Argipressin (Vasopressin)

Vasopressin in cirrhosis and sepsis: physiology and clinical implications

Arginine-vasopressin (AVP) is an important hormone in the regulation of plasma osmolality and blood volume/pressure. In clinical practice it is frequently used in the treatment of septic shock and decompensated cirrhosis. In this review the physiology of AVP and its analogues is presented. In addition the use of AVP in cirrhosis and sepsis is reviewed.

Increased complexity of vasopressin's vascular actions

Vasopressin is becoming a widely used pressor in conditions with severe hypotension. Like several other hormones important in cardiovascular and extracellular fluid control, however, vasopressin can activate several receptors that when pharmacologically or pathologically stimulated may result in conflicting effects. In the present issue of Critical Care, Rehberg and colleagues examined the hypothesis that blockade of vasopressin V2 receptor during septic shock may be beneficial. Their tantalizing results indicate that future work must consider the precise vasopressin receptors that are stimulated and/or inhibited.

Management of vasodilatory shock: defining the role of arginine vasopressin

The rationale for an arginine vasopressin (argipressin) infusion was put forward after it was discovered that patients in shock states might have an endogenous arginine vasopressin deficiency. Subsequently, several investigations impressively demonstrated that arginine vasopressin can successfully stabilise haemodynamics even in advanced vasodilatory shock. We report on physiological and pharmacological aspects of arginine vasopressin, and summarise current clinical knowledge on employing a continuous arginine vasopressin infusion in critically ill patients with catecholamine-resistant vasodilatory shock of different aetiologies. In view of presented experimental evidence and current clinical experience, a continuous arginine vasopressin infusion of approximately 2 to approximately 6 IU/h can be considered as a supplemental strategy to vasopressor catecholamines in order to preserve cardiocirculatory homeostasis in patients with advanced vasodilatory shock. Because data on adverse effects are still limited, arginine vasopressin should be reserved for patients in whom adequate haemodynamic stabilisation cannot be achieved with conventional vasopressor therapy or who have obvious adverse effects of catecholamines that result in further significant haemodynamic deterioration. For the same reasons, arginine vasopressin should not be used as a single, alternative vasopressor agent instead of catecholamine vasopressors. Future prospective studies will be necessary to define the exact role of arginine vasopressin in the therapy of vasodilatory shock.

Actualités autour de la prise en charge des diabètes insipides centraux: Management of central diabetes insipidus in 2016

Diabetes insipidus is a syndrome that associates both hypotonic polyuria and polydipsia, due to insufficient or ineffective arginine vasopressin (AVP) synthesis, or to AVP resistance. The diagnosis between central/renal origin, or an abnormal thirst regulation (primary polydipsia) is required to organize an adapted management. Because water deprivation tests are not reliable, it's often based on medical history, response to treatment and MRI. Copeptin is an AVP precursor which could be very helpful for the diagnosis. Its basal dosage may identify nephrogenic DI whereas osmotic stimulated dosage would discriminate central DI and primary polydipsia. Central DI is quite frequent after pituitary surgeries or traumatic brain injuries, and often transient. In case of early diagnosis and familial history of DI, a mutation of AVP gene is suspected, most of the time autosomal dominant. MRI is required to identify the other causes, i.e. tumors and inflammatory diseases (sarcoidosis, histiocytosis, hypophysitis). An advanced evaluation is required before idiopathic DI be retained, especially if a thickening of pituitary stalk is observed. The treatment of central DI is mainly based on lyophilisate of desmopressin administration.

Evolving role of vasopressin in the treatment of cardiac arrest

Sudden cardiac arrest is a major public heath problem, affecting more than 450,000 individuals annually. Response time and the initiation of cardiopulmonary resuscitation (CPR) remain the most important factors determining successful revival. During resuscitation, sympathomimetics are given to enhance cerebral and coronary perfusion pressures in an attempt to achieve restoration of spontaneous circulation. Epinephrine has been the preferred vasopressor since the inception of advanced cardiac life support, although the lack of definitive evidence regarding its effectiveness has created much controversy surrounding its use, including the optimum dosage. Vasopressin is an alternative vasopressor that, when given at high doses, causes vasoconstriction by directly stimulating smooth muscle V1 receptors. The 2000 American Heart Association (AHA) guidelines commented that vasopressin is a reasonable first-line vasopressor in patients with ventricular fibrillation or pulseless ventricular tachycardia. Since release of those guidelines, additional human studies support an expanded role for vasopressin, whereas other studies cast doubt regarding its efficacy compared with epinephrine. The AHA recently released revised guidelines for CPR and emergency cardiovascular care. The consensus was that vasopressors should remain a part of pulseless sudden cardiac arrest management, with epinephrine 1 mg every 3-5 minutes being the recommended adrenergic of choice. In these revised guidelines, the role of vasopressin expanded beyond previous recommendations, despite the recommendation being downgraded to class indeterminate. The guidelines comment that one dose of vasopressin 40 U may replace the first or second dose of epinephrine in all pulseless sudden cardiac arrest scenarios, including asystole and pulseless electrical activity. A consistent theme with all vasopressors in sudden cardiac arrest is that additional studies are necessary to clearly document greater efficacy compared with no treatment. Further evaluation is warranted to better assess the role of vasopressin in asystolic sudden cardiac arrest, as well as its use with epinephrine, and to determine its optimal timing of administration and potential synergistic effects.