Sleep and cardiac disorders

Carolina Lombardi MD PhD (Dr. Lombardi of the University of Milano-Bicocca and Head of the Sleep Disorders Center at San Luca Hospital has no relevant financial relationships to disclose.)
Paola Mattaliano MD (Dr. Mattaliano of the IRCCS Instituto Auxologico Italiano has no relevant financial relationships to disclose.)
Gianfranco Parati MD (Dr. Parati of the University of Milano-Bicocca and Instituto Auxologico Italiano IRCCS in Milan, Italy has no relevant financial relationships to disclose.)
Antonio Culebras MD, editor. (Dr. Culebras of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
Originally released November 4, 1993; last updated June 12, 2016; expires June 12, 2019

This article includes discussion of sleep and cardiac disorders, sleep disorders associated with congestive failure, sleep disorders associated with periodic respiration with apnea, sleep disorders associated with angina, sleep disorders associated with arrhythmias, and sleep disorders associated with heart failure. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

In normal subjects, sleep is characterized by physiological changes in cardiovascular parameters (blood pressure, heart rate), but sleep and, in particular, sleep disorders are also related to cardiovascular diseases. Patients with cardiovascular diseases may complain of several sleep disturbances, such as sleep fragmentation, insomnia, and breathing disorders, during sleep. On the other hand, patients with sleep disorders seem to be more frequently affected by cardiovascular disorders, so it is often difficult to determine which is the cause and the effect. Quality and duration of nocturnal sleep have been reported as factors affecting the health status of a population, particularly the cardiovascular risk profile. Specifically, sleep features and sleep disorders seem to play an important role in determining blood pressure levels, both in the office and over 24 hours, and in modulating the day-night blood pressure profile, which can have an impact on the prognosis of hypertensive patients. However, the most important sleep-related clinical condition affecting cardiovascular control seems to be represented by sleep-related breathing disorders. In this article, the author summarizes the evidence concerning the link between sleep disorders and cardiovascular diseases, and the effects of specific treatment.

Key points

 

Obstructive sleep apnea is common in the general population, but is increased in frequency in cardiovascular disorders.

 

Cheyne-Stokes respiration or periodic breathing is common in patients with congestive heart failure, but can occur in healthy individuals, including athletes.

 

• Heart failure is ultimately fatal, but relief of symptoms is paramount.

 

• Most cardiovascular symptoms result from congested lungs, inadequate cardiac output, or angina.

 

• Treatment is primarily focused on improving cardiac function and diuresis, but CPAP or mandibular advancement may be required.

Historical note and terminology

The link between sleep and cardiovascular system is a well-known phenomenon. Sleep, in fact, is normally characterized by major changes in the physiologic mechanisms responsible for cardiovascular (CV) regulation. Moreover, increasing evidence shows that there is also an important relationship between sleep, sleep disorders, and cardiovascular diseases (Levy et al 2013). Periodic breathing was the first breathing pattern during sleep described in patients with cardiovascular diseases. Periodic breathing is an abnormal ventilatory pattern in which apneas and hypopneas alternate with periods of hyperventilation. Periodic breathing was first observed by Hippocrates (approximately 460 to 377 BCE). Cheyne (Cheyne 1818) and Stokes (Stokes 1854) published descriptions of repeated respiratory cycles beginning with central apnea followed by several breaths before the next apnea. Central apneas occur when arterial pCO2 (paCO2) falls below the threshold required to stimulate breathing, whereas hyperpnea occurs with reduced arterial pO2 (paO2), pulmonary congestion, or increased chemosensitivity. Changes in paO2 represent the most important modulator of peripheral chemoreceptor activity, whereas paCO2 is the major stimulus for central chemoreceptors (Lahiri and Forster 2003). However, it has been proposed that the central and peripheral components of the chemoreflex are not functionally separate, but rather dependent on 1 another, and that this interaction may affect the appearance and frequency of periodic breathing (Smith et al 2010).

Pryor first demonstrated that most patients with Cheyne-Stokes respiration had cardiac enlargement and prolonged circulation time (Pryor 1951). Prolonged transit time had been demonstrated as producing periodic breathing in normal volunteers in breathing experiments (Douglas and Haldane 1909); this was also shown in experimental animals by delaying flow from the lungs to the brain (Guyton et al 1956). They also recognized that hypoxia from a decreased vital capacity from pulmonary edema or severe congestion could cause periodic breathing. However, their suggestion that periodic breathing could be caused by an increase in “gain” of the central controller of respiration has never been demonstrated except in mathematic models.

At sea level, periodic breathing has been reported to occur in patients with stroke, metabolic disorders, and heart failure (Yumino and Bradley 2008). In particular, periodic breathing during sleep in heart failure patients is associated with poor prognosis (Corra et al 2006). Periodic breathing has also been described during exposure to hypobaric hypoxia at high altitude in the original work by Angelo Mosso at the end of the XIX century (Mosso 1897), and this breathing pattern during sleep affects males more than females (Lombardi et al 2013) probably because of their increased hypoxic chemosensitivity (Caravita et al 2015).

Under conditions of hypobaric hypoxia, paO2 and paCO2 values are reduced close to the thresholds that induce hyperpnea and apnea, respectively, so the onset of a cyclic alternation between ventilatory stimulation and inhibition is facilitated at high altitude, thus leading to periodic breathing (Whitelaw 2006).

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