enalapril and Shock--Cardiogenic

enalapril has been researched along with Shock--Cardiogenic* in 4 studies

Other Studies

4 other study(ies) available for enalapril and Shock--Cardiogenic

ArticleYear
The use of low-dose insulin in cardiogenic shock due to combined overdose of verapamil, enalapril and metoprolol.
    Cardiology, 2006, Volume: 106, Issue:4

    We describe a case of severe heart failure due to the combined effect of verapamil and enalapril overdose in a patient treated regularly with metoprolol. The patient was dependent for 2 days on glucagon and dopamine infusion but remained oliguric, with deteriorating renal function. Marked improvement in all hemodynamic parameters was noted a short time after initiation of treatment with low-dose insulin infusion (1-2 units/h), which allowed the prompt withdrawal of glucagon and dopamine. We discuss the efficacy of glucose-insulin treatment in toxic cardiac depression and suggest that a low dose may be beneficial in similar cases.

    Topics: Antihypertensive Agents; Drug Synergism; Enalapril; Female; Humans; Hypoglycemic Agents; Insulin; Metoprolol; Middle Aged; Shock, Cardiogenic; Vasodilator Agents; Verapamil

2006
Partial left ventriculectomy: preoperative risk factors for perioperative mortality.
    International journal of cardiology, 1998, Dec-01, Volume: 67, Issue:2

    This study aimed at determining risk factors for perioperative mortality for patients undergoing partial left ventriculectomy. Fourteen patients with end-stage congestive heart failure underwent partial ventriculectomy at our institution from February, 1995 to October, 1997. Mean age was 48+/-11 years, symptoms duration 44+/-34 months, New York Heart Association symptoms score 4+/-0, systolic blood pressure 97.69+/-20.06 mmHg, diastolic blood pressure 65.38+/-13.91 mmHg, heart rate 91+/-15 beats/min, furosemide daily dose 121.66+/-96.65 mg and captopril daily dose 68.75+/-76.76 mg. Seven (50%) patients needed inotropic support for hemodynamic stabilization. On echocardiography, left ventricular diastolic dimension was 81.71+/-11.92 mm. Left ventricular ejection fraction determined by radionuclide ventriculography or echocardiography was 16.71+/-5.13. At heart catheterization, mean right atrial pressure was 12.50+/-7.72 mmHg, mean pulmonary capillary wedge pressure 23.60+/-7.79 mmHg, and mean pulmonary artery pressure 34.10+/-12.81 mmHg. Twelve patients had idiopathic dilated cardiomyopathy and two patients had a globally dilated heart with single vessel coronary artery disease. Aneurysmectomy, mitral valve surgery or coronary artery bypass surgery were not performed in any patient. Four (28%) patients died: three in the operating theatre and one from low output syndrome 2 days after surgery. The proportion of patients operated on with cardiogenic shock was four (100%) in nonsurvivors and 0% in survivors (P=0.001). Inotropic support was necessary in three (30%) survivors and in four (100%) nonsurvivors (P=0.06). Thus, preoperative hemodynamic instability may be associated with perioperative mortality after partial left ventriculectomy.

    Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Captopril; Cardiac Surgical Procedures; Cardiomyopathy, Dilated; Diuretics; Echocardiography; Electrocardiography; Enalapril; Female; Furosemide; Heart Failure; Heart Ventricles; Hemodynamics; Humans; Male; Middle Aged; Perioperative Care; Postoperative Complications; Preoperative Care; Risk Factors; Shock, Cardiogenic

1998
Hemodynamics of pancreatic ischemia in cardiogenic shock in pigs.
    Gastroenterology, 1997, Volume: 113, Issue:3

    Previous studies have shown that the renin-angiotensin axis plays a pivotal role in vasoconstriction of the gastric, intestinal, and hepatic circulations during cardiogenic shock. The aim of this study was to evaluate the fundamental hemodynamic mechanism of pancreatic ischemia during cardiogenic shock induced by pericardial tamponade.. Cardiogenic shock was induced by pericardial tamponade. Cardiac output (and total peripheral vascular resistance) was determined by thermodilution. Pancreatic blood flow (and vascular resistance) was determined with radiolabeled microspheres.. Graded increases in pericardial pressure produced corresponding decreases in cardiac output to 42% +/- 1% and arterial pressure to 67% +/- 3% of baseline and increases in total peripheral vascular resistance to 146% +/- 5% of baseline. Pancreatic blood flow decreased disproportionately to 30% +/- 3% of baseline, because of a disproportionate increase in pancreatic vascular resistance to 220% +/- 19% of baseline. Previously confirmed blockade of the renin-angiotensin axis ablated this response, whereas confirmed blockade of the alpha-adrenergic system or vasopressin system had no significant effect. Without shock, central intravenous infusions of angiotensin II closely mimicked this selective vasoconstriction.. Angiotensin-mediated selective pancreatic vasoconstriction results in significant pancreatic ischemia during cardiogenic shock.

    Topics: Adrenergic alpha-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Animals, Newborn; Cardiac Tamponade; Enalapril; Hemodynamics; Ischemia; Pancreas; Phenoxybenzamine; Regional Blood Flow; Shock, Cardiogenic; Swine

1997
Mesenteric vasoconstriction in cardiogenic shock in pigs.
    Gastroenterology, 1992, Volume: 102, Issue:6

    The quantitative impact of mesenteric vasoconstriction on the systemic hemodynamic response to cardiogenic shock induced by pericardial tamponade was evaluated. Graded increases in pericardial pressure produced corresponding decreases in cardiac output to 44% +/- 2% and arterial pressure to 64% +/- 3% of baseline and increases in total peripheral vascular resistance to 131% +/- 4% of baseline. Total mesenteric blood flow decreased disproportionately, to 28% +/- 3% of baseline, because of a disproportionate increase in mesenteric vascular resistance to 223% +/- 6% of baseline. Nonmesenteric vascular resistance increased only to 119% +/- 4% of baseline. Thus mesenteric vasoconstriction accounted for 42% of the increase in total peripheral resistance. Prior blockade of the renin-angiotensin axis ablated this response and eliminated the mesenteric contribution to systemic vascular resistance, while confirmed blockade of the alpha-adrenergic system or vasopressin system had no effect. Without shock, central intravenous infusions of angiotensin II (but not norepinephrine or vasopressin) closely mimicked this selective vasoconstriction. Angiotensin-mediated selective mesenteric vasoconstriction accounts for more than 40% of the overall increase in systemic vascular resistance in cardiogenic shock.

    Topics: Animals; Cardiac Tamponade; Enalapril; Mesenteric Arteries; Mesenteric Veins; Phenoxybenzamine; Shock, Cardiogenic; Swine; Vascular Resistance; Vasoconstriction

1992