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Sleep Apnoea and Systemic Hypertension

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Sleep Apnoea and Systemic Hypertension Thorax: first published as 10.1136/thx.44.12.984 on 1 December 1989. Downloaded from Thorax 1989;44:984-989 Review Sleep apnoea and systemic hypertension Gross obstructive sleep apnoea has two clear pitfalls and problems with these experimental and consequences, recurrent sleep disruption (with epidemiological data, which call for careful scrutiny daytime sleepiness) and repeated noctural hypox- before health screening programmes start to label aemia. The importance of the hypoxaemia is debated snoring as more than an auditory nuisance. but when it is severe, or perhaps in the presence of This review divides the lines of argument and ischaemic heart disease, it may trigger off serious evidence into five parts: (1) How does obstructive sleep arrhythmias.' When associated with even quite mild apnoea raise systemic blood pressure acutely? (2) Does lower airways obstruction, obstructive sleep apnoea obstructive sleep apnoea really raise diurnal systemic may lead to diurnal hypoxaemia and hypercapnia23 blood pressure in the long term and increase cardio- with all the well known sequelae of fluid retention, vascular complications? (3) What is the evidence that pulmonary hypertension, and right ventricular hyper- an important proportion of patients with essential trophy (cor pulmonale).4 Why profound intermittent hypertension have appreciable sleep apnoea? (4) What hypoxaemia may apparently be harmless is not clear, is the epidemiological evidence that snoring is an but the key may be in its short duration and the independent risk factor for systemic hypertension and recovery of arterial oxygen tension (Pao2) between cardiovascular events? (5) What evidence do we need episodes ofapnoea. For example, this pulsatile hypox- to establish whether snoring and sleep apnoea are aemia does not lead to raised erythropoietin concen- important and underdiagnosed causes of essential trations,5 which explains the rarity ofpolycythaemia in hypertension or cardiovascular events? copyright. obstructive sleep apnoea until daytime Pao2 is also low. How does obstructive sleep apnoea raise systemic blood What this recurrent asphyxia of obstructive sleep pressure acutely? apnoea does do, however, is to cause profound recurrent changes in haemodynamics. A rise in systolic During normal non-REM sleep systolic blood pres- blood pressure during the course of an episode of sure is about 5-14% lower than during relaxed http://thorax.bmj.com/ apnoea, with a further increase on arousal and wakefulness.7 The pressures are not constant but show termination of the apnoea, was documented early in smooth oscillations with 20-30 second cycles.'0 Blood the history ofobstructive sleep apnoea.6 Thus, whereas pressure is higher during REM than non-REM sleep normally sleep is associated with a low and relatively but does not reach the awake levels.7". stable systolic blood pressure,' in obstructive sleep With the onset of obstructed inspiratory efforts the apnoea arterial pressure is higher on average and recurrent falls in pleural pressure (sometimes as low as oscillates considerably.8 The early finding that many -80 cm H20) are reflected to a varying extent as with obstructive apnoea had diurnal recurrent dips in the systolic blood pressure.8 Because patients sleep on September 26, 2021 by guest. Protected systemic hypertension9 led most workers to assume the heart is in the chest, pleural pressures are added to that this was a consequence of recurrent cardio- and subtracted from the systolic blood pressure (pul- vascular instability during sleep. This premise led sus paradoxus). They are not, however, fully reflected some authors to search for hidden sleep apnoea among in systolic blood pressure swings owing to a com- patients with essential hypertension, and to look for plicated net effect of other factors and compensatory epidemiological evidence that people with a history of measures.'2 As the apnoea progresses systolic blood snoring (a marker of possible obstructive sleep pressure rises and this is thought to be due to the apnoea) might be at greater risk of cardiovascular concomitant fall in arterial oxygen saturation (Sao2). events such as stroke, angina, and myocardial infarc- The systolic blood pressure rise mirrors the fall in Sao2, tion. Indeed, the suggestion has even been made that as does the accompanying bradycardia. Whether the snoring alone, through bigger swings in pleural rise in blood pressure is a direct consequence of the pressure and cardiac loading, might increase the risk hypoxaemia, or the hypercapnic acidosis, or is due to of cardiovascular events in the absence of frank the increased (albeit frustrated) respiratory effort that obstructive sleep apnoea. There are, however, many these provoke is not clear. So called "irradiation" of the cardiovascular centre from the respiratory centre may be responsible. The accompanying bradycardia is Address for reprint requests: Dr J R Stradling, Osler Chest Unit, as it Churchill Hospital, Oxford OX3 7LJ. only partially accounted for by the hypoxaemia, 984 Thorax: first published as 10.1136/thx.44.12.984 on 1 December 1989. Downloaded from Sleep apnoea and systemic hypertension 985 requires apnoea (no lung expansion) and may be part expected during exercise, but clearly for those pres- of the diving reflex." '3 Stimulation of the carotid sures to be maintained throughout the night is body, in the absence of stretch receptor activity, extremely abnormal. produces bradycardia.'4 During awake held inspira- Recent evidence suggests that patients with obstruc- tory manoeuvres (Mueller) patients with obstructive tive sleep apnoea do have left ventricular hyper- sleep apnoea develop bradycardia apparently irrespec- trophy,25 but it is difficult to separate the relative tive ofany accompanying hypoxaemia.'5 In this study, contributions of nocturnal hypertension, diurnal however, the degree ofhypoxaemia was much less (4% hypertension, and obesity. fall in Sao2) than that experienced by the patients during their episodes ofsleep apnoea ofsimilar length (9% fall in Sao2), and a maintained Mueller Does obstructive sleep apnoea really raise diurnal manoeuvre is not at all like obstructive sleep apnoea, systemic blood pressure in the long term and increase where the inspiratory efforts are phasic until the cardiovascular events? apnoea breaks. At the moment of arousal and termination of an Whether the systemic hypertension that occurs during episode of apnoea there is a further rise in systolic recurrent apnoea is carried over to the waking hours is blood pressure, probably as a result of the release of by no means clear. Periods of stress from other causes the bradycardia (by stretch receptor activity), the rise that release catecholamines are thought to cause in sympathetic output occurring with arousal, and the sustained hypertension,26 and increased sympathetic continuing fall in arterial oxygenation-which, of activity is thought to underlie much essential hyper- course, takes a further 10-12 seconds to reverse at the tension.2' Excess sympathetic activity may also raise carotid body (and brain) owing to the circulation time. blood lipid concentrations.28 On average systolic blood pressure usually rises The prevalence of systemic hypertension in patients about 1 mm Hg for every 1% fall in Sao2 and the with obstructive sleep apnoea in most series exceeds diastolic pressure rises about 0 5 mm Hg.8 This is not 40%.9 Even in severe obstructive sleep apnoea the copyright. always the case and falls in systolic blood pressure hypertension is often only moderate, however. Until have been observed in association with apnoea in older recently the obstructive sleep apnoea was assumed to patients. 6 be the main cause but the confounding variable of The fall in Sao2 and rise in systolic blood pressure obesity (or, more particularly, upper body obesity) are associated with a rise in sympathetic nervous was rarely considered. As most patients with obstruc- output'7 and catecholamine production.'8 9 Thus tive sleep apnoea are obese it is difficult to be sure http://thorax.bmj.com/ much ofthe rise in systolic blood pressure is likely to be which factor is causing the hypertension. In a recent due to peripheral vasoconstriction, as cardiac output report Hoffstein et alQ used multiple linear regression has been shown to fall during the episodes ofapnoea, a to dissect out the contributory causes ofhypertension; result mainly of the bradycardia, though stroke obesity proved to be the dominant factor, apnoea volume may also fall.20 severity being very much ofsecondary importance. Of The recurrent subatmospheric pleural pressures 372 patients who snored, 194 had sleep apnoea (> 10 during each episode of obstructive apnoea, down to a events/hour ofsleep). Eight per cent ofthe variance in certain pressure at least,2' will aspirate venous blood diastolic blood pressure in the group was accounted into the right heart, and this may cause deviation ofthe for by body mass index (weight/height2, W/H2), 4% by on September 26, 2021 by guest. Protected interventricular septum and embarrassment of left age, and only 1-7% by number of apnoeic episodes/ ventricular filling by reducing its compliance.2223 On hour of sleep. In an epidemiological survey that the other hand, the left ventricle will also be subjected identified 15 individuals with obstructive sleep to a similar dilating force and thus a higher preload. apnoea, the prevalence of hypertension was no higher There is fluoroscopic evidence that both the left and in the 15 subjects with sleep apnoea than in 46 the right heart enlarge during obstructive apnoea.24 If without.' left ventricular transmural pressure stayed constant, After effective treatment for obstructive sleep the fall in systolic blood pressure would equal the fall apnoea (mainly in obese patients) the blood pressure in pleural pressure. Starling's law of the heart, falls to some extent, but not to normal.3' There are no however, will offset this to some extent if the left good data to show a significant fall in diurnal systemic ventricle can dilate. The rising peripheral resistance blood pressure after the institution of nasal contin- will present a raised afterload insofar as systolic uous positive airway pressure (CPAP).
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