Relationship Between Cardiac Disorders and Sleep Apnea

¶ … Cardiac Disorders and Sleep Apnea

The objective of this study is to ascertain the relationship between cardiac disorders and sleep apnea. Toward this end, this work will examine the research on this area of study.

An American Heart Association/American College of Cardiology Foundation Scientific Statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Strike Council, and Council on Cardiovascular nursing report states that "Sleep-related breathing disorders are highly prevalent in patients with established cardiovascular disease. Obstructive sleep apnea (OSA) affects an estimated 15 million adult Americans and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including coronary artery disease, stroke, and atrial fibrillation." (Somers, et al., 2008, p.1080) Central sleep apnea occurs primarily in patients with heart failure. (Somers, et al., 2008, paraphrased)

The work of Halberstadt (2010) states that many deaths that occur among individuals in their 40s and older which have been attributed to heart disease or automobile accidents "may actually be related to an unseen epidemic of snoring and sleep apnea. Apnea, a potentially deadly phantom, is the frequent stoppage of breathing caused by relaxed tissues in the throat during sleep. Snoring is caused by vibrations of the relaxed throat tissues and is often the precursor or companion of sleep apnea. Although effective medical treatment for sleep apnea exists, this information has not entered routine medical practice nor does the public recognize the dangers. Unfortunately, even when apnea is suspected, it may be difficult to obtain qualified care. As a result, 95% of the millions of people who suffer from sleep apnea have not and may never be diagnosed, let alone treated. Nevertheless, the informed person with sleep apnea can take the initiative to get appropriate diagnosis and treatment and take the steps necessary to assure recovery." (Halberstadt, 2010, p.1) Halberstadt reports that some cardiological problems associated with sleep apnea are known and their risk possible to reduce through treating the sleep apnea.

I. Obstructive Sleep Apnea

Obstructive Sleep Apnea is reported to be characterized by "repetitive interruption of ventilation during sleep caused by collapse of the pharyngeal airway. An obstructive apnea is a 10-second pause in respiration associated with ongoing ventilatory effort. Obstructive hypopneas are decreases in, but not complete cessation of, ventilation, with an associated fall in oxygen saturation or arousal. A diagnosis of OSA syndrome is accepted when a patient has an apnea-hypopnea index (AHI; number of apneas and hypopneas per hour of sleep)

It is reported that while hypopneas "constitute the majority of disordered breathing events, there is some controversy regarding the optimal criteria for definition of hypopneas." (Somers, et al., 2008, p. 1082) A recent analysis of data from >6000 adults participating in the Sleep Heart Health Study reported that "hypopneas accompanied by oxyhemoglobin desaturation of 4% were associated with prevalent cardiovascular disease independently of confounding covariates." (Somers et al., 2008, p. 1082)

II. Signs, Symptoms, and Risk Factors for Obstructive Sleep Apnea

Signs, symptoms, and risk factors for Obstructive Sleep Apnea including those as follows:

(1) disruptive snoring;

(2) witnessed apnea or gasping;

(4) obesity and/or enlarged neck size;

(5) hypersomolence (not common in children or in heart failure); and (6) Other signs and symptoms in clued male gender, crowded-appearing pharyngeal airway, increased blood pressure, morning headache, sexual dysfunction, and behavioral changes. (Somers et al., 2008, p. 1082))

IV. Screening and Diagnostic Testing

Screening and diagnostic testing used to detect Obstructive Sleep Apnea include the following:

(1) questionnaires;

(2) holter monitoring;

(3) overnight oximetry;

(4) home-based/ambulatory unattended polysomnography;

(5) in-hospital attended overnight polysomonography. (Somers et al., 2008, p. 1080)

V. Treatment Options

Treatment options include:

(1) positional therapy;

(2) weight loss;

(3) avoidance of alcohol and sedatives;

(4) positive airway pressure;

(5) oral appliances; and (6) surgery including: (a) Uvulopalatopharyngoplasty; (b) tonsillectormy; and (c) tracehostomy. (Somers, et al., 2008, p. 1082)

It is reported that pharyngeal collapse in patients with Obstructive Sleep Apnea "generally occurs posterior to the tongue, uvula, and soft palate or some combination of these structures. This portion of the pharyngeal airway has relatively little bony or rigid support and is therefore largely dependent on muscle activity to maintain patency." (Somers, et al., 2008, p. 1082) It is reported that the primary abnormality in patients with Obstructive Sleep Apnea is "an anatomically small pharyngeal airway resulting from obesity, bone, and soft tissue structures or in children, tonsils, and adenoids." (Somers, et al., 2008, p. 1082) The result in that while the individual is awake there is an increased airflow resistance and "greater intrapharyngeal negative pressure during inspiration." (Somers, et al., 2008, p. 1082)

VI. Diagnosis

In patients with suspected OSA required is a definitive diagnosis. The individual spends a night in a sleep laboratory and a polysomnography records multiple physiological variables continuously. Included are "sleep staging using the electroencephalogram, electromyogram, electroculogram, respiration (flow, effort, oxygen saturation) and snoring." (Somers et al., 2008, p. 1083) It is possible with these signals and the effect of sleep and oxygenation to quantify OSA. Somers et al. states that the importance of "the cardiovascular response to sleep as been recognized in the recently revised Sleep Scoring Manual form the American Association of Sleep Medicine (AASA) which not includes scoring of a continuous-lead ECG as a recommended component of poly somnography." (Somers, et al., 2008, p. 1083) Some controversy exists concerning whether disordered breathing during sleep can undergo adequate assessment through use of fewer recorded signals in the home as the majority of these systems have limitations in that they monitor the respiratory channels but are not inclusive of sleep staging and other non-respiratory signals." (Somers, et al., 2008, p. 1083)

VII. Epidemiology

Studies conducted in the United States, Europe Australia and Asia have documented the high prevalence and wide spectrum of the severity of Obstructive Sleep Apnea in adults. While there is noted a variation in measurement techniques and definitions studies have shown that one out of every five adults has at least mild OSA and 1 in 15 has moderate or severe OA. (Somers et al., 1084) Two population studies have shown significant progression in Obstructive Sleep Apnea over time. More than 85% of patients with clinically significant and treatable OSA have never been diagnosed. Somers et al. states "in addition to emphasizing the large burden of untreated OSA in the general population, the low level of medical detection demands caution in generalizing observations of OA patients diagnosed in sleep clinics to cardiovascular disease patients with occult OSA." (p.1084)

VIII. Relationship Between Congestive Heart Failure and Central Sleep Apnea

The work of Kohniein, Welte, Tan and Elliott (2002) states that there have been several studies that report the investigation of the relationship between chronic congestive heart failure and the central sleep apnea syndrome. This syndrome is reported to have a hypercapnic and hypocapnic form. The hypercapnic form is reported to result "from a chronically depressed respiratory drive or ability to breath, and is associated with hypercapnia during wakefulness and sleep." (Kohniein, Welte, Tan and Elliott, 2002, p.1)

Hypocapnic CSAS is reported as more prevalent and not caused by snoring or mechanical obstruction of the upper airway and to have a cause and pathophysiology that is completely different. Patients with hypocapnic CSAS has a general nocturnal breathing pattern of "periodic breathing, characterized by a regular, crescendo-decrescendo oscillation of tidal volume which is thought to be caused by dysfunction of central respiratory control. As the central drive to breathe slowly faces, ventilation temporarily ceases before resuming again. This results in an oscillation between central hyperpnoea or a decrease of more than fifty percent in the sum of thoracoabdominal movements lasting 10 seconds or more followed by a decrease of more than 4$ in peripheral oxygen saturation or central apnea or a reduction of more than 90% in thoracoabdominal movement or complete cessation of ventilator efforts and hyperventilation." (Kohniein, Welte, Tan and Elliott, 2002, p.1)

The typical length of one period may be between 30 to 60 seconds however, there has been observation of longer periods. During a prolonged hypopnoea or apnea there is a decrease in oxygen saturation and this is combined with a slow rise in the arterial carbon dioxide tension and a decline in blood and tissue pH. Central nervous system activity in the majority of cases is not affected until late apnea although it is reported that findings have shown changes in lower activity and deep sleep stages during apnea. Ventilation resumption is stated to be associated with EEG arousals, markers of central nervous system activation and sleep disturbances stated to be "drive back to a more superficial level." (Kohniein, Welte, Tan and Elliott, 2002, p.1)

The following illustration demonstrates the process of Central Sleep Apnea Syndrome (CSAS)

Figure 1

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

The following illustration shows a five-minute section of polysomnographic record of EEG (C3A1, C4A2), electrocardiogram (ECG), or nasal air flow (Flow), abdominal ventilatory effort (ABD), thoracic ventilatory effort (THO), and oxygen saturation measured at the finger tip of the left hand (SaO2) in a 57-year-old man with moderate ischemic CHF (NYHA II -- III). 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)