(Circulation. 1997;96:683-688.)
© 1997 American Heart Association, Inc.
Articles |
High-Energy Defibrillation Increases the Severity of Postresuscitation Myocardial Dysfunction
From the Institute of Critical Care Medicine, Palm Springs, Calif (J.X., M.H.W., S.S., W.T., Y.S., X.J., J.B.) and the University of Southern California School of Medicine, Los Angeles (M.H.W., S.S., W.T., J.B.).
Correspondence to Max Harry Weil, MD, PhD, The Institute of Critical Care Medicine, 1695 N Sunrise Way, Bldg 3, Palm Springs, CA 92262. E-mail weilm{at}aol.com
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Abstract |
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Background The fatal outcome of victims after initially successful resuscitation from cardiac arrest has been attributed both to global myocardial ischemia during the interval of cardiac arrest and to the adverse effects of reperfusion. The present study was prompted by earlier experimental observation that the magnitude of myocardial dysfunction was in part related to the energy delivered during electrical defibrillation.
Methods and Results Ventricular fibrillation (VF) was induced in 15 Sprague-Dawley rats. Precordial compression was begun together with mechanical ventilation after 4 minutes of untreated VF and continued for 6 minutes. Spontaneous circulation was restored in each animal after external defibrillation with a single stored 2-, 10-, or 20-J countershock. Cardiac index and the rate of left ventricular pressure rise at left ventricular pressure of 40 mm Hg (dP/dt40) and fall (negative dP/dt) during the 240-minute interval after successful resuscitation were decreased, and left ventricular diastolic pressure was increased. These decreases in myocardial function were closely related to the energy of electrical defibrillation. After a 20-J shock, animals survived for only 5±3 hours; after a 10-J shock, animals survived for 15±4 hours; and after a 2-J shock, all animals survived for >24 hours.
Conclusions The severity of postresuscitation myocardial dysfunction is related, at least in part, to the magnitude of the electrical energy of the delivered shock.
Key Words: contractility • death, sudden • ischemia • fibrillation • defibrillation • cardiopulmonary resuscitation
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Introduction |
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Rapid restoration of coronary perfusion and therefore myocardial blood flow has been the critical determinant of the success of CPR interventions after prolonged cardiac arrest.1 2 3 4 5 Even though the initial success rate of witnessed, in-hospital CPR is
40%, >60% of
victims succumb within 24 hours.6 Studies in
animals7 8 and in human patients9 10 support
the notion that deaths after initially successful CPR result, at least
in part, from postresuscitation myocardial dysfunction. The severity of postresuscitation myocardial dysfunction is related to the severity and duration of global myocardial ischemia during the interval of cardiac arrest. Most likely, it is also the consequence of reperfusion injury after spontaneous circulation is restored.7 8 11 12 However, there is currently no consensus on whether the quantity of electrical energy delivered during electrical defibrillation contributes to postresuscitation myocardial dysfunction. This issue was addressed in the present study.
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Methods |
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All animals received humane care in compliance with the institute's Animal Use and Care Committee Standards, the Principles of Laboratory Animal Care formulated by the National Society for Medical Research, and the Guide for the Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institute of Health (NIH publication 86-32, revised 1985).
Preparation
The experiments were performed in an established rodent model of
cardiac arrest and resuscitation and by methods previously
described.2 8 Briefly, 15 Sprague-Dawley rats (450 to
550 g) were fasted overnight except for free access to water. The
animals were anesthetized by injection of sodium pentobarbital
in a dose of 45 mg/kg IP. Anesthesia was supplemented by
additional injections of 10 mg/kg pentobarbital IP at hourly intervals.
No pentobarbital was administered during the 30 minutes that preceded
VF. The trachea was orally intubated with a 14-gauge cannula
(Quick-Cath, Vicra Division, Travenol Laboratories) mounted with a
blunt needle with a 145° angled tip. Expired gas was sampled through
a side manifold interposed between the tracheal cannula and the
respirator. PETCO2 was measured with a
sidestream infrared CO2 analyzer (model 200,
Instrumentation Laboratories). LV pressure and both dP/dt40
and negative dP/dt were measured through a polyethylene catheter (PE
50, Becton-Dickinson) that had been advanced into the left ventricle
from the right carotid artery. Through the left external jugular vein,
a polyethylene catheter (PE 50, Becton-Dickinson) was advanced into the
right atrium. Right atrial pressure was measured with a
high-sensitivity transducer (P-23-Gb, Spectramed). Through the right
external jugular vein, a 3F pediatric radial artery catheter (model
C-PUM-301J, Cook) was advanced into the right atrium. A precurved
guidewire supplied with the catheter was then advanced through the
catheter into the right ventricle until an endocardial electrogram was
obtained. A thermocouple microprobe 10 cm long and 0.5 mm in
diameter (9030-12-D-30, Columbus Instruments) was advanced from the
right femoral artery into the descending thoracic aorta. Blood
temperature and cardiac output were measured with this sensor. Through
the left femoral artery, a polyethylene catheter (PE 50,
Becton-Dickinson) was advanced into the thoracic aorta for measurement
of aortic pressure with a model TNF-R transducer (Abbott Critical Care)
and for sampling arterial blood. Through the left femoral
vein, a polyethylene catheter (PE 50, Becton-Dickinson) was advanced
into the inferior vena cava for sampling venous blood and
blood transfusion. Cardiac output was measured by the thermodilution
technique after injection of 200 µL isotonic saline maintained at
15°C into the right atrium. Duplicate thermodilution curves were
obtained with a cardiac output computer (model CO-100, ICCM).
Subcutaneous 25-gauge, 1/2-in needle electrodes were used for
recording the ECG (lead 2).
Experimental Procedure
Animals were randomly assigned to one of three groups of five
animals each. After baseline measurements had been completed, the
responsible investigator opened a sealed envelope, the contents of
which provided for assignment of the animal to electrical
defibrillation with a single stored energy of 2, 10, or 20 J.
The animals were mechanically ventilated with a high-frequency jet ventilator of our own design. Ventilation with room air was started before VF was induced. Tidal volume was established at 0.65 mL/100 g animal wt and a frequency of 100 breaths per minute. The tidal volume was then adjusted to maintain PETCO2 in the range of 30 to 35 mm Hg. VF was induced with an alternating current delivered to the right ventricular endocardium. Current flow was progressively increased from 0.5 to 3.5 mA and continued at one half of the maximal current for 3 minutes after VF had been induced to preclude spontaneous reversal of VF. Mechanical ventilation was discontinued immediately after VF appeared. Precordial compression was initiated after 4 minutes of untreated VF and continued for 6 minutes with a pneumatically driven mechanical chest compressor of our design. Compressions were at a rate of 200 per minute. Compression and relaxation intervals were equal, and depth of compression was adjusted to decrease the anteroposterior diameter of the chest by 30%. Coincident with the start of precordial compression, mechanical ventilation with 100% oxygen was started. Compression and ventilation were synchronized to maintain two compressions for each ventilation.
After 10 minutes of VF, the animals were defibrillated with a DC countershock of 2, 10, or 20 J delivered between a 4-cm-diameter paddle applied to the anterior chest and a 4-cm-diameter surface of conductive foil applied to the posterior chest of the supine animal. Direct countershocks were delivered from an experimental high-energy defibrillator (Life Pak 9 Cardiac Monitor, Physio-Control Corp) with a damped sine-wave pulse. Resuscitated animals were monitored for an additional 4 hours. All vascular catheters and electrodes were then removed. The animals were returned to their cages and observed for a total of 48 hours. Animals that survived at the end of 48 hours were recorded as 48-hour survivors for purposes of averaging the duration of survival. They were euthanized by intraperitoneal injection of pentobarbital. Autopsy was routinely performed to identify adverse effects of the interventions and especially traumatic injuries of thoracic and abdominal organs.
Measurements
A 1.5-mL bolus of arterial blood from a donor rat of
the same colony was transfused into the inferior vena cava
immediately after withdrawal of a total of 1.5 mL of
arterial and venous blood. PO2,
PCO2, and lactic acid were measured on these
samples with the aid of an automated pH/blood gas analyzer
(model 1306, Instrumentation Laboratories). Arterial and
mixed venous blood oxyhemoglobin saturation were measured with a
co-oximeter system adapted for rat blood (model 282, Instrumentation
Laboratories). Arterial lactate concentration was measured
with an electrode-based lactate analyzer (model 2300 STAT PLUS,
Yellow Springs Instruments). At 1 and 4 minutes after the start of
precordial compression and at 10, 30, 60, 120, 180, and 240 minutes
after restoration of spontaneous circulation, these measurements were
repeated. Aortic, LV, and right atrial pressures, ECG, and
PETCO2 were continuously monitored and
digitally recorded on a PC-based data acquisition system supported
by CODAS software (DATAQ Inc). Coronary perfusion pressure was
calculated as the difference between decompression
diastolic aortic and time-coincident right atrial pressure
measured at the end of each minute of precordial compression.
Myocardial function was assessed from measurements of LV pressure and cardiac index. With optimal damping, the frequency response of the system was 35 Hz. The rate of LV pressure increase was determined at an LV pressure of 40 mm Hg (dP/dt40), with digital differentiation of the LV pressure pulses as an index of isovolumic contractility.8 The rate of maximal LV pressure decline (-dP/dt) served as an indicator of myocardial relaxation,13 and the LV end-diastolic pressure was used as an index of LV compliance.8
The ratio of heart weight to body weight was measured at autopsy in five rats weighing between 495 and 534 g. For the measurement of the transthoracic impedance, a constant 30-kHz current was applied between the electrode paddle on the anterior chest and the conductive foil in contact with the posterior chest in three anesthetized rats. The impedance was calculated from the ratio of measured voltage and delivered current.
Statistical Analysis
Differences in hemodynamic and
metabolic measurements and duration of survival were
analyzed by ANOVA and Scheffé's multicomparison methods.
Comparisons between time-based measurements within each group were
performed with ANOVA with repeated measures. Measurements are reported
as mean±SD. A value of P<.05 was considered
significant.
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Results |
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Baseline hemodynamic and blood analytical measurements did not differ significantly among the three groups. Spontaneous circulation was restored in each animal after a single transthoracic countershock. There were no statistical differences in either arterial pressure or blood gas measurements among the three groups. LV dP/dt40, negative dP/dt, and cardiac index were significantly decreased and LV end-diastolic pressure was significantly increased in all animals after successful resuscitation. When the defibrillatory energy was increased from 2 to 10 and to 20 J, the dP/dt40 and negative dP/dt were correspondingly reduced, indicating impairment in contractile function and relaxation (Fig 1
). These
decreases in the rate of pressure development and relaxation were
accompanied by decreases in cardiac index and increases in LV
end-diastolic pressure (Fig 2) with
increasing electrical energy of the transthoracic shock.
Heart rate was minimally but significantly decreased by a maximum of
10% after defibrillation. Each of these abnormalities persisted during
the 4-hour interval of postresuscitation monitoring.
Arterial blood lactate, a metabolic measure of
the severity of postresuscitation perfusion failure, was maximal after
20 J and correspondingly less after 10 and 2 J (Fig 3).
Duration of survival was inversely related to the electrical energy
delivered during the single electrical shock. It was 35±11 hours after
2 J and decreased to 15±4 and 5±3 hours after 10 and 20 J,
respectively (Fig 4).
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The relationships among heart and animal weights and stored energy
measured in five animals are shown in the Table. The
transthoracic impedance was 144±5 
. The delivered
energy corresponded to between 91% and 97% of stored energy over the
impedance range of 95 to 160 .
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Discussion |
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After DC transthoracic defibrillation was introduced for the treatment of VF by Lown et al14 in 1962, the possibility that the electrical energy delivered during defibrillation impairs subsequent myocardial function has been an issue of continuous debate. Anecdotally, Guyton15 described an anesthetized dog that was shocked transthoracically 130 times without adverse effects. However, this study was done under physiological conditions rather than in more typical settings of cardiac arrest. During spontaneous circulation or transient VF of 15 seconds in dogs, Kerber et al16 observed that transthoracic shocks with a maximum of 460 J of delivered energy did not adversely affect heart rate, arterial pressure, or LV end-diastolic pressure. Nevertheless, in isolated tissue cultures of myocardial cells, irregularities of contraction followed a single shock with a peak intensity of either 80 or 200 V/cm.17 Synchronized shocks with an energy of 35 J applied directly to the heart of dogs significantly decreased cardiac output.18 When DC transthoracic countershocks of 400 J were applied to normal dogs, increased myocardial uptake of 99mTc stannous pyrophosphate provided evidence of myocardial injury,19 and after cardiac arrest, a transthoracic 400-J countershock produced histological injury to the myocardium.20 Complete heart block, postresuscitation hypotension, and decreased postresuscitation survival have been well documented after successful defibrillation both in animals and in human patients.21 22 23 24
The mechanism by which these electrical shocks produce injury is only partially understood. Free ascorbyl radicals are generated after defibrillation with electrodes applied directly to the epicardium.25 The ascorbyl free radical concentration of coronary sinus blood is also increased in direct proportion to the delivered energy. These free radicals may explain damaged sarcolemma and mitochondria, calcium overload, impaired mitochondrial function and cellular oxidative metabolism, and cellular swelling.26 27 Lysosomal rupture and persistent myofibrillar contractions have also been demonstrated.28 29 30 ACE inhibitors may attenuate free radical generation.31
In the setting of CPR, patients not infrequently receive multiple countershocks. The selectively high energy levels of 10 and 20 J were designed to simulate this cumulative energy. However, we also recognized that this is a compromise. With conventional CPR, multiple shocks would be delivered over a variable time interval contingent on successful resuscitation. Experimentally, this would introduce an important uncontrolled variable, namely, differing durations of myocardial ischemia. It is for this reason that only one shock was delivered, representing the total energy, rather than multiple shocks. However, we recognized that the effects of a single large-energy shock may differ from the cumulative effects of several lower-energy shocks. We also recognized that impaired postresuscitation myocardial function, although associated with substantial increases in fatalities, does not prove that myocardial dysfunction was the cause of the death.
Before applying the present findings of this animal model to human patients, we are prompted to confirm the findings on large animals and, ultimately, in clinical studies. However, past experiences with this model are reassuring. It initially exposed acid-base differences between arterial and venous blood, PETCO2 as a quantifier of blood flow generated during CPR, and postresuscitation myocardial dysfunction, all of which proved to be directly applicable to large animals and human victims.2 8 11 32 33 34 The results of the present study would therefore serve as an important incentive to reexamine the possibility that delivered energy levels would be best at minimally effective levels such that postresuscitation myocardial dysfunction is minimized and postresuscitation survival is increased.
In conclusion, we observed global myocardial dysfunction after cardiac resuscitation from VF, reminiscent of that observed after regional ischemia.35 36 37 The severity of postresuscitation myocardial dysfunction and the duration of survival corresponded to the magnitude of the electrical energy that was delivered for purposes of defibrillation. These observations provide concern that high-energy countershocks, which only marginally increase the success of immediate defibrillation, might increase the severity of life-threatening postresuscitation myocardial dysfunction.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by grants-in-aid from the Mary Pickford Foundation of Beverly Hills, Calif; the Laerdal Foundation of Stavanger, Norway; and Mr and Mrs Jack Samuelson.
Received August 13, 1996; revision received January 2, 1997; accepted January 15, 1997.
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T. Schneider, P. R. Martens, H. Paschen, M. Kuisma, B. Wolcke, B. E. Gliner, J. K. Russell, W. D. Weaver, L. Bossaert, and D. Chamberlain Multicenter, Randomized, Controlled Trial of 150-J Biphasic Shocks Compared With 200- to 360-J Monophasic Shocks in the Resuscitation of Out-of-Hospital Cardiac Arrest Victims Circulation, October 10, 2000; 102(15): 1780 - 1787. [Abstract] [Full Text] [PDF]
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 W. Tang, M. H. Weil, S. Sun, A. Pernat, and E. Mason KATP channel activation reduces the severity of postresuscitation myocardial dysfunction Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1609 - H1615. [Abstract] [Full Text] [PDF]
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T. Eftestol, K. Sunde, S. Ole Aase, J. H. Husoy, and P. A. Steen Predicting Outcome of Defibrillation by Spectral Characterization and Nonparametric Classification of Ventricular Fibrillation in Patients With Out-of-Hospital Cardiac Arrest Circulation, September 26, 2000; 102(13): 1523 - 1529. [Abstract] [Full Text] [PDF]
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D. Bansch, D. Bocker, J.u. Brunn, M. Weber, G.u. Breithardt, and M. Block Clusters of ventricular tachycardias signify impaired survival in patients with idiopathic dilated cardiomyopathy and implantable cardioverter defibrillators J. Am. Coll. Cardiol., August 1, 2000; 36(2): 566 - 573. [Abstract] [Full Text] [PDF]
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 S. Sun, M. H. Weil, W. Tang, H. P. Povoas, and E. Mason Combined Effects of Buffer and Adrenergic Agents on Postresuscitation Myocardial Function J. Pharmacol. Exp. Ther., November 1, 1999; 291(2): 773 - 777. [Abstract] [Full Text]
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W. Tang, M. H. Weil, S. Sun, H. Yamaguchi, H. P. Povoas, A. M. Pernat, and J. Bisera The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function J. Am. Coll. Cardiol., September 1, 1999; 34(3): 815 - 822. [Abstract] [Full Text] [PDF]
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