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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.

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Presentation on theme: "Coronary Artery Disease Angina Acute Coronary Syndrome J.O. Medina,RN,MSN,FNP,CCRN Education Specialist Nurse Practitioner Critical Care & Emergency Services."— Presentation transcript:

1 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

2 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

3 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

4 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

5 –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

6 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

7 Plaque

8 Plaque With Thrombus

9 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

10 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

11 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

12 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”

13 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

14 Angina  Management –  demands on heart NTG Beta blockers Calcium channel blockers –Relieve Pain MONA Demerol if bradycardia present

15 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

16 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

17 CABG

18 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

19 Acute Coronary Syndromes  Pathophysiology –90% fatal transmural ACS associated with thrombosis ; 10% caused by vasospasm –irreversible cell death occurs within 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

20 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

21 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

22 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

23 Acute Coronary Syndromes  Physical Examination –Precordial signs heart sounds –Pulmonary assessment –Systemic signs vital signs LOC JVD UO

24 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 minutes other myocardial injury defibrillation, CPR, CABG also release these enzymes

25 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 hours; returns to normal in 3 days –must be >4% of total CK for definitive diagnosis of MI

26 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

27 Cardiac Enzymes

28 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

29 Acute Coronary Syndromes  Complications –arrythmia - most common complication ventricular –PVC - 80% –VT - 10% –VF % bradycardias - common with inferior MI –AV block ( narrow Vs. wide QRS) SVT –pump failure - common with anterior

30 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

31 Acute Coronary Syndromes

32 Questions ? Thank You!


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