Acute Myocardial Infarction (Nursing)

Learning Outcome

  1. Describe the presentation of acute myocardial infarction (MI)
  2. Recall the nursing diagnosis of acute MI
  3. Summarize the treatment of acute MI
  4. Describe ways to reduce the risk of coronary artery disease


Acute myocardial infarction is one of the leading causes of death in the developed world. The prevalence of the disease approaches three million people worldwide, with more than one million deaths in the United States annually. Acute myocardial infarction can be divided into two categories, non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is similar to NSTEMI. However, cardiac markers are not elevated.[1][2][3]

An MI results in irreversible damage to the heart muscle due to a lack of oxygen. An MI may lead to impairment in diastolic and systolic function and make the patient prone to arrhythmias. In addition, an MI can lead to a number of serious complications. The key is to reperfuse the heart and restore blood flow. The earlier the treatment (less than 6 hours from symptom onset), the better the prognosis.

An MI is diagnosed when two of the following criteria are met:

  1. Symptoms of ischemia
  2. New ST-segment changes or a left bundle branch block (LBBB)
  3. Presence of pathological Q waves on the ECG
  4. Imaging study showing new regional wall motion abnormality
  5. Presence of an intracoronary thrombus at autopsy or angiography

Nursing Diagnosis

  • Acute pain
  • Activity intolerance
  • Fear/anxiety
  • Risk for decreased cardiac output
  • Risk for ineffective tissue perfusion
  • Risk for excess fluid volume
  • Deficient knowledge


The etiology of acute myocardial infarction is decreased coronary blood flow. The available oxygen supply cannot meet oxygen demand, resulting in cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Other etiologies of decreased oxygenation/myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.[4][5]

Risk Factors

Among patients suffering from acute myocardial infarction, 70% of fatal events are due to occlusion from atherosclerotic plaques. As atherosclerosis is the predominant cause of acute myocardial infarction, risk-factors for atherosclerotic disease are often mitigated in the prevention of disease. Modifiable risk factors account for 90% (men) and 94% (female) of myocardial infarctions. Modifiable risk factors include cigarette smoking, exercise, hypertension, obesity, cholesterol, LDL, and triglyceride levels. In contrast, age, sex, and family history are non-modifiable risk factors for atherosclerosis.[6][7]


The history of and physical exam is often inconsistent when evaluating for acute myocardial infarction. The history should focus on the onset, quality, and associated symptoms. Recent studies have found that diaphoresis and bilateral arm radiating pain most often are associated with myocardial infarction in men. Associated symptoms include:

  • Lightheadedness
  • Anxiety
  • Cough
  • Choking sensation
  • Diaphoresis
  • Wheezing
  • Irregular heart rate

Physical exam, most importantly, should note vital signs and patient’s appearance, including diaphoresis, as well as lung findings, and cardiac auscultation.

  • Heart rate may reveal tachycardia, atrial fibrillation or ventricular arrhythmia
  • Unequal pulses if the patient has an aortic dissection
  • Blood pressure is usually high, but hypotension if the patient is in shock
  • Tachypnea and fever are not uncommon.
  • Neck veins may be distended indicating right ventricular failure
  • Heart: lateral displacement of apical impulse, soft S1, palpable S4, new mitral regurgitation murmur. A loud holosystolic murmur radiating to the sternum may be indicative of ventricular septal rupture.
  • Wheezing and rales are common if the patient has developed pulmonary edema
  • Extremities may show edema or cyanosis and will be cold


Early and rapid ECG testing should be employed in all patients presenting with chest pain. Women often have atypical symptoms such as abdominal pain or dizziness and may present without chest pain at all. Elderly patients more often have shortness of breath as their presenting symptom for myocardial infarction. All of these presentations should prompt ECG testing, as well.[8][9][10]

The ECG is highly specific for MI (95% to 97%), yet not sensitive (approximately 30%). Right-sided, posterior lead placement, and repeat ECG testing can increase ECG sensitivity. For example, peaked T-waves on ECG, known as “hyperacute T waves,” often indicate early ischemia and will progress to ST elevation. When present, findings of  ST-elevations greater than 2 mm in two contiguous leads on ECG (inferior: leads II, III, aVF; septal equal V1, V2; anterior: V3, V4; lateral: I, aVL, V5, V6) are indicative of an ST-elevation myocardial infarction. Often, there are ST depressions that are visualized in opposite anatomical regions of the myocardium.

ECG diagnosis of STEMI can be difficult, particularly in patients with a left bundle branch block and pacemakers. Sgarbosa described criteria that can assist the physician or practitioner in diagnosing STEMI in these patients. Isolated ST-elevations in aVR are indicative of left main coronary artery occlusion in the appropriate clinical setting. Wellens noted deeply biphasic T waves in V2, V3, and found they are often predictive of an impending proximal left anterior descending artery occlusion, which may lead to devastating anterior wall myocardial infarction.

Patients that present with myocardial infarction may not have diagnostic ST-elevation ECG abnormalities. Patients with typical chest pain should be investigated for NSTEMI with subtle abnormalities on ECG, including ST-depressions and T wave changes. Serial ECGs can be helpful here as well to look for dynamic changes. ECG without acute changes or any abnormalities is common in NSTEMI.

There are diagnostic guidelines that can assist the practitioner in determining whether further testing is useful in identifying patients with NSTEMI. Given the poor sensitivity of ECG for STEMI, troponins are almost universally used for patients with a suspicious clinical history. The HEART score has been validated and popularized. It utilizes clinician’s suspicion, patient risk factors, ECG diagnostics, and troponin level to determine the “risk level” of the patient. 

Laboratory Features

  • Cardiac troponins should be the only marker ordered
  • CBC
  • Lipid profile
  • Renal function
  • Metabolic panel

Medical Management

All patients with STEMI and NSTEMI require immediately chewed aspirin 160 mg to 325 mg. Furthermore, the patient should have intravenous access and oxygen supplementation if oxygen saturation is less than 91%. Opioids may be used for pain control in addition to sublingual nitroglycerin if the blood pressure is adequate.[11][12][13]

Treatment for STEMI includes immediate reperfusion. Preference is for emergent percutaneous coronary intervention (PCI). Before PCI, patients should receive dual antiplatelet agents, including intravenous heparin infusion as well as an adenosine diphosphate inhibitor receptor (P2Y2 inhibitor), most commonly ticagrelor. Furthermore, glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may be given at the time of percutaneous intervention.

If percutaneous intervention is unavailable within 90 minutes of the diagnosis of STEMI, reperfusion should be attempted with an intravenous thrombolytic agent.

NSTEMI in a stable asymptomatic patient may not benefit from emergent percutaneous coronary intervention and should be managed medically with antiplatelet agents. Percutaneous coronary intervention can be done within 48 hours of admission and may lead to improved in-hospital mortality and decreased length of stay. In NSTEMI patients with refractory ischemia or ischemia with hemodynamic or electrical instability, PCI should be performed emergently

Before discharge for acute MI, patients may routinely be given aspirin, high-dose statin, beta-blocker, and/or ACE-inhibitor.

If PCI is contemplated, it should be done within 12 hours. If fibrinolytic therapy is considered, it should be done within 120 minutes. Parenteral anticoagulation, in addition to antiplatelet therapy, is recommended for all patients.

Nursing Management

  • Obtain ECG daily
  • Always make sure the patient has 2 large-bore IVs
  • Monitor cardiac enzymes
  • Initiate treatment for acute MI
  • Administer morphine for pain
  • Start aspirin and nitroglycerin (0.4 mg sublingual)
  • Provide oxygen if pulse oximetry is less than 94% at room air
  • Ensure patient seen by a cardiologist
  • Monitor vitals, daily weight, and urine output
  • Administer heparin as ordered for STEMI
  • If the patient has cardiac catheterization, check groin for hematoma and feel distal leg pulses

When To Seek Help

  • Hypotension
  • Nausea and vomiting
  • Continuing chest pain
  • Loss of distal leg pulses (think emboli or low blood pressure)
  • If a sudden change in mental status
  • Continuing oxygen desaturation
  • Tachycardia or arrhythmias
  • Sudden onset of a loud murmur (think new-onset mitral regurgitation or ventricular rupture)

Outcome Identification

  • Improve breathing
  • Chest pain relief
  • Improved tissue perfusion
  • Able to regain function as before


  • ECG
  • Cardiac enzymes
  • Oxygenation-pulse oximetry
  • Vital signs
  • The intensity of chest pain
  • Palpate leg pulses
  • Auscultate chest for rales and new murmurs

Coordination of Care

Acute myocardial infarction is managed by an interprofessional team that is solely dedicated to heart disease. Besides the cardiologist, the team usually consists of a cardiac surgeon, an interventional cardiologist, intensivist, cardiac rehabilitation specialist, critical care or cardiology nurses, and physical therapists. Because many patients die before even reaching the hospital, the key is to educate the patient on symptoms and early arrival to the emergency department.

The pharmacist, nurse practitioner, and primary care providers should educate patients on how to take nitroglycerin, and if there is no relief after three doses, then 911 should be called.

At triage, the nurse should immediately communicate with the interprofessional team as time to reperfusion is limited. The cardiologist may consider thrombolysis or PCI, depending on the duration of symptoms and contraindications. All patients need ICU monitoring. Nurses should be vigilant about the potentially life-threatening complications and communicate with the team if there are abnormal clinical signs or laboratory parameters. No patient should e prematurely discharged because complications of an MI can occur up to a week after an MI. After stabilization, patients need thorough education by the nurse on the reduction of risk factors for coronary artery disease. Besides a nurse practitioner, the social worker should be involved to facilitate home care, cardiac rehab, and the need for any support services while at home. The pharmacist should address and provide education concerning appropriate medication dosing and discuss potential side effects.

After discharge, the patient needs to enter a cardiac rehabilitation program, eat a healthy diet, discontinue smoking, abstain from alcohol, reduce body weight, and lower cholesterol and blood glucose levels. The patient should be educated on the importance of compliance with medications to lower blood pressure and blood cholesterol. [14][15][16] [Level 2] Pharmacists review prescribed medications, check for interactions, and provide patient education about the importance of compliance. [Level 5]


Acute myocardial infarction continues to have high mortality out of the hospital. Data indicate that at least one-third of patients die before coming to the hospital, and another 40%-50% are dead upon arrival. Another 5%-10% of patients will die within the first 12 months after their myocardial infarction. Readmission is common in about 50% of patients within the first 12 months after the initial MI. The overall prognosis depends on the ejection fraction, age, and other associated comorbidity. Those who do not undergo any revascularization will have a poorer outcome compared to patients who undergo revascularization. The best prognosis is in patients with early and successful reperfusion and preserved left the ventricular function.[17][18][19] [Level 2]

Health Teaching and Health Promotion

  • Eat health, low salt diet
  • Medication compliance
  • Maintain healthy body weight
  • Become physically active, enrol in cardiac rehabilitation
  • Control blood pressure, blood sugars and lipids
  • Do not smoke
  • Follow up with clinician

Risk Management

  • Do not disregard chest pain- call clinician
  • If vital signs abnormal, refer patient ASAP to cardiologist
  • If laboratory parameters abnormal, consult with physician right away

Discharge Planning

  • Eat healthy
  • Ambulate and become physically active
  • Take medications as prescribed
  • Follow up in clinic as scheduled
  • Do not smoke

Evidence-Based Issues

The earlier an MI is treated, the better the prognosis. Hence, nurses should be vigilant about MI symptoms and signs.

Reduce risk factors to improve outcomes.

(Click Image to Enlarge)
Specimen showing myocardial infarction in the left ventricle and the interventricular septum. The asterisk(*) also indicates left ventricular hypertrophy.
Specimen showing myocardial infarction in the left ventricle and the interventricular septum. The asterisk(*) also indicates left ventricular hypertrophy.
Contributed by Wikimedia Commons (CC by 4.0)

(Click Image to Enlarge)
Heart attack (myocardial infarction) warning signs in women.
Heart attack (myocardial infarction) warning signs in women.
Contributed by U.S. Department of Health and Human Services Office on Women's Health

(Click Image to Enlarge)
An ECG showing pardee waves indicating acute myocardial infarction in the inferior leads II, III and aVF with reciprocal changes in the anterolateral leads.
An ECG showing pardee waves indicating acute myocardial infarction in the inferior leads II, III and aVF with reciprocal changes in the anterolateral leads.
Contributed by Wikimedia Commons, Glenlarson (Public Domain-Self)

Contribute by Wikimedia Commons, Goslar T, Podbregar M. (CC by 2.0)
Article Details

Nurse Editor

Kim Ziegler

Article Author

Oren Mechanic

Article Author

Michael Gavin

Article Editor:

Shamai Grossman


8/11/2021 8:36:04 PM



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