Echocardiographic left ventricular remodeling and pseudohypertrophy as markers of hypovolemia. An experimental study on bleeding and volume repletion

• Published in: Journal of the American Society of Echocardiography Vol. 10; no. 9; p. 926
• Main Authors: Di Segni, E, Preisman, S, Ohad, D G, Battier, A, Boyko, V, Kaplinsky, E, Perel, A, Vered, Z
• Format: Journal Article
• Language: English
• Published: United States 01.11.1997
• Subjects: Animals; Blood Volume; Female; Heart Ventricles - diagnostic imaging; Hemodynamics; Hypertrophy, Left Ventricular - diagnostic imaging; Swine; Ultrasonography; Ventricular Function, Left
• ISSN: 0894-7317
• DOI: 10.1016/s0894-7317(97)80009-0

Monitoring intravascular volume during surgery, especially in major cardiovascular procedures is necessary for appropriate fluid restoration and the maintenance of an adequate cardiac output. In estimating preload, both standard hemodynamic and echocardiographic parameters have been limited. The purpose of this study was to further define the effects of induced hypovolemia on the echocardiographic parameters. In particular, we sought to show whether a decrease in echocardiographic left ventricular area and volume was associated with a significant increase in left ventricular wall thickness (left ventricular pseudohypertrophy) and with changes in LV function. In addition, we sought to investigate the effects of rapid restoration of blood volume on cardiac dimensions and function. Seven anesthetized pigs underwent systemic and right heart pressures and cardiac output measurements. Two-dimensional echocardiographic parasternal long- and short-axis views were obtained during graded bleeding by rapid withdrawal of blood from an arterial cannula, with increments of 5% each up to 30% of calculated blood volume. After completion of the bleeding, the entire amount of the blood withdrawn was retransfused within 4 to 5 minutes. Both hemodynamic and echocardiographic measurements were performed at baseline, immediately after the completion of each stage of bleeding and after blood restoration. Mean (+/- standard deviation) left ventricular wall thickness (mean of septal and posterior wall thickness) was 6.3 +/- 0.1 mm at baseline, 8.3 +/- 1.5 mm at peak bleeding, and 6.2 +/- 0.1 after restoration (p < 0.01). Left ventricular mass did not change during the experiment. Left ventricular end-diastolic volume was 62.8 +/- 20.3 ml at baseline, 37.5 +/- 12.4 ml at peak bleeding (p < 0.0001), and 65.9 +/- 16.7 ml after blood restoration (p < 0.001 compared with 30% bleeding). H/r ratio (posterior wall thickness divided by left ventricular radius) increased from 0.29 +/- 0.07 at baseline to 0.50 +/- 0.19 at peak bleeding returning to 0.26 +/- 0.04 after restoration. Left ventricular ejection fraction was 0.53 +/- 0.10 at baseline and 0.55 +/- 0.20 at peak bleeding (not significant), decreasing to 0.38 +/- 0.11 after blood restoration (p < 0.05 compared with 30% bleeding). End-diastolic volume correlated closely with right atrial pressure (r = -0.82), capillary wedge pressure (r = -0.78), and stroke volume (r = 0.74). Left ventricular ejection fraction inversely correlated with left ventricular end-diastolic volume (r = -0.48) and with end-systolic wall stress (r = -0.62). The changes in interventricular septal and posterior wall thickness were inversely related to left ventricular end-diastolic volume (r = -0.72 and -0.35, respectively). This study shows that transient concentric left ventricular remodeling (pseudohypertrophy), a phenomenon previously described in cardiac tamponade and during rapid atrial pacing is commonly seen during hypovolemia. This new sign may further enhance the echocardiographic estimation of left ventricular preload.