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NURS 313R > Exam 1: Coronary Artery Disease > Flashcards

Exam 1: Coronary Artery Disease Flashcards

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.

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2
Q

Theories of Atherogenesis

A
  1. Endothelial injury through hyperlipidemia
  2. Lipid infiltration of the smooth layer
  3. Aging can harden the blood vessels
  4. Thrombogenic
  5. Vascular dynamic: HTN if not controlled, it can damage the intima layer.
  6. Inflammation: can increase plaque formation.
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3
Q

Developmental Stages of CAD

A
  1. Fatty Streak: earliest lesion of atherosclerosis
  2. Raised Fibrous Plaque: beginning of progressive changes of arterial wall.
  3. Complicated Lesion: final stage in the development of atherosclerotic lesion
  4. ISCHEMIA - death of tissue
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4
Q

CAD Risk Factor Categories

A

Unmodifiable Risk Factors (age, gender, ethnicity)
Modifiable Major Risk Factors
Modifiable Contributing Factors

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5
Q

Modifiable Major Risk Factors

A
  1. Elevated Serum lipids
  2. Hypertension: BP > or = 140/90. (Above 120 - needs lifestyle changes; Above 130 - medications may be needed)
  3. Smoking: 2-6x at risk for developing CAD
  4. 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)
  5. Obesity: weight 30% above the standard weight.
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6
Q

Elevated Serum Lipid Levels include

A
  1. Serum cholesterol - above 200 mg/dL
  2. 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
  3. LDL above 160 mg/dL high risk for CAD
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7
Q

Modifiable Contributing Risk Factors include

A
  1. Diabetes Mellitus
  2. Stress and Behavior Problems: such as type A personality (perfectionists)
  3. Homecysteine (sulfur containing amino acid): increased level linked to increased risk for CAD
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8
Q

What is the leading cause of Cardiovascular disease death and death in general?

A

Heart attacks

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9
Q

Major Clinical Manifestations of CAD

A
  1. Angina Pectoris
  2. A Ute Coronary Syndrome
  3. Sudden Cardiac Death
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10
Q

Types of Angina

A
  1. Stable Angina Pectoris
  2. Silent Ischemia
  3. Prinzmetal’s Angina
  4. Nocturnal Angina and Angina Decubitus
  5. Unstable Angina
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11
Q

Stable Angina Pectoris

A

Controlled with medication

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12
Q

Silent Ischemia

A

asymptomatic

Increased in diabetes d/t diabetic neuropathy affecting the nerves innervating the cardiovascular system.

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13
Q

Prinzmetal’s Angina

A

Variant angina

Occurs at rest d/t spam of the coronary artery

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14
Q

Nocturnal Angina and Angina Decubitus

A

Occurs at night, patient doesn’t have to be laying down or sleeping.

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15
Q

Unstable Angina

A

New onset, unpredictable, worsening pattern

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16
Q

Clinical Manifestations of Angina

A

Appears substernally, in the neck, radiate to jaw, shoulder and down to the arm

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17
Q

Myocardial Infarction: Clinical Manifestations

A
  1. Pain: severe, immobilizing, not relieved by rest or nitrate administration.
  2. Describes as heaviness, pressure, tightness, burning, and crushing
  3. N/V and fever
  4. Cardiovascular manifestations
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18
Q

Myocardial Infarction: Cardiovascular manifestations

A 
Elevated HR
Decrease BP and urine output
Crackles
Hepatic Engorgement
Peripheral Edema
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19
Q

Complications of MI

A
  1. Arrhythmias: most common complication of MI (80%)
  2. CHF
  3. Cardiogenic Shock
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20
Q

Angina: Diagnostic Studies

A
  1. CXR
  2. ECG
  3. Laboratory Tests: serum lipids, cardiac markers and C-reactive protein.
  4. Treadmill Exercise Testing
  5. Nuclear Imaging (IV injection of radioisotope)
  6. PET scan
  7. Coronary Angiography
  8. Echocardiogram
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21
Q

Myocardial Infarction: Diagnostic Studies

A
  1. Pt. History
  2. ECG: changes in ST segment
  3. Serum Cardiac Marker: CK (creatine kinase; MB band is cardiac specific), Troponin (myocardial protein)
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22
Q

Angina Treatment Goal

A

Aimed at decreasing oxygen demand and/or increasing oxygen supply.

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23
Q

How can you treat angina?

A
  1. Drug Therapy
  2. Percutaneous Coronary Intervention (PCI)
  3. Stent Placement
  4. Atherectomy
  5. Laser Angioplasty
  6. Myocardial Revascularization (CABG)
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24
Q

What is the initial therapeutic intervention for angina?

A

Use of nitrate

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25
Q

What are the drugs used to treat angina?

A
  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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26
Q

In what ways can you administer nitrates?

A 
Sublingual
Nitroglycerin ointment
Transdermal controlled
Long acting nitrates
Intravenous nitroglycerin
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27
Q

Percutaneous Coronary Intervention

A

Insertion of catheter equipped with an inflatable tip to the coronary artery resulting in vessel dilation.

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28
Q

Stem Placement

A

Expandable mesh like structures designed to maintain vessel latency by compressing the arterial walls and resisting vasoconstriction.

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29
Q

Initial management of MI is best accomplished in

A

The ICU

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30
Q

What ways can you treat a myocardial infarction?

A
  1. Fibrinolytic Therapy
  2. Cardiac Catherization
  3. Drug Therapy
  4. Nutritional Therapy
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31
Q

Fibrinolytic therapy

A

Produce an open artery through lysis of a thrombus to reprefuse the myocardium

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32
Q

What kind of drugs can be used to treat a myocardial infarction?

A
  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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33
Q

Nursing Therapeutics/Plan of Care for patients with Angina

A
  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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34
Q

What are some acute interventions that can be carried out on patients with angina?

A

Administration of Oxygen.
Monitoring vital signs, ECG, and heart sounds.
Give nitrate followed by narcotic analgesic.
Position for comfort.

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35
Q

Nursing therapeutics for patient’s with myocardial infarction

A
  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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36
Q

What are some acute interventions that can be used on patients with myocardial infarction?

A 
Pain
Monitoring
Rest and Comfort
Control Anxiety
Emotional and Behavioral reactions
37
Q

What would you teach patients w/ myocardial infarction?

A
  • 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
Q

What are some things you should teach patients with MI about resumption of sexual activity?

A

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)

39
Q

CAD Complication: CHF Treatment

A
  • 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
Q

Nursing Plan of Care: Chronic CHF

A
  • Administer O2
  • Monitor O2 and ABG or pulse ox
  • Allow physical and emotional rest
  • Drug therapy
  • Dietary therapy
  • Ambulatory Home Care
41
Q

What kind of drugs are used to treat Chronic CHF?

A 
ACE inhibitor 
Diuretic therapy
Inotropic drugs
Vasodilator
Beta adrenergic drugs
42
Q

What kind of dietary therapy can be used in patients with chronic CHF?

A
  • 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
Q

What kind of ambulatory home care should the nurse implement in patients with chronic CHF?

A
  • 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)
44
Q

Atherosclerosis

A

Hardening of the arteries d/t fatty deposits.

Major cause of CAD

45
Q

Atherosclerosis is caused by

A

Endothelial lining injury d/t tobacco use, hyperlipidemia, HTN, toxins, DM, hyperhomocysteinemia and infection causing local inflammatory response.

46
Q

How does C-reactive protein (CRP) relate to CAD?

A

CRP is usually increased with CAD.

47
Q

C-Reactive Protein

A

Protein produced by the liver. Non specific marker of inflammation.
Systemic inflammation = increased CRP levels -> unstable plaques and oxidation of LDL cholesterol

48
Q

Fatty Streak

A

Earliest lesions of atherosclerosis.
Characterized by lipid-filled smooth muscle cells -> yellow tinge.
Tx that lowers LDL cholesterol may reverse this process.

49
Q

Fibrous Plaque

A

-Beginning of changes in the endothelium of arterial wall. (Usually endothelium can heal itself, but NOT with CAD)

50
Q

Fibrous Plaque: Pathophysiology

A
  • 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
51
Q

Complication Lesion

A

Final Stage of CAD. Most dangerous.

52
Q

Complicated Lesion Pathophysiology

A
  • As the plaque grows, continued inflammation occurs -> plaque instability, ulceration and rupture.
  • Compromised inner wall -> accumulation of platelets -> thrombus.
53
Q

Isotonic activity

A

Using weights

54
Q

Isometric activity

A

Planks, yoga

55
Q

How can omega-3 fatty acids affect CAD?

A

Decreases risk of CAD

56
Q

Lipid lowering drugs

A
  • 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
Q

Lipid Lowering Drug Therapy has 3 different mechanisms of action. What are they?

A

Decreases lipoprotein production
Increased lipoprotein removal
Decreased cholesterol absorption.

58
Q

Women intolerant of aspirin should take what drug?

A

Clopidogrel (Plavix)

59
Q

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!

A

Stopped right before page 5.

60
Q

Angina

A

Chest pain. Clinical manifestation of reversible myocardial ischemia.

61
Q

Myocardial ischemia

A

Myocardial O2 demand>ability of the coronary arteries to supply the heart with O2.

62
Q

What causes chest pain (angina)?

A

The myocardium becomes hypoxic within first 10 sec -> anaerobic metabolism produces lactic acid -> lactic acid irritates nerve fibers -> causes transmission of pain

63
Q

S&S of Unstable Angina in women

A

Fatigue, SOB, indigestion, anxiety

64
Q

How long can cardiac cells withstand ischemic conditions

A

20 minutes before cell death begins.

65
Q

How long does it take for the entire thickness of heart muscle to become necrosed?

A

4-6 hours (if artery not completely blocked by thrombus ~ 12 hours until complete necrosis.

66
Q

Blockage of the right coronary artery results in

A

Inferior wall MI

67
Q

Blockage of the left circumflex results in

A

Lateral/posterior MI

68
Q

How long does a myocardial infarction usually last?

A

20+ minutes

69
Q

Angina Decubitus

A

Occurs only while laying down, usually relieved by standing or sitting. (Decreased lung expansion -> decreased O2 supply to heart -> chest pain)

70
Q

Prinzmetal’s Angina can occur

A

W/ or w/o CAD

71
Q

Prinzmetal’s Angina: Factors causing spasm

A

Increased myocardial O2 demand
Increased levels of certain substances (tobacco smoke, alcohol, methamphetamines)
CCB and nitrates can be used to control.

72
Q

Complications of MI: Dysrhythmias

A

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.

73
Q

Life threatening dysrhythmias include

A

V-fib (can be w/ or w/out pulse, QRS takes over)
Ventricular Tachycardia (never has pulse)
Both must be treated immediately!!

74
Q

Left Sided HF Symptoms

A

Related to lungs

75
Q

Right Sided HF Symptoms

A

RT Heart

76
Q

Cardiogenic Shock

A

When O2 and nutrients supplied to tissues (BRAIN) are inadequate d/t severe left ventricular failure.
High mortality rate.

77
Q

Cardiogenic Shock can cause

A

Decrease in BP (Emergent!)

78
Q

How does pain create shock?

A

MASSIVE DILATION = decreased BP

79
Q

Goals of Cardiogenic shock

A

Maximize O2 delivery, O2 demand and prevent complications.

80
Q

MI Complications: Papillary Muscle Dysfunction

A

Rare, life-threatening

Occurs if infarcts are near papillary muscles attaching to mitral valve

81
Q

Papillary Muscle Dysfunction causes

A

Massive mitral valve regurgitation, dyspnea, pulmonary edema and decreased CO.

82
Q

Treatment for Papillary Muscle Dysfunction

A

Rapid afterload reductions, immediate cardiac surgery

83
Q

MI Complications: Ventricular Aneurysm

A

D/t infarcts myocardial wall being thin and bulging out during contraction

84
Q

MI Complications: Pericarditis

A

Inflammation of visceral and/or parietal pericardium

Usually occurs 2-3 hrs post-MI

85
Q

What can help relieve pericarditis?

A

Sitting in forward position often relieves pain

86
Q

What can irritate pericarditis?

A

Inspiration, coughing or upper body movement.

87
Q

Pericarditis Assessment

A

Friction rub
Fever
Hypotension
Narrow pulse pressure

88
Q

When should a patient notify the HCP in association with daily weights?

A

If they gain 4 lbs of weight over a 2 day period.

89
Q

End of pg 9 (under elctrocardiogram), pg 10, 6 and 7.

A

… need to add cards.

NURS 313R (18 decks)

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