The CI by thermodilution (CItd) correlated well with simultaneous measurements with the bioimpedance (CIbi), r2 = 0.915, r2 = 0.84, p < 0.001. The bias and precision of simultaneous measurements was -0.070 +/- 0.47 L/min/m2; agreement was considered satisfactory. In the initial resuscitation period of both monitoring systems, the CI, mean arterial blood pressure, SapO2, and tissue perfusion (reflected by invasive DO2 and VO2, and by noninvasive PtcO2/FiO2 ratio) were higher in survivors than in nonsurvivors, whereas heart rate values were higher in the nonsurvivors. We concluded that noninvasive hemodynamic monitoring provided a feasible, safe, inexpensive, accurate, continuous, on-line real-time graphic displays that are equivalent to the essential features of invasive pulmonary artery catheter monitoring.
The absence of respiratory movements is a major criterion recommended for use by bystanders for recognizing an out-of-hospital cardiac arrest (CA), as the persistence of eupneic breathing is considered to be incompatible with CA. The basis for CA-related apnea is, however, uncertain, since brain stem Po(2) is not expected to drop immediately to the critical level where anoxic apnea occurs. It is therefore essential on both clinical and physiological grounds to determine whether and when breathing stops after the onset of CA. In eight patients, we measured the ventilatory response at the onset of ventricular fibrillation (VF) for 12-15 s during the placement of an implantable cardioverter-defibrillator device. We found that regular eupneic breathing was maintained unchanged despite the cessation of systemic and pulmonary blood flow generated by the heart. We extended these findings in adult sheep and found that, as in humans, the normal ventilatory pattern persists unchanged for the first 15 s despite the drop in blood pressure, followed by a progressive increase in minute ventilation, which was sustained for up to 164 s. The ensuing apnea was disrupted by typical gasps occurring at a very slow frequency. These observations suggest a complete "decoupling" between the return of CO(2) to the pulmonary circulation and continued effective respiratory activity, contrary to what we predicted. This delayed cessation of eupneic breathing during the absence of cardiac pump function is likely related to the time needed for brain stem anoxia to develop. These findings challenge the notions that 1) ventilation stops as pulmonary blood flow/cardiac output ceases and 2) the presence of eupneic breathing is a reliable sign of effective cardiac pumping activity.
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