The Annals of Thoracic Surgery, Vol 32, 486-494, Copyright © 1981 by The Society of Thoracic Surgeons
The harmful effects of ventricular distention during postischemic reperfusion
SK Lucas, HV Schaff, JT Flaherty, VL Gott and TJ Gardner
To assess the effects of left ventricular distention during the early
reperfusion period following ischemic arrest, 16 canine heart preparations
were subjected to 45 minutes of hypothermic (27 degree C) cardioplegic
arrest and normothermic reperfusion. Isovolumic left ventricular developed
pressure and rate of rise of left ventricular pressure (dp/dt) were
measured with an intraventricular balloon; endocardial/epicardial flow
ratios were determined with microspheres; and myocardial gas tensions were
monitored with mass spectrometry. During early reperfusion, Group 1 hearts
(n = 8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n
= 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial
15 minutes of reperfusion. Group 2 hearts demonstrated impaired
subendocardial blood flow after 5 minutes of reflow (0.75 +/- 0.06 vs 0.96
+/- 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and
persistent elevation of intramyocardial carbon dioxide (CO2) tension (68
+/- 4 vs 51 +/- 4 mm Hg, Group 2 vs Group 1). In addition, postischemic
ventricular function was significantly worse in Group 2 hearts (60 +/- 7 vs
79 +/- 3% of control dP/dt, Group 2 vs Group 1, and 53 +/- 6 vs 81 +/- 5%
of control left ventricular developed pressure, Group 2 vs Group 1). These
data demonstrate that even mild distention during early reperfusion can
result in reduced subendocardial perfusion and delayed washout of tissue
CO2. Although myocardial blood flow and CO2 tension subsequently returned
to normal in the distended hearts, left ventricular performance remained
significantly depressed. This injury can occur clinically in nonvented
hearts prior to the resumption of effective ventricular contraction.
