pituitrin and Tachycardia--Ventricular

Advanced Life Support guidelines recommend the use of epinephrine during Cardiopulmonary Resuscitation (CPR), as to increase coronary blood flow and perfusion pressure through its alpha-adrenergic peripheral vasoconstriction, allowing minimal rises in coronary perfusion pressure to make defibrillation possible. Contrasting to these alpha-adrenergic effects, epinephrine's beta-stimulation may have deleterious effects through an increase in myocardial oxygen consumption and a reduction of subendocardial perfusion, leading to postresuscitation cardiac dysfunction.. The present paper consists of a systematic review of the literature regarding the use of beta-blockade in cardiac arrest due to ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT).. Studies were identified through MEDLINE electronic databases research and were included those regarding the use of beta-blockade during CPR.. Beta-blockade has been extensively studied in animal models of CPR. These studies not only suggest that beta-blockade could reduce myocardial oxygen requirements and the number of shocks necessary for defibrillation, but also improve postresuscitation myocardial function, diminish arrhythmia recurrences and prolong survival. A few case reports described successful beta-blockade use in patients, along with two prospective human studies, suggesting that it could be safe and effectively used during cardiac arrest in humans.. Even though the existing literature points toward a beneficial effect of beta-blockade in patients presenting with cardiac arrest due to VF/pulseless VT, high quality human trials are still lacking to answer this question definitely.

Topics: Adrenergic beta-Antagonists; Animals; Cardiopulmonary Resuscitation; Coronary Circulation; Epinephrine; Heart Arrest; Humans; Myocardium; Oxygen Consumption; Propanolamines; Propranolol; Tachycardia, Ventricular; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

Topics: Advanced Cardiac Life Support; Anti-Arrhythmia Agents; Humans; Practice Guidelines as Topic; Tachycardia, Ventricular; Takayasu Arteritis; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

Local anesthetic (LA) intoxication with cardiovascular arrest is a potential fatal complication of regional anesthesia. Lipid resuscitation has been recommended for the treatment of LA-induced cardiac arrest. Aim of the study was to compare four different rescue regimens using epinephrine and/or lipid emulsion and vasopressin to treat cardiac arrest caused by bupivacaine intoxication.. Twenty-eight piglets were randomized into four groups (4 × 7), anesthetized with sevoflurane, intubated, and ventilated. Bupivacaine was infused with a syringe driver via central venous catheter at a rate of 1 mg·kg(-1)·min(-1) until circulatory arrest. Bupivacaine infusion and sevoflurane were then stopped, chest compression was started, and the pigs were ventilated with 100% oxygen. After 1 min, epinephrine 10 μg·kg(-1) (group 1), Intralipid(®) 20% 4 ml·kg(-1) (group 2), epinephrine 10 μg·kg(-1) + Intralipid(®) 4 ml·kg(-1) (group 3) or 2 IU vasopressin + Intralipid(®) 4 ml·kg(-1) (group 4) were administered. Secondary epinephrine doses were given after 5 min if required.. Survival was 71%, 29%, 86%, and 57% in groups 1, 2, 3, and 4. Return of spontaneous circulation was regained only by initial administration of epinephrine alone or in combination with Intralipid(®). Piglets receiving the combination therapy survived without further epinephrine support. In contrast, in groups 2 and 4, return of spontaneous circulation was only achieved after secondary epinephrine rescue.. In cardiac arrest caused by bupivacaine intoxication, first-line rescue with epinephrine and epinephrine + Intralipid(®) was more effective with regard to survival than Intralipid(®) alone and vasopressin + Intralipid(®) in this pig model.

Topics: Anesthetics, Local; Animals; Blood Gas Analysis; Blood Pressure; Bupivacaine; Cardiopulmonary Resuscitation; Chromatography, High Pressure Liquid; Dose-Response Relationship, Drug; Electrocardiography; Emulsions; Epinephrine; Female; Heart Arrest; Male; Mass Spectrometry; Phospholipids; Soybean Oil; Survival Analysis; Swine; Tachycardia, Ventricular; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

The aim of the present study was to investigate the protective effect of various doses of exogenous vasopressin (AVP) against ischemia-reperfusion injury in anesthetized rat heart. Anesthetized rats were randomly divided into seven groups (n=4-13) and all of them subjected to prolonged 30 min regional ischemia and 120 min reperfusion. Group I served as saline control with ischemia, in treatment groups II, III, IV and V, respectively different doses of AVP (0.015, 0.03, 0.06 and 1.2 μg/rat) were infused within 10 min prior to ischemia, in group VI, an AVP-selective V1 receptor antagonist (SR49059, 1mg/kg, i.v.) was administrated prior to effective dose of AVP injection and in group VII, SR49059 (1 mg/kg, i.v.) was only administrated prior to ischemia. Various doses of AVP significantly prevented the decrease in heart rate (HR) at the end of reperfusion compared to their baseline and decreased infarct size, biochemical parameters [LDH (lactate dehydrogenase), CK-MB (creatine kinase-MB) and MDA (malondialdehyde) plasma levels], severity and incidence of ventricular arrhythmia, episodes and duration of ventricular tachycardia (VT) as compared to control group. Blockade of V1 receptors by SR49059 attenuated the cardioprotective effect of AVP on ventricular arrhythmias and biochemical parameters, but partially returned infarct size to control. AVP 0.03 μg/rat was known as effective dose. Our results showed that AVP owns a cardioprotective effect probably via V1 receptors on cardiac myocyte against ischemia/reperfusion injury in rat heart in vivo.

Topics: Anesthesia; Animals; Antidiuretic Hormone Receptor Antagonists; Arrhythmias, Cardiac; Blood Pressure; Cardiotonic Agents; Creatine Kinase, MB Form; Dose-Response Relationship, Drug; Electrocardiography; Heart Rate; Hemodynamics; Indoles; L-Lactate Dehydrogenase; Male; Malondialdehyde; Models, Animal; Myocardial Reperfusion Injury; Pyrrolidines; Rats; Tachycardia, Ventricular; Time Factors; Vasopressins

A 14-year-old boy with catecholamine-induced polymorphic ventricular tachycardia was treated for hypoxic brain injury after a 25-minute ventricular tachycardia arrest. He had been treated by the local paediatric cardiology service with ?-blockers for syncopal events related to episodes of ventricular tachycardia. As standard inotropic support was contraindicated, he was treated for hypoxic brain injury, with targeting of brain tissue oxygen levels (PtO2) with vasopressin. He was extubated after 7 days and discharged home with an automatic implantable cardioverter defibrillator, with no neurological sequelae. PtO2 is a reliable and effective clinical assessment tool that can aid in the management of patients with significant cerebral injury. Vasopressin proved a valuable adjunct in treatment of hypoxic brain injury when inotropic agents were contraindicated.

Topics: Adolescent; Brain; Catecholamines; Heart Arrest; Humans; Hypoxia, Brain; Intracranial Pressure; Male; Oxygen Consumption; Tachycardia, Ventricular; Vasoconstrictor Agents; Vasopressins

An increasing body of evidence from laboratory and clinical studies suggests that vasopressin may represent a promising alternative vasopressor for use during cardiac arrest and resuscitation. Current guidelines for cardiopulmonary resuscitation recommend the use of adrenaline (epinephrine), with vasopressin considered only as a secondary option because of limited clinical data.. The present study was conducted in a prehospital setting and included patients with ventricular fibrillation or pulseless ventricular tachycardia undergoing one of three treatments: group I patients received only adrenaline 1 mg every 3 minutes; group II patients received one intravenous dose of arginine vasopressin (40 IU) after three doses of 1 mg epinephrine; and patients in group III received vasopressin 40 IU as first-line therapy. The cause of cardiac arrest (myocardial infarction or other cause) was established for each patient in hospital.. A total of 109 patients who suffered nontraumatic cardiac arrest were included in the study. The rates of restoration of spontaneous circulation and subsequent hospital admission were higher in vasopressin-treated groups (23/53 [45%] in group I, 19/31 [61%] in group II and 17/27 [63%] in group III). There were also higher 24-hour survival rates among vasopressin-treated patients (P < 0.05), and more vasopressin-treated patients were discharged from hospital (10/51 [20%] in group I, 8/31 [26%] in group II and 7/27 [26%] group III; P = 0.21). Especially in the subgroup of patients with myocardial infarction as the underlying cause of cardiac arrest, the hospital discharge rate was significantly higher in vasopressin-treated patients (P < 0.05). Among patients who were discharged from hospital, we found no significant differences in neurological status between groups.. The greater 24-hour survival rate in vasopressin-treated patients suggests that consideration of combined vasopressin and adrenaline is warranted for the treatment of refractory ventricular fibrillation or pulseless ventricular tachycardia. This is especially the case for those patients with myocardial infarction, for whom vasopressin treatment is also associated with a higher hospital discharge rate.

Topics: Adult; Aged; Ambulatory Care; Cardiopulmonary Resuscitation; Cohort Studies; Female; Heart Arrest; Humans; Male; Middle Aged; Prospective Studies; Survival Rate; Tachycardia, Ventricular; Treatment Outcome; Vasopressins; Ventricular Fibrillation