Angina Pectoris in Emergency Medicine 

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



Angina pectoris (AP) represents the clinical syndrome occurring when myocardial oxygen demand exceeds supply. The term is derived from Latin; the literal meaning is "the choking of the chest;" angere, meaning "to choke" and pectus, meaning "chest." The first English-written account of recurrent angina pectoris was by English nobleman Edward Hyde, Earl of Clarendon. He described his father as having, with exertion, "a pain in the left arm…so much that the torment made him pale".[1] The first description of angina as a medical disorder came from William Heberden. Heberden, a prodigious physician, made many noteworthy contributions to medicine during his career. He presented his observations on "dolor pectoris" to the Royal College of Physicians in 1768. Much of his classic description retains its validity today.[2]

Angina pectoris has a wide range of clinical expressions. The symptoms most often associated to angina pectoris are substernal chest pressure or tightening, frequently with radiating pain to the arms, shoulders, or jaw. The symptoms may also be associated with shortness of breath, nausea, or diaphoresis. Symptoms stem from inadequate oxygen delivery to myocardial tissue. No definitive diagnostic tools that capture all patients with angina pectoris exist. This, combined with its varied clinical expression, makes angina pectoris a distinct clinical challenge to the emergency physician. The disease state can manifest itself in a variety of forms, including the following:

  • Stable angina pectoris is classified as a reproducible pattern of anginal symptoms that occur during states of increased exertion.

  • Unstable angina pectoris (UA) manifests either as an increasing frequency of symptoms or as symptoms occurring at rest.

  • Prinzmetal angina or variant angina occurs as a result of transient coronary artery spasms. These spasms can occur either at rest or with exertion. Unlike stable or unstable angina, no pathological plaque or deposition is present within the coronary arteries that elicits the presentation. On angiography, the coronary arteries are normal in appearance with spasm on angiography.

  • Cardiac syndrome X occurs when a patient has all of the symptoms of angina pectoris without coronary artery disease or spasm.


The past 2 decades has greatly expanded our overall understanding of the pathophysiology of myocardial ischemic syndromes. The primary dysfunction in angina pectoris is decreased oxygen delivery to myocardial muscle cells. The 2 predominant mechanisms by which delivery is impaired appear to be coronary artery narrowing and endothelial dysfunction. Any other mechanism that affects oxygen delivery can also precipitate symptoms.

Extracardiac causes of angina include, but are by no means limited to, anemia, hypoxia, hypotension, bradycardia, carbon monoxide exposure, and inflammatory disorders.[3] The end result is a shift to anaerobic metabolism in the myocardial cells. This is followed by a stimulation of pain receptors that innervate the heart. These pain receptors ultimately are referred to afferent pathways, which are carried in multiple nerve roots from C7 through T4. The referred/radiating pain of angina pectoris is believed to occur because these afferent pathways also carry pain fibers from other regions (eg, the arm, neck, and shoulders).

Coronary artery narrowing

Coronary artery narrowing appears to be the etiology of cardiac ischemia in the preponderance of cases. This has clinical significance when atherosclerotic disease diminishes or halts blood flow through the coronary arterial circulation, interfering with normal laminar blood flow. The significance of even a small change in the diameter of a blood vessel can be profound. The Poiseuille law predicts this outcome—the rate of flow is decreased exponentially by any change in the radius of the lumen. As with a smaller pediatric airway, even relatively minute changes in diameter have dramatic consequences in flow rates. Thus, when a lumen is narrowed by one fifth, the flow rate is decreased by about one half. This predicts that even a small change in a coronary artery plaque size can affect the oxygenation through that vessel's territory.

The epicardial vessel, where atherosclerosis often takes place, has the capacity to dilate via autoregulatory mechanisms to respond to increased demand. Angina occurs as this compensatory mechanism is overwhelmed either by large plaques (typically considered 70% or greater obstruction) or by significantly increased myocardial demand.[4]

Endothelial factors

Endothelial factors also play an important role in angina pectoris. During sympathetic stimulation, the endothelium is subjected to mediators of both vasoconstriction and vasodilatation. Alpha-agonists (catecholamines) directly cause vasoconstriction, while endothelial nitrous oxide synthase creates nitrous oxide (NO), which counteracts this constricting force via vasodilatation.

In the diseased coronary artery, NO production is reduced or absent. In this setting, the catecholamine drive can overwhelm the autoregulatory mechanisms. In addition, the endothelium of the plaque-laden artery may, in itself, be dysfunctional. This limits the ability of the intra-arterial endothelium to produce mediators, which, in a healthy artery, would protect against further vasoconstriction, assist dilatation, and provide protection from platelet aggregation. Small lesions in these vessels may produce incompletely obstructing aggregates of platelets. This would further impede flow through the affected vessel.[4]

In the diseased heart, these 2 factors, coronary artery narrowing and endothelial dysfunction, synergistically result in reduced oxygen delivery to the myocardium. The net result is angina pectoris.

Extrinsic factors

Extrinsic factors can also play a role in specific circumstances. The oxygen-carrying capacity of blood is based on a number of factors. The most important of which is the amount of hemoglobin. Any alteration in the ability of blood to carry oxygen can precipitate angina. Anemia of any degree can result in anginal symptoms. Given a scenario where demand is increased, such as climbing a flight of stairs, increased stress, or even sexual intercourse, the anginal symptoms may appear.[5] Abnormal hemoglobin, such as methemoglobin, carboxyhemoglobin, or any of a number of hemoglobinopathies, creates an environment at greater risk for precipitating angina.

Other extrinsic factors that affect hemoglobin formation, such as lead poisoning or iron-deficiency states, also lead to a similar decrease in oxygen-carrying capacity. Any mechanism that impedes oxygen delivery to the red blood cells has a similar effect. Therefore, any number of pulmonary causes, such as pulmonary embolism, pulmonary fibrosis or scarring, pneumonia, or congestive heart failure, can exacerbate angina. A decreased oxygen environment, such as travel to a higher elevation, has similar consequences due to the decrease in concentration of atmospheric oxygen.

Variant angina

The etiology of variant angina is currently not well understood. Research suggests that inflammatory mediators may result in focal coronary artery vasospasm. Another possibility is that perfusion is decreased through microvascular circulation. Spasm or intermittent narrowing of this microscopic lumen may result in transient areas of hypoperfusion and oxygen deprivation.[6]

Syndrome X

Syndrome X is the triad of angina pectoris, a positive ECG stress test result, and a normal coronary angiogram. The pathophysiology of this disease is not well understood. Many theories exist as to the underlying pathology. Decreased oxygenation of the underlying myocardium may be the result of impaired vasodilatation, dysfunctional smooth muscle cells, poor or deficient microvascular circulation, or even structural problems on a cellular level (eg, an inappropriately functioning sodium ion channel).[6]



United States

An average of 3.4 million US adults older than 40 years experience angina each year. Between 2007 and 2010, there were a total of 2.3 million office visits per year for angina.[7]

About 635,000 US adults with have a new coronary event (MI or CHD death), with an estimated 300,000 experiencing recurrent events.[7]

Conservative 2010 data show 625,000 acute coronary syndrome (ACS) discharges from hospitals.[7]


The prognosis of each patient is dependent upon individual factors and the progression of their underlying disease.

The majority of coronary attacks are NOT preceded by long-standing angina pectoris (AP) (only 18%).[7]


Cardiovascular diseases, including heart disease and stroke, account for more than onethird (33.6%) of all U.S. deaths.[7]

Coronary heart disease is the single greatest killer of American men and women.[7]

In 2010, the total costs of cardiovascular diseases in the United States were estimated to be $444 billion, with treatment of these diseases accounting for about $1 of every $6 spent on US healthcare.[7]


Complications may occur from the progression of the patient's underlying disease or from failure to intervene. Unfortunately, even the testing for underlying disease (eg, stress testing, angiography) can lead to complications including progression to myocardial infarction and renal failure. The risks and benefits of testing and treatment must be determined for and discussed with each patient.


The Centers for Disease Control and Prevention (CDC) note that the prevalence of angina and/or coronary heart disease is highest and increasing in Hispanics followed by whites and black non-Hispanics (5%, 4.2%, 3.7%, respectively). This information includes the 50 US states, the District of Columbia, Puerto Rico, and the US Virgin Islands.[8, 9]


Among US adults aged 40-59 years and 80 years and older, the age-adjusted prevalence of angina pectoris (AP) is higher among women than men; in those aged 60-79 years, it is higher men than women.[7]


The incidence of new and recurrent angina increases with age but then declines at around 85 years.




Classically, angina presents as substernal chest discomfort that occurs with exertion, but it also may occur at rest. The discomfort is frequently described as a pressure or heaviness. Other commonly used adjectives for anginal pain include dull, aching, or squeezing. Pain may radiate to one or both arms, to one or both shoulders, or to the neck or jaw. Symptoms are highly variable. The entity cannot be expected to present with the classic triad of chest pressure with exertion radiating to the left arm. The diversity of disease expression is likely related to a patient's age, sex, race, and culture.

The caveat is to have a high index of suspicion for the disease. Many factors influence the expression of anginal symptoms. Familiar terms such as anginal equivalent and atypical chest pain are frequently used in these cases. In addition, systemic diseases, such as diabetes mellitus or chronic pain syndromes, may alter presenting anginal symptoms; while other diseases, such as prior cerebral vascular accident or dementia, may limit the patient's reporting of symptoms. A pain-free variant of angina—sometimes referred to as silent chest pain—also exists. These patients can present with complaints of shortness of breath, nausea, altered mentation, or abdominal pain.[10]

Chest discomfort quality

Which of the following describes the patient's chest discomfort?

  • Pain

  • Pressure

  • Squeezing

  • Dullness

  • Burning

  • Heaviness

  • Absent chest discomfort (eg, dyspnea, vomiting, altered sensorium)

Location (often diffuse to any location of C7-T4 dermatomes)

Which of the following is the site of the patient's chest pain?

  • Retrosternal or substernal

  • Inframammary

  • Left sided

  • Right sided

  • Upper abdominal

  • Shoulder, neck, arm

  • Teeth, jaw, lower face (above C7 unclear etiology)

  • Back, scapular region


Which of the following areas does the patient's chest pain radiate to?

  • Unilateral or bilateral arms

  • Unilateral or bilateral shoulders

  • Back

  • Neck

  • Jaw, ear, or lower face


Which of the following describes the temporal relationship of the chest pain?

  • Onset to maximum discomfort is progressive: With exertion (with or without increasing frequency) or at rest

  • Alleviation to relief is progressive.

  • Alleviation mediators may include oxygen, nitroglycerin, reduction of stressful activity, pain medication, and the placebo effect (eg, "GI cocktail")


Which of the following describes the patient's pain severity?

  • Mild to severe (1/10 to >10/10)

  • "Like my heart pain" - Patients in the emergency department (ED) may refer to the pain as being consistent with prior heart pains.


The physical examination may reveal signs of a hyperadrenergic state. One might observe tachycardia, tachypnea, hypertension, and/or diaphoresis. In addition, ischemia may lead to the presence of crackles due to the loss in contractility with subsequent pulmonary edema or a reduction in the S1 intensity.[11]

That said, no definitive examination findings suggest angina. Much of the information obtained from the physical examination may suggest other comorbidities that place the patient at higher risk for anginal symptoms (eg, chronic obstructive pulmonary disease [COPD], tachycardia, pale conjunctiva). Therefore, the physical examination is necessary to qualify the patient's current physical state and comorbidities. In this manner, the emergency physician obtains a baseline physical examination. Also, as mentioned, comorbid illnesses that affect the patient's level of cardiac, pulmonary, and circulatory function can be assessed.

As with many presentations to the emergency department, the physical examination in angina pectoris also serves as a marker for response to therapy. Important comorbidities that can be identified on physical examination include aortic stenosis, gastrointestinal bleeding, and airway obstruction. Unfortunately, no examination findings are pathognomonic for angina pectoris. In addition, no physical examination findings rule out the disease state.

Of note, while the reproducibility of chest wall pain with palpation may lower the likelihood of angina, this alone cannot rule out angina or myocardial infarction.[12, 13]


See Pathophysiology.



Diagnostic Considerations

As previously stated, there is no standard presentation of angina. One must be vigilant for anginal equivalents, such as breathlessness or diaphoresis, in all subgroups of patients.

No amount of testing can routinely be performed in the emergency department setting to definitively rule out angina as the cause of a patient's chest pain or suspected anginal equivalent.

Reproducible chest wall pain is found in roughly 10% of all cases of AMI.[14]

Missed MIs account for approximately 10% of malpractice claims against emergency physicians and 24% of payout.[15, 16]

Other conditions to be considered in the differential diagnosis of patients with suspected angina include the following:

  • Abdominal aortic aneurysm

  • Anxiety disorders

  • Aortic dissection

  • Boerhaave syndrome

  • Biliary colic

  • Cardiomyopathy, hypertrophic

  • Cholecystitis

  • Coronary artery atherosclerosis

  • Coronary artery vasospasm

  • Gastric ulcers

  • Gastritis, acute

  • Gastroesophageal reflux disease

  • Hiatal hernia

  • Hypercholesterolemia, familial

  • Hypercholesterolemia, polygenic

  • Hypertension

  • Hyperventilation syndrome

  • Isolated coronary artery anomalies

  • Kawasaki disease

  • Panic disorder

  • Peptic ulcer disease

  • Pericardial effusion

  • Pericarditis, acute

  • Pleurodynia

  • Pneumothorax

  • Polyarteritis nodosa

  • Pott disease (tuberculous spondylitis)

  • Pulmonary hypertension, primary

  • Pulmonary hypertension, secondary

  • Scleroderma

  • Takayasu arteritis

  • Tietze syndrome

  • Varicella-zoster virus anemia

  • Esophageal spasm

  • Pneumonia with pleural involvement

Differential Diagnoses



Laboratory Studies

The laboratory workup of patients with angina includes the following tests:

  • CBC (anemia, leukocytosis may suggest an alternative diagnosis)

  • BUN and creatinine level, if intravenous contrast is anticipated

  • Electrolyte levels are of virtually no value unless the patient is on a diuretic and concern for an abnormality exists.

  • Cardiac enzyme levels, if positive may suggest non–ST-segment elevation myocardial infarction (NSTEMI); negative results do not rule out ischemia

  • Coagulation studies, if anticoagulation or antiplatelets are anticipated

  • Type and screen, if surgery or transfusions are considered

Imaging Studies

Chest radiography is used to rule out an alternative diagnosis or contributing factors (eg, pneumothorax [PTX], pneumonia [PNA], congestive heart failure); it is also used to evaluate the aorta prior to anticoagulant administration.

CT of the chest may be considered for evaluation of aortic or pulmonary disease; if evaluating the aorta, include the abdominal aorta. Of note, the forthcoming "triple rule out CT scan" exposes the patient to an exorbitantly high dose of radiation and should only be used in certain circumstances.

Limited CT coronary scans may help to reduce the posttest probability of coronary artery disease while utilizing potentially less radiation exposure than the "triple rule out scan." Coronary artery calcification suggests the presence of an atherosclerotic plaque. Calcium scores are determined by the density of calcium and the total area. Higher calcium scores may suggest a higher risk of current or future adverse cardiac events. Multiple sites are currently conducting trials to see if this modality will benefit patients in the emergency department.

Bamberg et al found that, in patients with acute chest pain and an inconclusive initial evaluation (nondiagnostic electrocardiographic findings, negative cardiac biomarkers), age and gender can serve as simple criteria to select patients who would derive the greatest diagnostic benefit from coronary computed tomographic angiography (CTA).[17] In an observational cohort study in 368 low-risk patients, positive findings on 64-slice coronary CTA led to restratification to high risk, and negative findings led to restratification to very low risk, in men younger than 55 years and women younger than 65 years. In contrast, in women older than 65 years and men older than 55 years, a negative result on CTA did not result in restratification to a low-risk category.

Nuclear imaging should include V/Q (PE evaluation) and resting Sestamibi (In the appropriate clinical setting, a normal study in a patient with ongoing chest pain may rule out myocardial ischemia.[18] ).

ECG results may be normal or show signs of ischemia. Main use is to establish a baseline and R/O acute ST-segment elevation myocardial infarction (STEMI).

Intraluminal coronary artery sonography (ICAS) is a highly invasive modality that may provide additional information to a patient's coronary artery anatomy and disease. Coronary atherosclerosis, which does not result in coronary artery narrowing, may be missed by conventional forms of coronary angiography. If clincially suspected, ICAS may be utilized to detect the presence or absence of such lesions. ICAS is not readily available; as such, it is highly unlikely that ICAS will be utilized from the emergency department in the foreseeable future.

The use of stress cardiac MRI in an observation unit may be a cost-saving alternative to inpatient management for emergency department patients with chest pain. In a randomized study in 110 patients, Miller et al reported that an observation unit strategy with stress cardiac MRI reduced median hospitalization cost by approximately $588, with no cases of missed acute coronary syndrome.[19]

While the recent ROMICAT trial showed the introduction of coronary CT imaging improved efficiency of the emergency clinical workup in comparison to the traditional ED care, patients who underwent cardiac CT imaging had increased subsequent workups and incurred a higher radiation burden without any reduction in overall cost.[20]



Prehospital Care

Often, patients with angina pectoris rest or lie down to alleviate the pain. If the patient is not naive to cardiac disease, he or she may have access to nitroglycerin. Often, the patient uses nitroglycerin at home to palliate his or her symptoms. A patient who has known stable angina often is able to report what exacerbates the condition and what (as well as how often) is a "normal" number of tablets for him or her to use prior to alleviation of anginal symptoms. Patients are often instructed by their physicians that the use of more than 3 tablets of nitroglycerin necessitates a higher level of care (eg, calling for an ambulance). Some patients are instructed to take aspirin as well. A knowledgeable patient who reports a change in the pattern or presentation of his or her symptoms should be suspected as having worsening or unstable angina. However, any patient who presents to the ED with symptoms of angina should be assessed promptly for signs of acute myocardial infarction (AMI).

Most prehospital care for angina pectoris consists of administering nitroglycerin, oxygen, and aspirin. The ability to obtain a prehospital ECG is becoming more prevalent.

Emergency Department Care

In the ED, the patient who complains of chest discomfort needs to be immediately assessed for AMI as well as other high-risk diagnoses (eg, aortic dissection, pulmonary embolism). Vital in this assessment is an early ECG and a rapid history and physical examination. Should this initial encounter not reveal a definitive diagnosis, then a more focused history and physical examination needs to be performed. Serial ECGs, especially in the setting of changing symptoms, is imperative. Labeling the ECGs with the patient's level of pain is often useful. A consecutive series of ECGs taken when a patient is having "10/10" pain, "3/10" pain, and "0/10" pain may yield valuable information that would not be readily apparent with an isolated cardiogram. Continuous telemetry monitoring is recommended for higher-risk patients.[21]

The patient who presents with chest pain is presumed to have underlying clinically significant cardiac pathology (ie, unstable angina or NSTEMI).

The initial treatment consists of administration of oxygen, aspirin, nitroglycerin, morphine, and a beta-blocker. Given an altered, yet nondiagnostic ECG and no contraindications, further treatment with heparin (low-molecular weight or unfractionated), clopidogrel, or other antiplatelet agents may be initiated. Most often, an additional abnormal marker (eg, an elevated serum troponin, myoglobin, or CPK level) will be verified prior to antiplatelet therapy.

For persistent symptoms unresponsive to initial therapy, glycoprotein inhibitors can be considered. These appear to demonstrate an additional benefit in the patient population who will be undergoing cardiac catheterization (PCI).[22] Persistent pain, in spite of this treatment, suggests either AMI or an alternative diagnosis. In the case of AMI, angioplasty or thrombolytics should be administered if available and not contraindicated. The American College of Cardiology offers an excellent evidenced-based online treatment resource (see American College of Cardiology Clinical Statements/Guidelines).

Atypical presentations of angina, unfortunately, are often diagnosed retrospectively. This subset of patients is identified either when their condition progresses to STEMI or through elevated serum marker levels or cardiac dysrhythmia (often ventricular tachycardia or fibrillation). It cannot be understated that the variance of expression of angina pectoris makes it imperative that the clinician have a high level of suspicion for the disease. Little value exists in relying on a constancy of expression or on ECG, history, or physical examination alone for making the diagnosis. Angina pectoris should be considered as well as an extensive differential diagnosis, in just about any patient who presents to the ED with chest pain with or without other nonspecific complaints.

Syndrome X and Prinzmetal angina are not diagnosed in the ED, but the patient's medical records or primary care physician may be helpful in recognizing these disorders.


In the setting of unstable angina or AMI, consultation with a cardiologist is warranted.


Admission is indicated for patients with unstable angina. Patients with angina pectoris who are admitted for alternative reasons do not routinely require telemetry monitoring.

Low-risk, pain-free patients who are admitted with nondiagnostic ECGs and negative cardiac marker results, often do not require telemetry monitoring as inpatients.

Patients admitted with UA/NSTEMI will likely undergo percutaneous transluminal coronary angioplasty (PTCA) if clinically indicated. If catheterization is not available, hospital transfer is suggested.


Transfer of the high-risk patient to an active catheterization center is recommended. This may be done from the inpatient setting after the patient has been stabilized in the ED.


Any discharged patient with suspected angina should have close primary or cardiology follow-up care.



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