MYOCARDIAL INFARCTION

MI refers to a dynamic process by which one

or more
regions of the heart experience a severe and
prolonged
decrease in oxygen supply because of
insufficient coronary blood flow;
subsequently, necrosis or death to the
myocardial tissue occurs.
The onset of the MI process may be sudden or
gradual, and the progression of the event to
completion takes approximately 3 to 6 hours.
 Pathophysiology and
Etiology
1. Acute coronary thrombosis (partial or total)associated
with 90% of MIs.
a. Severe CAD ( 70% narrowing of the artery)
precipitates
thrombus formation.
b. The first step in thrombus formation involves plaque
rupture. Platelets adhere to the damaged area.
c. Activation of the exposed platelets causes expression
of glycoprotein IIb/IIIa receptors that bind
fibrinogen.
d. Further platelet aggregation and adhesion occurs,
enlarging the thrombus and occluding the artery.
2. Other etiologic factors include
coronary artery spasm,
coronary artery embolism, infectious
diseases causing arterial
inflammation, hypoxia, anemia, and
severe exertion or stress on the heart
in the presence of significant CAD (ie,
surgical procedures or shoveling
snow).
3. Different degrees of damage occur to the
heart muscle:

. Zone of necrosisdeath to the heart

muscle caused by extensive and complete
oxygen deprivation; irreversible damage
. Zone of injuryregion of the heart muscle
surrounding the area of necrosis;
inflamed and injured, but still viable if
adequate oxygenation can be restored
 Zone of ischemiaregion of the
heart muscle surrounding the
area of injury, which is ischemic
and viable; not endangered
unless extension of the
infarction occurs
4. Classification of MI:
STEMIwhereby ST-segment elevations are
seen on ECG. The area of necrosis may or may
not occur through the entire wall of heart
muscle.
NSTEMIno ST-segment elevations can be
seen on ECG. ST depressions may be noted as
well as positive cardiac markers, T-wave
inversions, and clinical equivalents (chest
pain). Area of necrosis may or may not occur
through the entire myocardium.
5. The region(s) of the heart muscle
that becomes affected depends on
which coronary artery(s) becomes
obstructed
a. Left ventricle is a common and
dangerous location for an MI because
it is the main pumping chamber of
the heart.
b. Right ventricular infarctions
commonly occur with damage to the
inferior and/or posterior wall of the left
ventricle
 Clinical Manifestations
1. Chest pain
a. Severe, diffuse, steady substernal pain; may be
described as crushing, squeezing, or dull
b. Not relieved by rest or sublingual vasodilator
therapy,but requires opioids
c. May radiate to the arms (usually the left),
shoulders,neck, back, and/or jaw
d. Continues for more than 15 minutes
e. May produce anxiety and fear, resulting in an
increase in heart rate, BP, and respiratory rate
f. Some patients exhibit no complaints of pain.
2. Diaphoresis, cool clammy skin, facial
pallor
3. Hypertension or hypotension
4. Bradycardia or tachycardia
5. Premature ventricular and/or atrial
beats
6. Palpitations, severe anxiety,
dyspnea
7. Disorientation, confusion,
restlessness
8. Fainting, marked weakness
9. Nausea, vomiting, hiccups
10.Atypical symptoms: epigastric or
abdominal distress, dull aching or
tingling sensations, shortness of
breath, extreme fatigue.
 NURSING ALERT Many patients do
not have symptoms; these are silent
MIs. Nevertheless, there is still
resultant damage to the heart.
Women and diabetics usually present
with atypical and/or vague
complaints (eg, epigastric pain,
gas, feeling tired).
 GERONTOLOGIC ALERT Elderly
patients are more likely to
experience silent MIs or have
atypical symptoms, such as
hypotension, low body temperature,
shortness of breath, vague
complaints of discomfort, mild
perspiration, strokelike symptoms,
dizziness, or change in sensorium.
 Diagnostic Evaluation
ECG Changes:
1. Generally occur within 2 to 12 hours, but may
take 72 to 96 hours.
2. Necrotic, injured, and ischemic tissue alters
ventricular depolarization and repolarization.
a. ST-segment depression and T-wave inversion
indicate a pattern of ischemia.
b. ST elevation indicates an injury pattern.
c. Q waves indicate tissue necrosis and are
permanent.
A pathologic Q wave is one that is greater than 3
mm in depth or greater than one-third the height
of the R wave.
3. Location of the infarction (anterior wall,
 Cardiac Markers:
1. Nonspecific markers: These include lactate
dehydrogenase, aspartate aminotransferase,
and myoglobin.
. Specific cardiac markers: Troponinis a
contractile protein of the muscle cell and has
three subunits: troponin C, troponin I, and
troponin T. Troponin I and T are cardiac-specific.
. Troponin I is assessed more commonly
because the test is readily available.
 CKis a nonspecific marker, but is
more specific when broken down into
its subunits.
CK-MB is the CK isoenzyme found in
the heart.
 Other Findings:
1. Elevated CRP and lipoprotein(a) due to
inflammation in the coronary arteries.
2. Abnormal coagulation studies
(prothrombin time [PT], partial
thromboplastin time [PTT]).
3. Elevated white blood cell (WBC) count and
sedimentation rate due to the inflammatory
process involved in heart muscle cell
damage.
4. Radionuclide imaging allows recognition of
areas of decreased perfusion.
5. PET determines the presence of reversible
heart muscle injury and irreversible or
necrotic tissue; extent to which the injured
heart muscle has responded to treatment
can also be determined.
6. Cardiac muscle dysfunction noted on
echocardiography or cardiac magnetic
resonance imaging (MRI).
 Management
Pharmacologic Therapy
1. M (Morphine)given I.V. Used to treat chest pain.
Endogenous catecholamine release during pain imposes an
increase in the workload on the heart, thus causing an increase
in oxygen demand. Morphines analgesic effects decrease the
pain, relieve anxiety, and improve cardiac output by reducing
preload and afterload.
2. O (Oxygen)given via nasal cannula or face mask. Increases
oxygenation to ischemic heart muscle.
3. N (Nitrates)given sublingually, spray, or I.V. Vasodilator
therapy reduces preload by decreasing blood return to the
heart and decreasing oxygen demand.
4. A (Aspirin)immediate dosing by mouth is recommended to
halt platelet aggregation.
 Other Medications
Thrombolytic agents, such as tissue
plasma activator (Activase), streptokinase
(Streptase), and reteplase (Retavase),
reestablish blood flow in coronary vessels
by dissolving thrombus.
a. No effect on the underlying stenosis that
precipitated the thrombus to form.
b. b. Administered I.V. or I.C.
 Anti-arrhythmics, such as
amiodarone, decrease the ventricular
irritability that occurs after MI.
a. Given I.V. via bolus, then infusion
over 24 hours.
 Percutaneous Coronary Interventions:
1. Mechanical opening of the coronary vessel
can be performed during an evolving infarction.
2. Percutaneous coronary interventions (PCIs),
includin percutaneous transluminal coronary
angioplasty, coronary stenting, and atherectomy,
can be used instead of, or as an adjunct to,
thrombolytic therapy
3. Should be performed within 30 minutes of
initial diagnosis of MI.
 Surgical Revascularization
1. Emergency CABG surgery can be
performed within 6 hours of evolving
infarction.
 Complications
1. Dysrhythmias
2. Sudden cardiac death due to ventricular
arrhythmias
3. Infarct expansion (thinning and dilation of the
necrotic
zone)
4. Infarct extension (additional heart muscle necrosis
occurring after 24 hours of acute infarction)
5. Heart failure (with 20% to 35% left ventricle
damage)
6. Cardiogenic shock
7. Reinfarction
8. Ischemic cardiomyopathy
9. Cardiac rupture
10. Papillary muscle rupture
11. Ventricular mural thrombus
12. Thromboemboli
13. Ventricular aneurysm
14. Cardiac tamponade
15. Pericarditis (2 to 3 days after MI)
16. Dissection of coronary arteries
during angioplasty
17. Psychiatric problemsdepression,
personality changes
 Nursing Assessment
1. Gather information regarding the patients
chest pain:
a. Nature and intensitydescribe the pain in
patients own words and compare it with
pain previously experienced.
b. Onset and durationexact time pain
occurred as well as the time pain relieved
or diminished (if applicable).
c. Location and radiationpoint to the area
where the pain is located and to other
areas where the pain seems to travel.
d. Precipitating and aggravating
factors describe the activity
performed just before the onset of
pain and if any maneuvers and/or
medications alleviated the pain.
2. Question patient about other symptoms experienced
associated with the pain. Observe patient for
diaphoresis, facial pallor, dyspnea, guarding
behaviors, rigid body posture, extreme weakness, and
confusion.
3. Evaluate cognitive, behavioral, and emotional status.
4. Question patient about prior health status with
emphasis on current medications, allergies (opiate
analgesics, iodine, shellfish), recent trauma or surgery,
nonsteroidal anti-inflammatory drug (NSAID)
ingestion, peptic ulcers, fainting spells, drug and
alcohol use.
5. Analyze information for
contraindications for thrombolytic
therapy and PCI.
6. Gather information about presence or
absence of cardiac risk factors.
7. Identify patients social support
system and potential caregivers.
8. Identify significant others reaction to
the crisis situation.
NURSING DIAGNOSES
Acute Pain related to oxygen supply
and demand imbalance
1. Handle patient carefully while providing initial
care, starting I.V. infusion, obtaining baseline
vital signs, and attaching electrodes for
continuous ECG monitoring.
2. 2. Maintain oxygen saturation greater than 95%.
a. Administer oxygen by nasal cannula.
b. Encourage patient to take deep breathsmay
decrease incidence of dysrhythmias by allowing
the heart to be less ischemic and less irritable;
may reduce infarct size, decrease anxiety, and
resolve chest pain.
3. Offer support and reassurance to
patient that relief of pain is a priority.
4. Administer sublingual nitroglycerin
as directed; recheck BP, heart rate,
and respiratory rate before
administering nitrate therapy and
then 5 to 10 minutes after dose.
5. Administer opioids as prescribed (eg, morphine
decreases sympathetic activity and reduces heart
rate, respirations, BP, muscle tension, and anxiety;
reduces preload and afterload).
a. Use caution when administering opioids to
elderly patients and those with chronic obstructive
pulmonary disease, hypotension, or dehydration.
b. Remember that meperidine is rarely used
because it can have a vagolytic effect and cause
tachycardia, thus increasing myocardial oxygen
demands.
6. Obtain baseline vital signs before giving
agents and 10 to 15 minutes after each dose.
Place patient in a supine position during
administration to minimize hypotension.
7. Give I.V. nitroglycerin as prescribed. Monitor
BP continuously with automatic blood
pressure machine (contraindicated with
antithrombolytic therapy) or intraarterially or
every 5 minutes with auscultatory method
while titrating for pain relief.
Anxiety related to chest pain, fear of
death, threatening environment
1. Rule out physiologic etiologies for increasing or
new onset anxiety before administering as-
needed sedatives. Physiologic causes must be
identified and treated in a timely fashion to
prevent irreversible adverse or even fatal
outcomes; sedatives may mask symptoms,
delaying timely identification, diagnosis, and
treatment.
2. Assess patient for signs of hypoperfusion,
auscultate heart and lung sounds, obtain a rhythm
strip, and administer oxygen as prescribed. Notify
the health care provider immediately.
3. Document all assessment findings,
health care provider notification and
response, and interventions and response.
4. Explain to patient and family reasons for
hospitalization, diagnostic tests, and
therapies administered.
5. Explain equipment, procedures, and
need for frequent assessment to patient
and significant others.
6. Discuss with patient and family the anticipated nursing
and medical regimen.
a. Explain visiting hours and need to limit number of
visitors at one time.
b. Offer family preferred times to phone unit to check on
patients status.
7. Observe for autonomic signs of anxiety, such as
increases in heart rate, BP, respiratory rate, tremulousness.
8. Administer anti-anxiety agents as prescribed.
a. Explain to patient the reason for sedation: undue
anxiety can make the heart more irritable and require
more oxygen.
9. Maintain consistency of care with one
or two nurses regularly assisting
patient, especially if severe anxiety is
present.
10. Offer back massage to promote
relaxation, reduce muscle tension, and
improve skin integrity.
11. Use techniques, such as guided
imagery, to relieve tension and anxiety.
Decreased Cardiac Output related to
impaired contractility
1. Monitor BP every 2 hours or as
directed hypertension increases
afterload of the heart, increasing
oxygen demand; hypotension causes
reduced coronary and tissue perfusion.
2. Monitor respirations and lung fields
every 2 to 4 hours or as prescribed.
a. Auscultate for normal and abnormal
breath sounds (crackles may indicate
left-sided heart failure; diffuse crackles
indicate pulmonary edema).
b. Observe for dyspnea, tachypnea,
frothy pink sputum, orthopneamay
indicate left-sided heart failure,
pulmonary embolus, pulmonary edema.
3. Evaluate heart rate and heart sounds
every 2 to 4 hours or as directed.
a. Compare apical heart rate with radial
pulse rate, and determine the pulse deficit.
b. Auscultate heart for the presence of a
third heartsound (failing ventricle), fourth
heart sound (stiffening ventricular muscle
due to MI), friction rub (pericarditis),
murmurs (valvular and papillary muscle
dysfunction, intraventricular septal rupture).
4. Note presence of jugular vein
distention and liver engorgement.
a. Estimate right atrial pressure by
determining jugular venous pressure.
b. Observe for hepatojugular reflux.
5. Evaluate urine output (30 mL/hour)
decrease in volume reflects a decrease in
renal blood flow.
6. Monitor skin color and temperature (cool,
clammy skin and pallor associated with
vasoconstriction secondary to decreased
CO).
7. Be alert to change in mental status, such
as confusion, restlessness, disorientation.