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Post Resuscitation Left Ventricular Failure

Karl B. Kern, MD

Sarver Heart Center, University of Arizona, Tucson, Arizona, USA

INTRODUCTION
   Acute, reversible heart failure has been termed "myocardial stunning". This phenomenon was first described by Braunwald and Kloner in 1982. It describes patients with significant coronary artery disease who following a coronary occlusive event had prolonged myocardial dysfunction manifested by systolic contractile abnormalities long after restoration of coronary blood flow (1). Recently, examples of transient myocardial dysfunction after non-traditional ischemic events have been reported (2-7). Such non-traditional ischemic insults leading to transient myocardial dysfunction include toxic shock syndrome, Legionnaires' disease, respiratory arrest, and cardiac arrest.

   Significant left ventricular systolic and diastolic dysfunction has recently been documented after successful resuscitation from prolonged cardiac arrest (8-11). Much as acute coronary occlusion followed by reperfusion can effect regional wall motion, the loss of global perfusion with ventricular fibrillation cardiac arrest and subsequent restoration of such perfusion post-resuscitation, results in global myocardial dysfunction. The development of acute heart failure following resuscitation has been manifested by decreases in ejection fraction (11), a decrease in fractional shortening (11), a decrease in dP/dt-40 (9), a decrease in peak systolic left ventricular pressure/end systolic volume ratio (11), and a rightward shift in the pressure volume relationship (10). The dramatically global nature of this systolic dysfunction post-resuscitation has been demonstrated with echocardiography, as well as ventriculography (11). The following case report illustrates several key features of post-resuscitation acute heart failure.

Case Report
   A 29-year old gravida 1, para 0 was admitted to the University of Arizona Health Sciences Center for a term intrauterine pregnancy. The patient had no significant past medical history except for an allergic reaction to Penicillin as a child. A labor epidural was placed without difficulty and with good function. The patient was taken for an emergent C-section, secondary to failure to progress and lack of fetal descent. Dosing the pre-existing epidural with 2% Lidocaine plus epinephrine plus 50 mcg of intravenous fentanyl produced good sensor levels and adequate surgical anesthesia. Standard monitoring techniques were used and six liters of oxygen were delivered by mask. A low transverse cesarean incision was made and delivery was accomplished with good fetal Apgars (9/9).

   Post-delivery, the patient was noted to have uterine atony and ongoing brisk bleeding. No response to Pitocin or Hemabate was seen. Uterine bleeding continued in spite of vigorous efforts at surgical hemostasis. Bleeding was treated with fluid resuscitation, administration of calcium gluconate, and intermittent dosing with Phenylephrine and ephedrine for pressure support. Total blood loss was estimated at 5,500 ml. An interim hemoglobin and hematocrit were 9.7 and 25.4. Total fluids administered included 8 units of packed red blood cells and 7,000 cc of crystalloid. No pressors were required during the final hour of the operation that included an emergency hysterectomy and cystoscopy.

   In the post-operative recovery area, the patient received an additional 2 units of fresh frozen plasma for coagulopathy and, over a 10 minute period, had a rapid decompensation of respiratory status with onset of tachypnea (40-50/min) with associated cough, shortness of breath and desaturation to less than 80% while on 8 liters O2 by mask. Rapid sequence intubation was then performed with good bilateral breath sounds and no evidence of aspiration, but white frothy sputum was noted in the ET tube. Following intubation, the patient was found to have no pulse. Chest compressions were begun, followed by epinephrine 1.0 mg IV. A total of five minutes of cardiopulmonary resuscitation was performed. A single 200 joule DC countershock was given for ventricular fibrillation. Post-defibrillation a supraventricular rhythm with return of pulses was documented. Post-resuscitation, the patient received Lidocaine 100 mg, Furosemide 20 mg, adenosine 6 mg, calcium chloride 1 gram, epinephrine 20 micrograms, phenylephrine 0.2 mg, Versed 2 mg and CIS-atracurium 10 mg with restoration of sinus rhythm pulses and blood pressure.

   Upon arrival in the ICU a pulmonary artery floatation catheter was inserted through the left subclavian vein, and the initial values included a wedge pressure of 17, pulmonary artery pressure of 36/22, and a right atrial pressure of 14. A chest x-ray showed significant pulmonary edema with extensive peri-vascular interstitial edema and some perihilar alveolar edema. An EKG showed sinus tachycardia with minimal ST depressions and no evidence of acute infarction

   Because of the persistent sinus tachycardia and relatively low cardiac index, a transthoracic echocardiogram was obtained. This showed sinus tachycardia at 140 per minute with normal left ventricular size but generalized left ventricular hypokinesis producing an ejection fraction of 35%. Altered left ventricular diastolic function was also documented with evidence of increased end-diastolic pressure. There was no pericardial effusion. The patient was begun on Digoxin, and an ACE-inhibitor.

   Hemodynamically, the patient improved rapidly and, two days later the Digoxin and Captopril were stopped. A repeat echocardiogram at that time on October 13, 1997 showed normal sinus rhythm with normal left ventricular size and contractility. The left ventricular ejection fraction was now greater than 55%. A follow-up electrocardiogram on October 13, 1997 was normal.

   This is an excellent example of a healthy young woman with no prior evidence for abnormal myocardial function who, following fluid resuscitation, had volume overload, then cardiac arrest including five minutes of cardiopulmonary resuscitation and subsequently had echocardiographically proven left ventricular failure with rapid and full recovery within three days.

   Post-resuscitation syndrome has been well described, manifesting its cardiovascular aspects through increased cardiac filling pressures, decreased cardiac index and a decrease in both systolic and diastolic function (12). More recently, in vivo data has shown left ventricular systolic and diastolic dysfunction after 10 to 15 minutes of untreated cardiac arrest and successful resuscitation to be severe but temporary (11). Studying 28 domestic swine (mean weight =26±1kg), we found both invasive and non-invasive measurements of ventricular function to be dramatically altered after prolonged untreated cardiac arrest and subsequent resuscitation. Left ventriculography, ventricular pressures, cardiac index and hemodynamically measured isovolumic relaxation time (Tau) all confirmed left ventricular systolic and diastolic dysfunction. Concurrent transthoracic Doppler echocardiographic studies also showed depressed left ventricular function following resuscitation. Regional wall motion analysis revealed the dysfunction to be diffuse with global left ventricular systolic dysfunction. Ejection fractions fell from a pre-arrest baseline of 55% to 35% at 30 minutes post-resuscitation, and to 25% by five hours. Left ventricular end-diastolic pressure rose from a baseline of 11 mmHg to a peak of 22 mmHg by two hours post-resuscitation. Hemodynamic measurements of Tau revealed prolonged relaxation of the left ventricle following resuscitation (rising from 28 msec at baseline to 46 msec at two hours post-resuscitation). Follow-up studies revealed partial improvement by 24-hours with total resolution and return to baseline by 48-hours.

   This study was the first demonstration in an intact in vivo model that marked stunning of the myocardium does occur after successful resuscitation from cardiac arrest. This dysfunction includes both systolic and diastolic dysfunction. In our study, the maximal dysfunction occurred between two and five hours after resuscitation following 10 to 15 minutes of untreated cardiac arrest. Improvement was seen at 24 hours, although incomplete, and full recovery was found by 48 hours. However, all these study animals had normal coronary arteries, and normal left ventricles before the ischemic insult of cardiac arrest, and it is possible that cardiac arrest may effect an older heart or hearts with coronary disease even more dramatically, resulting in an even slower rate of recovery. Since the strict definition of myocardial stunning includes the persistence of left ventricular dysfunction after the return of normal myocardial blood flow, an additional three animals were studied in a post hoc fashion. Myocardial blood flow was unchanged between baseline levels and that found at five hours after resuscitation, even though left ventricular ejection fraction remained markedly decreased by five hours (11). These data convincingly show that this phenomenon of post-resuscitation myocardial dysfunction is an example of acute but reversible heart failure.

   The importance of this finding is the implication that aggressive support is indicated during the first 48-72 hours. Good long-term outcome is possible if this early severe period of dysfunction can be overcome.

   We next embarked on a second experimental trial to explore treatments of this post-resuscitation left ventricular dysfunction (13). Twenty-seven domestic swine were studied including 8 controls, 5 that received dobutamine at 5 mcg/kg/min and 14 receiving dobutamine at 10 mcg/kg/min. A similar cardiac arrest insult of 15 minutes of untreated ventricular fibrillation was utilized following which aggressive cardiac life-support was performed for successful resuscitation. Animals were then randomized to one of two treatment arms, including no therapy or dobutamine 10 mcg/kg/min. Five additional animals were studied post hoc using 5 mcg/kg/min of dobutamine. Post-resuscitation data on left ventricular function was collected at 30 minutes, two hours, and five hours. The control group had a decline in left ventricular ejection fraction from a baseline level of 56% down to 29% at five hours, while the 5 mcg/kg/min dobutamine group had a transient descent from 50% to 46% by 30 minutes, but by five hours was normal at 53%. A 10/mg/kg/min dobutamine had no decline, in fact a slight rise from baseline of 52% to 57% by two hours and 55% by five hours. Left ventricular end-diastolic pressure was normalized by either dose of dobutamine. The dramatic difference between dobutamine groups was the heart rate response. Ten mcg of dobutamine caused an impressive increase in heart rate from 130/min at baseline to 186/min at two hours in contrast to the control group, which rose some from 124/min at baseline to 146/min at two hours. This heart rate response was significantly different. Five mcg did not increase the two hour heart rate when compared to baseline. We concluded that, though left ventricular dysfunction is a prominent post-resuscitation problem, dobutamine at 10 mcg/kg/min, can completely ameliorate such dysfunction; however, an impressive tachycardia can result at this dose. Five mcg/kg/min of dobutamine, though slightly less effective at correcting the left ventricular dysfunction at 30 minutes and two hours post-resuscitation, results in much less heart rate increase and seems to be equally potent by five hours post-resuscitation.

   In conclusion, post-resuscitation acute reversible heart failure is a common problem following prolonged cardiac arrest. This appears to be a true "stunning" phenomenon and is transient. However, there is a substantial morbidity and even mortality associated with this period. Approximately 60% to 70% of patients originally resuscitated do not survive to be discharged from the hospital. The most common causes of post-resuscitation death appears to be either central nervous system failure or myocardial failure (14). An aggressive approach to treatment of the myocardial failure subgroup could include inotropic support with dobutamine. Clinically relevant experimental data suggest such therapy is effective.

REFERENCES

1. Braunwald E, Kloner RA. The stunned myocardium: prolonged, post- ischemic ventricular dysfunction. Circulation 1982;66:1146-1149.

2. Ascher EK, Stauffer J-C E, Gaasch WH. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. Am J Cardiol 1988;61:939-941.

3. Deantonio HJ, Kaul S, Lerman BB. Reversible myocardial depression in survivors of cardiac arrest. PACE 1990;13:982-985.

4. Crews JB, Harrison JK, Corey GR et al. Stunned myocardium in toxic shock syndrome. An Intern Med 1992;117:912-913

5. Zhu W. Olson DE, Karon BL, et al. Myocardial stunning after electro- convulsive therapy. Ann Intern Med 1992;117:914-915.

6. Rajan RT, Freeman I, Khan FA et al. Myocardial stunning with Legionnaires' disease. Cardiovasc Rev Rep 1994;15:65-71.

7. Bashir R, Padder FA, Khan FA. Myocardial stunning following respiratory arrest. Chest 1995;108:1459-1460.

8. Tang W, Weil MH, Sun S, Gazmuri RJ, Bisera J. Progressive myocardial dysfunction after cardiac resuscitation. Crit Care Med 1993;21:1046-1050.

9. Tang W, Weil MH, Sun S, Noc M, Yang L, Gazmuri RJ. Epinephrine increases the severity of postresuscitation myocardial dysfunction. Circulation 1995;92:3089-3093.

10. Gazmuir RJ, Weil MH, Bisera J, Tang W, Fukui M, Mckee D. Myocardial dysfunction after successful resuscitation from cardiac arrest. Crit Care Med 1996;24:992-1000.

11. Kern KB, Hilwig RW, Rhee KH, Berg RA. Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning. J Am Coll Cardiol 1996;28:232-240.

12. Cerchiari EL, Safar P, Klein E, Cantadore R, Pinsky M. Cardiovascular function and neurologic outcome after cardiac arrest in dogs. The cardiovascular post-resuscitation syndrome. Resuscitation 1993;25:9- 33.

13. Kern KB, Hilwig RW, Berg RA, Rhee KH, Sanders AB, Otto CW, Ewy GA. Postresuscitation left ventricular systolic and diastolic dysfunction-treatment with dobutamine. Circulation 1997;95:2610-2613.

14. Schoenenberger, RA, von Planta M, von Planta I. Survival after failed out-of-hospital Resuscitation. Arch Intern Med 1994;154:2433-2437.

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2nd Virtual Congress of Cardiology

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