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Transcript
18 Apnea-induced hypoxia and heart failure By Regina Patrick, RPSGT H eart failure is a condition in which the heart does not pump blood efficiently. Inefficient pumping can occur if the heart can not fill with enough blood or if heart contractions are not sufficiently strong enough. A person with heart failure may have either of these problems or both. An estimated 40 percent of people with heart failure have obstructive sleep apnea (OSA, the intermittent cessation of breathing during sleep).1 Heart failure patients have a worse prognosis if they also have OSA. Why OSA worsens the course of heart failure is unclear. One possibility may be that changes in intrathoracic pressures during apnea episodes alter the heart’s pumping action, further impairing an alreadyweakened heart’s ability to pump blood. Another possibility may be that repeated arousals resulting from hypoxia in OSA induce activation of the sympathetic nervous system; this increases blood pressure, the heart rhythm, and the heart’s oxygen needs, further stressing an already-weakened heart.2,3 Recent studies point to hypoxia, rather than arousals, as the factor that worsens heart failure. The right atrium of the heart collects unoxygenated blood and, on contracting, expels it into the right ventricle. Once the right ventricle is filled, it contracts, sending the unoxygenated blood to the lungs. After the blood is oxygenated in the lungs, it is transported to the left atrium. When the left atrium contracts, it expels the oxygenated blood into the left ventricle. The subsequent contraction of the left ventricle sends the oxygenated blood through the aorta. The blood then travels throughout the body, bringing oxygen to the body’s tissues. Heart failure typically involves damage to one or both ventricles, although damage to the atria can increase the risk of heart failure. Heart failure due to dysfunction of the left ventricle primarily produces pulmonary symptoms (e.g., dyspnea [difficulty breathing], wheezing, hypoxia, cyanosis), while heart failure due to dysfunction of the right ventricle produces primarily systemic symptoms (e.g., peripheral edema, jugular vein distention, ascites [fluid retention in the abdominal cavity], fainting). Heart failure symptoms may be treated by medications (e.g., diuretics, vasodilators, digoxin); lifestyle changes (e.g., bed rest, dietary changes); devices (e.g., defibrillator); or surgery (e.g., heart transplant). OSA has long been associated with an increased risk of cardiovascular problems such as cardiac arrhythmias, coronary artery disease, left ventricular dysfunction, and hypertension (i.e., high blood pressure).3 In OSA, the cessation of breathing (i.e., apnea) occurs when upper airway tissue collapses into and obstructs the upper airway during sleep, preventing air flow through the respiratory tract. During an obstructive apnea episode, a person continues Regina Patrick, RPSGT Regina Patrick, RPSGT, has been in the sleep field for more than 20 years and works as a sleep technologist at the St. Anne Mercy Sleep Disorders Center in Toledo, Ohio. to make efforts to breathe, but no air − or an insufficient amount of air − enters the lungs. The effort involved in trying to breathe, and the reduction of oxygen, impacts the heart’s function in several different ways. The inspiratory efforts during an apneic episode can significantly decrease intrathoracic pressure, which allows the right ventricle to expand and fill with an increased amount of blood.2 This distends the right ventricle, which leaves less room for the left ventricle to expand. As a result, the left ventricle is less able to fill with blood. The decreased amount of blood in the left ventricle, combined with the increased force exerted against it by the extra blood in the right ventricle, increases the left ventricle’s afterload (i.e., the pressure against which the ventricle contracts). A chronically increased left ventricular afterload can result in hypertrophy (i.e., increased muscle mass) of the left ventricle. This stiffens the ventricle and reduces its ability to contract efficiently. In a person with heart failure, left ventricular hypertrophy can decrease the pumping action of the heart, thereby worsening heart failure. Another impact of OSA on the heart is that frequent OSAinduced arousals increase sympathetic activity, which triggers vasoconstriction of the peripheral blood vessels (thereby increasing blood pressure) and the release of catecholamines such as epinephrine (thereby increasing the heart rate and the heart’s oxygen needs).2 In people with heart failure for whom the heart is already insufficiently providing oxygen to the body’s tissues, the increased oxygen demand may worsen heart failure by further depleting the heart of needed oxygen. Scientists remain unsure which aspect of OSA – arousals or hypoxia – is more responsible for worsening the course of heart failure. Researchers Joshua Gottlieb and colleagues investigated this subject in a recent study.1 They used brain (B-type) natriuretic peptide (BNP) as a marker of heart stress. This peptide is secreted by heart muscle cells in response to stretching. They hypothesized that the stress placed on the heart during an apneic episode would increase the ventricular production of BNP and, therefore, people with severe apnea would have a significantly greater amount of BNP than someone with no or mild apnea. The patients involved in the study were being treated for heart failure. All of the patients underwent a baseline sleep study. Afterward, they were divided into three groups: a no/mild OSA group (an apnea-hypopnea index [AHI] of less than 5 respiratory events per hour); an intermediate OSA group (an AHI of 6 to 39.9); and a severe OSA group (an AHI greater than 40). The intermediate OSA group was not studied after the baseline night. By comparing the no/mild OSA group with the severe OSA group, the researchers aimed to maximize the sensitivity of their results in detecting significant effects of sleep apnea on BNP levels. The no/mild OSA group and the severe OSA group underwent a second sleep study during which their blood was sampled for BNP levels every 20 minutes throughout the night. Two weeks later the severe OSA group came back for a third night, during which the patients were administered oxygen during sleep while their blood was sampled every 20 minutes for BNP levels. The researchers measured the ejection fraction of each patient’s heart to assess its pumping ability. The ejection fraction is the portion of blood that is ejected A2Zzz 19.1 | March 2010 19 from the ventricles on contraction. About 68 percent of the blood volume is normally ejected on the contraction of the ventricles; an ejection fraction less than 68 percent can indicate ventricular dysfunction. The researchers found that patients with moderate or severe apnea had a lower ejection fraction (i.e., less efficient cardiac pumping) than the no/mild OSA group. The ejection fraction of patients in the severe OSA group was less than that of the moderate OSA group. They concluded that the heart’s ability to pump is increasingly reduced with increasing severity of OSA. They also found that, although the addition of oxygen in the severe OSA group reduced the total amount of apneic events by 27 percent, there was no significant difference between the BNP levels on night two and night three in this group. This indicated that the number of apnea episodes did not stress the heart. Then they analyzed the collective BNP level results of the no/ mild OSA group and severe OSA group to compare the impact of apnea vs. hypoxia on BNP levels. In doing this, the researchers noted that the BNP levels rose and fell in association with the rise and fall of blood oxygen saturation. By contrast, the BNP level did not rise and fall in association with the frequency of apneic events. Gottlieb and colleagues concluded that changes in the level of BNP were related to the severity of hypoxemia, but not to the frequency of the apnea episodes. A Brazilian research team, headed by Cristiana Marques de Araújo, similarly found that the frequency of apnea events may not be correlated with heart dysfunction.4 Rather than using BNP, the researchers used ischemia (i.e., low blood flow) as a marker of cardiac stress and a measure of the impact of OSA on heart function. The study involved 53 patients who had OSA and were being treated for angina or for ischemic heart disease resulting from myocardial infarction, narrowing of the coronary arteries or multivessel disease. The patients underwent simultaneous polysomnography and continuous electrocardiographic recording using a Holter monitor. From the patients’ electrocardiograms, the researchers determined the number of ischemia episodes that occurred. Based on the patients’ AHI, they were placed in either a control group (an AHI of less than 15); an apnea group (an AHI greater than 15); or a severe apnea group (an AHI greater than 30). They found that the number and duration of ischemic episodes significantly decreased during sleep in all groups. During wakefulness, patients with severe apnea had fewer and shorter ischemic episodes than the controls. From this, they concluded that there was no link between the frequency of apnea episodes (i.e., severity of OSA) and myocardial ischemia. Several studies indicate that OSA treatment – in particular, continuous positive airway pressure (CPAP) therapy – significantly improves heart function in people with heart failure. For example, Canadian researcher Yasuyuki Kaneko and colleagues treated one group of heart failure patients with the normal medical therapy alone.5 They treated a second group of heart failure patients with the normal medical therapy plus CPAP therapy, which prevents apnea by blowing pressurized air into the airway to prevent collapse of tissues into the upper airway during sleep. By preventing apnea, a person’s blood oxygen saturation remains at normal levels, and arousals are eliminated during sleep. The researchers assessed the left ventricular ejection fraction in both groups and found no improvement in the group that received medical therapy alone. By contrast, the left ventricular ejection fraction improved by 35 percent in the group that had been treated with medical therapy and CPAP. Kaneko and colleagues concluded that CPAP treatment could improve left ventricular function in heart failure patients. Another group of Canadian researchers assessed the left ventricular ejection fraction in heart failure patients before and after CPAP therapy.6 They found that the ejection fraction increased, on average, by 32 percent after one month of treatment with CPAP. Some of the patients were then withdrawn from CPAP treatment for one week, and the ejection fraction was re-assessed. This time the researchers found that the ejection fraction decreased by 15 percent. From these results, they also concluded that CPAP can improve left ventricular function. About 5 million people (both children and adults) in the U.S. have heart failure, and about 300,000 people die from heart failure every year.7 Improving heart function can improve the course of heart failure in some people. People with both OSA and heart failure have a worse prognosis, and treating OSA in people with heart failure improves left ventricular function and other aspects of heart function. Therefore, treating OSA could improve the prognosis of some people with heart failure. However, studies have not yet proven that treating OSA reduces cardiac mortality in heart failure patients. The finding that BNP increases with hypoxia – indicating increased stress on the heart – suggests that preventing hypoxia may be especially important in heart failure patients. Therefore, patients with heart failure may need to be assessed and treated for OSA or other sleep-disordered breathing problems to reduce the impact of intermittent episodes of hypoxia on the heart. REFERENCES 1. Gottlieb JD, Schwartz AR, Marshall J, et al. Hypoxia, not frequency of sleep apnea, induces acute hemodynamic stress in patients with chronic heart failure. J Am Coll Cardiol. 2009 Oct 27;54(18):1706-12. 2. Dorasamy P. Obstructive sleep apnea and cardiovascular risk. Ther Clin Risk Manag. 2007 Dec;3(6):1105-11. 3. Chaicharn J, Carrington M, Trinder J, Khoo MCK. The effects on cardiovascular autonomic control of repetitive arousal from sleep. Sleep. 2008 Jan 1;31(1):93-103. 4. Marques de Araújo C, Solimene MC, Grupi CJ, et al. Evidence that the degree of obstructive sleep apnea may not increase myocardial ischemia and arrhythmias in patients with stable coronary artery disease. Clinics (Sao Paulo). 2009;64(3):223-30. 5. Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003 Mar 27;348(13):1233-41. 6. Malone S, Liu PP, Holloway R, et al. Obstructive sleep apnea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet. 1991 Dec 14;338(8781):1480-4. 7. Department of Health and Human Services. National Institutes of Health (NIH). National Heart, Lung, and Blood Institute. Heart failure: what is heart failure? 2007 December. Available at: http://www.nhlbi.nih.gov/health/ dci/Diseases/Hf/HF_WhatIs.html. Accessed Dec. 17, 2009. A2Zzz 19.1 | March 2010