Recent Observations on Pharmacological Interventions During CPR

  • G. Cammarata
  • M. H. Weil


Myocardial dysfunction, accounts for death during the first 72 h after resuscitation from cardiac arrest. When the heart stops beating, ischemic injury of myocytes follows cessation of coronary blood flow. The severity of injury is contingent on the duration of the “no-flow” interval. When ventricular fibrillation (VF) was electrically induced in 20 male pigs and animals were randomized to 4 or 7 min of untreated cardiac arrest, the severity of post-resuscitation myocardial dysfunction was proportional to the duration of untreated VF [1]. This conclusion is also supported by human data reported by Schultz et al. [2]. Even precordial compression fails to fully supply coronary blood flow in amounts that fulfill myocardial oxygen needs during VF [3]. With the aid of esophageal echocardiographic measurements, our research team has demonstrated ischemic contracture of the heart with increased thickness of the inter-ventricular septum and the left ventricular free wall during prolonged CPR. This accounts for the “stony heart” [4]. Compliance of the left ventricle is greatly reduced with progressive reductions in stroke volumes. On a cellular level, the stone heart is best explained by intracellular calcium overload during ischemie injury and probably due to reperfusion.


Cardiac Arrest Cardiopulmonary Resuscitation Coronary Blood Flow Coronary Perfusion Pressure Left Ventricular Free Wall 
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© Springer-Verlag Italia 2004

Authors and Affiliations

  • G. Cammarata
  • M. H. Weil

There are no affiliations available

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