Acute Myocardial Infarction

4.0 ANCC Contact Hours



Upon completion of this activity, participants should be able to:

  • Discuss the pathophysiology and causes of acute myocardial infarction (AMI)
  • Describe treatment guidelines for AMI
  • Discuss nursing management for patients with AMI
  • List how to apply the nursing processing in caring for patients with AMI


A myocardial infarction (MI) occurs when irreversible necrosis from ischemia occurs to the myocardium. The leading cause of MI is coronary artery disease (CAD), and it is also the leading cause of death worldwide. (The Centers for Disease Control and Prevention, [CDC], 2017).  

Every 42 seconds, one American person will have an acute myocardial infarction (AMI). AMI is a frequent cause of hospital admission in the United States and is associated with significant mortality and morbidity. Survivors of AMI are at increased risk for recurrent cardiovascular events, and its cost burden on the health care system remains substantial (Ibanez et al., 2018). 

The CDC (2018), also found that in the US, 790,000 AMI occur yearly and that 210,000 of these cases occur to individuals who have already had an MI. Upon completion of this module you will be able to discuss the pathophysiology and causes of AMI, describe the national treatment guidelines for AMI, and discuss how to manage and apply the nursing process in caring for patients with AMI.

Pathophysiology of AMI

An MI indicates irreversible myocardial injury resulting in necrosis of a significant portion of the myocardium generally >1 cm. The term "acute" denotes infarction less than 3-5 days old, when the inflammatory infiltrate is primarily neutrophilic. AMI may be either of the non-reperfusion type, in when the obstruction to blood flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow is long enough in duration usually hours to induce cell death but is reversed or restored afterwards (Urden, Stacy & Lough, 2018).

AMI generally refers to segmental by regional myocardial necrosis, typically endocardium-based, secondary to occlusion of an epicardial artery. In contrast, concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of prolonged cardiac arrest with resuscitation. Areas of myocardial infarction may be subepicardial if there is occlusion of smaller vessels by thromboemboli originating from coronary thrombi. In the majority of patients, there is obstructive coronary disease at angiography (Urden et al., 2018).

The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. There is often extension to the anterior portion of the ventricular septum with proximal left coronary occlusions (Urden et al., 2018).

In hearts with a right coronary dominance with the right artery supplying the posterior descending branch, a right coronary artery occlusion causes a posterior inferior infarct. With a left coronary dominance which includes about 15% of the population, a proximal circumflex occlusion will infarct the posterior wall; in the right dominant pattern, a proximal obtuse marginal thrombus will cause a lateral wall infarct only, and the distal circumflex is a small vessel (Urden et al., 2018).

The anatomic variation due to microscopic collateral circulation, which is not evident at autopsy, plays a large factor in the size of necrosis and distribution. Unusual patterns of supply to the posterior wall, such as wraparound left anterior descending or posterior descending artery supplied by the obtuse marginal artery, may also result in unexpected areas of infarct in relation to the occluded proximal segment (Urden et al. 2018).

Figure 1: Coronary Arteries and CAD
Figure 1 includes anterior and posterior views of the coronary arteries and veins. In addition, vessel layers and fatty deposit with in the arterial lumen up are shown.

Causes of acute angina and AMI

An AMI means that some portion of the heart muscle has died. Heart attacks almost always happen when the blood supply to the heart muscle has been cut off. In most cases, it is an acute event, resulting from the sudden rupture of an atherosclerotic plaque in the wall of a coronary artery in a person with typical CAD. However, there are other conditions that can also produce an AMI. (Urden, et al., 2018).

Table 1: Causes and examples of angina and AMI

Acute coronary syndrome (ACS)
Acute coronary syndrome associated with typical CAD is, by far, the most common cause of myocardial infarction
Unstable angina, ST elevationMI (STEMI) or non -ST elevation MI (NSTEMI)
Coronary artery spasm
Otherwise known as Prinzmetal angina
Duration of angina is less but with longer durations it can lead to more damage to the heart
Microvascular angina
Otherwise known as Cardiac Syndrome X
Occurs with the microvascular smaller cardiac vessels and may lead to an AMI
Stress cardiomyopathy
Otherwise known as Broken Heart Syndrome
Endothelial tissue dysfunction that can cause heart failure as a result of stressful life events
Viral myocarditisViral infection directly affecting the heart muscle. It seems to occur by producing extensive localized inflammation in cardiac muscle, with the interruption of the local blood supply
Blood clotting disordersCertain disorders of the blood clotting mechanism, such as Factor V Leiden predispose to abnormal blood clotting. People with such conditions can develop acute thrombosis of a coronary artery even without any underlying CAD, and thus, can experience myocardial infarctions
Coronary artery embolismA myocardial infarction can occur if a blood clot, usually originating within the heart, breaks free and becomes lodged in a coronary artery, interrupting the blood supply to part of the heart muscle
Several conditions predispose to blood clot embolization, including:
  • Atrial fibrillation
  • Dilated cardiomyopathy
  • Artificial heart valves
These patients are usually treated with anticoagulants.
GeneticsThe risk of premature heart attacks tends to have a genetic link. Evidence of familial hypercholesterolemia or Factor V Leiden places a patient at higher risk for CAD and cardiac events

Treatment Guidelines for AMI

MIs are classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). The term acute myocardial infarction (AMI) should be used when there is evidence of myocardial injury which is defined as an elevation of cardiac troponin values with at least one value above the 99th percentile upper reference limit with necrosis in a clinical setting consistent with myocardial ischemia (Ibanez et al., 2018).

The American College of Cardiology (ACC) and the American Heart Association (AHA) as well as the European Society of Cardiology (ESC), have developed guidelines for management of patients with STEMI (Ibanez et al., 2018; Jneid et al., 2017).

Before reading the recommendations review table 1 and table 2 for classes of recommendations and level of evidence. Class of recommendations include the strength of a recommendation, while level of evidence refers to the quality of evidence for a recommendation. (Ibanez et al., 2018)

Figure 2: STEMI
Stemi on an ECG. Note difference of ST elevation in STEMI

Figure 3: NSTEMI
NSTEMI on an ECG. Note ST depression

Table 2: Classes of Recommendations

Classes of RecommendationsDefinitionSuggested wording to use
Class IEvidence/general agreement that a given treatment or procedure is beneficial, useful, effectiveIs indicated/recommended
Class IIConflicting evidence and/or a divergence of opinion about the usefulness/efficacy of the given treatment or procedure
Class IIaWeight of evidence/opinion is in favor of usefulness/efficacyShould be considered
Class IIbUserfulness/efficacy is less well established by evidence/opinionsMay be considered
Class IIIEvidence or general agreement that the given treatment or procedure is not useful/effective, and in some cases may be harmfulIs not recommended

Table 3: Levels of Evidence

Level of Evidence A

Data derived from multiple random clinical trials or meta-analyses.

Level of Evidence B

Data derived from a single random clinical trial or large non-randomized studies.

Level of Evidence C

Consensus of opinion of the experts or small studies, retrospective studies registries.

Emergency Care

Initial Diagnosis

A diagnosis of AMI can be made based on clinical signs and symptoms as well as the results from diagnostic tests. Some signs and symptoms that are consistent with myocardial ischemia include:

  • Persistent chest pain
  • Radiating pain to the neck, lower jaw, or left arm
  • Atypical symptoms: (females more) shortness of breath, nausea, fatigue, palpitations, or syncope
  • 12-lead ECG: ST elevation - obtain as soon as possible to detect arrhythmias and provide prompt defibrillation if needed (Ibanez et al., 2018)

Review the 2017 treatment recommendations from the ESC

In cases of symptom relief after administration of nitroglycerin, another 12-lead ECG should be obtained. If complete normalization of the ST-segment elevation occurs along with symptom relief it is suggestive of coronary spasm with out without associated MI. In cases like these, it is recommended to obtain an early coronary angiography (within 24 hours). In cases with recurrent episodes of ST-segment elevation or chest pain, immediate angiography is required.

ECG monitoring should occur as soon as possible in all patients with suspected STEMI in order to assess and treat life-threatening arrhythmias and allow for prompt defibrillation if indicated. If STEMI is suspected, then a 12-lead ECG should be done as soon as possible. Take a look at the recommendations for time target recommendations for ECG and routine blood sampling in the table below.

Table 4: Recommendations for initial diagnosis for ECG monitoring and blood sampling

12-lead ECG within a maximum target of 10minsIB
ECG monitoring with a defibrillator capacity as soon as possible for those suspected for STEMIIB
For high suspicion of posterior wall MI (circumflex occlusion) use additional leads V7-V9IIaB
For inferior wall MI use additional right precordial leads (V3R and V4R) to identify RV infarctionIIaB
Routine blood sampling for serum markers as soon as possible but should not delay reperfusion treatmentIC

Challenging cases where ECG diagnosis may be more difficult

These cases require prompt management and include bundle branch block, ventricular pacing non-diagnostic ECG, isolated posterior MI and left main coronary obstruction. 

  • Bundle branch block:  In Left bundle branch block, a diagnosis of AMI is challenging but often possible if marked ST-segment abnormalities are present. The prognosis for right bundle branch block and ischemia is poor. It may be difficult to detect transmural ischemia in patients with chest pain and right bundle branch block. In these instances, emergent coronary angiography and percutaneous coronary intervention percutaneous coronary intervention (PCI) should be considered when persistent ischemic symptoms occur in the presence of right bundle branch block
  • Ventricular pacing: Pacemaker rhythm may also prevent interpretation of ST-segment changes and may require urgent angiography to confirm the diagnosis and begin therapy
  • Non-diagnostic ECG: Some patients with acute coronary occlusion may initially have an ECG without ST-segment elevation because they are seen very early after the onset of symptoms. In those cases, it’s important to repeat and monitor for ST-segment changes. In addition, there are other patients (e.g. left main disease, occult occlusion of a coronary artery, occlusion of a vein graft, and occluded circumflex coronary artery). These patients may be denied reperfusion therapy, which may result in a larger infarction and worse outcomes
  • Isolated Posterior MI: In AMI of the inferior and basal portion of the heart, often corresponding to the left circumflex territory, isolated ST-segment depression ≥ 0.5 mm in leads V1–V3 represents a significant finding. These should be managed as a STEMI. The use of additional posterior chest wall leads [elevation V7–V9 ≥ 0.5 mm (≥1 mm in men, 40 years old)] is recommended to detect ST-segment elevation consistent with inferior and basal MI
  • Left main coronary obstruction: The presence of ST depression ≥ 1 mm in eight or more surface leads (inferolateral ST depression), coupled with ST-segment elevation in aVR and/or V1, suggests multivessel ischemia or left main coronary artery obstruction, particularly if the patient presents with hemodynamic compromise (Ibanez et al., 2018)

Atypical ECG presentations that require prompt primary percutaneous coronary intervention (PCI)

PCI should be done promptly in patients with ongoing ischemic symptoms such as:

  • Bundle branch block: Criteria should be used to improve the diagnosis of right and left bundle branch block. The presence of right or left bundle branch block may confound the diagnosis of STEMI
  • Ventricular paced rhythm: During right ventricular right ventricular (RV) pacing, the ECG shows left bundle branch block and MI during pacing needs to be ruled out
  • Isolated posterior myocardial infarction: Isolated ST depression ≥ 0.5 mm in leads V1-V3 and ST-segment elevation ≥ 0.5 mm in posterior chest wall leads V7-V9
  • Ischemia from left main coronary artery occlusion or multi-vessel disease: ST depression ≥ 1mm in eight or more surface leads, couples with ST-segment elevation in a VR and or V1 suggest left main or left main or equivalent coronary obstruction or severe three vessel ischemia (Ibanez et al., 2018)

Relief of Symptoms

Relief of pain is of primary concern as well as breathlessness and anxiety. Pain is associated with sympathetic activation, which causes vasoconstriction and increases the workload of the heart. Some of the medications used are titrated such as morphine or opioids (Ibanez et al., 2018). Review when oxygen is indicated as well as treatment considerations for pain and anxiety relief.

Table 5: Relief of hypoxemia and symptoms



Oxygen is indicated for patients with hypoxemia (SaO2 < 90% or Pao2 < 60 mmHg)


Routine oxygen is not recommended in patients with saO2 ≥ 90%



Pain relief with titrated opioids should be considered to relieve pain


For anxiety a mild tranquilizer should be considered for very anxious patients


Cardiac Arrest

Many deaths occur early after a STEMI and happen outside of the hospital setting.  The primary lethal arrhythmia that occurs is ventricular fibrillation (VF). It is indicated that all medical and paramedical personnel caring for patients with suspected MI have access to defibrillation equipment and are trained in cardiac life support, and that ECG monitoring be implemented immediately for all patients with suspected MI (Ibanez et al., 2018).

As a result of the high prevalence of coronary occlusions and the potential difficulties in interpreting the ECG in patients after cardiac arrest, urgent angiography as within 2 hours should be considered in survivors of cardiac arrest, including unresponsive survivors, when there is a high index of suspicion of ongoing infarction as in the presence of chest pain before arrest, a history of established CAD, and abnormal or uncertain ECG results.

Unconscious patients admitted to critical care units after out-of-hospital cardiac arrests are at high risk for death, and neurologic deficits are common among those who survive. Recommendations for cardiac arrest are listed below and include guidelines for PCI, temperature control and medical management (Ibanez et al., 2018).

Table 6: Recommendations for Cardiac Arrest
(European Society of Cardiology (ESC), *AHA/ACC, 2017)


Primary PCI for patients with resuscitated cardiac arrest and an STEMI on the ECG


Targeted temperature is indicated early for those in cardiac arrest in patients who remain unresponsive


Transfer patients when MI suspected so they have access to defibrillation equipment and are trained in basic cardiac life support
*Within 120mins or less (Class I, B)


All medical and paramedical staff should have be trained access to defibrillation equipment


Urgent angiography and PCI if indicated should be available for all resuscitated cardiac arrest without a high suspicion of ongoing myocardial ischemia


Rapid cooling with large volumes of cold IV fluid immediately after return of spontaneous circulation is not recommended


Reperfusion Therapy

In patients with myocardial ischemia, STEMI reperfusion therapy should begin as soon as possible. Primary PCI is the preferred reperfusion strategy in patients with STEMI within 12 hours of symptom onset, provided it can be performed within 120 min from STEMI diagnosis. If the goal is to inject the bolus of fibrinolytics, the time goal is to do it within 10 minutes from diagnosis of STEMI. It is also recommended if possible, to shorten the time to treatment that fibrinolysis be started in the pre-hospital setting if possible. Review the recommendations for reperfusion therapy. Review the recommendations in table 7 for reperfusion therapy according to time goals and related diagnosis of STEMI or NSTEMI. (Ibanez et al., 2018; Jneid et al., 2017).

Table 7: Recommendations for reperfusion therapy

For patients with symptoms of ischemia of ≤ 12 hours duration and persistent ST elevation


Primary PCI is recommended over fibrinolysis within indicated time frames


If primary PCI cannot be performed after STEMI diagnosis, fibrinolytic therapy is recommended within 12 hours of symptom onset without contraindications
*Fibrinolytic therapy is recommended if door to device time exceeds 120 mins (Class I, B)


In patients with NSTEMI, a primary PCI is indicated with suspected active ischemic MI symptoms and at least one of the following criteria should be present:

  • Acute heart failure
  • Mechanical complications of MI
  • Life threatening arrhythmia or cardiac arrest
  • Recurrent ongoing angina refractory to medical treatment
  • Cardiogenic shock or hemodynamic instability
  • Recurrent dynamic ST-segment or T-wave changes especially with intermittent ST-segment elevation

*In the absence of contraindications, fibrinolytic therapy should be given to patients with STEMI onset of ischemic symptoms within the previous 12 hours when it’s anticipated that a primary PCI cannot be performed with 120 mins of entry into the hospital. (Class I, A)


Early angiography within 24 hours if symptoms are completely resolved and ST-segment elevation is completely normalized spontaneously or as a result of nitroglycerin


For patients with ongoing symptoms suggestive of ischemia, hemodynamic or instability a time frame from symptom onset that is less than 12 hours a primary PCI strategy is recommended


For patients presenting with late onset of symptoms (12-48 hours) after symptom onset, a routine primary PCI should be considered


In asymptomatic patients, a routine PCI of an occluded infarct-related artery greater than 48 hours after onset of STEMI is not indicated


Table 8: Treatment time targets
(Ibanez et al., 2018; Jneid et al., 2017)

IntervalsTime Targets (Max time)

First medical contact with ECG and diagnosis

≤10 min

STEMI diagnosis to choose primary PCI (wire crossing)

≤120 min

Time to wire crossing from STEMI diagnosis to wire crossing in patients who present at primary PCI hospitals

≤60 min

*Primary PCI should be performed in patients with STEMI and ischemic symptoms if less than 12 hours’ duration. (Class I, A)

< 12 hrs

For STEMI diagnosed transferred patients to wire crossing

≤90 min

For STEMI diagnosis to bolus or infusion start of fibrinolysis in patients unable to meet primary PCI times
*In patients where fibrinolytic therapy is chosen as an initial therapy, it should be given within 30 mins (Class I, B)

≤10 min

Time delay from the start of fibrinolysis to the evaluation of its effectiveness

60-90 min

Time delay from the start of fibrinolysis to angiography (if fibrinolysis is successful)

2-4 hrs

Table 9: AHA/ACC Guideline for the Management of Patients with STEMI 
The figure below compares treatment guidelines for patients who have STEMI and who are initially seen at a PCI capable hospital verses a non-PCI capable hospital. Review the various recommended treatment options.

Initially seen at a PCI capable hospital

1To cath lab for primary PCI if door to device time ≤ 90 mins (Class I, A)
2Diagnostic Angiogram
3Medical therapy

Initially seen at a non-PCI capable hospital

1Door in and out time ≤ 30 mins
2Transfer for primary PCI (Door to device time ≤ 120 mins/Class I, B)
3Administer fibrinolytic therapy within 30 min of arrival time when time from door to device is anticipater to be ≤ 120 mins
4Urgent transfer for PCI for patients with evidence of reocclusion or evidence of failed reperfusion
5Transfer for angiography and revascularization within 3-14 hrs for other patients as part of an insurance strategy

The AHA/ACC (2017) have listed 13 measure sets for STEMI/NSTEMI:

Table 10: Performance measures for STEMI/NSTEMI

1. Aspirin at arrival

  • 162-325mg before primary PCI (class I, B)
  • 162-325mg loading dose and clopidogrel 300mg loading dose for those < 75 years old > 75 years old should receive 75mg) for those who have an STEMI who receive fibrinolytic therapy
  • Non-enteric coated chewable aspirin (162 to 325 mg) to all patients with NSTEMI-ACS without contraindications as soon as possible after presentation and a maintenance dose of 81mg-162 mg (Class I, A)
  • Patients not on aspirin therapy should be given non-enteric coated aspirin 325mg before PCI (Class I, B)
  • For patients that cannot take aspirin who have NSTEMI-ACS should take a loading dose of clopidogrel followed by a daily maintenance dose (Class I, B)

2. Aspirin at discharge

  • Continue aspirin indefinitely after PCI
  • Aspirin should be continued indefinitely and clopidogrel 75mg daily should be continued for 2 weeks (Class I, A) and up to 1 year for patients who have fibrinolytic therapy (Class I, C)
  • After PCI aspirin should be continued at 82mg-325mg daily indefinitely
  • Aspirin should be continued indefinitely. The maintenance dose should be 81mg daily in patients treated with tricagrelor and 81mg-325mg daily in all other patients (Class I, A)

3. Beta-blocker at discharge

  • For patients without contraindications for use, beta-blockers should be continued (Class I, B)
  • In patients with stabilized heart failure and reduced systolic beta-blocker therapy should occur with 1 of the 3 drugs proven to reduce mortality in patients with heart failure, sustained-release succinate, carvedilol or bisopropol. (Class I, C)
  • Beta-blockers should not be administered to patients with ACS with a recent history of methamphetamine or cocaine use who demonstrate signs of acute intoxication due to the risk of coronary spasm. (Class III, C).

4. High intensity statin at discharge

(Titrated by age, side effects and diagnosis)

To reduce Atherosclerotic Cardiovascular Risk in Adults:
  • For those ≤ 75 years old who have clinical atherosclerotic disease (even though with an MI) with high intensity statin (Class I, A)
  • For those >75 who have contraindications to high dose statins, a moderate dose statin should be recommended (Class IIA, B)

5. Evaluation of left ventricular ejection fraction (LVEF)

  • LVEF should be measured in all patients with STEMI (Class I, C)
  • A non-invasive imaging test is recommended to evaluate LV function in patients with definite ACS (Class I, C)

6. Angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) for LVSD at discharge

  • An ACE should be administered within the first 24 hours to all patients with STEMI with anterior location, HF, or ejection fraction (EF) less than or equal to 0.40, unless contraindicated (Class I, A)
  • An ARB should be given to patients with STEMI who have indications for but are intolerant of ACE inhibitors (Class I, B)
  • ACE inhibitors should be started and continued indefinitely in all patients with LVEF < 0.40 and in those with hypertension, stable chronic kidney disease and diabetes mellitus unless contraindicated. (Class I, A)
  • ARBs are recommended in patients with heart failure or MI with LVEF < 0.40 who are unable to take an ACE inhibitor. (Class I, A)

7. Door to needle time

  • In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI at non–PCI-capable hospitals when the anticipated arrival-to-device time at a PCI-capable hospital exceeds 120 minutes because of unavoidable delays. (Class I, B)
  • When fibrinolytic therapy is indicated or chosen as the primary reperfusion strategy, it should be administered within 30 minutes of hospital arrival (Class I, B)
  • In the absence of contraindications, fibrinolytic therapy should be given to patients with STEMI and onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI cannot be performed within 120 minutes of entry to the hospital (Class I, A)
  • Fibrinolytic therapy should not be administered to patients with ST depression except when a true posterior (MI is suspected or when associated with ST elevation in lead aVR. (Class III, B)
  • In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and cardiogenic shock who are unsuitable candidates for either PCI or CABG. (Class I, B)

8. First medical contact to device time

  • Primary PCI is the recommended method of reperfusion when it can be done in a timely manner. (Class I, A)
  • EMS transport directly to a PCI-capable hospital for primary PCI is the recommended triage strategy for patients with STEMI, with an ideal door-to-device time system goal of 90 minutes or less (Class 1, B)
  • Primary PCI should be performed in patients with STEMI and ischemic symptoms of less than 12 hours’ duration (Class I, A)

9. Reperfusion Therapy

  • Reperfusion therapy should be administered to all eligible patients with STEMI with symptom onset within the prior 12 hours (Class I, A)
  • In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI at non–PCI-capable hospitals when the anticipated door-to-device time at a PCI-capable hospital exceeds 120 minutes because of unavoidable delays. (Class I, B)
  • In the absence of contraindications, fibrinolytic therapy should be given to patients with STEMI and onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI cannot be performed within 120 minutes of entry into the hospital (Class I, A)

10. Door in door out time

  • Immediate transfer to a PCI-capable hospital for primary PCI is the recommended triage strategy for patients with STEMI who initially arrive at or are transported to a non–PCI-capable hospital, with an FMC-to-device time system goal of 120 minutes or less (Class I, B)
  • Immediate transfer to a PCI-capable hospital for coronary angiography is recommended for suitable patients with STEMI who develop cardiogenic shock or acute severe HF, regardless of the time delay from MI onset (Class I, B).

11.Time to primary PCI among transferred patients

Immediate transfer to a PCI-capable hospital for primary PCI is the recommended triage goal for patients with STEMI who initially arrive at or are transported to a non–PCI-capable hospital, with a door-to-device time system goal of 120 minutes or less (Class I, B)

12. Cardiac rehab referral

  • For all CABG patients (Class I, B)
  • STEMI patients (Class I, B)
  • NSTEMI patients (Class I, B)
  • Chronic Angina (Class I, B)
  • Disease prevention in women: ACS or risk for new onset angina, stroke rehab (Class I, A)
  • Recent PTCA intervention (CLass I, B)

13. PY12 Inhibitor prescribed at discharge
(Examples: clopidogrel, prasugrel or tricagrelor)

  • P2Y12 inhibitor therapy should be given for 1 year to patients with STEMI who receive a stent (bare-metal or drug-eluting) during primary PCI (Class I, B)
  • A P2Y12 inhibitor in addition to aspirin should be administered for up to 12 months to all patients with NSTE-ACS without contraindications who are treated with either an early invasive or ischemia-guided strategy (Class I B)

(Jneid et al., 2017)

Nursing Assessment

Nurses play a vital role in management of an AMI. They must respond rapidly and efficiently to patients who are experiencing symptoms of acute MI. In addition, they must quickly work to assess patients; administer sublingual nitroglycerin and aspirin, if indicated; obtain a 12-lead ECG; and notify the physician (Urden et al, 2018).

When assessing patients with suspected AMI, the nurse's priority is to assess the ABCs: airway, breathing, and circulation as well as level of consciousness and cardiac arrhythmias. Since the incidence of sudden death is very high during the first hour of an MI, it is essential to monitor the patient closely and be prepared for an emergency (Urden et al, 2018).

Emergency departments (ED) often have devices that can detect (point of care devices) cardiac enzymes in blood within seconds after labs are drawn. However, nurses in other areas of the hospital may not have access to this rapid-acting diagnostic equipment. Although nurses may draw stat labs, the results are not readily available. Immediately obtain a 12-lead ECG and assess the patient's signs and symptoms. Show the ECG to the physician immediately for interpretation as well as communicate your physical assessment to the provider. Completing these tasks while labs are pending will help prevent delay of diagnosis (Urden et al, 2018).

One of the most important assessments that nurses can do with suspected AMI is the pain assessment. Chest pain can occur with pulmonary edema, congestive heart failure, pericarditis, pneumothorax, and unstable angina. Therefore, it is helpful to use a systematic method for assessing chest pain. Areas to consider include precipitating factors, quality, region, and radiation (Urden et al, 2018).

Precipitating factors – Ask the patient the following questions:

  • What brought on the symptoms? 
  • What time did they begin? 
  • What were you doing at the time? 
  • What did you do to relieve the pain, and did it help? 

The nurse should also document if the patient was doing any particular activity and if cessation of the activity helped the pain to decrease (Urden et al, 2018).

Quality - MI-associated chest pain is often very intense; therefore, it is important to obtain an objective description of the patient's discomfort. Ask the patient to describe the pain to determine whether the pain feels like pressure, burning, squeezing, or aching. Ask the patient to rate the pain on a scale of 0–10, with 0 being no pain and 10 being the worst pain ever experienced. Be sure to document the quality of the pain on your initial assessment to establish a baseline. This baseline will help you determine whether the patient experiences any changes in condition later, and it will help nurses in other units if the patient transfers to their care (Urden et al, 2018).

Region and radiation – Chest pain associated with MI often begins in the center of the chest and radiates to other areas. Common areas include the left arm, the neck, the jaw, and the back. Ask the patient to point to where it hurts. Also, keep in mind that the patient may only have pain in the arms, neck, or jaw. Some patients who complain of a toothache have been found to actually be suffering an acute MI. The patient history is the primary step in the nursing clinical assessment of patients presenting with AMI. The gathered information is useful for nursing as well as medical decisions. For a patient in acute distress a focused assessment includes asking a few questions regarding the chief complaint.  
The focused assessment includes assessing the patient in these four areas:

  • Review of the presenting symptoms/illness
  • Overview of general cardiac history (surgeries, interventions, diagnostic studies, medications/herbs/vitamins)
  • Examination of general health status and family history of CAD, hypertension, peripheral artery disease, stroke or diabetes mellitus (DM)
  • Survey of lifestyle including risk factors for CAD (Urden et al, 2018)

Table 11: Subjective and Objective Assessment Examples

Chest pain/pressure/squeezingECG: STEMI
P - provoke, precipitate, palliate
Q - quality
R - radiate
S - severity/symptoms
T - time
Decreased oxygenation
Reports of impending doomSigns of left ventricular failure (e.g. S3 heart sound)
Shortness of breathTachycardia/Bradycardia
Elevated cardiac enzymes

Nursing Diagnoses, Planning, Implementation

Upon the completion of the nursing assessment a plan of care will begin. There is a range of medical diagnosis and as a result nursing diagnoses for hemodynamic monitoring that center around these 3 nursing diagnoses (Urden et al, 2018)

  1. Ineffective Tissue Perfusion
  2. Decreased Cardiac Output
  3. Deficient/Excess Fluid Volume

The following are some of the nursing interventions and rationales (Check with the provider’s orders to assure accuracy):

MONA: Morphine, Oxygen, Nitroglycerin, and Aspirin (ASA)

(This is a mnemonic and not the correct order of administration)

Initial treatment NSTEMI/STEMI:

Morphine: Given if ASA and nitroglycerin do not relieve chest pain. Initial dose is 2-4 mg IVP.

Oxygen: If under 94% or if patient is short of breath give 2L NC initially. Oxygen can cause vasoconstriction thus worsening the situation and decreasing blood flow. Administer oxygen when clinically relevant.

Nitroglycerin (NTG): This is the initial medication given, along with aspirin. Nitroglycerin dilates the blood vessels to help allow any blood flow that might be impeded. Give 0.4 mg sublingual tab, wait 5 minutes, if the chest pain is not relieved administer another dose. This can happen 3 times total. Monitor a patient’s blood pressure, hold for a systolic BP of less than 90 mmHg.

Aspirin: given to thin the blood. A total of 4 baby aspirin (81 mg each) can be given for a total of 324 mg. Refer back to the guideline recommendations for STEMI and NSTEMI (Urden et al, 2018).

Additionally, the following may also occur and varies per patient situation:

  1. 12 lead ECG: If initial 12-lead ECG indicates inferior MI, do a right-sided 12 lead ECG.
    • Assess a 12 lead ECG immediately on anyone complaining of chest pain to determine if a STEMI is occurring.
    • Right sided 12 lead ECG shows the right side of the heart to assess for right ventricular ischemia. Inferior MI’s require a different treatment approach.
  2. 3 or 5 Lead monitoring
    • All patients should be on continuous monitoring after a 12 lead ECG. Monitor  for worsening condition such as cardiac arrest.
  3. Cardiac Catheterization with Percutaneous Coronary Intervention (PCI)
    • A patient who has an STEMI will be rushed to the cath lab so they can locate the clot and place a stent to regain cardiac artery patency.
    • A patient may also go to the cath lab without having a STEMI, and they may still find a clot. Most NSTEMI’s are treated without catheterization.
  4. BP Monitoring: It can be measured by the systolic BP or the Mean Arterial Pressure 
    • Monitoring blood pressure assures that pressure is not going to dislodge a clot or put too much stress on damaged cardiac tissue
  5. Heparin
    • An anticoagulant that breaks/prevents up cardiac thrombi
    • Monitor a PTT or Factor HA Inhibition (Anti-Xa) to adjust and maintain therapeutic levels
      • For STEMI: 
        Bolus: 60 units/kg (max 4,000 units)
        Continuous infusion: 12 units/kg/hr
      • For NSTEMI:
        Bolus: 60-70 units/kg (max 5,000 units)
        Continuous Infusion: 12-15 units/kg/hr
  6. Insert Large Bore IV and draw initial Cardiac Enzymes
    • IV access is important for administration of medications, possible interventions if angina worsens, and any scans that may be needed to rule out thrombi
    • Cardiac enzymes further serve to rule out AMI and can give an indication to the extent of myocardial damage
      • Troponin I
      • CK
      • CK-MB
      • Myoglobin
  7. Monitor Cardiac Enzymes: Troponin I Creatine Kinase-MB (CKMB)
    The values of these enzymes are based on institutional laboratory technique. If they are elevated it indicates that the cardiac muscle is stressed out or injured.
    • Troponin I is an enzyme that helps the interaction of myosin and actin in the cardiac muscle. When necrosis of the myocyte happens, the contents of the cell eventually will be released into the bloodstream. Troponin can become elevated 2-4 hours after in ischemic cardiac event and can stay elevated for up to 14 days.
    • Creatine Kinase MB (CKMB): This enzyme is found in the cardiac muscle cells and catalyses the conversion of ATP into ADP providing cells energy to contract. When the cardiac muscle cells are damaged the enzyme is eventually released into the bloodstream.CKMB increases within 3-6 hours of symptoms and peak levels occur between 16-30 hours. As a result they should be checked at admission, and then every 8 hours afterwards.
      • CK: This test’s values are influenced by gender, race and activity. The normal range is 22-198 U/L. Increased valued can indicate muscle damage either acute or chronic.
      • MB: This enzyme is found in the muscles of most mammals and is found in the bloodstream after muscle injury.

(Urden et al, 2018)

Complications Associated with AMI

As nurses, it’s imperative to understand the complications for AMI so that prompt identification and treatment can occur. Many impressive advances have been made in the treatment of acute MI over the past several years; however, it is still one of the leading causes of death. This is due to the serious complications usually associated with an infarction. These include coronary artery reocclusion, heart failure and cardiogenic shock, and arrhythmias (Urden et al, 2018).

Coronary Artery Reocclusion

A small number of patients will experience reocclusion of the artery after thrombolytic therapy even when preventative measures are taken. This happens because the clot in the artery has been dissolved, the athersclerotic plaque is still present. If anticoagulation is inadequate, another thrombus may form. About 50% of the reocclusions occur within the first 24 hours following thrombolytic therapy. Symptoms such as chest pain, nausea, diaphoresis, and ST segment elevation will usually be similar to those experienced with the original MI. With this in mind, it is crucial to monitor the patient closely and be aware of changes indicative of reocclusion. Since readministration of a thrombolytic agent is not recommended, the patient will need to have a percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) if angioplasty is not an option or unsuccessful (Urden et al, 2018).

Heart Failure and Cardiogenic Shock

Congestive heart failure following a myocardial infarction can range from mild to severe, depending on the extent of ventricular damage. Heart failure occurs when myocardial tissue is damaged, and the ventricle no longer works as an efficient pump. In right-sided failure, the compromised right ventricle causes fluid to back up in the peripheral circulation. In left-sided heart failure, fluid backs up in the pulmonary circulation. The nurse should monitor for signs of heart failure, including shortness of breath; hypoxia; production of pink, frothy sputum; hypotension; oliguria; confusion or changes in level of consciousness; and tachycardia (Urden et al, 2018).

Treatment of heart failure depends on the severity. Expect to administer supplemental oxygen, diuretics, a continuous nitroglycerin infusion, morphine, inotropic agents to improve cardiac contractility, and an angiotensin-converting enzyme (ACE) inhibitor. These patients will be quite ill and may require transfer to the critical care unit. Mechanical ventilation may also be required (Urden et al, 2018).

Patients with heart failure can rapidly decline into cardiogenic shock. Cardiogenic shock occurs when 40% or more of the myocardium has been affected by the infarction. Because the heart is incapable of contracting with sufficient force to pump enough blood, the vital organs and peripheral tissues cease to function as a result of ischemia. The patient may experience the following symptoms: pulmonary congestion, diaphoresis, cool extremities, and mental confusion. Treatment for cardiogenic shock is aggressive and can include fluid replacement, inotropic drugs, and an intra-aortic balloon pump which is an invasive device used to decrease ventricular workload and improve coronary artery perfusion (Urden et al, 2018).

Unfortunately, death occurs in about 85% of patients who develop cardiogenic shock. Therefore, nursing interventions should include assisting patients and families to work through end of life issues (Urden et al, 2018).


Successful thrombolysis can cause a variety of cardiac arrhythmias, such as ventricular tachycardia, premature ventricular contractions, accelerated idioventricular rhythm, and sinus bradycardia. These are generally accepted as normal consequences of coronary reperfusion, and treatment is not necessary unless the patient becomes unstable (Urden et al, 2018).

Ventricular fibrillation (VF)

The majority of sudden cardiac deaths are because of ventricular fibrillation, or v fib. This arrhythmia results in an ineffective quivering of the ventricles and no cardiac output. Treatment includes basic life support (airway, breathing, and circulation), defibrillation, and advanced cardiac life support. The sooner the ventricular fibrillation is treated, the greater the chance of survival for the patient. Nurses in all areas of health care should be able to recognize the signs of cardiac arrest and intervene appropriately (Urden et al, 2018).

Ventricular tachycardia (VT)

Patients who have suffered an acute MI may experience ventricular tachycardia, or v tach. This ventricular arrhythmia can be benign or it can be life threatening. Patients may be asymptomatic or they may experience shortness of breath, chest discomfort, palpitations, and syncope. Patients may be given an antiarrhythmic, such as lidocaine, procainamide, or amiodarone, to reestablish sinus rhythm. If the patient is unstable, electrical cardioversion may be conducted in an attempt to convert the myocardium to a sinus rhythm. This arrhythmia is most common in patients who have experienced an anterior or anterolateral MI (Urden et al, 2018).

Sinus bradycardia and heart block (SB)

Bradycardia is a slowing of the heart rhythm. The patient may experience hypotension and syncope which usually responds to oxygen and atropine. Heart blocks occur as a result of problems in the atrioventricular (AV) node of the conduction system. Electrical impulses are not conducted from the atrium to the ventricles, which can cause a decrease in cardiac output. To correct the arrhythmia, patients may need transcutaneous (external) pacing or surgery to insert a transvenous (internal, temporary) pacemaker (Urden et al, 2018).

Patient and Family Education/Support for AMI

Nurses play an important role in educating the patient and family. The patient and family will need education about the MI. The education should begin as soon as the patient comes in contact with the healthcare system. Initial information should be simple and concise and focus on what to expect. It may also be necessary to educate the patient and family about thrombolytic agents and PCI so that informed decisions can be made. Nurses need to remember to use familiar terms when describing medications and procedures. For example, the nurse may want to describe the thrombolytic agent as a "clot-buster" or medicine used to dissolve clots in the arteries of the heart. Nurses should also explain that these drugs "thin the blood" and may cause bleeding complications. Most important, nurses should offer emotional support and attempt to relieve anxiety (Urden et al, 2018).

It is appropriate in most cases to begin more detailed education once the patient's condition has stabilized and some of the initial feelings of fear and anxiety have subsided. This is a good time to begin explaining exactly what happened. It may be helpful to use pictures and diagrams of the heart and provide educational information that the patient can take home and review (Urden et al, 2018).

Nurses should take into account the patient's learning style, learning challenges, and home language. Give information in a way that will be most beneficial to the patient. Provide written materials in the patient's native language and use a translation service or professional translator if needed. To address individual learning needs, nurses can offer the patient choices such as "Would you like to read a booklet about what to expect after your heart attack or would you prefer to watch a 15 minute video?" Always remain open to queries and don't give the patient and family a sense that they are asking irreverent questions (Urden et al, 2018).

The next step in the patient education process usually occurs once the patient transfers from an intensive care unit to a monitored floor or intermediate care area. Patients and families may be less anxious at this point and may begin making plans for discharge. Patients may also begin to ask questions about lifestyle changes. Keep in mind that each individual may have different ideas about what caused the MI. One patient may attribute it to smoking while another patient may think it was brought on by workplace stress. The nurse should discuss the patient's perceptions and talk about making lifestyle changes specific to these perceptions, keeping in mind that patients will usually have more motivation to change the things that are most meaningful to them (Urden et al, 2018).

Discharge teaching is an essential part of nursing care. The nurse should give the patient verbal and written instructions about medications, smoking cessation, exercise and daily activities, ability to return to work, and dietary changes. Most patients will also be discharged with medication prescriptions, including anticoagulants, beta-blockers, ACE inhibitors, and an lipid-lowering drug. It is helpful to provide verbal and written instructions about the medications. It is also valuable to assess if the patient has the necessary resources to acquire medications. If not, a social worker may be able to assist the patient. The patient and family also should be given specific instructions regarding what to do if chest pain reoccurs (Urden et al, 2018).

Most health care facilities offer an outpatient cardiac rehabilitation program. Nurses should be familiar with available resources and promote development of a healthy lifestyle. A hospital case manager can assist patients in establishing a rehab plan. (Urden et al, 2018)

When an individual experiences an acute MI, healthcare professionals focus most of their attention on meeting the eminent physical needs of the patient. However, an acute MI usually occurs suddenly and without warning and can be an extremely stressful experience for the patient and family. Many patients often ignore symptoms when they first begin or contribute them to heartburn or muscle pain. They may also delay seeking medical care because they are in denial, refusing to believe they could be having a heart attack. When symptoms become more serious, patients often appear apprehensive and fearful. They may have a feeling of impending doom and ask questions such as "Am I going to die?" (Urden et al, 2018).

The emotional stress can have a profound effect on physiological functions as well. During times of anxiety and apprehension, the sympathetic nervous system causes changes to occur (the "fight or flight" response). The heart rate increases, cardiac contractility becomes stronger, blood vessels constrict, and, initially, cardiac output increases. These responses in turn increase the myocardial oxygen demand in a compromised patient. As the heart demands more oxygen and the supply diminishes, the patient may experience more chest pain and other signs of hemodynamic instability. These changes then create more fear and anxiety in the patient.

In the hospital, the patient's anxiety may increase due to unfamiliarity of the surroundings and procedures. For this reason, attempt to make the environment less stressful. Prevent unnecessary intrusions, conversations, disturbances, and interruptions. If possible, schedule lab tests, ECGs, x-rays, and other diagnostic tests to be done within the same time frame. Rest is an essential part of the recovery process and allowing for uninterrupted periods of rest and sleep is helpful. Reducing bright lights and noise is also important. During patient transfers from one unit to the next, avoid having large gatherings of nurses at the bedside. One or two nurses calmly and confidently admitting the patient usually helps to decrease patient and family anxiety. During the admission process, explain each procedure, treatment, and piece of equipment to the patient, offering reassurance that the patient is being closely monitored (Urden et al, 2018).


In the critical care situation of AMI, patient assessment findings guide treatment decisions in very timely manner. Evaluation occurs immediately after each treatment and changes are made along the way. In addition, there is a range of diagnostic tools available to the critical care nurse, which will continue to be more complex and expand in the care of the patient with AMI. (Urden et al, 2018).

Case Study Review

During change of shift, Marco and Maria sat at the nursing station on the general adult orthopedic unit. Marco, the day-shift nurse quickly reported off to Maria on the patient in room 701: "Mr. Olsen is a 58-year-old male patient who was admitted to our floor Tuesday after a left knee replacement. He has a dry and intact dressing on his knee. He has a fentanyl PCA and his pain seems to be under control. He has been pretty sleepy all evening and really has not had any complaints. He is a large guy. He's 6'0" and he weighs about 115 kg. He is a smoker, but his anxiety level is under control now. I also read in his chart earlier this evening in the history and physical that he has a family history of heart disease. He’s healthy except for a bad knee. I cannot think of anything else to tell you about this patient. It should be a quiet night for you."

After gathering report on every patient, Maria performed her assessments and passed her evening meds. During that time, Mr. Hamilton described some vague knee pain, but overall said he was feeling good. Around 3 a.m., when everything was quiet, Mr. Hamilton put on his call signal and indicated that he was having pain. Maria assumed he was referring to his knee pain, and just needed couple Norco to reduce his pain enough to sleep.

She stopped by the medication dispensary and withdrew a couple hydrocodone tablets on her way to his room. Mr. Hamilton looked extremely anxious. When Maria inquired about the intensity and location of his pain, he stated that his knee felt fine, but he was experiencing a tight, squeezing sensation in the center of his chest and rated the pain a 9 on a scale of 1–10. He indicated that just before he called the nurse's station, he awoke with serious discomfort. Maria quickly assessed the patient and noted his blood pressure was 167/89, his pulse was 100, and his respirations were 24. His skin was pale, cool, and clammy. A quick chest auscultation revealed clear and equal breath sounds and normal heart sounds.

Maria realized that the symptoms were most likely unrelated to his knee surgery and recalled the classic signs and symptoms of acute MI. She also remembered the importance of early treatment and immediately called Mr. Hamilton’s attending physician. The doctor ordered a 12-lead ECG. She ordered nitroglycerin sublingual 0.4 mg q 5 minutes × 3 as long as the patient's blood pressure remained elevated. She also ordered 162 mg aspirin to be chewed. After reviewing the faxed ECG, the physician called Maria and told her that the cardiologist and the cardiac catheterization lab team were on their way to take the patient for an urgent cardiac catheterization. The 12-lead ECG showed significant ST-segment elevation in leads II, III, and AVF. Maria recalled her ECG training and knew that Mr. Hamilton was having an inferior MI. The doctor ordered STAT lab draws for cardiac enzymes, as well as a complete blood count, a coagulation study, and a basic metabolic panel. She also ordered 5 mg morphine IV to be administered immediately.

Within 15 minutes, the cath lab team arrived to take Mr. Hamilton for percutaneous coronary intervention, where the cardiologist placed a stent to open what was a 95% occlusion of the right coronary artery. Afterward, Mr. Hamilton was transferred to the cardiac care unit for further monitoring. Twenty-four hours later, he was transferred to a telemetry unit and continued his recovery until he was discharged from the hospital. (Urden, et al., 2018)

Nursing diagnosis for Mr. Hamilton:

Based on the assessment, Maria identifies the following nursing diagnoses:

  • Acute pain related to ischemic myocardial tissue
  • Anxiety and fear related to change in health status
  • Ineffective protection related to the risk of bleeding secondary to thrombolytic therapy
  • Risk for decreased cardiac output related to altered cardiac rate and rhythm

Expected outcomes - Mr. Hamilton will:

  • Rate chest pain as 2 or lower on a pain scale of 0 to 10.
  • Verbalize reduced anxiety and fear.
  • Demonstrate no signs of internal or external bleeding.
  • Maintain an adequate cardiac output during and following reperfusion therapy.

Planning and implementation
The following interventions are planned and implemented during the immediate phase of Mr. Hamilton’s hospitalization.

 Instruct to report all chest pain and:

  • Monitor and evaluate pain using a scale of 0 to 10.

    Titrate intravenous nitroglycerin infusion for chest pain; stop infusion if systolic BP is below 100 mmHg.

  • Administer 2 to 4 mg morphine intravenously for chest pain unrelieved by nitroglycerin infusion.

  • Encourage verbalization of fears and concerns.

  • Respond honestly, and correct misconceptions about the disease, therapeutic interventions, or prognosis.

  • Assess knowledge of CAD

  • Explain the purpose of thrombolytic therapy to dissolve the fresh clot and reperfuse the heart muscle, limiting heart damage.

  • Explain the need for frequent monitoring of vital signs and potential bleeding.

  • Assess for manifestations of internal or intracranial bleeding: complaints of back or abdominal pain, dysrhythmias or other cardiac events per protocol.

  • Notify the physician.

  • Discuss continuing cardiac care and rehabilitation.

  • Headache, decreased level of consciousness, dizziness, bloody secretions or excretions, or pallor. Test all stools, urine, and vomitus for occult blood. Notify physician immediately of any abnormal findings.

  • Monitor for signs of reperfusion: decreased chest pain, return of ST segment to baseline, reperfusion dysrhythmias (e.g., PVCs, bradycardia, and heart block).

  • Continuously monitor ECG for changes in cardiac rate, rhythm, and conduction. Assess vital signs.


Centers for Disease Control and Prevention (CDC). (2017). Heart Attack Facts and Statistics.

Retrieved on December 8, 2018 from

Jneid, H., Addison, D., Bhatt, D.L., Fonarow, G.C., Gokak, S., Grady, K.L.,. Pancholy, S. (2017)

AHA/ACC clinical performance and quality measures for adults with ST-elevation and non–ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. Circulation: Cardiovascular Quality and Outcomes, 10, e000032. doi: 10.1161/HCQ.0000000000000032.

Ibanez, B., James, S., Agewall, S., Antunes, M. J., Bucciarelli-Ducci, C., Bueno, H., Widimský, P. (2018)

2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). European Heart Journal, 39(2), 119-177. doi: 10.1093/eurheartj/ehx393.

Urden, L., Stacy, K, & Lough, M. (2018).

Critical Care Nursing: Diagnosis and Management, 8th Ed. Cardiovascular Alterations (pp 184-199). Maryland Heights, MO: Elsevier.