Myocardial Infarction NCLEX Review (Part 1)

Definition: The heart’s myocardial tissue layer dies from decreased blood flow due to:

Causes:

Blockage in the coronary artery from coronary artery disease (most common)

Coronary spasms from illicit drug usage drugs like cocaine or hypertension. This causes constriction of the coronary
artery and stops blood flowing to the heart muscle.

Damage to the coronary artery due to coronary artery dissection. This is a tear in the inner layer “tunica intima” of
the artery which causes blood to leak in the “tunica media”. This restricts the flow of blood through the coronary
artery. It can happen spontaneously and occurs more likely in young, active women.

Pathophysiology of MI:

The coronary arteries supply the heart with nutrients. They branch off from the aorta into the left and right coronary
artery.

Left Coronary Arteries:

Important to note: Blockages in the left coronary arteries can cause the worst damage from a myocardial infarction.
This is because blockages in the left coronary artery can cause anterior wall death which affects the left ventricle.
Anterior MIs affect the most myocardial tissue, especially if the blockage occurs before it branches off and this can
extend into the septum and lateral wall.

Left anterior descending artery: supplies right and left ventricle and septum. This is the most common site for
blockages.

Left circumflex: supplies the left atrium and ventricle

Right Coronary Arteries:

Right coronary artery: supplies the right atrium and ventricle

Right marginal artery: supplies the right ventricle and septum

What happens to the heart muscle after an MI?

When a coronary artery becomes 100% blocked the muscle cells die. Cell death is irreversible after about 30 minute.
The cells are gone forever and can never be replaced.

Early signs of an MI…no physical changes to heart muscle yet (until about 6-8 hours), but when the myocytes die
cardiac enzymes are released: CK-MB (4 to 6 hours after MI), troponin (2-4 hours…most regarded) myoglobin (1
hours after injury…show injury but not too specific).

Within 24-36 hours inflammation sets in and neutrophils come on the scene and congregate at the damaged tissue
site. This causes complication of possible pericarditis. In addition, within 24 hours the heart fails to pump efficiently
(cardiogenic shock) and arrhythmias can develop (atrial and ventricular dysrhythmia along with AV blocks).

Within 10 days, granulation occurs when the macrophages come on the scene. They are WBCs who’ve came to clean
up the dead cells and other components. However, the new tissue formed from granulation is not well formed and is
weak. This increases the chance of cardiac rupture.

Within 2 months scarring occurs, and the heart is affected in size and functionality due to increased collagen.
Other Complications:
Heart failure, depression, and ventricular aneurysm

Signs & Symptoms of Myocardial Infarction

Remember the mnemonic: CRUSHING

 Chest pain (intense, heavy)

 Radiating chest pain that goes to left arm, jaw, back
 Unrelieved by nitroglycerin or rest (chest pain)
 Sweating (cold)
 Hard to breathe (shortness of breath)
 Increased heart rate, blood pressure or irregular heart rate
 Nausea with vomiting
 Going to be anxious and scared

Note: Women can present differently by not having “heavy” chest pain. Their chest pain may be felt in the lower
part of the chest, experience shortness of breath, and feel extremely fatigued. They may not seek immediate help
because they think they are “just ill” with a sickness.

Silent MIs: this is where the patient has no symptoms of chest pain. Mainly occurs in diabetics due to diabetic
neuropathy where the nerves that feel pain are damaged in the heart.

Diagnosing with Cardiac Markers & Other Tools

When the heart muscle is injured it releases cardiac markers overtime. This will help the health care provider know
that something is going on along with a 12-lead EKG (and other tools).

Blood Tests Cardiac markers:

Troponins: gold standard now used by most hospitals in assessing for an MI. It is a protein released from the heart
when damage is present from a myocardial infarction. They are drawn in a series (troponin levels will elevate 2-4
after injury). They are usually drawn every 6 hours for 3 sets. The nurse’s role is to collect levels and monitor them
for an upward trend. If levels are increasing, the physician will need to be notified.

Myoglobin: an early cardiac marker released after heart injury (1 hour after injury). However, not very cardiac
specific…used in early detection..will need more blood tests to further evaluate.

CK: protein released when there is muscle damage (not specific to just the heart)…so CK-MB may be ordered to tell if
it is the heart since CK-MB represents heart muscle (it elevates 4-6 hr after injury).

Other tools used:

Echocardiogram: ultrasound of the heart to look at the heart to see if there is damaged from an MI.

Heart Cath: a procedure where a special dye is injected into the coronary arteries and an X-Ray is taken to see if
there are any blockages, their locations, and if there is any muscle damage. If there is a blockage, the cardiologist will
assess the need for stent placement or other techniques used to open the artery.

Stress test with Myocardial Perfusion Imaging: assesses how the heart responses to stress and evaluate the blood
flow to the myocardial muscle.

EKG:

Shows ischemia, injury, and infarction.

Nurses role: obtaining EKG (or delegating it to be done) looking for any EKG changes and notifing md of them

Compare newly obtained EKG to previous EKGs

What are you looking for on the EKG? Please watch the lecture video above for an in depth explanation on this. This
explanation starts at time mark: 18:33

1. ST-segment depression or elevation

2. T-wave inversion or hyperacute
3. Pathological Q-wave

Know the views of the heart based on an EKG reading:

1. I, AVL, V5, V6: Lateral

2. II, III, AVF: Inferior
3. V 1, V2: Septal
4. V 3, V4: Anterior

Nursing Interventions for Myocardial Infarction

Monitoring & Assessing Cardiovascular system:

 Obtain a 12-lead EKG, have continuous bedside cardiac monitoring

 Monitoring blood pressure and heart rate
 Place on oxygen via nasal cannula per MD order 2-4 L
 Working IV access (multiple…may start drips and administer other IV medications)
 Monitor respiratory system: lung sounds “crackles”..represent heart failure
 Strict bedrest (activity puts strain on heart)
 Collect cardiac enzymes as ordered by the physician

Administering medications per MD order:

Mnemonic: Acute Angina Means Nasty Artery Blockages And Cardiac Complications

 Antithrombotic agents: prevent formation of clot

 Lovenox (subq injection) monitor for bleeding (assess gums of mouth, stool (dark tarry), drop in blood
pressure and increase in heart rate, blood in urine)
 Heparin (drip usually or subq injection) monitor for bleeding just as with Lovenox, but watch platelet count
which may start to decrease after several days while being on Heparin. This could represent Heparin-
Induced Thrombocytopenia (<150,000 platelets)…. if this develops patient may be be switched to
Argatroban or Angiomax . Monitor PTT (Partial thromboplastin time) normal 25-35 seconds ,60-80
therapeutic range (depends on facility)
 Antiplatelets: decrease platelets aggregation and thrombus formation
 Aspirin: low dose (decrease the chances of a clot forming and decrease the chance of another heart attack).
Watch for signs and symptoms of GI bleeding, especially if patient has a history.
 Plavix: taken if can’t take aspirin (may be prescribed short term for up to a year after the myocardial
infarction)

monitor for:

1. Thrombotic Thrombocytopenic Purpura (TTP): clotting disorder where clots form in blood vessels in the body
which causes decreased blood flow to vital organs…low platelet count, neuro changes, bruising, anemia,
renal failure, fever
2. **will need to discontinue medication for 5-7 days before a planned surgical procedure because of the
increase chance of hemorrhage while taking this drug. Patients need to let their surgeon know they are
taking Plavix because they will be switched to another antiplatelet prior to the surgery. Plavix takes a while
to clear in the body’s system.
3. Morphine: for chest pain relief (may find that morphine only relieves the chest pain rather than nitro)
hypotension, respiratory depression.
 Nitrates: Nitroglycerin (ointment, sublingual, IV, patch, or oral “Imdur”): causes vasodilation and increases
blood flow to the heart, hence better blood flow to the area experiencing ischemia
 Monitor blood pressure, assess patient’s chest pain, monitor EKG and BP continuously if on drip.
 Side effects: headache, flushing, dizzy
 Ace Inhibitors: end in “pril” Lisinopril, Ramipril, Enalapril, Captopril
 ACEI work by allowing more blood to get to the heart muscle and this allows it to work easier. It does this by
blocking the conversion of Angiotensin I or Angiotensin II (this causes vasodilation, lowers blood pressure,
and allows kidneys to secrete sodium because it decreases aldosterone)
 Side effects: dry, nagging cough and can increase potassium level (it does this by inhibiting angiotensin II
which decreases aldosterone in the body which causes the body to retain more potassium and excrete
sodium)
 Beta blockers: “Coreg, Lopressor” decreases work load on the heart…slows heart rate and decreases blood
pressure
 monitor for bradycardia, masking signs and symptoms of hypoglycemia in diabetics, breathing problems in
asthmatics and COPD…educate patient not to take beta blockers with grapefruit juice because it slows the
absorption of beta blockers
 ARBS Angiotensin II receptor blockers: end in “sartan” like Losartan, Valsartan
 used in place of ACE inhibitors if patient can’t tolerate them
 ARBs work by blocking angiotensin II receptors which causes vasodilation. This lowers blood pressure and
helps the kidneys to excrete sodium and water (due to the affects that blocking angiotensin II has on the
kidneys…decreases aldosterone).
 Side effects: increases potassium levels….NO dry nagging cough
 Cholesterol lowering medication such as Statins: “Lipitor, Crestor, Zocor” (goal: LDL less than 100 mg/dL)
helps lower LDL, total cholesterol, lower triglycerides, and increase HDL.
 Educate not to replace diet and exercise
 Notify doctor if they develop muscle pain or tenderness
 Monitor CPK (creatine kinase) levels…. which if elevated it can cause muscle problems
 Monitor liver function because statins act on the liver to block it from producing too much cholesterol.
 Calcium Channel Blockers: Norvasc, Cardizem
 This medications work by stopping the transport of calcium to the myocardium and into smooth muscle
which causes vasodilation on the coronary arteries.
 Monitoring heart rate, orthostatic hypotension, educate about good oral hygiene due to gum enlargement.