Research Paper: Cardiac Disorders and Sleep Apnea

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[. . .] Typical breathing pattern with Cheyne-Stokes respiration with hyperpnoeic and apnoeic sequences in sleep stage 2. There are fluctuations in oxygen saturation in response to periodic breathing, with delay of the transit time from the lungs to the fingertip of the left hand.

Figure 2

Source: Kohniein, Welte, Tan and Elliott (2002)

It is reported that the presence of period breathing during sleep in patients with congestive heart failure (CHF) has implications that are of a significant nature. Patients with congestive heart failures and periodic breathing "are more limited in their physical performance and develop dyspnoea at lower workloads than patients with disease of similar severity but without periodic breathing. On average, the left ventricular ejection fraction is lower in patients with periodic breathing and the prevalence of cardiac arrhythmia is significantly higher in patients with the same degree of heart failure but without periodic breathing." (Kohniein, Welte, Tan and Elliott, 2002, p.1) In addition the prognosis of patients with congestive heart failure is worse when they also have a sleep apnea syndrome. In a study conducted by Hanly and colleagues of patients in chronic congestive heart failure with and without nocturnal CSR which were matched for age, sex, body mass index, severity and duration of heart rate that the "cumulative survival and transplant free rates was significantly worse for patients with CSR (100% v 66% after 1 year, 86% v 56% after two years). " (Kohniein, Welte, Tan and Elliott, 2002, p.1)

The study conducted by Andreas and colleagues reports "an increased likelihood of dying within a few months in patients with CHF and CSR during wakefulness." (Kohniein, Welte, Tan and Elliott, 2002, p.1) In addition, patients with CSR are more likely to experience "complex arrhythmias, including (non-sustained) ventricular tachycardia…" (Kohniein, Welte, Tan and Elliott, 2002, p.1) The following figure shows the cumulative survival and transplant free rate for CHF patients with CSR.

Figure 3

Patients with left ventricular dysfunction and low cardiac output generally have a prolonged circulation time and it was speculated approximately 50 years ago in the work of Pryor that this might result in a "time delay between changes in blood gas tension in the lung and their detection in the central nervous system, adversely affecting the control of ventilation." (Kohniein, Welte, Tan and Elliott, 2002, p.1) It is reported however, that recent studies have not shown a "predisposition or statistical association between low cardiac output and periodic breathing in patients with CHF." (Kohniein, Welte, Tan and Elliott, 2002, p.1) The following illustration shows the interactions between left ventricular failure and instabilities in ventilation.

Figure 4

Source: Kohniein, Welte, Tan and Elliott (2002)

The work of Parati, Lombardi and Narkiewicz (2007) states that the mechanisms that link sleep apnea to cardiovascular disease are little understood however, it is stated that the most likely of all hypotheses is that of "a multifactorial process involving a diverse range of mechanisms including sympathetic overactivity, selective activation of inflammatory pathways, endothelial dysfunction, and metabolic dysregulation, the latter particularly involving insulin resistance and disorders in lipid metabolism." (Parati, Lombardi and Narkiewicz, 2007, p.1)

In regards to increased sympathetic nerve activity, it is stated that OSA "is responsible for repeated blood oxygen desaturations and for concomitant increases in arterial carbon dioxide levels." (Parati, Lombardi and Narkiewicz, 2007, p.1) During the apnea, it is reported that sympathetic nerve activity rises progressively and becomes further enhanced by the arousal. One breathing resumes, cardiac output experience increases "on the background of constricted peripheral vasculature. " (Parati, Lombardi and Narkiewicz, 2007, p.1) This may result in "marked increases in arterial pressure which induce a reflex and transient reduction in sympathetic efferent traffic." (Parati, Lombardi and Narkiewicz, 2007, p.1)

In chronic OSA, it is reported that an elevated sympathetic drive is present "even during daytime wakefulness when subjects are breathing normally and both arterial oxygen saturation and carbon dioxide levels are also normal." (Parati, Lombardi and Narkiewicz, 2007, p.1) An increase in sympathetic activity can be observed in normal weight OA patients through use of microneurography. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased)

It is reported as well that the high levels of sympathetic activity noted in OSA patients as being due to baroreflex and chemoreflex dysfunction are "associated with profound abnormalities in cardiovascular variability during both wakefulness and sleep. This alteration occurs even in the absence of hypertension or heart failure. In OSA patients, blood pressure variability is markedly increased, heart rate is faster, and the R-R variability is decreased during daytime, whereas it is increased at night due to the effects of changes in intrathoracic pressure and in the patterns of ventilation due to OSA. The degree of derangement in cardiovascular variability is closely linked to the severity of OSA." (Parati, Lombardi and Narkiewicz, 2007, p.1)

Sympathetic overactivation and abnormal cardiovascular variability in sleep apnea patients are varied and have the potential to contribute to a risk that is increased for hypertension in the future and hypertensive end-organ damage. OSA patients show that CPAP ventilation is successful in treating the occurrence of OSA episodes. Even in patients that have little evidence of cardiovascular disease, endothelial dysfunction has been shown to occur in patients with OSAS. OSAS has been identified as a risk factor for impaired flow-mediated vasodilatation in older participants. CPAP treatment has been shown in studies to bring about a reversal in endothelial dysfunction. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased)

Nitric oxide (NO) is an important vasodilator substance that the endothelium releases and which shows decreased production or activity as an early sign of atherosclerosis. Studies show that NO levels were decreased in OSAS patient and that these levels increased following CPAP therapy. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased) In addition, vasoconstrictor substances are produced by the endothelium including endothelin and angiotensin II which levels are decreased in OSAS patients but show an increase with effective CPAP therapy. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased)

It is reported by (Parati, Lombardi and Narkiewicz, that the reduction of NO release combined with the increase of endothelin 1 levels may be a contributor to OSA-related hypertension" however, they caution that more research is required in this area. In regards to inflammation and oxidative stress it is reported that one of the postulated links between OSA and increased cardiovascular morbidity is inflammation. It has been indicated in several studies showing elevated levels of inflammatory markers in OSA patients when compared with matched healthy subjects. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased) Additionally reported in the work (Parati, Lombardi and Narkiewicz is that elevated C-reactive protein (CRP), IL06, TNF -- a or adhesion molecules in OSA syndrome may be contributors to acceleration of atherosclerosis." (2007, p.1)

Treatment with nasal CPAP has been found in studies to be associated with decreased levels of these markers. (Parati, Lombardi and Narkiewicz, 2007, p.1) Evidence has been stated that links OSA to arterial hypertension. It is related that in 1980 the association of systemic hypertension and snoring was reported in the San Marino epidemiological study by Lugaresi and colleagues. (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased) One decade later reported was "a high prevalence of cardiovascular disease (systemic hypertension, coronary artery disease, and cerebrovascular disease in OSAS patients at diagnosis, and a dose-response effect between cardiovascular involvement and OSAS severity, reported by the Stanford group." (Parati, Lombardi and Narkiewicz, 2007, p.1)

Evidence presently exists that suggests that OSAS "may represent an important independent risk factor for systemic hypertension. Multi-variate analysis and careful case control studies have confirmed that the association of sleep apnea and increased blood pressure is independent of confounders such as obesity." (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased) There is additionally reported to be a "high prevalence of OSAS in patients with drug-resistant hypertension (96% in men and 65% in women), which suggests that OSAS might be one of the most important causes of refractory hypertension." (Parati, Lombardi and Narkiewicz, 2007, p.1, paraphrased)

Summary and Conclusion

The literature reviewed in this study indicates that Obstructive Sleep Apnea and cardiac disorders are inherently linked and that it is possible and in fact, very likely that Obstructive Sleep Apnea is a contributor to cardiac disorders. Obstructive Sleep Apnea in the patient with Congestive Heart Failure is a dangerous condition placing the individual at risk for early death in heart failure. There are still many questions remaining in this area of inquiry and it is emphasized by researchers that much more is needed in the way of research studies to gain a better understanding of this condition and to be better informed about treating Obstructive Sleep Apnea and most particularly in patients with cardiac dysfunction.


Halberstadt, Jerry (2010) Sleep Apnea, The Phantom Cause of Heart Disease and Accidents. Healthy Resources. 2010. Retrieved from:

Kohnlein, T., Welte, T., Tan, LB and Elliott, MW (2002) Central… [END OF PREVIEW]

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APA Format

Cardiac Disorders and Sleep Apnea.  (2012, April 16).  Retrieved April 21, 2019, from

MLA Format

"Cardiac Disorders and Sleep Apnea."  16 April 2012.  Web.  21 April 2019. <>.

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"Cardiac Disorders and Sleep Apnea."  April 16, 2012.  Accessed April 21, 2019.