Coronary Artery Disease & CAD & ACS Coronary Artery Disease Cardiovascular diseases are the major cause of death in the United States Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general Coronary Artery Disease A type of blood vessel disorder that is included in the general category of atherosclerosis Begins as soft deposits of fat that harden with age Referred to as hardening of arteries Can occur in any artery in the body Preference for the coronary arteries Coronary Artery Disease Etiology and Pathophysiology Atherosclerosis: major cause of CAD Occurs in 3 stages 1. Streaks of fat develop within smooth muscle cells of arteries 2. Raised fibrous plaque, in which endothelial injury results in fatty lesions covered with collagen tissue & elastic fibers 3. Complicated lesion, plaque consists of a core of lipid that continues to grow by incorporating lipids, thrombi, Ca, & damaged tissue End result is partial or total occlusion of artery 1
Coronary Artery Disease Pathophysiology C-reactive protein (CRP) Nonspecific marker of inflammation Increased in many patients with CAD Chronic exposure to CRP triggers the rupture of plaques Coronary Artery Disease Collateral circulation Growth and extent of collateral circulation is attributed to two factors Inherited predisposition to develop new vessels (angiogenesis) Presence of chronic ischemia When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing Risk Factors for CAD Nonmodifiable risk factors Age Gender Ethnicity Family history Genetic predisposition Risk Factors for CAD Modifiable risk factors Elevated serum lipids Hypertension Tobacco use Physical inactivity Obesity Diabetes Stress 2
CAD Health Promotion Health-promoting behaviors Physical fitness Regular physical activity contributes to:» Weight reduction» Reduction of >10% in systolic BP» In some men more than women, an increase in HDL cholesterol Nutritional therapy»omega-3 fatty acids CAD Health Promotion Cholesterol-lowering drug therapy Drugs that restrict lipoprotein production: Statins, niacin Drugs that increase lipoprotein removal Drugs that decrease cholesterol absorption: Ezetimibe (Zetia) CAD Health Promotion Antiplatelet therapy ASA Blocks formation of thromboxane A2, which causes platelets to aggregate and arteries to constrict Clopidogrel (Plavix) inhibits platelet aggregation by inhibiting binding of ADP to its platelet receptor Clinical Syndromes of CAD Angina & Unstable angina CP caused by myocardial ischemia Reversible cellular injury Non-ST segment elevation MI (NSTEMI) Non-ST segment elevation MI (NSTEMI) ST segment elevation MI (STEMI) STEMI & NSTEMI result in irreversible cellular injury, necrosis Sudden cardiac death may occur with each syndrome 3
ACS Pathophysiology 1. Rupture of plaque (some causes may be turbulent blood flow, inflammation that weakens the plaqe, vessel anatomy) 2. Platelets cover the surface of ruptured plaque (platelet aggregation) 3. Coagulation system activated with thrombin generation Results in partial or total occlusion Clinical Manifestations of CAD Chronic Stable Angina Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms Pain usually lasts 3 to 5 minutes Subsides when the precipitating factor is relieved Pain at rest is unusual ECG reveals ST segment depression Chronic Stable Angina Types Silent ischemia (atypical s/s) Up to 80% of patients with myocardial ischemia are asymptomatic Associated with diabetes mellitus and hypertension Confirmed by ECG changes S/S may include SOB, dizziness Chronic Stable Angina Types of Angina Prinzmetal s (variant) angina Occurs at rest usually in response to spasm of major coronary artery Seen in patients with a history of migraine headaches and Raynaud s phenomenon Spasm may occur in the absence of CAD 4
Chronic Stable Angina Nursing and Collaborative Management Drug therapy: Goal: O 2 supply Short-acting nitrates O 2 demand and/or Sublingual/Spray Administer up to 3 doses; 1 spray or SL tab q 3-5 minutes as long as SBP>90 Long-acting nitrates Nitroglycerin ointment Chronic Stable Angina Nursing and Collaborative Management Drug therapy: Goal: O 2 demand and/or O 2 supply β-adrenergic blockers Calcium channel blockers If β-adrenergic blockers are poorly tolerated, contraindicated, or do not control anginal symptoms Angiotensin-converting enzyme inhibitors Chronic Stable Angina Nursing and Collaborative Management Diagnostic Studies 12 lead EKG Stress Testing Cardiac catheterization Diagnostic Coronary revascularization: Percutaneous coronary intervention Balloon angioplasty Stent When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops ACS encompasses: Unstable angina (UA) Non ST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation (STEMI) 5
Etiology and Pathophysiology Deterioration of a once stable plaque rupture platelet aggregation thrombus Result Partial occlusion of coronary artery: Unstable Angina or NSTEMI Total occlusion of coronary artery: STEMI Unstable Angina Unstable angina New in onset Occurs at rest Has a worsening pattern UA is unpredictable and represents a medical emergency (MI) Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) Necrosis of entire thickness of myocardium takes 4 to 6 hours The degree of altered function depends on the area of the heart involved and the size of the infarct Contractile til function of the heart is disrupted in areas of myocardial necrosis Most MIs involve the left ventricle (LV) 6
Pain Total occlusion anaerobic metabolism and lactic acid accumulation severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration Pain Described as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: substernal, retrosternal, or epigastric areas; pain may radiate Sympathetic nervous system stimulation results in Release of glycogen Diaphoresis i Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch Cardiovascular Initially, HR and BP, then BP (secondary to in CO) Crackles Crackles Jugular venous distention Abnormal heart sounds S 3 or S 4 New murmur 7
Nausea and vomiting Can result from reflex stimulation of the vomiting center by the severe pain Feverer Systemic manifestation of the inflammatory process caused by cell death Healing Process Within 24 hours, leukocytes infiltrate the area of cell death Enzymes are released from the dead cardiac cells (important indicators of MI) Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by second or third day Healing Process Development of collateral circulation improves areas of poor perfusion Necrotic zone identifiable by ECG changes and nuclear scanning 10 to 14 days after MI, scar tissue is still weak and vulnerable to stress Healing Process By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed, but less compliant Ventricular remodeling In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate 8
Complications of Dysrhythmias Most common complication Present in 80% of MI patients Most common cause of death in the prehospital period Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock Diagnostic Studies Unstable Angina and Detailed health history and physical 12-lead ECG: Changes in QRS complex, ST segment, and T wave can rule out or confirm UA or MI Serum cardiac markers Elevated troponin = MI Coronary angiography Others: Exercise stress testing, echocardiogram Diagnostic Studies Lab Cardiac Markers Death of heart cells leads to release ofmacromolecules in the blood stream Myoglobin Detected 1-2 hours but nonspecific CK-MB isoforms, Troponins I & T Specific to myocardial necrosis, not detected for 4-6 hours Troponin I & T preferred biomarker for dx AMI Collaborative Care Emergency management <10 minute Assessment VS, EKG, 12 lead EKG, targeted history and cardio resp assess, start IV, draw cardiac markers, lytes, & coagulation studies Treatment: MONA <10 minutes Start O2 at 4L Aspirin, NTG, Morphine 9
Acute Intervention Anxiety Emotional and behavioral reaction Maximize patient s social support systems Consider open visitation Collaborative Care Emergent PCI Treatment of choice for confirmed MI Balloon angioplasty + drug-eluting stent(s) Ambulatory 24 hours after the procedure Collaborative Care Fibrinolytic therapy Reteplase Indication STEMI or new LBBB, chest pain<12hrs Contraindication BP>180/110 or closed head/face trauma within 3 months, surgery within 6 weeks, bleeding or clotting disorder, CPR>10 minutes Marker of reperfusion: Return of ST segment to baseline Prevent reocclusion Heparin Weight based bolus and gtt Rescue PCI if thrombolysis fails Major complication: Bleeding Drugs Oxygen - 4L maintain SpO2>90% Aspirin- decreases platelet aggregation to reduce coronary reocclusion Nitroglycerin: SL, spray, IV Dilates coronary arteries and vascular smooth muscle in veins, arteries, and arterioles Morphine sulfate Dilates arteries and veins, redistributing blood volume and reducing ventricular preload & afterload. Analgesic effect reduces CP Titrate 2-4 mg IV at 5-15 minute intervals until CP gone as long as SBP>90 10
Drugs β-adrenergic blockers Blocks sympathetic stimulation of heart and vasoconstriction. Decrease myocardial O2 use, reduces of ventricular ectopy & fibrillation Angiotensin-converting erting enzyme inhibitors Reduces mortality and CHF associated with AMI Helps prevent LV remodeling Collaborative Care Coronary surgical revascularization Fail medical management Presence of left main coronary artery or three-vessel disease Not a candidate for PCI (e.g., lesions are long or difficult to access) Failed PCI with ongoing chest pain Collaborative Care Coronary surgical revascularization Coronary artery bypass graft (CABG) surgery Requires cardiopulmonary bypass Uses arteries and veins for grafts Minimally invasive direct coronary artery bypass (MIDCAB) Alternative to traditional CABG ACS Coronary revascularization: ICU for first 24 to 36 hours Pulmonary artery catheter for measuring CO, other hemodynamic parameters Intraarterial line for continuous BP monitoring Pleural/mediastinal chest tubes for chest drainage Continuous ECG monitoring to detect dysrhythmias (esp. atrial dysrhythmias) 11
ACS Coronary revascularization: ICU for first 24 to 36 hours Endotracheal tube connected to mechanical ventilation Extubation within 12 hours Epicardial pacing wires for emergency pacing of the heart Urinary catheter to monitor urine output NG tube for gastric decompression ACS Coronary revascularization: Complications related to cardiopulmonary bypass Bleeding and anemia from damage to RBCs and platelets Fluid and electrolyte imbalances Hypothermia as blood is cooled as it passes through the bypass machine ACS Chronic Stable Angina and ACS Coronary revascularization: Care is focused on Assessing the patient for bleeding (e.g., chest tube drainage, incision sites) Monitoring fluid status Replacing electrolytes PRN Restoring temperature (e.g., warming blankets) Nursing Diagnoses Acute pain Ineffective tissue perfusion (cardiac) Ineffective tissue perfusion (cardiac) Anxiety Activity intolerance 12
Chronic Stable Angina and ACS Planning: Overall goals Relief of pain Preservation of myocardium Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors ACS Evaluation Relief of pain Preservation of myocardium Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors Summary Time is heart muscle Aggressive Treatment with MONA Our goal is for the patient to rate pain 0/10. 13