pituitrin and esmolol

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

A rapid increase in the end-tidal concentration of desflurane to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating epinephrine and vasopressin concentrations. We hypothesized that drugs that block sympathetic activity or decrease sympathetic outflow (an opioid, a beta-adrenergic antagonist, and an alpha 2-adrenergic agonist) would blunt these responses.. After induction of anesthesia with intravenous propofol 2 mg/kg in ten healthy male volunteers age 25 +/- 1 yr (mean +/- standard error), anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. Controlled ventilation provided normocapnia. We then increased the end-tidal desflurane concentration within 1 min to 8% (1.1 MAC) and maintained this concentration for 10 min. On separate days, five of these volunteers were similarly anesthetized except that 5 min before the increase to 8% desflurane, we administered intravenous fentanyl 1.5 micrograms/kg and on another day 4.5 micrograms/kg (dose randomly assigned). On 2 separate days, intravenous esmolol 0.75 mg/kg was given to five volunteers 1.5 min before, or clonidine 4.3 micrograms/kg by mouth to four volunteers 90 min before, the increase from 4% to 8% desflurane.. Without pretreatment, the increase to 8% desflurane increased heart rate (from 57 +/- 2 to 118 +/- 6 beats/min at peak, mean +/- standard error) and mean arterial blood pressure (from 66 +/- 2 to 118 +/- 5 mmHg). At the time of peak hemodynamic changes (within 1-2 min of the increase in desflurane concentration), plasma epinephrine and norepinephrine concentrations increased (from 22 +/- 6 to 339 +/- 83 pg/ml and from 205 +/- 19 to 283 +/- 30 pg/ml, respectively). Fentanyl 1.5 and 4.5 micrograms/kg attenuated the heart rate increase by 61 +/- 14% and 70 +/- 7% and the mean arterial blood pressure increase by 31 +/- 16% and 46 +/- 11% but did not alter the epinephrine or norepinephrine response at the time of peak cardiovascular changes. Esmolol attenuated the heart rate response but no other response. Clonidine attenuated all responses except that of norepinephrine and also caused postanesthesia sedation.. Fentanyl, esmolol, and clonidine blunt the transient cardiovascular response to a rapid increase in desflurane concentration. Fentanyl may be the most clinically useful of these drugs because it blunts the increase in heart rate and blood pressure, has minimal cardiovascular depressant effects, and imposes little postanesthetic sedation.

Topics: Adrenergic beta-Antagonists; Anesthesia, Inhalation; Anesthetics; Blood Pressure; Chromatography, High Pressure Liquid; Clonidine; Desflurane; Dose-Response Relationship, Drug; Epinephrine; Fentanyl; Heart Rate; Humans; Injections, Intravenous; Isoflurane; Male; Norepinephrine; Propanolamines; Vasopressins

Long-term survival after cardiac arrest (CA) due to shock-refractory ventricular fibrillation (VF) is low. Clearly, there is a need for new pharmacological interventions in the setting of cardiopulmonary resuscitation (CPR) to improve outcome. Here, hemodynamic parameters and cardiac damage are compared between the treatment group (milrinone, esmolol and vasopressin) and controls (vasopressin only) during resuscitation from prolonged CA in piglets.. A total of 26 immature male piglets were subjected to 12-min VF followed by 8-min CPR. The treatment group (n=13) received i.v. (intravenous) boluses vasopressin 0.4 U/kg, esmolol 250 μg/kg and milrinone 25 μg/kg after 13 min, followed by i.v. boluses esmolol 375 μg/kg and milrinone 25 μg/kg after 18 min and continuous esmolol 15 μg/kg/h infusion during 180 min reperfusion, whereas controls (n=13) received equal amounts of vasopressin and saline. A 200 J monophasic counter-shock was delivered to achieve resumption of spontaneous circulation (ROSC) after 8 min CPR. If ROSC was not achieved, another 200 J defibrillation and bolus vasopressin 0.4 U/kg would be administered in both groups. Direct current shocks at 360 J were applied as one shot per minute over maximally 5 min. Hemodynamic variables and troponin I as a marker of cardiac injury were recorded.. Troponin I levels after 180 min reperfusion were lower in the treatment group than in controls (P<0.05). The treatment group received less norepinephrine (P<0.01) and had greater diuresis (P<0.01). There was no difference in survival between groups.. The combination of milrinone, esmolol and vasopressin decreased cardiac injury compared with vasopressin alone.

Topics: Acid-Base Equilibrium; Adrenergic beta-Antagonists; Animals; Cardiopulmonary Resuscitation; Cardiotonic Agents; Fluid Therapy; Heart Arrest; Heart Diseases; Male; Milrinone; Myocardium; Propanolamines; Survival Analysis; Swine; Troponin I; Vasoconstrictor Agents; Vasopressins

The aim of this study was to determine the influence of different therapeutic interventions and positions on catecholamine and vasopressin levels in the pneumoperitoneum (PN) in a porcine model.. In 43 pigs, a 14-mm-Hg PN was established and plasma concentrations of epinephrine, norepinephrine and vasopressin were measured in head-up, supine and head-down positions. Additionally, the effects of the following changes were studied: (1) increase in intrathoracic blood volume (ITBV) by means of hydroxyethyl starch infusion; (2) vasodilatation induced by sodium nitroprusside, or (3) selective sympathicolysis induced by esmolol. Again, catecholamines (ELISA) and vasopressin (RIA) were determined.. After PN, epinephrine levels did not significantly increase in the head-up position (p = 0.075) and remained also unchanged in the supine or head-down position. Plasma norepinephrine statistically significantly decreased in the head-up position (p = 0.046). Vasopressin concentrations remained unaltered. After increased ITBV, neither catecholamine nor vasopressin concentrations changed in any body position. Application of sodium nitroprusside or esmolol caused no changes.. Changes in endogenous catecholamine levels safely prevent cardiocirculatory instability in small pigs. Volume substitution might reduce endocrine responses to PN in the head-up position.

Topics: Animals; Epinephrine; Head-Down Tilt; Hemodynamics; Laparoscopy; Models, Animal; Nitroprusside; Norepinephrine; Pneumoperitoneum, Artificial; Posture; Propanolamines; Supine Position; Swine; Vasopressins

A 52-year-old woman with hypertension and Graves' disease was scheduled for surgical removal of a meningioma. Intraoperative events were significant for hypotension requiring a vasopressin infusion. Prophylactic dolasetron was administered to the patient before emergence. The patient's trachea was easily extubated and she was neurologically intact at the end of the surgical procedure. On transport to the neurological intensive care unit, the patient developed torsades de pointes, requiring cardiopulmonary resuscitation, before a return to normal sinus rhythm.

Topics: Adrenergic beta-Antagonists; Amiodarone; Anti-Arrhythmia Agents; Antiemetics; Cardiopulmonary Resuscitation; Electrocardiography; Female; Follow-Up Studies; Graves Disease; Humans; Hypertension; Hypotension; Indoles; Intraoperative Complications; Intubation, Intratracheal; Meningeal Neoplasms; Meningioma; Middle Aged; Postoperative Complications; Propanolamines; Quinolizines; Risk Factors; Torsades de Pointes; Vasoconstrictor Agents; Vasopressins