Medication SummaryVasopressors 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. Show
Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output. 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. Inotropic AgentsClass SummaryThese agents augment coronary and cerebral blood flow during the low-flow state associated with cardiogenic shock. They also improve cardiac output in refractory hypotension and shock. Norepinephrine (Levophed)
Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic blood pressure < 70 mm Hg) or hypotension unresponsive to other medication. Dopamine
Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction. Dobutamine
Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It produces systemic vasodilation and increases the inotropic state. Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia. Milrinone
Milrinone is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with positive inotropic and vasodilator effects; it has little chronotropic activity. This agent's mode of action differs from that of either digitalis glycosides or catecholamines. Inamrinone
Formerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity. It produces vasodilation and increases the inotropic state. Inamrinone is more likely to cause tachycardia than is dobutamine, and it may exacerbate myocardial ischemia. VasodilatorsClass SummaryVasodilators decrease preload and/or afterload. Nitroglycerin IV
This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in preload and blood pressure (ie, afterload). Antiplatelet Agents, CardiovascularClass SummaryAgents that irreversibly inhibit platelet aggregation may improve morbidity. Aspirin (Anacin, Ascriptin Regular Strength, Bayer Aspirin Regimen Regular, Bufferin, Ecotrin)
Aspirin is an odorless, white, powdery substance available in 81 mg, 325 mg, and 500 mg, for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids. It is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid derivatives. The acetyl group is responsible for inactivation of cyclo-oxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics. Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclo-oxygenase. This, in turn, inhibits the conversion of arachidonic acid to prostaglandin 12 (a potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (a potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for the life of the cell (approximately 10 d). Aspirin may be used at a low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. It reduces the likelihood of myocardial infarction (MI) and is also very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute MI may reduce cardiac mortality in the first month. Opioid AnalgesicsClass SummaryAnalgesics reduce pain, which decreases sympathetic stress and provides some preload reduction. Morphine sulfate (Duramorph, Astramorph, MS Contin, Kadian, Oramorph SR)
Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various intravenous doses are used; the drug is commonly titrated until the desired effect is achieved. Diuretics, LoopClass SummaryThese drugs cause diuresis to decrease plasma volume and edema and thereby decrease cardiac output and, consequently, blood pressure. The initial decrease in cardiac output causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, extracellular fluid and plasma volumes return almost to pretreatment levels. Peripheral vascular resistance decreases below that of the pretreatment baseline. Furosemide (Lasix)
Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule. Individualize the dose to the patient. Depending on the response, administer furosemide at increments of 20-40mg no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants, titrate the drug in increments of 1mg/kg/dose until a satisfactory effect is achieved. Cardiovascular, OtherClass SummaryThese drugs cause arterial and venous dilation by binding to the cyclic guanosine monophosphate (GMP) receptors on vascular smooth muscle, causing smooth muscle relaxation. Natriuretic peptides produce dose-dependent decreases in pulmonary capillary wedge pressure and systemic arterial pressure. Nesiritide (Natrecor)
Nesiritide is a recombinant deoxyribonucleic acid (DNA) form of human B-type natriuretic peptide (hBNP), which dilates veins and arteries. Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to the receptor causes an increase in cyclic GMP, which serves as a second messenger to dilate veins and arteries. Pulmonary capillary wedge pressure is reduced and dyspnea is improved in patients with acutely decompensated congestive heart failure. Nesiritide may be considered in the treatment of patients with cardiogenic shock. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains US Food and Drug Administration (FDA) approval. However, it should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.
Author Coauthor(s) Andrew Lenneman, MD Associate Professor of Medicine (Cardiovascular Disease, Scientist, Comprehensive Cardiovascular Center, University of Alabama School of Medicine Disclosure: Nothing to disclose. Chief Editor Henry H Ooi, MD, MRCPI 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. Acknowledgements Ethan S Brandler, MD, MPH Clinical Assistant Professor, Attending Physician, Departments of Emergency Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital Ethan S Brandler, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US Disclosure: Nothing to disclose. Mark A Hostetler, MD, MPH Associate Professor of Pediatrics, University of Chicago; Chief, Section of Emergency Medicine, Department of Pediatrics, Medical Director of Pediatric Emergency Department, University of Chicago Children's Hospital Disclosure: Nothing to disclose. A Antoine Kazzi MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon A Antoine Kazzi is a member of the following medical societies: American Academy of Emergency Medicine Disclosure: Nothing to disclose. 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. 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 Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association Disclosure: Nothing to disclose. Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine 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 Which type of heart failure would indicate the need for nesiritide Natrecor to be administered?NATRECOR (nesiritide) is indicated for the treatment of patients with acutely decompensated heart failure who have dyspnea at rest or with minimal activity.
Which medication would be prescribed to reduce preload for a patient with heart failure?Nitroglycerin IV (Nitro-Bid, Minitran, Nitrostat)
NTG is the drug of choice (DOC) for patients who are not hypotensive. It provides excellent and reliable preload reduction, and high dosages provide mild afterload reduction.
Which medication is a negative Chronotropic agent used to treat acute heart failure?Digoxin has a negative chronotropic action on the sinus node and decreases the cardiac rate, especially in patients with heart failure.
Which clinical manifestation is first to be observed in children who may be developing digoxin toxicity?In infants and small children, the earliest signs of overdose are changes in the rate and rhythm of the heartbeat. Children may not show the other symptoms as soon as adults.
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Which effect is expected when administering a vasodilator to a patient in acute heart failure
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