Assessment of left ventricular function and hemodynamic reserve by volume loading in acute myocardial infarction.
Volume manipulations in 27 patients (volume loading n = 22; phlebotomy n = 5) with acute myocardial infarction (AMI) and 7 normal subjects has been performed in order to evaluate left ventricular performance in terms of cardiac index (CI) and pulmonary artery enddiastolic pressure (EDPAP). An EDPAP in the range of 18-22 mm Hg was in general associated with maximal cardiac output. In patients with AMI maximal cardiac performance was significantly lower compared to normal subjects (p less than 0.01). Volume loading that increased the EDPAP beyond the level of 18-22 mm Hg usually deteriorated cardiac performance in AMI. A phlebotomy in 5 subjects with severe pulmonary congestion decreased EDPAP significantly from 32 to 24 mm Hg (p less than 0.1) without a change of cardiac index (2.2 - 2.5 1/min/m2;NS). In 11 patients left ventricular performance was assessed during the acute and convalescent period. 4-6 weeks after AMI resting EDPAP decreased from initially 16 to 11 mm Hg (p less than 0.02), whereas cardiac index did not change significantly (3.1-3.3. 1/min/m2;NS) and even did not rise markedly after volume loading (3.3-3.4 1/min/m2;NS). By plotting the relative change of cardiac index after volume loading against the individual infarct size (n = 16), left ventricular hemodynamic reserve was assessed and revealed a significant depression compared to normal subjects (n = 7). A rough reverse relationship (r = -0.69) between left ventricular hemodynamic reserve and infarct size was observed.
D000328:Adult; D000368:Aged; D001794:Blood Pressure; D002302:Cardiac Output; D002306:Cardiac Volume; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D011312:Pressure; D011651:Pulmonary Artery / Q000503:physiopathology*