End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2 from 4.0 + 0.2% to less than 0.7 + 0.2%. With precordial compression, it increased to 1.9 + 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2 increased from 1.9 + 0.3% to 4.9 + 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2 were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2 and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2 and CO was also demonstrated during open-chest cardiac massage (r = .95). ETCO2 therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals, ETCO2 during precordial compression averaged 1.7 + 0.2%, whereas it was only 0.5 ± 0. 1% in five animals in whom resuscitation procedures were unsuccessful (p<.001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation. Circulation 77, No. 1, 234-239, 1988. PRIMARY INTERVENTIONS during cardiopulmonary resuscitation (CPR) include external ventilation after establishing airway patency, and precordial compression.t It is precordial compression that maintains forward flow of blood in amounts that temporarily sustain the viability of major organs and especially the heart and the brain. The cardiac output measured during experimental closed-chest cardiac massage has ranged between 17% and 27% of prearrest values.2-5 Except for arterial or intracardiac pressure measurements, there are currently no reliable options for continuously monitoring the efficacy of precordial compression in terms of the blood flow that is generated. We therefore searched for practical, and preferably noninvasive, options with which the efficacy of precordial compression could be quantitatively monitored. Received Aug. 12, 1987; accepted Sept. 24, 1987. 234 In prior studies in a porcine preparation of cardiac arrest and subsequently on human patients, measurements of arterial blood gases demonstrated hypercarbia in mixed venous blood and hypocarbia in arterial blood during CPR.6-9 There was venous acidemia and arterial alkalemia. A large venoarterial Pco2 gradient was associated with decreases in end-tidal CO2 concentration (ETCO2). We hypothesized that this was related to a critical reduction in pulmonary blood flow during CPR accounting for a critical curtailment of CO2 excretion.10 11 In the present study, we observed a close relationship between ETCO2 and cardiac output. We further demonstrated the potential usefulness of ETCO2 as a prognosticator of resuscitability. Moreover, ETCO2 was an immediate in...

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We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

The effects on cardiac resuscitability of iso-osmolal solutions of tris-hydroxymethyl-aminomethane (tromethamine), sodium bicarbonate (NaHCO3) and sodium chloride placebo were compared in 30 domestic pigs using a well-established model of electrically induced cardiac arrest and resuscitation. We hypothesized that a carbon dioxide (CO2) consuming buffer like tromethamine would reduce and sodium bicarbonate would increase the respiratory acidosis of mixed venous blood, which had recently been demonstrated in our laboratory, Tromethamine did decrease and sodium bicarbonate did increase both arterial and mixed venous CO2 during cardiopulmonary resuscitation (CPR). Both concentrations of end-tidal CO2 and coronary venous PCO2 were significantly lower after tromethamine than after bicarbonate. However, tromethamine produced an unexpected vasodilator effect with reduction of mean aortic and coronary perfusion pressures to levels that are known to reduce resuscitability and survival independently of its buffer action. Neither resuscitability nor survival was altered by bicarbonate therapy in comparison with sodium chloride placebo.