CAD Flashcards
Is the narrowing or blockage of the coronary artery, usually caused by atherosclerosis
Coronary Artery Disease (CAD)
Risk factors of CAD in Nonmodifiable Risk Factors
-Family history of CAD
-Age (> 45 years for men; 55 years for women)
-Gender: Men develop CAD at an earlier age
-Race: African American
Risk factors of CAD in Modifiable Risk Factors
-Hyperlipidemia
-Cigarette smoking, tobacco use
-Hypertension
-Diabetes
-Metabolic Syndrome
-Obesity
-Physical inactivity
Is an abnormal accumulation of lipid and fibrous tissue in the lining of arterial blood vessel walls
Coronary atherosclerosis
Involves a repetitious inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties of the arterial walls
Coronary Atherosclerosis
Medical Management of Coronary Atherosclerosis
Goal: Prevent, modify, or slow progression of the disease
-Health Promotion
-Diet Therapy
-Physical Acitvity
-Drug Therapy
All adults 20 years and older should have a fasting lipid profile performed once every 5 years, and more often if the profile is abnormal
Fasting Lipid Profile
Preparation for Fasting Lipid Profile
NPO for 10-12 hours
Low-Density Lipoprotein (LDL)
<100 mg/dl (<70 mg/dl for very high risk)
Total Cholesterol
<200 mg/dl
High-Density Lipoprotein
> 40 mg/dl for males, >50 mg mg/dl for females
Triglyceride
<150 mg/dl
Diet Therapy
Therapeutic Lifestyle Changes (TLC) Diet
TLC Diet Characteristics
-Decreased consumption of saturated fat and cholesterol
-Increase in complex carbohydrates and fiber
Reduces risk of CAD when eaten regularly
Omega- 3 fatty acids
Without CAD:
Fatty fish (i.e., salmon, tuna) 2x a week as these contain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)
With CAD:
EPA and DHA supplements together with diet
Intensity aerobic activity for at least 150 minutes per week
Moderate
Intensity aerobic activity at least 75 minutes per week
Vigorous
If weather is hot and humid:
-Exercise during the early morning, or indoors
-Wear loose-fitting clothing
If weather is cold:
-Layer clothing
-Wear a hat
Drug Therapy for Coronary Atherosclerosis
HMG-CoA Reductase Inhibitors Drugs
-Atorvastatin (Lipitor)
-Simvastatin (Zocor)
Therapeutic Effects of HMG-CoA Reductase Inhibitors
Decrease total cholesterol, decrease LDL, increase HDL, decrease TG
Drug Therapy for Coronary Atherosclerosis
Fibric Acids Drugs
Fenofibrate (Tricor)
Therapeutic effects of Fibric Acids Drugs
Increase HDL, decrease TG
Drug Therapy for Coronary Atherosclerosis
Bile Acid Sequestrants Drugs
Cholestyramine (Questran)
This drug is used as an adjunct therapy if statins alone are not effective in controlling lipid levels
Bile Acid Sequestrants
Therapeutic effects of Bile Acid Sequestrants Drugs
Decrease LDL, slight increase in HDL, oxidizes cholesterol into bile acids
A clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest
Angina Pectoris
Etiology of Angina Pectoris
Coronary Atherosclerosis
Types of Angina
-Stable Angina
-Unstable Angina
-Intractable Angina
-Prinzmetal’s Angina
Characteristics of Stable Angina
PORN
-Predictable and consistent pain
-Occurs on exertion
-Rest
-NTG
Characteristics of Unstable Angina
-Symptoms increase in frequency and severity
-May not be relieved by rest and/or NTG
-Unstable: Up
Characteristics of Intractable Angina
-Severe, incapacitating pain
-Intractable: Incapacitating
Characteristics of Prinzmetal’s Angina
-Pain at rest
-Reversible ST-segment elevation
-Prinzmetal’s: Pain at Rest
Clinical Manifestations of Angina Pectoris
-Deep behind sternum (retrosternal area)
-Radiates to the neck, jaw, shoulder, and inner aspects of upper left arm
-Accompanied by apprehension and a feeling of impending death
-Feeling of weakness or numbness in the arms, wrists, and hands
-SOB
-Pallor
-Diaphoresis
-Dizziness
-N/V
Diagnostics of Angina Pectoris
-12-Lead ECG
-Treadmill Stress Test
-Dobutamine Stress Test
Reveals an inverted T-wave
12-Lead ECG
Medical Management of Angina Pectoris
Goal: increase oxygen supply while decreasing oxygen demand
-Oxygen therapy
-Drug Therapy
-Initiated at onset of chest pain
-Attempts to increase the amount of oxygen delivered to the myocardium and to decrease pain
Oxygen Therapy
Drug therapy for Angina Pectoris is
Nitroglycerin (NTG)
A potent vasodilator and a treatment of choice
Nitroglycerin
Placed under tongue or in the cheek and ideally alleviates pain within 3 minutes
Sublingual NTG
May be given to hospitalized patients with recurring s/sx of ischemia or after a revascularization procedure
Continuous/Intermittent IV infusion of NTG
Major S/E of Nitroglycerin (NTG)
Headache
Nursing Responsibility of Nitroglycerin
Educate on proper administration of “as needed” doses of NTG
T/F NTG is dispensed in a dark glass bottle to prevent being inactivated by sunlight
True
Metoprolol is a
Beta-Blockers
Decreased myocardial oxygen consumption by blocking beta-adrenergic sympathetic
Metoprolol (Neobloc)
Metoprolol result
Reduced HR, slowed conduction of impulses, decreased BP, and reduced myocardial contractility
S/E of metoprolol
Depressed mood, fatigue, decreased libido, dizziness
Decreases sinoatrial node automaticity and Atrioventricular node conduction resulting in a slower heart rate (negative chronotropic) and decreased strength of myocardial contractility (negative inotropic)
Calcium-channel blockers
S/E of calcium-channel blockers
Hypotension, AV block, bradycardia, and constipation
Prevents platelet aggregation and reduces incidence of MI and death in patients with CAD
Aspirin
Initial dose of Aspirin
162-mg to 325-mg dose
Maintenance dose of Aspirin
81 to 325 mg
Side Effects of Aspirin
GI upset
May take a few days to achieve antiplatelet effects
Clopidogrel
Side Effects of Clopidogrel
GI bleeding and bleeding from other sites
Prevents formation of new blood clots and reduces risk of MI in unstable angina
Unfractionated Heparin IV
Therapeutic level of heparin
aPTT is 2 to 2.5 times normal
Enoxaparin SQ
is a subcutaneous injection of low-molecular-weight heparin
Treatment for unstable angina or Non-ST-elevation MI
Enoxaparin SQ
Provides effective and stable anticoagulation, potentially reducing the risk of rebound ischemic events, and eliminating the need to monitor aPTT.
Enoxaparin SQ
Unfractionated Heparin and LMWH side effects
Risk for bleeding
When using an unfractionated heparin and LMWH you need to watch out for internal and external bleeding such as:
-Hypotension
-Tachycardia
-Decreased serum hemoglobin and hematocrit
Bleeding Precautions are
-Applying pressure to the site of any needle puncture
-Avoiding IM injections
-Avoiding tissue injury and bruising from trauma or use of constrictive devices
Is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death if definitive interventions do not occur promptly.
Acute Coronary Syndrome (ACS)
Presenting Symptom of Acute Coronary Syndrome
CHEST PAIN
Clinical Manifestations of Acute Coronary Syndrome (ACS)
-Chest Pain
-Acute, substernal chest pain radiating to the left arm, jaw.
-crushing, vice-like
- “Stepped on by an elephant”
-Diaphoresis
-SOB
-Anxiety
-Tachycardia
-Tachypnea
-Cool, pale, moist skin
Clench fist held over the anterior chest
Levine Sign
Diagnostic of ACS
-12-Lead ECG
Should be obtained within 10 minutes from the time the patient reports pain or arrives in the ER
12-Lead ECG
Ischemia alters and delays myocardial repolarization
T wave inversion
Injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line
ST segment elevation
-Develops within 1 to 3 days because of the absence of depolarization current conducted from necrotic tissue.
- ≥ 0.04 second and 25% of R wave depth
Abnormal Q wave
Diagnostic of Acute Coronary Syndrome
- Troponin
-Creatine kinase- MB (CK-MB)
-Myoglobin
A protein found in myocardial cells which regulates the myocardial contractile process
Troponin
Cardiac specific
Troponin I and T
An enzyme found in cardiac cells
Creatine kinase-MB (CK-MB)
Indicator of acute MI and begins to rise in 4-14 hours and return to normal after 36 to 48 hours
Creatine kinase- MB (CK-MB)
A heme protein that helps transport oxygen
Myoglobin
Found in cardiac and skeletal muscle
Myoglobin
Rises in 1 to 3 hours and normalized within 24 hours
Myoglobin
Troponin elevation is
4-12 hours
CK-MB Elevation is
4-14 hours
Myoglobin elevation is
1-3 hours
Normal Level of Troponin
0.4 - 2 ng/ml
Normal Level of CK-MB is
0-6 mg/ml
Normal Level of Myoglobin is
17.4-105.7 ng/ml
Opioid Agonist
Morphine Sulfate
Morphine Sulfate in Indications of MI:
-Reduce pain and anxiety
-Reduces preload and afterload thereby decreasing the workload of the heart
Side Effects of Morphine Sulfate
-Hypotension
-Respiratory depression
Volume of blood in ventricles at end of diastole (end diastolic pressure)
Preload
Resistance left ventricle must overcome to circulate blood
Afterload
Preload increase in
-Hypervolemia
-Regurgitation of cardiac valves
-Heart Failure
To prevent further clot formation
Unfractionated heparin or LMWH+ platelet
Used to open occluded coronary artery and promote reperfusion to the area that has been deprived of oxygen and must be performed in less than 60 minutes from time of admission.
Percutaneous Coronary Intervention
Initiated when primary PCI is not available or the transport time to a PCI-capable hospital is too long.
Thrombolytic Therapy
Must be given within 30 minutes of presentation to the hospital
Thrombolytic Therapy
Drugs used during Thrombolytic Therapy
-Alteplase (Activase)
-Reteplase (Retavase)
-Tenecteplase (TNKase)
