CORONARY ARTERY DISEASES

Coronary Artery Disease

Refers to the diseases of the heart that may result from an impaired blood flow to the myocardium
usually due to the accumulation of atherosclerotic plaque.
Atherosclerosis
Is a progressive disease characterized by atheroma (plaque) formation, which affects the intimal and
medial layers of large and midsize arteries and results to the occlusion of the coronary arteries.
Causes the coronaries to become narrowed or blocked that may result in impaired blood flow to the
myocardium
Risk factors for CHD
Non-modifiable major risk factors
- hereditary, including race
- Age
- Gender
Modifiable
- Cigarette smoking
- Hypertension
- Elevated serum cholesterol
- DM
- Physical inactivity
- Obesity
- Inflammatory process
A. NON-MODIFIABLE RISK FACTORS
1. AGE
Symptomatic C.A.D. appears predominantly in clients over 40y/o
Clients in their 30’s, and even in their 20’s sometimes suffer from anginal attacks or M.I
50% of w Attacks occur in individual >65y/o
2. GENDER
Men are at a greater risk for the development of CVD
Risk for women increases significantly at menopause
3. RACE
Black Americans have a higher risk for developing CVD than the general population because of their
high incidence of HPN.
4. FAMILY HISTORY
The presence of Coronary Atherosclerosis in a parent or sibling under 50y/o is associated w/ the
same findings in another family member.
B. MODIFIABLE RISK FACTORS
1. CIGARETTE SMOKING
Major contributing factor of CVD
♂ adult smokers have a 70% higher mortality rate than ♂ non-smokers
All smokers have more than 2x the risk of w attack than the non-smokers
Smoking triples the risk of MI in women and doubles the risk of MI in men.
2. HYPERTENSION
♂ over 45y/o and with BP ↑ 140/90 & adult ♀ w/ BP ↑ 160/95 have a 50% ↑ chance of
mortality
HPN can be prevented through adherence to medical regimen
3. ↑SERUM CHOLESTEROL (HYPERLIPIDEMIA)
Hyperlipidemia ↑ the risk of developing C.A.D. among clients w/cholesterol level of >300mg/dl;
is 3x more likely to develop C.V.D than in clients with <200mg/dl of cholesterol level
A diet high in saturated fat, cholesterol and calories is thought to be a major factor in the
development of hyperlipidemia
4. DIABETES MELLITUS
Diabetes leads to early atherosclerosis
Clients w/ DM are at much risk for CAD
5. OBESITY
↑ workload & O2 demand of the heart
Associated w/ ↑ caloric intake and elevated levels of LDL
6. LACK OF EXERCISE
Exercise can improve the efficiency of the w
Exercise may reduce the risk of CAD by
↓ weight, ↓ BP & ↑ protective lipoprotein HDL
7. DIET
Intake of food with ↑Na, Cholesterol, Saturated fat content & caffeine
Nurse also assess attitudes toward food
Cultural beliefs and economic status can affect the choice of food.
8. HABITS
Alcohol intake
Drug abuse
Contributing Factors
- Stress
- Homocysteine level
Factors unique to women:
- Premature menopause / menopause
- Oral contraceptive use
- Non-compliance with hormonal replacement therapy
STRESS
Stress stimulates the CVS by the release of Catecholamines
Type A personality = found to have 2x risk of developing CVD compared w/ the Type B person
ORAL CONTRACEPTIVES
Use of oral contraceptives or birth control pills has been associated with an increased risk of
CVD
Pathophysiology: ATHEROSCLEROSIS
Injury of inflammation of the endothelial lining the artery----Platelet adhesion and aggregation---
Migration of leukocytes and other macrophages to the area---Collection of atherogenic
lipoprotein---Abnormal proliferation of smooth muscles cells and connective tissue within the vessel
wall----Development of an early lesion in the inner lining of the artery---Enlargement of smooth
muscle, proliferation of collagen fiber an accumulation of lipid---Fibrous plaque development----
Occlusion of the blood vessel and inability to dilate in response to increased oxygen demand----
Atheroma formation----Stenosis and occlusion of the blood vessel ----Angina/Myocardial infarction---
Sudden cardiac death

Diagnostics:
- Total serum cholesterol
- C – reactive protein/ESR
- Exercise stress test
- Electron beam CT
- Myocardial perfusion testing
- ECG

Management:
Medical (Pharmacologic)
1. Statins
 Lovastatin (Mevacor)
 Pravastatin (Pravachol)
 Simvastatin (Zocor)
2. Bile acid sequestrants
 Cholesteramine (Questran)
 Colestipol (Colestid)
3. Nicotinic acid
 Niacin (Nicobid)
4. Fibric acid derivatives
 Gemfibrosil (Lopid)
 Fenofibrate (Tricor)
 Clofibrate (Atromid-S)
5. Prophylactic low dose aspirin therapy
6. ACE inhibitors, beta blockers, and nitrates
7. Insulin and OHA

PERCUTANEOUS CORONARY REVASCULARIZATION

Revascularization Procedures
(Interventional cardiology)
Percutaneous Coronary Revascularization (PCR) / Percutaneous Coronary Interventions (PCI)
 Balloon Angioplasty (Percutaneous Transluminal Coronary Angioplasty or PTCA)
  Intracoronary Stents
 Directional Coronary Atherectomy (DCA)
 Laser Ablation
BALLOON ANGIOPLASTY
[PERCUATNEOUS TRANSLUMINAL CORONARY ANGIOPLSTY (PTCA)]

INTRACORONARY STENTS

CORONARY ATHERECTOMY
1. ROTATOR ATHERECTOMY
2. EXTRACTIONATHERECTOMY
3. DIRECT ATHERECTOMY
LASER ABLATION
Complications after PCR procedures
Hematoma at the catheter insertion site
Pseudoaneurysm
Embolism
Hypersensitivity to contrast dye
Dysrhythmias
Bleeding
Vessel perforation
Restenosis or reocclusion of the treated vessel

Nursing responsibilities for PCR

Administer Aspirin, Heparin, Ca channel blockers or Nitrates before the procedure as ordered
Administer intravenous NTG infusion, anticoagulant and antiplatelet
Maintain bed rest w/ head of the bed at 30° or less. Prevent flexion of the leg on the affected side
Apply pressure dressing
Monitor CSM on the affected leg every 15 min for the first hour, every 30 min for the next hour and
hourly for the next 8 hours, then q 4°
Monitor renal function
Monitor electrolyte levels
Monitor cardiac enzymes
Keep atropine at bedside

CORONARY ARTERY BYPASS GRAFTING (CABG)

Complications after CABG

Post operative bleeding
Wound infection and dehiscence
Intra-operative stroke
MI
Blood clots
Multiple organ system failure
 Death
Nursing responsibilities for CABG
Monitor VS
Auscultate heart and BS at least q4°
Assess for signs of decreased CO
Measure I&O
Report a chest tube drainage of greater than 70 ml/hr or that is warm, red and free flowing

Risk factor management

- Smoking cessation
- Diet
Reduce saturated fat
Take non-fat dairy products, fish and poultry
Take monosaturated fats (veg oil, olive oil, canola oil, peanut oil)
Take foods containing Omega-3 fatty acids (cold water fish such as tuna, salmon, and mackerel)
Increase intake of Vitamin E, fruits and vegetables
Moderate alcohol intake
Reduce caloric intake
- Regular physical exercise
- DM control
- Weight loss
- Reduce fat intake
- Exercise
- Blood glucose management
Angina Pectoris
 Chest pain resulting from reduced coronary blood flow, which causes a temporary imbalance
between myocardial blood supply and demand.
 Chest pain resulting from myocardial ischemia (inadequate blood supply to the myocardium).
- Seen in clients w/ aortic stenosis, hypertension, hypertropic stenosis cardiomyopathy
- Acute or Chronic blockade
 
Acute
- Rupture or disruption of vulnerable atherosclerotic plaques that cause platelet aggregation and
thrombus formation
- Associated w/ unstable angina & MI
Chronic
- Episode of angina is precipitated by conditions that increase myocardial O2 demand (physical
exertion, emotion, exposure to extreme cold)
- Associated w/ calcified or fibrotic atherosclerotic lesion that occlude more than 75% of the
vessel lumen
PATTERNS OF ANGINA
 Stable Angina
Most common
Predictable form
 Unstable Angina
Occurs with increasing frequency, severity and duration.
Occurs unpredictably
 Prinzmetal’s (Variant) Angina
Occurs unpredictably and often at night due to coronary artery spasm with or without
atherosclerotic lesion.
 Angina Decubitus
Chest pain that occurs when the client reclines and lessens when the client sits or stands
up. 
 Intractable Angina
Chronic incapacitating angina that is unresponsive to intervention
 Post-infarction Angina
Occurs after MI, when residual ischemia may cause episodes of angina.

ASSESSMENT
ETIOLOGIES:
 Disorder of Coronary artery
Atherosclerosis, Arterial spasm, Coronary arteritis
 Disorder of circulation
Hypotension, aortic stenosis and regurgitation
 Disorder of the Blood
Anemia, hypoxemia, polycythemia
 Conditions that increase demand on the heart
Exercise, emotion, exertion, stress, digestion of large meals, hyperthyroidism,
hypertension

Pathophysiology: ANGINA PECTORIS

Myocardial oxygen needs are greater than the partially occluded vessels can supply---Ischemia of
myocardial cells---Anaerobic metabolism---Lactic acid production---Stimulation of nerve endings---CHEST
PAIN---Dyspnea,Pallor,Tachycardia,Anxiety

MANIFESTATIONS:
Chest pain
Dyspnea
Pallor
Tachycardia
Great anxiety and fear
Clinical Manifestation of Angina
Characteristics of the Chest Pain
Onset: can develop quickly or slowly
Location: 90% retrosternal
Radiation: usually to the left shoulder & upper arm and may then travel down the inner aspect
of the left arm to the elbow, wrist and 4 th or 5th finger. It may also radiate to the right shoulder
and epigastric area
Duration: usually < 5 minutes
- Sometimes 15-20 min
Sensation: squeezing, burning, choking, aching, or bursting pressure
- Anginal pain is not described as sharp or knife-like
Severity: mild to moderate
- “discomfort” not “pain”
Associated characteristics:
- Dyspnea, pallor, sweating, faintness, palpitation and dizziness
Atypical presentation:
- Elderly and WOMEN
Treatment: should be relieved by NTG

DIAGNOSTIC TESTS:
 Electrocardiography
 Stress Electrocardiography
 Radionuclide Testing/ Radioisotope Imaging
 Electron-Beam (Ultrafast) Computed Tomography (EBCT)
 Echocardiography
 Coronary Angiography

Levels of Prevention
Primary prevention
- life-long commitment to reducing the risk factors for CHD
Secondary prevention
- Recognition and early treatment of anginal attacks
Tertiary prevention
- Resolution of angina before myocardial damage occurs

“ABCDE” of Angina
A – aspirin and anti-anginal tx
B – beta blockers and BP control
C – cigarettes and cholesterol control
D – diet and DM
E – education and exercise
For patient’s with CHEST PAIN:
Remember:
 “ALL PATIENTS WITH CHEST PAIN GET MONA”
  Morphine sulfate
  Oxygen therapy
  Nitrates
  Aspirin
MEDICAL MANAGEMENT
Pharmacologic Management
 Nitrates
 Nitroglycerin
Sublingual
Oral
Ointment
Transdermal patches
 Beta-Blockers
 Propranolol
 Metoprolol
 Nadolol
 Atenolol
 Calcium Channel Blockers
 Verapamil
 Diltiazem
 Nifedipine
 Aspirin and other Antiplatelets
 Opiate Analgesic

Revascularization Procedures
 Percutaneous Coronary Revascularization (PCR)
 Balloon Angioplasty (Percutaneous Transluminal Coronary Angioplasty or PTCA)
 Intracoronary Stents
 Atherectomy
 
 Coronary Artery Bypass Grafting (CABG)

NURSING MANAGEMENT
INEFFECTIVE TISSUE PERFUSION: CARDIAC
 Keep NTG at bedside
 Administer oxygen therapy at 4-6LPM
 Instruct to take SL NTG before engaging in activities that precipitate angina
 Encourage exercise
  Encourage smoking cessation
RISK FOR INEFFECTIVE THERAPEUTIC REGIMEN MANAGEMENT
 Assess knowledge and understanding of angina
 Teach about angina and atherosclerosis
 Educate clients to avoid activities that precipitates angina
 Provide written and verbal instructions about the medications and their use
 Stress the importance of taking chest pains seriously while maintaining a positive attitude

MYOCARDIAL INFARCTION
A life-threatening condition characterized by the necrosis (death) of myocardial cells
ASSESSMENT
 ETIOLOGIES:
 Age
 Gender
 Heredity
 Race
 Smoking
 Obesity
 Hyperlipidemia
 Hypertension
 Diabetes
 Sedentary lifestyle
 Physical and Emotional Stress
 Diet
 Drugs
MANIFESTATIONS:
 Chest pain
 Sympathetic Stimulation
 Tachycardia
 Tachypnea
 Anxiety
 Diaphoresis
 Vasoconstriction
 Cool, clammy, mottled skin
 Sense of impending doom and death
 Palpitations
 Nausea or dizziness
 ANGINA MI

Time 5-15 min 30 min

Severity Mild Severe
Location Retrosternal (left sternum) Radiates bilateral but usually on the left side

Treatment Rest, nitroglycerine, O2

COMPLICATIONS:
Dysrhythmias
Pump Failure
Cardiogenic Shock
Infarct Extension
Structural Defects
Pericarditis
DIAGNOSTIC TESTS:
Serum Cardiac Markers
CBC
ABG
Electrocardiography
Positron Emission Tomography (PET)
Magnetic Resonance Imaging (MRI)
Echocardiography
Radionuclide Imaging
Hemodynamic Monitoring

Serum Cardiac Markers

 Myoglobin
 Heme protein found in striated muscle fibers that elevates within 2 hours after
AMI.
 Sensitive if serum level doubles on the 2 nd sample
 CK-MB
 Increases 3-6 hours after the onset of chest pain, peaks in 12-18 hours, and
return to normal in 3-4 days
 Cardiac Specific TROPONIN T
 Increases within 3-6 hours after pain has started, remain elevated for 14 to 21
days.
 More useful for confirmation of distant MI
 Cardiac Specific TROPONIN I
  Increases 7-14 hours after.
 Very specific and sensitive. It is not affected by other disease or injury except
the cardiac muscle
 Lactic Dehydrogenase (LDH) (1-5); LDH1 & LDH2
 Elevate 14-24 hours after onset, peak within 48-72 hours, and return to normal
over the next 7-14 days.
 if concentration of LDH1 > LDH2; pattern is said to have “flipped”, signifying
infarction.
 Serum Aspartate Transaminase
 Peaks within 12-18 hours, and return to normal within 3 to 4 days.
ECG:
 Tall, peaked T waves in the area of ischemia may be the first sign of tissue injury.
 ST segment elevation is seen in early transmural infarction. The ST elevation is seen in the leads
directed towards the area of injury.
 ST segment depression may also be seen in infarction. It may be: 1) primary ST depression due
to a large area of relative ischemia surrounding a small area that is infarcting
ECG showing ISCHEMIA:

ECG result of a client with MI

ECG:
 The last sign of infarction to occur is the Q wave. Q waves appear only with larger, transmural
infarctions. Most often, the Q waves become a permanent reminder of the infarct.

Positron Emission Tomography

 a nuclear medicine imaging technique which produces a three-dimensional image or picture of
functional processes in the body.
Used to evaluate cardiac metabolism and to assess tissue perfusion.
Magnetic Resonance Imaging
provides the best information on chamber size, wall motion, valvular function and great vessel
blood flow
Info on morphology and structural changes, presence of lesions, blood flow quantifications
within vessels & chamber, tissue characterization
Echocardiography (2D Echo)
based on the principles of ultrasound
It is used to evaluate structural & functional changes in a wide variety of heart ailments.
Can assess the ability of the heart walls to contract and relax.
Hemodynamic Monitoring
pressures provide information about blood volume, fluid balance and how well the heart is
pumping. (CVP, Pulmonary Artery Pressure, Cardiac output measurement, Intra-arterial pressure
monitoring)
Radionuclide Imaging Studies
Provide information on the presence of CAD as well as the location of ischemic and infarcted
tissues.
Perfusion imaging can show areas of ‘cold spots’ because the radioisotopes in the bloodstream
is not taken up by ischemic or infarcted areas.
Other tests:
Cardiac Catheterization – involves the insertion of a catheter into the heart and surrounding
vessels to obtain detailed information about the structure and performance of the heart, valves
and circulatory system. May include the studies of the right, left side of the heart and coronary
arteries.
Angiography – invaluable tool in cardiac diagnosis and offers a great assistance in understanding
heart and vessel disease. Injection of contrast agent via IV at the desired locations under study.
MEDICAL MANAGEMENT
Pharmacologic Management
 Aspirin
 Thrombolytic Therapy
 Streptokinase
 Anisoylated Plasminogen Streptokinase Activator Complex (APSAC)
 Tissue Plasminogen Activator
 Reteplase
 Anticoagulant
 Heparin, Enoxaparin
 Oxygen
 Analgesia
 Niroglycerin (SL)
 MORPHINE SULFATE
  Diazepam (Valium)
 Antidysrhythmics
 IV Atropine 0.5 to 1mg
 Verapamil
 Brevibloc
 Beta blockers
 Propranolol (Inderal)
 Atenolol (Tenormin)
 Metoprolol (Lopressor)
 ACE Inhibitor
 Dopamine
 Antilipemic Agents
 Diuretics
 Anti-platelet
 Lactulose
 Omega 3 Fatty Acids
Diet
Liquid Diet
Low Fat, Low Cholesterol, Reduced Sodium Diet in Small Frequent Feedings
Limit drinks containing caffeine, very hot and cold foods
Activity
CBR without BRP
Sitting in the chair at bedside
Gradual increase in activity level
Revascularization Procedures
 Percutaneous Coronary Revascularizaton (PCR)
 Angioplasty (PTCA)
 Stent Placement
 CABG
 Intra-Aortic Balloon Pump (IABP
 Ventricular Assist Device (VAD)

NURSING MANAGEMENT
ACUTE PAIN r/t myocardial ischemia
(The client will experience improved comfort in the chest AEB decrease in the rating of the chest pain)
 Assess verbal and nonverbal signs of pain
 Administer oxygen at 2 to 5 LPM per nasal cannula
 Promote physical and psychological rest
 Titrate intravenous Nitroglycerine as ordered
 Administer 2 to 4 mg Morphine by intravenous push for chest pain as needed
 Administer Nitrates as ordered
INEFFECTIVE TISSUE PERFUSION
(The client will demonstrate improved cardiac tissue perfusion AEB decrease in the rating of pain and
resolving ST segment)
 Assess and document vital signs
 Assess for changes in LOC; decreased urine output, moist, cool, pale, mottled or cyanotic skin;
dusky or cyanotic mucous membranes and nail beds; diminished to absent peripheral pulses;
delayed capillary refill.
 Auscultate heart and breath sounds
 Monitor ECG
 Monitor oxygen saturation levels and administer oxygen as ordered.
 Elevate the client’s head and loosen tight clothing around the neck.
 Administer Thrombolytics as ordered
 Administer antidysrhythmic medications as needed
 Obtain serial CK isoenzymes, and troponin levels as ordered
INEFFECTIVE COPING
 Establish an environment of caring and trust
 Accept denial as a coping mechanism but do not reinforce it.
 Note any aggressive behaviors and failure to comply with treatments.
 Help the patient identify positive coping skills used in the past
 Provide opportunities for the client to make decisions about the plan of care.
OTHER NURSING DIAGNOSES:
 Decreased cardiac output r/t negative inotrophic changes in the heart secondary to myocardial
ischemia
 Impaired gas exchange r/t decreased cardiac output
 Anxiety and Fear r/t hospital admission and fear of death
 Risk for constipation r/t bed rest
  HOME INSTRUCTIONS
 Home should be conducive to rest
 Strict adherence to treatment regimen
 Resumption of sexual activity at 4-8 weeks
 Avoid alcohol and smoking
 Encourage frequent walks and regular exercise
 Return to work at the end of week 8 0r 9
 Cardiac rehabilitation program: 4-6 months