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What are the nonmodifiable risk factors for CAD?
age, gender, ethnicity, family history, genetic inheritance
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What are the modifiable risk factors for CAD?
- elevated serum lipids
- elevated blood pressure
- elevated homocysteine level
- tobacco use
- physical inactivity
- obesity
- diabetes
- metabolic syndrome
- psychological states
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Elevated serum lipids are a major modifiable risk factor for CAD. What values specifically present a risk?
Total Cholesterol: ?
Triglycerides: ?
LDL cholesterol: ?
HDL cholesterol:?
- Total Cholesterol: > 200 mg/dL
- Triglycerides: > or equal to 150 mg/dL
- LDL cholesterol: > 160 mg/dL
- HDL cholesterol: < 40 mg/dL in men
- < 50 mg/dL in women
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Obesity is a major modifiable risk factor for CAD. How is obesity measured and what measure shows risk?
- In this case, waist circumference is more important than BMI.
- > or equal to 40 inches for men
- > or equal to 35 inches for women
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Patients at high risk for having a nonfatal MI or of dying from a coronary event based on low-density lipoprotein levels and other factors used to generate a risk score have a goal LDL level of ______.
They should consider drug therapy for LDL levels of ____.
<100 mg/dL
The high risk category includes patients who have CAD, peripheral vascular disease, or ACS
They should consider drug therapy for LDL levels of >100. 70-100 is reasonable to treat to < 70.
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Patients at moderately high risk for having a nonfatal MI or of dying from a coronary event based on low-density lipoprotein levels and other factors used to generate a risk score have a goal LDL level of __.
They should consider drug therapy for LDL levels of ____.
<130 mg/dL (optional goal of <100 mg/dL)
The moderately high risk category includes patients with 2 or less risk factors and a 10 year risk score between 10 and 20%.
They should consider drug therapy for LDL levels of > or equal to 130. 100-129, drug therapy is optional.
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Patients at moderate risk for having a nonfatal MI or of dying from a coronary event based on low-density lipoprotein levels and other factors used to generate a risk score have a goal LDL level of __.
They should consider drug therapy for LDL levels of ____.
< 130 mg/dL
The moderate risk category includes patients with 2 or less risk factors and < 10% 10 year risk score.
They should consider drug therapy for LDL levels of > or equal to 160.
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Patients at low risk for having a nonfatal MI or of dying from a coronary event based on low-density lipoprotein levels and other factors used to generate a risk score have a goal LDL level of __.
They should consider drug therapy for LDL levels of ____.
<160 mg/dL
The low risk category includes patients with 1 or no risk factors.
They should consider drug therapy for LDL levels of > or equal to 190. 160 - 189, drug therapy is optional.
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HMG-CoA Reductase Inhibitors (Statins)
Mechanism of action and effects?
Side effects?
- Mechanism of action and effects:
- Block synthesis of cholesterol and increase LDL receptors in liver.
- Decrease LDL
- Decrease Triglycerides
- Increase HDL
-
- Side effects:
- Rash, GI disturbances, elevated liver enzymes, myopathy, rhabdomyolysis
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What are the nursing considerations for HMG-CoA Reductase Inhibitors?
- Statins
- Well-tolerated with few side effects. Monitor liver enzymes and creatinine kinase (if muscle pain or weakness occurs)
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Niacin
Mechanism of action and effects?
Side effects?
- Mechanism of action and effects
- Inhibits synthesis and secretion of VLDL and LDL.
- Decrease LDL
- Decrease Triglycerides
- Increase HDL
- Side effects
- Flushing and pruritis in upper torso and face, GI disturbances (nausea, vomiting, dyspepsia, diarrhea), orthostatic hyptension, can elevate homocysteine levels.
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What are the nursing considerations for Niacin?
Most side effects subside with time; decreased liver function may occur with high doses. Taking aspirin or NSAIDs 30 minutes before drug may prevent flushing; take drug with food. Treat elevated homocysteine levels with folic acid.
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Fibric Acid Derivatives
Mechanism of action and effects?
Side effects?
- Mechanism of action and effects
- Decrease hepatic synthesis and secretion of VLDL; reduce triglycerides by lowering VLDL.
- Decrease LDL
- Decrease Triglycerides
- Increase HDL
- Side effects?
- Rashes, mild GI disturbances (nausea, diarrhea, elevated liver enzymes)
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What are the nursing considerations for fibric acid derivatives?
May increase effects of warfarin (Coumadin) and some antihyperglycemic drugs. When used in combination with statins, may increase adverse effects of statins, especially myopathy.
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What classes of drugs reduce lipoprotein production?
- HMG-CoA Reductase inhibitors (Statins)
- Niacin
- Fibric Acid Derivatives
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______ increase lipoprotein removal while _____ decrease cholesterol absorption.
- Bile Acid Sequestrants
- Cholesterol Absorption Inhibitor ( ezetimibe (Zetia) )
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Bile Acid Sequestrants
Mechanism of action and effects?
Side effects?
- Mechanism of action and effects
- Binds with bile acids in the intestine, forming insoluble complex and excreted in feces. Binding results in removal of LDL and cholesterol.
- Decreased LDL.
- Side effects
- Unpleasant quality to taste, GI disturbances ( indigestion, constipation, bloating)
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What are the nursing considerations for Bile-Acid Sequestrants?
Effective and safe for long-term use; side effects diminish with time. Interfere with absorption of many drugs ( digoxin, thiazide diuretics, warfarin, some antibiotics)
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ezetimibe (Zetia) is a ______.
Mechanisms of Action and Effects?
Side Effects?
- Cholesterol Absorption Inhibitor
- Mechanisms of Action and Effects
- Inhibits the intestinal absorption of cholesterol.
- Decreases LDL
- Increases HDL
- Side Effects?
- Infrequent, but may include headache and mild GI distress.
-
What are nursing considerations for cholesterol absorption inhibitors?
When used with a statin, LDL is further reduced. Should not be used by patients with liver impairment.
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PQRST Assessment of angina
- P-- Precipitating events-- what events or activities precipitated the pain?
- Q-- Quality of pain-- What does the pain feel like (Pressure, dull, aching, tight, squeezing, heaviness)?
- R-- Radiation of Pain-- Where is the pain located? Does the pain radiate to other areas (neck, back, arms, jaw, shoulder, elbow)?
- S-- Severity of pain-- On a scale of 0-10, rate pain.
- T-- Timing-- when did the pain begin? Has the pain changed since this time? Have you had pain like this before?
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Chronic Stable Angina
Etiology?
Characteristics?
- Etiology
- Myocardial ischemia, usually secondary to CAD
- Characteristics
- Episodic pain lasting 5 to 15 minutes
- Provoked by exertion
- Relieved by rest or nitroglycerin
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Prinzmetal's Angina
Etiology?
Characteristics?
- Etiology
- Coronary Vasospasm
- Characteristics
- Occurs primarily at rest
- Triggered by smoking and increased levels of some substances (eg histamine, angiotensin epinephrine)
- May occur in presence or absence of CAD
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Microvascular Angina
Etiology?
Characteristics?
- Etiology
- Myocardial ischemia secondary to microvascular disease affecting the distal branches of the coronary arteries.
- Characteristics
- More common in women
- Triggered by activities of daily living (shopping, work) vs. physical exercise (exertion)
- Treatment may include nitroglycerin
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Unstable Angina
Etiology?
Characteristics?
- Etiology
- Rupture of thickened plaque exposing thrombogenic surface
- Characteristics
- New-onset angina
- Angina of increasing frequency, duration, or severity
- Occurs at rest or with minimal exertion
- Pain refractory to nitroglycerin.
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Antiplatelet /Anticoagulant Agents
- --Inhibits cyclooxygenase, which in turn produces thromboxane A2, a potent platelet activator
- -- Should be administered as soon as ACS is suspected
- -- Inhibits platelet aggregation
- -- Alternative for patient who cannot use aspirin
- -- Inhibit platelet aggregation
- -- Used as an alternative to clopidogrel
- -- Interferes with hepatic synthesis of vitamin K-dependant clotting factors
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Nitrates
Promote peripheral vasodilation decreasing preload and afterload, coronary artery vasodilation. Relieves pain in about 3 minutes and lasts approximately 30 to 60 minutes, may repeat every 5 minutes a maximum of 3 times.
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Beta-Adrenergic Blockers
- Inhibit sympathetic nervous stimulation of the heart
- Reduce heart rate, contractility, and blood pressure
- Decrease afterload
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Calcium-Channel Blockers
- Prevent calcium entry into vascular smooth muscle cells and myocytes (cardiac cell)
- Coronary and peripheral vasodilation
- Reduce heart rate, contractility, and blood pressure.
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Angiotensin-Converting Enzyme (ACE) inhibitors
- Prevent conversion of angiotensin I to angiotensin II resulting in vasodilation.
- Decrease endothelial dysfunction
- Useful with heart failure, tachycardia, MI, hypertension, diabetes, and chronic kidney disease
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Angiotensin II Receptor Blockers
- Inhibit binding of angiotensin II to AT1 receptors resulting in vasodilation.
- Useful for patients intolerant of ACE inhibitors
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Unfractionated Heparins
Prevent conversion of fibrinogen to fibrin and prothrombin to thrombin.
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Low-Molecular-Weight Heparins
- Bind to antithrombin III, enhancing its effect
- Heparin-antithrombin III complex inactivates activated factor X and thrombin
- Prevents conversion of fibrinogen to fibrin.
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Glycoprotein IIb/IIIa Inhibitors
- Prevent the binding of fibrinogen to platelets, thereby blocking platelet aggregation.
- Standard antiplatelet therapy in combination with aspirin for patients at high risk for unstable angina
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Opioid Analgesics
- Functions as an analgesic and sedative
- Acts as a vasodilator to reduce preload and myocardial O2 consumption
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Fibrinolytic Therapy
- Breaks up fibrin meshwork in clots
- Used only in ST-segment elevation MI
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P Wave
Description
Normal duration
Source of Possible Variation
- Description
- Represents time for the passage of electrical impulse through the atrium causing atrial depolarization (contraction); should be upright
- Normal Duration
- 0.06 - 0.12 seconds
- Source of Possible Variation
- Disturbance in conduction within atria
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PR Interval
Description
Normal duration
Source of Possible Variation
- Description
- Measured from beginning of P wave to beginning of QRS complex; represents time taken for impulse to spread through the atria, AV node and bundle of His, the bundle branches, and purkinjie fibers, to a point immediately preceding ventricular contraction.
- Normal duration
- 0.12 - 0.20
- Source of Possible Variation
- Disturbance in conduction usually in AV node, bundle of His, or bundle branches but can be in atria as well.
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ST Segment
Description
Normal duration
Source of Possible Variation
- Description
- Measured from the S wave of the QRS complex to the beginning of the T wave; represents the time between ventricular depolarization and repolarization (diastole); should be isolelectric (flat)
- Normal duration
- 0.12 seconds
- Source of Possible Variation
- Disturbances usually acused by ischemia, injury, or infarction.
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QRS Interval
Description
Normal duration
Source of Possible Variation
- Description
- Measured from beginning to end of QRS complex; represents time taken for depolarization (contraction) of both ventricles (systole).
- Normal duration
- < 0.12 seconds
- Source of Possible Variation
- Disturbance in conduction in bundle branches or in ventricles.
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T Wave
Description
Normal duration
Source of Possible Variation
- Description
- Represents time for ventricular depolarization; should be upright
- Normal duration
- 0.16
- Source of Possible Variation
- Disturbances usually caused by electrolyte imbalances, ischemia, or infarction
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QT Interval
Description
Normal duration
Source of Possible Variation
- Description
- Measured from beginning of QRS complex to end of T wave; represents time taken for entire electrical depolarization and repolarization of the ventricles
- Normal duration
- 0.34- 0.43 seconds
- Source of Possible Variation
- Disturbances usually affecting repolarization more than depolarization and caused by drugs, electrolyte imbalances, and changes in heart rate.
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Normal Sinus Rhythm
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- 60 - 100 bpm and regular
- P wave
- normal
- PR Interval
- normal
- QRS Complex
- normal
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Sinus Bradycardia
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- < 60 bpm and regular
- P wave
- Normal
- PR Interval
- Normal
- QRS Complex
- Normal
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Sinus Tachycardia
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- 101-200 bpm and regular
- P wave
- normal
- PR Interval
- normal
- QRS Complex
- normal
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Premature Atrial Contraction
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- Usually 60 to 100 bpm and irregular
- P wave
- abnormal shape
- PR Interval
- normal
- QRS Complex
- usually normal
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Paroxysmal Supraventricular Tachycardia
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- 150-220 bpm and regular
- P wave
- Abnormal shape, may be hidden in the preceding T wave.
- PR Interval
- Normal or shortened
- QRS Complex
- Usually normal
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Atrial Flutter
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- Atrial: 200-350 bpm and regular
- Ventricular: > or < 100 bpm and may be regular or irregular.
- P wave
- Flutter (F) waves (sawtooth pattern); more flutter waves than QRS complexes; may occur in a 2:1, 3:1, 4:1, etc pattern.
- PR Interval
- Not measurable
- QRS Complex
- Normal (usually)
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Atrial Fibrillation
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- Atrial: 350-600 bpm and irregular
- Ventricular: > or < 100 bpm and irregular
- P wave
- Fibrillatory (f) waves
- PR Interval
- Not measurable
- QRS Complex
- Normal (usually)
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Junctional Dysrhythmias
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- 40-180 bpm and regular
- P wave
- inverted, may be hidden in QRS complex
- PR Interval
- Variable
- QRS Complex
- Normal (usually)
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First Degree AV block
Rate and Rhythm
P wave
PR Interval
QRS Complex
- Rate and Rhythm
- normal and regular
- P wave
- Normal
- PR Interval
- > 0.20 seconds
- QRS Complex
- Normal
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Second Degree AV Block, Type 1
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