• Bengt Sandstedt, Johan Pontén, S Bertil Olsson, and Nils Edvardsson.
• Division of Cardiology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. bengt.sandstedt@swipnet.se
• Scand. Cardiovasc. J. 2004 May 1;38(2):113-20.

ObjectiveVentricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis.DesignThe immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement.ResultsDuring VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p < 0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p < 0.001), an increased release of lactate from 32 to 137 micromol/min (p < 0.001) and potassium from 29 to 73 micromol/min (p < 0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p < 0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%).ConclusionVF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF.

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