Asthma, 413.9
Myocardial infarction, 410.9
II. Incidence/predisposing factors/general comments
A. Incidence
1. Heart disease is the leading cause of death in the U.S.
2. Approximately 7 million people in the U.S. have angina.
3. Over 1.5 million people in the U.S. experience an acute MI each year.
4. Most (55%) patients who experience MI are older than 65 years of age.
5. Eighty percent of deaths related to MI occur among individuals older than 65 years of age.
6. Classically, MI is precipitated by events that increase myocardial oxygen demand.
a. Physical exertion (e.g., exercise, sex)
b. Extremes in weather conditions
c. Consumption of a heavy meal
e. Smoking
B. Predisposing factors
1. Coronary artery disease/Hyperlipidemia
2. Hypertension
3. Metabolic syndrome
4. Obesity/Being overweight with increased measured visceral fat
5. Other—such as male gender (more prevalent until age 65; then incidence is equal in men and women) and family history
C. General comments
1. Misdiagnosis of MI is the leading cause of liability among emergency room physicians.
2. For ST elevation myocardial infarction (STEMI), national recommendations stipulate that all emergency departments should treat patients with acute MI within 30 minutes (door to fibrinolytics) and 90 minutes (door to angioplasty) upon arrival at hospital.
3. Occurrence of MI and sudden cardiac death peaks between 6 AM and noon. A significant number of deaths related to MI also occur between 4 am and 6 am.
III. Types of angina
A. Stable (chronic or classic)
1. Intermittent chest pain over time with the same onset, intensity, and duration
2. Usually induced by exercise or exertion
3. Pain at rest is unusual; pain usually lasts 1 to 5 minutes to a maximum of 10 minutes.
4. ECG usually shows ST segment depression (ischemia).
5. Results from atherosclerotic blockage over time
6. Nitroglycerin relieves pain.
7. With lifestyle changes and medication, angina may be controlled without severe complications.
B. Prinzmetal’s (variant)
1. Pain often occurs at rest and may last up to 30 minutes.
2. Pain is not usually precipitated by an increase in oxygen demand.
3. Pain may occur in the absence of atherosclerosis.
4. Pathology is related to spasms of the coronary arteries. Spasms are strong contractions of smooth muscle in the coronary arteries caused by an increase in intracellular calcium levels.
5. ECG usually shows ST segment elevation.
C. Unstable (preinfarction, rest or crescendo, coronary syndrome)
1. Chest pain lasting longer than 20 to 30 minutes
2. Pain is more severe than with stable angina and is experienced at rest or with low activity levels.
3. Pattern of attacks usually progresses, with increased frequency, duration, and intensity.
5. Nitrates are usually insufficient to relieve pain.
6. Increased incidence of MI within 6 months after the start of angina
D. Microvascular angina (syndrome X/metabolic syndrome)
1. Chest pain mimics angina.
2. Exercise stress test is positive.
3. No evidence of abnormal angiogram or coronary spasm
4. Postulated defective mechanism resulting in dilatation of the coronary microcirculation
IV. “P-Q-R-S-T” method of pain assessment
P = Provocative: What activities elicit pain?
Q = Quality: What does the pain feel like? Do other symptoms occur simultaneously?
R = Region/Radiation: Where is the pain? Does the pain radiate? If so, to where?
S = Severity: How would you rate the pain on a scale of 0 to 10? (Some institutions now use a 0 to 5 scale.)
T = Timing/Treatment: When did the pain begin? How long does it last? What did you do to relieve the pain? Were such measures effective?
V. Pain of angina vs myocardial infarction
A. Generally, anginal pain is more diffuse and vague than pain resulting from an MI.
B. With MI, pain may be described as “viselike,” “crushing” substernal pressure that may or may not radiate to the jaw and/or left arm.
C. Pain from myocardial infarction may radiate to the jaw, back, shoulders, arms, or abdomen.
D. Approximately 15% of patients who experience MI have no pain; lack of pain is particularly common among diabetic patients who have MIs.
E. Generally, women who experience angina/MI complain of more gastrointestinal-like symptoms than are reported by men.
1. Administration of a “GI cocktail” consisting of Maalox or Mylanta, viscous lidocaine, and Donnatal should immediately relieve pain related to acute GI causes such as esophagitis, gastritis, and gastric/duodenal ulcers.
2. If pain is not relieved, cardiac-related causes should be thoroughly investigated.
VI. Subjective/physical examination findings of angina/MI
A. Note: History and physical examination findings are very important for early detection and diagnosis.
B. Nausea
C. Vomiting
D. Diaphoresis
E. Cool, clammy skin
F. Chest pain, usually substernal; in MI, not relieved by nitroglycerin
G. Dyspnea
H. Feeling of impending doom
VII. Diagnostics/laboratory findings of angina/MI
A. 12-lead ECG changes
1. Signs of MI progression: Heightening or peaking of T waves → ST segment elevation → Inversion of T waves → Formation of Q waves → Diminished height of R waves
2. Note: Approximately 30% of patients who experience MI show no immediate 12-lead ECG changes.
3. Hallmarks of ischemia versus injury versus infarction include the following:
a. Ischemia—T-wave inversion, peaked T waves, and ST segment depression. Note: With angina, cardiac changes usually do not persist once pain has been alleviated.
b. Injury—ST segment elevation greater than 1 mm above baseline
c. Infarction—Q waves (pathologic) greater than 25% of QRS complex height or more than 1 mm wide (0.04 s)
4. Expected site of MI based on ECG changes
a. Inferior: leads II, III, aVF; diaphragmatic involving the right coronary artery (80%-90%) or the left circumflex artery (10%-20%)
b. Inferolateral: leads II, III, aVF, V5, and V6; site = left circumflex artery
c. Anterior: V3 and V4; site = left anterior descending artery
d. Anterolateral and lateral: leads I, aVL, V5, and V6; site = left anterior descending artery or left circumflex artery
e. Anteroseptal: V1, V2, and V3; site = left anterior descending artery
f. Posterior: Reciprocal changes noted in V1 and V3, broad or tall R waves, and ST depression without T-wave inversion may be seen; site = right coronary artery or left circumflex artery.
g. Right ventricular: V4 to V6; elevations in all precordial leads may be seen; site = right coronary artery
B. Serum cardiac enzymes (Table 11-1)
1. Because neither troponin nor creatine kinase isoenzyme MB (CK-MB) consistently appears in the blood during the first 6 hours post MI, serial testing is needed (i.e., on admission and every 6 to 8 hours × 3).
| CK-MB, Creatine kinase isoenzyme MB; CK, creatine kinase; LD^ human heart LD1 isoenzyme; LD, human lactate dehydrogenase isoenzyme. | ||||
| Serum marker | Earliest increase, hours | Peak, hours | Duration | Other causes of elevation |
|---|---|---|---|---|
| Troponin T | 4-6 | 10-24 | 14-21 days | Regenerative muscular disorders, unstable angina |
| Troponin I | 4-6 | 10-24 | 5-7 days | 100% specific for myocardial necrosis |
| Myoglobin | 2-3 | 6-9 | 3-15 hours | Regenerative muscular disorders, unstable angina |
| CK-MB | 4-8 | 15-24 | 48-72 hours | Post cardioversion, cardiac contusion, cardiac surgical procedures, myocarditis, and acute pericarditis with myocardial involvement |
| Total CK | 3-6 | 24-36 | 18-30 hours | Smooth muscle injury, nonspecific |
| LD1 | 8-12 | 72-144 | 7-12 days | Hemolytic and megaloblastic anemias, acute renal infarction, hemolysis, and testicular cancer |
| Total LD | 10-12 | 48-72 | 10-14 days | Smooth muscle injury, nonspecific |
C. Laboratory analyses
1. C-reactive protein (CRP) or high-s ensitivity CRP (hs-CRP)—high levels consistently predict new coronary events in patients with unstable angina and acute MI; higher hs-CRP levels also are associated with lower survival rates; recent studies suggest that higher rates are associated with reclosure of coronary arteries after angioplasty.
a. Low risk: hs-CRP level less than 1 mg/L
b. Average risk: hs-CRP level 1 to 3 mg/L
c. High risk: hs-CRP level greater than 3 mg/L
2. B-type natriuretic peptide (BNP)—Elevated levels are strongly correlated with myocardial ischemia/damage and may serve to predict severity of future cardiac complications, including heart failure and mortality.
b. Mean levels
i. Ages 55 to 64: 26 pg/ml
ii. Ages 65 to 74: 31 pg/ml
iii. Ages 75 and older: 63 pg/ml
c. Expected levels associated with MI: 100 to 400 pg/ml
3. CBC with electrolytes, hemoglobin, and hematocrit levels
4. Prothrombin time (PT) and partial thromboplastin time (PTT)
5. Lipoprotein profile
VIII. Management of angina/acute MI (Figure 11-1; TABLE 11-2TABLE 11-3 and TABLE 11-4)
A. Emergency management of acute angina/MI
1. Aspirin, 162-325 mg PO; chew and swallow. If the patient is aspirin-allergic, consider clopidogrel as a substitution.
2. Nitroglycerin, sublingual (1 every 5 minutes × 3); IV nitroglycerin may subsequently be used after narcotic administration (e.g., morphine), yet it should be used with extreme caution in patients with inferior MI because hypotension may especially occur related to dramatic preload changes.
4. Bedside monitor: Evaluate potentially life-threatening arrhythmias.
5. IV access: Blood for cardiac enzymes and other laboratory values may be drawn at this time.
6. Continuous pain assessment
8. 12-lead ECG
9. If pain is not relieved, consider morphine (0.1 mg/kg) IV, or hydromorphone (Dilaudid) (0.015 mg/kg) IV; may repeat with low doses every 15 minutes until pain is relieved, unless other adverse effects occur. This completes adherence to national recommendations for the use of MONA (morphine, oxygen, nitroglycerin, and aspirin) in emergent pharmacologic management of angina/MI.
10. Consider admitting the patient to the coronary care unit to rule out acute MI, pending results of cardiac enzymes.
11. If diagnosis of unstable angina or acute MI is made or suspected, continue immediately as follows:
12. For hemodynamically stable patients, institute beta blocker therapy intravenously, for example, as follows:
a. Metoprolol (Lopressor), 5 mg IV × 3 doses, administered 2 minutes apart, followed by 25-50 mg PO every 6 hours, starting 15 minutes after the last IV dose; maintenance doses range from 50-100 mg twice daily, or
b. Atenolol (Tenormin) 5 mg IV over 5 minutes; if well tolerated, repeat in 10 minutes and then start PO dose (i.e., 50 mg every day, increasing to 100 mg every day as tolerated) within 10 minutes after the last IV dose.
13. Consider heparin continuous IV drip (e.g., 80 units/kg IV bolus followed by 18 units/kg/hour continuous infusion to maintain a PTT at 1.5 to 2 × the patient control. Note: The emergency antagonist for heparin is protamine sulfate. Low molecular weight heparin (e.g., Enoxaprin [Lovenox], 1 mg/kg every 12 hours subcutaneously for 2 to 8 days) may be used as an alternative to the use of unfractionated heparin; especially indicated in patients with non–Q-wave MI and patients with unstable angina; monitor therapeutic coagulation values.
14. Consider administration of an antiplatelet agent glycoprotein IIb/IIIa inhibitor such as tirofiban (Aggrastat) in combination with heparin for patients with non–Q-wave MI. Initial dose, 0.4 mcg/kg/minute IV for 30 minutes, continued at 0.1 mcg/kg/minute. Dosing should be continued through angiography and for 12 to 24 hours after angioplasty. Monitor for bleeding. Other preparations include abciximab (ReoPro), 0.25-mg/kg bolus 10 to 60 minutes before therapy, followed by 10 mcg/minute continuous infusion × 12 hours; or eptifibatide (Integrilin), 180 mcg/kg IV (maximum, 22.6 mg) over 1 to 2 minutes, then 2 mcg/kg/minute (maximum 15 mg/hour) by continuous infusion for up to 72 hours. If patient is to undergo percutaneous coronary intervention, reduce infusion to 0.5 mcg/kg/minute and continue for 20 to 24 hours after the procedure, up to 96 hours of therapy.
15. Consider nitroglycerin continuous IV drip (Tridil) if pain is not relieved by sublingual nitroglycerin and morphine or hydromorphone (Dilaudid); begin nitroprusside at 5-10 mcg/minute, and titrate up by 5-10 mcg/minute every 5 to 10 minutes until pain is relieved or the patient becomes hypotensive (i.e., systolic blood pressure less than 90 mmHg.)
16. Consider fibrinolytic/thrombolytic therapy, or
17. Consider cardiac catheterization/percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI), and then
18. Consider coronary artery bypass graft surgery.
19. Admit to critical care unit for continuous monitoring.
20. Following emergent therapy, consider the steps presented in the following section.
B. After an acute ischemic event, consider additional testing.
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1. Exercise/stress test: use of a treadmill to monitor ECG changes for signs of ischemia, as well as heart rate and BP
a. Usually requires 10 to 15 minutes
b. A maximal test requires that the patient exercise until at least 85% of predicted capacity is reached (based on age and measured by heart rate).
c. Exercise continues until chest pain, fatigue, or other adverse effects are experienced, including the following:
i. Extreme weakness
ii. Severe dyspnea
iii. Syncope or dizziness
iv. Ataxia
v. Claudication
vi. Appearance of S3 or S4 heart sounds
vii. ST segment elevation or depression of 1 mm or greater
viii. Systolic BP above 250 mmHg
ix. Decrease in systolic BP greater than 10 mmHg
x. Rise in diastolic BP to higher than 90 mmHg or by more than 20 mmHg over the patient’s baseline measurement
xi. “Glassy-eyed” appearance, cold sweats, or confusion
d. Submaximal tests are usually conducted on patients who have experienced an acute MI and are stopped once the patient reaches a specific, calculated target heart rate. Usually, the targeted heart rate (THR) is calculated with use of this formula: (220 – age) × 0.85 = THR
e. Abnormal results/positive stress test: downsloping or flat ST segment of 1 mm or farther than 1 mm from an originally depressed ST segment
2. Thallium stress test: use of a radionuclide to detect perfusion of the myocardium
a. Test is conducted similarly to the treadmill test.
c. Patient is then placed on a nuclear imaging scanner, where the myocardium is scanned for distribution of the radionuclide/tracing agent.
d. Scan is repeated in 3 to 4 hours.
e. Abnormal results: Light distribution indicates decreased or absent perfusion on the first scan. Defects depicted on the first scan, but not on the second, indicate ischemia. Defects on both scans indicate areas of scar tissue that have resulted from MI.
3. Pharmacologic stress test: use of pharmacologic agents to increase coronary blood flow in patients unable to exercise to the point of reaching their target heart rates
a. Drugs of choice to increase coronary artery perfusion include dipyridamole (Persantine) and adenosine (Adenocard). Dobutamine (Dobutrex) is given primarily to increase cardiac output, rather than to increase coronary blood flow (i.e., perfusion); subsequently, coronary blood flow will increase.
b. If dipyridamole (Persantine) is used, give thallium 201 approximately 5 minutes after the intravenous dose, followed by a nuclear scan. Give aminophylline, 50-125 mg, to reverse the adverse effects of dipyridamole, which may include chest pain, nausea, dizziness, or headache. Two to three hours later, administer a second dose of thallium, and conduct a second scan.
c. Abnormal results/positive test: downsloping or flat ST segment 1 mm or greater for longer than 0.08 second, or greater than 1 mm depression from an initial ST segment depression of the patient’s baseline measurement
4. Ultrasonographic testing: Consider use of the following:
