An Unusual
Cause
for Reintervention
After Coronary
Artery Bypass
Grafting
Raymond G.G.M.P. Ruijters, MD, Sjef M.P.G. Ernst, MD, PhD, Paul J. Knaepen, MD, Johanna J.M. Langemeijer, MD, PhD
A
myocardial infarction (MI) may be followed by severe complications leading to rapid hemodynamic deterioration. Well-known examples are pump failure secondary to loss of left ventricular mass, ventricular fibrillation, ventricular septal rupture, and papillary muscle rupture. Any patient with a recent MI who has to undergo coronary artery bypass grafting (CABG) because of postinfarction angina can sustain these complications in the postoperative period. This case describes a patient who developed cardiovascular collapse in the early postoperative period of a CABG, probably as a sequela of the recent myocardial infarction. CUTE
CASE REPORT A 67-year-old woman with a long-standing history of coronary artery disease (CAD), hypertension, and hypercholesterolemia was admitted to the coronary care unit of this hospital for an acute anterolateral myocardial infarction. The peak serum CPK level was 2310 IU/L (normal < 175 IUIL) with a CK-MB level of 78 IUiL (normal < 15 IUIL). Medical therapy consisted of the administration of nitroglycerin (IV), 25 mg daily, captopril, 12.5 mg three times per day, orally, isosorbide dinitrate. 40 mg three times per day, sublingually, diltiazem, 60 mg three times per day, orally, and furosemide, 40 mg daily, orally. Two days after admission to the hospital the patient developed ventricular fibrillation, which was treated by direct current defibrillation. Because of postinfarction unstable angina, coronary angiography was carried out 10 days after the myocardial infarction. It showed severe three-vessel CAD and impaired function of the anterior wall of the left ventricle. There were no signs of mitral regurgitation. The following hemodynamic data were found at catheterization: sinus rhythm of 72 beatsimin, blood pressure (BP) 115180 mmHg, pulmonary artery pressure (PAP) 34110 mmHg, and right atrial pressure 2 mmHg. The patient was scheduled for CABG. Until the operation, 18 days after the MI, medication was continued. Premeditation consisted of morphine, 10 mg, and haloperidol, 5 mg, intramuscularly. The patient was monitored by a three-lead electrocardiogram (XC), radial arterial catheter, right internal central venous pressure (CVP) catheter, electroencephalogram, urinary catheter, and nasopharyngeal, rectal, and blood temperature probes. Transesophageal echocardiography was not used. Before induction of anesthesia, the ECG showed a sinus rhythm of 85 beatsimin, the BP was 1.50/70 mmHg with a CVP of 7 mmHg. Anesthesia was induced with etomidate, 0.3 mgikg, fentanyl, 20 *g/kg, and pancuronium, 0.12 mgikg. After tracheal intubation, mechanical ventilation was started, using 30% 0: and 70% N20. During the precardiopulmonary bypass (CPB) period the patient remained stable. CPB was initiated uneventfully and the patient was cooled to 28°C nasopharyngeally. Cardioplegia consisted of cold crystalloid solution administered via the aortic root after
From the Departments of Anesthesiolog)i, Cardiology, and Cardiothoracic Surgery St. Antonius Hospital, Nieuwegein, The Netherlands. Address reprint requests to Johanna J.M. Langemeijer, MD, PhD. Department OfAnesthesiology, St. Antonius Hospital, Koekoekslaan 1, 3435 CM Nieuwegein, The Netherlands. Copyright 0 I992 by WB. Saunders Company 1053-0770192/0606-OOlS$O3.OOJO Key words: coronav artery surgery, reoperation, complications 728
aortic clamping and supplemented with topical myocardial cooling. Bypasses were performed to the left anterior descending coronary artery using the left internal mammary artery, to the posterolateral branch of the circumflex artery and to the posterolateral branch of the right coronary artery using a venous sequential graft. At the end of CPB a pulmonary artery catheter (PAC) was inserted. After rewarming, the patient was weaned from CPB with the aid of dobutamine at a dose of 2 kgikgimin. Total CPB time was 97 minutes and cross-clamping of the aorta lasted 66 minutes. After termination of CPB the heart rate (HR) was 78 beatsimin, BP was 105155 mmHg, PAP 2317 mmHg, and CVP 1 mmHg. During the post-CPB period the patient remained stable and she was transported to the intensive care unit. On arrival in the unit. the ECG showed a sinus rhythm of 82 beatsimin, BP 110150 mmHg, PAP 32112 mmHg, and CVP 6 mmHg. Blood gases obtained from the PAC demonstrated values for mixed venous oxygen saturation of 70% or more. Initially these hemodynamic parameters did not change significantly and the patient recovered uneventfully. Extubation of the trachea was accomplished within 24 hours postoperatively and the chest tubes were removed. On the first postoperative day the infusion of dobutamine was terminated and the PAC was removed. On the second postoperative day, after initial mobilization. the patient suddenly became extremely dyspneic, BP dropped to 60135 During auscultation of the mmHg, and HR fell to SO beatsimin. heart no systolic murmur suggesting mitral regurgitation (MR) could be heard. The ECG showed no signs of myocardial ischemia. A bolus injection of atropine. 0.S mg, was given and a dobutamine infusion at 6 pg/kg/min was started, followed by an epinephrine infusion of 0.04 pg/kg/min. After administration of etomidate. 0.08 mgikg, and pancuronium, 0.12 mgikg, endotracheal intubation was performed and mechanical ventilation was initiated with 100% 02. At first, the cardiovascular collapse was ascribed to the development of acute bleeding. most probably in the pericardial space. However, opening of the distal part of the sternum revealed no pericardial effusion and hemodynamics did not improve. A PAC was inserted. Hemodynamic parameters at this time showed a sinus tachycardia of 127 heatsimin. BP 70140 mmHg. CVP 12 mmHg. and cardiac output (CO) of 2.0 Limin. PAP, which had been 30! I3 mmHg early postoperatively. now was 63126 mmHg, and the pulmonary wedge tracing showed large V waves. This strongly suggested MR and transesophageal echocardiography (TEE) was used. It demonstrated massive MR and signs of a flailled anterior leaflet of the mitral valve. An echogenic structure attached to the anterior leaflet prolapsed into the left atrium. The left ventricle was hyperdynamic with a dilated left atrium and there were no signs of a pericardial effusion. Hence, papillary muscle rupture was the cause of the sudden cardiovascular collapse and immediate surgical intervention was indicated. Despite increasing infusion rates of inotropes, hemodynamics rapidly deteriorated. An intra-aortic balloon pump (IABP) was inserted through the right femoral artery. to support the circulation preoperatively and to facilitate weaning from CPB at the end of the operation. With the IABP at ]:I, an arterial pressure of 70/30 mmHg could he achieved and the patient was transferred to the operating room. After injection of etomidate, 0.3 mg/kg, fentanyl, 15 kg/kg, and pancuronium, 0.12 mgikg, the thorax was reopened. Hemodynamics remained very unstable with a BP of 60135 mmHg despite continuous infusions of dohutamine, 10 p,g/kg/min, epinephrine, 0.10 p,g/kg/min, holus injections of 1 to 2 mL of norepinephrine (1 mg diluted in 20 mL of saline) and the IABP at l:l. During the period of resuscitation, the arterial blood gases
JournalofCardiothoracic and VascularAnesthesia, Vol6, No 6 (December),
1992: pp 728.730
EMERGENCY
REOPERATION
AFTER CABG
showed a severe metabolic acidosis: pH was 7.07, PaOz 150 mmHg, PaCOz 35 mmHg, HCOj 9.7 mmol/L, base excess -17.5 mmol/L, and Sa02 97.3%. During the resuscitation, a total of 250 mmol of NaHCOj was given. Before initiation of CPB, metabolic acidosis was corrected: pH was 7.35, Pa02 105 mmHg, PaC02 48 mmHg, HCO; 26.4 mmol/L, base excess +0.8 mmol/L, and Sa02 96.8%. CPB was initiated and the patient was cooled to 32°C nasopharyngeally. Cardioplegia consisted of cold crystalloid solution administered via the aortic root after aortic clamping and supplemented with topical myocardial cooling. After incision of the left atrium, rupture of one head of the anterolateral papillary muscle became clearly visible.
An adequate valvular repair was not possible, so the mitral valve had to be excised and replaced by a Sorin prosthesis (Biomedica SpA, Saluggia, Italy). At the end of the procedure and after rewarming of the patient, the ECG showed asystole, which necessitated the insertion of pacemaker leads. With sequential atrioventricular pacing of the heart, the IABP could be started again as well as infusions of dopamine, 6 kg/kg/min, dobutamine, 6 pglkgimin, epinephrine, 0.1 p,g/kg/min, and nitroprusside, 1 kglkgimin. Initially, the patient could not be weaned from CPB. Over 2 hours of reperfusion, and with increasing infusion rates of dobutamine, 10 kg/kg/ min, dopamine 10 Fgikgimin, and epinephrine, 0.1 kglkgimin, CO gradually improved. Having achieved a perfusion pressure of 50 mmHg a successful attempt was made to separate the patient from CPB (total CPB time was 225 minutes). In the next 45 minutes, the BP improved to 90130 mmHg with a PAP of 2718 mmHg and CVP of 12 mmHg. After surgical closure, the patient was transferred to the intensive care unit. On arrival in the unit, the ECG showed a sinus rhythm of 95 beats/min, and the pacemaker was turned off. The BP was 80135 mmHg, PAP 22110 mmHg, and CVP 16 mmHg. The CO was 3.3 Limin with an SVR of 750 dyne.s.cmm5 and PVR of 145 dyne.s.cm-5. Over the next 24 hours, CO increased to 4.9 L/min and the patient remained hemodynamically stable. The IABP and the infusions of inotropes were gradually reduced. On the third postoperative day, the IABP was removed and the inotropes were discontinued. Only the infusion of a low dose of dopamine, 4 kg/kg/min, was continued until the fifth postoperative day because of a transient rise of the serum creatinine level to 227 FmoliL. With the aid of pressure support, the patient could be weaned from the ventilator, and extubation of the trachea was accomplished on the eleventh postoperative day. There were no signs of neurologic disturbances or infections. Cardiac enzymes were not elevated during the entire postoperative period. The patient was discharged from the intensive care unit on the 14th postoperative day. Echocardiography after 3 months showed good function of the mitral valve prosthesis.
DISCUSSION
Rupture of a papillary muscle is a complication in 1% of acute myocardial infarctions (MI).’ Its reported incidence among fatal MI ranges from 1% to 5%.2,3 In the majority of cases, the infarction involves the inferior left ventricular wal1.2%3Because the blood supply to the posteromedial papillary muscle entirely depends on the posterior descending artery, the posteromedial muscle ruptures three to eight times more frequently than the anterolateral one, which derives arterial blood from both the marginal branches of the circumflex artery and the diagonal branches of the left anterior descending artery.* Rupture usually occurs between 1 to 7 days after the myocardial infarction.2,4 In this case, the 20-day interval between the infarction and the
729
papillary muscle rupture is exceptional, but not unique, as intervals of 4 weeks or more have been described. It is a striking feature that rupture occurred shortly after the CABG. This cannot be explained by a new perioperative MI, because the postoperative ECG was not changed in comparison with the preoperative ECG, there was no elevation of the cardiac enzymes, and the TEE demonstrated no severe reduction of left ventricular function. Possibly, cross-clamping of the aorta and the subsequent myocardial ischemia worsened the ischemia of the papillary muscle, which already had a marginal blood supply because of the previous myocardial infarction. However, it is possible that ischemia and rupture of the papillary muscle occurred unrelated to the previous myocardial infarction. It could have been the consequence of the revascularization procedure itself (secondary to inadequate revascularization, the insult of ischemic arrest, or vein occlusion). This possibility cannot be completely ruled out by the normal enzymes and ECG in the postoperative period. TEE during revascularization procedures might be useful for the detection of ischemia of the papillary muscle, but it is not yet routinely used for this purpose. The clinical picture after an MI is characterized by acute massive MR and subsequent pulmonary edema, cardiogenie shock, or both. On auscultation, a loud systolic murmur is common, but the murmur may be soft or absent. Nishimura et al described seven patients with acute MR after acute myocardial infarction.5 Only two of the seven patients had signilicant systolic murmurs on auscultation, three patients had soft systolic murmurs, and two patients had no audible murmur. A possible explanation for the lack of an audible murmur may be the extreme left atria1 hypertension, which reduces the flow across the mitral vaIve.z Without adequate treatment the majority of patients die within a few days. The overall mortality of partial and total ruptures approximates 90%,3 whereas complete transection of the entire papillary muscle is generally viewed to be incompatible with life.6 Because rapid hemodynamic deterioration is the usual clinical course, an immediate and definitive diagnosis is crucial. Transthoracic two-dimensional echocardiography is a safe and rapid diagnostic modality in the differentiation of causes of acute mitral regurgitation.? However, mechanical ventilation is frequently required in patients sustaining papillary muscle rupture, making the interpretation of transthoracic echocardiography difficult. This case and other reports8,9 illustrate that TEE can be used on an emergency basis and is capable of providing a definitive diagnosis in patients in whom the usefulness of transthoracic imaging may be limited. In this case, additional coronary angiography was not carried out because there were no signs of new myocardial ischemia. The first step in the treatment should be support of the circulation by an IABP and positive inotropic agents in combination with a vasodilator unless the patient is hypotensive.6 However, even after initial stabilization, a labile course with rapid clinical deterioration and death is usually seen. On the other hand, autopsy studies on patients who died of postinfarction papillary muscle rupture showed
RUIJTERS ET AL
relatively small sizes of the MI, leaving many patients with fairly good ventricular function.3J0 Because of the relatively small involvement of the myocardium, a good prognosis may be expected if the hemodynamic abnormality itself can be corrected. Successful mitral valve replacement (MVR) in a patient with papillary muscle rupture was first accomplished by Austen et all’ in 1965. De Busk et al described the first case of postinfarction papillary muscle rupture and subsequent MVR.12 Since then other reports of successful surgical treatment, usually combined with CABG, have followed.s~13-‘sAlthough the mortality rates of surgical intervention remain high, ranging from 14% to 40%, most authors now recommend emergency MVR in patients with postinfarction papillary muscle rupture.s.10x’3,‘4 In this case, weaning from CPB after the MVR was not possible without the aid of inotropes. Infusions of the inotropes were started with a combination of dobutamine, 6 kgikgimin, and dopamine, 6 pg/kg/min. This combination of drugs was
chosen to produce potent /31-stimulation while at the same time attempting to exert minimal effects on the peripheral circulation. However, CO only slightly improved; thus, epinephrine, 0.1 bg/kg/min, was started, combined with nitroprussidc, 1 kgikglmin, to blunt the cY,-stimulation and subsequent vasoconstriction produced by epinephrine. Phosphodiesterase inhibitors might have been effective in this case, but these drugs were not available at the time of the operation. This case describes a patient who, probably as a sequela of a previous MI, had a rupture of a papillary muscle in the early postoperative period after a CABG. Thus, if a patient who has undergone a CABG after a recent MI suddenly develops signs of pulmonary congestion or cardiovascular collapse, the possibility of papillary muscle rupture should be considered. Immediate confirmation of the diagnosis. hemodynamic stabilization, and emergency MVR can significantly improve the outcome of this highly fatal entity.
REFERENCES 1. Sanders RJ, Neuberger KT, Ravin A: Rupture of papillary muscles: Occurrence of rupture of the posterior muscle in posterior myocardial infarction. Dis Chest 31:316-323, 1957 2. De Pace NL, Nestico PF, Morganroth J: Acute severe mitral regurgitation: Pathophysiology, clinical recognition, and management. Am J Med 78:293-306,1985 3. Wei JY, Hutchins GM, Bulkley BH: Papillary muscle rupture in fatal acute myocardial infarction: A potentially treatable form of cardiogenic shock. Ann Intern Med 90:149-153, 1979 4. Barbour DJ, Roberts WC: Rupture of a left ventricular papillary muscle during acute myocardial infarction: Analysis of 22 necropsy patients. J Am Coil Cardio18:558-565, 1986 5. Nishimura RA. Schaff HV, Gersch BJ: Early repair of mechanical complications after acute myocardial infarction. JAMA 256:47-50, 1986 6. Pasternak RC, Braunwald E, Sobel BE: Acute myocardial infarction, in Braunwald E (ed): Heart Disease. A Textbook of Cardiovascular Medicine, vol 2. Philadelphia, PA, Saunders, 1988, pp 1283-1284 7. Mintz GS, Victor MF, Kotler MN, et al: Two-dimensional echocardiographic identification of surgically correctable complications of acute myocardial infarction. Circulation 64:91-96, 1981 8. Koenig K, Kasper W, Hofmann T. et al: Transesophageal echocardiography for diagnosis of rupture of the ventricular
septum or left ventricular papillary muscle during acute myocardial infarction. Am J CardiolS9:362. 1987 9. Stoddard MF, Keedy DL, Kupersmith J: Transesophageal echocardiographic diagnosis of papillary muscle rupture complicating acute myocardial infarction. Am Heart J 120:690-692, 1990 10. Nishimura RA, Schaff HV, Shub C. et al: Papillary muscle rupture complicating acute myocardial infarction: Analysis of 17 patients. Am J Cardiol51:373-377. 1983 Il. Austen WG, Sanders CA, Averill JH, et al: Ruptured papillary muscle: Report of a case with successful mitral valve replacement. Circulation 32:597-601, 1965 12. De Busk RF, Kleiger RE, Ebnother CL, et al: Successful early operation for papillary muscle rupture. Chest 58:17517X. 1970 13. Killen DA, Reed WA, Wathanacharoen S, et al: Surgical treatment of papillary muscle rupture. Ann Thorac Surg 35:243248, 1983 14. Tepe NA, Edmunds LH: Operation for acute postinfarction mitral insufficiency and cardiogenic shock. J Thorac Cardiovasc Surg 89:525-530. 1985 15. Loisance DY, Deleuze Ph. Hillion ML, et al: Are there indications for reconstructive surgery in severe mitral regurgitation after acute myocardial infarction? Eur J Cardiothorac Surg 4:394397, 1990
Cause
for Reintervention
After Coronary
Artery Bypass
Grafting
Raymond G.G.M.P. Ruijters, MD, Sjef M.P.G. Ernst, MD, PhD, Paul J. Knaepen, MD, Johanna J.M. Langemeijer, MD, PhD
A
myocardial infarction (MI) may be followed by severe complications leading to rapid hemodynamic deterioration. Well-known examples are pump failure secondary to loss of left ventricular mass, ventricular fibrillation, ventricular septal rupture, and papillary muscle rupture. Any patient with a recent MI who has to undergo coronary artery bypass grafting (CABG) because of postinfarction angina can sustain these complications in the postoperative period. This case describes a patient who developed cardiovascular collapse in the early postoperative period of a CABG, probably as a sequela of the recent myocardial infarction. CUTE
CASE REPORT A 67-year-old woman with a long-standing history of coronary artery disease (CAD), hypertension, and hypercholesterolemia was admitted to the coronary care unit of this hospital for an acute anterolateral myocardial infarction. The peak serum CPK level was 2310 IU/L (normal < 175 IUIL) with a CK-MB level of 78 IUiL (normal < 15 IUIL). Medical therapy consisted of the administration of nitroglycerin (IV), 25 mg daily, captopril, 12.5 mg three times per day, orally, isosorbide dinitrate. 40 mg three times per day, sublingually, diltiazem, 60 mg three times per day, orally, and furosemide, 40 mg daily, orally. Two days after admission to the hospital the patient developed ventricular fibrillation, which was treated by direct current defibrillation. Because of postinfarction unstable angina, coronary angiography was carried out 10 days after the myocardial infarction. It showed severe three-vessel CAD and impaired function of the anterior wall of the left ventricle. There were no signs of mitral regurgitation. The following hemodynamic data were found at catheterization: sinus rhythm of 72 beatsimin, blood pressure (BP) 115180 mmHg, pulmonary artery pressure (PAP) 34110 mmHg, and right atrial pressure 2 mmHg. The patient was scheduled for CABG. Until the operation, 18 days after the MI, medication was continued. Premeditation consisted of morphine, 10 mg, and haloperidol, 5 mg, intramuscularly. The patient was monitored by a three-lead electrocardiogram (XC), radial arterial catheter, right internal central venous pressure (CVP) catheter, electroencephalogram, urinary catheter, and nasopharyngeal, rectal, and blood temperature probes. Transesophageal echocardiography was not used. Before induction of anesthesia, the ECG showed a sinus rhythm of 85 beatsimin, the BP was 1.50/70 mmHg with a CVP of 7 mmHg. Anesthesia was induced with etomidate, 0.3 mgikg, fentanyl, 20 *g/kg, and pancuronium, 0.12 mgikg. After tracheal intubation, mechanical ventilation was started, using 30% 0: and 70% N20. During the precardiopulmonary bypass (CPB) period the patient remained stable. CPB was initiated uneventfully and the patient was cooled to 28°C nasopharyngeally. Cardioplegia consisted of cold crystalloid solution administered via the aortic root after
From the Departments of Anesthesiolog)i, Cardiology, and Cardiothoracic Surgery St. Antonius Hospital, Nieuwegein, The Netherlands. Address reprint requests to Johanna J.M. Langemeijer, MD, PhD. Department OfAnesthesiology, St. Antonius Hospital, Koekoekslaan 1, 3435 CM Nieuwegein, The Netherlands. Copyright 0 I992 by WB. Saunders Company 1053-0770192/0606-OOlS$O3.OOJO Key words: coronav artery surgery, reoperation, complications 728
aortic clamping and supplemented with topical myocardial cooling. Bypasses were performed to the left anterior descending coronary artery using the left internal mammary artery, to the posterolateral branch of the circumflex artery and to the posterolateral branch of the right coronary artery using a venous sequential graft. At the end of CPB a pulmonary artery catheter (PAC) was inserted. After rewarming, the patient was weaned from CPB with the aid of dobutamine at a dose of 2 kgikgimin. Total CPB time was 97 minutes and cross-clamping of the aorta lasted 66 minutes. After termination of CPB the heart rate (HR) was 78 beatsimin, BP was 105155 mmHg, PAP 2317 mmHg, and CVP 1 mmHg. During the post-CPB period the patient remained stable and she was transported to the intensive care unit. On arrival in the unit. the ECG showed a sinus rhythm of 82 beatsimin, BP 110150 mmHg, PAP 32112 mmHg, and CVP 6 mmHg. Blood gases obtained from the PAC demonstrated values for mixed venous oxygen saturation of 70% or more. Initially these hemodynamic parameters did not change significantly and the patient recovered uneventfully. Extubation of the trachea was accomplished within 24 hours postoperatively and the chest tubes were removed. On the first postoperative day the infusion of dobutamine was terminated and the PAC was removed. On the second postoperative day, after initial mobilization. the patient suddenly became extremely dyspneic, BP dropped to 60135 During auscultation of the mmHg, and HR fell to SO beatsimin. heart no systolic murmur suggesting mitral regurgitation (MR) could be heard. The ECG showed no signs of myocardial ischemia. A bolus injection of atropine. 0.S mg, was given and a dobutamine infusion at 6 pg/kg/min was started, followed by an epinephrine infusion of 0.04 pg/kg/min. After administration of etomidate. 0.08 mgikg, and pancuronium, 0.12 mgikg, endotracheal intubation was performed and mechanical ventilation was initiated with 100% 02. At first, the cardiovascular collapse was ascribed to the development of acute bleeding. most probably in the pericardial space. However, opening of the distal part of the sternum revealed no pericardial effusion and hemodynamics did not improve. A PAC was inserted. Hemodynamic parameters at this time showed a sinus tachycardia of 127 heatsimin. BP 70140 mmHg. CVP 12 mmHg. and cardiac output (CO) of 2.0 Limin. PAP, which had been 30! I3 mmHg early postoperatively. now was 63126 mmHg, and the pulmonary wedge tracing showed large V waves. This strongly suggested MR and transesophageal echocardiography (TEE) was used. It demonstrated massive MR and signs of a flailled anterior leaflet of the mitral valve. An echogenic structure attached to the anterior leaflet prolapsed into the left atrium. The left ventricle was hyperdynamic with a dilated left atrium and there were no signs of a pericardial effusion. Hence, papillary muscle rupture was the cause of the sudden cardiovascular collapse and immediate surgical intervention was indicated. Despite increasing infusion rates of inotropes, hemodynamics rapidly deteriorated. An intra-aortic balloon pump (IABP) was inserted through the right femoral artery. to support the circulation preoperatively and to facilitate weaning from CPB at the end of the operation. With the IABP at ]:I, an arterial pressure of 70/30 mmHg could he achieved and the patient was transferred to the operating room. After injection of etomidate, 0.3 mg/kg, fentanyl, 15 kg/kg, and pancuronium, 0.12 mgikg, the thorax was reopened. Hemodynamics remained very unstable with a BP of 60135 mmHg despite continuous infusions of dohutamine, 10 p,g/kg/min, epinephrine, 0.10 p,g/kg/min, holus injections of 1 to 2 mL of norepinephrine (1 mg diluted in 20 mL of saline) and the IABP at l:l. During the period of resuscitation, the arterial blood gases
JournalofCardiothoracic and VascularAnesthesia, Vol6, No 6 (December),
1992: pp 728.730
EMERGENCY
REOPERATION
AFTER CABG
showed a severe metabolic acidosis: pH was 7.07, PaOz 150 mmHg, PaCOz 35 mmHg, HCOj 9.7 mmol/L, base excess -17.5 mmol/L, and Sa02 97.3%. During the resuscitation, a total of 250 mmol of NaHCOj was given. Before initiation of CPB, metabolic acidosis was corrected: pH was 7.35, Pa02 105 mmHg, PaC02 48 mmHg, HCO; 26.4 mmol/L, base excess +0.8 mmol/L, and Sa02 96.8%. CPB was initiated and the patient was cooled to 32°C nasopharyngeally. Cardioplegia consisted of cold crystalloid solution administered via the aortic root after aortic clamping and supplemented with topical myocardial cooling. After incision of the left atrium, rupture of one head of the anterolateral papillary muscle became clearly visible.
An adequate valvular repair was not possible, so the mitral valve had to be excised and replaced by a Sorin prosthesis (Biomedica SpA, Saluggia, Italy). At the end of the procedure and after rewarming of the patient, the ECG showed asystole, which necessitated the insertion of pacemaker leads. With sequential atrioventricular pacing of the heart, the IABP could be started again as well as infusions of dopamine, 6 kg/kg/min, dobutamine, 6 pglkgimin, epinephrine, 0.1 p,g/kg/min, and nitroprusside, 1 kglkgimin. Initially, the patient could not be weaned from CPB. Over 2 hours of reperfusion, and with increasing infusion rates of dobutamine, 10 kg/kg/ min, dopamine 10 Fgikgimin, and epinephrine, 0.1 kglkgimin, CO gradually improved. Having achieved a perfusion pressure of 50 mmHg a successful attempt was made to separate the patient from CPB (total CPB time was 225 minutes). In the next 45 minutes, the BP improved to 90130 mmHg with a PAP of 2718 mmHg and CVP of 12 mmHg. After surgical closure, the patient was transferred to the intensive care unit. On arrival in the unit, the ECG showed a sinus rhythm of 95 beats/min, and the pacemaker was turned off. The BP was 80135 mmHg, PAP 22110 mmHg, and CVP 16 mmHg. The CO was 3.3 Limin with an SVR of 750 dyne.s.cmm5 and PVR of 145 dyne.s.cm-5. Over the next 24 hours, CO increased to 4.9 L/min and the patient remained hemodynamically stable. The IABP and the infusions of inotropes were gradually reduced. On the third postoperative day, the IABP was removed and the inotropes were discontinued. Only the infusion of a low dose of dopamine, 4 kg/kg/min, was continued until the fifth postoperative day because of a transient rise of the serum creatinine level to 227 FmoliL. With the aid of pressure support, the patient could be weaned from the ventilator, and extubation of the trachea was accomplished on the eleventh postoperative day. There were no signs of neurologic disturbances or infections. Cardiac enzymes were not elevated during the entire postoperative period. The patient was discharged from the intensive care unit on the 14th postoperative day. Echocardiography after 3 months showed good function of the mitral valve prosthesis.
DISCUSSION
Rupture of a papillary muscle is a complication in 1% of acute myocardial infarctions (MI).’ Its reported incidence among fatal MI ranges from 1% to 5%.2,3 In the majority of cases, the infarction involves the inferior left ventricular wal1.2%3Because the blood supply to the posteromedial papillary muscle entirely depends on the posterior descending artery, the posteromedial muscle ruptures three to eight times more frequently than the anterolateral one, which derives arterial blood from both the marginal branches of the circumflex artery and the diagonal branches of the left anterior descending artery.* Rupture usually occurs between 1 to 7 days after the myocardial infarction.2,4 In this case, the 20-day interval between the infarction and the
729
papillary muscle rupture is exceptional, but not unique, as intervals of 4 weeks or more have been described. It is a striking feature that rupture occurred shortly after the CABG. This cannot be explained by a new perioperative MI, because the postoperative ECG was not changed in comparison with the preoperative ECG, there was no elevation of the cardiac enzymes, and the TEE demonstrated no severe reduction of left ventricular function. Possibly, cross-clamping of the aorta and the subsequent myocardial ischemia worsened the ischemia of the papillary muscle, which already had a marginal blood supply because of the previous myocardial infarction. However, it is possible that ischemia and rupture of the papillary muscle occurred unrelated to the previous myocardial infarction. It could have been the consequence of the revascularization procedure itself (secondary to inadequate revascularization, the insult of ischemic arrest, or vein occlusion). This possibility cannot be completely ruled out by the normal enzymes and ECG in the postoperative period. TEE during revascularization procedures might be useful for the detection of ischemia of the papillary muscle, but it is not yet routinely used for this purpose. The clinical picture after an MI is characterized by acute massive MR and subsequent pulmonary edema, cardiogenie shock, or both. On auscultation, a loud systolic murmur is common, but the murmur may be soft or absent. Nishimura et al described seven patients with acute MR after acute myocardial infarction.5 Only two of the seven patients had signilicant systolic murmurs on auscultation, three patients had soft systolic murmurs, and two patients had no audible murmur. A possible explanation for the lack of an audible murmur may be the extreme left atria1 hypertension, which reduces the flow across the mitral vaIve.z Without adequate treatment the majority of patients die within a few days. The overall mortality of partial and total ruptures approximates 90%,3 whereas complete transection of the entire papillary muscle is generally viewed to be incompatible with life.6 Because rapid hemodynamic deterioration is the usual clinical course, an immediate and definitive diagnosis is crucial. Transthoracic two-dimensional echocardiography is a safe and rapid diagnostic modality in the differentiation of causes of acute mitral regurgitation.? However, mechanical ventilation is frequently required in patients sustaining papillary muscle rupture, making the interpretation of transthoracic echocardiography difficult. This case and other reports8,9 illustrate that TEE can be used on an emergency basis and is capable of providing a definitive diagnosis in patients in whom the usefulness of transthoracic imaging may be limited. In this case, additional coronary angiography was not carried out because there were no signs of new myocardial ischemia. The first step in the treatment should be support of the circulation by an IABP and positive inotropic agents in combination with a vasodilator unless the patient is hypotensive.6 However, even after initial stabilization, a labile course with rapid clinical deterioration and death is usually seen. On the other hand, autopsy studies on patients who died of postinfarction papillary muscle rupture showed
RUIJTERS ET AL
relatively small sizes of the MI, leaving many patients with fairly good ventricular function.3J0 Because of the relatively small involvement of the myocardium, a good prognosis may be expected if the hemodynamic abnormality itself can be corrected. Successful mitral valve replacement (MVR) in a patient with papillary muscle rupture was first accomplished by Austen et all’ in 1965. De Busk et al described the first case of postinfarction papillary muscle rupture and subsequent MVR.12 Since then other reports of successful surgical treatment, usually combined with CABG, have followed.s~13-‘sAlthough the mortality rates of surgical intervention remain high, ranging from 14% to 40%, most authors now recommend emergency MVR in patients with postinfarction papillary muscle rupture.s.10x’3,‘4 In this case, weaning from CPB after the MVR was not possible without the aid of inotropes. Infusions of the inotropes were started with a combination of dobutamine, 6 kgikgimin, and dopamine, 6 pg/kg/min. This combination of drugs was
chosen to produce potent /31-stimulation while at the same time attempting to exert minimal effects on the peripheral circulation. However, CO only slightly improved; thus, epinephrine, 0.1 bg/kg/min, was started, combined with nitroprussidc, 1 kgikglmin, to blunt the cY,-stimulation and subsequent vasoconstriction produced by epinephrine. Phosphodiesterase inhibitors might have been effective in this case, but these drugs were not available at the time of the operation. This case describes a patient who, probably as a sequela of a previous MI, had a rupture of a papillary muscle in the early postoperative period after a CABG. Thus, if a patient who has undergone a CABG after a recent MI suddenly develops signs of pulmonary congestion or cardiovascular collapse, the possibility of papillary muscle rupture should be considered. Immediate confirmation of the diagnosis. hemodynamic stabilization, and emergency MVR can significantly improve the outcome of this highly fatal entity.
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