Exam 1: Coronary Artery Disease Flashcards
(89 cards)
1
Q
Coronary Artery Disease
A
Type of blood vessel disorder affecting the coronary artery resulting in atherosclerosis or hardening of the artery due to fatty deposits.
2
Q
Theories of Atherogenesis
A
- Endothelial injury through hyperlipidemia
- Lipid infiltration of the smooth layer
- Aging can harden the blood vessels
- Thrombogenic
- Vascular dynamic: HTN if not controlled, it can damage the intima layer.
- Inflammation: can increase plaque formation.
3
Q
Developmental Stages of CAD
A
- Fatty Streak: earliest lesion of atherosclerosis
- Raised Fibrous Plaque: beginning of progressive changes of arterial wall.
- Complicated Lesion: final stage in the development of atherosclerotic lesion
- ISCHEMIA - death of tissue
4
Q
CAD Risk Factor Categories
A
Unmodifiable Risk Factors (age, gender, ethnicity)
Modifiable Major Risk Factors
Modifiable Contributing Factors
5
Q
Modifiable Major Risk Factors
A
- Elevated Serum lipids
- Hypertension: BP > or = 140/90. (Above 120 - needs lifestyle changes; Above 130 - medications may be needed)
- Smoking: 2-6x at risk for developing CAD
- Physical Inactivity: Regular exercise 3-5 times a week for at least 30 min (needs to cause perspiration and increase HR by 30-40 bpm)
- Obesity: weight 30% above the standard weight.
6
Q
Elevated Serum Lipid Levels include
A
- Serum cholesterol - above 200 mg/dL
- HDL (caries lipids to liver where it can be metabolized, therefore it is not left circulating in the blood): lower than 35 mg/dL major risk factor
- LDL above 160 mg/dL high risk for CAD
7
Q
Modifiable Contributing Risk Factors include
A
- Diabetes Mellitus
- Stress and Behavior Problems: such as type A personality (perfectionists)
- Homecysteine (sulfur containing amino acid): increased level linked to increased risk for CAD
8
Q
What is the leading cause of Cardiovascular disease death and death in general?
A
Heart attacks
9
Q
Major Clinical Manifestations of CAD
A
- Angina Pectoris
- A Ute Coronary Syndrome
- Sudden Cardiac Death
10
Q
Types of Angina
A
- Stable Angina Pectoris
- Silent Ischemia
- Prinzmetal’s Angina
- Nocturnal Angina and Angina Decubitus
- Unstable Angina
11
Q
Stable Angina Pectoris
A
Controlled with medication
12
Q
Silent Ischemia
A
asymptomatic
Increased in diabetes d/t diabetic neuropathy affecting the nerves innervating the cardiovascular system.
13
Q
Prinzmetal’s Angina
A
Variant angina
Occurs at rest d/t spam of the coronary artery
14
Q
Nocturnal Angina and Angina Decubitus
A
Occurs at night, patient doesn’t have to be laying down or sleeping.
15
Q
Unstable Angina
A
New onset, unpredictable, worsening pattern
16
Q
Clinical Manifestations of Angina
A
Appears substernally, in the neck, radiate to jaw, shoulder and down to the arm
17
Q
Myocardial Infarction: Clinical Manifestations
A
- Pain: severe, immobilizing, not relieved by rest or nitrate administration.
- Describes as heaviness, pressure, tightness, burning, and crushing
- N/V and fever
- Cardiovascular manifestations
18
Q
Myocardial Infarction: Cardiovascular manifestations
A
Elevated HR Decrease BP and urine output Crackles Hepatic Engorgement Peripheral Edema
19
Q
Complications of MI
A
- Arrhythmias: most common complication of MI (80%)
- CHF
- Cardiogenic Shock
20
Q
Angina: Diagnostic Studies
A
- CXR
- ECG
- Laboratory Tests: serum lipids, cardiac markers and C-reactive protein.
- Treadmill Exercise Testing
- Nuclear Imaging (IV injection of radioisotope)
- PET scan
- Coronary Angiography
- Echocardiogram
21
Q
Myocardial Infarction: Diagnostic Studies
A
- Pt. History
- ECG: changes in ST segment
- Serum Cardiac Marker: CK (creatine kinase; MB band is cardiac specific), Troponin (myocardial protein)
22
Q
Angina Treatment Goal
A
Aimed at decreasing oxygen demand and/or increasing oxygen supply.
23
Q
How can you treat angina?
A
- Drug Therapy
- Percutaneous Coronary Intervention (PCI)
- Stent Placement
- Atherectomy
- Laser Angioplasty
- Myocardial Revascularization (CABG)
24
Q
What is the initial therapeutic intervention for angina?
A
Use of nitrate
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What are the drugs used to treat angina?
1. Anti-platelet Aggregation Therapy: First line treatment (ex. Aspirin, ticlid, plavix)
2. Nitrates
3. B-Adrenergic Blockers
4. Calcium Channel Blockers
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In what ways can you administer nitrates?
```
Sublingual
Nitroglycerin ointment
Transdermal controlled
Long acting nitrates
Intravenous nitroglycerin
```
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Percutaneous Coronary Intervention
Insertion of catheter equipped with an inflatable tip to the coronary artery resulting in vessel dilation.
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Stem Placement
Expandable mesh like structures designed to maintain vessel latency by compressing the arterial walls and resisting vasoconstriction.
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Initial management of MI is best accomplished in
The ICU
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What ways can you treat a myocardial infarction?
1. Fibrinolytic Therapy
2. Cardiac Catherization
3. Drug Therapy
4. Nutritional Therapy
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Fibrinolytic therapy
Produce an open artery through lysis of a thrombus to reprefuse the myocardium
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What kind of drugs can be used to treat a myocardial infarction?
1. IV nitroglycerin
2. Antiarrhythmic drugs
3. Morphine Sulfate
4. B-Adrenergic blockers
5. Angiotensin-Converting Enzyme Inhibitors
6. Stool Softeners
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Nursing Therapeutics/Plan of Care for patients with Angina
1. Health promotion: aimed to decrease risk factors.
2. Acute interventions
3. Ambulatory/Home Care: pt assurance, health teaching and counseling.
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What are some acute interventions that can be carried out on patients with angina?
Administration of Oxygen.
Monitoring vital signs, ECG, and heart sounds.
Give nitrate followed by narcotic analgesic.
Position for comfort.
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Nursing therapeutics for patient’s with myocardial infarction
1. Acute Interventions (Prioritize Action)
2. Ambulatory/Home Care: Patient teaching, physical exercise and resumption of sexual activity (use matter of fact approach)
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What are some acute interventions that can be used on patients with myocardial infarction?
```
Pain
Monitoring
Rest and Comfort
Control Anxiety
Emotional and Behavioral reactions
```
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What would you teach patients w/ myocardial infarction?
- Anticipatory guidance: tells patient what they can anticipate about their care -> gives them a sense of control.
- Physical Exercise: uncomplicated MI - ambulation can begin on day 3; isotonic exercise such as shortening and lengthening of muscle.
- Resumption of Sexual Activity
38
What are some things you should teach patients with MI about resumption of sexual activity?
No viagra
Avoid anal intercourse because of vasovagal response = decreases HR
Safe to resume sexual activity 7 days post uncomplicated MI
Can resume sexual activity if ale to climb stairs w/out (listen to audio for more)
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CAD Complication: CHF Treatment
- Use of diuretics (d/t water retention)
- Position patient in high Fowler’s position (to maximize lung expansion)
- IV nitroglycerin (drug of choice for pt w/ pulmonary edema)
- Morphine administration (causes vasodilation which decreases workload of the heart)
- O2 administration
- Digitalis administration (positive inotrope = increases strength of contractility of the heart)
- Potassium supplements (d/t use of diuretics)
40
Nursing Plan of Care: Chronic CHF
- Administer O2
- Monitor O2 and ABG or pulse ox
- Allow physical and emotional rest
- Drug therapy
- Dietary therapy
- Ambulatory Home Care
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What kind of drugs are used to treat Chronic CHF?
```
ACE inhibitor
Diuretic therapy
Inotropic drugs
Vasodilator
Beta adrenergic drugs
```
42
What kind of dietary therapy can be used in patients with chronic CHF?
- Sodium restriction (2 g sodium diet): avoid/limit milk, cheese, bread, cereal, canned goods
- Diet education
- Weight management
- Fluid restriction (if there is renal insufficiency)
43
What kind of ambulatory home care should the nurse implement in patients with chronic CHF?
- Teach patient the physiologic changes of CHF (such as wedding band getting tight or sudden weight gain)
- Encourage to take medications regularly
- Teach patient to take his/her own pulse in one full minute.
- Alert on S&S of hypo/hyperkalemia
- Discuss energy saving energy efficient behaviors (periods of rest, pacing of activity)
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Atherosclerosis
Hardening of the arteries d/t fatty deposits.
| Major cause of CAD
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Atherosclerosis is caused by
Endothelial lining injury d/t tobacco use, hyperlipidemia, HTN, toxins, DM, hyperhomocysteinemia and infection causing local inflammatory response.
46
How does C-reactive protein (CRP) relate to CAD?
CRP is usually increased with CAD.
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C-Reactive Protein
Protein produced by the liver. Non specific marker of inflammation.
Systemic inflammation = increased CRP levels -> unstable plaques and oxidation of LDL cholesterol
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Fatty Streak
Earliest lesions of atherosclerosis.
Characterized by lipid-filled smooth muscle cells -> yellow tinge.
Tx that lowers LDL cholesterol may reverse this process.
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Fibrous Plaque
-Beginning of changes in the endothelium of arterial wall. (Usually endothelium can heal itself, but NOT with CAD)
50
Fibrous Plaque: Pathophysiology
- LDL’s growth factors from platelets stimulates thickening of arterial wall -> leads to endothelial injury -> endothelial injury causes lipoproteins to transport cholesterol and other lipids into intima -> collagen covers fatty streak and forms fibrous plaque (white/gray appearance)
- RESULT: narrowing of vessel and reduction of BF
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Complication Lesion
Final Stage of CAD. Most dangerous.
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Complicated Lesion Pathophysiology
- As the plaque grows, continued inflammation occurs -> plaque instability, ulceration and rupture.
- Compromised inner wall -> accumulation of platelets -> thrombus.
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Isotonic activity
Using weights
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Isometric activity
Planks, yoga
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How can omega-3 fatty acids affect CAD?
Decreases risk of CAD
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Lipid lowering drugs
- Statin Drugs - inhibits synthesis of cholesterol in liver
- Simvastatin: liver able to remove LDLs from blood
- Niacin: Water-soluble Vit B; decreased LDL, triglyceride; interferes w/ synthesis; increased HDL.
- Fibric Acid Derivatives: No effects on LDL; Increases HDL & lowers triglycerides
- Bile acid sequestrants: increases conversion of biles acids and decreases hepatic cholesterol -> decreases total cholesterol and LDLs.
57
Lipid Lowering Drug Therapy has 3 different mechanisms of action. What are they?
Decreases lipoprotein production
Increased lipoprotein removal
Decreased cholesterol absorption.
58
Women intolerant of aspirin should take what drug?
Clopidogrel (Plavix)
59
Study all information in flash cards and add in information you don’t know from the Exam 1- CAD and HF study guide on Pages!
Stopped right before page 5.
60
Angina
Chest pain. Clinical manifestation of reversible myocardial ischemia.
61
Myocardial ischemia
Myocardial O2 demand>ability of the coronary arteries to supply the heart with O2.
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What causes chest pain (angina)?
The myocardium becomes hypoxic within first 10 sec -> anaerobic metabolism produces lactic acid -> lactic acid irritates nerve fibers -> causes transmission of pain
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S&S of Unstable Angina in women
Fatigue, SOB, indigestion, anxiety
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How long can cardiac cells withstand ischemic conditions
20 minutes before cell death begins.
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How long does it take for the entire thickness of heart muscle to become necrosed?
4-6 hours (if artery not completely blocked by thrombus ~ 12 hours until complete necrosis.
66
Blockage of the right coronary artery results in
Inferior wall MI
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Blockage of the left circumflex results in
Lateral/posterior MI
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How long does a myocardial infarction usually last?
20+ minutes
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Angina Decubitus
Occurs only while laying down, usually relieved by standing or sitting. (Decreased lung expansion -> decreased O2 supply to heart -> chest pain)
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Prinzmetal’s Angina can occur
W/ or w/o CAD
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Prinzmetal’s Angina: Factors causing spasm
Increased myocardial O2 demand
Increased levels of certain substances (tobacco smoke, alcohol, methamphetamines)
CCB and nitrates can be used to control.
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Complications of MI: Dysrhythmias
MI -> cardiac cell’s sensitivity to nerve impulses (when tissue is affected from necrosis, it affects the sinus rhythm)
Can cause tachycardia, bradycardia and irregular pulse.
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Life threatening dysrhythmias include
V-fib (can be w/ or w/out pulse, QRS takes over)
Ventricular Tachycardia (never has pulse)
Both must be treated immediately!!
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Left Sided HF Symptoms
Related to lungs
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Right Sided HF Symptoms
RT Heart
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Cardiogenic Shock
When O2 and nutrients supplied to tissues (BRAIN) are inadequate d/t severe left ventricular failure.
High mortality rate.
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Cardiogenic Shock can cause
Decrease in BP (Emergent!)
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How does pain create shock?
MASSIVE DILATION = decreased BP
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Goals of Cardiogenic shock
Maximize O2 delivery, O2 demand and prevent complications.
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MI Complications: Papillary Muscle Dysfunction
Rare, life-threatening
| Occurs if infarcts are near papillary muscles attaching to mitral valve
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Papillary Muscle Dysfunction causes
Massive mitral valve regurgitation, dyspnea, pulmonary edema and decreased CO.
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Treatment for Papillary Muscle Dysfunction
Rapid afterload reductions, immediate cardiac surgery
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MI Complications: Ventricular Aneurysm
D/t infarcts myocardial wall being thin and bulging out during contraction
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MI Complications: Pericarditis
Inflammation of visceral and/or parietal pericardium
| Usually occurs 2-3 hrs post-MI
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What can help relieve pericarditis?
Sitting in forward position often relieves pain
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What can irritate pericarditis?
Inspiration, coughing or upper body movement.
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Pericarditis Assessment
Friction rub
Fever
Hypotension
Narrow pulse pressure
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When should a patient notify the HCP in association with daily weights?
If they gain 4 lbs of weight over a 2 day period.
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End of pg 9 (under elctrocardiogram), pg 10, 6 and 7.
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