Extramyocardial acidosis impairs cardiac resuscitability in isolated, perfused, rat hearts.
OBJECTIVE
Patients suffering out-of-hospital cardiac arrest have various degrees of acidemia when cardiopulmonary resuscitation is initiated. Myocardial hypercarbia, rather than decreases in myocardial pH, may determine cardiac resuscitability. Accordingly, we questioned whether different degrees of acidemia accompanying cardiac arrest affect cardiac resuscitability. We evaluated the effect of different degrees of extramyocardial acidosis on cardiac performance and resuscitability after ventricular fibrillation using isolated, perfused, rat hearts.


METHODS
Prospective, randomized, controlled study.


METHODS
Experimental animal laboratory in a university hospital.


METHODS
Thirty-one male, Sprague-Dawley rats.


METHODS
Rat hearts were perfused with N-[2-hydroxyethyl]piperazine-N-[2-ethanesulfonic acid] (HEPES) buffered solution (sodium chloride 145 mM, potassium chloride 4 mM, sodium dihydrogen phosphate dihydrate 1.25 mM, magnesium chloride 1.5 mM, calcium chloride 2 mM, HEPES 6 mM, glucose 10 mM), which was bubbled with 100% oxygen and adjusted to a pH of 7.4. The perfusion pressure was held constant at 60 mm Hg. After 60 mins of stabilization, the control perfusion solution was switched to one of the solutions titrated to pH 6.2, 6.5, 6.8, 7.1, or 7.4, using 1 N of sodium hydroxide. Hearts were allocated randomly to each group. After 15 mins of perfusion, the perfusion was discontinued, and artificial ventricular fibrillation was induced by electrical stimulation for 5 mins. The hearts were then perfused again in one of the same acidotic solutions for 30 mins.


RESULTS
Left ventricular developed pressure (left ventricular pressure minus end-diastolic left ventricular pressure), positive change in left ventricular pressure over time, heart rate (HR), and coronary flow were continuously measured. After 60 mins of stabilization, the values of left ventricular developed pressure, positive change in left ventricular pressure over time, HR, and coronary flow were not significantly different between groups. After 5 mins of ventricular fibrillation, all hearts were asystolic and left ventricular developed pressure, positive change in left ventricular pressure over time, HR, and coronary flow were all zero. After 30 mins of reperfusion, all values in the acidotic groups were significantly lower than the values in the pH 7.4 group. When we judged the recovery of left ventricular developed pressure at > 35 mm Hg as "resuscitated," resuscitability was impaired at a pH of < 7.1. No hearts recovered after perfusion below a pH of 6.5.


CONCLUSIONS
Extramyocardial acidosis below pH 7.1 decreased cardiac performance and resuscitability after ventricular fibrillation. This result indicates that progressive acidemia during cardiac arrest is one of the important determinants of cardiac resuscitability.
Morimoto
Y
Y
Department of Anesthesiology and intensive Care, Hokkaido University School of Medicine, Sapporo, Japan.
Kemmotsu
O
O
Morimoto
Y
Y
D000138:Acidosis / Q000150:complications* / Q000503:physiopathology; D000818:Animals; D016887:Cardiopulmonary Resuscitation; D003326:Coronary Circulation; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D006339:Heart Rate; D066298:In Vitro Techniques; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014693:Ventricular Fibrillation / Q000503:physiopathology; D016277:Ventricular Function, Left; D017725:Ventricular Pressure