. Put simply, his condition was as serious as it gets.” 

    A multidisciplinary heart team convened to understand the full picture of Mr. Morgan’s condition and determine the best course of treatment to resolve the clotting. A thrombectomy was successful in removing the blockages from his pulmonary arteries. 

    After a four-day stay at CaroMont Regional Medical Center, Mr. Morgan remembers two things: his view of the Christmas tree on top of the hospital, and the care team he credits with saving his life and helping ease his anxiety and discomfort during a time of great challenge. 

    “Everyone, from the housekeepers to my night nurse, Corey, were special people,” remembers Mr. Morgan. “Eusther Toussaint, the Nurse Practitioner who cared for me in the ICU, took the time to check on me once I moved to the recovery unit. Her support filled me with great peace and her presence was restorative.” 

    While the emergency procedure gave Mr. Morgan immediate relief, it took another several weeks for him to regain the confidence to return to everyday activities. He keeps regular, follow-up visits with his CaroMont Heart cardiologist, Dr. Anthony Arn, with whom he shares a strong sense of faith. 

    “I haven’t felt this good in a long time,” said Mr. Morgan. “I have a whole new lease on life and with that, I feel I’m here for a reason. And I'm going to do what I can to now find my purpose.” 

    For now, that purpose includes getting back to the things he loves: walking Pepper, visiting Myrtle Beach for the music and dancing, and finding as much time as possible to spend with his two daughters and their children. He’s also committed to sharing an important health message:  

    “Every day, get up and move, go for a walk and look after your health. It’s so important, especially as you age. So, watch your diet and the time you spend on the couch. Get out and walk a little bit. You’ve just got to get up and move.” 


    Mr. Morgan with his two daughters and grandchildren, who serve as motivation for him to stay active, stay healthy and stay well.

    And for the surgeon he credits with saving his life? Dr. Schindler and Mr. Morgan reunited recently to share a handshake, hug and exchange words of kindness and encouragement. 

    “Different people have different skills,” Mr. Morgan told Dr. Schindler. “Some people build buildings, some pave driveways and make patios. I told Dr. Schindler to take those pictures of what he removed from my lungs and use it to show people the truly incredible work he does every day.” 


    Mr. Morgan and Dr. Schindler reunite at CaroMont Regional Medical Center in Gastonia for the first time since Morgan's hospitalization.

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    Singer and guitarist Dilbert Aguilar died of respiratory failure yesterday Severe pneumonia cases, For this reason, he was admitted to the intensive care unit (ICU). According to the Spanish Society of Internal Medicine (SEMI), pneumonia can be an extremely serious disease if not diagnosed promptly. Therefore, it is important to understand its symptoms and the signs that occur during respiratory failure.

    According to experts at the Mayo Clinic, pneumonia is an infection that causes inflammation of one or both of the air sacs in the lungs. During this process, the air sacs fill with fluid or pus, causing coughing up phlegm, fever, chills, difficulty breathing, and respiratory failure. “Not all respiratory illnesses are pneumonia and require a chest X-ray to identify them,” emphasizes Dr. Javier Jauregui, a pulmonologist at the Ricardo Palma Clinic.

    What are the symptoms of pneumonia?

    Research from the Mayo Clinic shows: The signs and symptoms of pneumonia vary depending on several factors, such as age, the type of bacteria causing the infection, and the patient’s overall health. However, they point out mainly:

    • Chest pain when breathing or coughing
    • Disorientation or changes in mental perception (adults 65 years or older)
    • Coughing can produce phlegm
    • fatigue
    • Fever, sweats, chills, and shivering
    • Lower than normal body temperature (adults over 65 and people with weakened immune systems)
    • Nausea, vomiting, or diarrhea
    • Difficulty breathing
    Cough is one of the most common symptoms of pneumonia.

    It should be pointed out that Newborns do not show the same symptoms, Well, in addition to having a fever and cough, they may appear restless or tired. Additionally, they may have trouble breathing and eating.

    In addition to symptoms, it is important to consider risk factors that may indicate a severe case of pneumonia. Among them, Mayo Clinic patients include patients over 65 years old, children under 2 years old, patients with undiagnosed health conditions, weakened immune systems and patients undergoing chemotherapy.

    What does respiratory failure include?

    In the words of Dr. Jauregui, Respiratory failure does not usually occur in anyone with pneumonia because risk factors must be present.

    “Respiratory failure symptoms occur due to one of the following reasons: Various lung conditions and diseases, such as acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, Cystic fibrosis, pulmonary edema, pulmonary embolism, pulmonary fibrosis and pneumonia, said Dr. Ivan Romero Legro, a pulmonary specialist at the Cleveland Clinic.

    Dr. Romero said other causes of respiratory failure include:
    Heart or circulatory (blood flow) conditions and diseases. This includes heart attack, congenital heart disease, heart failure and shock.
    A disease that affects the nerves and muscles that help you breathe. This includes muscular dystrophy, amyotrophic lateral sclerosis (ALS), severe scoliosis and Guillain-Barre syndrome.
    Injury to the chest, spinal cord, or brain (including stroke).
    Surgery requiring sedation or anesthesia.
    Taking drugs or drinking too much alcohol.
    Smoking or exposure to other lung irritants. This includes chemical fumes, dust, air pollution and asbestos.
    Taking drugs or drinking too much alcohol.
    age. Newborns (especially premature infants) and adults over 65 years of age are at higher risk of developing respiratory failure.

    To identify it, Dr. Romero said, The most common symptoms are shortness of breath, shortness of breath (shortness of breath), extreme tiredness (fatigue), increased heart rate, and behavioral changes. From a physical perspective, this is also very common Cough with blood, excessive sweating, pale skin, headache, blue skin, lips, or nails.

    “While many causes of acute respiratory failure are treatable, if left untreated, it can be fatal. As many as one-third of patients hospitalized with acute respiratory failure do not survive. “Chronic respiratory failure is often caused by an ongoing condition that worsens over time,” the Cleveland Clinic experts added.

    therefore, Dr. Jauregui concluded by emphasizing the importance of correct treatment of respiratory diseases to avoid severe respiratory failure. Especially if the patient has other risk factors.

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    Vittorio Cecchi Gori is hospitalized in intensive care at the Gemelli Polyclinic in Rome due to respiratory failure. What is that? What is it due to? It is “a pathological condition caused by the inability of the respiratory system to guarantee adequate exchanges of oxygen between the environment and the blood”, with consequent “inability to obtain adequate blood values ​​of oxygen and carbon dioxide”.

    Respiratory failure, what it is and causes

    Respiratory failure “can be acute, when its onset is rapid and sudden, or chronic, when it occurs progressively to stabilize or evolve over time”. There are different causes at the origin, explains Laura Mancino, pulmonologist at the Angelo hospital in Mestre (Venice), in an in-depth analysis on the 'Let's take breath' portal, dedicated to breathing diseases.

    “The most frequent causes of acute respiratory failure are acute pulmonary edema, massive pulmonary embolism, tension pneumothorax, asthmatic crisis, pneumonia causing acute respiratory distress syndrome such as Covid-19 related pneumonia”, i.e. associated with Sars-CoV-2 infection. Precisely due to pulmonary complications from Covid, Cecchi Gori had already been hospitalized at the beginning of 2022. The cause of acute respiratory failure can then be “traumas, intoxications from drugs or toxins”, lists the specialist. “The most common causes of chronic respiratory failure are” instead “chronic lung diseases such as chronic obstructive pulmonary disease (COPD) or interstitial lung diseases (pulmonary fibrosis), neurological diseases such as amyotrophic lateral sclerosis (ALS), obesity syndrome -hypoventilation (or Pickwick syndrome), cystic fibrosis, pulmonary hypertension, congenital or chronic worsening heart diseases”.

    Symptoms

    What are the symptoms? “Common manifestations of respiratory insufficiency are dyspnea, or shortness of breath – describes the pulmonologist – the reduction in oxygen saturation”, which is why Cecchi Gori arrived at Gemelli before having a respiratory crisis that left him led to hospitalization, or even “the use of the accessory muscles of ventilation, but also drowsiness to the point of coma”.

    “Respiratory insufficiency can therefore” determine alterations in the values ​​of oxygen in the blood, but also of carbon dioxide. In the sense of a decrease or, what is much more serious, an increase. This distinction – specifies Mancino – is necessary to keep in mind” when it comes to deciding on treatment.

    “When the partial pressure of oxygen in the blood falls below 55 mmHg – explains the expert – then it is necessary to treat respiratory failure”. We begin with the administration of oxygen through simple nasal cannulas, if the oxygen requirement is low, then moving on to special masks, up to high flow oxygen therapy through nasocannulae if the oxygen requirement is very high. “These measures are useful in correcting respiratory failure defined as hypoxemic and normocapnic, i.e. with normal carbon dioxide values”.

    However, “some pathologies (the most common is COPD) are characterized not only by low oxygen values ​​but also by high carbon dioxide values” or hypercarbia. The accumulation of carbon dioxide in the blood “initially manifests itself with hyper-reactivity and agitation, and then leads to a reduction in the state of consciousness (the patient appears drowsy), up to coma”. In this case the administration of oxygen is not enough, the pulmonologist points out, in fact it must be controlled because “the excess would lead to a further increase in carbon dioxide. It will therefore be necessary to reduce the carbon dioxide values ​​using non-invasive ventilation devices (patient in sub-intensive or home therapy) and in the most serious cases invasive (patient intubated in intensive care or tracheotomised)”.

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    Deep vein thrombosis (DVT) is a blood clot that forms inside a vein deep in the body, whereas superficial thrombophlebitis (STP) is inflammation of the veins just below the skin’s surface. STP can occur due to a blood clot in a superficial vein.

    DVT is a medical emergency. Without immediate treatment, it may lead to severe complications or even sudden death.

    In contrast, STP may resolve without the need for medical treatment. However, it may also increase the risk of developing DVT. If a person has symptoms of DVT or STP, it is best to seek medical help.

    This article compares the symptoms and causes of DVT and STP, outlines their treatments and outlooks, and provides tips on how to help prevent blood clots.

    The following sections outline the potential symptoms of DVT and STP.

    DVT symptoms

    DVT can develop in any of the body’s deep veins, but it typically develops in deep veins in the pelvis, thigh, or calf.

    According to the American Academy of Orthopaedic Surgeons (AAOS), DVT often does not cause symptoms. However, when symptoms do occur, they affect the part of the body where DVT occurs.

    DVT in the leg may cause the following symptoms in that leg:

    For some people, a pulmonary embolism may be the first sign of DVT. This is a blood clot in the lung and may cause the following symptoms:

    STP symptoms

    According to the United Kingdom’s National Health Service (NHS), STP usually affects the superficial veins in the legs but can also affect the superficial veins of the arms or neck.

    STP may cause the following symptoms in the affected part of the body:

    • pain, tenderness, or swelling
    • warmth and itchiness
    • changes to skin color, such as redness
    • changes to skin texture, such as thickness or hardness
    • firmness or thickening of the vein called a “cord” that a person may be able to feel

    Below are some causes of DVT and STP, as well as some of the risk factors associated with each of these conditions.

    DVT risk factors

    DVT forms when blood flow within one of the body’s deep veins slows or stops. According to the Centers for Disease Control and Prevention (CDC), some factors that can increase the risk include:

    • injury to the vein, such as from one of the following:
      • fracture
      • severe muscle injury
      • major surgery
    • slow blood flow, often due to:
      • limited movement
      • long periods of inactivity
      • paralysis
    • increased estrogen, often due to:
    • certain chronic medical conditions, such as:
    • a previous or family history of DVT or pulmonary embolism
    • aging
    • obesity
    • placement of a catheter in a central vein

    STP risk factors

    According to the NHS, STP does not always have a clear cause. Inflammation may occur due to:

    • varicose veins, which are swollen, enlarged veins
    • conditions that cause the blood to clot more easily, such as thrombophilia
    • autoimmune conditions that cause inflammation of the blood vessels, such as Behçet’s disease
    • receiving injections into a vein or having an intravenous (IV) line in a vein

    Other risk factors for STP include:

    • having a prior history of phlebitis
    • aging
    • obesity
    • pregnancy
    • cancer

    Below are the different treatment approaches for DVT and STP.

    DVT treatment

    According to the AAOS, DVT treatment aims to prevent the clot from getting larger, minimize the risk of complications, such as a pulmonary embolism, and reduce the risk of other clots.

    Treatment options include:

    • Observation and monitoring: If the DVT is in the lower part of the leg, a doctor may recommend observation and monitoring using a series of ultrasound scans.
    • Anticoagulant medications: These medications help dissolve existing blood clots and prevent further clotting. Examples include:
      • direct oral anticoagulants (DOAC)
      • heparin
      • low molecular weight heparin
      • warfarin (Coumadin)
    • Thrombolytics: These are medications that a doctor injects directly into a blood clot to help dissolve the clot. Doctors may use thrombolytics in cases where there is a very high risk of pulmonary embolism.
    • Surgical options: This may include surgery to remove a blood clot from the veins or lungs or surgery to fit a device called a vena cava filter, which captures blood clots traveling to the lungs.

    Nonsurgical DVT treatments are the most common. However, doctors may recommend surgical treatment for DVT in cases where anticoagulants are ineffective or a person is unable to take anticoagulants.

    STP treatment

    According to the NHS, STP that causes only mild symptoms may not require treatment.

    However, severe or persistent STP may require treatments such as:

    The outlooks for those with DVT and STP differ, with DVT presenting the greatest risk to health.

    DVT outlook

    According to the CDC, between 60,000 and 100,000 Americans die of DVT every year, with sudden death being the first symptom in approximately 25% of cases.

    Of those who survive DVT, around 1 in 3 will experience long-term complications. The most severe is a pulmonary embolism. Another is a condition called post-thrombotic syndrome (PTS).

    PTS develops in roughly 1 in 3 people who survive DVT. The condition occurs due to clot-induced damage to the valves within the vein. Symptoms develop in the affected body part and may include:

    The CDC also estimates that 1 in 3 people who survive the initial DVT will experience DVT again within 10 years.

    STP outlook

    According to the NHS, STP is not typically a medical emergency and usually resolves without treatment within 1–2 weeks.

    However, a 2017 review notes that STP often occurs alongside asymptomatic DVT. Therefore, the reviewers recommend that all individuals presenting with STP symptoms receive an ultrasound scan to check for DVT.

    According to the review, STP can also progress to DVT in some cases. The authors recommend that individuals at risk of developing DVT receive low dose anticoagulant medications as a preventive measure.

    The American Heart Association (AHA) recommends strategies for helping prevent blood clots in high risk situations, such as during periods of inactivity due to surgery, hospitalization, or long-distance travel.

    Methods to help prevent blood clots include:

    • making an effort to move around if possible
    • wearing compression devices
    • taking prescription medications
    • performing exercises, such as:
      • flexing and extending the ankles
      • contracting the calf muscles
    • changing positions regularly
    • staying hydrated

    It is best to contact a doctor as soon as possible if a person develops symptoms of STP. Although STP is rarely dangerous, research suggests that it can occur alongside DVT or progress to DVT.

    Anyone who develops symptoms of DVT should seek emergency medical care immediately. DVT is a life threatening condition that can lead to sudden death. Emergency medical treatment with anticoagulation medication can save a person’s life.

    Potential DVT symptoms to look out for include:

    • throbbing or cramping pain in the leg, arm, or neck
    • sudden swelling in the leg, arm, or neck
    • swollen veins that are hard or sore to the touch
    • warm, red, or darkened skin around the painful area

    Deep vein thrombosis (DVT) and superficial thrombophlebitis (STP) are conditions of the circulatory system. DVT is a blood clot that forms in a deep vein, whereas STP is inflammation of the superficial veins close to the skin’s surface.

    STP is typically not a medical emergency. However, research suggests that STP may increase a person’s risk of developing DVT. Anyone who experiences symptoms of STP should speak with their doctor for a thorough medical evaluation.

    DVT is a medical emergency. Anyone who experiences symptoms should phone the emergency services immediately. Prompt treatment with anticoagulant medications or surgery can help prevent complications, including death.

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    Pulmonary embolism (PE) is a serious condition that arises when a blood clot forms in the pulmonary arteries. This can lead to life-threatening complications, making early detection and treatment of paramount importance. However, diagnosis of this condition is often missed, leading to delayed treatment and potentially severe health complications. In this article, we aim to raise awareness about the signs and symptoms of pulmonary embolism, diagnostic methods, and the importance of early detection and medical intervention.

    Missed Diagnosis of Pulmonary Embolism

    Research suggests that diagnosis of pulmonary embolism is often overlooked, with 12-36% of patients misdiagnosed during initial evaluation. This issue is more prevalent in older adults, patients with chronic cardiopulmonary disease, and those with a low pre-test risk of PE. However, the use of D-dimer thresholds adjusted for age or probability may help reduce false positive results and unnecessary computed tomography pulmonary angiography (CTPA) scans, thereby improving diagnostic accuracy.

    Causes and Risk Factors of Pulmonary Embolism

    Pulmonary embolism usually occurs when a dislodged deep vein thrombosis (DVT) travels to an artery in the lungs. Risk factors for both PE and DVT are virtually identical, including lifestyle-related factors such as smoking, sedentariness, and certain medical conditions like cancer, obesity, pregnancy, and coagulation disorders. Certain medications and hormone replacement therapy can also increase the risk of blood clots. Despite the overall risk of PE being very low, it’s worth noting that it is higher for pregnant women than for nonpregnant women on hormonal contraceptives. Specific forms of hormonal birth control, such as birth control patches and pills containing higher levels of the progestin drospirenone, pose a higher risk compared to other forms of hormonal birth control.

    The Importance of Recognizing Symptoms

    Public figures like Serena Williams have shared their experiences with pulmonary embolism, emphasizing the importance of recognizing symptoms and advocating for personal health. According to the Centers for Disease Control and Prevention, up to 100,000 people die from DVT and PE each year in the United States, further highlighting the importance of raising awareness about the signs and symptoms of vascular diseases.

    Diagnostic Methods for Pulmonary Embolism

    For the diagnosis of pulmonary embolism, healthcare providers typically rely on imaging tests, blood tests, and clinical evaluation. Imaging tests such as CT pulmonary angiography (CTPA) and ventilation-perfusion scans are commonly used. Additionally, clinical assessment and D-dimer blood tests are crucial components of the diagnostic process, helping to confirm the presence of a clot or, conversely, rule it out.

    Early diagnosis is crucial for the successful treatment of pulmonary embolism. By understanding the causes, recognizing symptoms, and being aware of diagnostic methods, patients can improve their chances of early detection and prompt treatment, thereby enhancing their overall outcomes.

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