Pathophysiology of Obstructive Sleep Apnea

In this article, we will discuss about Pathophysiology of Obstructive Sleep Apnea. So, let’s get started.


During inspiration, the intraluminal pressure becomes negative creating a suctioning force and since there is no bone or cartilage present in the pharyngeal airway the stabilization completely relies on the pharyngeal dilator muscles. These muscles are continuously activated during wakefulness, neuromuscular output declines with sleep onset. In patients with collapsible airway, the reduction in neuromuscular output results in transient episodes of pharyngeal collapse (apnea) or near collapse (hypopnea). The episodes are terminated when ventilatory reflexes are activated and cause arousal and then stimulating an increase in neuromuscular activity and opening the airway. Obstructive sleep apnea may be most severe during rapid eye movement sleep when the neuromuscular output to the skeletal muscles is particularly low, and also in supine position due to gravitation force.

Individuals with small pharyngeal lumen are more predisposed to excessive airway collapsibility during sleep as they require high levels of neuromuscular innervation to maintain patency during wakefulness. The airway lumen may be narrowed because of the enlargement of soft tissue structures such as tongue, palate, uvula, etc. Craniofacial factors such as mandibular retroposition, genetic variation or developmental influences also can reduce lumen dimension.

Additionally, lung volumes influence the caudal traction on the pharynx causing stiffness of the pharyngeal wall. Low lung volumes in the supine position (particularly in obese individuals) contribute to pharyngeal collapse. High-level nasal resistance can also contribute to pharyngeal collapse because of negative intraluminal suction pressure.

Pharyngeal muscle activation is integrally linked to ventilatory drive. Thus, factors related to ventilatory control, particularly ventilatory sensitivity, arousal threshold, and neuromuscular responses to CO2, contribute to the pathogenesis of Obstructive Sleep Apnea. Pharyngeal collapse can also occur when the ventilatory control system is overly sensitive to CO2, with resultant wide fluctuations in ventilation and ventilatory drive and in upper airway instability. Increased level of CO2 during sleep results in CNS arousal and moves an individual from a deeper to a lighter level of sleep or can also awaken. A low arousal threshold can forestall the CO2-mediated process of pharyngeal muscle compensation and prevent airway stabilization. A high arousal threshold conversely may prevent appropriate termination of apneas, prolonging apnea duration, and exacerbating oxyhemoglobin desaturation severity. Finally, any impairment in the ability of the muscles to compensate during sleep can contribute to the collapse of the pharynx.


Investigations required for diagnosing Pulmonary Venous Thromboembolism

In this article, we will discuss about various Investigations required for diagnosing Pulmonary Venous Thromboembolism. So, let’s get started.


The chest x-ray may be normal; however, in case of positive x-ray following findings are frequently noted:


Elevated hemidiaphragm

Enlargement of cardiac shadow

Enlarged pulmonary conus

Pleural effusion

Lung consolidation

Avascular lung zone (Westermark sign), wedge-shaped opacity above hemidiaphragm (Hampton’s hump) and enlarged right descending pulmonary artery (Palla’s sign) are also noted in the chest x-ray.

The ECG may be normal in mild to moderate cases with 70-80% cases just show sinus tachycardia. In severe cases, ECG shows P pulmonale wave acute right ventricular strain (T wave inversion in V1-V4) or myocardial ischemia (ST-segment depression I and II) or both. Right axis deviation and clockwise rotation are common. the SIQIII, TIII syndrome in which there is S wave in lead I and Q wave in lead III with inversion if present is highly suggestive of acute pulmonary embolism. The transient development of incomplete RBBB is indicative of acute pulmonary embolism. Recurrent episodes of arrhythmias, sinus tachycardia, atrial fibrillation may also occur.

Arterial blood gas analysis shows hypoxemia with respiratory alkalosis.

CT pulmonary angiography is considered a gold standard for the diagnosis of pulmonary embolism. It provides direct visualization of intraluminal filling defects or abrupt cut-off the vessel caused by pulmonary embolism.

Plasma D-dimer analysis helps in the diagnosis of pulmonary embolism.

The 2-D echocardiogram reveals right ventricular dilatation/dysfunction, hypokinesia, septal flattening, and tricuspid regurgitation.

Radioisotopic ventilation-perfusion ratio (V/Q scan) is the second line diagnostic test for pulmonary embolism. The hypoperfusion or under-perfused area of the lung is shown as cold spots or avascular zone in the scan. A high probable scan is defined as two or more segmental perfusion defects with normal ventilation indicates pulmonary embolism.

Spiral contrast chest CT is the principal imaging test for the diagnosis of pulmonary embolism. This approach is best suited for the identification of the emboli that are situated in the proximal pulmonary vessels; however, is unsuitable for the identification of emboli present in the distal vascular bed.

Diagnostic test (Doppler ultrasound, impedances plethysmography, contrast venography, contrast MRI, etc) which confirms the diagnosis of DVT raises the possibility of pulmonary thromboembolism.