Coronary Artery Disease

Description:
• The coronary arteries that deliver a constant supply of blood to the heart muscle
begin to develop fatty plaques that can lead to restriction of blood flow to the
heart.

• Fatty plaques are caused by a condition called ATHEROSCLEROSIS which creates

fatty plaques in the artery walls.

• Happens overtime
• Limits blood supply to the heart muscle and can rupture which can lead to thrombosis
formation (hence causing a myocardial infarction)
• Atherosclerosis can also lead to hypertension, chest pain, and heart failure.
 Main Arteries that supply the heart muscle:

❖ Left coronary artery which branches off to:

• Left circumflex artery provides blood to left atrium & side and back of the left
ventricle.

• Left anterior descending artery provides blood to the front and bottom of
the left ventricle and front of the septum.

❖ Right coronary artery which branches off to:

• Right marginal artery provides blood to the right atrium and ventricle.

• Posterior descending artery provides blood to the bottom part of the right ventricle
and back of the septum.
Factors that increase atherosclerotic plaque:
• Smoking
• Unhealthy: obese or overweight
• High cholesterol
• Sedentary lifestyle
• Diabetes
• Family history
 Pathophysiology of Atherosclerosis:
• Blood flows through the artery which contains the red blood cells and lipids (LDL). LDL
(low-density lipoproteins…the bad cholesterol) starts to adhere to the artery wall and
grows overtime (risks factors can increase the rate at which it grows).
• As it grows the patient is usually asymptomatic until the plaque becomes so big the
artery starts to become narrow and blood flow to the heart becomes restricted. The
patient can experience stable angina when the artery is blocked enough to slightly
impede blood flow (however, blood is still able to get to the heart muscle), but the
patient only has the chest pain during ACTIVITY. The activity increases the heart rate
and puts strain on the heart which already has compromised blood flow, but when the
activity STOPS the pain STOPS too.

****Collateral circulation can develop if chronic ischemia is experienced. This is

where more than one artery forms to re-route blood to the heart muscle to make up for
the decreased blood flow due to the blockage.
• Patients with fatty plaque buildup in the arteries are at risk for the plaques to rupture.
This can lead to coronary thrombosis where clotting material aggregates at the site of
rupture and this leads to a significant or complete blockage of the coronary artery.
• Patients will have acute coronary syndrome with unstable angina or experience a
myocardial infraction. This is a MEDICAL EMERGENCY.
Signs and Symptoms of CAD:
Many patients are asymptomatic during the early phases of CAD development.
• Chest pain during activity (stable angina…not a medical emergency but patients
need to let their doctor know about this chest pain so diagnostic testing can be
performed). The pain may feel like heaviness on chest…. can progress to unstable
angina where the patient will have pain at rest, and it is more intense…may not be
relieved by Nitroglycerin.
• Shortness of breath easily gets short of breath during activity because the blood
supply is impeded to the heart muscle.
• Very tired, feeling run down especially with activity
Diagnoses of CAD:
❖ Blood tests: Lipoprotein profile: total cholesterol, LDL, HDL, triglycerides
❖ EKG: assesses if there are any changes in the ST segments or T-waves (shows if
there is a heart attack in the progress, previous heart attack, or compromised blood
flow)
• ST segment depression demonstrates ischemia that is reversible
• ST segment elevation: infarction where there is injury to the heart muscle

❖ Holter Monitoring: A 24- or 48-hour Holter monitor may be ordered to watch the
heart rhythm during the patient’s regular activities of daily living.
❖ Stress Test: monitor the heart rate and rhythm during exercise and see if there
are any EKG changes.
• During activity, if blood flow is reduced ST segment depression will occur and
patient may have chest pain and then as activity stops the ST segment will return
to normal. A patient will probably then be ordered a heart catheterization to
assess where the potential blockage is located.
• Also, a nuclear stress test may be ordered. This is where a tracer is injected, and
pictures of the heart are taken to assess blood flow of the heart muscle during
activity.
❖ Heart Catheterization: A special catheter is inserted into the femoral or radial artery
to assess for blockages in the artery. Dye is injected into the coronary arteries to
assess if they are blocked (coronary angiography) …moderate sedation is used, and
the patient breathes on their own.
Treatment of CAD
Cardiac doctor makes the decision if the artery needs:
❖ PCI (also called angioplasty): Percutaneous Coronary Intervention
o Balloon angioplasty: inflates a balloon in the blocked artery to compress the
plaque against the artery wall and a stent is placed to allow blood to flow back
through the artery.
o Atherectomy: removal of plaque from the artery
 • Sometimes, arteries cannot be stented, and the patient will have to have surgery
known as Coronary Artery Bypass Graft.

Note: Patients with stable angina will complete a stress test to assess the need for a
heart catheterization. The most non-invasive testing is performed first to assess the need
of more invasive procedures.
 Nursing Interventions for CAD
Goal: prevent further progression of CAD

❖ Educating patient about treatment, preventive measure, medications, and

management
• Educate the patient about the significance and complications of CAD (Modifying
lifestyle:
o How to manage with diet (Low fat, Low calorie)
o Exercise program
o Smoking cessation and why it is important
o Weight loss
o Monitoring heart rate and blood pressure
o Signs and symptoms and when to seek help (Chest Pain, Exhaustion)
o Education about procedures: EKG, stress test, heart catheterization, lipid profile
blood test.

Medications for CAD

❖ Anti-platelets: prevent clots from forming or growing which decrease the chances
of ischemia.

• Aspirin: watching for GI bleeding.

• Clopidogrel (Plavix): for patients who can’t tolerate Aspirin or just had a stent
placed.
 Monitor for:
✓ 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
✓ **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 blood thinner prior to the surgery. Plavix takes a while to
clear in the body’s system.
❖ Nitrates:
• Nitroglycerin: dilates vessels to allow more blood to get the heart muscle.
 Educate about how to take: sublingual (underneath the tongue)
✓ Take right when having chest pain.
✓ Place one tab or one spray under the tongue.
✓ Call 911 immediately after 1st dose of Nitroglycerin.
✓ Patient may feel dizzy or hot flushing after taking Nitro. As a nurse, we will need
to monitor their blood pressure because Nitro causes hypotension.
✓ If not relieved in 5 minutes take another dose of Nitro a 2nd dose and
✓ If not relieved in 5 minutes take another one for a 3rd dose. The patient is NOT
to take more than 3 total doses.
❖ Cholesterol Lowering Medication:

• 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 (low fat, low calorie) and exercise.
• Notify doctor if they develop muscle pain or tenderness. (Risk for Renal Tubular
Necrosis)
• Monitor CPK-MM (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.
❖ Beta Blockers:
• End in “lol” Propranolol, Metoprolol
• Lowers heart rate and blood pressure which reduces workload on the heart. This
will help decrease episodes of chest pain.
• Side effects: mask hypoglycemia signs and symptoms (like sweating and
tachycardia in diabetics), bradycardia, breathing problems in patients with COPD or
asthma, don’t take with grapefruit juice.
❖ ACE Inhibitors:
• End in “pril” Lisinopril
• Blocks the conversion of angiotensin I to angiotensin II which caused vasodilation….
lowers blood pressure…this decreases the workload on the heart.
• Side effect: nagging dry cough
 Myocardial Infarction
Description:
The heart’s myocardial tissue layer dies from decreased blood flow due to:

• 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 Note: Blockages in the left coronary arteries can cause the worst
damagefrom 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 minutes. 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 6hours after MI),
troponin (2­4 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, 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 isa 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 hrs after injury).

❖ Echocardiogram: ultrasound of the heart to look at the heart to see if there

isdamaged from an MI.

❖ Heart Catheterization: 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 notifying MD of them
• Compare newly obtained EKG to previous EKGs

 What are we looking for on the EKG?

✓ ST--segment depression or elevation
✓ T--wave inversion or hyperacute
✓ Pathological Q--wave
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 “crackled”. Represents heart failure
• Strict bedrest (activity puts strain on heart)
• Collect cardiac enzymes as ordered by the physician
Medications for MI
Mnemonic: Acute Angina Means Nasty Artery Blockages And Cardiac
Complications
➢ Antithrombotic/Thrombolytic agents: prevent formation of clot
• Lovenox LMWH: (SC injection) monitor for bleeding (assess gums of
mouth, stool (darktarry), drop in blood pressure and increase in heart rate,
blood in urine)
• Heparin (drip usually or SC 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
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
yearafter the myocardial infarction)
 Monitor for:
o 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
o **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.
➢ Morphine: for chest pain relief (may find that morphine only relieves the chest
painrather 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 BPcontinuously 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
AngiotensinII (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 workload 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
totake 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: LDLless 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
muscleproblems
• Monitor liver function because statins act on the liver to block it from
producing toomuch cholesterol.
➢ Calcium Channel Blockers: Norvasc, Cardizem
• These medications work by stopping the transport of calcium to the
myocardium and into smooth muscle which causes vasodilation on the
coronary arteries.
• Monitor heart rate, orthostatic hypotension, educate about good oral hygiene
due to gum enlargement.