3 12 Lead EKG Interpretation and EKG Manifestation of CAD STUDENTS.pptx

12 Lead EKG Interpretation and EKG Manifestations of CAD R. C. Ward, PhD, CRNA, FAANA Spring 2024 1 Objectives Compare and contrast ischemia, injury and infarction Discuss how ischemia, injury, and infarction are observed on 12-lead EKG. Describe coronary artery blood supply in terms of the region o...

12 Lead EKG Interpretation and EKG Manifestations of CAD R. C. Ward, PhD, CRNA, FAANA Spring 2024 1 Objectives Compare and contrast ischemia, injury and infarction Discuss how ischemia, injury, and infarction are observed on 12-lead EKG. Describe coronary artery blood supply in terms of the region of the heart that each vessel supplies. Be able to identify, on 12-lead EKG, which coronary blood vessel is affected, along with the region of the heart. Describe lead placement for 12-lead EKG to include limb leads and precordial leads. Describe the view of the heart that is ‘seen from precordial and limb leads. Describe the type of infarction when ST changes are seen in various leads of the 12-lead EKG. Given a clinical scenario, describe the cardiac condition associated with the 12-lead EKG. 2 3 4 Blood Supply LAD: anterior wall of LV, anterior septum, bundle branches Left circumflex: left atrium, lateral wall LV, posterior wall LV RCA: right atrium, right ventricle, bottom of LV, posterior septum 5 Limb Leads: Bipolar Leads I, II, and III Two electrodes (+ and -) equi-distant from heart Records electricity flow from negative to positive electrode A wave of depolarization moving toward a positive electrode produces a positive deflection on the ECG Depolarization moving away from a positive electrode records a negative deflection Lead axis is the direction of electrical depolarization 6 Einthoven’s Triangle Formed by 3 bipolar limb leads Heart at center Willem Einthoven developed electrocardiogram in early 1900s. 7 Axial reference system Three limbs of Einthoven’s triangle are broken apart, collapsed, and superimposed over the heart Lead I is at 0 degrees Lead II is at + 60 degrees Lead III is at +120 degrees 8 Limb Leads: Unipolar Leads aVR, aVL, aVF Letter a refers to augmented Letter V refers to voltage Letters R, L, and F refer to where positive electrode is placed (right arm, left arm and left leg) Records electricity flow from center of heart toward positive electrodes 9 10 Limb Lead Placement 11 Precordial Leads V1 and V2 are on either side of sternum at 4th ICS V4 is midclavicular line, 5th ICS V3 is halfway between V2 and V4 V6 is at midaxillary line, 5th ICS V5 is halfway between V4 and V6, 5th ICS 12 13 Precordial Lead Electrode Placement Correct anatomical placement imperative! Sternal angle (angle of Louis) used as reference point Run finger down the sternum, from the sternal notch at the top until a boney horizontal ridge, the sternal angle is met With your finger on this ridge, slide down and to the right side to locate the second intercostal space Count down to the third and fourth space Locate the edge of the sternum and place V1 In women, V4, V5, and V6 are place under the left breast 14 View from Precordial Leads V1 Right ventricle V2/V3 Septum V4 Apex V5/V6 LV; left lateral wall 15 Myocardial Infarction (MI) Necrotic development within the myocardium as a result of severe deprivation of blood supply. 16 Evolution of an Acute Myocardial Infarction Ischemia: deficient blood supply to an area of tissue, resulting in hypoxia; usually 70% of vessel is occluded; O2 demand exceeds supply (reversible). Injury: a degree of tissue hypoxia severe enough to cause damage to cells. Cells may survive if blood flow is reestablished (reversible). Infarction: a degree of tissue hypoxia severe enough to cause death of cells (not reversible). 17 EKG Changes with MI: The Classic Triad ST segment elevation – occurs immediately after occlusion. T wave inversion / ST depression – occurs 6-24 hours after the infarction. Pathological Q waves – indicator of myocardial tissue death. 18 ST Elevation Denotes myocardial injury Seen in early hours of injury Merges with T wave ST elevation more than 1mm above baseline should be investigated Reversible if treated early 19 T Wave Inversion and/or ST Depression Denotes myocardial ischemia Ischemia also denoted by ST depression of 1-2 mm for duration of 0.08 seconds in leads facing the ischemic area. T waves invert as the ST segment begins to return to baseline Reversible 20 Pathologic Q Waves Denote myocardial infarction Irreversible Common to have small Q waves in Leads I, II aVL, V4, V5 & V6 Pathologic Q waves are unusually large At least 0.04 seconds in duration Deeper than 1/3 the height of the R wave 21 22 Sites of Infarction Relative to Coronary Distribution and Indicative/Reciprocal Leads , V5, V6{some or all} * * Usually occur in context of an inferior MI or II, III, aVF 23 Depolarization Vectors in Infarcted Tissue Infarcted (necrotic) tissue in the heart is not excitable and becomes electrically inert. Necrotic tissue can be thought of as a physiologic ‘hole’ in the heart No longer excitable tissue; acts as passive conductor of the potentials generated from the viable opposite wall of the heart. Depolarization vector shifts and points away from area of necrosis. Q waves develop. 24 25 26 27 Inferior Wall MI Supplied by RCA Leads II, III, and aVF Reciprocal changes in lateral leads Damage may extend into RV Possible left axis deviation Biventricular dysfunction SA node dysfunction Bradyarrhythmias Heart blocks 28 Clinical Case: Anterior Wall MI Supplied by LAD Changes in precordial leads V1-V4 ST elevation Q waves Reciprocal changes in inferior leads Possible damage to septum and bundle branches Arrhythmias 69 yo white male w/ generalized weakness x 1 day, progressing to pain that awakened him from sleep, prompting a call to EMS. History of HTN. Medication included Metoprolol. No PSHx. Smoking history unknown. Cath lab upon arrival to hospital revealed 100% LAD occlusion. Stent placed Ventricular (PVCs) Bundle branch blocks 2nd or 3rd degree AVBs – prognosis poorer 30 Significant ST elevation in V1V4, with some also in V5-V6 anterolateral MI * What is the QRS axis? Reciprocal leads = II, III, aVF 31 33 Lateral Wall MI Supplied by left circumflex artery Leads I, aVL, V5 and V6 Reciprocal changes in inferior leads Possible right axis deviation Potential for reduction in LV function, but not as great as with anteroseptal wall MI Arrhythmias from SA node dysfunction Sinus arrest Bradyarrhythmias 34 35 Posterior Wall MI Often accompanies inferior MI ST elevation in II, III, aVF Isolated posterior MI less common Posterior myocardium not directly visualized by standard 12-lead EKG Reciprocal changes in anteroseptal leads V1, V2 Tall R waves in V1 and V2 ST segment depression Arrythmias Junctional rhythm Heart blocks 36 37 38 Summary of vessels and locations 39 Evolution of Infarction Stage I: Injury -A degree of hypoxia severe enough to cause damage to cells. Cells may survive if blood flow is reestablished. -Manifests within minutes or hours after the onset of ischemia. -Persists until recovery or manifestations of cell death occur, usually within 2448hr. Stage II: Infarction -Part of the myocardium dies and becomes electrically inert. Necrotic tissue acts as a passive conductor of the potentials generated from the viable opposite wall of the heart. The depolarization vector will shift and point away from the necrotic area. Stage III: Resolution -Occurs over weeks or months as the damaged tissue is replaced by scar. Sequence of Changes in Myocardial Infarction Taken from URL: Sequence of Changes in Myocardial Infarction 41 Resources: Dubin, D. (2000). Rapid Interpretation of EKG’s-6th edition. Fort Myers: COVER Publishing. Dubin Chapter 7 & 9. URL: Sequence of Changes in Myocardial Infarction - Platelet Aggregation - Acute Coronary Syndrome - Cardiology Te aching Package - Practice Learning - Division of Nursing - The University of Nottingham 42