Downloaded 1,689 times
Uploaded byLPS Institute of Cardiology Kanpur UP India
Ecg in acs
The document discusses electrocardiograms (ECGs) in the context of acute coronary syndrome. It begins by describing the normal conduction system and the 12 standard ECG leads. It then explains how ECGs are recorded and the positioning of limb and precordial leads. The document discusses ST segments, T waves, and how to evaluate for ST elevations. It defines acute coronary syndrome and describes the classifications of ST-elevation MI, non-ST-elevation MI, and unstable angina based on ECG and cardiac enzyme findings. Specific ECG patterns for lateral, inferior, septal, and posterior wall MIs are also shown.
More Related Content
More from LPS Institute of Cardiology Kanpur UP India
Ecg in acs
- 1. ECG in Acute Coronary Syndrome DrAwadhesh Kumar sharma Deptt of Cardiology
- 2. The Normal ConductionSystem
- 5. ECG Leads • Thestandard EKG has 12 leads: – 3 Standard Limb Leads – 3 Augmented Limb Leads – 6 Precordial Leads
- 6. ECG Limb Leads •Leads are electrodes which measure the difference in electrical potential between either: 1. Two different points on the body (bipolar leads) 2. One point on the body and a virtual reference point with zero electrical potential, located in the center of the heart (unipolar leads)
- 7. Recording of theECG • Limb leads are I, II, II. • Each of the leads are bipolar; i.e., it requires two sensors on the skin to make a lead. • If one connects a line between two sensors, one has a vector. • There will be a positive end at one electrode and negative at the other. • The positioning for leads I, II, and III were first given by Einthoven (Einthoven’s triangle).
- 8.
- 9.
- 10. Standard Chest LeadElectrode Placement The Right-Sided 12-Lead ECG The 15-Lead ECG
- 11. Contiguous Leads • • • • • Lateral wall:I, aVL, V5, V6 Inferior wall: II, III, avF Septum: V1 and V2 Anterior wall: V3 and V4 Posterior wall: V7-V9 (leads placed on the patient’s back 5th intercostal space creating a 15 lead EKG)
- 12.
- 14. Coronary Circulation • Coronaryarteries and veins • Myocardium extracts the largest amount of oxygen as blood moves into general circulation • Oxygen uptake by the myocardium can only improve by increasing blood flow through the coronary arteries • If the coronary arteries are blocked, they must be reopened if circulation is going to be restored to that area of tissue supplied
- 16. ST segment • Connectsthe QRS complex and T wave • Duration of 0.08-0.12 sec (80-120 msec)
- 17. S – TSegment I V1 Normal Elevated V3 Depressed 7
- 18. T waves • Representsrepolarization or recovery of ventricles • Interval from beginning of QRS to apex of T is referred to as the absolute refractory period
- 19. T wave morphology AVR I UprightT 8 Inverted T
- 20. Acute Coronary Syndrome Definition:a constellation of symptoms related to obstruction of coronary arteries with chest pain being the most common symptom in addition to nausea, vomiting, diaphoresis etc. Chest pain concerned for ACS is often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Chest pain is often categorized into typical and atypical angina.
- 21. Acute coronary syndrome •Based on ECG and cardiac enzymes, ACS is classified into: – STEMI: ST elevation, elevated cardiac enzymes – NSTEMI: ST depression, T-wave inversion, elevated cardiac enzymes – Unstable Angina: Non specific EKG changes, normal cardiac enzymes
- 22. Unstable Angina • Occursat rest and prolonged, usually lasting >20 minutes • New onset angina that limits activity • Increasing angina: Pain that occurs more frequently, lasts longer periods or is increasingly limiting the patients activity
- 23. ECG • First pointof entry into ACS algorithm • Abnormal or normal • Neither 100% sensitive or 100% specific for AMI • Single ECG for AMI – sensitivity of 60%, specificity 90% • Represents single point in time –needs to be read in context • Normal ECG does not exclude ACS – 1-6% proven to have AMI, 4% unstable angina
- 24. • GUIDELINES: • Initial12 lead ECG – goal door to ECG time 10min, read by experienced doctor (Class 1 B) • If ECG not diagnostic/high suspicion of ACS – serial ECGs initially 15 -30 min intervals (Class 1 B) • ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B) • Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs (Class 2a B)
- 25. Evaluating for STSegment Elevation • Locate the J-point • Identify/estimate where the isoelectric line is noted to be • Compare the level of the ST segment to the isoelectric line • Elevation (or depression) is significant if more than 1 mm (one small box) is seen in 2 or more leads facing the same anatomical area of the heart
- 26. The J Point •J point – where the QRS complex and ST segment meet • ST segment elevation - evaluated 0.04 seconds (one small box) after J point
- 27. • Coved shape usually indicates acute injury •Concave shape is usually benign especially if patient is asymptomatic
- 28. Significant ST Elevation •ST segment elevation measurement – starts 0.04 seconds after J point • ST elevation – > 1mm (1 small box) in 2 or more contiguous chest leads (V1-V6) – >1mm (1 small box) in 2 or more anatomically contiguous leads (ie: II, III, aVF; I, aVL, V5, V6) • Contiguous lead – limb leads that “look” at the same area of the heart or are numerically consecutive chest leads (ie: V1 – V6)
- 29. EKG STEMI: Qwaves , ST elevations, hyper acute T waves; followed by T wave inversions. Clinically significant ST segment elevations: > than 1 mm (0.1 mV) in at least two anatomical contiguous leads or 2 mm (0.2 mV) in two contiguous precordial leads (V2 and V3) Note: LBBB and pacemakers can interfere with diagnosis of MI on EKG
- 30. EKG • NSTEMI: – STdepressions (0.5 mm at least) or T wave inversions ( 1.0 mm at least) without Q waves in 2 contiguous leads with prominent R wave or R/S ratio >1. – Isolated T wave inversions: • can correlate with increased risk for MI • may represent Wellen’s syndrome: – critical LAD stenosis – >2mm inversions in anterior precordial leads • Unstable Angina: – May present with nonspecific or transient ST segment depressions or elevations
- 31. Evolution of AMI A- pre-infarct (normal) B - Tall T wave (first few minutes of infarct) C - Tall T wave and ST elevation (injury) D - Elevated ST (injury), inverted T wave (ischemia), Q wave (tissue death) E - Inverted T wave (ischemia), Q wave (tissue death) F - Q wave (permanent marking)
- 32.
- 33.
- 34.
- 35.
- 36.
- 37.
- 38. Lateral Wall MI:I, aVL, V5, V6 Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
- 39. Inferior Wall MIII, III, aVF Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
- 40. Septal MI: LeadsV1 and V2 Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
- 41. Anterior Wall MIV3, V4 Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
- 42. Posterior MI –Reciprocal Changes ST Depression V1, V2, V3 Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
- 43.
- 44. Evolution of acuteanterior myocardial infarction at 3 hours
- 45.
- 46.
Editor's Notes
- #21 Typical chest pain: met 3/3 criteria v.s. atypical chest pain, only met 2/3 criteria. 3 criteria are: 1. the presence of substernal chest pain or (2) discomfort that was provoked by exertion or emotional stress and (3) was relieved by rest and/or nitroglycerin.
- #22 There is a subset of Q-wave v.s. non Q-wave MI (can fall under either NSTEMI or STEMI). Patients with nonQwave MI seem to have a better prognosis.
- #30 Remember 50% of patients with history of LBBB do not present with chest pain in addition to difficult ECG interpretation patient with LBBB is difficult to diagnose and manage and should have low threshold for acute MI in these patients.