Vasopressin as adjunct vasopressor for vasodilatory shock due to non-occlusive mesenteric ischemia

We present the case of an 83-year-old patient who underwent cardiac surgery and developed postoperative non-occlusive mesenteric ischemia (NOMI), which was treated with a local intra-arterial papaverine and prostaglandin E1 infusion. After successful mesenteric reperfusion, a multiple organ dysfunction syndrome with severe cardiovascular failure developed. High norepinephrine dosages (1.09 microg/kg body weight/min) and catecholamine-related complications (tachycardiac atrial fibrillation) required initiation of supplementary argininevasopressin (AVP) infusion (4 U/h). AVP stabilized vasodilatory shock, ensured adequate gut perfusion pressure and had no adverse clinical or angiographic effects on restitution of gut integrity. In conclusion, after reperfusion of NOMI in this patient, adjunct AVP therapy combined with local vasodilator infusion was beneficial as a potentially life-saving vasopressor.     

Arginine vasopressin as a rescue vasopressor to treat epidural anaesthesia-induced arterial hypotension

Epidural anaesthesia is a well-established and recognized technique in anaesthetic practice. Its benefits are multiple and range from positive effects on the respiratory and cardiocirculatory system, a reduced need for analgesics and decreased costs to earlier hospital discharge. Disadvantages like sympathetic blockade followed by hypotension, bradycardia, and cardiac arrest, however, must be taken into consideration. Treatment of these side effects consists of fluid infusion and vasopressor drugs. During epidural anaesthesia, plasma arginine vasopressin (AVP) concentrations are increased. In case reports and a small clinical study, administration of AVP or one of its analogues could rapidly reverse hypotension and restore cardiovascular stability. Because no major controlled clinical trial has yet evaluated the effects of AVP on morbidity, AVP can so far not be recommended as a first-line drug to treat cardiovascular instability during epidural anaesthesia. In refractory cases, however, the use of AVP as a rescue vasopressor may be beneficial.     

Vasopressin and shock.

Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of a variety of shock states. Increasing interest in the clinical use of vasopressin has resulted from the recognition of its importance in the endogenous response to shock and from advances in understanding of its mechanism of action. From animal models of shock, vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds (particularly the brain) than does adrenaline. Although vasopressin has similar direct actions to the catecholamines, it may uniquely also inhibit some of the pathologic vasodilator processes that occur in shock states. There is current interest in the use of vasopressin in the treatment of shock due to ventricular fibrillation, hypovolaemia, sepsis and cardiopulmonary bypass. This article reviews the physiology and pharmacology of vasopressin and all of the relevant animal and human clinical literature on its use in the treatment of shock following a MEDLINE (1966-2000) search.     

Vasopressin analogues in the treatment of shock states: potential pitfalls

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.     

Phaeochromocytoma as an unusual aetiology of cardiogenic shock

The authors reported a case involving a young patient with a cardiogenic shock associated to an acute pulmonary oedema. According to the seriousness of the shock, an external ventricular assist device (VAD) was initially inserted and replaced thereafter because of the cardiovascular instability, by an external pneumatic biventricular assist device. A cardiogenic shock induced by an acute adrenergic myocarditis due to a phaeochromocytoma was diagnosed. The patient was weaned from the VAD on day 84 and was scheduled for elective surgery of the phaeochromocytoma on day 93. The authors discussed the time of the surgery according to the anticoagulation therapy necessary to the VAD and the necessary caution taken if a cardiogenic shock appeared around surgery.     

Employing vasopressin as an adjunct vasopressor in uncontrolled traumatic hemorrhagic shock

Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.     

Acute experimental study of Abiomed BVS5000 as a V-A bypass to cardiogenic shock models.

PURPOSE: Abiomed BVS5000 is generally used as a ventricular assist device, and there have been no reports of its application to a veno-arterial bypass (V-A bypass). In the present study, we developed a new V-A bypass system using this pump and examined its usefulness experimentally. MATERIALS AND METHODS: Pigs (n=21; 37.4+/-2.2 kg) with cardiogenic shock were divided into the following three groups: (1) Abiomed group (Abiomed BVS5000); (2) nonpulsatile pump (NP)+intra-aortic balloon pump (IABP) group (centrifugal pump and IABP); and (3) NP group. In all three groups, assisted circulation using the pumps was performed for 3 h after the shock. Hemodynamic data and blood specimens were measured before and immediately after the shock, and again at 1, 2, and 3 h after. The individual variations were reduced by evaluation of the measured value/preshock value ratio, not by evaluation of the absolute values. RESULTS: The coronary arterial blood flows at 3 h after the shock were significantly larger in the Abiomed and NP+IABP groups than in the NP group (1.32+/-0.34 and 1.24+/-0.05 vs. 1.05+/-0.11, P<0.05), and the renal arterial and renal cortical tissue blood flows were significantly larger in the Abiomed group than in the NP+IABP and NP groups (renal artery: 1.30+/-0.17 vs. 0.89+/-0.20 and 0.68+/-0.10, P<0.05; renal cortical tissue: 0.74+/-0.25 vs. 0.62+/-0.05 and 0.43+/-0.18, P<0.05). The lactate/pyruvate ratios were significantly lower in the Abiomed groups than in the NP group (25.2+/-1.6 vs. 36.0+/-3.1, P<0.05). CONCLUSION: The results suggest that a V-A bypass using an Abiomed BVS5000 is a useful treatment for organ blood flow redistribution after shock.     

Treatment of cardiogenic shock with the Hemopump left ventricular assist device

A multiinstitutional study is in progress to evaluate the Hemopump in the treatment of cardiogenic shock. Fifty-three patients with refractory cardiogenic shock were selected for Hemopump assistance. The hemodynamic definition of cardiogenic shock included (1) a cardiac index of less than 2.0 L.min-1.m-2, (2) pulmonary capillary wedge pressure of greater than 18 mm Hg, and (3) a systolic blood pressure of less than 90 mm Hg or a left ventricular work index of less than 1,500 g-m.m-2.min-1. The Hemopump was successfully inserted in 41 of 53 patients (77.3%). A significant improvement in the hemodynamic status was seen during Hemopump assistance. A minimal level of hemolysis was observed. No leg ischemia was observed. The 30-day overall survival of the Hemopump group was 31.7%. Criteria establishing indications for use and clinical utility are proposed. We conclude that the Hemopump provides significant hemodynamic support of the patient in cardiogenic shock allowing for recovery from ventricular stunning in marginal ventricles, and that in select patients the Hemopump may offer a major improvement in survival over conventional therapy.     

Treatment of cardiogenic shock with levosimendan in combination with beta-adrenergic antagonists

Levosimendan, a calcium sensitizer, was used in combinationwith ß-adrenergic antagonists in a man aged 56 yrwith cardiogenic shock, complicating acute myocardial infarction,who developed severe tachycardia after dobutamine administration.The patient's trachea was intubated, his lungs were ventilated,and he was started on dopamine 5 µg kg^–1 min^–1and dobutamine 5 µg kg^–1 min^–1, titrated toa mean arterial pressure 65 mm Hg. He progressively became tachycardiac(>120 beats min^–1) with a cardiac index (CI) of 1.4litre min^–1 m^–2 despite adequate preload. Levosimendan6 µg kg^–1 was administered intravenously over 10min followed by a continuous infusion of 0.2 µg kg^–1min^–1 for 24 h. Within 30 min, the patient's CI increasedto 2.2 litre min^–1 m^–2, but the heart rate (HR)also increased from 142 to 155 beats min^–1. Esmolol 1mg kg^–1 i.v. was administered with a consequent transientdecrease in HR to 110 beats min^–1 without adverse haemodynamiceffects; however, HR increased again shortly afterwards. Carvedilol3.125 mg orally twice a day was then administered, and the dosewas increased to 6.25 mg orally twice daily on the followingday. Subsequently, HR decreased over time and both catecholamineswere discontinued 14 h after starting levosimendan infusion.The trachea was extubated within 20 h and the patient was dischargedto the ward on day 4 after admission. In conclusion, levosimendanin combination with a ß-adrenergic antagonist mayhave beneficial effects in patients with cardiogenic shock whoexhibit tachycardia in response to inotropic agents.     

Hemofiltration as therapy in acute pulmonary failure in cardiogenic shock

In 29 cardiosurgical patients in cardiogenic shock after extracorporal circulation complicated by acute pulmonary failure, it was impossible to restore normal postoperative arterial oxygen tension, in-spite of optimal pharmacotherapy and ideal conditions with a conventional volume-controlled respirator. These patients were subject to continuous arteriovenous haemofiltration; in all of them the start of haemofiltration immediately led to a significant reduction of respiratory oxygen supply with an increase in arterial oxygen tension. Pulmonary shunt volume decreased. At the same time there was an increase in arteriovenous oxygen difference, arterial oxygen content and oxygen transport capacity. Pulmonary artery pressure as well as pulmonary vascular resistance decreased noticeably, whereas there was an increase in total peripheral vascular resistance. Starting haemofiltration with decreasing left ventricular filling pressure, accompanied by a rise in blood pressure and an increase in total peripheral resistance, led to an improvement of the haemodynamic situation as well as pulmonary oxygen diffusion, thereby ensuring oxygen perfusion of peripheral tissue. The results suggest a causal relation between the improvement of the clinical condition of the patient and the elimination of cardiopulmonary toxic agents like myocardial depressant factor (MDF) and shock mediators due to arteriovenous haemofiltration.     

Cardiac transplantation: treatment for cardiogenic shock.

Eighty-six patients received orthotopic cardiac transplants at the Royal Victoria Hospital in Montreal between 1985 and 1989. Of these, 16 mortally ill, being sustained in hospital by the intravenous administration of inotropic agents (15 patients [94%]) or intra-aortic balloon counterpulsation (6 [38%]). There was one early death (at 7 days), for a death rate of 6.3% (versus 8.6% for the 70 "elective" transplants). Two others died of delayed infection: one of viral hepatitis at 6 weeks, and one of pneumonia due to Pneumocystis 4 months after transplantation. The other 13 patients are alive and well 12 to 66 months postoperatively. Nine have returned to their preoperative work, three have decreased activity levels but are functioning well, and one is retired.     

Treatment of cardiogenic shock in peripartum cardiomyopathy: Case series from a tertiary ECMO center

Peripartum cardiomyopathy (PPCM) occurs toward the end of pregnancy or in the months after delivery without previously known structural heart disease. Development of therapy-refractory cardiogenic shock is described in the literature with a limited number of overall presented cases in this young patient cohort. To provide differences and key points in the therapy of end-stage PPCM patients, we present a case series of four young women with PPCM referred to our department for potential VA ECMO support.