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Coronary Artery Disease Angina Acute Coronary Syndrome J.O. Medina,RN,MSN,FNP,CCRN Education Specialist Nurse Practitioner Critical Care & Emergency Services California Hospital Medical Center Coronary Artery Disease Pathophysiology – Atherosclerosis : progressive, diffuse disease that narrows artery lumen by abnormal thickening, hardening of artery wall resulting in non-compliant vessels – CAD: characterized by development of atherosclerotic plaques, called atheromas or “lesions” that blocks coronary artery blood flow Coronary Artery Disease – Development of lesions, starting in childhood, progress through phases, caused by injury to intima of artery – Progression of CAD • Phase I : fatty streaks – do not obstruct flow • Phase II: fibrous plaque- elevated lesion protruding into lumen obstructs flow to varying degrees • Phase III: complicated lesions – partially or totally occlude lumen – Occurs largely at points of artery bifurcation, usually more prominent at proximal end of artery – Process causes reduced supply of oxygen and nutrients to heart cells and inability to meet metabolic demands of the heart Coronary Artery Disease – Process causes reduced supply of oxygen and nutrients to heart cells and inability to meet metabolic demands of the heart • MVO2 is dependent on – – – – Preload Afterload Contractility Heart rate • Myocardial oxygen supply is dependent on – Arterial oxygen content – Coronary artery perfusion – Imbalance between supply/demand ratio leads to myocardial ischemia Coronary Artery Disease – Major effects of myocardial ischemia • Decreased contractility – pump failure • Electrical instability- arrythmias – Risk Factors • Non-modifiable risk factors – – – – Age: death from CAD with age Sex Family history Race: afro-Americans have = 45% > hypertension than Caucasians Coronary Artery Disease • Modifiable Risk Factors – Cigarette smoking: 2X increased risk for CAD – HTN: damages blood vessels leading to plaque formation and atherosclerosis – Hyperlipidemia: CAD and atherosclerosis by causing build up in artery walls – Physical Inactivity: risk of CAD 2X – Diabetes: risk 2X in men; 3X in women – Obesity – Stress : increased catecholamine release; sympathetic response Plaque Plaque With Thrombus Angina Chest discomfort caused by transient myocardial ischemia without cell death Usually brought on by physical or emotional stress Precipitated by 4 “E’s” – – – – Extreme emotion Extreme temperature Excessive eating Exercise Angina Types – Angina Pectoris (classic angina): occurs at least 50-60% of one or more main coronary arteries • Stable – does not increase in severity or duration over months; promptly relieved by rest and/or NTG • Unstable Angina – (crescendo, preinfarction) progressively increases in severity, duration, quality, not relieved promptly by rest/NTG • Prinzmetal’s Angina – (variant) usually occurs at rest; due to coronary artery spasm • Silent Ischemia – no symptoms Angina Clinical Presentation – History – look for risk factors – Pain Profile • Onset: sudden • Location: precordial, substernal, diffuse, ache in arm (usually left) • Duration: 3-5 min; rarely longer than 20 minutes • Characteristics – P,Q,R,S,T • Associated Symptoms: weakness, dizziness, sweating, nausea, vomiting, dyspnea • Relief: rest • Treatment: NTG Angina – Physical Examination – Diagnostics • EKG : 3 “I’s” • Echocardiogram – wall motion abnormalities – estimates ejection fraction • EF = EDV - ESV x 100 EDV • Normal EF 65% ( 10%) – measures cavity size and wall thickness of ventricles – may be used with EKG exercise tolerance test or Dobutamine to stress heart without exercise • Thallium Scans – radioisotope will be diminished in ischemic zones ; absent in infarcted zones referred as “cold spots” Angina • Positron Emission Tomogaphy (PET) / Single Photon Emission Computed Tomography (SPECT) – differentiates normal, ischemic, infarcted tissue by assessing myocardial metabolism • Cardiac catheterization – “gold standard “ for diagnosing CAD – demonstrates location and degree of blockages – can identify type of blockage (i.e. calcium, clots, or spasm) – measure right and left heart pressure, EF, CO – demonstrates wall motion abnormalities – used to evaluate type of interventional therapies most suited: angioplasty, atherectomy, stenting, LASER) surgery, medication only Angina Management – demands on heart • NTG • Beta blockers • Calcium channel blockers – Relieve Pain • MONA • Demerol if bradycardia present Angina – Coronary Artery supply • Pharmacological agents – – – – oxygen NTG calcium channel blocking agents ASA • PTCA – increases inner diameter of coronary artery – achieved by advancing balloon catheter • Atherectomy - removal of plaque from the artery Angina • Coronary artery stents - creates larger luminal diameter by physically compressing plaque against arterial wall – restenosis rate lower than PTCA • LASER - ablate plaque • Coronary artery bypass graft (CABG) – anastomosis of saphenous vein graft or internal mammary artery (IMA) bypassing blockage – selection criteria • angina not responsive to medical therapy • left main disease • failed PTCA CABG Acute Coronary Syndromes Irreversible necrosis or death of myocardial tissue due to inadequate blood supply 1.5 million Americans suffer ACS annually 60% die prior to hospitalization; 15-25% will die within next 4 weeks from complications frequently occurs at rest, sleep or usual activities ; most common 0600-1200 Acute Coronary Syndromes Pathophysiology – 90% fatal transmural ACS associated with thrombosis ; 10% caused by vasospasm – irreversible cell death occurs within 20-40 minutes of cessation of blood flow – subendocardium is first affected due to highest O2 demands and most tenuous blood supply – wavefront of cellular death - endo to epicardium Acute Coronary Syndromes – Wavefront produces zones: • zone of necrosis - electrically and mechanically dead tissue • zone of injury- severe cellular injury; may be viable • zone of ischemia - reduced blood flow, but salvageable – amount of damage/necrosis depends on • duration of occlusion • artery blocked • degree of collateral blood flow Acute Coronary Syndromes – Metabolic changes as cells convert to anerobic metabolism due to cellular ischemia – arrythmias – decreased contractility - pump failure – ANS response can be either • sympathetic nervous system response – HR, contractility, SVR • parasympathetic nervous response – HR, BP, CO, heart blocks Acute Coronary Syndromes Clinical Presentation – chest pain • 80% experience chest pain ; 15-30% no chest pain • pain similar to angina, usually more severe, lasting > 30 minutes, not relieved by NTG or rest – associated signs and symptoms • nausea / vomiting • weakness, cold perspiration, sense of doom • dizziness, palpitations, dyspnea Acute Coronary Syndromes Physical Examination – Precordial signs • heart sounds – Pulmonary assessment – Systemic signs • • • • vital signs LOC JVD UO Acute Coronary Syndromes Diagnosis – 12/13/15/18/21 Lead EKG • limitations • 3 Is of ACS – zone of ischemia - T wave inversion – zone of injury - ST elevation – zone of infarction - Q wave – Cardiac Enzymes • ACS damages cell membranes, releasing enzymes into plasma within 30-60 minutes • other myocardial injury defibrillation, CPR, CABG also release these enzymes Acute Coronary Syndromes – CK (CPK) - creatine phosphokinase • rises in 3-6 hours post MI; peaks at 24 hours; returns to normal in 3-4 days • composed of 3 isoenzymes: MB (found in heart); MM (found in skeletal muscles); BB (found in brain) • CK-MB (CK#2) very sensitive to MI – rises within hours; peaks at 18-24 hours; returns to normal in 3 days – must be >4% of total CK for definitive diagnosis of MI Acute Coronary Syndromes – LDH - lactic dehydrogenase • consists of 5 isoenzymes; LDH 1most specific for myocardial damage • LDH 1 occurs after CK elevation • helpful in delayed presentation – Other biochemical markers • myoglobin - found both in skeletal muscles and heart; rises within 2 hours; but not specific • Troponin I and T - more specific than CKMB; rise within 4 hours ; stay elevated 1-2 weeks Cardiac Enzymes Acute Coronary Syndromes Management – Goals of therapy • • • • re-establish supply and demand balance salvage ischemic cells relieve pain prevent/treat complications – AHA ischemic chest pain algorithm Acute Coronary Syndromes Complications – arrythmia - most common complication • ventricular – PVC - 80% – VT - 10% – VF - 5-15% • bradycardias - common with inferior MI – AV block ( narrow Vs. wide QRS) • SVT – pump failure - common with anterior Acute Coronary Syndromes – RVMI – Pericarditis • early within first week or up to 12 weeks post MI • dressler’s syndrome – Thromboemboli • from mural thrombi • atrial fibrillation – DVT • up to 30 % • due to immobility and hypercoagulable state Acute Coronary Syndromes Questions ? 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