Definition
A.Acute myocardial infarction (MI) is a prolonged lack of myocardial oxygenation leading to necrosis of a portion of the heart muscle. It is caused by atherosclerotic coronary artery disease (CAD), which alone or in association with other factors causes complete blockage of one of the coronary arteries.
Incidence
A.The estimated annual incidence of heart attack in the United States is 720,000 new attacks and 335,000 recurrent attacks. Average age at the first heart attack is 65.6 years for males and 72.0 years for females. Approximately every 40 seconds, an American will have a heart attack. Despite a marked decrease in incidence and mortality during the past three decades, MI continues to be the leading cause of death in this country, accounting for one-fourth of all fatalities. More women die from heart disease than men.
Pathogenesis
A.Abrupt coronary artery occlusion is the primary cause of most MIs. Occlusions can result from atherosclerotic plaque, intracoronary thrombus formation, or arterial spasm.
Predisposing Factors
A.Hypercholesterolemia: Increased low-density lipoprotein (LDL), decreased high-density lipoprotein (HDL).
B.Hypertriglyceridemia.
C.Premature familial onset of coronary heart disease (CHD), formerly called CAD, before age 55.
D.Smoking.
E.Hypertension (HTN).
F.Obesity.
G.Sedentary lifestyle.
H.Diabetes mellitus.
I.Aging.
J.Stress.
Common Complaints
A.Primary complaint: Pain somewhere in the chest, often described as worst pain ever experienced.
B.Nausea.
C.Vomiting.
D.Diaphoresis.
E.Indigestion.
Other Signs and Symptoms
A.Pain in abdomen, arm, back, jaw, and neck.
B.Chest heaviness or tightness.
C.Anxiety.
D.Cough.
E.Dyspnea.
F.HTN or hypotension.
G.Weakness, lightheadedness, syncope.
H.Pallor.
I.Orthopnea.
J.Fatigue.
K.Malaise.
Potential Complications
A.Arrhythmias.
B.Heart failure (HF).
C.Cardiogenic shock.
D.Rupture of left ventricular (LV) papillary muscle.
E.Ventricular septal rupture.
F.Pericarditis or Dressler’s syndrome.
G.Ventricular aneurysm.
H.Thromboembolism.
I.Death.
Subjective Data
A.Ask the patient if they were participating in some type of activity and what it was that brought about or preceded the episode of chest pain.
B.Ask the patient to describe the duration of pain and what time of day symptoms began.
C.Ask the patient to describe pain, for example, crushing, stabbing, or burning.
D.Ask the patient where sensation began and in what direction it radiates.
E.Identify the degree of pain by using a pain scale of 0 to 10, with 0 being no pain.
F.Ask the patient to list all medications currently being taken, particularly substances not prescribed and illicit drugs such as cocaine.
Physical Examination
Patients presenting with acute chest pain should be quickly assessed for the need to call emergency services/911 for immediate transport to the hospital.
A.Check pulse, respirations, blood pressure (BP), and pulse oxygenation.
B.Inspect:
1.Inspect general appearance, noting dyspnea and weakness.
2.Inspect skin for pallor and diaphoresis.
3.Inspect legs for edema.
4.Inspect chest wall for visible pulsations.
5.Inspect neck for jugular vein distension.
6.Observe nail beds for signs of cyanosis and note capillary filling time.
C.Palpate:
1.Palpate abdomen for organomegaly.
2.Palpate peripheral pulses in legs.
3.Palpate femoral pulses.
D.Auscultate:
1.Auscultate carotid arteries.
2.Auscultate abdomen.
3.Conduct a complete heart exam, checking for dysrhythmias.
4.Conduct a complete lung exam.
E.Mental status: Assess for confusion and anxiety.
Diagnostic Tests
A.ECG: Shows inverted T waves, ST segment elevation, and Q waves. One normal ECG initially does not always rule out MI; perform serial ECGs if MI suspected.
B.Laboratory testing:
1.Cardiac biomarkers/enzymes.
2.Troponin levels: A protein that is released when necrosis of the cardiac muscles occurs.
3.Creatine kinase (CK): Creatine kinase-muscle/brain (CK-MB) levels increase 3 to 12 hours after the chest pain begins, peak at 24 hours, and return to normal in 48 to 72 hours.
4.Myoglobin: Urine myoglobin levels rise 1 to 4 hours after the chest pain begins.
5.Complete blood count (CBC).
6.Chemistry profile.
7.Lipid profile.
8.C-reactive protein (CRP) and inflammatory markers.
C.Cardiac imaging: Coronary angiogram.
Differential Diagnoses
A.Acute MI.
B.Unstable angina pectoris.
C.Aortic dissection.
D.Pulmonary embolism (PE).
E.Pericarditis.
F.Esophageal spasm.
G.Pancreatitis.
H.Biliary tract disease.
Plan
A.General interventions:
1.Educate the patient and family regarding the signs and symptoms of an acute MI.
2.Long-term care and treatment should be reinforced at each patient visit.
B.Patient teaching:
1.Educate the patient about modifying controllable risk factors such as keeping diabetes and HTN under control, diet, exercise, and smoking cessation.
2.If known CHD is present:
a.Instruct the patient on signs and symptoms of an acute MI.
b.Advise the patient to have a plan in seeking medical attention or dialing 911 if signs and symptoms occur.
c.Advise the patient to carry nitroglycerin at all times and to take the nitroglycerin at the first sign of chest pain. If there is no relief after 5 minutes, 911 should be called. Nitroglycerin may be repeated every 5 minutes times three doses.
d.Encourage cardiopulmonary resuscitation (CPR) training for family members and close friends.
e.Exercise regimen: Encourage routine exercise for the patient most days of the week, such as walking, treadmill use, and so on, once released by the cardiologist.
f.
See Section III: Patient Teaching Guide Nicotine Dependence.
C.Dietary management: Counsel the patient on nutrition and low-fat, low-cholesterol, and low-sodium diets. Recommend dietary approaches to stop hypertension (DASH) diet and lifestyle changes. Provide dietary handouts on the DASH diet and a low-fat/low-cholesterol/low-sodium diet. See Appendix B for the DASH diet.
D.Pharmaceutical therapy:
1.When MI is suspected: Aspirin 160 to 325 mg (four 81 mg baby aspirin) chewed or swallowed as soon as possible. Enteric-coated aspirin delays absorption and therefore is not recommended.
2.Instruct the patient on how to take sublingual nitroglycerin tablets and other medications.
3.Nitrates: Nitroglycerin sublingual 0.2 to 0.6 mg every 5 minutes for ischemic chest pain in the absence of hypotension.
4.If pain persists after three doses of nitroglycerin:
a.Morphine sulfate intravenous (IV); 2 to 4 mg IV, repeating every 5 minutes until pain resolves. Dose may be increased to 2 to 8 mg per dose as tolerated. Monitor side effects: Nausea/vomiting, dizziness, hypotension, respiratory depression.
5.Oxygen therapy: 2 to 4 L per nasal cannula.
6.If there are no contraindications (bradycardia, HF, second- or third-degree heart block, asthma, shock), beta-blockers may be started IV during the acute phase and changed to oral therapy during the course of treatment.
7.Fibrinolytic therapy may be used for patients with suspected MI with ST-elevation myocardial infarction (STEMI) or non-ST-elevation myocardial infarction (NSTEMI) with left bundle branch block.
8.After an MI, if the patient is not currently on a statin, a statin should be started.
Follow-Up
A.Follow-up is determined by patient’s needs, severity of acute MI, and whether complications are present.
Emergent Issues/Instructions
A.If MI is suspected, refer patient for immediate hospitalization.
B.Administer four aspirin 81 mg swallowed or chewed while waiting for emergency medical service (EMS).
Consultation/Referral
A.According to the 2015 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of a patient who is a candidate for reperfusion who is seen at a percutaneous coronary intervention (PCI)-capable hospital, this patient should be sent to the cath lab for primary PCI in less than or equal to 90 minutes. If the patient is at a facility that is non-PCI capable, then a transfer should be made to a PCI facility as soon as possible and in less than or equal to 120 minutes. If the time lapse will be greater than 120 minutes, then it is recommended to administer fibrinolytic therapy within 30 minutes of arrival.
B.Follow up with cardiologist as scheduled when discharged from the hospital.
Individual Considerations
A.Geriatrics:
1.The approach to the older adult with MI is similar to that of younger adults with some key, potential differences in symptoms:
a.Non-ST elevation MI is more common than STEMI in older adults, and both recurrent MI and HF as a result of MI are more common in the elderly.
b.In the first hours of MI, the elderly are more likely to complain about symptoms other than typical coronary chest pain. They often describe dyspnea, fatigue, and dizziness. Confusion or altered mental status may be the presenting manifestation of acute MI in up to 20% of patients older than 85 years of age.
c.Even when classic ischemic precordial discomfort is present, it tends to be less severe and less well defined. The elderly appear to have reduced pain perception.
d.Older patients are also more likely to have silent
or unrecognized MIs compared to younger patients. These facts often result in delays in MI diagnosis in the elderly. The length of time from symptom onset to hospital admission is significantly longer for the elderly compared to the younger patient.
2.Post-MI pharmaceutical therapy for the elderly is similar to treatment for those in younger age groups with some key potential differences based on individual considerations and renal function:
a.An older adult (over age 65) treated for an acute coronary syndrome (MI or angia) should discontinue nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs (other than aspirin) are independent risk factors for cardiovascular disease.
b.Unless contraindicated, older adults who have had an MI should take aspirin, a beta-blocker, and an angiotensin-converting enzyme inhibitor (ACEI).
c.Long-acting nitrates (e.g., isosorbide mononitrate) or long-acting calcium channel blockers (CCBs) may be used for chronic angina if beta-blockers are contraindicated.
3.Beers Criteria precautions:
a.Use nitrates with caution due to an increased risk for syncope.
b.Avoid nondihydropyridine CCBs in HF with reduced ejection fraction due to increased risk of fluid retention and exacerbation of HF.