LETTER TO THE EDITOR
The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function
Shije Sun, MDa,
Kada Klouche, MDa,
Wanchun Tang, MDa and
Max Harry Weil, MD, PhD, FACCa
a Institute of Critical Care Medicine, 1695 North Sunrise Way, Building #3, Palm Springs, California 92262-5309, USA
weilm{at}aol.com
In a recent study, Niemann et al. (1) compared the effects of 150-J biphasic truncated exponential waveform shocks and conventional 200-, 300- and 360-J monophasic truncated exponential waveform shocks on the success of defibrillation and on postresuscitation myocardial function in pigs. After 5 min of untreated ventricular fibrillation, there was no difference in the number of animals successfully defibrillated. Postresuscitation left ventricular (LV) function was evaluated with measurements of peak LV pressure, the first derivative of LV pressure (LV dP/dt) and cardiac output measured by the thermodilution method. Again, the authors found no differences between the two groups with respect to measurements that the authors regarded as quantitative indicators of postresuscitation myocardial function.
Their observations contrast with earlier reports (2–4) and a recent report from our own laboratory (5), which had demonstrated that equally effective low-energy biphasic waveform shocks produced less postresuscitation myocardial injury. We believe that the differences are best explained by the experimental procedures employed by the authors.
Baseline mean aortic pressure reported by Niemann et al. (1) was only 70%, and dP/dt was approximately 50% of those measurements observed by our group in a comparable porcine model of more mature pigs (5,6). The hemodynamic differences are summarized in Table 1. Most important, experiments were terminated 60 min after successful resuscitation. Our group has observed that more precise measurements of postresuscitation myocardial function, including stroke volume, fractional area change and pressure-volume relationships are progressively impaired over 240 min following resuscitation (5,6). Finally, although cardiac output was reported by the authors, it was not normalized against heart rate. Earlier observations pinpointed that decreases in stroke volumes are compensated for by disproportionate increases in heart rate (5,6). Finally, the isovolumetric phase index of maximal rate of pressure rise (dP/dt max) is preload dependent (7–10). Without accounting for preload, dP/dt measurements are suspect.
We applaud the efforts of the authors for investigating the effects of new defibrillation energies and waveforms. However, the limitations of this study preclude their challenge to the earlier findings that lower-energy biphasic waveforms minimize postresuscitation myocardial function that evolves over the 4-h interval after successful resuscitation.
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References
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1. Niemann JT, Burian D, Garner D, Lewis RJ. Monophasic versus biphasic transthoracic countershock after prolonged ventricular fibrillation in a swine model. J Am Coll Cardiol. 2000;36:932–938[Abstract/Free Full Text]
2. Bardy GH, Marchlinski FE, Sharma AD, et al. Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Circulation. 1996;94:2507–2514[Abstract/Free Full Text]
3. Mittal S, Ayati S, Stein KM, et al. Comparison of a novel rectilinear biphasic waveform with a damped sine wave monophasic waveform for transthoracic ventricular defibrillation. J Am Coll Cardiol. 1999;34:1595–1601[Abstract/Free Full Text]
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5. Tang W, Weil MH, Sun SJ, et al. The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function. J Am Coll Cardiol. 1999;34:815–822[Abstract/Free Full Text]
6. Gazmuri 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[CrossRef][Medline]
7. Kass DA, Maughan WL, Guo ZM, Kono A, Sunagawa K, Sagawa K. Comparative influence of load versus inotropic states on indexes of ventricular contractility: experimental and theoretical analysis based on pressure-volume relationships. Circulation. 1987;76:1422–1436[Abstract/Free Full Text]
8. Perlini S, Meyer TE, Foëx P. Effects of preload, afterload and inotropy on dynamics of ischemic segmental wall motion. J Am Coll Cardiol. 1997;29:846–855[Abstract]
9. Yamada H, Oki T, Tabata T, Iuchi A, Ito S. Assessment of left ventricular systolic wall motion velocity with pulsed tissue Doppler imaging: comparison with peak dP/dt of the left ventricular pressure curve. J Am Soc Echocardiogr. 1998;11:442–449[CrossRef][Medline]
10. Greaves SC. Assessment of left ventricular systolic function in research and in clinical practice. Heart. 2000;83:493–494[Free Full Text]
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