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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
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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
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
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
Rounds • H&P’s/discharges • Physical exams • Evaluation/initiation of plan of care • diagnostics • pharmacotherapy • clinical interventions
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
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.
Occlusion of the Vessel • Ischemia • Injury • Infarct
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
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
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
Common Manifestations • Uncomfortable pressure • Fullness in chest • Radiation to shoulder, jaw, neck, arm • Diaphoretic • SOB • N&V
Other Manifestations • Palpitations • Fatigue • Reduced urine output • Systolic murmur • Decreased or abnormal heart sounds • Tingling of extremities • Syncope or confusion
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
Diagnosis • EKG • ST elevation • New LBBB • ST depression with T-wave inversion - ischemia • New Q waves
ECG Leads • ECG Leads • Bipolar • Leads I, II, and II • Unipolar • Leads aVR, aVL, and aVF • Precordial • V1, V2, V3, V4, V5, V6
ECG Leads • Precordial Leads • Lead V1 • Lead V2 • Lead V3 • Lead V4 • Lead V5 • Lead V6
LEADS • II, III, aVf • V1, V2 • V3, V4 • V5, V6, I, aVl • VIEW • Inferior • Septal • Anterior • Lateral
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
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
Infarct Recognition Process • Are Indicative Changes Present? • If so, in which Leads? • Presence and Location of AMI
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
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
ST SEGMENT • Normally is isoelectric and indicates ventricular repolarization • Can become depressed or elevated in the presence of injury, ischemia or infarction
Pathology associated with ST segment changes • Ischemia or Infarction • Digitalis • Tachycardia • Hypothermia • Hypokalemia • Ventricular Hypertrophy • LBBB • Vasospastic Angina • Pericarditis • Early Repolarization
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
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
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
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
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
Acute MI Evolution A B C D E F
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
INDICATIVE CHANGES LEADS II, III, aVf V1 – V4 V5, V6, I and aVl LOCATION Inferior Wall Antero/Septal Wall Lateral Wall
Ischemia: T-wave inversion I, aVL, V5, V6, II and V4
Infarction: ST elevation V1-V4
Posterior Wall MI (PWMI) • Usually an extension of an inferior or lateral MI • Common with proximal RCA occlusions • Occurs with LCX occlusions
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