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ECG INTERPRETATION Sahana MaheshSmith, John QRS: 100ms Sinus rhythm QT/QTc: 398 ms Normal ECG 07/09/1957 PR: 156 ms Z82630 25 mm/s 10 mm/mV Remember ‘R R P W Q S T ‘ R ate W idth R hythm QT interval P wave S T segment 25 mm/smm/mV T wave1 SMALL SQUARE 1 BIG SQUARE 0.04 s 0.2 s 40 ms 200 ms 1 big square = 5 small squares 25 mm/s 10 mm/mV CALCULATING RATE ~4 big boxes Rate = 300 No. of big boxes How many big Between 2 R-waves boxes between 2 R- NUMBER OF RATE waves? BIG BOXES 1 300 bpm 2 150 bpm If irregular rhythm, count number of 3 100 bpm QRS complexes on rhythm strip and multiply by 6 4 75 bpm 5 60 bpm 25 mm/s 10 mm/mV THE CARDIAC AXIS & TERRITORIES SEPTAL ANTERIOR LATERAL SEPTAL INFERIOR LATERAL LATERAL INFERIOR INFERIOR ANTERIOR LATERAL FIRST DEGREE AV BLOCK PR INTERVAL > 200ms RRPWST CAUSES HR: 100 bpm Mitral valve surgery Rhythm: sinus rhythm Myocarditis e.g. Lyme disease P: present Hyperkalemia W: QRS complex normal Beta-blodigoxinCa2+ blockers, ST: isoelectric SECOND DEGREE AV BLOCK TYPE 1 WENCKEBACK AV BLOCK PROGRESSIVE PR PROLONGATION CULMINATING IN A NON -CONDUCTED P-WAVE RRPWST CAUSES HR: 75 bpm Beta-blockers, Ca2+ blockers, Rhythm: sinus rhythm with digoxin, amiodarone intermittent missed QRS AthletesInferior MI vagal tone) complexes Myocarditis P: present W: QRS complex normal Cardiac surgery ST: isoelectric2 : 1, 3 : 1 or 4 : 1 block may indicate a need for 2ND DEGREE AV temporary or permanent BLOCK pacing, especially if the ventricular rate is slow. MOBITZ I WENCKEBACH MOBTIZ II PROGRESSIVE LENGTHENING OF SINGLE OR INTERMITTENT PR INTERVAL UNTIL A BEAT IS NONCONDUCTED P WAVES DROPPED (P WAVE NOT WITHOUT QRS COMPLEXES FOLLOWED BY QRS COMPLEX) PR INTERVAL REMAINS CONSTANT PATIENTS OFTEN ASYMPTOMATIC CAN PROGRESS TO THIRD DEGREE BLOCK, PTS MUST BE ADMITTED! COMPLETE HEART BLOCK SEVERE BRADYCARDIA DUE TO ABSENCE OF AV CONDCTION AV DISSOCIATION WITH INDEPENDENT ATRIAL AND VENTRICULAR RATES RRPWST CAUSES HR: 50 bpm Inferior myocardial infarction Rhythm: Complete AV Beta-blockers, Ca2+ blockers, dissociation Idiopathic degeneration of the P: present conducting system ( Lenegre’s or W: QRS complex normal but not associated with p-waves Lev’s disease) ST: isoelectric High risk of ventricular standstill & sudden cardiac death! CAUSES RVH/cor pulmonale PE IHD Rheumatic heart disease Myocarditis Cardiomyopathy RIGHT BUNDLE BRANCH BLOCK (RBBB) QRS DURATION > 120 ms RSR’ PATTERN IN V1 -V3 (“M shaped” QRS complex) Wide, slurred S wave in lateral leads (1, aVL, V5-6) ANTERIOR NON-ST ELEVATION MYOCARDIAL INFARCTION RRPWST HR: 62bpm Rhythm: Sinus P: present W: normal QT: normal ST: isoelectric T waves inverted in V3, V4 and biphasic in V2 & V5 ATRIAL FIBRILLATION VNETRICULAR RATE ~ OR > 200 bpm IRREGULARLY IRREGULAR RHYTHM NO P WAVES RRPWST HR: 180 bpm CAUSES Rhythm: irregularly irregular IHD, HTN, valve disease P: absent Acute infections Hypokalemia, W: narrow complex hypomagnesemia (<120ms) Thyrotoxicosis ST: loss of isoelectric Alcohol baseline, “sagging” ST Pre-excitation syndromes segment depression visible Cardiomyopathies in V6, II, III and aVF, suggestive of digoxin effect TORSADES DE POINTES A TYPE OF POLYMORPHIC VENTRICULAR TACHYCARDIA QT PROLONGATION CAUSES OF QT PROLONGATION RRPWST HR: 90 bpm DRUGS: macrolides, Rhythm: irregular metoclopramide, haloperidol, P: present initially methadone, TCAs W: broad, polymorphic pattern Hypokalemia, hyperklaemia, ST: loss of isoelectric hypomagnesemia, hypocalcemia baseline Hypothermia QT prolongation Structural heart diseases HYPERKALAEMIA PEAKED T WAVES P WAVE WIDENDING PR PROLONGATION RRPWST BRADYARRHYTHMIAS CONDUCTION BLOCKS HR: 100 bpm QRS WIDENING WITH BIZARRE MORPHOLOGY Rhythm: Sinus P: present , widened and merged with QRS W: broad, bizarre merging with preceding P wave and subsequent T wave Peaked T waves PLEASE FILL OUT THE FEEDBACK FORM PLEASE TUNE IN TO OUR REMAINING SESSIONS THIS WEEK! @OSCEazyOfficial @osceazyofficial OSCEazy Osceazy@gmail.com