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Coronary Artery Disease Angina Acute Coronary Syndrome

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Presentation on theme: "Coronary Artery Disease Angina Acute Coronary Syndrome"— 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 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

6 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

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 Relieve Pain NTG Beta blockers
Calcium channel blockers Relieve Pain MONA Demerol if bradycardia present

15 Angina  Coronary Artery supply Pharmacological agents PTCA
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


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 % 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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