Sleep Apnea Types, Pathogenesis & Diagnostic Tests

Sleep Apnea Types, Pathogenesis & Diagnostic Tests

The two main categories of sleep apnea include OSA (Obstructive Sleep Apnea) or CSA (Central Sleep Apnea). Here, learn more about the two sleep apnea types, pathogenesis, and diagnostic testing.

More than 18 million American adults have one of the two sleep apnea types – obstructive sleep apnea or central sleep apnea – where breathing repeatedly stops and starts during sleep. It is thought to be associated with a drop in arterial oxyhemoglobin saturation and/or an electroencephalographic arousal. “Apnea” actually owes its name to a Greek word meaning “want of breath”. “Sleep apnea” is cycles of significant pauses in breathing (absence of inspiratory airflow for at least 10 seconds) and partial neurological arousals that ultimately have an impact on sleep quality and overall health. The disordered breathing events are associated with a profile of perturbations. These include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction.

Types of Sleep Apnea

Sleep apnea is classified as either obstructive or central. Regardless of the sleep apnea type, it is a result of an absence of brainstem neural output to upper airway muscles. The pattern of this neural output absence determines the phenotype of OSA (Obstructive Sleep Apnea) or CSA (Central Sleep Apnea). In OSA, there is a complete or partial upper airway occlusion even though inspiratory muscles are working normally. Here, one can see the tongue falling backward with absent air flow. In contrast, CSA occurs when there is a transient reduction in breathing rhythm driven by the brainstem. Obstructive Sleep Apnea (OSA): OSA is repeated episodes of complete upper airway obstruction during sleep. OSA symptoms include loud snoring, periods of apnea and hypoxia, and sudden arousals from sleep. Studies support that OSA can lead to the development and progression of a number of cardiovascular disorders, including hypertension, cardiac arrhythmias, myocardial ischemia, infarction, and HF. In addition, OSA is known to be an independent risk factor for postoperative complications. The apnea-hypopnea index (AHI) is used to classify the severity of OSA. This is the number of apnea and hypopnea events per hours of sleep during overnight polysomnography (PSG) monitoring. An AHI of more than 30 is usually defined as a severe OSA. Central Sleep Apnea (CSA): CSA is not very common in the general population. Rather, it is usually seen among patients with heart failure, stroke, atrial fibrillation, or opioid use with the two most common causes of CSA being heart failure and opioid use. Studies show that CSA occurs in 30% to 50% of HF patients. CSA is a temporary withdrawal of central (brainstem-driven) respiratory drive. This withdrawal results in the cessation of respiratory muscle activity and airflow. It appears as a form of periodic breathing with recurring cycles of Cheyne-stokes respiration. In other words, a person will have a breathing pattern that is a progressively deeper and faster, followed by a gradual decrease with a temporary stop or an apneic episode.


Sleep has multiple pronounced effects on the respiratory system and breathing control. A complex matrix of peripheral and central receptors, as well as rhythm generators, interact continuously to control the respiratory system. This includes interaction with the lungs, chest wall, and arterial blood gas content. Pathogenesis of OSA: In OSA, studies show decreased activity of the diaphragm and dilator muscles of the upper airway when there is a decrease in electrical activity in the medullary inspiratory neurons. Individuals with altered mechanical properties of the upper airway are prone to upper airway obstruction. Several anatomic, as well as non-anatomic processes, may be responsible for upper airway patency. Enlarged tonsils, upper airway edema, decreased lung volume, obesity, as well as alterations in craniofacial structures, are some examples of anatomical factors. In contrast, non-anatomical factors cause OSA in 20 to 40% of individuals. Here, upper airway dilator muscle dysfunction, higher chemosensitivity, low arousal threshold, and fluid around the upper airway explain the apneic episodes during sleep. Pathogenesis of CSA: Understanding pathogenesis for CSA is more complex. Research supports that an increased respiratory control in response to changes in PaCO2 above and below the apneic threshold is in center to the pathogenesis of CSA. During the day, several metabolic and behavioral factors affect the rate of production of CO2. However, during sleep metabolic factors affect the breathing control. Therefore, during sleep, any increase in PaCO2 will stimulate ventilation where any decrease in PaCO2 will suppress it. When PaCO2 falls below the apneic threshold, respiration ceases.

Diagnosis of Sleep Apnea

A team of sleep disorder specialists is involved in making a definitive diagnosis of sleep apnea. This team can include a primary care physician, pulmonologist, or neurologist along with other sleep disorder specialists. Diagnostic tests are usually performed in a sleep center. With newer technology, it is also possible to perform a sleep study in the patient’s home:
  • Multiple Sleep Latency Test (MSLT) – a measurement of how quickly a person falls asleep. It measures the degree of excessive daytime sleepiness and helps to rule out other types of sleep disorders.
  • Polysomnography – a test that records a variety of body functions during sleep, which include eye movement, muscle activity, heart rate, respiratory effort, air flow, and blood oxygen This helps in diagnosis of sleep apnea as well as determine the severity of the sleep apnea.


Left untreated, sleep apnea can have serious and life-shortening consequences. Studies support that sleep apnea is associated with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, stroke, automobile accidents caused by falling asleep at the wheel, diabetes, depression, and other ailments. Patients can find help for their sleep apnea here: References:
  1. Deflandre, P.E., Bonhomme, V.L., Brichant, O.J., Joris, J.L., What mediates postoperative risk in obstructive sleep apnea: airway obstruction, nocturnal hypoxia, or both? Can J Anesth/J Can Anesth (2016) 63:1104–1105.
  2. National Institutes of Health - National Heart - Lung and Blood
  3. Costanzo, R.M.; Khayat, R.; Ponikowski, P.; Augostini, R.; Stellbrink, C.; Mianulli, M.; Abraham, t. W. Mechanisms and Clinical Consequences of Untreated Central Sleep Apnea in Heart Journal of the American College of Cardiology. (2015) 65; 72-84.
  4. Hudgel, D. Critical Review: CPAP and weight management of obstructive sleep apnea cardiovascular co-morbidities. Sleep Medicine Reviews. (2018) 37; 14-23.
  5. Floras, J. Sleep apnea and cardiovascular risk. Journal of Cardiology. (2014) 63; 3-8.
  6. Javaheri; Barbe, F.; Campos-Rodriguez, F.; Dempsey, A.J.; Khayat, R.; Javaheri, S.; Malhotra, A.; Martinez-Garcia, A, M., Mehra, R.; Pack, I. A.; Polosky, Y. V.; Redline, S.; Somers, K.V. Sleep Apnea: types, Mechanisms and Clinical Cardiovascular Consequences. Journal of the American College of Cardiology. (2017) 69; 841-858.
  7. McEvoy, R.; Antic, A.N.; Heeley, E.; Luo, Y.; Ou, Q.; Zhang, X.; Mediano, O.; Drager,
  8. L.; Liu, Z.; Chen, G.; Du, B. CPAP for PREvention of Cardiovascular Events in Obstructive Sleep Apnea. The New England Journal of Medicine. (2016); 375: 919-931.
This article was written by Bijal Shah, Clinical Educator

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