PubMed1975
Hemorrhagic shock was induced in 20 spontaneously breathing adult greyhounds by lowering the mean arterial pressure to 40 millimeters of mercury. In the first group of six dogs, reinfusion was carried out without delay; in a second group of six dogs, hypovolemia was continued for two hours, during which time the arterial pressure was permitted to rise in response to intact cardiovascular reflexes; in a third group of eight dogs, the mean arterial pressure was artificially maintained at 40 millimeters of mercury for two hours, initially by further bleeding. In all dogs in the latter group, take-up of blood from the reservoir was required during the second hour to maintain the arterial pressure, this being indicative of irreversible shock. In two of this group, fatal arrhythmias developed during reinfusion. All three groups showed evidence of ventricular dysfunction during and immediately after reinfusion, as indicated by disproportion between left ventricular stroke work and left ventricular end diastolic pressure, these data being used to construct ventricular function curves. Measurement of dP/dt maximum suggested that this dysfunction was due to impairment of myocardial contractility. The first two groups recovered normal function within one hour; the third group failed to have such a recovery. Evidence indicates that generalized tissue hypoxia, in addition to myocardial hypoxia, is important in the cause of cardiac dysfunction in irreversible shock.