Hemodynamic Response to Volume Expansion in Ischemic Heart Disease

Abstract

In order to asses the cardiac function of ischemic heart disease, 31 patients (6 stable angina and 25 old myocardial infarction) without overt heart failure were studied. Pulmonary artery diastolic pressure (PADP), mean right atrial pressure (mRAP) and cardiac index (CI) were measured by SWAN GANZ catheter prior to infusion (control) and at every 100 ml infusion of 6 % hydroxyethyl starch (infusion rate was 20 ml/min. ). Slope of cardiac function curve was calculated from maximum change of CI divided by PADP. We terminated the infusion when the PADP rearched 18 mmHg or the total infusion volume of 400 ml. The patients in this study were subdivided into 5 groups according to the ECG findings and clinical features in acute phase.
Group I consists of 6 patients with stable angina. Control PADP was 6.5 ± 2.1 mmHg mean ± 1SD), mRAP was 1.8 ± 1.0 mmHg and CI was 3.58 ± 0.54 L/min/m². Group II consists of 9 patients with /inferior myocardial infarction. Control PADP was 6.5 ± 2.1, mRAP was 1.3 ± 0.9 and CI was 3.15 ± 0.46. Group 3 consists of 5 patients with anteroseptal myocardial infarction. Control PADP was 9.6 ± 2.1, mRAP was 2.8 ± 1.9 and CI was 3.25+ 0.55. Group IV consists of 6 patients of myocardial infarction with previous history of myocardial infarc tion. Control PADP was 10.2 ± 4.3, mRAP was 1.2 ± 1.6 and CI was 2.97 ± 0.87. Group V consists of 5 patients with right ventricular infarction. Control PADP was 8.0 ± 4.1, mRAP was 3.8 ± 1.6 and Cl was 2.96 ± 0.87. Control PADP and CI were normal in all groups there were no significant differences between earch groups. Group V showed significantly higher mRAP than other groups. Although the patients in group I showed significant increase in PADP (2.7± 1.0 ), mRAP (0.8 ± 0.4) and CI (0.22 ± 0.13) from control, these changes were smaller than other groups. Group 11 showed significant increase in PADP (7.8 ± 2.0), mRAP (1.9 ± 1.2)and Cl (0.95 ± 0.37) from control. Group II showed significant increase in PADP (8.4 ± 2.7), mRAP (1.6 ± 1.5) and Cl (0.47 ± 0.33) from control. Group IV showed significant increase in PADP (10.0 ± 3.8), mRAP (3.0+1.3) and CI (0.45+0.34) from control. One patient in group III and four patients in group N, the PADP increased over 18 mmHg and CI decreased at this higher pressure. The slope of cardiac function curve of group III (0.06+0.04) and group IV (0.07 ± 0.07) were significantly smaller than group II (0.13+0.06). Group V showed significant increase in PADP (5.2± 1.6) and mRAP (3.6± 1.7), but there was no significant increase in CI (0.28+0.36). The change of mRAP from control in this group was significantly larger than other groups.
Hemodynamics being identical among the 5 groups (mRAP in group V was higher than other groups but was in normal range), the cardiac function and reserve could not be assesed prior to volume expansion. Our findings by volume expansion suggests: 1) In group I cardiac reserve was maintained by the neuro-humoral regulatory mechanisms.2) Regulatory mechanism to preload augumentation is fairly well reserved in group II, but compromised in group III and was severly compromised in group IV.4)In group V right ventricular failure which was suggested in control became overt after volume expansion.
Volume loading test is a interesting test to understand the natural history and pathologic phisiology of ischemic heart disease.