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)
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
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
Unmodifiable risk factors for CAD
Age Gender (males are more at risk initially; women catch up after menopause) Ethnicity Genetic inheritance
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)
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)
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)
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)
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
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
Factors increasing myocardial oxygen demand
Hypertension Cardiomegaly Exertion (physical or emotional) Hyperthyroidism (increases metabolism) Aortic stenosis (has to work harder to push blood through)
Types of angina
Stable Unstable Prinzmetal's
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
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
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
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)
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
Treatment of stable angina
Risk factor modification (low fat diet, smoking cessation, control of BP and diabetes) : ASA or Plavix (decreases platelet aggregation) Antiplatelets 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
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 : headache, dizziness, tachycardia, orthostatic hypotension, can cause fatal hypotension and MI side effects Avoid using with Viagra, Levitra, or Cialis Store in cool dry place Discard 6 months after opening Use of : rotate patches; nitrate free period; remember to remove transdermal nitroglycerin
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)
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
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
What complications can result from an MI involving the right coronary artery?
What complications can result from an MI involving the left anterior descending artery?
Valvular problems (acute mitral regurgitation) Systolic murmurs
Atypical presentation of an MI
Women - less pain, more shortness of breath Diabetics - silent MI Elderly - syncope, change in mental status, pulmonary edema
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
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)
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)
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
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
Aspirin Morphine sulfate IV nitroglycerin Heparin Beta blocker (decreases myocardial O2, increases myocardial O2 supply, decreases mortality)
How will you titrate nitroglycerin?
Based on pain level and BP
Vital signs and pulse oximetry EKG ischemic changes and arrhythmias Chest pain Associated symptoms (dyspnea, dizziness, nausea, vomiting, shortness of breath, diaphoresis) Cardiopulmonary assessment
Chest x-ray (CKR) Serial 12 lead EKG Serial cardiac enzymes
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
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
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
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
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)
What is a CABG?
Coronary artery bypass graft Grafting of vessels around an area that is blocked
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)
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
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
Relative contraindications of thrombolytic therapy
Patient on Coumadin Recent CPR CVA or TIA in last 12 months Severe renal or liver disease Hemorrhagic retinopathy
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)
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
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)