Influence of alterations in loading produced by lower body negative pressure on aortic blood flow acceleration

Abstract

The objectives of this study were to evaluate the effects of alterations in loading induced by lower body negative pressure on aortic blood flow velocity and acceleration. Twenty-seven normal men were studied during various levels of lower body negative pressure (0 to −60 mm Hg) during which echocardiographic, Doppler and hormonal measurements were obtained. Lower body negative pressure induced a decrease in left ventricular diastolic diameter from 5.18 ± 0.08 to 4.41 ± 0.1 cm (p < 0.0001) and in left ventricular systolic diameter from 3.33 ± 0.09 to 2.84 ± 0.1 cm (p < 0.0001). Shortening fraction remained unchanged.The decrease in diastolic diameter resulted in a reduction in flow velocity integral from 13.8 ± 0.8 to 7.5 ± 0.4 cm (p < 0.0001) and, therefore, in stroke volume from 89.6 ± 4.7 to 49.5 ± 2.8 ml (p < 0.0001). Heart rate reflexly increased from 62.5 ± 1.9 to 82.2 ± 2.3 beats/min (p < 0.0001) as did systemic vascular resistance from 1,280.8 ± 69.5 to 1,863.4 ± 121.4 dyne·s·cm−5 (p < 0.0001). The increase in heart rate was insufficient to maintain cardiac output, which decreased from 5.53 ± 0.29 to 3.99 ± 0.21 liters/min (p < 0.0001). Systolic, diastolic and mean arterial blood pressure was maintained.The negative pressure resulted in a concomitant significant increase in norepinephrine levels from 1.46 ± 0.09 to 2.056 ± 0.2 nmol/liter (p = 0.0019) but no change in plasma epinephrine: 0.845 ± 0.22 to 0.78 ± 0.11 nmol/liter (p = NS). Despite the presumed increase in contractility (increased heart rate, augmented norepinephrine level and unchanged shortening fraction in the face of an adverse change in loading), there was a significant decrease in aortic blood flow acceleration (16.96 ± 0.66 to 13.11 ± 0.63 m/s2 (p < 0.0001) and velocity (0.79 ± 0.02 to 0.56 ± 0.02 m/s (p < 0.0001).Thus, lower body negative pressure effectively decreases preload, with a concomitant reflex increase in systemic vascular resistance. Aortic blood flow acceleration and velocity were affected by these hemodynamic alterations and, therefore, cannot be used to assess left ventricular systolic performance independent of loading.