Reduced left ventricular filling following blood volume extraction does not result in compensatory augmentation of cardiac mechanics

Abstract

An acute non-invasive reduction in preload has been shown to augment cardiac mechanics to maintain stroke volume and cardiac output. Such interventions induce concomitant changes in heart rate, whereas blood volume extraction reduces preload without changes in heart rate. Therefore, the purpose of this study was to determine whether a preload reduction in isolation resulted in augmented stroke volume achieved via enhanced cardiac mechanics. Nine healthy volunteers (four female, age 29 ± 11 years) underwent echocardiography for the assessment of left ventricular (LV) volumes and mechanics in a supine position at baseline and end extraction after the controlled removal of 25% of total blood volume (1062 ± 342 ml). Arterial blood pressure was monitored continuously by a pressure transducer attached to an indwelling radial artery catheter. Heart rate and total peripheral resistance were unchanged from baseline to end extraction, but systolic blood pressure was reduced (from 148 to 127 mmHg). From baseline to end extraction there were significant reductions in left ventricular end-diastolic volume (from 89 to 71 ml) and stroke volume (from 56 to 37 ml); however, there was no change in LV twist, basal or apical rotation. In contrast, LV longitudinal strain (from -20 to -17%) and basal circumferential strain (from -22 to -19%) were significantly reduced from baseline to end extraction. In conclusion, a reduction in preload during blood volume extraction does not result in compensatory changes in stroke volume or cardiac mechanics. Our data suggest that LV strain is dependent on LV filling and consequent geometry, whereas LV twist could be mediated by heart rate.

Cardiac performance with chronic hypoxia: mechanisms regulating stroke volume

“…Recently, a number of groups have tried to quantify how chronic hypoxemia influences the rate of diastolic relaxation using LV untwisting velocity derived from speckle tracking echocardiography. Whilst untwist velocity is load-dependent, and will be markedly influenced by gravitational forces (Negishi et al, 2017), it does correlate with invasive measurements of LV stiffness and pressure decay (Zhou et al, 2013) and remains unchanged following a marked reduction in end-diastolic volume (Lord et al, 2018). Virtually all investigators report an increase in LV untwist velocity despite the decrease in LV filling (Dedobbeleer et al, 2015;Osculati et al, 2015;Stembridge et al, 2015).…”

“…Recent studies of LV mechanics at high altitude have also been performed at rest in young healthy individuals who will possess a substantial ability to vasodilate so that delivery can easily meet demand (Duncker & Bache, 2008). Secondly, it is unlikely that changes in LV geometry secondary to decreased LV filling results in such marked changes in LV twist, as even during extraction of 25% blood volume, twist remains unchanged (Lord et al, 2018). Moreover, when plasma volume is restored to sea level values at high altitude via saline infusion, LV twist remains elevated from sea level (Stembridge et al, 2018).…”

Acute impact of changes to hemodynamic load on the left ventricular strain-volume relationship in young and older men

“…The ability to provide sufficient cardiac output is constantly challenged by beat-to-beat changes in hemodynamic loading (preload, afterload), contractility, and heart rate (8,15,23). Acute changes in left ventricular (LV) hemodynamics and heart rate will alter LV mechanics (1,4,5,14,17,24), such as LV peak longitudinal strain (ε) (4,14,24), circumferential ε (1,4,14,24), and peak torsion (5), and thus LV function. Chronic exposure to such changes can lead to LV remodeling, affecting both LV structure and function (15).…”