Coronary Artery Disease Angina Acute Coronary Syndrome

1. Coronary Artery DiseaseAnginaAcute 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 • 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 0600-1200

19. 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

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 30-60 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 18-24 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 - 5-15% • 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!