Prolongation of the Agonal Phase in the DCD Donor Results in Impairment of Myocardial Contractility Following DCD Heart Resuscitation

Abstract

Purpose Circulatory arrest follows withdrawal of supportive therapy in the DCD donor. The agonal phase following withdrawal can be prolonged and may be associated with hypoxia and hypotension. Our aim was to evaluate the impact of the duration of the agonal period on the capacity for cardiac resuscitation. Methods Rats (n = 6/group) were subjected to hypoventilation using a mechanical ventilator and exposed to either brief (5 mins), moderate (30 mins) or prolonged (60 mins) hypoxia and hypotension prior to circulatory arrest. This method was used to simulate an agonal phase of varying duration. Following circulatory arrest 15 minutes of warm ischemia was observed prior to reperfusion with extracorporeal membrane oxygenation (ECMO). ECMO reperfusion was followed by cardiac resuscitation. Load independent left ventricular (LV) contractility was assessed at baseline and following resuscitation via the end-systolic pressure volume relationship (ESPVR). Results Hypoventilation was followed by a decrease in oxygen saturation (pre 96% vs post 48%), mean arterial pressure (pre 72 +/- 14 vs. post 41 +/- 5 mm Hg) and pH (pre 7.49 +/- 0.1 vs. post 6.99 +/- 0.1). There was no difference between groups in LV contractility at baseline. Following circulatory arrest and cardiac resuscitation all groups demonstrated a decline in contractile function from baseline. There was marked reduction in LV contractility in animals with a 60-minute agonal phase (ESPVR: 60 minutes; 0.17 +/- 0.08, 30 minutes; 0.66 +/- 0.16, 5 minutes; 0.47 +/- 0.09, p Conclusion Brief or moderate exposure to hypoxia and hypotension prior to circulatory arrest was associated with satisfactory recovery of contractile function. Prolonged exposure to these conditions was associated with a significant decline in LV contractility. In the human DCD donor marked prolongation of the agonal phase may limit cardiac donation.