ACUTE CORONARY SYNDROMES

1. Practice and Education of EBP Critical Care ACUTE CORONARY SYNDROMES Christopher Manacci, MSN, ACNP Director, ACNP Flight Nursing Program The National Flight Nurse Academy Frances Payne Bolton School of Nursing Case Western Reserve University Acute Care Nurse Practitioner Cleveland Clinic Critical Care Transport

2. Registered nurses who: • Have a master’s degree or doctorate • Are nationally certified • Have advanced training and education in a specialized area of health care • CNP functions include: management of acute and chronic illnesses and disease prevention to a variety of age ranges in a variety of care settings

3. Written guideline which defines responsibilities, accountabilities, and obligations of the specific CNP practice. • Limited by: • State legislation • Standard Care Agreement • Credentialing institution • Collaborating Physician Scope of Practice

4. Rounds • H&P’s/discharges • Physical exams • Evaluation/initiation of plan of care • diagnostics • pharmacotherapy • clinical interventions

5. Key elements of the acute care nurse practitioner : • Diagnosing and management of patients • Utilization and performance of invasive and non invasive interventions and procedures to promote physiologic stability or obtain diagnostic information • Surveillance of care • Accountability and authority for patient care outcomes across settings and boundaries

6. Acute Coronary Syndromes • Sudden onset of coronary insufficiency, presenting with chest pain, resulting from thrombotic occlusion. • Three conditions: • ST- segment elevation MI (STEMI)- Q-wave • Non- ST – segment elevation MI (NSTEMI)- non Q-wave • Unstable angina • Rule out other significant chest pathology, such as acute aortic dissection. Chest Xray and CT scan.

7. Aorta Pathology

8. Occlusion of the Vessel • Ischemia • Injury • Infarct

9. The Stages of Infarction • Ischemia - temporary shortage of oxygen at the cellular level • Injury - supply fails to meet the demand; can result in decreased pump function or electrical conductivity if hypoxia is not corrected • Infarct - death from anoxia

10. Time is Muscle

11. Risk Factors + family history Gender (men and post menopausal women) Hypertension Smoking Abnormal cholesterol obesity Excessive intake of saturated fats Sedentary lifestyle Aging Stress Drug use – cocaine and amphetamines

12. TIMI Risk Score • Age > 65 years • At least 3 risk factors for CAD • Significant coronary stenosis • ST –segment deviation on ECG at presentation • Severe anginal symptoms • Use of aspirin in last 7 days • Elevated serum cardiac markers

13. Common Manifestations • Uncomfortable pressure • Fullness in chest • Radiation to shoulder, jaw, neck, arm • Diaphoretic • SOB • N&V

14. Other Manifestations • Palpitations • Fatigue • Reduced urine output • Systolic murmur • Decreased or abnormal heart sounds • Tingling of extremities • Syncope or confusion

15. Diagnosis • Cardiac Enzymes – released upon necrosis of cardiac muscle • CK-MB – • >2 times the upper limit of normal • Low levels found in healthy people so specificity limited • Troponin I and T • More sensitive • Degree of elevation correlated with rate of mortality • Not released until 6 hours after symptoms

16. Diagnosis • EKG • ST elevation • New LBBB • ST depression with T-wave inversion - ischemia • New Q waves

17. Basic QRS complex data

18. ECG Leads • ECG Leads • Bipolar • Leads I, II, and II • Unipolar • Leads aVR, aVL, and aVF • Precordial • V1, V2, V3, V4, V5, V6

19. ECG Leads • Precordial Leads • Lead V1 • Lead V2 • Lead V3 • Lead V4 • Lead V5 • Lead V6

20. Lead placement for diagnostics

21. Normal electrophysiology

22. LEADS • II, III, aVf • V1, V2 • V3, V4 • V5, V6, I, aVl • VIEW • Inferior • Septal • Anterior • Lateral

23. I II III aVr aVl aVf V1 V2 V3 V4 V5 V6 Location of Acute MI Anterior/Septal: V1-V4 Inferior: II, III, aVf Lateral: I, aVl, V5, V6

24. Diagnosing Acute MI Type aVr Non-diagnostic I Lateral V1 Septal V4 Anterior II Inferior aVl Lateral V2 Septal V5 Lateral III Inferior aVf Inferior V3 Anterior V6 Lateral

25. Infarct Recognition Process • Are Indicative Changes Present? • If so, in which Leads? • Presence and Location of AMI

26. Practice EKG

27. Practice EKG

28. Q WAVES • Can signify presence of MI • Can be completely normal • Challenge is to differentiate physiological (normal) ‘Q’ waves from pathological (significant) ‘Q’ waves indicating infarction

29. Q Wave Determination • Determine the width and depth of the ‘Q’ wave • physiologic = less than 40 ms and an amplitude less than 1/3 the height of the ‘R’ wave • pathologic = more than 40 ms and may exceed 1/3 the height of the ‘R’ wave

30. ST SEGMENT • Normally is isoelectric and indicates ventricular repolarization • Can become depressed or elevated in the presence of injury, ischemia or infarction

31. Pathology associated with ST segment changes • Ischemia or Infarction • Digitalis • Tachycardia • Hypothermia • Hypokalemia • Ventricular Hypertrophy • LBBB • Vasospastic Angina • Pericarditis • Early Repolarization

32. DETERMINING ST SEGMENT CHANGES • Locate the ‘J’ point - junction between the QRS complex and the ST segment • Use the ‘TP’ segment and the ‘PR’ segment to estimate the position of the isoelectric line • Compare the level of the ST segment to the isoelectric line • Deviation of 1 mm or more is considered significant as measured 2 boxes after the end of the QRS • can be in the form of depression or elevation

33. R WAVE PROGRESSION • Morphologies of QRS complexes in chest leads follow a predictable pattern from V1-V6 • Begins with rS in V1 and progresses to become a more positive R wave increasing in height as the impulse travels toward the LV • The S wave respectively becomes smaller • Transition Zone is between V3-V4 or at V3 • Infarction can affect the R wave progression • Not strong enough evidence to support the diagnosis of infarction alone

34. EKG CHANGES DUE TO INFARCTION • Infarct recognition in the EKG relies on the detection of morphologic changes of the QRS complex, the T wave and the ST segment • Occurs in a predictable pattern which is recognizable on the EKG

35. EKG CHANGES • The first change may be the development of tall T waves - this may occur within the first few minutes of infarction - known as the Hyperacute phase • Tall T waves alone are not strong enough evidence to support the diagnosis of MI

36. EKG CHANGES • Signs of myocardial injury may develop with evidence of ST segment elevation • primary indicator of injury in progress • may occur within first hour or first few hours of infarction • Known as the ACUTE phase • may also see T wave inversion • can occur simultaneously with ST segment elevation

37. Acute MI Evolution A B C D E F

38. Pathologic ‘Q’ Wave • Evidence that tissue death has occurred is seen with the development of a Pathologic ‘Q’ • greater than 40 ms (wider than 1 small box) • After healing process, ‘Q’ wave may remain as evidence that infarction has occurred • ST depression in non-Q-wave MI = subendocardial MI which effects the inner most myocardial layer • ST elevation in Q-wave MI = transmural MI with damage extending through all myocardial layers

39. INDICATIVE CHANGES LEADS II, III, aVf V1 – V4 V5, V6, I and aVl LOCATION Inferior Wall Antero/Septal Wall Lateral Wall

40. Ischemia: T-wave inversion I, aVL, V5, V6, II and V4

41. Infarction: ST elevation V1-V4

42. Practice Strip #1

43. Practice Strip #2

44. Practice Strip #3

45. Practice Strip #4

46. Practice Strip #5

47. Last One

48. Posterior Wall MI (PWMI) • Usually an extension of an inferior or lateral MI • Common with proximal RCA occlusions • Occurs with LCX occlusions

49. Pathology Findings

50. BUNDLE BRANCH BLOCK - Significance • New onset in setting of MI carries increased mortality rate of 40-60% • Cardiogenic Shock increases to 70% • indicates extensive infarct affecting the bundles • LAD coronary artery occlusion • More common in patients suffering from septal and anteroseptal infarcts • LBBB can mimic infarct pattern