pituitrin and Systemic-Inflammatory-Response-Syndrome

Vasopressin and terlipressin are increasingly used as alternative non-adrenergic vasopressors for hemodynamic support of septic patients with arterial hypotension. Despite excellent vasopressive effects, vasopressin analogues may potentially impair macro-hemodynamics, oxygen transport and microvascular blood flow. Due to those unwanted side-effects, vasopressin and terlipressin may potentially compromise organ function and possibly foster the development of multiple organ failure. This review article discusses the results of clinical and experimental studies to judge the effects of vasopressin and terlipressin on microcirculation, oxygen supply, metabolism and organ function in patients with sepsis or systemic inflammatory response syndrome (SIRS). Although vasopressin analogues are emerging as promising alternatives to treat catecholamine-refractory hypotension, there is no evidence that vasopressin receptor agonists improve outcome. To date, vasopressin and terlipressin can, therefore, not be recommended for routine clinical use.

Topics: Animals; Humans; Lypressin; Microcirculation; Oxygen Consumption; Sepsis; Systemic Inflammatory Response Syndrome; Terlipressin; Vasoconstrictor Agents; Vasopressins

Although nearly 10% of patients experience profound vasodilatory shock after cardiopulmonary bypass, some patients remain refractory to traditional resuscitation. Among this subset are patients who have inappropriately low levels of endogenous vasopressin. Thus, vasopressin replacement is an intuitively attractive intervention. The purposes of this review are to outline the pathophysiology of vasodilatory shock after cardiopulmonary bypass, to discuss the physiological role of endogenous vasopressin, to explore the clinical basis for vasopressin replacement, and to review the pharmacology and dosing guidelines.

Topics: Cardiopulmonary Bypass; Coronary Care Units; Education, Continuing; Humans; Practice Guidelines as Topic; Shock, Surgical; Systemic Inflammatory Response Syndrome; United States; Vasopressins

Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasopressin, clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.

Topics: Animals; Humans; Kidney; Osmosis; Shock, Hemorrhagic; Shock, Septic; Systemic Inflammatory Response Syndrome; Vasoconstriction; Vasodilation; Vasopressins

Cardiopulmonary bypass (CPB) is associated with a systemic stress hormonal response, which can lead to changes in hemodynamics and organ perfusion. We examined perioperative stress hormone release in low-risk patients undergoing coronary artery bypass grafting with and without cardiopulmonary bypass.. Fifty-two patients undergoing primary coronary artery bypass grafting by the same surgeon were randomly assigned into either on-pump (n = 26) or off-pump (n = 26) groups. The on-pump coronary artery bypass grafting group underwent mildly hypothermic (35 degrees C) pulsatile cardiopulmonary bypass with arterial line filtration. Arterial blood samples were collected preoperatively, at the end of operation, and at 1, 6, and 24 hours postoperatively. Plasma levels of vasopressin and cortisol were measured using radioimmunoassay. Anesthetic management was standardized.. Both groups had similar demographic makeup and extent of revascularization (on-pump coronary artery bypass grafting, 2.8 +/- 1.0 grafts versus off-pump coronary artery bypass grafting, 2.4 +/- 0.9 grafts; p = 0.20). No mortality or major morbidity was observed and there were no crossovers. The cardiopulmonary bypass and aortic cross-clamp times in the on-pump coronary artery bypass grafting group were 63 +/- 24 and 33 +/- 11 minutes, respectively. In both groups there was a similar and significant rise in cortisol and vasopressin levels in the early postoperative phase, with a partial recovery toward baseline values observed at 24 hours postoperatively. Repeated measures analysis of covariance showed no significant difference between the groups with time for both hormones (cortisol, p = 0.40; vasopressin, p = 0.30).. Despite the avoidance of cardiopulmonary bypass, off-pump coronary artery bypass grafting surgery triggers a systemic stress hormone response that is comparable to conventional surgical revascularization. The neurohormonal environment during beating-heart surgery should be further explored.

Topics: Aged; Biomarkers; Cardiopulmonary Bypass; Coronary Artery Bypass; Coronary Artery Bypass, Off-Pump; Female; Humans; Hydrocortisone; Hypothermia, Induced; Intraoperative Complications; Male; Middle Aged; Postoperative Complications; Prospective Studies; Stress, Physiological; Systemic Inflammatory Response Syndrome; Vasopressins

Severe right ventricular failure complicated a postoperative systemic inflammatory response in a 33-year-old woman after surgical repair of congenital cardiac malformations. Volume loading, and high doses of catecholamines, failed to produce improvement, but treatment with vasopressin improved all haemodynamic parameters, and also allowed reduction of the other inotropes. After 10 days, the patient was discharged in stable condition from the intensive care unit.

Topics: Adult; Female; Hemodynamics; Humans; Systemic Inflammatory Response Syndrome; Vascular Resistance; Vasoconstrictor Agents; Vasopressins; Ventricular Dysfunction, Right

Topics: Cardiopulmonary Bypass; Coronary Care Units; Shock, Surgical; Systemic Inflammatory Response Syndrome; Vasoconstrictor Agents; Vasopressins

A 54-year-old patient, admitted to the intensive care unit with a diagnosis of severe pancreatitis, developed circulatory shock that failed to respond to standard vasopressor treatment: epinephrine and norepinephrine. Addition of vasopressin helped reduce standard catecholamine need while maintaining adequate arterial blood pressure. Vasopressin appears to be a promising agent for maintaining arterial pressure during septic shock or systemic inflammatory response syndrome, but due to limited data and potential side effects, its use as first-line treatment for these indications is not recommended.

Topics: Blood Pressure; Fatal Outcome; Female; Humans; Middle Aged; Pancreatitis; Shock; Systemic Inflammatory Response Syndrome; Vasoconstrictor Agents; Vasopressins