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What is coronary artery disease?
- Narrowing of coronary vessels with atherosclerotic plaques (compromises blood flow to myocardium)
- Major cause of death in the US (CV disease is #1 cause of death in women; more women die than men)
- Normally asymptomatic (sudden death is most common symptom)
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Pathophysiology of CAD
- Endothelial injury predisposes artery to lipid deposits and platelet activation
- Initiated by elevated blood pressure, high cholesterol, heredity, smoking, and immune reactions
- Platelets release growth factors which cause smooth muscle proliferation further trapping lipids
- Lipids adhere to the damaged blood vessel wall and gradually increase in size and calcify over time
- Platelets accumulate at the site in large numbers which lead to thrombus formation
- An unstable plaque can rupture and precipitate an MI
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What is collateral circulation?
- New vessels form in order to perfuse an area of the heart that is not adequately perfused
- Smaller vessels grow around to bypass obstruction
- Attributes to two factors: arterial branching due to chronic ischemia or inherited predisposition to develop new blood vessels
- Greater chance of collateral circulation developing when the occlusion of an artery happens slowly
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Unmodifiable risk factors for CAD
- Age
- Gender (males are more at risk initially; women catch up after menopause)
- Ethnicity
- Genetic inheritance
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Modifiable risk factors for CAD
- Elevated serum cholesterol (200mg/dl associated with risk of developing CAD)
- Hypertension
- Smoking (6x greater risk; proportional to number of cigarettes smoked)
- Physical inactivity
- Obesity (heart grows in size causing increase in myocardial O2 consumption)
- Diabetes
- hs-CRP > 2mg/L (indicative of inflammation in coronaries)
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List serum lipids
- Low density lipoprotein "LDL" ("bad cholesterol" deposits cholesterol in artery walls; less than 130 is ideal)
- High density lipoprotein "HDL" ("good cholesterol" cleans up cholesterol from arteries; greater than 60 is ideal)
- Triglycerides (contributes to atherosclerosis; less than 150 is ideal)
- Total cholesterol (least important; ideal less than 200)
- Determined by fasting lipid profile (12 hr fast)
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Treatment of hyperlipidemia
- Low fat, low cholesterol diet (decrease intake of red meat, eggs, butter, high fat dairy products; more fruits and vegetables)
- Exercise and weight loss (raises HDL)
- If target not met consider drug therapy
- Statins (proven to decrease morbidity/mortality; lowers LDL)
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Nursing implications of statins
- Monitor LFTs and myositis (inflammation of skeletal muscle)
- Muscle tissue breakdown can cause kidney damage (rhabdomyolysis)
- Ask patient if have weakness, pain, muscle aches, perform CPK test to look for breakdown
- Often give drug in the evening (liver makes cholesterol mostly at night)
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What is angina pectoris?
- Chest pain resulting from reversible myocardial ischemia
- Imbalance between myocardial oxygen supply and demand
- Results from anaerobic metabolism and lactic acid build up (pain caused by irritation of nerve fibers by lactic acid build up)
- Ischemia is evidenced by ST depression on EKG
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Factors that decrease myocardial oxygen supply
- Atherosclerotic plaques
- Anemia (lack of hemoglobin makes O2 supply worse)
- Hypoxia
- CHF (lose cardiac output)
- Tachycardia (decreases supply because blood perfuses to coronaries during diastole; decreases time in diastole)
- Arrhythmias
- Coronary spasm
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Factors increasing myocardial oxygen demand
- Hypertension
- Cardiomegaly
- Exertion (physical or emotional)
- Hyperthyroidism (increases metabolism)
- Aortic stenosis (has to work harder to push blood through)
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Types of angina
- Stable
- Unstable
- Prinzmetal's
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What is stable angina?
- Classic type, predictable
- Chest pain occurring intermittently over 3 to 5 minutes with the same pattern of onset, duration and intensity of symptoms
- Usually exercise induced and subsides with rest or nitroglycerin
- Discomfort is mild or disabling
- Can be controlled with mediations as an outpatient
- ECG: ST depression
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What is unstable angina?
- Progressive and unpredictable (patient with stable can develop unstable)
- Increasing frequency of pain provoked by minimal or no exercise
- Associated with plaque that has ruptured (increased risk of complete thrombosis of the lumen with progression to MI)
- Requires immediately hospitalization
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What is Prinzmetal's angina?
- Often occurs at rest, rare form of angina
- Thought to be caused by coronary artery spasm (vasospastic)
- Clean coronaries
- Treat with calcium channel blockers or nitroglycerin
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Precipitating factors for angina
- Physical exertion (increases HR; decreases time heart spends in diastole)
- Strong emotions (stimulates SNS and increases work of heart; increases HR, BP, and contractility)
- Consumption of a heavy meal (blood shunted to GI system causing low flow rate to the coronary arteries)
- Temperature extremes (hot or cold; increases workload of heart)
- Cigarette smoking (vasoconstriction, increases HR, diminishes available O2 by increasing level of CO2)
- Sexual activity (increases cardiac workload and sympathetic stimulation)
- Stimulants (cocaine & crack; vasoconstriction increases HR and myocardial O2 demand)
- Circadian rhythm patterns (symptoms tend to occur early in the morning after wakening)
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Characteristics of anginal pain?
- Usually substernal pressure, may radiate to arm or jaw
- May be associated with diaphoresis or dyspnea
- Not positional, sharp, or pleuritic (does not hurt worse if cough or breathe deeply)
- Cannot easily be localized
- Atypical presentation: females, diabetics (neuropathy, syncope), and elderly - less pain, may be fatigue, weakness, dizziness, dyspnea
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Treatment of stable angina
- Risk factor modification (low fat diet, smoking cessation, control of BP and diabetes)
- Antiplatelets: ASA or Plavix (decreases platelet aggregation)
- Statins (decreases risk of MI)
- Nitroglycerin (vasodilates venous side, decreases preload, afterload, and O2 demand; monitor BP)
- Beta blockers (decreases HR, contractility, BP and myocardial O2 demand)
- Calcium channel blockers (vasodilation; decreases influx of calcium into muscle; decreases myocardial O2 demand by decreasing afterload and contracility; contraindicated in acute MI or CHF)
- Possible PTCA or CABG
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Patient teaching on Nitroglycerin
- Administer sublingually (one tab under tongue q5 minutes x3)
- Call 911 if pain worsens or fails to improve after 5 minutes (may be an MI)
- Common side effects: headache, dizziness, tachycardia, orthostatic hypotension, can cause fatal hypotension and MI
- Avoid using with Viagra, Levitra, or Cialis
- Store in cool dry place
- Discard 6 months after opening
- Use of transdermal nitroglycerin: rotate patches; nitrate free period; remember to remove
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Treatment of unstable angina
- Hospitalization
- Bedrest
- Continuous EKG monitoring
- Administer ASA with or without Heparin
- Nitro drip titrated to pain and BP (monitor for decrease in BP)
- Beta blockers (decreases mortality)
- Consider PTCA (inflation of balloon to compress plaque; stent placed to keep vessel open)
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What is myocardial infarction?
- Ischemic intracellular changes that become irreversible and necrosis results
- Infarction results from sustained ischemia causing irreversible cellular death; cell death begins in 20 minutes
- Contractile function of heart stops in the area of necrosis (degree of altered function depends on the area of the heart involved and size of infarct)
- Most infarcts involve the left ventricle
- MI is usually described by the area of occurrence as anterior, inferior, lateral, or posterior wall
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What are the types of MI's by location and coronary anatomy?
- Right coronary artery - inferior wall and AV node; 90% of MIs (arrhythmias, heart blocks)
- Left main artery - massive anteriolateral; "widowmaker"
- Left anterior descending - anterior wall, papilllary muscles and chordae tendineae; risk for valvular problems (acute mitral regurgitation), systolic murmur (5th ICS midclavicular line)
- Circumflex - lateral and posterior wall of ventricle
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What complications can result from an MI involving the right coronary artery?
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What complications can result from an MI involving the left anterior descending artery?
- Valvular problems (acute mitral regurgitation)
- Systolic murmurs
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Atypical presentation of an MI
- Women - less pain, more shortness of breath
- Diabetics - silent MI
- Elderly - syncope, change in mental status, pulmonary edema
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Three areas of damage after an MI
- Area of infarction - O2 deprived, damage irreversible; causes Q wave on EKG
- Area of injury - next to infarct, tissue is viable as long as circulation remains adequate; causes ST segment elevation on EKG
- Area of ischemia - viability may not be damaged as long as MI doesn't extend and collateral circulation is able to compensate; causes depressed ST segment
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MI "timeline"
- Initial myocardial necrosis
- Inflammatory processes occurs in 2 to 3 days (macrophages and neutrophils remove necrotic tissue; can be associated with low grade fever)
- Scar formation in 10 to 14 days (initial scar tissue is fragile)
- In 6 weeks the scar is formed
- Myocardial remodeling (surrounding myocardium dilates and increases O2 demand; can lead to late-onset CHF; remodeling minimized with ACE inhibitors and beta blockers)
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General complications of an MI
- Arrhythmias (most common; v-fib most likely to kill patient)
- CHF (anterior is the most common; inadequate cardiac output, pulmonary edema)
- Cardiogenic shock (severe left ventricular failure, renal failure, worsened myocardial ischemia; requires intubation, vasopressors)
- Pericarditis (chest pain aggravated by inspiration, coughing and upper body movement; pain relieved by sitting in a forward position; heard as a friction rub)
- Dressler's syndrome (pericarditis that develops in 1 to 4 weeks post MI; caused by immune response to necrotic heart tissue)
- Pulmonary embolism (due to immobility)
- Papillary muscle dysfunction (ischemia or injury)
- Papillary muscle rupture (sudden, severe mitral regurgitation; flash pulmonary edema)
- Ventricular aneurysm (bulging of ventricular wall)
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How do you detect arrhythmias, CHF, and pericarditis?
- Arrhythmias - EKG, telemetry, peripheral pulses, cardia auscultation
- CHF - perfusion, lung sounds (crackles), pulmonary edema, peripheral edema
- Pericarditis - auscultation of heart, chest pain when moving or positioning
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What is the nursing care for a patient with chest pain?
- Administer O2 at 4L
- Establish IV access
- Continuous EKG monitoring
- Labs
- Administer meds (nitrates, aspirin, morphine)
- On-going assessment
- Emotional support
- Acute chest pain is considered an MI until proven otherwise
- "Time is muscle" - the sooner you intervene the more myocardium that can be salvaged
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MI medications
- Aspirin
- Morphine sulfate
- IV nitroglycerin
- Heparin
- Beta blocker (decreases myocardial O2, increases myocardial O2 supply, decreases mortality)
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How will you titrate nitroglycerin?
Based on pain level and BP
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Nursing assessments
- Vital signs and pulse oximetry
- EKG ischemic changes and arrhythmias
- Chest pain
- Associated symptoms (dyspnea, dizziness, nausea, vomiting, shortness of breath, diaphoresis)
- Cardiopulmonary assessment
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Diagnostic tests
- Chest x-ray (CKR)
- Serial 12 lead EKG
- Serial cardiac enzymes
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What are the cardiac enzymes?
- CK-MB - rise 3 to 12 hours after onset of an MI; peaks in 24 hours; returns to baseline in 2 to 3 days
- Troponins - rise in 3 hours; peaks in 24 to 48 hours; returns to baseline in 5 to 14 days
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Treatment of NSTEMI
- Admit to CCU
- Bedrest
- Continuous monitoring
- Assess for complications
- Consider PCI (PTCA) or CABG
- Emergent PCI (PTCA) or thrombolytics (clot busters)
- Goal is to get patient into the cath lab in 20 to 30 minutes to stent the artery
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What is a PCI (PTCA)?
- Alternative to surgical intervention
- Catheter with balloon on end is inserted
- Patient is ambulatory after the procedure; decreased length of hospital stay
- Complications: dissection of dilated artery causing death, cardiac tamponade, ischemia, MI, allergic reaction to dye
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What is a stent?
- Treats abrupt or threatened closure following a PTCA
- Mesh-like structure that maintains vessel patency
- Complications: hemorrhage, vascular injury, acute MI, emergency CABG, stent embolization, coronary spasm
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What is the nursing care following a PCI (PTCA)?
- Post procedure sheaths in place (to keep artery patent)
- Continue to monitor vital signs, pulse ox, telemetry, cardiopulmonary assessment
- Care of femoral artery site as per cardiac cath (look for hematoma, bleeding, peripheral perfusion)
- Continue ASA and Plavix post stent placement (for at least 1 year)
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What is a CABG?
- Coronary artery bypass graft
- Grafting of vessels around an area that is blocked
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Nursing care post-CABG
- Assess both surgical sites
- Sternotomy
- Chest tube care
- Patient will initially be intubated
- Critical care monitoring of vital signs, CVP, telemetry, urine output (tells perfusion of kidneys, marker for cardiac output)
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Thrombolytic therapy
- Produces lysis of clots
- Indication: STEMI within 6 to 12 hours of onset
- Need to make sure there are no contraindications or active bleeding before starting therapy
- Types: tPa, streptokinase
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Absolute contraindications of thrombolytic therapy
- Active bleeding
- Coagulation defects
- Peptic ulcer disease
- GI bleed within 6 months
- Past hemorrhagic stroke
- Pregnancy
- Surgery within 3 months
- Suspected aortic dissection
- SBP>180
- DBP>110
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Relative contraindications of thrombolytic therapy
- Patient on Coumadin
- Recent CPR
- CVA or TIA in last 12 months
- Severe renal or liver disease
- Hemorrhagic retinopathy
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Nursing care for thrombolytic therapy
- Draw labs prior
- Establish 2 to 3 IV lines
- Initiate infusion with close monitoring
- Observe for reperfusion
- Observe for bleeding (monitor BP, HR, IV sites, change in LOC, hematuria, blood in stool)
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Post-MI nursing care
- Gradually advance activity
- Educate patient on meds, diet, activity
- Encourage smoking cessation
- Confirm activity prescription with cardiologist
- Refer to cardiac rehab
- Possible follow-up stress test
- Reinforce need to control diabetes, hypertension, lipids
- Screen for depression
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What is sudden cardiac death?
- Unexpected sudden cardiac arrest (no known history)
- Usually underlying CAD
- Usually results from v-fib
- Death is first symptom of CAD in 25% of cases
- 20% are discharged without brain damage
- For sudden cardiac death survivors: perform work-up for MI, cardiac catheterization, EPS study (to see if patient is prone to having lethal arrhythmias), CABG if indicated, ICD (implanted cardioversion defibrillator)
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