Living Without a Pulse

Abstract

Pulsatility seems to have a teleological role because evolutionary hierarchy favors higher ordered animals with more complex, multichamber circulatory systems that generate higher pulse pressure compared with lower ordered animals. Yet despite years of such natural selection, the modern generation of continuous-flow left ventricular assist devices (CF-LVADs) that have been increasingly used for the last decade have created a unique physiology characterized by a nonpulsatile, nonlaminar blood flow profile with the absence of the usual large elastic artery Windkessel effect during diastole. Although outcomes and durability have improved with CF-LVADs, patients supported with CF-LVADs have a high rate of complications that were not as frequently observed with older pulsatile devices, including gastrointestinal bleeding from arteriovenous malformations, pump thrombosis, and stroke. Given the apparent fundamental biological role of the pulse, the purpose of this review is to describe the normal physiology of ventricular-arterial coupling from pulsatile flow, the effects of heart failure on this physiology and the vasculature, and to examine the effects of nonpulsatile blood flow on the vascular system and potential role in complications seen with CF-LVAD therapy. Understanding these concomitant vascular changes with CF-LVADs may be a key step in improving patient outcomes as modulation of pulsatility and flow characteristics may serve as a novel, yet simple, therapy for reducing complications.

Non-pulsatile blood flow is associated with enhanced cerebrovascular carbon dioxide reactivity and an attenuated relationship between cerebral blood flow and regional brain oxygenation

“…In the field of cardiac surgery and at many ICUs and emergency departments of tertiary care centres, it is daily practice to subject patients to a non-physiological condition where systemic blood flow either completely lacks pulsatility or pulsatility is greatly diminished [1]. Non-pulsatile flow, however, has been linked to increased vascular resistance, raised muscular sympathetic nervous activity, decreased oxygen consumption, endothelial dysfunction with loss of endothelial integrity and deterioration of microvascular perfusion.…”

The Relation Between Viscous Energy Dissipation And Pulsation For Aortic Hemodynamics Driven By A Left Ventricular Assist Device

“…Wall elasticity is related to vessel wall stiffening, which in itself is a consequence of aging, or other vascular pathologies. Frequency and pulsation have emerged as critical factors for consideration in LVAD design and operation, and our study provides some additional insights into the role of pulse-modulation in LVAD therapy as outlined in other works [31,43] . We have ensured that the parametric analysis of VDR due to anastomosis and pulsation remained decoupled from specific pump hardware features such as blade sweep and pump part design.…”

“…This methodology enabled quantifying the extent by which the LVAD jet driven flow differs from baseline; which is information that may not be otherwise available or generated. There is increasing interest in clinical community on what physiological flow features are adversely altered during LVAD operations [31] , and our study provides the foundations to develop relevant hemodynamic descriptors for this altered flow state for improved understanding of etiology of post-surgical complications in VAD therapy. Flow imaging is conventionally done using techniques like 4D flow MRI, which is not suitable for LVAD.…”

Computational Design of a Soft Robotic Myocardium for Biomimetic Motion and Function

“…High-speed rotary pumps or continuous flow VADs are associated with high shear stress and non-physiologic flows, leading to complications including gastrointestinal bleeding, arteriovenous malformations, hemolysis, and pump thrombosis. [22][23][24] In vitro simulators that replicate dynamic flow often suffer from inverse pressure-volume relationships, and unnatural hemodynamics and flow patterns. [25] Devices that reinstate physiologic pressure-volume relationships by external compression of the heart have been developed.…”