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(Chest. 2002;122:1006-1011.)
© 2002 American College of Chest Physicians

Evolution of the Stone Heart After Prolonged Cardiac Arrest*

Kada Klouche, MD; Max Harry Weil, MD, PhD, Master FCCP; Shijie Sun, MD; Wanchun Tang, MD, FCCP; Heitor P. Povoas, MD; Takashi Kamohara, MD and Joe Bisera, MSEE

* From The Institute of Critical Care Medicine (Drs. Klouche, Weil, Povoas, and Kamohara), Palm Springs; and The Keck School of Medicine of the University of Southern California (Drs. Weil, Sun, Tang, and Prof. Bisera), Los Angeles, CA.

Correspondence to: Max Harry Weil, MD, PhD, Master FCCP, The Institute of Critical Care Medicine, 1695 North Sunrise Way, Building 3, Palm Springs CA; e-mail: weilm{at}911research.org


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Objectives: We hypothesized that progressive impairment in diastolic function during cardiopulmonary resuscitation (CPR) precedes evolution of the "stone heart" after failure of CPR. We therefore measured sequential changes in left ventricular (LV) volumes and free-wall thickness of the heart during CPR in an experimental model.

Design: Prospective, observational animal study.

Setting: Medical research laboratory in an university-affiliated research and educational institute.

Subjects: Domestic pigs.

Methods: Ventricular fibrillation (VF) was induced in 40 anesthetized male domestic pigs weighing between 38 kg and 43 kg. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Failing to reverse VF in each instance, precordial compression at a rate of 80/min was begun coincident with mechanical ventilation. Coronary perfusion pressures (CPPs) were computed from the differences in time-coincident diastolic aortic and right atrial pressures. Left ventricular (LV) systolic and diastolic ventricular volumes and thickness of the LV free wall were estimated with transesophageal echocardiography. The stroke volumes (SVs) were computed from the differences in decompression diastolic and compression systolic volumes. Free-wall thickness was measured on the hearts at autopsy.

Results: Significantly greater CPPs were generated with the 4 min of untreated cardiac arrest. Progressive reductions in LV diastolic and SV and increases in LV free-wall thickness were documented with increasing duration of untreated VF. A stone heart was confirmed at autopsy in each animal that failed resuscitative efforts. Correlations with indicator dilution method and physical measurements at autopsy corresponded closely with the echocardiographic measurements.

Conclusion: Progressive impairment in diastolic function terminates in a stone heart after prolonged intervals of cardiac arrest.

Key Words: cardiopulmonary resuscitation • left ventricular diastolic volume • left ventricular compliance • left ventricular wall thickness • stone heart


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Current methods of closed-chest cardiac resuscitation lose effectiveness when the duration of cardiac arrest prior to attempted cardiac resuscitation increases to > 8 min.1 2 Accordingly, the success of current methods of closed-chest compression after protracted intervals of untreated cardiac arrest > 8 min is remote.3 4 5 The duration of cardiac arrest prior to the start of cardiopulmonary resuscitation (CPR) in human victims is the best single predictor of outcome.6 7

In settings of regional myocardial ischemia due to coronary artery disease, decreases in ventricular compliance with myocardial stunning are well documented.8 9 Decreases in ventricular compliance have also been documented during the global myocardial ischemia of cardiac arrest.10 Reductions in left ventricular (LV) end-diastolic volumes would explain, at least in part, progressive decreases in stroke volume (SV) during CPR. We therefore anticipated that decreases in LV chamber size with increases in wall thickness would correspond to the duration of untreated ventricular fibrillation (VF) and terminate in an anatomically "stony heart." In the present study, we validated transesophageal echocardiography in a porcine model of cardiac arrest to quantitate the dynamic changes in LV volumes and wall thickness after untreated cardiac arrest for intervals of 4 min, 7 min, and 10 min and failed resuscitation. We subsequently related these to physical measurements at autopsy.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Animals received humane care in compliance with principles of laboratory animal care formulated by the National Society for Medical Research, and care and use of laboratory animals as mandated by the Institute of Laboratory Animal Resources. The protocols were approved by the Institutional Animal Care and Use Committee of the Institute of Critical Care Medicine.

Animal Preparation
Male domestic pigs from a single source breeder weighing between 38 kg and 45 kg were investigated. Animals were fasted overnight except for free access to water. Anesthesia was initiated by IM injection of ketamine, 20 mg/kg, followed by ear vein injection of sodium pentobarbital, 30 mg/kg. Additional doses of sodium pentobarbital, 8 mg/kg, were injected at intervals of approximately 1 h to maintain anesthesia. After endotracheal intubation, the animals received mechanical ventilation with a tidal volume of 15 mL/kg and a peak flow of 40 L/min of room air with the aid of a volume-controlled ventilator (Model MA-1; Puritan Bennett; Carlsbad, CA). End-tidal PCO2 (PETCO2) was monitored with a mainstream infrared analyzer (Model 01R-7101A; Nihon Kohden; Tokyo, Japan). Respiratory frequency was adjusted to maintain PETCO2 between 35 mm Hg and 40 mm Hg prior to cardiac arrest without adjustment thereafter. Conventional ECG scalar limb leads were continuously recorded. The femoral artery and vein were surgically isolated under aseptic conditions. An 8F angiographic catheter (Model 6523; USCI, C.R. Bart; Billerica, MA) was advanced through the right femoral artery into the descending thoracic aorta for measurement of aortic pressure. A multilumen, thermistor and balloon-tipped pulmonary artery catheter (41216–01; Abbott Critical Care; Anaheim, CA) was flow directed from the right femoral vein into the pulmonary artery. The atrial port was utilized for measurement of atrial pressure and for injection of thermal tracer. Positions of the catheters were guided by characteristic pressure pulse morphology and confirmed by fluoroscopy.

For the measurements of LV volumes, a 5-MHz, single-plane, transesophageal echocardiographic transducer with 5-MHz continuous-wave Doppler echocardiography with four-way flexure capability (Model 21363A; Hewlett-Packard, Medical Products Group; Andover, MA) was utilized as a noninvasive option so that the bony chest was preserved for conventional chest compression. The probe was advanced from the incisor teeth into the esophagus for a distance of approximately 35 cm. Feasibility studies in our porcine model demonstrated that biplane transducers yielded less consistent images for mensuration during precordial compression.

For inducing VF, a 4F pacing wire (EP Technologies; Mountain View, CA) was advanced through a surgically isolated right cephalic vein into the right ventricle. The tip of the pacing wire was impinged on the apical endocardium during fluoroscopic imaging. A characteristic endocardial injury current confirmed appropriate placement.

Experimental Procedures
Baseline recordings of hemodynamic and echocardiographic parameters were obtained. Blood temperature was maintained at 38 ± 0.5°C with infrared heating lamps. VF was induced by progressively increasing the alternating current delivered to the endocardium from 0 to 2 mA. Mechanical ventilation was discontinued after confirmation of VF. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Up to three 150-J biphasic electrical shocks were delivered between the positive right infraclavicular electrode and the negative apical electrode. If VF was not reversed after a sequence of three shocks, precordial compression was started with a pneumatic chest compressor (Thumper, Model 1000; MI Instruments; Grand Rapids, MI) at a rate of 80 compressions per minute. Coincident with start of precordial compression, the animals received mechanical ventilation with a tidal volume of 15 mL/kg and a fraction of inspired oxygen of 1.0. Chest compression was synchronized to provide a compression/ventilation ratio of 5:1 with equal compression-relaxation intervals (ie, a 50% duty cycle). The compression force was adjusted to decrease the anteroposterior diameter of the chest by 25%. After each min of precordial compression, another sequence of up to three shocks was delivered. Successful resuscitation was defined as a return of a supraventricular rhythm that generated a mean aortic pressure of >= 60 mm Hg, for an interval > 5 min. When we failed to restore spontaneous circulation after 15 min, resuscitation efforts were discontinued and autopsy was performed.

Measurements
Dynamic data, including aortic pressure, right atrial pressure, PETCO2, and lead 2 of the scalar ECG, together with the digital output of the Hewlett-Packard Acoustic Quantification system, were recorded continuously on a personal computer-based data acquisition system, supported by CODAS hardware and software (Dataq Instruments; Akron, OH). Sixteen channels were provided for continuous recording at optimal sampling frequencies. The coronary perfusion pressure (CPP) was digitally computed from the differences in time-coincident diastolic (compression) aortic and right atrial pressures and displayed in real-time.

Echocardiographic measurements were made frame-by-frame on the long axis, two-chamber view. Compression systole was defined as the minimal chamber dimension of the LV during chest compression. Compression diastole was defined as the maximal chamber dimension of the LV following release of chest compression. LV areas were calculated by the method of discs (Acoustic Quantification Technology; Hewlett Packard; Andover, MA). LV systolic and diastolic volumes and SV were computed using the simplified Simpson’s rule.11 LV wall thickness was measured in the posterior wall, 1 cm distal to the mitral valve. This site provided more consistent images in contrast to the anterior and lateral walls.

Free-wall thickness was physically measured at autopsy in the four animals for comparison with echocardiographic measurements. It was only after analyses of the ultrasound data pointed to the evolution of the stone heart that we performed anatomic correlation at autopsy within 5 min of failed CPR in the final four animals enrolled in this experimental study.

Additional studies were performed in five animals in whom VF was induced and maintained for 7 min. The same procedure described earlier was used but, in addition, thermodilution cardiac outputs were measured during CPR with the aid of a cardiac computer (Model 9520A; American Edwards Laboratories; Irvine, CA) following injection of 5 mL of saline solution maintained at 4°C. Duplicate measurements of thermodilution cardiac output in each instance differed by < 5% and were averaged. These measurements of cardiac output were compared with echocardiographic estimates of cardiac output.

Statistical Analysis
Data are presented as mean ± SD. Differences in LV volumes and free wall thickness between groups of animals were analyzed by analysis of variance. Comparisons between time-based measurements within each group were performed with analysis of variance repeated measurements with adjustments for multiple comparisons (Newman-Keuls). Correlations were computed by linear regression analyses utilizing STAT VIEW II software (Abacus Concepts; Berkeley, CA). The outcome differences were analyzed with the Fisher exact test and {chi}2 square test. A p value < 0.05 was regarded as statistically significant.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
No differences in baseline hemodynamic measurements and values of LV volumes and free-wall thickness between the three groups of animals were observed. After 4 min of untreated VF, all five animals obtained spontaneous circulation within 2 min of the start of CPR. As anticipated, survival significantly decreased after 7 min and 10 min of untreated cardiac arrest with respect to the 4-min group. Differences were, however, not statistically significant between 7 min and 10 min of untreated VF. The principal outcomes are shown in Table 1 .


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  		Table 1. The Effects of Arrest Time on Resuscitation and Left Ventricular Function*

 
Consistently greater CPP was documented in animals after 4 min of untreated VF, as shown in Figure 1 . However, the differences between the 7-min and 10-min groups were not statistically significant. PETCO2 was greater after both 4 min and 7 min when compared to 10 min of untreated VF. However, the differences between the 7-min and 10-min groups once again were numerically but not statistically different (Fig 2 ).



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  		Figure 1. CPPs during the initial 11 min of precordial compression and after 4 min, 7 min, or 10 min of untreated VF. The numbers in parentheses refer to the number of unresuscitated animals. BL = baseline.

 


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  		Figure 2. PETCO2 during the initial 11 min of precordial compression and after 4 min, 7 min, or 10 min of untreated VF. The number of unresuscitated animals included in each time interval is shown in Figure 1 , as is the expansion of abbreviation.

 
End-systolic volumes did not differ among the three groups. The most impressive change was an early and highly significant decrease in diastolic volumes with increasing duration of cardiac arrest (Fig 3 ). This accounted for progressive reductions in SV (Fig 4 ). After 7 min of untreated cardiac arrest and at 10 min after start of resuscitation efforts, the diastolic volume was reduced to one third of control values. After 10 min of untreated cardiac arrest and 10 min of CPR, the diastolic volume reduced to only 15% of baseline values. Concurrently, progressive increases in the thickness of the free wall of the LV were documented (Fig 5 ). The differences in wall thickness between the 7-min and 10-min groups proved to be highly significant. Autopsy demonstrated a strikingly firm and contracted heart that, in each instance, was characteristic of the stone heart previously described.12 13 Ventricular chamber dimensions were markedly decreased, and the thickness of the septum and the free wall were markedly increased. The correlation between echocardiographic measurements and physical measurement of free-wall thickness on four animals that failed resuscitation attempts after 7 min of untreated cardiac arrest are shown in Figure 6 . In the five animals in which echocardiographic estimates of SV were compared with thermodilution measurements during CPR, the correlation (r2) was 0.94, p < 0.0001 (Fig 7 ).



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  		Figure 3. Diastolic LV volumes during the initial 11 min of precordial compression and after 4 min, 7 min, or 10 min of untreated VF. The number of unresuscitated animals included in each time interval is shown in Figure 1 . ML = milliliter; see Figure 1 for expansion of other abbreviation.

 


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  		Figure 4. SVs during the initial 11 min of precordial compression and after 4 min, 7 min, or 10 min of untreated VF. The number of unresuscitated animals included in each time interval is shown in Figure 1 . See Figures 1 and 3 for expansions of abbreviations.

 


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  		Figure 5. LV free-wall thickness during the initial 11 min of precordial compression and after 4 min, 7 min, or 10 min of untreated VF. The number of unresuscitated animals included in each time interval is shown in Figure 1 , as is the expansion of abbreviation.

 


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  		Figure 6. The relationship between echocardiographic and physical measurements at autopsy of LV free-wall thickness on four animals.

 


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  		Figure 7. The relationship between echocardiographic and thermodilution measurements of SVs during CPR on five animals.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
When immediate defibrillation fails, the success of CPR becomes contingent on prompt restoration of CPP and therefore myocardial blood flow.14 15 Closed-chest compression provides sufficient forward blood flow in the early intervals following cardiac arrest. However, when CPR is started after 7 min or 10 min of untreated cardiac arrest, as in the present investigations, precordial compression typically fails to generate sufficient forward blood flow and perfusion pressures to be predictive of successful resuscitation.1 5 15 16 Progressive decreases in LV diastolic volumes and increases in LV wall thickness characterize the diastolic dysfunction that is associated with decreased SV. The findings are consistent with a progressive loss of LV compliance associated with ischemic contracture following global myocardial ischemia as previously reported by our group.17 After VF is induced in the isolated beating heart, progressive increases in LV diastolic pressure during VF were documented.18 Whether compression of the chest with increases in intrathoracic pressure also accounts for decreases in preload and therefore SV is postulated and such may be potentially minimized by active compression decompression CPR.19

Our findings of ischemic contracture are reminiscent of observations reported in settings of regional ischemia.8 9 20 21 The concept of ischemic contracture of the myocardium is associated with myocardial stunning. The same concept may be applicable to the global myocardial ischemia of cardiac arrest. Visner et al10 compressed the left main coronary artery and produced decreases in LV compliance, much like those observed by us in the settings of failed cardiac resuscitation. Augmented crossbridging between actin and myosin followed depletion of high-energy phosphates.13 22 Neumar et al23 24 found a strong temporal correlation between the duration of global myocardial ischemia of cardiac arrest and high-energy phosphates. These time-dependent changes were associated with reductions in ventricular diastolic volumes and increases in myocardial stiffness. These, in turn, accounted for decreased effectiveness of chest compression for producing forward blood flow during CPR.25 Increases in ventricular wall stiffness of themselves account for reductions in diastolic and SVs because of ischemia consequent to increased mechanical resistance to coronary blood flow.26 Accordingly, both ischemic stunning and increased coronary arterial resistance to blood flow are implicated. Histopathologic examinations of stone hearts following prolonged cardiac arrest in human victims have demonstrated myocardial edema with increased myocardial tissue water as an additional feature.27 28 Ultrastructural studies on hearts following cardiac resuscitation are eagerly awaited to explain both the hemodynamic and gross anatomic abnormalities herein described.

We acknowledge potential limitations in the interpretation of our findings. Pentobarbital, which is well established as an anesthetic in CPR settings, is a cardiac depressant and a coronary dilator.29 30 31 32 33 Because all animals in the present study received the same doses by weight, which are less than those recognized as cardiodepressant, the differences between groups are not likely to reflect the effects of the anesthetic agent.34

LV volume, free-wall thickness, and dynamic changes associated with progressive impairment of diastolic function are consistent with decreased compliance. However, we elected to forego measurements of LV pressures to minimize previously observed obfuscating effects of intracardiac catheters for computation of ventricular compliance. The decreases in LV chamber volumes in association with increases in wall thickness provide us with secure evidence of a contracted ventricle. A monoplane transducer comparable to that employed by earlier investigators was utilized to obviate major artifacts induced by chest compression.35 36 The single-plane, area-length method of measurement was utilized with the assumption that the LV is best represented by a conical ellipsoid.11 However, LV volumes when measured in the transesophageal long-axis view, yield comparable values in pigs to those measured through a transgastric window.37 38 Nevertheless, we have independently validated this method under the conditions of the present study.

Finally, we caution against direct extrapolation of the present findings to clinical CPR. The porcine model was chosen because the porcine thorax is comparable to that of humans, and this model has been extensively exercised and validated against human observations during CPR.29 30 31 39 Nevertheless, the animals were young, healthy pigs, free of atherosclerotic disease. It is within the context of these limitations that the present study traces the evolution of the stone heart.


   Footnotes
 
Abbreviations: CPP = coronary perfusion pressure; CPR = cardiopulmonary resuscitation; LV = left ventricular; PETCO2 = end-tidal PCO2; SV = stroke volume; VF = ventricular fibrillation

Supported in part by National Institutes of Health grant HL-54322 from the National Heart, Lung, and Blood Institute, Bethesda, MD, the Desert Health Care District and the Mason Foundation, Inc.

Received for publication April 28, 2000. Accepted for publication March 18, 2002.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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