Circulation
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Comparative Study
Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis.
Carbicarb is a mixture of Na2CO3/NaHCO3 that buffers similarly to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% O2/92% N2). ⋯ Muscle O2 consumption rose with carbicarb, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (-12 vs -46 mm Hg, p less than .006) and the cardiac output was stable with carbicarb but decreased with NaHCO3 (from 143 to 98 ml/kg/min, p less than .004). Stroke volume also improved with carbicarb but there was no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility.(ABSTRACT TRUNCATED AT 250 WORDS)
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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%. ⋯ 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 less than .001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation.
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The influence of chest compression rate on initial resuscitation success and 24 hr survival after prolonged manual cardiopulmonary resuscitation (CPR) was investigated in 26 morphine-anesthetized dogs (17 to 30 kg). After placement of aortic and right atrial micromanometers and induction of ventricular fibrillation, manual CPR was commenced immediately and continued for 30 min. One group of 13 dogs underwent manual CPR at a compression rate of 60/min, and the other group at a rate of 120/min. ⋯ One 24 hr survivor in each group had difficulty walking. Improved survival with the high-rate compression technique was consistent with the significantly higher mean aortic (systolic and diastolic) and coronary perfusion pressures attained with high-rate compressions (all p less than .002). Although the clinical applicability of these findings has yet to be demonstrated, they provide empirical support for the recent decision to increase the chest compression rate for manual CPR recommended by the American Heart Association, and indicate that the hemodynamic and survival benefits of faster compression rates in this experimental preparation were not dependent on covariant alterations in compression duration.