Cardiogenic Shock Medication

  • Author: Andrew Lenneman, MD; Chief Editor: Henry H Ooi, MBBCh   more...
 
Updated: Aug 25, 2011
 

Medication Summary

Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.

Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output. Adequate pain control is essential for quality patient care and patient comfort. Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.

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Vasopressors/inotropic agents

Class Summary

Augment coronary and cerebral blood flow during low-flow state associated with cardiogenic shock.

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Dopamine (Intropin)

 

Stimulates adrenergic and dopaminergic receptors. Hemodynamic effect depends on dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.

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Dobutamine (Dobutrex)

 

Sympathomimetic amine with stronger beta than alpha effects. Produces systemic vasodilation and increases the inotropic state. Higher doses may cause increase in heart rate, exacerbating myocardial ischemia.

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Phosphodiesterase enzyme inhibitors

Class Summary

Induce peripheral vasodilation and provide inotropic support.

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Milrinone (Primacor)

 

Positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from either cardiac glycosides (digoxin) or catecholamines.

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Inamrinone (Inocor)

 

Formerly known as amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.

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Vasodilators

Class Summary

Decrease preload and/or afterload.

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Nitroglycerin IV (Nitro-Bid)

 

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in preload and blood pressure (ie, afterload).

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Analgesics

Class Summary

Reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.

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Morphine sulfate (Duramorph, Astramorph, MS Contin)

 

DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used, commonly titrated until desired effect is achieved.

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Diuretics

Class Summary

Decrease plasma volume and peripheral edema. Excessive reduction in plasma volume and stroke volume associated with diuresis may decrease cardiac output and, consequently, blood pressure.

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Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Individualize dose to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until satisfactory effect is achieved.

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Contributor Information and Disclosures
Author

Andrew Lenneman, MD 

Disclosure: Nothing to disclose.

Coauthor(s)

Henry H Ooi, MBBCh  Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Russell F Kelly  MD, Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald J Oudiz, MD, FACP, FACC, FCCP  Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society

Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MBBCh  Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Sat Sharma, MD, FRCPC, and Michael E Zevitz, MD, to the original writing and development of this article.

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This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient subsequently developed cardiogenic shock.
ECG tracing shows further evolutionary changes in a patient with cardiogenic shock.
ECG tracing in a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.
Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery. Following angioplasty of the critical stenosis, coronary flow is reestablished. The patient recovered from cardiogenic shock.
Echocardiogram image from a patient with cardiogenic shock shows enlarged cardiac chambers; the motion study showed poor left ventricular function. Courtesy of R. Hoeschen, MD.
 
 
 
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