Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation.
OBJECTIVE
To define changes in intramyocardial pH and PCO2 during cardiac arrest and resuscitation.


METHODS
Prospective and observational trial.


METHODS
Mammalian research laboratory utilizing a porcine model of cardiac arrest.


METHODS
Sixteen domestic pigs.


METHODS
Ventricular fibrillation was induced by an alternating current delivered to the epicardium. Precordial compression was begun after 3 mins of untreated cardiac arrest and was initially adjusted to produce a coronary perfusion pressure of 10 mm Hg. Electrical defibrillation was attempted after an additional 8 mins of precordial compression.


RESULTS
A rapid-response, ion-selective field effect transistor sensor was adapted for measurement of intramyocardial PCO2. Intramyocardial PCO2 progressively increased from 54 to 346 torr (7.2 to 46.1 kPa) during the 11-min interval of cardiac arrest. Intramyocardial hydrogen ion concentrations were simultaneously measured with a glass electrode. The intramyocardial hydrogen ion value increased from 65 nmol/L (pH 7.20) to 441 nmol/L (pH 6.38) over the same interval. The increases in myocardial PCO2 were inversely correlated with coronary perfusion pressure and with the likelihood of successful resuscitation. Within 30 mins after successful cardiac resuscitation, myocardial PCO2 had almost completely returned to prearrest levels.


CONCLUSIONS
Striking increases in myocardial PCO2 and hydrogen ion values accompany the global myocardial ischemia of cardiac arrest. The increases in myocardial PCO2, rather than decreases in pH, reflected more precisely the hemodynamic efficacy of the resuscitation effort, correlated inversely with coronary perfusion pressure, and predicted the likelihood of successful resuscitation.
Kette
F
F
Department of Medicine, University of Health Sciences, Chicago Medical School, IL.
Weil
M H
MH
Gazmuri
R J
RJ
Bisera
J
J
Rackow
E C
EC
D000142:Acidosis, Respiratory / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D000818:Animals; D002245:Carbon Dioxide / Q000032:analysis; D004195:Disease Models, Animal; D006323:Heart Arrest / Q000150:complications* / Q000628:therapy; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007477:Ions; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D017202:Myocardial Ischemia / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D012151:Resuscitation; D013552:Swine; D014173:Transistors, Electronic
D007477:Ions; D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid