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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 (usually will kill the patient)
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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
- Ex: 40 year old and 60 year old both have an infarct at the same vessel, who is more at risk to die? The 40 year old because has no or less collaterals
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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)
- Elevations in certain types of lipids can increase propensity for them to be deposited in coronaries
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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 narrow valve)
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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)
- Associated with unstable plaque
- 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 for females, diabetics, and elderly: less pain, may be fatigue, weakness, dizziness, dyspnea
- Diabetics may not feel pain due to neuropathy; initially present with syncope, heart failure, 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; increases time in diastole, perfusion of coronaries, and supply)
- Calcium channel blockers (vasodilation in periphery on arterial side; 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 for acute relief (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 to prevent symptoms (rotate patches; nitrate free period to avoid tolerance; 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
- Occluded artery caused by unstable plaque
- 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 - perfuses right side of heart, inferior wall of left ventricle and AV node; 90% of MIs (arrhythmias, heart blocks)
- Left main artery - goes through entire left side of heart (both lateral and anterior wall of left ventricle); "widowmaker"
- Left anterior descending - perfuses anterior wall, papilllary muscles and chordae tendineae of mitral valve; 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 (indicates permanent damage; person has had an MI at some point)
- 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; need to get patient on leads)
- 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 (autoimmune 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 (max O2 delivery of myocardium)
- Establish IV access
- Continuous EKG monitoring (looking to detect arrhythmias and ST segment abnormalities)
- Labs (troponin, CK-MB, CBC, lipid panel, platelets, electrolytes, Cr, clotting)
- Administer meds (nitrates, aspirin, morphine - relieves pain and anxiety which decreases heart strain; also vasodilates on arterial side which decreases afterload)
- 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
- "MONA"
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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 (heart sounds, lung sounds, peripheral pulses)
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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
- Goal is to get patient into the cath lab in 20 to 30 minutes to stent the artery
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Treatment of STEMI
- Emergent PCI (PTCA) or thrombolytics (clot busters; risk for hemorrhage)
- Goal is to get into cath lab in 20 to 30 minutes to stent the artery
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What is a PCI (PTCA)?
- Percutaneous translumenal coronary angioplasty
- 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 (sternal incision and femoral or radial artery incision)
- 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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