• M Müllner, H Domanovits, F Sterz, H Herkner, G Gamper, I Kürkciyan, and A N Laggner.
• Department of Emergency Medicine, Vienna General Hospital-University of Vienna, Medical School, Austria. marcus.muellner@univie.ac.at
• Resuscitation. 1998 Oct 1;39(1-2):51-9.

AbstractAfter successful resuscitation from cardiac arrest, prolonged contractile failure has been demonstrated in animal experiments. No systematic evaluation of myocardial contractility following successful resuscitation after human cardiac arrest exists. The aim of this study was to assess left ventricular contractility following human cardiac arrest with successful resuscitation. In 20 adult patients after cardiac arrest and in four control patients, the relation between meridional wall stress (MWS) and rate-corrected mean velocity of circumferential fibre shortening (Vcf(c)), a load independent and rate corrected index of left ventricular contractility was measured within 4 h after return of spontaneous circulation and after 24 h by means of transoesophageal echocardiography. As the normal values of Vcf(c) depend on MWS, a normal deviate (z) was calculated. A normal z-score is defined as 0+/-2, < -2 indicates reduced contractility, > + 2 increased contractility. Data are presented as median and the interquartile range (IQR). For the comparison of related samples the Wilcoxon sign test was used. In most patients after cardiac arrest contractility was severely impaired within 4 h after successful resuscitation [z - 7.0 (IQR - 8.9 - (-2.5))]. Contractility did not significantly improve within the observational period [z after 24 h - 3.7 (IQR - 7.9 - (-1.8))] (P = 0.3). The four control patients had normal left ventricular contractility on arrival (z 0.0, range - 0.9-0.8) and after 24 h (z 0.7, range - 1.5-2.7). In conclusion non-invasive wall stress analysis can be applied to quantitate systolic left ventricular function, which was severely compromised in most patients within the first 24 h after successful resuscitation. Whether depression of left ventricular function is caused by cardiac arrest itself or by the underlying disease remains speculative.

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