1. 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)
  2. 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
  3. 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
  4. Unmodifiable risk factors for CAD
    • Age
    • Gender (males are more at risk initially; women catch up after menopause)
    • Ethnicity
    • Genetic inheritance
  5. 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)
  6. 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)
  7. 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)
  8. 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)
  9. 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
  10. 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
  11. Factors increasing myocardial oxygen demand
    • Hypertension
    • Cardiomegaly
    • Exertion (physical or emotional)
    • Hyperthyroidism (increases metabolism)
    • Aortic stenosis (has to work harder to push blood through)
  12. Types of angina
    • Stable
    • Unstable
    • Prinzmetal's
  13. 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
  14. 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
  15. 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
  16. 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)
  17. 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
  18. 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
  19. 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
  20. 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)
  21. 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
  22. 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
  23. What complications can result from an MI involving the right coronary artery?
    • Arrhythmias
    • Heart blocks
  24. What complications can result from an MI involving the left anterior descending artery?
    • Valvular problems (acute mitral regurgitation)
    • Systolic murmurs
  25. Atypical presentation of an MI
    • Women - less pain, more shortness of breath
    • Diabetics - silent MI
    • Elderly - syncope, change in mental status, pulmonary edema
  26. 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
  27. 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)
  28. 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)
  29. 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
  30. 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
  31. MI medications
    • Aspirin
    • Morphine sulfate
    • IV nitroglycerin
    • Heparin
    • Beta blocker (decreases myocardial O2, increases myocardial O2 supply, decreases mortality)
  32. How will you titrate nitroglycerin?
    Based on pain level and BP
  33. 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
  34. Diagnostic tests
    • Chest x-ray (CKR)
    • Serial 12 lead EKG
    • Serial cardiac enzymes
  35. 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
  36. 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
  37. 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
  38. 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
  39. 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)
  40. What is a CABG?
    • Coronary artery bypass graft
    • Grafting of vessels around an area that is blocked
  41. 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)
  42. 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
  43. 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
  44. Relative contraindications of thrombolytic therapy
    • Patient on Coumadin
    • Recent CPR
    • CVA or TIA in last 12 months
    • Severe renal or liver disease
    • Hemorrhagic retinopathy
  45. 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)
  46. 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
  47. 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)
Card Set
CAD - Med-Surg I Quiz 3