Acute myocardial infarction causes depression of left ventricular function, but the capacity of the ventricle to recover from such an injury remains unknown. This problem was explored by measuring left ventricular function in eight intact conscious dogs before, 1 hr after, and again 6-8 days after myocardial infarction. Acute myocardial infarction was produced using a technique which entails gradual inflation over an average period of 1 hr of a balloon cuff previously implanted around the left anterior descending coronary artery. Occurrence of anterior wall infarction was detected electrocardiographically and later confirmed by postmortem examination. Left ventricular function was evaluated from the relationship between left ventricular developed pressure (left ventricular peak systolic pressure minus left ventricular end-diastolic pressure) and left ventricular end-diastolic pressure during transient aortic occlusion with a balloon catheter. Left ventricular function curves were obtained by plotting left ventricular-developed pressure at increasing left ventricular end-diastolic pressures up to 50 mm Hg. Acute myocardial infarction caused marked depression of left ventricular function measured 1 hr after onset of infarction, but 1 wk later all eight animals showed improvement with return of function toward the control levels. A small but significant descending limb was noted at left ventricular end-diastolic pressures above 35 mm Hg. Quantitatively, the descending limb was similar before, 1 hr after, and 1 wk after myocardial infarction. Hemodynamic data revealed evidence of left ventricular failure in all animals, but variability in individual hemodynamic parameters was noted. The data indicate that the marked depression of left ventricular function observed immediately after experimental acute myocardial infarction undergoes considerable resolution within 1 wk, but that functional recovery remains incomplete.

Acute Disease↗

PubMed1970

Hemodynamic effects of pneumonia. II. Expansion of plasma volume.

Previous work has demonstrated that approximately one-third of patients with pneumonia have a hypodynamic circulatory response. This response is characterized by an abnormally wide arteriovenous oxygen difference, a low cardiac output, increased peripheral resistance, and an increased hematocrit. This state was found to abate in convalescence. In an attempt to elucidate the pathogenesis of this hypodynamic state, nine additional patients were studied hemodynamically during the acute phase of pneumonia before and during acute expansion of blood volume by low molecular weight dextran (seven patients) or normal saline (two patients). Five patients were restudied before and during acute blood volume expansion in convalescence. Three patients with pneumonia had a normal arteriovenous oxygen difference (< 5.5 vol%), and six patients were hypodynamic in that their arteriovenous oxygen differences were greater than 5.5 vol%. With expansion of blood volume in the acute phase of pneumonia, all patients showed an increase in cardiac output, a decrease in arteriovenous oxygen difference, and a decrease in peripheral vascular resistance; however, the percentage change in the hypodynamic patients was not as great as occurred in the patients with normal hemodynamics nor as great as occurred when restudied in convalescence. Likewise, all patients had a normal or near normal hemodynamic profile in convalescence. In addition, ventricular function in the acute phase of pneumonia was depressed. The findings suggest that the hypodynamic state associated with acute pneumonia is due to depressed myocardial contractility to which relative hypovolemia may contribute.

Acute Disease↗

PubMed1970

Experimental myocardial infarction. IV. Reduction of left ventricular compliance in the healing phase.

Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.

Animals↗

PubMed1970