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MedSurgExam1 > Coronary Artery Disease > Flashcards

Coronary Artery Disease Flashcards

1
Q

Coronary Artery Disease (CAD)?

A

The most prevalent type of Cardiovascular Disease in Adults

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2
Q

Most common cause of CAD?

A

*Atherosclerosis:
Abnormal Accumulation of lipid or fatty substances and fibrous tissue in the lining of arterial blood vessel walls.

*These substances create blockages and narrow the coronary vessels, reducing blood flow to the myocardium.
Repetitious, inflammatory response to the arterial wall

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3
Q

Pathophysiology of CAD?

A

*Atherosclerosis begins as fatty streaks of lipids (lesions)deposited in arterial wall

  • Progression of the lesions depends on:
    1. Genetics
    2. Environmental Factors
    3. Continued development of atherosclerosis begins an inflammatory response
  • ——Collection of plaque, thrombus formation and continued narrowing of the vessels
    4. Result: Blockage of blood vessel, depriving the myocardial tissue of oxygen
  • All 3 major coronary arteries have multiple branches
  • Atherosclerotic lesions most often form where the arteries have branches
  • Any obstruction of blood flow which cuts off oxygen to the myocardium results in ischemia= acute myocardial infarction
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4
Q

What is Angina Pectoris?

A
  • Chest pain that is brought about by myocardial ischemia
  • ——-Usually caused by significant coronary atherosclerosis
  • ——-Major predecessor of MI
  • If the decrease in blood supply is great enough and of a long enough duration, it can cause death of myocardium cells
  • Death of myocardium cells is irreversible
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4
Q

Signs and Symptoms of CAD?

A
  1. Chest Pain: Most common manifestation of myocardial ischemia
  2. 15% of men & women discovered to have had a myocardial infarction report no symptoms
  3. Shortness of breath
Women often present atypical symptoms:
             Nausea
             Dyspnea
             Weakness
             Jaw Pain
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5
Q

Risk Factors for CAD?

A
  1. Atherosclerosis
  2. Diabetes
  3. Peripheral Artery Disease
  4. Abdominal Aortic Aneurysm
  5. Smoking
  6. Family History of CAD
  7. Hyperlipidemia
  8. Increasing Age
  9. African American
  10. Male Sex
  11. Lack of Estrogen
  12. Obesity
  13. Physical Inactivity
  14. Metabolic Syndrome
    - obesity
    - high blood pressure
    - HDL Cholesterol
    - Try-glycerides




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6
Q

High Density Cholesterol vs. Low Density Cholesterol

A
  • **Low Density Cholesterol= The ‘Bad’ Cholestrol
    - LDL Particles can be easily transported into vessel lining
  • **HDL (High Density Cholesterol)= The ‘Good’ Cholesterol
    - Helps transport the LDL to the liver for breakdown and excretion
  • LDL breaks down and can stick to the blood vessels
  • HDL helps transport the LDL to the liver, where it is metabolized and excreted

Goal: Higher levels of HDL, lower levels of LDL

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7
Q

Prevention & Teaching of CAD?

A
  • Prevention and Patient Teaching aimed at 4 modifiable high risk factors:
    1. Cholesterol Abnormalities
    2. Tobacco Use
    3. Hypertension
    4. Diabetes

Prevention aimed at these 4 modifiable risk factors significantly lower risk for MI

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8
Q

Hyperlipidemia Medications: CAD

Statins?

A

‘Statins’: Most often used to lower LDH and raise HDH levels

  1. Lovastatin (Mevacor)
  2. Prevastatin (Pravachol)
  3. Simvastatin (Zocor)
  4. Atorvastatin (Lipitor)
  5. Rosuvastatin (Crestor)
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9
Q

Hyperlipidemia Medications: CAD

Contraindications?

A
  • Liver Disease
  • Concomitant use of anti-fungal medications
  • Grapefruit Juice
  • Amiodarone
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10
Q

what is Angina Pectoris?

A

Definition: A clinical symptom usually characterized by episodes or paroxysms of pain or pressure in the anterior chest

Caused by:
Insufficient coronary blood flow

An increased demand for oxygenated blood in response to physical exertion or emotional stress

  • Chest pain that is brought about by myocardial ischemia
  • ——-Usually caused by significant coronary atherosclerosis
  • ——-Major predecessor of MI
  • If the decrease in blood supply is great enough and of a long enough duration, it can cause death of myocardium cells
  • Death of myocardium cells is irreversible
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11
Q

Oxygen Supply vs. Oxygen Demand on Angina Pectoris

A

***Angina results when the heart’s demand
For oxygen exceeds the supply

***The severity of angina (and pain) is based
On the precipitating activity and its effect
On ADLs

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12
Q

Types of Angina?

A
  1. Stable Angina: Predictable and consistent
    - Occurs on exertion, relieved by rest
  2. Unstable Angina: (also called pre-infarction angina or crescendo angina)
    - Symptoms occur more frequently and last longer
    - Threshold for pain lower; pain may occur at rest
    - Intractable or refractory angina: Severe incapacitating chest pain
  3. Variant Angina: (Prinzmetal’s angina)
    - Pain at rest with (ECG) ST-segment elevation
    - Thought to be caused by coronary artery vasospasm
  4. Silent Ischemia: Objective evidence of ischemia (such as ECG changes with stress test) but patient reports no symptoms
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13
Q

Pathophysiology of Angina Pectoris?

A
  1. Usually caused by atherosclerotic disease
    - Almost always associated with a significant obstruction of a major coronary artery
  2. Myocardium demands large supply of oxygen to meet continuous demands
  3. Increase in demand necessitates an increase in supply
  4. If coronary artery blocked, it prevents the increased oxygen from getting to the myocardium, resulting in ischemia
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14
Q

Factors Associated With Typical Anginal Pain?

A
  1. Physical Exertion
  2. Exposure to Cold
    • Causes vasoconstriction & elevates BP, with increased oxygen demand
  3. Eating a Heavy Meal
    - Increases blood flow to GI tract for digestion, reducing blood supply available to heart(Shunt can be necessary)
  4. Stress: Causes release of catecholamines, increases BP, heart rate and myocardial workload
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15
Q

Assessment & Diagnostic Findings of Angina Pectoris?

A
  1. Patient’s history related to the clinical manifestations of ischemia
  2. 12 Lead Electrocardiogram
  3. Stress Test: The heart is monitored by ECG, Echocardiogram
  4. Laboratory Testing
    C-Reactive Protein (CRP): a marker for inflammation of vascular endothelium (CAD)
16
Q

Medical Management:

Objective?

A

Objective: Decrease oxygen demand of the myocardium and increase oxygen supply

17
Q

Medical Management : angina pectoris

Pharmacological Therapy

A
  1. Nitroglycerin
    - Reduces Oxygen demand
    - Vasodilator
    - Sublinqual, paste, IV drip (for hospitalized patients)
  2. Beta Blockers
    - Reduces Myocardial Demands (oxygen consumption)by lowering heart rate & reducing force of contractions
  3. Calcium Channel Blockers
    - Act upon the electrical impulses (nodes) slowing down the conduction, resulting in reduced workload
    - Also relaxes blood vessels, decreasing BP
  4. Antiplatelet/Anticoagulant Medications
    -Prevents platelet formation & subsequent thrombosis
    Aspirin
    Clopidogrel (Plavix)
    Ticlopidine (Ticlid)
    Heparin
    Lovenox
  5. Control of Risk Factors
    - Stress Reduction, Anxiety
  6. Oxygen Administration
  7. **Percutaneous Transluminal Coronary Angioplasty (PTCA)
    Balloon inflated within a coronary artery to break an atheroma and open the vessel lumen, improving coronary artery blood flow
  8. Intracoronary Stents
  9. Atherectomy
18
Q

Nursing Diagnosis of Angina Pectoris?

A
  1. Ineffective Cardiac Tissue Perfusion, secondary to CAD, As E/B: chest pain
  2. Anxiety secondary to CAD, Angina, chronic chest pain, As E/B: Verbalization, anxious demeanor
  3. Knowledge Deficiency, re: disease process, risk factors,
19
Q

Pathophysiology of Myocardial Infarction (MI)?

A
  1. In a Myocardial Infarction (MI) an area of the myocardium is permanently destroyed due to lack of oxygen to myocardial tissue.
  2. Tissue Death results from lack of oxygenated blood to myocardium
  3. Unstable Angina and Acute MI are both usually caused by a blockage to a coronary artery

CAD—>Unstable Angina—-> MI

20
Q

Acute Coronary Syndrome(ACS) applies to any of the 3 conditions?

A
  1. CAD
  2. Angina
  3. MI
21
Q

Myocardial Infarction(MI) also known as:

A

Heart attack

Coronary occlusion

22
Q

Causes of Myocardial Infarction(MI)?

A
  1. Majority caused by the rupture of atherosclerotic plaque, causing a blockage of a coronary artery blood vessel
  2. Other Causes:
    - Vasospasm (sudden constriction/narrowing)
    - Decreased Oxygen Supply (anemia, blood loss, low blood pressure
    - Increased demand (rapid heart rate, thyrotoxicosis, cocaine)
23
Q

facts about Myocardial Infarction (MI)?

A
  • Tissue death occurs rapidly – minutes to hours
  • As the cells are deprived of oxygen, tissue death occurs (Infarction)
    - —Time is muscle
  • 900,000 in U.S. per year
    - —-¼ of those die
    - —-Half of those who die never make it to a hospital
24
Q

Clinical Manifestations of MI?

A

Chest pain that occurs suddenly and continues despite medication and resting is the cardinal sign of an MI

25
Q

Sign & Symptoms of Acute MI:

Respiratory

A

Respiratory:

  1. Shortness of Breath
  2. Dyspnea
  3. Tachypnea
  4. Crackles on Auscultation, if the MI has 4. caused pulmonary congestion
  5. Possibly pulmonary edema
26
Q

Sign & Symptoms of Acute MI:

  1. Gastrointestinal
  2. Genitourinary
  3. Skin
A
  1. Gastrointestinal
    - Nausea & Vomiting
  2. Genitourinary
    • Decreased Urinary output, if Cardiogenic shock
  3. Skin
    • Cool, Clammy
    • Diaphoretic
    • Pale
27
Q

Sign & Symptoms of Acute MI:

  1. Neurological
  2. Psychological
A
  1. Neurological
    • Anxious, Restlessness
    • Lightheadedness (if cardiogenic shock)
  2. Psychological
    • Fear, Feeling of Impending Doom
    • Patient may deny that anything is wrong
28
Q

Assessment & Diagnostic Findings MI?

A
  1. Diagnosis of MI is based on presenting symptoms, ECG results and lab tests
  2. **Prognosis depends on severity of the coronary artery obstruction and extent of damage to myocardial tissue*
  3. Patient History has 2 parts
    - Description of presenting symptoms (ie:pain)
    - Previous history- Risk Factors
  4. Electrocardiogram: Provides valuable info to assist in diagnosis of MI
    • Should be done within 10 minutes of onset of symptoms or arrival to ER
    • Continual monitoring can show location, evolution and resolution
  5. Echocardiogram: Used to evaluate ventricular function and determine ejection fraction
  6. Laboratory Tests: Cardiac Biomarkers used to diagnose an MI
    • Myoglobin and Troponin Levels: Present when myocardial cells die; released into the circulation upon cell death
      a. Myoglobin level increases in 1-3 hours, peaks within 12 hours of onset of symptoms; Useful in ruling out acute MI
      b. Troponin Level evident within a few hours, lasts up to 3 weeks
  7. Three Creatine Kinase (CK) Isoenzymes
    * CK-MM – Skeletal muscle*
    * CK-MB- Heart Muscle**
    * CK-BB- Brain Tissue**
29
Q

Medical Management: Goal of Acute MI?

A 
Goal: To minimize myocardial damage, preserve myocardial function and prevent complications
   - Reduce myocardial oxygen demand
        1. Medication
        2. Bedrest 
   - Increase oxygen supply to the heart
Supplemental Oxygen

Supply & Demand of oxygen are in equilibrium when pain subsides and ECG stable

30
Q

Medical Management of MI?

A

Pharmacologic Therapy
-The patient with a suspected acute MI is given aspirin, nitroglycerin, morphine, a beta-blocker and other medications as indicated while the diagnosis is being confirmed

31
Q

Medical Management of MI:

Thrombolytics

A

Thrombolytics

- To dissolve and lyse the thrombus in the coronary artery
- May be given IV or directly into the coronary artery via cardiac catheterization
       a. Allows reperfusion (flow of blood resumes through the coronary artery)
       b. Minimizes the size of the infarction
       c. Given as early as possible, if no contraindications
32
Q

Medical Management of MI:

Analgesics

A

Analgesics

       - Morphine to reduce pain and anxiety
       - Reduces preload and afterload
       - Relaxes bronchioles, promoting oxygenation
33
Q

Medical Management of MI:

Angiotensin-Converting Enzyme (ACE) Inhibitors

A

Angiotensin-Converting Enzyme (ACE) Inhibitors

    - Prevents conversion of Angiotensin I to Angiotensin II 
    - BP decreases, kidneys excrete excess   sodium and fluid, resulting in decreased workload on the heart
34
Q

Medical Management of MI:

Percutaneous Coronary Intervention

A

Percutaneous Coronary Intervention
-Done in Cardiac Catheterization Lab
-Opens the occluded coronary artery and allows reperfusion
-Should be done within 1 hour of patient’s arrival to the ED
The duration of oxygen deprivation is directly related to the number of cells that die

35
Q

Medical Management of MI:

Cardiac Rehabilitation

A

Cardiac Rehabilitation
Goals:
1. to extend life and improve quality of life

  1. Limit effects and progression of atherosclerosis
  2. Return patient to home & work and pre-illness lifestyle
  3. Promote activity and exercise tolerance
36
Q

Nursing Diagnosis of Acute MI?

A
  1. Ineffective Cardiac Tissue Perfusion R/T reduced coronary artery blood flow
  2. Risk for Imbalanced Fluid Volume
  3. Risk for Ineffective Peripheral Tissue Perfusion R/T Decreased Cardiac Output
  4. Death Anxiety
  5. Knowledge Deficit: Post MI Care

MedSurgExam1 (6 decks)

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