Sleep apnoea is a type of breathing disorder which occurs during sleep. Breathing occurs automatically in healthy individuals but can become disordered in various ways as part of different conditions.
The commonest form of sleep breathing disorder is snoring in which partial collapse of the airway occurs during sleep, breathing effort increases and overcomes the obstruction to breathing but makes a noise in the process. Snoring is common and thought not to have adverse health effects.
If breathing is reduced we call that hypopnoea, and when it stops altogether for at least 10 seconds it is called apnoea. If breathing efforts are increased with these hypopnoeas or apnoeas and there are 5 or more per hour of sleep it is called obstructive sleep apnoea or OSA.
There are other types of sleep disorder where breathing is reduced or stops altogether without an increase in breathing efforts. This is called central apnoea because the brain stem has turned off breathing efforts. The cut off for diagnosis is 5 or more breathing events per hour. The common type of central sleep apnoea (CSA) is due to heart failure. It is also seen in patients with stroke although less commonly than OSA and occurs in healthy individuals at altitude (altitude sickness) such as during visits to Machu Picchu in Peru.
Cardiologists are aware that the common type of sleep apnoea – obstructive sleep apnoea or OSA – is linked to a number of heart and blood vessel (cardiovascular) problems including high blood pressure (hypertension), artery disease – including coronary, aortic and carotid arteries – cardiomyopathy and heart failure.
Snoring is a marker of risk of OSA but most snorers (2 in 3) don’t have sleep apnoea; it is possible to have OSA and not be known to snore. In sleep apnoea, the airway collapses, partly or completely during sleep and normal breathing recovers because the brain briefly wakes up from sleep (called an ‘arousal’) promptly followed by sleep, snoring and obstruction. This cycle is repeated literally 100’s of times a night in more severely affected patients. It is often more severe in the deeper stages of sleep called slow wave and REM sleep. This loss or duration and quality of sleep can affect daytime performance greatly but most sufferers of OSA have no identifiable daytime symptoms.
OSA is often thought of as a disease of overweight middle-aged men, but it occurs at all ages, in men and women- including during pregnancy- and in slim as well as the obese.
Recent research has shown that heart rhythm problems such as atrial fibrillation (AF), slow heart rhythms (sinus bradycardia and heart block) as well as potentially serious arrhythmias like ventricular tachycardia (VT), are common in OSA especially when it is severe.
The consequences of these conditions may be heart attacks, strokes and even sudden death. Undetected or untreated OSA can adversely impact on treatment of heart disease with medications, electrical cardioversion, pacemakers or defibrillators.
A recent study from the Mayo Clinic showed that 80% of those admitted for electrical cardioversion of atrial fibrillation had OSA and only 1 in 3 (35%) were sleepy using the Epworth Sleepiness Scale. In a previous study the same group showed those with untreated or inadequately treated OSA were twice as likely to have gone back into AF over the next year.
Detecting and treating OSA can be beneficial to quality and length of life in those with risk factors or diagnosed heart disease. The lack of daytime sleepiness or tiredness in patients with OSA can make treatment by lifestyle changes, dental splints (MAS) or CPAP harder to adjust to than OSA patients motivated by improvement in daytime symptoms.
The condition is traditionally diagnosed by an overnight study in a sleep laboratory but increasingly we use simpler home testing equipment to screen for OSA.
This type of breathing disorder occurs during sleep in those with heart failure. Known to occur since the early 1900s it results in alternating cycles of over breathing, or hyperventilation, followed by breathing stoppages without an attempt to breathe during them called central (sleep) apnoeas. The traditional medical term has been paroxysmal nocturnal dyspnoea or PND. Although OSA can cause heart failure, this condition is due to heart failure, not the other way around. As the sufferer is not attempting to breathe during the apnoea, it is relatively silent and those who had snoring or OSA before heart failure developed, are noticed to have gone quiet but this is not as good as it might seem. The condition is conventionally diagnosed by a full diagnostic sleep study (PSG) but is a very variable condition which changes between sleep stages, with sleeping posture, disease progression and in response to heart failure treatment.
Central sleep apnoea/Cheyne-Stokes respiration forms part of a downward spiral in heart failure and although CSA is common in heart failure at worst only 70% of heart failure sufferers will develop it. This condition will change as heart failure status changes; it may improve in response to drug or device-based treatments for heart failure.
The physiology of CSA in heart failure is complex but leads to unstable breathing patterns in which there are alternating cycles of over-breathing (hyperventilation) and under-breathing (hypoventilation or apnoeas). Hyperventilation lowers CO2 in the blood (hypocapnia) which acts on the breathing control centres in the brainstem and reduces or actually stops breathing efforts. When breathing resumes it is excessive and hyperventilation recurs.
Treating this type of sleep apnoea starts with optimising the conventional treatment of heart failure but positive airway pressure either simple (CPAP, BiPAP®, or VPAP™) or more complex treatment (Adaptive Servoventilation or ASV) can improve both the sleep apnoea and heart failure. Major clinical trials are underway to answer these and other questions.