The Heart in Chronic Obstructive Pulmonary Disease

The Heart in Chronic Obstructive Pulmonary Disease

CHEST VOLUME 75 I NUMBER 1 I JANUARY, 1979 EDITORIALS Abnormalities of cardiac rhythm in patients with severe COPD, although recognized for many ye...

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CHEST VOLUME 75

I NUMBER 1 I JANUARY, 1979

EDITORIALS

Abnormalities of cardiac rhythm in patients with severe COPD, although recognized for many years, have been getting a fresh look lately. This scrutiny stems from the widespread use of cardiac monitoring during intensive care and the development of light-weight cardiac monitoring tape recorders that can be worn by ambulatory patients. Studies employing monitoring in COPD have confirmed two suspicions. First, atrial and ventricular arrhythmias are common among patients with COPD when they require intensive care;8 and, secondly, arrhythmias are often present among patients with severe COPD, regardless of acute illness," Indeed, atrial arrhythmias may occur in patients with COPD with greater frequency than in patients with coronary arterial disease, while the incidence of ventricular arrhythmias is about the same," With recognition that arrhythmias are prevalent in advanced COPD, at least two major areas of study now deserve attention. The first concerns etiologic factors. A leading candidate is hypoxemia. In this issue (see page 8), Flick and Block confirm the high occurrence of arrhythmias in patients with COPD and show that the arrhythmias often reach their maximum during sleep, a time when the patients are apt to become most hypoxemic. Arterial hypoxemia might wen be the important factor in promoting arrhythmias in some patients with COPD but does not appear to be an adequate explanation in all instances. Flick and Block observed that therapy with supplemental oxygen during the night ameliorated arrhythmias in four of ten patients, yet these patients did not have lower values for arterial oxygen saturation than the others. A better relationship between arrhythmias and oxygenation might be detected from determinations of mixed venous oxygen tension and saturation, since a more ·critical aspect may be the transport of oxygen and its eifect on the oxygenation of tissue, rather than simply the level of arterial oxygenation. Other factors that may be at play include pulm0nary hypertension and drugs. Perhaps the patients with COPD who are most prone to arrhythmias are those with the highest pulmonary arterial pressures and associated enlargement of the right side of the

The Heart in Chronic Obstructive Pulmonary Disease Arrhythmias

Tchronic he performance of the heart in patients with obstructive pulmonary disease (COPD)

has been attracting attention steadily for several decades. Cardiac catheterization was first done in patients with COPD about 30 years ago and led to the fundamental principle that therapy for right-sided heart failure due to COPD is best directed at the lungs and not the heart. This conclusion followed the demonstration that improving alveolar ventilation and especially arterial oxygenation ameliorates pulmonary hypertension, the abnormality that provokes right ventricular failure.' Ever since then, the standard drugs for heart failure (ie, digitalis and diuretics) have played a minor role in the management of heart disease related to COPD, although these agents may be beneficial. For example, recent evidence suggests that therapy with the "loop" diuretics may aid in reducing pulmonary hypertension in COPD, but not primarily as a result of their diuretic properties.t Instead, these drugs may help by relaxing peripheral vascular tone and favoring redistribution of blood away from the pulmonary circulation. While the right ventricle deservedly has received most of the research, the left ventricle in patients with COPD has not been ignored. Initially, the possibility of left ventricular dysfunction in COPD gained support from ( 1) studies showing abnormalities of the left ventricle in experimentally induced right ventricular failure, (2) the finding of elevated left ventricular end-diastolic pressures in cattle with right ventricu1ar failure following exposure to high altitude, and (3) descriptions of occasional patients with COPD and unexplained left ventricular failure; however, it now appears to be established that patients with COPD, even those with superimposed acute respiratory failure, usually have normal left ventricular function. a,~ Notably, left ventricular hypertrophy infrequently accompanies COPD associated with right ventricular hypertrophy.1

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heart Use of the balloon Hotation pulmonary arterial catheter to study pulmonary hemodynamics may help to identify an association with arrhythmias. The potential of drugs such as digitalis, aminophylline, adrenergic bronchodilator drugs, and diuretics to produce arrhythmias in an individual patient with COPD should not be overlooked, but in the report by Flick and Block, as well as in other studies," these agents could not be implicated. Further insight into the cause of arrhythmias in COPD may come from looking at other forms of severe chronic pulmonary disease. Little information is available now. Patients with cystic fibrosis would appear to be particularly interesting, since their youth should exclude underlying degenerative myocardial abnormalities and coronary arterial disease. The second area of interest is the relationship of arrhythmias to morbidity and mortality. In acutely ill patients with COPD, the occurrence of ventricular tachycardia or multifocal atrial tachycardia has been associated with a poor prognosis;S.8 however, there are no studies dealing with the course of patients with COPD who have serious arrhythmias during clinically stable periods. The likelihood that such arrhythmias are important seems strong, since complex ventricular arrhythmias seen on long-term electrocardiographic monitoring of patients with COPD resemble the types of arrhythmias associated with sudden death in patients with coronary arterial disease, congestive cardiomyopathy, and mitral valve prolapse." One report describes sudden death in 11 of 109 deaths among patients with COPD, but the antecedent cardiac rhythms were not characterized. 10 To settle the question of whether arrhythmias in COPD have clinical importance, prospective serial studies will have to be done. The issue bears directly on the role of therapy with antiarrhythmic drugs in COPD. In any event, the physician caring for patients with advanced COPD should recognize that arrhythmias are common and that treating hypoxemia, whether it is severe continually or only during sleep, is at present likely to be the best therapy.

Robert M. Senior, M.D., F.C.C.P.; Stephen S. Lefrak, M.D., F.C.C.P.; and Roberl E. Kleiger, M.D., F.C.C.P. St. Louis

Department of Medicine, Washington University at the Jewish Hospital of St. Louis.

1b:FERENCES 1 Harvey RM, Ferrer MI, Richards DW Jr, et at: InBuence of chronic pulmonary disease on the heart and ciradafion.

2 EDITORIALS

Am J Moo 10:719-738, 1951 2 Heinemann HO: Right-sided heart failure and the use of diuretics. Am J Med 64:367-369, 1978 3 Steele P, Ellis JH Jr, Van Dyke D, et al: Left ventricular ejection fraction in severe chronic obstructive airways disease. Am J Med 59:21-28, 1975 4 Kline LE, Crawford MH, MacDonald WJ Jr, et at: Noninvasive assessment of left ventricular performance in patients with chronic obstructive pulmonary disease. Chest 72:558-564,1977 5 Murphy ML, Adamson J, Hutcheson F: Left ventricular hypertrophy in patients with chronic bronchitis and emphysema. Ann Intern Med 81:307-313,1974 6 Hudson LD, Kurt TL, Petty TL, et at: Arrhythmias associated with acute respiratory failure in chronic airway obstruction. Chest 63:661·665, 1973 7 Kleiger RE, Senior RM: Longterm electrocardiographic monitoring of ambulatory patients with chronic airway obstruction. Chest 65:483-487, 1974 8 Shine KI, Kastor JA, Yurchak PM: Multifocal atrial tachycardia. N Eng} J Med 279:344-349,1968 9 Kennedy HL, Caralis DC: Ambulatory electrocardiography: A clinical perspective. Ann Intern Moo 87 :729739, 1977 10 Burrows B, Earle RH: Course and prognosis of chronic obstructive lung disease: A prospective study of 200 patients. N Eng} J Med 280:397-404,1969

Duration of Action of Isosorbide Dinitrate a century since the report on amyl nitrite F byor over Sir Lauder Brunton,' who was a house physi-

cian at the time of his discovery, physicians have been aware of the clinical utility of nitrates to assuage the fearsome oppressive sensation of angina pectoris. Both inhalation of amyl nitrite, as described by Brunton, I and sublingual therapy with nitroglycerin have been accepted by physicians and their patients without question, probably in large part due to the speed of the pharmacologic efficacy; however, dissatisfaction with the duration of the effectiveness of these compounds led to attempts to develop agents that would provide longer freedom from angina following administration. Such an agent has been isosorbide dinitrate. Early studies of the clinical effectiveness of this agent administered sublingually in a dosage of 5 mg found that therapy with isosorbide dinitrate did not reduce the number of anginal episodes, improve exercise tolerance on a bicycle ergometer over that noted following administration of a placebo," or was oral therapy with isosorbide dinitrate (10 to 20 mg three or four times daily) more effective than a placebo in relieving daily episodes of angina or improving exercise tolerance on a multistage treadmill exercise test or step test. ll.4 Others found that a dose of 5 to 10 mg did prolong the exercise capability measured on a bicycle ergometer ten minutes follow-

CHEST, 75: 1, JANUARY, 1979