Relationship between pulmonary hypertension and sleep apnea

Pulmonary Hypertension And Sleep Apnea

relationship between pulmonary hypertension and sleep apnea

However, most studies have reported no association between severity of OSA (as . Management of Obstructive Sleep Apnea – Pulmonary Hypertension. Keywords: pulmonary hypertension, obstructive sleep apnea, heart failure, . concluded that there was a direct causal relationship between hypoxia and PH. Pulmonary hypertension is a rare and serious lung disorder. is the connection between sleep apnea and pulmonary hypertension (PH)?.

Prevalence data on resting, awake PH in OSA is based primarily on retrospective case series or prospective cohort studies with poorly defined entry criteria Table 1. In addition, several comorbidities including left-sided cardiac disease, COPD, and obesity may have an impact on the occurrence of PH and were not always excluded. Female preponderance has been described in several other forms of PH and has been attributed to genetic predisposition, the role of estrogen, and higher prevalence of autoimmune disease in females.

On the other hand, even studies of patients without significant cardiopulmonary disease have included patients with small airway abnormalities83 or mild hypoxemia. Unlike patients with PAH who have chronic RV pressure overload and markedly elevated pulmonary vascular resistance, OSA patients may have chronic volume overload with milder elevation in pulmonary vascular resistance, suggesting that these patients may not have a large decrease in the cross-sectional area of the pulmonary vasculature.

Current evidence, however, suggests that the occurrence of RV systolic failure in OSA requires the presence of additional comorbidities such as chronic lung disease or left ventricular dysfunction. In addition to causing vasoconstriction and shear stress, chronic hypoxia exerts its effect on the vascular endothelium and smooth muscle cells mainly the small muscular pulmonary arteries and nonmuscular precapillary arterioles to release vasoconstrictive, pro-proliferative, and mitogenic mediators.

Several mediators including endothelin-1, vascular endothelial growth factor, angiotensin II, nitric oxide, endothelial apoptotic factors, angiotensin converting enzyme, inflammatory mediators IL-8, IL-6reactive oxygen species, and various transcription factors such as hypoxia-inducible factor-1 have been implicated in this process.

Extreme capillary proliferation may also be seen in some patients with severe OSA and RV hypertrophy. Individual variation in ventilatory responsiveness to hypoxia demonstrated in awake OSA patients could also modulate the magnitude of PAP changes, although its role in PH remains controversial.

So far it has not been convincingly demonstrated that a reduced chemosensitivity, possibly secondary to repetitive nighttime hypoxemic and hypercapnic episodes, can lead to daytime hypoxemia or PH. Whether the repetitive upper airway collapse and large intrathoracic negative pressure swings with nocturnal oxygen desaturation and hypercapnia leading to marked variation in PAP underlies the chronic PAP elevation in OSA requires further study.

The role of comorbidities Several studies have shown that OSA patients with PH often have concomitant cardiac or pulmonary disease, leading to the speculation that such comorbidities are a prerequisite for the development of significant PH and RV failure in OSA.

It has been suggested that PH in association with OSA is mainly precapillary in nature; however, given the prevalence of morbid obesity, hypertension, and left ventricular systolic and diastolic dysfunction in this population, it is likely that postcapillary factors play an important role. Diastolic dysfunction and left ventricular hypertrophy with elevated PCWP have been demonstrated in OSA patients without any other evidence of underlying cardiac disease and may contribute to the diagnosis of PH during rest and exercise.

Two other studies have reported similar findings, suggesting that PVH due to diastolic dysfunction is an important factor in patients with OSA. Chronic obstructive pulmonary disease is often the primary cause of alveolar hypoventilation in OSA. Discrepancies in the findings among the series in the literature could be accounted for by the differences in the prevalence of severe obesity in each series and across continents where these studies were conducted.

Pulmonary Hypertension and Sleep Apnea

Role of humoral factors The effect of humoral factors on awake PAP remains speculative. Clinical Significance of Pulmonary Hypertension in Obstructive Sleep Apnea Pulmonary hypertension can lead to functional decline and poor prognosis in several diseases, including connective tissue diseases, pulmonary fibrosis, and COPD. This study further showed that mortality was increased in patients with PH Figure 3 and that in addition to factors such as age, forced expiratory volume in 1 second, diffusion capacity for carbon monoxide, and AHI, pulmonary hemodynamics were important correlates of increased mortality in patients with OSA.

In addition, exertional and nocturnal hypoxia should be corrected with oxygen supplementation or CPAP therapy as appropriate. It is unclear whether the mild PH found among OSA patients without concomitant cardiopulmonary diseases requires treatment. In addition to relieving the upper airway obstruction and minimizing the intrathoracic pressure swings, long-term treatment with CPAP can produce significant improvement in daytime arterial oxygenation, raising the expectation of improvement or stabilization of PH, similar to that seen in COPD patients receiving long-term oxygen supplementation.

A prospective, uncontrolled, single-center case series by Sajkov et al showed significant decrease in the daytime PAP and pulmonary vascular response to hypoxia after 4 months of nasal CPAP treatment in 5 of the 20 OSA patients with mild PH. These were followed by larger prospective, controlled trials. Based on the current limited data, we can conclude that CPAP therapy has a modest role in improving pulmonary hemodynamics in OSA and is less likely to normalize the more severe elevations in PAP.

Matilde et al showed a significant improvement in pulmonary hemodynamics following a marked reduction in body weight and resolution of OSA following bariatric surgery. Development of PH is likely multifactorial, involving both precapillary and postcapillary processes. Due to a lack of population-based studies, the true prevalence of PH is not known; however, it is clear that patients with comorbidities are at higher risk. In patients with milder elevations in PAP, CPAP therapy has the potential to improve pulmonary hemodynamics, although the role of adjunctive vasomodulatory therapy should be explored in those with more significant elevations.

relationship between pulmonary hypertension and sleep apnea

Longer-term studies of various treatment options with an emphasis on functional improvement, quality of life, and survival are required to properly assess their role. Key Words—obstructive sleep apnea, pulmonary hypertension, right heart failure, right ventricular hypertrophy Address for reprints and other correspondence: Pulmonary hypertension associated with chronic respiratory disease.

Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol. Epidemiology of obstructive sleep apnea: Cardiovascular outcomes of CPAP therapy in obstructive sleep apnea syndrome. Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines.

Obstructive sleep apnea and pulmonary hypertension. Frequency and impact of pulmonary hypertension in patients with obstructive sleep apnea syndrome. Pulmonary hypertension in the obstructive sleep apnoea syndrome: Prevalence, causes and therapeutic consequences. Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea. Screening, early detection, and diagnosis of pulmonary arterial hypertension: Diagnosis and differential assessment of pulmonary arterial hypertension.

Pulmonary arterial hypertension in patients with sleep apnoea syndrome. Pulmonary hypertension in patients with obstructive sleep apnea syndrome. Severe pulmonary hypertension and chronic obstructive pulmonary disease.

Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med. Importance in the assessment of pulmonary hypertension in obstructive sleep apneas. Marrone O, Bonsignore MR.

relationship between pulmonary hypertension and sleep apnea

Pulmonary haemodynamics in obstructive sleep apnoea. Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep.

Influence of sleep state and sleep disordered breathing on cardiovascular function. Continuous recording of the pulmonary and systemic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing. Bull Physiopathol Respir Nancy. Hemodynamic and respiratory aspects of the pickwickian syndrome. Manifestation of pulmonary hypertension during REM sleep in obstructive sleep apnea syndrome.

Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: Pulmonary hemodynamics in the obstructive sleep apnea syndrome.

Results in consecutive patients. Pulmonary hypertension in obstructive sleep apnoea. Haemodynamic studies in sleep apnea. Guilleminault C, Dement WC, eds. Sleep apnea and pulmonary hypertension. Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease.

Am Rev Respir Dis. Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome. Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome.

Daytime pulmonary hypertension in patients with obstructive sleep apnea: Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity. Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease. If PH is severe and does not improve with the treatment of the sleep disorder, then other reasons for PH need to be investigated.

Can pulmonary hypertension PH cause a reduction in oxygen during sleep? This is a very good question. Yes, patients with PH can have low oxygenation during sleep. Interestingly, patients with sleep apnea—a condition associated with low oxygenation during sleep—can also be a cause of mild PH.

At what point do I begin therapy for pulmonary hypertension PH? Treatments for PH are approved for patients with some degree of shortness of breath with activity. If you have no symptoms, the echocardiogram is normal, and the blood work is normal, then you can be followed closely by a physician with experience treating the disease. Can having pulmonary ablations for atrial fibrillation cause pulmonary hypertension? Can having sarcoid of the lungs in childhood that has been in remission for 30 years cause pulmonary hypertension?


Sarcoidosis and Pulmonary Hypertension Batyah: What is the connection between sarcoidosis and pulmonary hypertension PH? As a sarcoidosis patient, what can I do to prevent or minimize the risk of having PH? As a sarcoidosis patient, what are the treatments for PH? A limited number of patients with sarcoidosis develop PH. It is hard to predict which patients with sarcoidosis will develop the disease. A regular follow up would be able to determine if you develop this.

For a person who already has pulmonary sarcoidosis, what are the symptoms of developing pulmonary hypertension PH? Symptoms of PH include worsening of the respiratory symptoms, edema, and dizziness or passing out. A higher need for oxygen is another presentation. Do you have any statistics on the prevalence of pulmonary hypertension in sarcoidosis?

relationship between pulmonary hypertension and sleep apnea

I do not have a statistic on its prevalence, but it is rare. It is hard to tell as there are many patients with sarcoidosis that have limited symptoms and remain undiagnosed. What are the initial tests to confirm or exclude pulmonary hypertension PH?


Stress echo is usually not regularly done in pulmonary hypertension PH patients unless there is suspicion of ischemic coronary artery disease. Rarely echocardiograms are done during exercise to see if the estimated right ventricular systolic pressure increases with activity exercise-induced PH. There are limited studies that can be done at this point to help in the diagnosis. We order several blood studies to help determine the cause of pulmonary hypertension.

This is a biomarker that helps determine if you have volume overload excessive fluid. Can a CAT scan offer any help with diagnosis? CT scan of the chest can reveal a dilated pulmonary artery that can suggest the diagnosis. However, this alone is not enough and further evaluation is needed. Some patients have PH related to lung diseases and these most of the time can be seen in a CT of the chest. In addition, patients with unresolved clots in the lung can be identified during a CT with contrast.

My heart catheterization in showed right ventricular systolic pressure of 41, and the echocardiogram echo was normal. Now the echo shows a pressure of Should the right heart catheterization be repeated? The right ventricular systolic pressure estimated by echocardiogram is not very precise. It uses tricuspid flow to estimate a pressure and variations of more than and less than 20 mmHg are not uncommon.


Pulmonary Hypertension



If you have higher pressure than the normal pressure of 25 in your right ventricle, how do you know if you have pulmonary hypertension PH? If your mean pulmonary artery pressure during a right heart catheterization is 25 mmHg or above, you do have pulmonary hypertension.

If your systolic right ventricular pressure on an echocardiogram is 25 mmHg—this is in normal range. However, echocardiogram is not the best tool to exclude or include PH. Further investigation with a right heart catheterization is decided on a case-by-case basis. I have just had a right heart catheterization that confirmed pulmonary arterial hypertension PAH. What can I expect my life expectancy to be? It would depend on a variety of factors. However, none of these tools are perfect. Fortunately, there are 10 pulmonary hypertension medications available and most patients improve.

The classes of PH include: PH originating at the pulmonary arteries i. Progression of treatment depends on different factors, such as symptoms, distance walked, right ventricular function on echocardiogram, and so on. Can you tell us something about the new medications that were approved by the FDA and how they related to the present medications?

Are they to be used instead of the present medications or to be added to the "cocktail"? Instead would be the answer. Therefore, they cannot be used together. I have idiopathic pulmonary arterial hypertension. How do the new medications recently approved by the FDA relate to the present medications that are available? For these conditions there were no FDA approved therapies. Surgery and Pulmonary Hypertension nutzy: What is your recommendation for a year-old female who needs mitral valve surgery, but the doctor also discovered severe pulmonary hypertension PH of ?

Should I start medical treatment before the surgery? A patient with mitral valve disease commonly will have pulmonary hypertension.

Usually the risks of surgery increase in the presence of advanced PH. Some physicians will consider sildenafil. However, this needs to be done very carefully as some patients could get worse. Can losing weight and doing cardio aerobic exercise help with mild pulmonary hypertension. Weight loss and exercise increase your capacity to do more, almost as much as some oral pulmonary hypertension therapies.