Objectives: Cardiac arrest (CA) is a hemostatic state only reversible via dynamic intracardiac action potentials following hemorheological–biochemical reactions of adequate blood volumes (BVs). Undeniable electrophysiological processes begun since intrauterine life compromised by cardiopulmonary resuscitation (CPR). Apart from mechanical circulatory support (MCS), CPR induces an ineffective back-and-forth perfusion mode that worsens the stalled cellular metabolism. This is probably due to the arrested cardiopulmonary pumps—the main generators of endothelial shear stress (ESS) that control microcirculation, thereby, cellular metabolism. The goal is to highlight and address shortcomings of CPR, including its incompatibilities with human cardiotorsal anatomy and thoracic biomechanics. 

Method: Prompt ESS restorations: mechanically with a noninvasive MCS inducing pulsatile circulatory flow restoration (CFR) regardless of return of spontaneous circulation (ROSC). And manually, with a novel chest compression technique allowing refill-recoil–rebound (3R/CPR) the heart and ribcage in a near-circumferential manner through the left 5th intercostal space. The technique can provide adequate BV inducing intracardiac water hammer-like mechanism and atrial wall stress promoting less traumatic ROSC. 

Results: Obtained data shown significant improvement of tissue perfusion with CFR device in CA animal models  and the potential advantages of 3R/CPR following its inevitable applications in two drownings after unsuccessful CPR. Additionally, an invasive pulsatile MCS data shown significant advantages of ESS-mediated endothelial function restoration over steady-flow perfusion in beatless-heart model.

Conclusions: Prompt ESS restoration can preserve cellular metabolism during CA. In-depth analysis of the proposal could evolve the strict doctrine of CPR, thus opening new horizons to improve the dismal outcomes of victims.