Our research supports the role of vasopressin as an efficient vasopressor during out-of-hospital CPR in blunt trauma patients, who are in cardiac arrest with initial PEA. In our previous studies about prehospital CPR we established the relationship between PETCO2
, MAP, and the prognosis [5
]. The average and final PETCO2
in vasopressin-treated patients with ROSC were significantly higher as well as the initial and the final MAP values. Therefore, vasopressin could be more potent than epinephrine in increasing the cardiac output. Results from the study by Bell and colleagues [16
] indicate that to secure cerebral perfusion and prevent secondary cerebral injury MAP should be kept at a level higher than commonly accepted. In our study, MAP was kept at a normal level (approximately 100 mmHg), thus securing coronary perfusion and preserving cerebral perfusion in the critical post-resuscitation period of absent cerebral autoregulation.
Some studies confirmed that the traumatic cardiac or pulmonary arrest is often associated with a dismal outcome and is considered to be an example of medical futility and inappropriate use of resources [7
]. On other hand, the use of guidelines regarding the termination or withholding of CPR in traumatic cardiac arrest patients remains controversial because several survivors met criteria for nontreatment according to the proposed clinical guidelines [8
]. Vasopressin is a promising agent in the treatment of traumatic cardiac arrest, especially in hemorrhagic shock [17
]. Voelckel et al. in two experimental studies [13
] concluded that treatment of hypovolemic cardiac arrest with vasopressin, but not epinephrine, resulted in sustained vital organ perfusion with less metabolic acidosis in the post-resuscitation phase, decreased gut perfusion in the post-resuscitation phase without impairing renal function, and subsequently in improved survival. Similarly, Sanui et al. [15
] have found that early supplemental arginine vasopressin (AVP) rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury. In severe chest trauma early AVP decreased mortality, reduced fluid requirements, improved pulmonary function, and did not increase the risk for bleeding in uncontrolled hemorrhage [19
]. In case reports of uncontrolled hemorrhagic shock with subsequent cardiac arrest some authors confirmed these results [20
The study by Friesenecker and colleagues [22
] showed that, under normal physiological conditions, vasopressin exerted significantly stronger vasoconstriction on large arterioles than norepinephrine.
This observation could explain, in part, why vasopressin can be effective in advanced shock unresponsive to therapeutic increases of catecholamines. In a clinical study, Westerman et al. [23
] confirmed significantly increased levels of endogenous vasopressin in multiple trauma patients.
That seems to be an integral part of the neuroendocrine response to severe injury; therefore, the natural response to trauma may be enhanced by additional exogenous vasopressin. Some clinical observations suggest that endogenous vasopressin insufficiency may be an underlying mechanism of refractory hypotension after prolonged hemorrhagic shock. Another beneficial effect of vasopressin may be that the blood is shifted away from a subdiaphragmatic region to the heart and brain, thus optimizing vital organ perfusion. This effect of vasopressin may be especially lifesaving in patients with uncontrolled hemorrhage resulting from subdiaphragmatic injury [24
]. In the historical group, resuscitation efforts lasted longer and a significantly higher quantity of additional epinephrine was needed. Adrenergic stimulation by additional doses of epinephrine is associated with adverse cardiac effects, including post-resuscitation myocardial dysfunction and increased myocardial oxygen consumption. In our trial in the vasopressin group we combined vasopressin with hypertonic HHS. Søreide and Deakin reported [29
] that the ideal prehospital fluid regimen may be a combination of an initial hypertonic solution given as a 10- to 20-min infusion, followed by crystalloids, and in some cases, artificial colloids. Meybohm et al. [27
] suggested the combination of HHS and vasopressin during the initial 10 min of therapy; cerebral perfusion pressure of the HHS group was significantly higher compared to the fluid group and increased more rapidly in the HHS with vasopressin group. HHS has a positive effect on hemodynamic parameters (systemic vascular resistence index, pulmonary vascular resistence index), microcirculation, and oxygen transport [31
]. The interesting study of Giusti-Paiva et al. can explain one additional synergistic effect of HHS and vasopressin [32
]. In this study they confirmed the effects of hypertonic saline solution administration on vasopressin secretion and mean arterial pressure in endotoxic shock. The hypertonic saline administration was followed by an immediate recovery of blood pressure and also by an increase in plasma vasopressin levels compared with isotonic saline solution. The vasopressin V1 receptor antagonist blocked the pressor response to hypertonic saline solution. These data suggest that the recovery of blood pressure after hypertonic saline solution administration during endotoxic shock is mediated by vasopressin secretion. Maybe a similar mechanism was responsible for the positive effect of HHS and vasopressin in traumatic cardiac arrest. The higher initial MAP after ROSC and lower average dose of epinephrine and average volume of resuscitation (without HHS) with similar ISS in both groups suggest that vasopressin could be more potent than epinephrine in increasing the cardiac output.
This small study has all the inherent problems associated with observational studies, but despite these limitations suggests a resuscitation strategy involving vasopressin in combination with HHS as a potentially lifesaving treatment in blunt trauma cardiac arrest. Our observations should be confirmed in future by larger multicenter prospective clinical trials.