CLINICAL PROBLEMS IN CARDIOPULMONARY DISEASE Complicated Myocardial Infarction with Chronic Pulmonary Disease Problems in Management
Clinical Evaluations by Robert C. Schlant, M.D., and Jay N. Cohn, M.D.
CASE SUMMARY
William B. Bauman, M.D.o A 69-year-old white man with known Buerger's disease and chronic obstructive pulmonary disease came to the emergency room after four hours of crushing substernal chest pain, shortness of breath, and diaphoresis. Physical examination revealed an alert, uncomfortable patient with pain in the chest. His blood pressure was 148/88 mm Hg; the pulse rate was 56 beats per minute and irregular. In the sitting position, the external jugular veins were distended to the angle of the jaw. An increased thoracic anteroposterior diameter was noted, together with decreased breath sounds at both bases. Wheezing was absent, but there were a few scattered rales. Heart sounds were distant, and no murmurs were heard. The liver was not tender and was palpable 9 cm below the right costal margin in the midclavicular line. The arms were warm and well perfused. The legs were cool, cyanotic, and pulseless. A portable chest roentgenogram disclosed a heart which was at the upper limits of normal in size. An electrocardiogram showed an axis of -30 0 , sinus rhythm with frequent premature ventricular contractions, and acute anterolateral myocardial infarction with Q waves and ST-segment elevation in leads V1 to V5' I, and AVL. The hematocrit reading was 55 percent, and the white blood cell count was 17,800/cu mm. Laboratory studies revealed the following levels: sodium, 137 mEq/L; potassium, 4.5 mEq/L; chloride, 9 mEq/L; carbon dioxide, 32 mEq/L; blood urea nitrogen, 9 mg/1oo ml; and creatinine, 0.9 mg/IOO mI. Initial blood gas levels were an arterial pH of 7.32, an arterial carbon dioxide tension (PaCO.» of 54 mm Hg, and an arterial oxygen pressure (PaO.) of 59 mm Hg. The level of lactate in the serum was 3.1 nig/100 ml (0.5 to 1.6). Initially, the patient was given intravenous therapy with morphine and lidocaine and therapy with supplemental oxygen. His blood pressure was 120/80 mm Hg, the pulse rate was 96 beats per minute. He was somnolent but easily aroused. Inspirational and expirational wheezing was heard over the anterior portion of the chest. Repeat determinations of blood gas levels during the administration of 24 percent oxygen revealed the following: pH, 7.24; PaC0 2 , 65 mm Hg; °Cardiology Fellow, Indiana University School of Medicine, Indianapolis. Reprint requests: Dr. Bauman, Indiana University School of Medicine, Indianapolis 46233
178 SCHLANT, COHN
and PaD.), 50 mm Hg. A repeat ECG during a recurrence of pain in the chest showed an axis of -45 0 , right bundlebranch block, and continued evidence of acute anterior wall myocardial infarction. A Swan-Ganz catheter was then inserted. The pulmonary arterial pressure was 70/40 rom Hg, the mean pulmonary capillary wedge pressure was 30 mm Hg, the cardiac output was 3.8 L/min, and the cardiac index was 2.1 L/min/sq m, QUESTIONS
1. Do you agree with the decision to insert a SwanGanz catheter? If so, why? 2. What is the likely cause of the patient's wheezing? 3. What is the most likely cause of the pulmonary hypertension? 4. What would be the treatment of choice for the patient's cardiac failure, and discuss each of the following possibilities: ( a) reduction in afterload? (b) diuretics? ( c) digitalis? ( d) inotropic agents, ie, dopamine? 5. Would you insert a temporary pacemaker as a prophylactic measure?
Comments by RobertC. Schlant, M.D. o O I would agree with the decision to insert a SwanGanz catheter to monitor the pulmonary arterial and pulmonary capillary wedge pressures and cardiac output, since the patient has evidence of a significant early deterioration in cardiac performance, with the onset of new wheezing, an episode of recurrent pain in the chest (of unknown duration), a decrease in Pa02 from 49 to 50 mm Hg, and an increase in PaC02 from 54 to 65 mm Hg following the adminiso °Professor
of Medicine (Cardiology) and Director, Division of Cardiology, Emory University School of Medicine, Atlanta.
CHEST, 75: 2, FEBRUARY, 1979
tration of lidocaine, morphine, and supplemental oxygen (24 percent by an unknown route). In addition, the patient has developed right bundle branch block and a shift in his electrical axis from -30 0 to -45 0 • Information is not provided regarding the urinary output or changes in respiratory rate or depth. We do not know whether or not a ventricular gallop sound (S3) was audible over the right clavicle or whether or not there was evidence of changes in the pulmonary vasculature on serial chest x-ray films (such as an increased ratio of upper lobe to lower lobe perfusion, early interstitial edema, and even alveolar pulmonary edema) . In this patient, wheezing is most probably due to left ventricular failure superimposed upon chronic obstructive pulmonary disease. Actually, some patients with acute or subacute left ventricular failure may develop wheezing or even clinical "asthma," even in the absence of preexisting pulmonary disease. One should also consider the possibility of pulmonary embolus in this setting. The pulmonary hypertension is likewise probably due to the combination of left ventricular failure superimposed on chronic obstructive pulmonary disease, probably with mild preexisting pulmonary hypertension. My initial treatment of choice would be very cautious reduction in afterload with intravenous therapy with sodium nitroprusside, avoiding a significant decrease in the aortic diastolic pressure. Intravenous therapy with sodium nitroprusside decreases both afterload and preload. The direct arterial pressure (radial artery) and the pulmonary capillary wedge pressure should be carefully monitored, preferably with serial measurements of cardiac output. The fact that the pulmonary capillary wedge pressure is significantly less than the pulmonary arterial diastolic pressure implies a probably significant increase in the pulmonary vascular resistance. It also implies that one should use the pulmonary capillary wedge pressure (rather than the pulmonary arterial diastolic pressure) to monitor the left ventricular filling pressure. One might also consider the use of intravenous therapy with nitroglycerin in this patient. Therapy with diuretic agents to decrease left ventricular filling pressure, as well as systemic venous pressure, would be appropriate. In this patient, intravenous administration of furosemide (Lasix; 20 to 80 mg) would have some beneficial effects by producing a diuresis, as well as having some direct effect to decrease venous tone. Both of these decrease venous return and decrease left ventricular IDling pressure (preload) . Since the agent being used might also decrease preload, I would tend to
CHEST, 75: 2, FEBRUARY, 1979
use a rather small dose (20 mg) of furosemide initially; however, in most patients with heart failure, there is little advantage to be gained from the use of intravenous or rapid-acting diuretic drugs, and most patients with chronic heart failure are better managed by oral therapy with diuretic agents with a more prolonged duration of action. We would cautiously administer digoxin, but in a smaller than usual dosage. The patient has heart failure, and most patients with heart failure probably benefit from therapy with digitalis, even in the setting of acute infarction; however, such therapy should be used with greater caution, because the ischemic myocardium appears to be more susceptible to digitalis-induced arrhythmias. In addition, the patient has evidence of chronic obstructive pulmonary disease and hypoxemia. In patients who have left ventricular dilatation associated with heart failure, therapy with digitalis may help to decrease left ventricular diastolic pressure and may decrease the left ventricular internal diameter, both of which would tend to decrease the myocardial requirements for oxygen and to improve the myocardial How of blood, especially to the left ventricular endocardium. In the setting of acute infarction with heart failure, therapy with digitalis may even help to preserve myocardium. At this time, I would not think that therapy with dopamine or norepinephrine would be indicated; however, if there were a further decrease in the patient's systemic blood pressure or cardiac index that was unresponsive to therapy, I would use dopamine if the pulmonary capillary wedge pressure was still elevated. If the pulmonary capillary wedge pressure fell below 18 to 20 mm Hg in this situation, I would consider increasing it (with therapy with dextran) back to this level. In some patients with severe left ventricular failure (or early preshock) following acute myocardial infarction, combined therapy with sodium nitroprusside and dopamine has been of benefit and, I think, has prevented the further development of full-blown cardiogenic shock. At this point, I would not insert a temporary pacemaker as a prophylactic measure. I think that the insertion has some risk of inducing arrhythmias itself, and I would generally prefer to wait if the patient is being monitored in a coronary care unit. At present, his ventricular rate appears to be adequate, and there is evidence of right bundle-branch block and an electrical axis of -45 0 , but the atrioventricular conduction does not appear to be significantly prolonged; however, I would be prepared to insert a pacemaker if complete heart block developed.
COMPLICATED MYOCARDIAL INFARCTION 179
Comments by Jay N. Cohn, M.D.t Measurement of left ventricular filling pressure is necessary in this patient, because it is difficult to assess on clinical grounds whether chronic cor pulmonale with an acute exacerbation or left ventricular failure from an acute myocardial infarction is the predominant physiologic abnormality. Since treatment of these two disorders might be quite different, knowledge of the severity of left ventricular dysfunction is necessary to plan therapy. A satisfactory measurement of pulmonary capillary wedge pressure may not always be obtained in such patients, and the pulmonary arterial diastolic pressure cannot be used as a guide to left ventricular filling pressure. Fortunately, in this patient a measurement of pulmonary capillary wedge pressure was obtained. The value of 30 mm Hg indicates severe left ventricular dysfunction and the gradient of 10 mm Hg from pulmonary arterial diastolic pressure is consistent with the preexisting pulmonary vascular disease. The pulmonary capillary wedge pressure is high enough to cause pulmonary edema, which could be a factor in the inspirational and expirational wheezing, particularly in a patient with chronic obstructive pulmonary disease and perhaps a tendency for bronchospasm. The pulmonary hypertension represents a combination of chronic pulmonary vascular disease with high pulmonary arteriolar resistance, possible acute pulmonary vasoconstriction due to hypoxia, and "backward" failure from the high left atrial pressure. In the absence of left ventricular failure, the pulmonary hypertension would likely be quite mild (about 20 mm Hg lower). Vasodilator therapy might be effective in lowering the pulmonary capillary wedge pressure and raising the cardiac output without inordinately reducing the arterial pressure. It would also probably relieve the pulmonary hypertension. Sodium nitroprusside would be the drug of choice, but care must be taken to avoid further aggravation of the hypoxemia as a result of such therapy. Cautious administration of supplemental oxygen at a low flow would be indicated, with frequent measurement of blood gas levels. Therapy with diuretic agents is certainly indicated. Furosemide administered intravenously would be the agent of choice; however, the diuretic agent alone would likely reduce the cardiac output further, and therefore this agent should be given in this patient only in combination with a vasodilator or inotropic drug. tProfessor of Medicine and Head, Cardiovascular Division, University of Minnesota Medical School, Minneapolis.
180 SCHLANT, COHN
Therapy with digitalis is contraindicated in this setting. Dopamine or dobutamine would be an appropriate choice if nitroprusside lowered the arterial pressure without satisfactorily correcting the low cardiac output. In that case, dopamine or dobutamine and nitroprusside could be administered in combin-ation. The left axis deviation and right bundle branch block are an ominous combination in anterior infarction. Insertion of a temporary pacemaker as a standby would be prudent. FOLLOW-UP
As suggested by our consultants, therapy with sodium nitroprusside was begun, resulting in a gradual drop in the pulmonary arterial pressure from 70/40 mm Hg to 58/35 mm Hg and a decrease in the pulmonary capillary wedge pressure from 30 to 20 mm Hg. The cardiac output did not change. Additionally, 40 mg of furosemide was administered intravenously, resulting in a diuresis of 800 ml. The nitroprusside was continued for six days, during which time the patient's left ventricular filling pressure remained satisfactory at around 20 mm Hg, with a cardiac index of approximately 2.1 L min/sq m. Subsequently, oral prazosin was used in an effort to maintain the left ventricular filling pressure at approximately 20 mm Hg. The patient's wheezing did not resolve with the drop in the pulmonary capillary wedge pressure. Endotracheal intubation and therapy with a volume-controlled respirator became necessary because of increasing effort of breathing and a rising PaCO.). Corticosteroids were administered intravenously for 48 hours in an effort to control the patient's bronchospasm, Morphine might have contributed to the bronchospasm, owing to its release of histamine. The patient's bronchospasm resolved within 24 hours of admission. Inotropic agents, including digitalis, were not administered during the acute phase of the patient's infarction. A temporary transvenous pacemaker was inserted as a prophylactic measure because of the bifascicular block. The patient did not develop high-degree atrioventricular block during his myocardial infarction, and he never required the use of the pacemaker. The pacemaker was removed on the seventh day of hospitalization, and a normal His-ventricle time was recorded at the time of the removal of the transvenous pacemaker. The patient was convalescing well in the hospital when, on the 14th day of hospitalization, he had mild recurrent pain in the chest of approximately 30 minutes' duration, which was followed by a syncopal episode during which time no arrhythmia or changes in the S-T segment or T wave were noted in the ECC. He subsequently died within a few hours, despite vigorous therapeutic measures. No autopsy was obtained.
Department Editor's Comment The use of digitalis during the acute phase of myocardial infarction is controversial. As Schlant points out, in patients with left ventricular dilatation associated with heart failure, therapy with digitalis may indeed decrease the left ventricular diastolic pressure and internal dimension, resulting
CHEST, 75: 2, FEBRUARY, 1979
in a decrease in the tension of the wa", which would decrease the myocardial requirements for oxygen and perhaps help preserve myocardium; however, in the absence of left ventricular dilatation, it is weU known that the myocardial requirement for oxygen is increased by therapy with digitalis, resulting potentially in a detrimental eDect.1 Schlant also points out that the ischemic myocardium appears to be more susceptible to digitalis-induced arrhythmias. There are data from animals to support this view;2-4 however, no clinical studies to date have shown that patients with acute myocardial infarction are more prone to ventricular arrhythmia. 5 The prophylactic insertion of a temporary transvenous pacemaker in patients with acute myocardial infarction (and, in particular, anterior wall myocardial infarction and bifascicular block) may provide some adoantage" Although no clinical studies have demonstrated an improved mortality due to transvenous pacing in complete heart.block, it is possible that occasional patients might otherwise die suddenly if a prophylactic pacemaker were not inserted. On the other hand, a pacing catheter may certainly cause arrhythmias; however, on balance, I believe that the prophylactic standby pacing was less hazardous and facilitated greater ease of management than would have been the case if emergency insertion
CHEST, 75: 2, FEBRUARY, 1979
of a transoenous catheter had become necessary at the time of high degree atrioventricular block. This case demonstrates the multifaceted approach that is necessary in a patient with severe chronic obstructive pulmonary disease who sustains an acute, severe myocardial infarction. Invasive hemodynamic monitoring is often essential in order to guide therapy. Despite these measures, many patients unfortunately still die during the course of their myocardial infarction.
1 Brunwald E, Morrocco P: Limitation of infarct size. Curr Probl CardioI3:46, 1978 2 Bellet S, Johnston CG, Schecter A: The effect of cardiac infarction on the tolerance of dogs to digitalis. Arch Intern Med 54:509-516, 1934 3 Travell J, Gold H, Modell W: The effect of experimental cardiac infarction on response to digitalis. Arch Intern Med 61: 184-197, 1938 B, Lown B: Myocardial infarction 4 Hood WB Jr, ~1cCarthy following coronary ligation in dogs: Hemodynamic effects of isoproterenol and acetyl strophanthidin. eire Res 21: 191199, 1967 5 Lown B, et al: Sensitivity to digitalis drugs in acute myocardial infarction. Am J Cardiol 30: 388-395, 1972 6 Mullins CB, Atkins JM: Prognosis and management of ventricular conduction blocks in acute myocardial infarction. Mod Cone Cardiovasc Dis 45:129, 1976
COMPLICATED MYOCARDIAL INFARCTION 181
Clinical Evaluations by Robert C. Schlant, M.D., and Jay N. Cohn, M.D.
CASE SUMMARY
William B. Bauman, M.D.o A 69-year-old white man with known Buerger's disease and chronic obstructive pulmonary disease came to the emergency room after four hours of crushing substernal chest pain, shortness of breath, and diaphoresis. Physical examination revealed an alert, uncomfortable patient with pain in the chest. His blood pressure was 148/88 mm Hg; the pulse rate was 56 beats per minute and irregular. In the sitting position, the external jugular veins were distended to the angle of the jaw. An increased thoracic anteroposterior diameter was noted, together with decreased breath sounds at both bases. Wheezing was absent, but there were a few scattered rales. Heart sounds were distant, and no murmurs were heard. The liver was not tender and was palpable 9 cm below the right costal margin in the midclavicular line. The arms were warm and well perfused. The legs were cool, cyanotic, and pulseless. A portable chest roentgenogram disclosed a heart which was at the upper limits of normal in size. An electrocardiogram showed an axis of -30 0 , sinus rhythm with frequent premature ventricular contractions, and acute anterolateral myocardial infarction with Q waves and ST-segment elevation in leads V1 to V5' I, and AVL. The hematocrit reading was 55 percent, and the white blood cell count was 17,800/cu mm. Laboratory studies revealed the following levels: sodium, 137 mEq/L; potassium, 4.5 mEq/L; chloride, 9 mEq/L; carbon dioxide, 32 mEq/L; blood urea nitrogen, 9 mg/1oo ml; and creatinine, 0.9 mg/IOO mI. Initial blood gas levels were an arterial pH of 7.32, an arterial carbon dioxide tension (PaCO.» of 54 mm Hg, and an arterial oxygen pressure (PaO.) of 59 mm Hg. The level of lactate in the serum was 3.1 nig/100 ml (0.5 to 1.6). Initially, the patient was given intravenous therapy with morphine and lidocaine and therapy with supplemental oxygen. His blood pressure was 120/80 mm Hg, the pulse rate was 96 beats per minute. He was somnolent but easily aroused. Inspirational and expirational wheezing was heard over the anterior portion of the chest. Repeat determinations of blood gas levels during the administration of 24 percent oxygen revealed the following: pH, 7.24; PaC0 2 , 65 mm Hg; °Cardiology Fellow, Indiana University School of Medicine, Indianapolis. Reprint requests: Dr. Bauman, Indiana University School of Medicine, Indianapolis 46233
178 SCHLANT, COHN
and PaD.), 50 mm Hg. A repeat ECG during a recurrence of pain in the chest showed an axis of -45 0 , right bundlebranch block, and continued evidence of acute anterior wall myocardial infarction. A Swan-Ganz catheter was then inserted. The pulmonary arterial pressure was 70/40 rom Hg, the mean pulmonary capillary wedge pressure was 30 mm Hg, the cardiac output was 3.8 L/min, and the cardiac index was 2.1 L/min/sq m, QUESTIONS
1. Do you agree with the decision to insert a SwanGanz catheter? If so, why? 2. What is the likely cause of the patient's wheezing? 3. What is the most likely cause of the pulmonary hypertension? 4. What would be the treatment of choice for the patient's cardiac failure, and discuss each of the following possibilities: ( a) reduction in afterload? (b) diuretics? ( c) digitalis? ( d) inotropic agents, ie, dopamine? 5. Would you insert a temporary pacemaker as a prophylactic measure?
Comments by RobertC. Schlant, M.D. o O I would agree with the decision to insert a SwanGanz catheter to monitor the pulmonary arterial and pulmonary capillary wedge pressures and cardiac output, since the patient has evidence of a significant early deterioration in cardiac performance, with the onset of new wheezing, an episode of recurrent pain in the chest (of unknown duration), a decrease in Pa02 from 49 to 50 mm Hg, and an increase in PaC02 from 54 to 65 mm Hg following the adminiso °Professor
of Medicine (Cardiology) and Director, Division of Cardiology, Emory University School of Medicine, Atlanta.
CHEST, 75: 2, FEBRUARY, 1979
tration of lidocaine, morphine, and supplemental oxygen (24 percent by an unknown route). In addition, the patient has developed right bundle branch block and a shift in his electrical axis from -30 0 to -45 0 • Information is not provided regarding the urinary output or changes in respiratory rate or depth. We do not know whether or not a ventricular gallop sound (S3) was audible over the right clavicle or whether or not there was evidence of changes in the pulmonary vasculature on serial chest x-ray films (such as an increased ratio of upper lobe to lower lobe perfusion, early interstitial edema, and even alveolar pulmonary edema) . In this patient, wheezing is most probably due to left ventricular failure superimposed upon chronic obstructive pulmonary disease. Actually, some patients with acute or subacute left ventricular failure may develop wheezing or even clinical "asthma," even in the absence of preexisting pulmonary disease. One should also consider the possibility of pulmonary embolus in this setting. The pulmonary hypertension is likewise probably due to the combination of left ventricular failure superimposed on chronic obstructive pulmonary disease, probably with mild preexisting pulmonary hypertension. My initial treatment of choice would be very cautious reduction in afterload with intravenous therapy with sodium nitroprusside, avoiding a significant decrease in the aortic diastolic pressure. Intravenous therapy with sodium nitroprusside decreases both afterload and preload. The direct arterial pressure (radial artery) and the pulmonary capillary wedge pressure should be carefully monitored, preferably with serial measurements of cardiac output. The fact that the pulmonary capillary wedge pressure is significantly less than the pulmonary arterial diastolic pressure implies a probably significant increase in the pulmonary vascular resistance. It also implies that one should use the pulmonary capillary wedge pressure (rather than the pulmonary arterial diastolic pressure) to monitor the left ventricular filling pressure. One might also consider the use of intravenous therapy with nitroglycerin in this patient. Therapy with diuretic agents to decrease left ventricular filling pressure, as well as systemic venous pressure, would be appropriate. In this patient, intravenous administration of furosemide (Lasix; 20 to 80 mg) would have some beneficial effects by producing a diuresis, as well as having some direct effect to decrease venous tone. Both of these decrease venous return and decrease left ventricular IDling pressure (preload) . Since the agent being used might also decrease preload, I would tend to
CHEST, 75: 2, FEBRUARY, 1979
use a rather small dose (20 mg) of furosemide initially; however, in most patients with heart failure, there is little advantage to be gained from the use of intravenous or rapid-acting diuretic drugs, and most patients with chronic heart failure are better managed by oral therapy with diuretic agents with a more prolonged duration of action. We would cautiously administer digoxin, but in a smaller than usual dosage. The patient has heart failure, and most patients with heart failure probably benefit from therapy with digitalis, even in the setting of acute infarction; however, such therapy should be used with greater caution, because the ischemic myocardium appears to be more susceptible to digitalis-induced arrhythmias. In addition, the patient has evidence of chronic obstructive pulmonary disease and hypoxemia. In patients who have left ventricular dilatation associated with heart failure, therapy with digitalis may help to decrease left ventricular diastolic pressure and may decrease the left ventricular internal diameter, both of which would tend to decrease the myocardial requirements for oxygen and to improve the myocardial How of blood, especially to the left ventricular endocardium. In the setting of acute infarction with heart failure, therapy with digitalis may even help to preserve myocardium. At this time, I would not think that therapy with dopamine or norepinephrine would be indicated; however, if there were a further decrease in the patient's systemic blood pressure or cardiac index that was unresponsive to therapy, I would use dopamine if the pulmonary capillary wedge pressure was still elevated. If the pulmonary capillary wedge pressure fell below 18 to 20 mm Hg in this situation, I would consider increasing it (with therapy with dextran) back to this level. In some patients with severe left ventricular failure (or early preshock) following acute myocardial infarction, combined therapy with sodium nitroprusside and dopamine has been of benefit and, I think, has prevented the further development of full-blown cardiogenic shock. At this point, I would not insert a temporary pacemaker as a prophylactic measure. I think that the insertion has some risk of inducing arrhythmias itself, and I would generally prefer to wait if the patient is being monitored in a coronary care unit. At present, his ventricular rate appears to be adequate, and there is evidence of right bundle-branch block and an electrical axis of -45 0 , but the atrioventricular conduction does not appear to be significantly prolonged; however, I would be prepared to insert a pacemaker if complete heart block developed.
COMPLICATED MYOCARDIAL INFARCTION 179
Comments by Jay N. Cohn, M.D.t Measurement of left ventricular filling pressure is necessary in this patient, because it is difficult to assess on clinical grounds whether chronic cor pulmonale with an acute exacerbation or left ventricular failure from an acute myocardial infarction is the predominant physiologic abnormality. Since treatment of these two disorders might be quite different, knowledge of the severity of left ventricular dysfunction is necessary to plan therapy. A satisfactory measurement of pulmonary capillary wedge pressure may not always be obtained in such patients, and the pulmonary arterial diastolic pressure cannot be used as a guide to left ventricular filling pressure. Fortunately, in this patient a measurement of pulmonary capillary wedge pressure was obtained. The value of 30 mm Hg indicates severe left ventricular dysfunction and the gradient of 10 mm Hg from pulmonary arterial diastolic pressure is consistent with the preexisting pulmonary vascular disease. The pulmonary capillary wedge pressure is high enough to cause pulmonary edema, which could be a factor in the inspirational and expirational wheezing, particularly in a patient with chronic obstructive pulmonary disease and perhaps a tendency for bronchospasm. The pulmonary hypertension represents a combination of chronic pulmonary vascular disease with high pulmonary arteriolar resistance, possible acute pulmonary vasoconstriction due to hypoxia, and "backward" failure from the high left atrial pressure. In the absence of left ventricular failure, the pulmonary hypertension would likely be quite mild (about 20 mm Hg lower). Vasodilator therapy might be effective in lowering the pulmonary capillary wedge pressure and raising the cardiac output without inordinately reducing the arterial pressure. It would also probably relieve the pulmonary hypertension. Sodium nitroprusside would be the drug of choice, but care must be taken to avoid further aggravation of the hypoxemia as a result of such therapy. Cautious administration of supplemental oxygen at a low flow would be indicated, with frequent measurement of blood gas levels. Therapy with diuretic agents is certainly indicated. Furosemide administered intravenously would be the agent of choice; however, the diuretic agent alone would likely reduce the cardiac output further, and therefore this agent should be given in this patient only in combination with a vasodilator or inotropic drug. tProfessor of Medicine and Head, Cardiovascular Division, University of Minnesota Medical School, Minneapolis.
180 SCHLANT, COHN
Therapy with digitalis is contraindicated in this setting. Dopamine or dobutamine would be an appropriate choice if nitroprusside lowered the arterial pressure without satisfactorily correcting the low cardiac output. In that case, dopamine or dobutamine and nitroprusside could be administered in combin-ation. The left axis deviation and right bundle branch block are an ominous combination in anterior infarction. Insertion of a temporary pacemaker as a standby would be prudent. FOLLOW-UP
As suggested by our consultants, therapy with sodium nitroprusside was begun, resulting in a gradual drop in the pulmonary arterial pressure from 70/40 mm Hg to 58/35 mm Hg and a decrease in the pulmonary capillary wedge pressure from 30 to 20 mm Hg. The cardiac output did not change. Additionally, 40 mg of furosemide was administered intravenously, resulting in a diuresis of 800 ml. The nitroprusside was continued for six days, during which time the patient's left ventricular filling pressure remained satisfactory at around 20 mm Hg, with a cardiac index of approximately 2.1 L min/sq m. Subsequently, oral prazosin was used in an effort to maintain the left ventricular filling pressure at approximately 20 mm Hg. The patient's wheezing did not resolve with the drop in the pulmonary capillary wedge pressure. Endotracheal intubation and therapy with a volume-controlled respirator became necessary because of increasing effort of breathing and a rising PaCO.). Corticosteroids were administered intravenously for 48 hours in an effort to control the patient's bronchospasm, Morphine might have contributed to the bronchospasm, owing to its release of histamine. The patient's bronchospasm resolved within 24 hours of admission. Inotropic agents, including digitalis, were not administered during the acute phase of the patient's infarction. A temporary transvenous pacemaker was inserted as a prophylactic measure because of the bifascicular block. The patient did not develop high-degree atrioventricular block during his myocardial infarction, and he never required the use of the pacemaker. The pacemaker was removed on the seventh day of hospitalization, and a normal His-ventricle time was recorded at the time of the removal of the transvenous pacemaker. The patient was convalescing well in the hospital when, on the 14th day of hospitalization, he had mild recurrent pain in the chest of approximately 30 minutes' duration, which was followed by a syncopal episode during which time no arrhythmia or changes in the S-T segment or T wave were noted in the ECC. He subsequently died within a few hours, despite vigorous therapeutic measures. No autopsy was obtained.
Department Editor's Comment The use of digitalis during the acute phase of myocardial infarction is controversial. As Schlant points out, in patients with left ventricular dilatation associated with heart failure, therapy with digitalis may indeed decrease the left ventricular diastolic pressure and internal dimension, resulting
CHEST, 75: 2, FEBRUARY, 1979
in a decrease in the tension of the wa", which would decrease the myocardial requirements for oxygen and perhaps help preserve myocardium; however, in the absence of left ventricular dilatation, it is weU known that the myocardial requirement for oxygen is increased by therapy with digitalis, resulting potentially in a detrimental eDect.1 Schlant also points out that the ischemic myocardium appears to be more susceptible to digitalis-induced arrhythmias. There are data from animals to support this view;2-4 however, no clinical studies to date have shown that patients with acute myocardial infarction are more prone to ventricular arrhythmia. 5 The prophylactic insertion of a temporary transvenous pacemaker in patients with acute myocardial infarction (and, in particular, anterior wall myocardial infarction and bifascicular block) may provide some adoantage" Although no clinical studies have demonstrated an improved mortality due to transvenous pacing in complete heart.block, it is possible that occasional patients might otherwise die suddenly if a prophylactic pacemaker were not inserted. On the other hand, a pacing catheter may certainly cause arrhythmias; however, on balance, I believe that the prophylactic standby pacing was less hazardous and facilitated greater ease of management than would have been the case if emergency insertion
CHEST, 75: 2, FEBRUARY, 1979
of a transoenous catheter had become necessary at the time of high degree atrioventricular block. This case demonstrates the multifaceted approach that is necessary in a patient with severe chronic obstructive pulmonary disease who sustains an acute, severe myocardial infarction. Invasive hemodynamic monitoring is often essential in order to guide therapy. Despite these measures, many patients unfortunately still die during the course of their myocardial infarction.
1 Brunwald E, Morrocco P: Limitation of infarct size. Curr Probl CardioI3:46, 1978 2 Bellet S, Johnston CG, Schecter A: The effect of cardiac infarction on the tolerance of dogs to digitalis. Arch Intern Med 54:509-516, 1934 3 Travell J, Gold H, Modell W: The effect of experimental cardiac infarction on response to digitalis. Arch Intern Med 61: 184-197, 1938 B, Lown B: Myocardial infarction 4 Hood WB Jr, ~1cCarthy following coronary ligation in dogs: Hemodynamic effects of isoproterenol and acetyl strophanthidin. eire Res 21: 191199, 1967 5 Lown B, et al: Sensitivity to digitalis drugs in acute myocardial infarction. Am J Cardiol 30: 388-395, 1972 6 Mullins CB, Atkins JM: Prognosis and management of ventricular conduction blocks in acute myocardial infarction. Mod Cone Cardiovasc Dis 45:129, 1976
COMPLICATED MYOCARDIAL INFARCTION 181
