In an isolated heart model, ventricular fibrillation decreases distensibility and causes myocardial oxygen consumption to increase with ventricular distention, unlike in potassium-induced arrest.
Pressure-volume relationships and myocardial oxygen consumption (V · O 2 ) were obtnined in an isolated heart during ventricular fibrillation, potassium-induced arrest, and isovolumetric contractions. The heart was found to be less distensible in fibrillation than in diastole or arrest. The V · O 2 increased from 4.6 to 14.6 cc./100 Gm. LV/min. as the fibrillating ventricle was distended. During arrest the V · O 2 remained constant despite ventricular distention. When the fibrillating ventricle was distended beyond a critical point coronary flow was compromised and the V · O 2 decreased. Beyond and only beyond this point could the V · O 2 be increased by the greater coronary flow induced by a higher perfusion pressure.
MONROE et al. (1960) studied this question.