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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 nontraditional 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 4872 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 postresuscitation 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;61:939941.
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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