Acute Myocardial Infarction (Coronary Occlusion)
Myocardial infarction results when arterial blood flow to the myocardium is suddenly decreased or interrupted. It is usually due to atherosclerotic coronary artery disease with plaque rupture and sudden occlusion by thrombus; vasculitis or emboli are less common causes. Complete occlusion, most often with thrombus, is found in 80–90% of patients with chest pain and ST segment elevation who are studied by coronary angioplasty within several hours of onset. Occasionally, patients dying of myocardial infarction are found to have nonoccluded coronary arteries, and infarction in such cases is presumably due to spasm of a coronary artery or thrombosis with complete lysis. Cocaine use has been associated with acute myocardial infarction, probably as a result of coronary spasm with or without intravascular thrombus formation. In myocardial infarction, severely ischemic and infarcted muscle contracts and relaxes poorly or not at all; if infarction is extensive, decreased cardiac output with heart failure or shock may result. After myocardial infarction, the ventricle may become aneurysmal or may even rupture. If conducting tissue is ischemic or infarcted, conduction abnormalities may occur. The infarcted endocardium attracts platelets and fibrin that may form mural clots, which can subsequently embolize. During acute myocardial infarction, the myocardium can become electrically unstable, resulting in arrhythmias that are frequently life-threatening.
Upon occlusion of a coronary artery, necrosis occurs in a time-dependent course, proceeding from endocardium to epicardium, generally over 4–6 hours. When residual perfusion by collateral vessels is present or lysis or thrombus occurs—either spontaneously or as a result of therapy—there will be salvage of myocardium. The earlier the reperfusion, the more myocardium is salvaged.
Most patients with myocardial infarction have chest discomfort that is typically substernal and may radiate to the neck or left arm. However, pain can occur in atypical areas such as the right arm, shoulders, back, or epigastrium. The pain is classically oppressive or squeezing in character and may be associated with shortness of breath, dizziness, syncope or pre-syncope, anxiety, restlessness, nausea and vomiting, abdominal bloating, dyspnea, and diaphoresis. Patients' descriptions of “pain” and symptoms can vary greatly. Symptoms frequently begin at rest, worsens gradually, and persist for hours. Occasionally, myocardial infarction is painless—especially in elderly or diabetic patients—and is manifested by the acute onset of left heart failure, hypotension, or cardiac arrhythmias. Up to 25% of patients with an acute myocardial infarction may not develop any significant symptoms that would prompt the patient to seek medical attention.
Physical findings vary, and none are specific or diagnostic of myocardial infarction. An S4 gallop or at times an S3 gallop may be present. Occasionally, an apical systolic murmur or mitral insufficiency due to papillary muscle and left ventricular dysfunction is present. In patients with uncomplicated myocardial infarction, there may be no abnormal findings on physical examination. When cardiopulmonary physical findings are present, they tend to reflect the presence of complications (see below).
The electrocardiogram (ECG) can show signs of infarction (eg, hyperacute T waves, flipped T- waves, elevated ST segments, ST segment elevation myocardial infarction, and abnormal Q waves) in about half of patients. In the remainder, the initial ECG shows only nonspecific ST or T wave changes, or may be normal. It is important to try to compare EKG findings with previous ECG's to assess for changes.
Note: A normal ECG does not rule out the possibility of myocardial infarction or ACS. Continuous ST segment monitoring or serial ECGs and serial laboratory testing provide additional information and may demonstrate an evolving acute coronary syndrome in patients with initially nondiagnostic ECGs.
CK-MB is found not only in the myocardium but also in brain and skeletal muscle, it is less specific for a myocardial ischemic event than some other markers. The CK-MB serum level elevates usually within 4–6 hours after the onset of an acute myocardial infarction and peaks within 12–24 hours. Levels return to baseline generally within 2–3 days of an acute myocardial infarction. Within 6 hours of an acute myocardial infarction, the sensitivity and specificity of elevations in the serum CK-MB levels are 17–62% and 92–100%, respectively. Many clinicians do not order CK-MB levels any longer because of the superior sensitivity and specificity of the cardiac troponin marker.
Troponin is a complex of three specific proteins found in striated muscle. Two of the subunits, cardiac troponin T (cTnt) and I (cTni), are useful as clinical markers of myocardial injury. Because these cardiac proteins are genetically unique, cTnt and cTni are the most cardiac-specific biochemical markers. With recent improvements in the assay, microinfarctions are diagnosed when elevations in cTnt or cTni occur without elevations in the CK-MB levels. After an acute myocardial infarction, cardiac troponin serum levels generally elevate within 2–6 hours, peak at 12–24 hours, and may stay elevated for 7–10 days. The sensitivities of elevations of cTnt and cTni within 6 hours of an acute myocardial infarction are 50–59 and 6–44%, respectively. The specificities of elevations of cTnt and cTni within 6 hours of an acute myocardial infarction are 74–96 and 93–99%, respectively.
One of the first cardiac markers used clinically, myoglobin, is still used by some today. Myoglobin is the most sensitive early marker of cardiac injury although it has very poor specificity. After an acute myocardial infarction, elevation occurs within 1–3 hours, levels peak within 4–12 hours, and levels remain elevated for 12–36 hours. The sensitivity of myoglobin for detecting myocardial infarction within 6 hours of symptom onset is considered very good at 55–100%. Some believe that because myoglobin is released in a noncontinuous manner and is very nonspecific, it is less helpful than other markers and should not be included in the standard evaluation for myocardial ischemia.
For a complete differential diagnosis of chest pain, see Chapter 14. Aortic dissection, aneurysm, pericarditis, and gastrointestinal disorders (eg, peptic ulcer disease and pancreatitis) must be clinically excluded in patients being considered for thrombolytic therapy.
Note: The diagnosis of myocardial infarction is suggested by the history, and a decision to admit the patient to the coronary care unit immediately should be based on this information alone. No amount of laboratory data obtained in the emergency department will definitely rule out ACS. Further testing such as stress test, echocardiogram, and cardiac catheterization are needed to further assess for cardiac disease. In some institutions, once acute myocardial infarction is ruled out in low risk patients, patients are referred for early stress testing. If timely referral is unavailable, then these patients are best served by admission for stress testing. Though AMI can be ruled out with serial troponins and serial ECGs, unstable angina cannot be excluded without further evaluation. Patients discharged without stress testing should be advised to take a baby aspirin and avoid exertion until evaluation is completed.
Patients experiencing acute coronary syndromes should receive aggressive treatment with the goal of rapidly reperfusing ischemic myocardium. The two methods currently available are pharmacologic thrombolysis via plasminogen activators and percutaneous coronary intervention (PCI). The effectiveness of either modality in reducing mortality and myocardial damage depends on how early it is given after the onset of symptoms.
Upon arrival, a patient being evaluated for ACS should be placed on cardiac monitor, given oxygen via nasal canula or mask and have 2 peripheral IV's placed.
Aspirin is the first and most important medication given to ACS patients early in their course. 162–325 mg nonenteric, and chewed is most effective. If contraindicated, use 300 mg clopidogrel. Coumadin use is not a contraindication to single aspirin dose, and does not substitute for aspirin as mechanism of action is different. NSAIDS should not be used to treat chest pain thought to be cardiac in origin.
A12 lead ECG should be obtained as rapidly as possible, ideally within 10 minutes of arrival.
If chest pain is present, give nitroglycerin, 0.4 mg sublingually or one spray delivered to the oral mucosa. Repeat if no effect occurs in 5 minutes. If chest pain returns or continues and systolic blood pressure is above 100 mm Hg, start intravenous nitroglycerin at 10 μg/min and increase by 5 μg/min every 3–5 minutes until systolic blood pressure falls by 10% or chest pain is relieved. The systolic blood pressure should not drop below 90 mm Hg.
Morphine may be still be used for analgesia, particularly for STEMI patients. However for UA/NSTEMI patients it may have increased adverse effects.
Current AHA guidelines recommend beta blockers be initiated within 24 hours of presentation. IV beta blockers are not useful if being used to reduce blood pressure. Contraindications to giving beta blockers include CHF, bradycardia, conduction blocks and hypotension. Also be aware of higher risks if given in elderly, patients with suspected cocaine use, and COPD/asthma patients.
Establish a laboratory test database including complete blood count (CBC) with differential, serum creatinine and electrolyte measurements, blood urea nitrogen determinations, enzyme levels (cTni or cTnt). Platelet count, prothrombin time, partial thromboplastin time, and blood for typing (and cross-matching if needed) should be obtained for patients to be given thrombolytic therapy. Monitor urine output.
Option 1: Thrombolytic Therapy
If a patient experiences an acute ST segment elevation myocardial infarction and no contraindications are present, pharmacologic revascularization is indicated especially if PCI is unavailable for more than 90 minutes. Many thrombolytic agents are available, including streptokinase, anistreplase (APSAC), alteplase (tissue plasminogen activator: t-PA), reteplase (r-PA), and tenecteplase (TNK). Thrombolytics should be initiated in the emergency department because the benefit of pharmacologic thrombolysis decreases with each passing hour after myocardial infarction. Some patients with myocardial infarction may benefit from thrombolytics up to 12 hours after the onset of chest pain, although 6 hours is generally considered the cutoff. Alteplase administration over 90 minutes improved survival when compared to streptokinase or 3-hour alteplase infusion. Even though intracranial bleeding events increased, alteplase demonstrated a long-term survival advantage presumably secondary to earlier thrombolysis and reperfusion of thrombosed coronary arteries. Compared to alteplase, TNK may offer advantages of a single bolus administration and fewer intracranial hemorrhage complications. Intracranial hemorrhage is the most devastating complication of thrombolytic therapy, occurring in 0.5–3.3% of patients.
The indications for pharmacologic revascularization are as follows:
- ST segment elevation of at least 0.1 mV in two or more contiguous leads (II, III, aVF or V1–V6, I, aVL) suggests acute injury in the absence of left bundle branch block. An acute true posterior myocardial infarction (with ST depression in leads V1–V4) is also an indication for thrombolysis. Patients with ongoing chest pain and a new (or not known to be old) left bundle branch block should also be considered for pharmacologic reperfusion.
- Both chest pain and ST elevation are not relieved by two to three sublingual nitroglycerin tablets.
- Patient is alert and oriented, or a family member or friend familiar with the patient's medical history is present.
- No contraindications to thrombolytic therapy or anticoagulation therapy are present (see below).
Absolute contraindications are as follows:
- History of any hemorrhagic cerebrovascular event (stroke, arteriovenous malformation, or aneurysm) or any nonhemorrhagic cerebrovascular event or transient ischemic attack (within the last year)
- Any intracranial neoplasm
- Active, internal bleeding (eg, serious gastrointestinal bleeding) excluding menses
- Suspected aortic dissection
In the following conditions, the risks associated with thrombolytic therapy may be increased, and clinical judgment should be used in evaluating expected benefits:
- Recent (within 10 days) puncture of a noncompressible blood vessel
- Poorly controlled hypertension of several years' duration or severe, uncontrolled arterial hypertension (diastolic blood pressure greater than 110 mm Hg or systolic blood pressure greater than 180 mm Hg)
- Diabetic hemorrhagic retinopathy or hemorrhagic ophthalmic condition
- Current treatment with an anticoagulant with international normalized ratio greater than two to three or other bleeding diathesis
- Any other condition associated with a predisposition to bleeding (eg, ulcerative colitis, active peptic ulcer disease, polycystic kidneys, gastrointestinal arteriovenous malformation, vascular tumors) or bleeding within 4 weeks
- Prolonged (>5 minutes) or traumatic external cardiac compression or traumatic endotracheal intubation
- History of nonhemorrhagic cerebrovascular accident beyond 1 year
- Recent (within 4 weeks) trauma or major surgery at a noncompressible site (eg, coronary artery bypass surgery, organ biopsy, intra-abdominal surgery, or obstetric delivery)
If indicated, the dosage regimens recommended are as follows:
The recommended dosage is 1.5 million units in 250 mL of 5% dextrose in water, given intravenously over 1 hour. Because of the risk of serious allergic reactions, streptokinase is contraindicated in patients who have ever received streptokinase previously.
The recommended dosage is 15 mg intravenous bolus followed by 0.75 mg/kg (maximum 50 mg) intravenous infusion over 30 minutes and then 0.5 mg/kg (maximum 35 mg) over 60 minutes. Alteplase has a very short half-life (5 minutes); therefore, unfractionated heparin must be used to prevent reocclusion. Heparin should be started as a bolus of 60 units/kg at the start of the alteplase infusion followed by a maintenance dose of 12 units/kg. The reduction in mortality with alteplase thrombolysis (if used within 6 hours of symptom onset) is 23–30%, which translates into a number needed to treat of between 3 and 5 patients.
Anisoylated plasminogen streptokinase activator complex (APSAC)
The recommended dosage is 30 mg intravenously infused slowly over 5 minutes. Because of the risk of serious allergic reaction, patients who have received streptokinase or APSAC previously cannot be given the drug again.
The recommended dosage is a loading dose of 0.5 million units over a 10-minute period. This is followed by infusion doses of 1.6–4.5 million units over 18–24 hours.
r-PA, a variation of t-PA, has a half-life of 13–16 minutes and is simpler to administer than t-PA. The dose is two 10-unit intravenous boluses over 2 minutes, with 30 minutes between each dose.
TNK is a third-generation variation of t-PA. It has improved fibrin specificity and a longer half-life, allowing single bolus administration. The dose is based on weight, ranging from 30 to 50 mg rapid bolus. Overall mortality compared to t-PA was equal; however, in patients presenting later in the course of an acute myocardial infarction, those given TNK had fewer episodes of nonintracranial bleeding.
Excellent evidence indicates that myocardial reperfusion salvages myocardium—resulting in better ventricular function than conventional management—and improves survival if reperfusion occurs within 6 hours after the onset of symptoms of myocardial infarction. Thrombolytic therapy may be beneficial in patients with persistent chest pain for up to 24 hours after onset of symptoms. t-PA results in a higher percentage of vessel patency (60–80%) than does streptokinase (30–60%) within the first hour with an associated improvement in survival.
Heparin or anti-coagulant such as enoxaparin, or fondaparinux should be used in conjunction with any thrombin-specific thrombolytic agent such as alteplase. Because of the systemic fibrinolysis achieved by streptokinase or APSAC, anticoagulation with heparin is not indicated. Intravenous heparin, 60 units/kg bolus followed by 12 units/kg/h, should be given in a separate line while alteplase is infusing because of the short half-life of alteplase and the danger of recurring thrombosis. Anti-coagulation should be continued for 48 hours or longer.
Transfer patients given thrombolytic therapy to an intensive care unit as soon as possible after initiation of treatment. Monitor the following:
- blood pressure every 15 minutes during infusion and every 30–60 minutes thereafter
- ECG rhythm strip for reperfusion arrhythmias and ST segment changes
- bleeding complications and changes in neurologic status; avoid venous or arterial punctures and unnecessary trauma
- 12-lead ECG 4 hours after the start of therapy and as needed (eg, for recurrence of chest pain)
- cTni or cTnt 4 hours after initiation of treatment and at 4-hour intervals for 24 hours
Option 2: Percutaneous Coronary Intervention
Formerly termed angioplasty, PCI involves cardiac catheterization and various techniques to assess and restore vessel patency on an emergency basis. Coronary artery stenting has become the procedure of choice. When performed early in the course of an acute myocardial infarction, PCI has demonstrated improved survival rates over pharmacologic thrombolysis. Increased rates of normal flow and decreased rates of reocclusion in the infarct-related artery are much more likely when PCI is chosen over pharmacologic thrombolysis. In addition, early definition of coronary anatomy can be used to tailor therapy and improve risk stratification. One study comparing PCI with t-PA found a reduction in mortality of 4% with PCI. Major complications associated with thrombolytics such as intracranial bleeding do not occur with PCI. In patients with contraindications to thrombolytics, PCI is the only option available to restore perfusion and salvage myocardium. Rescue PCI is useful for patients who have received thrombolytics but whose chest pain or ST segment elevation has failed to resolve (50% decrease in ST elevation in 90 min after fibrinolysis begins). Unfortunately, PCI is not widely available; fewer than 18% of US hospitals are equipped to perform the procedure. If the time to PCI is expected to exceed 90 minutes for a patient with a ST segment elevation myocardial infarction, thrombolytics should be strongly considered in order to salvage as much myocardium as possible.
Facilitated PCI, as defined by administration of a fibinolytic agent at partial or full dosing, with PCI performed immediately after is not currently recommended. This differs from rescue PCI as defined by PCI performed after fibrinolysis failure.
Hospitalize all patients with clinical histories suggesting myocardial infarction. For patients with ST segment elevation MI, ideally, a hospital capable of performing PCI will have a mechanism in place that allows an emergency physician to directly activate the cardiac catheterization laboratory so as to get the patient to definitive treatment as rapidly as possible. Patients with suspected myocardial infarction and normal initial ECGs and initial cardiac enzymes may be admitted to a monitored intermediate care unit.
Complications of Myocardial Infarction
About 10–15% of patients reaching the hospital with myocardial infarction die during hospitalization. One or more complications occur in over half of all patients with myocardial infarction.
Shock (Cardiogenic Shock)
Shock complicating myocardial infarction occurs in 7–8% of patients and may be caused by extensive myocardial infarction with decreased cardiac output (most common), inappropriate reflex peripheral vasodilatation, arrhythmias, hypovolemia, right ventricular infarction, and mechanical complications such as ruptured ventricular septum and severe mitral regurgitation. Free-wall myocardial rupture results in tamponade and shock. The mortality rate is as high as 70–80% among patients with cardiogenic shock as a complication of acute myocardial infarction.
Hypotension accompanied by confusion, obtundation or restlessness, cool skin, oliguria, and metabolic acidosis suggests shock. Mild to moderate hypotension alone is common in myocardial infarction and does not itself indicate shock. Shock in myocardial infarction may be due to many causes (see Table 11–1), which may be difficult to differentiate noninvasively (Table 34–1).
Table 34–1. Differential Diagnosis by Hemodynamics of Heart Failure and Hypotension after Myocardial Infarction. ||Download (.pdf)
Table 34–1. Differential Diagnosis by Hemodynamics of Heart Failure and Hypotension after Myocardial Infarction.
|Arterial Pressure||Central Venous Pressure||Pulmonary Arterial Wedge Pressre||Stroke Volume Index||Diagnosis||Treatment|
|→||→ or ↑||↑||→ or ↓||Heart failure||Diuretics; preload and afterload reduction|
|→ or ↓||→ or ↓||↓||↓||Hypovolemia||Saline volume loading|
|→ or ↓||↑||→ or ↓||→ or ↓|
Right ventricular myocardial infarction
|Ventilation/perfusion scan; saline or dextran; volume loading; no diuretics|
|↓||→ or ↑||↑||↓||Cardiogenic shock||Inotropic agents; diuretics; preload and afterload reduction if arterial pressure can be maintained; counterpulsation|
Use any or all of the measures discussed here as necessary (see also Chapter 11).
Give oxygen by mask or nasal cannula. Patients in shock with respiratory failure require endotracheal intubation.
Venous Pressure Monitoring
Consider monitoring central pressure with a Swan-Ganz pulmonary artery catheter (or, far less desirably, a central venous pressure catheter, since in acute myocardial infarction, left ventricular filling pressure can be markedly elevated with normal right ventricular filling pressure, and vice versa). Use an arterial line to measure blood pressure.
Give a fluid challenge (200 mL of saline intravenously over 20 minutes) if the patient is not in congestive heart failure (ie, no rales and no pulmonary edema on chest X-ray). Repeat as needed if congestive heart failure does not develop. Correct arrhythmias (see below). Insert a Foley catheter, and measure urine output hourly.
Give dopamine (or dobutamine), 2.5–20 mg/kg/min by continuous intravenous infusion. Use the smallest effective dose, guided by hemodynamic response. When shock is caused by inappropriate vasodilatation (rare), α-adrenergic drugs such as norepinephrine are useful.
Percutaneous Coronary Intervention
Evidence indicates that acute revascularization by PCI might be particularly effective in patients who develop cardiogenic shock early (within 3–6 hours) after onset of myocardial infarction. PCI acutely should be seriously considered in such patients because thrombolytics are ineffective in cardiogenic shock associated with an acute myocardial infarction. An intra-aortic balloon pump (IABP) can also be placed, typically in the cath lab. IABP counterpulsation can increase cardiac output and improve both coronary and systemic perfusion. IABP counterpulsation is contraindicated in patients with aortic valve disease or those with aortic dissection.
All patients with cardiogenic shock must be hospitalized, preferably in an intensive care unit. Therapy is directed at the likely causes of shock.
Congestive heart failure is caused by extensive myocardial infarction, volume overload, arrhythmias, acute mitral regurgitation, or ventricular septal rupture.
Symptoms and signs of congestive heart failure include dyspnea, anxiety, tachypnea, tachycardia, pulmonary rales or frank pulmonary edema, jugular venous distention, hypoxemia, and typical findings on chest X-ray (cardiomegaly, pulmonary vascular plethora, Kerley B lines, pleural effusion, or pulmonary infiltrates consistent with pulmonary edema). Wheezing may also be a sign of congestive heart failure (cardiac asthma). Suspect right ventricular infarction in inferior myocardial infarction if signs of right heart failure (right ventricular gallops, elevated central venous pressure, hepatomegaly, peripheral edema) are prominent in the absence of signs of left heart failure (dyspnea, rales, pulmonary congestion on chest X-ray).
Give oxygen by mask or nasal cannula. Treat respiratory failure if present.
Nitroglycerin—Give NTG either sublingual or spray, followed by IV infusion. NTG will decrease preload as well as afterload. In patients with inferior or right ventricular acute myocardial infarction, nitrates are relatively contraindicated because they may precipitate profound hypotension. Hypotension related to nitrates is treated with reduction or discontinuation of the infusion depending on the degree of symptomatic hypotension. Intravascular volume expansion with intravenous fluid infusions will often quickly correct hypotension.
Furosemide—Give furosemide as an intravenous bolus of at least the patient's normal total daily dose. If the patient is not already taking furosemide, administer a 40-mg intravenous bolus initially, and observe the diuretic response by monitoring the patient's symptoms and urine output. Diuretics are contraindicated if right ventricular infarction is suspected.
ACE or ARB inhibitors can be used to decrease afterload.
Noninvassive positive pressure ventilation (CPAP/Bipap) has been shown to decrease need for intubation. Alveoli are kept open with positive pressure and work of the heart is reduced.
Treatment of congestive heart failure in the emergency department is directed at reducing the intravascular volume through diuretics or vasodilation. Patients with respiratory failure may require intubation in the emergency department. Hemodynamic monitoring with a pulmonary artery catheter may assist in assessing volume status. In the setting of an acute myocardial infarction, patients with congestive heart failure should be closely monitored in an intensive care unit.
Acute Mitral Regurgitation and Ventricular Septal Rupture
Mechanical failure of infarcted tissue (eg, rupture of the ventricular septum or of papillary muscle supporting the chordae tendineae) is a common cause of acute mitral regurgitation and ventricular septal rupture. Minimal-to-moderate mitral regurgitation is common after myocardial infarction as a result of papillary muscle and left ventricular wall dysfunction. Severe degrees of mitral regurgitation can result from marked ischemia with little or no infarction and can be completely reversed with revascularization.
Abrupt, severe congestive heart failure with pansystolic regurgitation murmur suggests acute mitral regurgitation or ventricular septal rupture. Echocardiography to detect mitral regurgitation or the abnormal velocity jet of a ventricular septal defect can establish the diagnosis.
Treat heart failure with diuretics, morphine, and nitroglycerin.
Obtain urgent cardiologic and cardiac surgical consultation. IABP is a useful temporizing measure while the patient is being prepared for surgery.
The only life-saving treatment for most patients is emergency cardiac catheterization followed by surgery.
Hospitalize all patients in a critical care unit for treatment and surgery.
The chief cause of myocardial rupture is mechanical failure of an infarcted ventricular wall.
Myocardial rupture is an uncommon cause of sudden death during acute myocardial infarction; it is responsible for only about 5% of deaths. Myocardial rupture is suggested by abrupt onset of hypotension with increased venous pressure (ie, cardiac tamponade). Pulseless electrical activity often occurs.
Treatment and Disposition
If echocardiography or bedside emergency ultrasound demonstrates a pericardial effusion, pericardiocentesis is indicated and can be performed under ultrasound guidance (Chapter 6). When emergent ultrasound is not available to assess a patient for possible pericardial tamponade, blind pericardiocentesis may be life saving.
Obtain emergency cardiac surgical consultation for immediate cardiac surgery. This is successful in the few cases in which rupture has been minimal with slow intrapericardial hemorrhage.
Systemic or Pulmonary Embolization
Systemic or pulmonary embolization is commonly caused by intracardiac mural thrombosis or phlebothrombosis.
The most common findings in pulmonary embolism are sudden unexplained dyspnea and tachycardia. Occasionally, pleuritic pain, signs of right heart strain, or abnormal chest X-ray may occur. Patients at greatest risk are those with thrombus visualized in the left or right ventricle by two-dimensional echocardiography. The diagnosis may be confirmed by computed tomography (CT) scan of the chest, lung scan, or arteriography (Chapter 33). Systemic embolization is suspected when symptoms and signs of arterial occlusion occur. The clinical picture depends on the artery occluded, for example, flank pain and hematuria with renal artery embolism; pallor, pain, and loss of pulse with brachial or femoral artery embolism; stroke with cerebral artery embolism.
Treatment and Disposition
Give oxygen, draw blood for determination of prothrombin and partial thromboplastin times, and then begin systemic anticoagulation with heparin, 80 units/kg bolus followed by 18 units/kg/h infusion, or a low-molecular-weight heparin such as enoxaparin, 1 mg/kg subcutaneous administration every 12 hours. Pericarditis is a relative contraindication to anticoagulation because of the risk of bleeding into the pericardial sac, with resulting cardiac tamponade. Heparin is also contraindicated in patients with recent stroke, active duodenal ulcer, or active bleeding that cannot be controlled by direct pressure. Even though it does not cross the placenta, heparin must be used with caution in pregnant patients, especially during the third trimester. (Acute myocardial infarction during pregnancy is quite rare.)
With a massive pulmonary embolism with right heart failure or shock, intravenous fibrinolysis with streptokinase, urokinase, or t-PA has been recommended in doses similar to those given for acute myocardial infarction. Occasionally, mechanical disruption of the embolic thrombus by a catheter has been life saving.
Seek appropriate surgical consultation (with a thoracic, general, or vascular surgeon) for patients with persistent hypotension, contraindications to thrombolytic therapy, or systemic embolization who may benefit from surgical intervention (eg, angioplasty and embolectomy for a pulseless and ischemic extremity).
Patients who have received TPA or have hemodynamic instability should be hospitalized in an intensive care unit.
When transmural myocardial infarction causes pericardial inflammation over the area of necrosis, pericarditis may occur within the first week. Pericarditis occurring more than 1 week after myocardial infarction may be the result of Dressler syndrome, an autoimmune reaction.
Pericarditis usually does not appear until 2–3 days after the onset of myocardial infarction. The appearance of a friction rub is often the only manifestation; pain and ECG changes are often absent. Frequently, a small pericardial effusion may be detected by echocardiography. If a pericardial friction rub is heard in the first 24 hours after onset, suspect pericarditis as a primary diagnosis rather than as being due to acute myocardial infarction. Early ECG signs of pericarditis include diffuse ST segment elevation (with a concave upslope and indistinct J point) and diffuse PR segment depression (except in AVR, where the PR segment is elevated).
Treat pain with a nonsteroidal anti-inflammatory agent such as indomethacin, 25–50 mg orally three times a day. If pain is severe, give morphine, 2–4 mg intravenously every 5–10 minutes, and repeat as necessary.
Hospitalize the patient in a coronary care unit for pain control and monitoring for possible cardiac tamponade (rare).
Myocardial ischemia (with attendant angina pectoris) results from an imbalance between myocardial oxygen supply and demand. Clinical findings vary depending on the severity of ischemia and on the frequency, duration, and rapidity of onset of ischemic episodes. If the demand for myocardial blood flow exceeds the capacity of the obstructed coronary arterial tree to supply it, the discomfort (angina pectoris) lasts until the excessive demand for coronary flow is reduced.
Discomfort is more intense and lasts longer when coronary blood flow decreases markedly, as occurs with sudden marked increase in coronary artery obstruction resulting from abrupt development of thrombus over an atherosclerotic plaque, embolization to a coronary artery, or sudden occlusion by coronary artery spasm. If myocardial necrosis then occurs, the condition is termed myocardial infarction; otherwise, the episode is one of acute coronary insufficiency, or preinfarction angina.
If obstruction is so severe that coronary blood flow is barely adequate to meet resting demands, even small increases in myocardial oxygen demand may cause angina. In addition, small aggregations of platelets on a ruptured plaque, spasm, or increased vasomotor tone can cause minor changes in the caliber of the severely obstructed coronary artery and precipitate angina.
Myocardial ischemia can exist in the absence of any chest discomfort. In patients with severe ischemia, 24-hour ECG monitoring shows that 80% of the episodes of ST segment depression lasting for a minute or more are present without angina (so-called silent ischemia). Painless myocardial infarction is not unusual in elderly or diabetic patients.
Stable Angina (Angina of Effort)
By definition, the pattern of discomfort, its frequency of occurrence, and precipitating factors have remained the same for 3 or more months.
Discomfort is usually substernal but may originate in other areas (eg, elbow, forearm, shoulder, neck inter-scapular region, or jaw), although substernal discomfort eventually occurs. It is usually precipitated by activities that increase myocardial oxygen consumption (eg, exercise, eating, or emotional upset), lasts longer than 1 minute and usually less than 15 minutes, and is usually relieved by rest or nitroglycerin. Pain that meets these criteria usually indicates the presence of fixed coronary obstruction. The most important feature suggesting the diagnosis of angina pectoris is discomfort precipitated by exercise or emotion.
Anginal pain that begins in a patient previously free of pain (ie, pain of less than 1 month's duration) is called new-onset angina. Unstable angina is that which has changed in pattern, becoming more frequent (crescendo angina) and longer lasting. It is precipitated by a lesser degree of activity and may respond less to rest and nitroglycerin than does stable angina. Angina that occurs at rest without any obvious precipitating factor (rest angina) is the most serious form of unstable angina.
Sudden changes in angina not associated with increased myocardial oxygen demand (eg, increased blood pressure or heart rate) are presumed to be caused by a change in the anatomy of the coronary artery, for example, new vessel obstruction caused by progression of heart disease, development of thrombus, or other factors such as platelet aggregation or coronary spasm.
Atypical Angina, or Prinzmetal (Variant) Angina
Prinzmetal angina occurs as a result of a sudden, reversible, severe coronary artery obstruction (coronary artery spasm). It may occur in patients with fixed atherosclerotic coronary lesions and less often in those with minimal or no fixed coronary obstruction. Chest discomfort usually occurs without a precipitating cause. It frequently occurs at rest or awakens the patient at night. The discomfort frequently lasts longer than the usual episode of angina and is often accompanied by ST segment elevation (current of injury) that is transient and reversed in minutes after administration of nitroglycerin. With lesser degrees of spasm, ST segment depression may occur. Ventricular ectopy and ventricular tachyarrhythmias may also occur.
Treatment and Disposition
Nitroglycerin, 0.4 mg sublingually, is the drug of choice when pain starts. It may also be taken prophylactically several minutes before activities that regularly precipitate angina. Pain is usually relieved in 1–2 minutes. Nitroglycerin tablets deteriorate in about 6 months; headache and sublingual tingling are common side effects of active tablets.
Current recommendations for patients who have previously been prescribed NTG for angina, is to take one dose, and if not improving after 5 minutes, to call 911 before taking any more. If pain is improved, NTG can be repeated every 5 minutes up to 3 doses, and then 911 called only if pain not resolved.
Unstable Angina, Rest Angina, and Prinzmetal Angina
Give oxygen by mask or nasal cannula. Hospitalize the patient immediately in the coronary care unit and obtain daily ECGs and myocardial enzyme determinations (cTni or cTnt) to detect possible myocardial infarction.
Start nonenteric-coated aspirin, 160–325 mg orally. Aspirin has been shown to reduce the incidence of myocardial infarction and death by about 50%.
Apply nitroglycerin paste, 1.25 cm (½ in), to the skin under an occlusive dressing every 4 hours, or transdermal nitroglycerin patches may be substituted. Topical nitroglycerin can be used if the patient is pain free. If the pain persists, an intravenous infusion of nitroglycerin is indicated at an initial rate of 10 μg/min.
Add a β-adrenergic blocking agent (eg, metoprolol, 25 mg orally) unless contraindicated (heart rate less than 60 beats/min, atrioventricular block, severe asthma, or chronic obstructive pulmonary disease). Calcium channel blockers are usually used for long-term treatment of patients with vasospastic or Prinzmetals angina. Beta blocker use is recommened in first 24 hours of unstable angina.
Give morphine, 2–3 mg intravenously every 5–10 minutes, to relieve prolonged pain. Monitor blood pressure. Morphine's use in cardiac chest pain, particularly NSTEMI has been diminished as some observational studies showed worsened outcomes. Do not use NSAIDS for suspected cardiac chest pain as they have been shown to increase mortality.
Antiocoagulation may also be helpful in these patients. Use unfractionated heparin at 80 units/kg intravenous bolus followed by 18 units/kg/h intravenous infusion or a low-molecular-weight heparin such as enoxaparin, 1 mg/kg administered subcutaneously every 12 hours. In the SYNERGY trial in which enoxaparin and unfractionated heparin were compared, the primary end point of death or myocardial infarction at 30 days was statistically similar although bleeding complications were slightly more common in the enoxaparin group. Other drugs that are currently being studies and now used include fondaparinux and bivalirudin.
Glycoprotein IIB/IIIA receptor antagonists such as abciximab and the newer agents tirofiban and eptifibatide are approved for use in patients with acute coronary syndrome. These agents block platelet binding at the receptor site that cross-links fibrinogen to the platelets. Although these agents have shown promise when used in conjunction with PCI, their role in unstable angina is still being defined. In the future, there may be a role for combining these agents with lower dose fibrinolytics to improve reperfusion while curtailing bleeding complications.
Percutaneous Coronary Intervention
If pain continues despite treatment, consider PCI. If acute myocardial infarction has occurred and pain continues despite optimal medical management or thrombolytics, PCI must be considered. Percutaneous aortic balloon counterpulsation may also be useful in patients with cardiogenic shock.
ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction—Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons
Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol 2007;50(7):e1-e157 657–668
ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol 2005;46(6):e1–82
ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Intervention—summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). Circulation 2006;113(1):156–175
Antman EM: Decision making with cardiac troponin tests. N Engl J Med 2002;346:2079
Diop D, Aghababian RV: Definition, classification, and pathophysiology of acute coronary ischemic syndromes. Emerg Med Clin North Am 2001;19:259
Karras DJ, Kane DL: Serum markers in the emergency department diagnosis of acute myocardial infarction. Emerg Med Clin North Am 2001;19:321
Lee TH, Goldman L: Evaluation of the patient with acute chest pain. N Engl J Med 2000;342:1187
Llevadot J, Giugliano RP, Antman EM: Bolus fibrinolytic therapy in acute myocardial infarction. JAMA 2001;286:442
McPherson JA, Gibson RS: Reperfusion therapy for acute myocardial infarction. Emerg Med Clin North Am 2001;19:433
Mishra PK: Variations in presentation and various options in management of variant angina. Eur J Cardiothorac Surg 2006;29:748–759
Shannon AW, Harrigan RA: General pharmacologic treatment of acute myocardial infarction. Emerg Med Clin North Am 2001;19:417
SYNERGY Executive Committee: Superior Yield of the New strategy of Enoxaparin
, Revascularization and Glycoprotein IIb/IIIa inhibitors. Am Heart J 2002;143;952–960