ADVERTISEMENT
Management of a Patient with Severe Coronary Artery Disease
and Cardiogenic Shock after Prolonged Cardiopulmonary
Resuscitatio
July 2004
Case Report. We present the case of a 74-year-old male with a history of hypertension and smoking who was urgently referred for evaluation after he suffered a cardiac arrest after a transurethral prostate resection (TURP) in a community hospital without coronary intervention capabilities. The patient initially presented to the emergency room with progressively worsening abdominal distension and was found to have a distended urinary bladder and bilateral hydronephrosis due to an enlarged prostate. The patient underwent a TURP without complications. While in the recovery room, he was noted to be hypotensive and suddenly had ventricular tachycardia, which progressed to ventricular fibrillation. Advanced cardiac life support measures were immediately implemented, and the patient underwent multiple electrical cardioversions, received several doses of intravenous epinephrine, lidocaine, and atropine, and was intubated. After 20 minutes of resuscitation, he regained a pulse with a systolic blood pressure of 70 mmHg. His 12-lead electrocardiogram showed sinus tachycardia with diffuse 4 mm ST segment elevation in the anterior and inferior leads. Even with escalating doses of intravenous norephinephrine and neosynephrine, he remained hypotensive with a systolic blood pressure in the 70–80 mmHg. A repeat 12 lead electrocardiogram revealed resolution of the inferior ST segment elevation, however there was persistent 3 mm ST elevation in anterior precordial leads in V3 and V4. Physical examination revealed a blood pressure of 72/40 mmHg, a heart rate of 120 beats/minute, a respiratory rate of 20 breaths/minute, and a temperature of 97.8. He had evidence of fractured ribs with paradoxical motion of his chest with the ventilator. He was tachycardic with a regular rate and rhythm, he had a normal S1 and S2 without an appreciable S3 or S4. He had a 2/6 holosystolic murmur heard loudest in the apex radiating to the axilla. There were no thrills or rubs. He had bilateral rales up to half of his lung fields. He had diminished but equal pulses bilaterally in the extremities without periphral edema. His neurological examination was grossly non-focal. His laboratory examination revealed a BUN of 29 mg/dL and creatinine of 1.6 mg/dL. His complete blood count and coagulation profile was within normal limits. His chest radiograph showed bilateral alveolar infiltrates consistent with pulmonary edema. An intraaortic balloon pump was immediately inserted, and he had an augmented blood pressure of 110 mmHg post-procedure. He was immediately transferred to a tertiary care center with for further management.
At the tertiary medical center, coronary angiography demonstrated the following: the left main had a diffuse 30% lesion, the proximal left anterior descending artery (LAD) had a diffuse 70% lesion, and the mid LAD had a tubular 90% lesion. The distal circumflex had a diffuse 90% stenosis (Figures 1 and 2). The right coronary artery (RCA) had a proximal 70% lesion and a diffuse 90% stenosis in its midportion. A pulmonary artery catheter was placed and the mean right atrial pressure was 9 mmHg, the right ventricular pressure was 31/8 mmHg, the pulmonary artery pressure was 25/15 with a mean of 20 mmHg, and the pulmonary capillary wedge pressure was 9 mmHg. The arterial saturation 99% and the mixed venous saturation was 47%. Left ventriculography revealed normal left ventricular function with an estimated ejection fraction of 47% with mild anterolateral hypokinesis, and severe posterobasal, diaphragmatic, and apical hypokinesis. There was severe (4+/4+) mitral regurgiation (with the intraaortic balloon pump on stand-by). *Almeda 4.jpgsubendsub**
Ramesh Daggubati, MD
Cardiology Fellow
Joshua DeLeon, MD
Director, Coronary Care Unit
Winthrop-University Hospital, Mineola, New York
We would like to commend the authors who described the successful management of a patient with acute myocardial infarction and cardiogenic shock. Briefly, a 74-year-old man developed post-operative (TURP) acute ST elevation MI with malignant ventricular arrhythmias who is successfully resuscitated. He was treated with inotropic agents and intra-aortic balloon counterpulsation. The patient had fractured ribs and developed acute mitral regurgitation clinically. Thrombolytics were not given in this patient, presumably because of the fractured ribs and post-operative status. The patient was subsequently transferred to a tertiary care hospital where catheterization revealed three-vessel disease for which he underwent PCI of the RCA, followed by CABG with mitral valve repair three days later.
At our center, which is a tertiary hospital, the initial management would have included inotropic agents, an intra-aortic balloon pump (IABP) and an emergency cardiac catheterization, similar to the management described by the authors. However, once the patient had a satisfactory augmented blood pressure with the IABP, with three vessel disease noted on the catheterization, this patient probably would have been sent for urgent CABG with mitral valve repair. Presumably, despite persistent ST elevation in the anterior rather than the inferior distribution, the authors intervened on the RCA with the thought that ischemia in this distribution was the cause of the mitral regurgitation. Neither vessel appears easily amenable to intervention, but of the two, the LAD would probably be more difficult. We assume this, or perhaps persistent significant mitral valve regurgitation is the reason for CABG rather than follow-up PCI. Again, we commend the authors for successful management of this patient, but at our institution, the patient probably would have undergone emergent surgery with MVR.
The patient described above is similar to patients enrolled in the SHOCK trial. In this trial, patients were aggressively managed with inotropic agents, intra-aortic balloon pump, thrombolytics and randomized either to early invasive therapy or medical stabilization with revascularization. The early revascularization group showed a 12-month mortality benefit of 55% compared to the medical stabilization group (70%). The greatest benefit was in patients Lloyd W. Klein, MD
Professor of Medicine and Director, Clinical Services
Rush-Presbyterian-St. Luke’s Medical Center
Chicago, Illinois
The clinical problem posed in this case required a series of complex clinical judgements based on precise interpretation of laboratory data and a dose of intuition. As difficult as it is to formulate a logical plan well after the fact, with full knowledge of what ultimately happened, the uncertainty is further magnified when such decisions have to be made at the bedside, without the benefit of being able to see the future.
The case is that of a 74-year-old man who has a cardiac arrest soon after TURP. The resuscitation is prolonged, and immediately after the patient is hypotensive, requiring pressors and IABP, and there are ECG changes suggesting a resolving inferior wall event and an ongoing posterior wall infarction. Additionally, catheterization shows severe three-vessel disease, more than one culprit lesion and severe mitral regurgitation (MR).
The two basic management choices are: 1) send the patient for CABG and MVR right away; or 2) perform a temporizing intervention. The argument favoring immediate surgery is that an operation will likely be necessary for a definitive repair and anything less may not reverse the shock. As high-risk as an immediate operation would be, waiting may result in further deterioration and loss of the window of opportunity. The counter argument favoring an intervention is that perhaps the MR and shock are ischemic, not mechanical in origin, and that temporizing might improve the odds later. If one takes this approach, it would be optimal if the ST depressions were still present and an echocardiogram did not show a flail leaflet. Additionally, determining the most appropriate timing for the bypass operation would necessitate consultation among the cardiologist, surgeon and family.
In the case presented, the right heart catheterization shows a completely normal wedge pressure without a large “V” wave, mildly abnormal RV diastolic pressure and normal PA pressure. Complete hemodynamic resolution of 4+ MR by an IABP despite its angiographic appearance with the IABP turned off is most likely due to acute ischemia rather than papillary muscle rupture. An echocardiogram to confirm this suspicion would have been helpful. Although the mid-LAD stenoses appear to be ulcerated, the presence of acute ischemic MR strongly suggests that the long RCA lesion is the key to this case. For these reasons, I believe the decision to proceed with RCA intervention was the right call. Of course, knowing that only a ring to repair the mitral valve was subsequently necessary, and consequently, no irreversible mechanical abnormality was found, is an advantage that the doctors in this case could surmise but not be certain about. I would like to know more about the immediate post-PCI course and the time frame in which the bypass operation was eventually performed. If the patient stabilized post-intervention, delaying the operation for a week might be one reasonable choice. Conversely, more urgent surgery should be considered if the intervention does not improve the clinical situation within a few hours. It is also possible that papillary muscle necrosis may develop days after the ischemic event, so the decision not to replace the mitrial valve, even in the absence of frank mechanical disruption, could be debated.
John G. Webb MD
St. Paul’s Hospital, University of British Columbia
Vancouver, Canada
The great majority of patients presenting with cardiogenic shock following an acute myocardial infarction have multivessel coronary artery disease.1 Although shock may be the consequence of acute left ventricular dysfunction superimposed on prior infarction of another vascular territory. This was not the case in this individual.
“Ischemia at a distance” to the infarct site as a consequence of multivessel disease is commonly present in shock patients. In the setting of routine myocardial infarction, culprit artery angioplasty alone is often prudent. However, in the setting of shock, reperfusion of the infarct artery alone may not be adequate to halt progressive hemodynamic deterioration. Many would argue for multivessel stenting and complete revascularization.2 Initial stabilization with stenting followed by delayed surgery is of some concern. Should the stented artery be grafted? Will the graft or stent occlude peri-operatively? Surgical revascularization may be a more desirable initial option when relatively complete percutaneous revascularization cannot be safely achieved.
It is unusual for an isolated inferior infarction to result in cardiogenic shock due to left ventricular dysfunction. Severe acute mitral regurgitation may not be clinically apparent in a hypotensive, ventilated shock patient and is often a critical factor. For this reason, echocardiography is part of our routine practice on the way to the catheterization laboratory in shock patients or where left ventricular angiography is not reassuring. Although severe mitral regurgitation may sometimes improve with revascularization, more often it does not. In the absence of mitral valve surgery, patients with acute cardiogenic shock and severe mitral insufficiency generally do very poorly.3,4
Medicine is an art and every case has its nuances. However, in patients with shock, multivessel disease is not amenable to relatively complete revascularization. Severe mitral regurgitation has an extremely high rate of mortality and prompt surgery is often desirable.
1. Sanborn TA, Sleeper LA, Webb JG, et al. Angiographic findings from the SHOCK Trial: left ventricular ejection fraction, culprit vessel, and absence of mitral regurgitation are independent correlates of one-year survival. J Am Coll Cardiol 2003;42:1373–1379.
2. Webb JG, Lowe A, Sanborn TA, et al. Percutaneous coronary intervention for cardiogenic shock in the SHOCK Trial. J Am Coll Cardiol 2003;42:1380–1386.
3. Thompson CR, Buller C, Sleeper LA, et al. Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36:1102–1109.
4. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med 1999;341:625–634.
