Can Obstructive Sleep Apnea Cause Pulmonary Hypertension?

Can Obstructive Sleep Apnea Cause Pulmonary Hypertension?

There is data that confirms that obstructive sleep apnea syndrome (OSAS) is a cardiovascular risk factor. The events of airway obstruction during sleep prompt to alterations such as systemic hypertension, ischemic heart disease and cerebrovascular disease, representing a negative impact on the public health of our environment. The OSS is also associated with endothelial dysfunction, arrhythmias, cardiac insufficiency and pulmonary hypertension (PH).

OSAS is characterized by events of airway obstruction that lead to episodes of hypoxemia, changes in intrathoracic pressure, and activation of the sympathetic system. These mechanisms during sleep lead to an increase in systemic blood pressure, increased ventricular afterload and decreased cardiac output, and chronically lead to endothelial dysfunction, cardiac arrhythmias, sustained diurnal systemic hypertension, PH, and heart failure.

Alterations in breathing during sleep impact on the pulmonary circulation, hypoxia (it is a state of oxygen deficiency in the blood) and hypercapnia (it is a medical term that designates the abnormal elevation in the concentration of dioxide carbon in the arterial blood) have been recognized as the main mechanisms; although ventricular dysfunction, the generation of oxidation products, the increase of endothelin 1 levels and the reduction of alveolar nitric oxide are also involved. This contributes to the high prevalence of PH in patients with OSAS.

Can Obstructive Sleep Apnea Cause Pulmonary Hypertension?

Association Of OSAS With Pulmonary Hypertension:

PH is a cardiopulmonary condition of various etiologies and pathophysiological mechanisms that lead to right ventricular dysfunction. The mean pressure of the pulmonary artery (mPAP), measured by right cardiac catheterization is considered normal from 8 to 20 mmHg, above 25 mmHg, at rest it is considered PH.

According To The Etiological And Therapeutic Characteristics, PH Is Classified Into The Following Groups:

  1. Pulmonary arterial hypertension
  2. PH secondary to left cardiovascular disease
  3. PH secondary to pulmonary disease and/or hypoxemia
  4. PH due to pulmonary thromboembolic disease
  5. PH of indeterminate or multifactorial origin.

OSAS belongs to the third group because chronic hypoxemia, secondary to periods of airway obstruction during sleep, is considered the etiology of PH in these patients. The increase in pressure in the pulmonary artery generates resistance to flow and produces greater load for the right ventricle. This condition chronically produces structural and functional changes in the right ventricle that deteriorate the prognosis of these patients.

Hypoxia is a common factor in chronic respiratory disorders. Intermittent hypoxia experiments in animal models have shown that this state produces an increase in pulmonary arterial pressure. In rodents subjected to hypoxia every 30 seconds for eight hours a day for five days of the week for five weeks, a significant increase in pulmonary arterial pressure was found. In addition, there is an increase in the size of the right ventricle and the hematocrit (it is the volume percentage of red cells in the blood).

However, in humans it seems difficult to identify the true impact of OSAS as an independent cause of PH due to the existence of comorbidities such as obesity and chronic obstructive pulmonary disease.

The answer to this question seems to be approached through studies that evaluate the therapeutic impact on PH in patients with OSAS.

It is recognized that hypoxia is the main trigger of endothelial dysfunction and as a consequence it facilitates atherogenesis and the development of comorbidities that appear as the main causes of death. It is important to document the development of PH in the patients, since it is known that without treatment they evolve to ventricular dysfunction, which continues to have high mortality despite current therapeutic measures.

Positive pressure treatment is effective in most of the published reports, although there is a lack of benefit significant in secondary prevention of cardiovascular events.

Conclusion

It is important to mention that studies designed to demonstrate the impact of OSAS challenge researchers to continue developing strategies that allow knowing with greater precision and certainty the association between heart disease and respiratory disorders during sleep. In clinical practice patients look for the best strategy for an integral treatment.

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