Vasopressin Can Increase Coronary Perfusion Pressure during Human Cardiopulmonary Resuscitation
ABSTRACT To determine the hemodynamic effect of vasopressin on coronary perfusion pressure (CPP) in prolonged human cardiac arrest.
A prospective, open-label clinical trial of vasopressin during cardiac resuscitation was performed. Ten patients presenting in cardiac arrest initially received resuscitative measures by emergency physicians according to Advanced Cardiac Life Support (ACLS) guidelines. A central venous catheter for fluid and drug administration and a femoral artery catheter for measurement of CPP (aortic minus right atrial relaxation phase pressures) were placed. When each patient was deemed nonsalvageable, 1.0 mg epinephrine was given and CPP was measured for 5 minutes, followed by a dose of vasopressin (1.0 U/kg). CPP measurements were continued for another 5 minutes.
The mean duration of cardiac arrest (out-of-hospital interval plus duration of ED ACLS) was 39.6 +/- 16.5 min. There was no improvement in CPP after 1.0 mg of epinephrine. Vasopressin administration resulted in a significant increase of CPP in 4 of the 10 patients. Patients responding to vasopressin had a mean increase in CPP of 28.2 +/- 16.4 mm Hg (range: 10-51.5), with these peak increases occurring at 15 seconds to 4 minutes after administration. The increases in the vasopressin levels after administration did not differ between the responders and nonresponders.
In this human model of prolonged cardiac arrest, 40% of the patients receiving vasopressin had a significant increase in CPP. This pilot study suggests that investigation of earlier use of vasopressin as a therapeutic alternative in the treatment of cardiac arrest is warranted.
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- "In a recent study by Stiell et al of in-hospital CPR, 87% of the patients in the vasopressin group also received epinephrine and the usefulness of the combination regimen was demonstrated by clinical observations such as significantly improved coronary perfusion pressure, increased likelihood of restoration of spontaneous circulation and 24-hour survival rates. No randomized control trials have yet been done to determine the cost-effectiveness of vasopressin. "
ABSTRACT: Vasopressin or antidiuretic hormone is a potent endogenous hormone, which is responsible for regulating plasma osmolality and volume. In high concentrations, it also raises blood pressure by inducing moderate vasoconstriction. It acts as a neurotransmitter in the brain to control circadian rhythm, thermoregulation and adrenocorticotropic hormone release. The therapeutic use of vasopressin has become increasingly important in the critical care environment in the management of cranial diabetes insipidus, bleeding abnormalities, esophageal variceal hemorrhage, asystolic cardiac arrest and septic shock. After 10 years of ongoing research, vasopressin has grown to a potential component as a vasopressor agent of the anesthesiologist's armamentarium in the treatment of cardiac arrest and severe shock states.Indian Journal of Critical Care Medicine 04/2011; 15(2):71-7. DOI:10.4103/0972-5229.83006
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- "In a study using a pig model of ventricular fibrillation cardiac arrest, Lindner and colleagues  concluded that administration of vasopressin led to a significantly higher CPP, myocardial blood flow, and total cerebral flow during CPR. In a study conducted by Morris and colleagues  using a human model of prolonged cardiac arrest, 40% of the patients receiving vasopressin had a significant increase in CPP. Our study shows that higher values of petCO2 and MAP in patients treated with vasopressin are consistent with the better outcomes in the vasopressin group. "
ABSTRACT: Clinical data considering vasopressin as an equivalent option to epinephrine in cardiopulmonary resuscitation (CPR) are limited. The aim of this prehospital study was to assess whether the use of vasopressin during CPR contributes to higher end-tidal carbon dioxide and mean arterial blood pressure (MAP) levels and thus improves the survival rate and neurological outcome. Two treatment groups of resuscitated patients in cardiac arrest were compared: in the epinephrine group, patients received 1 mg of epinephrine intravenously every three minutes only; in the vasopressin/epinephrine group, patients received 40 units of arginine vasopressin intravenously only or followed by 1 mg of epinephrine every three minutes during CPR. Values of end-tidal carbon dioxide and MAP were recorded, and data were collected according to the Utstein style. Five hundred and ninety-eight patients were included with no significant demographic or clinical differences between compared groups. Final end-tidal carbon dioxide values and average values of MAP in patients with restoration of pulse were significantly higher in the vasopressin/epinephrine group (p < 0.01). Initial (odds ratio [OR]: 18.65), average (OR: 2.86), and final (OR: 2.26) end-tidal carbon dioxide values as well as MAP at admission to the hospital (OR: 1.79) were associated with survival at 24 hours. Initial (OR: 1.61), average (OR: 1.47), and final (OR: 2.67) end-tidal carbon dioxide values as well as MAP (OR: 1.39) were associated with improved hospital discharge. In the vasopressin group, significantly more pulse restorations and a better rate of survival at 24 hours were observed (p < 0.05). Subgroup analysis of patients with initial asystole revealed a higher hospital discharge rate when vasopressin was used (p = 0.04). Neurological outcome in discharged patients was better in the vasopressin group (p = 0.04). End-tidal carbon dioxide and MAP are strong prognostic factors for the outcome of out-of-hospital cardiac arrest. Resuscitated patients treated with vasopressin alone or followed by epinephrine have higher average and final end-tidal carbon dioxide values as well as a higher MAP on admission to the hospital than patients treated with epinephrine only. This combination vasopressor therapy improves restoration of spontaneous circulation, short-term survival, and neurological outcome. In the subgroup of patients with initial asystole, it improves the hospital discharge rate.Critical care (London, England) 02/2007; 11(2):R39. DOI:10.1186/cc5726 · 4.48 Impact Factor
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- "Furthermore, prolonged hemorrhage, cardiogenic shock, and sepsis may evolve into a refractory phase characterized by unresponsiveness to either fluid replacement or catecholamines  . Recently, AVP was found to effectively restore systemic circulation in some of these conditions       . This counterintuitive finding has prompted a resurgence of interest in this hormone. "
ABSTRACT: In the past few years, arginine vasopressin (AVP) has emerged as a rational alternative to catecholamines for the hemodynamic support of refractory vasodilatory shock and cardiopulmonary arrest. The therapeutic potential of AVP in traumatic shock is now being evaluated. Our laboratory investigations have revealed an apparent benefit of AVP when compared to standard fluid resuscitation in clinically relevant models of brain injury and chest injury. Further experimental work and subsequent clinical trials appear justified to validate the efficacy of AVP for resuscitation of trauma patients.