Myocardial depression in shock; a survey of cardiodynamic studies.

The question as to whether myocardial depression occurs in hemorrhagic shock and, if so, its importance was reinvestigated. For this purpose the cardiodynamic changes which occur after simple hemorrhage, during prolonged hypotension (50 to 30 mm. Hg), during reinfusion of all the withdrawn blood, and during spontaneous circulatory failure following infusion, were studied in the same animal. In different series of experiments in which the same standard technique was used, we studied changes in calibrated arterial pressure pulses, cardiac output by a modified Stewart method, alterations in effective venous pressure, ventricular volume and pressure curves, inferior vena cava flow, and electrocardiograms by standard and chest leads. Following simple hemorrhage sufficient to reduce mean arterial pressure to 50 mm. Hg, the changes in ventricular action are all secondary to reduction in venous return and decrease in effective central venous pressure. Electrocardiograms reveal no significant changes. Changes in the contour of the central arterial pulse consist in abridgement of the period of systolic ejection and development of a primary spike followed by a peaked summit, and this is followed by a deep incisura. As a result of decreased venous pressure, ventricular filling is slower, initial tensions decrease in both ventricles, and their diastolic size is smaller. Pressure and volume curves indicate that the ventricles expel their diminished volumes with good velocity. If severe posthemorrhagic hypotension is prolonged for 135 minutes, death results from an oligemic type of failure unless blood is reinfused. However, such reinfusion is of only temporary benefit; a slow spontaneous circulatory failure and eventually death follow. Irreversibility develops during the period of prolonged hypotension. This includes depression of the myocardium, for while venous return continues to decrease slightly, effective venous and initial ventricular pressures return to or above control levels and the diastolic size of the ventricles augment. Nevertheless, the stroke volume and cardiac output decrease. Myocardial depression is further indicated by a subminimal stroke volume when venous pressures are elevated to normal levels and by development of S-T depression in electrocardiograms. Reinfusion of blood restores arterial pressures and pulses as well as cardiac output to normal, but in order to do so the ventricles are required to operate under supernormal conditions of high venous pressure and initial tensions. As soon as these re-establish at normal levels, cardiac output decreases, and the ventricles pump less efficiently due to a depressed state of the myocardium. As arterial pressure declines to ca. 70 mm. Hg, reduction in venous return becomes so great that the myocardial depression is obscured but is detectable by special tests. A progressive circulatory failure develops despite the fact that blood volumes are not significantly decreased. This represents a form of normovolemic shock due solely to default of the peripheral circulation and of the myocardium. The preduction of venous return is of paramount importance, but circulatory failure is hastened by coexistent myocardial depression. Since the functional state of the myocardium and the capacity of the coronary responses at the time of shock-producing catastrophies may often be below par, myocardial depression may play as significant a subsidiary role in some cases of human shock as it did in our animals submitted to a particular type of hemorrhage and shock. The problem deserves further careful exploration by cardiologists.