Arginine vasopressin in advanced cardiovascular failure during the post-resuscitation phase after cardiac arrest

Summary

Arginine vasopressin (AVP) has been employed successfully during cardiopulmonary resuscitation, but there exist only few data about the effects of AVP infusion for cardiovascular failure during the post-cardiac arrest period.

Cardiovascular failure is one of the main causes of death after successful resuscitation from cardiac arrest. Although the “post-resuscitation syndrome” has been described as a “sepsis-like” syndrome, there is little information about the haemodynamic response to AVP in advanced cardiovascular failure after cardiac arrest. In this retrospective study, haemodynamic and laboratory variables in 23 patients with cardiovascular failure unresponsive to standard haemodynamic therapy during the post-cardiac arrest period were obtained before, and 30 min, 1, 4, 12, 24, 48, and 72 h after initiation of a supplementary AVP infusion (4 IU/h). During the observation period, AVP significantly increased mean arterial blood pressure (58 ± 14 to 75 ± 19 mmHg, p < 0.001), and decreased noradrenaline (norepinephrine) (1.31 ± 2.14 to 0.23 ± 0.3 μg/kg/min, p = 0.03), adrenaline (epinephrine) (0.58 ± 0.23 to 0.04 ± 0.03 μg/kg/min, p = 0.001), and milrinone requirements (0.46 ± 0.15 to 0.33 ± 0.22 μg/kg/min, p < 0.001). Pulmonary capillary wedge pressure changed significantly (p < 0.001); an initial increase being followed by a decrease below baseline values. While arterial lactate concentrations (95 ± 64 to 21 ± 18 mg/dL, p < 0.001) and pH (7.27 ± 0.14 to 7.4 ± 0.14, p < 0.001) improved significantly, total bilirubin concentrations (1.12 ± 0.95 to 3.04 ± 3.79 mg/dL, p = 0.001) increased after AVP. There were no differences in the haemodynamic or laboratory response to AVP between survivors and non-survivors.

In this study, advanced cardiovascular failure that was unresponsive to standard therapy could be reversed successfully with supplementary AVP infusion in >90% of patients surviving cardiac arrest.

Introduction

Unfortunately, initial resuscitation from cardiac arrest does not ensure long-term survival¹; up to 70% of patients successfully resuscitated die before hospital discharge.² The main causes of post-resuscitation deaths are irreversible neurological injury, uncontrollable cardiovascular failure, and severe multiple organ dysfunction syndrome.³

Negovsky, a Russian, first described a systemic “post-resuscitation syndrome” with multiple organ dysfunction after successful resuscitation from cardiac arrest,⁴ and investigators from Pittsburgh have identified a specific “cardiovascular post-resuscitation syndrome”.⁵ Cardiovascular failure after return of spontaneous circulation is characterised by hypovolaemia⁶, myocardial dysfunction,2, 7 and excessive vasodilatation,³ Thus, cardiovascular failure after successful resuscitation of cardiac arrest is similar to inflammation-induced haemodynamic failure. Accordingly, the “post-resuscitation syndrome” has recently been reported to be a “sepsis”⁸ or “SIRS like” syndrome.⁹

AVP has been employed successfully during cardiopulmonary resuscitation,10, 11 but not to treat vasodilatation in successfully resuscitated cardiac arrest patients. AVP has frequently been administered as a supplementary vasopressor in advanced cardiocirculatory failure in sepsis and after major surgery.12, 13 Since resuscitated cardiac arrest patients are especially vulnerable to catecholamine-mediated complications, infusion of AVP may be beneficial in the treatment of excessive vasodilatation unresponsive to standard haemodynamic therapy due to the catecholamine-sparing effects. In refractory cardiogenic shock after myocardial infarction, AVP was associated with increased MAP and no adverse effect on other haemodynamic variables.¹⁴

This retrospective analysis evaluates the haemodynamic, and laboratory response to a supplementary AVP infusion in 23 patients with advanced cardiovascular failure following resuscitation from cardiac arrest.