Angina Pectoris in Emergency Medicine Medication

  • Author: Marc D Haber, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
Updated: Feb 18, 2015

Medication Summary

The goal of all of the following medications is either to improve myocardial oxygen and glucose supply or to reduce myocardial oxygen and glucose demand.

The use of thrombolytics in unstable angina and NSTEMI are not useful and potentially harmful. They should be reserved for use in STEMI when indicated.[23] (For more information, see American College of Cardiology Clinical Statements/Guidelines.)


Anti-platelet agents

Class Summary

These agents inhibit platelet aggregation.

Aspirin (Anacin, Bayer Aspirin, Ascriptin)


Aspirin inhibits platelet cyclooxygenase-1, which blocks the formation of thromboxane A2, thus inhibiting platelet aggregation. Aspirin is arguably the most cost-effective medication in medicine.

Clopidogrel (Plavix)


Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

May have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis not only through inhibition of platelet function but also through changes in the hemorrhagic profile.

May have additive effect when used in combination with aspirin. Useful alternative therapy in patients with a salicylate allergy.

Ticlopidine (Ticlid)


A thienopyridine that irreversibly alters the platelet membrane and inhibits platelet aggregation. Second-line antiplatelet therapy for patients who cannot tolerate or fail aspirin therapy. Toxicity includes neutropenia and diarrhea.



Class Summary

These agents relieve chest discomfort by improving myocardial oxygen supply, which, in turn, dilate epicardial and collateral vessels, improving blood supply to the ischemic myocardium.

Nitroglycerin topical (Nitro-Bid, Deponit)


Reduces preload and ventricular pressures, thus reducing myocardial oxygen demand. NTG also promotes coronary vasodilatation, which promotes improved myocardial blood flow. Reflex tachycardia may be harmful, concomitant beta-blocker usage may offset this reaction.



Class Summary

These agents reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.

Morphine sulfate (Astramorph, MS Contin, MSIR)


Reduces pain and possibly anxiety associated with angina pectoris. Use judiciously in setting of hypotension.


Beta-adrenergic blockers

Class Summary

This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand, secondary to elevations in heart rate and inotropy.

Metoprolol (Lopressor, Toprol XL)


These agents decrease myocardial oxygen demand by reducing heart rate, contractility, and arterial pressure. Shown to improve survival in patients with MI.


Calcium channel blockers

Class Summary

When beta-blockade is contraindicated in the setting of continuing angina, a nondihydropyridine calcium antagonist (eg, verapamil, diltiazem) may be used as initial therapy in the absence of severe LV dysfunction or other contraindications (see ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).

Though controversial, long-acting nifedipine may have some benefit in stable angina.[24]

Verapamil (Calan SR, Covera-HS, Verelan)


During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.

Diltiazem (Cardizem CD, Dilacor, Tiazac)


During depolarization, inhibits the influx of extracellular calcium across both the myocardial and vascular smooth muscle cell membranes. Serum calcium levels remain unchanged. The resultant decrease in intracellular calcium inhibits the contractile processes of myocardial smooth muscle cells, resulting in dilation of the coronary and systemic arteries and improved oxygen delivery to the myocardial tissue.

Decreases conduction velocity in AV node. Also increases refractory period via blockade of calcium influx. This, in turn, stops reentrant phenomenon.

Decreases myocardial oxygen demand by reducing peripheral vascular resistance, reducing heart rate by slowing conduction through SA and AV nodes, and reducing LV inotropy.



Class Summary

Anticoagulants interfere with platelet aggregation and clot formation thus reducing arterial clot burden and promoting continued myocardial oxygen and glucose delivery. These agents do not digest present clots, they help prevent secondary formation during and after spontaneous fibrinolysis. Often, the decision of when and which anticoagulant to use is decided jointly by the emergency physician and cardiologist.



Unfractionated heparin potentiates the effect of antithrombin, an enzyme that inactivates factors IIa, IXa, and Xa. This leads to an anticoagulant effect. Because of a relatively narrow therapeutic window, laboratory monitoring is required.

Enoxaparin (Lovenox)


Low molecular weight heparin produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). Binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin).

Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Advantages include intermittent dosing and decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing.

LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa compared with UFH.


Platelet aggregation inhibitors

Class Summary

These agents block the GP IIb/IIIa receptor on platelets. Once the platelet is activated, these receptors change configuration, facilitating fibrinogen and ligand binding. GP IIb/IIIa receptor binding of fibrinogen is the final step leading to platelet aggregation. Thus, these agents stymie platelet aggregation.

Abciximab (ReoPro)


Chimeric human-murine monoclonal antibody approved for use in elective/urgent/emergent percutaneous coronary intervention. Binds to receptor with high affinity and reduces platelet aggregation by 80% for up to 48 h following infusion.

Eptifibatide (Integrilin)


Antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, which reversibly prevents von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP IIb/IIIa receptor. Inhibits platelet aggregation. Effects persist over duration of maintenance infusion and are reversed when infusion ends.

Tirofiban (Aggrastat)


Nonpeptide antagonist of GP IIb/IIIa receptor. Reversible antagonist of fibrinogen binding. When administered IV, more than 90% of platelet aggregation inhibited. Approved for use in combination with heparin for patients with unstable angina who are being treated medically and for those undergoing PCI.



Promotes a higher PaO2, thus improving myocardial oxygen delivery

Contributor Information and Disclosures

Marc D Haber, MD Assistant Professor, Department of Emergency Medicine, Tufts University School of Medicine; Clinical Associate of Radiology, Baystate Medical Center; Past President of Young Physician Section, AAEM

Marc D Haber, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Radiology, Radiological Society of North America, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Thomas A Brunell, MD, MA, FACEP, FAAEM Director, Emergency Medicine Education, St Francis Hospital and Medical Center; Assistant Professor of Traumatology and Emergency Medicine, University of Connecticut Medical Center

Thomas A Brunell, MD, MA, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Massachusetts Medical Society, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Jerry R Balentine, DO, FACEP, FACOEP Vice President, Medical Affairs and Global Health, New York Institute of Technology; Professor of Emergency Medicine, New York Institute of Technology College of Osteopathic Medicine

Jerry R Balentine, DO, FACEP, FACOEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, American College of Osteopathic Emergency Physicians, American Association for Physician Leadership, American Osteopathic Association

Disclosure: Nothing to disclose.

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