Adequate sleep duration with normal ventilation is crucial for normal cardiovascular function. Reductions in sleep timing (aka circadian rhythm disorders) or sleep duration (aka sleep deprivation) are independently thought to be harmful to normal CV function. Disturbances to ventilation are usually caused by either upper airway collapse (aka obstructive sleep apnoea [OSA]) or a "loop gain" disturbance between brain and lung interaction (aka central sleep apnoea [CSA]). OSA is thought to be injurious to the cardiovascular system, by virtue of hypoxia-hyperoxia, hypercapnia, large negative intrathoracic swings and fragmented sleep associated with autonomic dysfunction and inflammation. Accordingly the risk of developing systemic hypertension, arrhythmias, myocardial ischaemia, heart failure and stroke are elevated with OSA as shown by several large epidemiological (prevalance and incidence) studies controlled for the usual CV factors. Animal and human experimental data is also supportive. We await randomised controlled trials to determine whether OSA treatment improves CV outcomes and ultimately survival. In contrast, CSA occurs primarily in end stage heart failure, and is characterised by hyperventilation, increased pulmonary capilliary wedge pressure and low cardiac output. Symptoms may include orthopnoea, paroxysmal nocturnal dyspnoea and fatigue, often in the absence of snoring or sleepiness. CSA usually indicates severe CHF and may indeed involve mechanisms which offset CHF: these will be discussed.