I. Pathophysiology
a. Marked reduction or loss of blood flow through one or more
of the coronary arteries, resulting in cardiac muscle
ischemia, and over a finite period, resulting in necrosis
b. Occurs most often due to coronary artery disease (CAD)
c. Cellular ischemia and necrosis can affect the heart’s rhythm,
pumping action, and blood circulation.
d. Other problems may also ensue, such as heart failure, lifethreatening
arrhythmias, and death.
e. Delay in seeking treatment is the largest barrier to receiving
therapy quickly.
II. Classification
a. Type of myocardial infarction (MI) can be identified on the
electrocardiogram (ECG).
i. ST-segment elevation (also called STEMI)
ii. Non-ST elevation
b. Location of MI can be identified on the ECG.
i. Anterior wall of the ventricle
ii. Inferior wall of the ventricle
iii. Posterior wall of the ventricle
iv. Lateral wall of the ventricle
c. Infarcts are usually classified by size.
i. Microscopic (focal necrosis)
ii. Small (<10% of the left ventricle)
iii. Medium (10% to 30% of the left ventricle)
iv. Large (>30% of the left ventricle)
d. Point of time can be identified on the ECG by the Q wave
and the client’s history.
i. Acute or evolving infarction is characterized by the presence
of polymorphonuclear leukocytes unless the interval
between the onset of infarction and death is brief (e.g.,
6 hours), minimal, or no polymorphonuclear leukocytes
may be seen.
ii. Old or healed infarction is manifested as scar tissue
without cellular infiltration, a process usually requiring
5 to 6 weeks or more.
III. Etiology
a. CAD common cause with plaque formation narrowing
vessels and pieces of plaque breaking off, creating emboli
b. Severe spasm of a coronary artery is less common cause
c. Risk factors—age, being overweight or obese, smoking,
hyperlipidemia, family history
d. Greater risk in presence of kidney problems, peripheral
arterial disease, or prior MI
IV. Statistics (Centers for Disease Control and Prevention
[CDC],2007b; National Heart, Lung and Blood Institute
[NHLBI], 2007)
a. Morbidity: Approximately 1.1 million people in the United
States suffer from MI annually.
b. Mortality: almost 50% die, approximately 460,000 annually.
i. CAD is leading killer of both men and women in the
United States.
ii. Leading cause of death for American Indians, Alaskan
Natives, African Americans, Hispanics, and whites, and
second leading cause of death for Asians and Pacific
Islanders
c. Cost: Projected $258 billion spent for heart disease in 2006.
Care Setting
Myocardial infarctions are treated in the emergency room,
inpatient acute hospital, critical care unit (CCU), intensive
care unit (ICU), step-down unit, or medical unit.
Nursing Priorities
1. Relieve pain and anxiety.
2. Reduce myocardial workload.
3. Prevent, detect, and assist in treatment of life-threatening
dysrhythmias or complications.
4. Promote cardiac health and self-care.
Discharge Goals
1. Chest pain absent or controlled.
2. Heart rate and rhythm sufficient to sustain adequate cardiac
output and tissue perfusion.
3. Achievement of activity level sufficient for basic selfcare.
4. Anxiety reduced and managed.
5. Disease process, treatment plan, and prognosis understood.
6. Plan in place to meet needs after discharge, including
follow-up appointments.
NURSING DIAGNOSIS: acute Pain
May be related to
Tissue ischemia (coronary artery occlusion)
Possibly evidenced by
Reports of chest pain with or without radiation
Facial grimacing
Restlessness, changes in level of consciousness
Changes in pulse, BP
Desired Outcomes/Evaluation Criteria—Client Will
Pain Level
Verbalize relief or control of chest pain within appropriate period for administered medications.
Display reduced tension, relaxed manner, and ease of movement.
Pain Control
Demonstrate use of relaxation techniques.
ACTIONS/INTERVENTIONS
Pain Management
Independent
Monitor and document characteristics of pain, noting verbal
reports, nonverbal cues, for example, moaning, crying,
restlessness, diaphoresis, clutching chest, rapid breathing,
and hemodynamic response (BP and heart rate changes).
Obtain full description of pain from client including location,
intensity (0 to 10), duration, characteristics (dull or
crushing), and radiation. Assist client to quantify pain by
comparing it to other experiences.
Review history of previous angina, anginal equivalent, or MI
pain. Discuss family history if pertinent.
Instruct client to report pain immediately.
Provide quiet environment, calm activities, and comfort measures,
for instance, dry or wrinkle-free linens and backrub.
Approach client calmly and confidently.
Assist or instruct in relaxation techniques, such as deep, slow
breathing and distraction.
Check vital signs before and after administration of opioid
medication.
Collaborative
Administer supplemental oxygen by means of nasal cannula
or face mask, as indicated.
Administer medications, as indicated, for example:
Aspirin (ASA)
Anti-anginals, such as nitroglycerin (Nitro-Bid, Nitrostat,
Nitro-Dur), isosorbide dinitrate (Isordil), and mononitrate
(Imdur)
Angiotensin-converting enzyme (ACE) inhibitors, such as
lisinopril (Zestril), captopril (Capoten), and benazepril
(Lotensin)
Angiotensin receptor blockers (ARBs), such as candesartan
(Atacand), olmesartan (Benicar), and valsartan (Diovan)
Aldosterone blockers, such as eplerenone (Inspra) and
spironolactone
Analgesics, such as morphine sulfate
RATIONALE
Variation of appearance and behavior of clients in pain may
present a challenge in assessment. For example, men and
women consistently present differently, or an individual may
present differently from one episode to another. However,
most clients with an acute MI appear ill, distracted, and
focused on pain. Verbal history and deeper investigation of
precipitating factors should be postponed until pain is
relieved. Respirations may be increased as a result of pain
and associated anxiety; release of stress-induced catecholamines
increases heart rate and BP.
Pain is a subjective experience and must be described
by client. Provides baseline for comparison to aid in determining
effectiveness of therapy, resolution or progression
of problem.
May differentiate current pain from preexisting patterns as
well as identify complications, such as extension of
infarction, pulmonary embolus, or pericarditis.
Delays in reporting pain hinders pain relief and may necessitate
increased dosage of medication to achieve relief. In
addition, severe pain may induce shock by stimulating the
sympathetic nervous system, thereby creating further damage
and interfering with diagnostics and relief of pain.
Decreases external stimuli, which may aggravate anxiety and
cardiac strain and limit coping abilities and adjustment to
current situation.
Helpful in decreasing perception of or response to pain.
Provides a sense of having some control over the situation,
increase in positive attitude.
Hypotension and respiratory depression can occur as a result
of opioid administration. These problems may increase
myocardial damage in presence of ventricular insufficiency.
Increases amount of oxygen available for myocardial uptake
and thereby may relieve discomfort associated with tissue
ischemia.
Giving aspirin as soon as possible (unless contraindicated)
inhibits platelet activity, interrupting platelet aggregation at
the site of plaque rupture—a key mechanism in the unfolding
acute MI. Patients who receive aspirin in the acute
phase have a 15% lower mortality rate than those who
don’t (Lackey, 2006).
Nitrates are useful for pain control by coronary vasodilating
effects, which increase coronary blood flow and myocardial
perfusion. Peripheral vasodilation effects reduce the volume
of blood returning to the heart (preload), thereby
decreasing myocardial workload and oxygen demand.
May be given to reduce hypertension and reduce risk of developing
heart failure following MI in client with diminished
ventricular EF and in those with hypertension, diabetes, or
chronic kidney disease, unless contraindicated (Smith et al,
2006).
May be used in patients who are intolerant to ACE inhibitors
and have heart failure (HF) or have had an MI with left ventricular
EF less than or equal to 40%. They block the action
of angiotensin II that causes the blood vessels to dilate and
reduce BP.
May be used in post-MI patients who have had an MI, ACS, or
left ventricular dysfunction with or without HF symptoms,
unless contraindicated. They block the effects of aldosterone
on the kidneys, allowing the kidneys to excrete
extra sodium and water, thereby reducing BP.
Although intravenous (IV) morphine is the usual drug of
choice, other injectable opioids may be used in acute-phase
or recurrent chest pain unrelieved by nitroglycerin to
reduce severe pain, provide sedation, and decrease
myocardial workload. IM injections should be avoided, if
possible, because they can alter the CPK diagnostic indicator
and are not well absorbed in underperfused tissue.
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