Key result
Progressive cooling of Starling heart-lung preparations resulted in ventricular fibrillation in 70% of cases at a mean temperature of 17.9°C, with acid administration sensitizing the heart to fibrillation.
Hypothermia sensitizes the heart to hydrogen ions, making acid-base shifts a primary trigger for ventricular fibrillation during cooling.
Acid-base shifts may trigger VF during hypothermia; hypothesis-generating for pH management but leaves clinical translation open pending human data.
On progressive cooling of Starling heart-lung preparations variations in cardiac excitability and behavior were assesssed from recordings of electrocardiogram, cardiac output, arterial and venous pressures and coronary outflow. These variations were related to changes occurring in the acid-base balance and percentage O2 saturation of the blood perfusate.Following the characteristic cardiac irregularities and changes in cardiac behavior on cooling, ventricular fibrillation set in 70% of preparations, at a mean temperature of 17.9°C. The Coh/CH ratio, indicating the true state of acid-base balance in conditions other than the normothermie, was found to be diminished in the fibrillatory cases, while no apprecieable change occurred in those which did not fibrillate.Acid administration to hypothemic preparations resulted in either a prompt or a 5–20 minute delayed onset of ventricular fibrillation in all cases. On the other hand, acid delivery to preparations working under normothermic conditions produced some cardiac irregularites, but did not initiate fibrillation. On subsequent cooling of these acid-injected preparations, fibrillation was the outcome in all. On the basis of these results, it was concluded that cooling, which by itself produces disturb bancs in acid-base balance of the perfusate, sensitizes the heart to the action of H-ions. Therefore, it was postulated that a shift towards acidity in the reaction of blood, be it brought about physically, physiologically or both, is one of the factors responsible for the initiation of fibrillation in the intact organism during the course of hypothermia.The inconsistent changes in arterial CO2 contents of the various hypothermic groups were explained by changes in the magnitude of ventilation. The reduction in CO2 content and increase in percentage oxygen saturation of venous blood was attributed to reduced tissue metabolism during the course of hypothermia. Due to the diminution in protein ionization at low temperatures, alkali reserve was found to be augmented.Of the various parameters related to cardiac behavior, heartrate, cardiac output were reduced during the course of hypothermia; pulse pressure, venous pressure were greatly augmented, while the coronary outflow was gradually increased, with a tendency to be lowered to the pre-cooling level at the lowest temperature range. This reduction in coronary flow occurred at the time of increased excitability and conductivity of the ventricular muscle, just before the onset of fibriller activity.
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Terziogclu et al. (1959) studied Hypothermia-induced ventricular fibrillation. Progressive cooling and acid administration vs. Normothermic conditions was evaluated on Ventricular fibrillation. Progressive cooling of Starling heart-lung preparations resulted in ventricular fibrillation in 70% of cases at a mean temperature of 17.9°C, with acid administration sensitizing the heart to fibrillation.
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