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OSCEAZY THE ECG STATION Sahana MaheshECGs for OSCEs Performing an ECG Rate & Rhythm ECG territories The cardiac axis Bundle & fascicular blocks Abnormalities of p waves, QRS complexes and T waves Common arrythmias, ischemia Role Foundation Year 1 Doctor (FY1) Setting Emergency Department Patient Mr Steve Rodgers, a 84 y/o male STUDENT presents with crushing central chest pain INSTRUCTIONS Student Take a focused history and initiate a task management plan including pertinent investigations.RECORDING AN ECG PERFORMING AN ECG INTRODUCTION LEADS 10 ELECTRODES, 6 ON CHEST + WIPE 4 ON LIMBS CHAPERONE FOR FEMALE PATIENT CONSENT CHECK EXPIRY DATE ON ELECTRODES EXPOSE chest, lower legs and wrists ENSURE GOOD SKIN CONTACT ADJUST BED TO 45 DEGREES WITH ELECTRODES CHECK FOR PAIN (CLEAN IF NECESSARY (clean area, offer shaving)PERFORMING AN ECG PERFORMING AN ECG RECORDING FINISH 1. TURN ON ECG MACHINE & ENSURE PAPER HAS BEEN 1. SWITCH OFF MACHINE LOADED 2. DETACH LEADS AND 2. DOUBLE CHECK REMOVE ELECTRODES ELECTRODES (CAREFULLY, MAY BE 3. ASK PATIENT TO REMAIN UNCOMFORTABLE) STILL 4. PRESS BUTTON TO RECORD 3. THANK PATIENT TRACE 4. LABEL ECG WITH PATIENT DETAILSECG INTERPRETATION QRS complex R Ventricular NORMAL ECG depolarization = T wave Repolarization of 1 P WA VE + 1 ventricular muscle QRS COMPLEX P wave T Depolarization of + 1 T-WA VE atrial muscle P Q S ST segment PR interval Interval between ventricular Conduction of electrical impulse depolarization and repolarization through AV node & bundle of HisSmith, John QRS: 100ms Sinus rhythm 07/09/1957 QT/QTc: 398 ms Normal ECG 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 RHYTHM Regular or irregular? Is the number of squares between each QRS complex the same or is it variable? 25 mm/s 10 mm/mV RHYTHM COMMON REGULAR RHYTHMS Atria & ventricles working normally One P wave for each QRS complex SINUS RHYTHM Electrical activation starts in eitherP waves may or may not be visible Narrow QRS complex SA node, Rate usually > 120 bpm SINUS TACHYCARDIA NARROW Atrial muscle or AV node Electrical activation starts in either SA node but slow transmission via Rate < 60 bpm SINUS BRADYCARDIA bundles Ventricles no longer synchronized, P waves visible but do not relate to QRS working independently. complexes. But both atria and ventricles are beatQRS usually wide but can be narrow regularly due to intrinsic activity Rate is slow but still regular COMPLETE HEART BLOCK RHYTHM COMMON IRREGULAR RHYTHMS Atria & ventricles working normally One P wave for each QRS complex SINUS ARRHYTHMIA Electrical activation starts in either P waves may or may not be visible Narrow QRS complex SA node, Rate usually > 120 bpm EXTRASYSTOLES/ECTOPIC BEATS Atrial muscle or AV node Bursts of electrical activity from P waves not visible automatic foci near pulmonary Rate > 200 bpm ATRIAL FIBRILLATION veins or diseased atrial tissue Ventricles no longer synchronized, P waves visible but do not relate to QRS working independently. complexes. But both atria and ventricles are beatinQRS usually wide but can be narrow regularly due to intrinsic activity Rate is slow but still regular VENTRICULAR FIBRILLATION P P wave Depolarization of atrial muscle • KEY to RHYTHM identification 1. Can you identify a P-wave P-PULMONALE: PEAKED P WAVES RIGHT ATRIAL HYPERTROPHY every QRS complex? (tricuspid stenosis or pulmonary hypertension)• No P waves? • More than 1 P wave before each QRS P-MITRALE: BROAD & BIFID P WAVES LEFT ATRIAL HYPERTROPHY (Mitral stenosis) 2. Unusually tall? 3. Unusually broad? R QRS Complex Ventricular depolarization BUNDLE BRANCH BLOCK Q S NORMAL QRS BUNDLE BRANCH BLOCK 1. No longer than 120 ms (3 ABNORMALLY VENTRICULAR ESCAPE BEATS, WIDE EXTRASYSTOLES small squares) TACHYCARDIA VENTRICULAR ECTOPIC 2. In a left ventricular lead (V5 or V6), the height of the R wave < 25 MM R QRS Complex Ventricular depolarization Q S Upright QRS in V1, Deep S in V6 NORMAL QRS 1. No longer than 120 ms (3 RIGHT VENTRICULAR HYPERTROPHY small squares) • Peaked P waves 2. In a left ventricular lead (V5 • Right axis deviation INCREASE IN PULMONARY (S waves in lead I) or V6), the height of the R VENTRICULAR EMBOLISM • Tall R waves in V1 MUSCLE MASS RVH • RBBB wave < 25 MM LEFT VENTRICULAR • Tall R wave in V5 or V6YPERTROPHY • Deep S wave in V1 or V2 • If significant, inverted T waves in leads I, VL, V5, V6LEFT VENTRICULAR HYPERTROPHY • Sinus rhythm, rate 83 bpm • Tall R waves in leads V5-V6 • Deep S waves in leads V1-V2 • Inverted T waves in leads I, VL, and V5-V6 QRS Complex Ventricular depolarization Q DEEP Q WA VES If the QRS complex starts with a deep downward deflection, may be a sign of an old myocardial infarction ST Segment T Interval between ventricular depolarization and repolarization S ü Normally isoelectric ELEVATION DEPRESSION LOCALISED? DIFFUSE? HORIZONTAL DOWNWARD DEPRESSION SLOPING • ST depression + Digoxin CONSIDER upright T wave, MYOCARDIAL CONSIDER INFARCTION PERICARDITIS may be a sign of ischaemia ANTERIOR DAMAGE SHOWS IN CHEST LEADS • May appear during 'reversed tick’ INFERIOR DAMAGE IN LEADS II, III, aVF exercise + AF, narrow QRS, inverted T T T wave Repolarization of ventricular muscle NORMALLY INVERTED IN aVR & V1 ABNORMAL INVERSION MYOCARDIAL VENTRICULAR INFARCTION HYPERTROPHY DIGOXIN T-wave LVH: T inversion in inversion I, II, aVL, V5-V6 usually later RVH: T inversion in V3 (white adults) onset Remember ‘ R R P W Q S T ‘ R ate W idth INTERVAL NORMAL RANGE (ms) P-R INTERVAL 120 – 200 ms R hythm QT interval QRS COMPLEX 120 ms P wave S T segment QT INTERVAL 360 – 440 ms 25 mm/s0 mm/mV T waveLET’S HAVE A BREATHER!THE CARDIA C AXIS & TERRITORIES THE CARDIA C AXIS & TERRITORIES aVR aVL Right atrium Left lateral surface I III II aVF Inferior surface THE CARDIA C AXIS & TERRITORIES- normal axis aVR aVL Right atrium Left lateral surface I III II aVF THE CARDIA C AXIS & TERRITORIES- normal axis aVR aVL Right atrium Left lateral surface I III II aVFRIGHT AXIS DEVIA TION aVR aVL Right atrium Left lateral surface I III II aVFRIGHT AXIS DEVIA TION aVR aVL Right atrium Left lateral surface I III II aVF RIGHT AXIS DEVIA TION aVR aVL COMMON CAUSES Left lateral surface Right atrium • Right ventricular • Right ventricular strain I e.g. PE, COPD, pulmonary III pulmonary stenosis II • RBBB • Normal variant e.g. neonates, congenital aVF LEFT AXIS DEVITION aVR aVL I III II aVF LEFT AXIS DEVITION aVR aVL I III II aVF LEFT AXIS DEVIA TION COMMON CAUSES aVR aVL • Left ventricular I hypertrophy • Left anterior III fasicular block II • WPW syndrome aVF THE CARDIC AXIS SUMMAR Y aVR aVL LEAD LEAD aVF I NORMAL 👍 👍 QRS LBBB 👍 III COMPLEX 👍 II RBBB 👍👍 aVF 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) CAUSES Aortic stenosis IHD, HTN Dilated cardiomyopathy Anterior MI Hyperkalemia Digoxin toxicity LEFT BUNDLE BRANCH BLOCK (LBBB) QRS DURATION > 120 ms DOMINANT S WAVE IN V1 BROAD MONOPHASIC R WAVE IN LATERAL LEADS (1, aVL, V5-6) ABSENCE OF Q WAVES IN LATERAL LEADS BUNDLE BRANCH BLOCK LBBB RBBB • Broad QRS • Broad QRS • Downward QRS deflection in • Upward QRS deflection in V1 V1 • MarroW • WilliAMPSUEDO RBBB with ST-elevation V1-V3 BRUGADA SYNDROME ECG CAN PRESENT WITH POLYMORPHIC VENTRICULAR TACHYCARDIA/VF1.Septum depolarized AV NODE BUNDLE OF HIS from LEFT TO RIGHT LEFT BUNDLE BRANCH RIGHT BUNDLE BRANCH 1.Excitation spreading towards a lead ANTERIOR causes an upward deflection within an FASCICLE ECG CARDIAC AXIS depends on the AVERAGE direction of depolarization of the ventricles POSTERIOR FASCICLE LV more muscle than right so has more influence on axis1.Septum depolarized AV NODE BUNDLE OF HIS from LEFT TO RIGHT LEFT BUNDLE BRANCH RIGHT BUNDLE BRANCH 1.Excitation spreading towards a lead ANTERIOR causes an upward deflection within an FASCICLE ECG CARDIAC AXIS depends on the AVERAGE direction of depolarization of the ventricles POSTERIOR FASCICLE LV more muscle than right so LEFT AXIS DEVIATION DUE TO LEFT has more influence on axis ANTERIOR FASCICULAR BLOCK LEFT AXIS DEVIATION DUE TO UNIFASCICULAR BLOCK Sinus rhythm, 80 bpm Left axis deviation • QRS upright in lead 1 But downward in aVF Normal QRS complexes, ST segments and T waves1.Septum depolarized AV NODE BUNDLE OF HIS from LEFT TO RIGHT LEFT BUNDLE BRANCH RIGHT BUNDLE BRANCH 1.Excitation spreading towards a lead ANTERIOR causes an upward deflection within an FASCICLE ECG CARDIAC AXIS depends on the AVERAGE direction of depolarization of the ventricles POSTERIOR FASCICLE LV more muscle than right so RIGHT AXIS DEVIATION DUE TO LEFT has more influence on axis POSTERIOR FASCICULAR BLOCK1.Septum depolarized AV NODE BUNDLE OF HIS from LEFT TO RIGHT LEFT BUNDLE BRANCH RIGHT BUNDLE BRANCH 1.Excitation spreading towards a lead ANTERIOR causes an upward deflection within an FASCICLE ECG CARDIAC AXIS depends on the AVERAGE direction of depolarization of the ventricles POSTERIOR FASCICLE LV more muscle than right so NO AXIS DEVIATION DUE TO RIGHT has more influence on axis BUNDLE BLOCK1.Septum depolarized AV NODE BUNDLE OF HIS from LEFT TO RIGHT LEFT BUNDLE BRANCH RIGHT BUNDLE BRANCH 1.Excitation spreading towards a lead ANTERIOR causes an upward deflection within an FASCICLE ECG CARDIAC AXIS depends on the AVERAGE direction of depolarization of the ventricles POSTERIOR FASCICLE LV more muscle than right so RBBB AND LEFT AXIS DEVIATION DUE has more influence on axis TO BIFASCICULAR BLOCK LEFT AXIS DEVIATION & RBBB DUE TO BIFASCICULAR BLOCK Sinus rhythm, 90 bpm Left axis deviation (downward QRS in II & III) RBBB (RSR pattern in V1 and deep, wide S wave in V6) THE CARDIA C AXIS & TERRITORIES SEPTAL ANTERIOR LATERAL SEPTAL INFERIOR LATERAL LATERAL INFERIOR INFERIOR ANTERIOR LATERAL THE CARDIA C AXIS & TERRITORIES LCx or LAD LAD diagonal branch LAD LCx or LCx or LAD diagonal branch LAD diagonal RCA and/or LCX branch LAD ECG RED FLAGS VENTRICULAR RATE > COMPLETE HEART BLOCK ABNORMAL T-WAVE 120 bpm OR < 45 bpm INVERSION Ischaemia, Infarction, ischaemia, Any heart disease hypotension, sepsis PE ST-SEGMENT ELEVATION ATRIAL FIBRILLATION OR DEPRESSION WIDE QRS WIDTH Valve disease, alcoholism, ischaemia, Infarction, ischaemia Any heart disease infection 25 mm/s 10 mm/mVLET’S HAVE A BREATHER! 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-blockers, Ca2+ blockers, ST: isoelectric digoxin 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 Athletes (increased vagal tone) complexes Inferior MI P: present Myocarditis W: QRS complex normal Cardiac surgery ST: isoelectric2 : 1, 3 : 1 or 4 : 1 block may ND indicate a need for 2 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 digoxin P: present Idiopathic degeneration of the W: QRS complex normal but conducting system (Lenegre’s or not associated with p-waves Lev’s disease) ST: isoelectric High risk of ventricular standstill & sudden cardiac death!TACHYARRHYTHMIAS SINUS TACHYCARDIA SINUS RHYTHM WITH RESTING HR > 100BPM (IN ADULTS) CAUSES Pulmonary embolism RRPWST Cardiac tamponade HR: 150 bpm Hyperthyroidism Rhythm: Sinus rhythm Alcohol withdrawal P: present, but hidden with Exercise, anxiety, hypovolemia each preceding T wave Sepsis, pyrexia W: Normal wdith Anemia Beta-agonists, ST: isoelectric sympathomimetics, antimuscarinics, caffeine ATRIAL FLUTTER NARROW COMPLEX TACHYCARDIA VNETRICULAR RATE (~150-175 bpm) SAW-TOOTH PATTERN OF P-WAVES RRPWST HR: 150 bpm Rhythm: Sinus rhythm P: present, ‘saw-toothed’ W: narrow complex (<120ms) ST: loss of isoelectric baseline ATRIAL FIBRILLATION NARROW COMPLEX TACHYCARDIA VNETRICULAR RATE ~ OR > 200 bpm IRREGULARLY IRREGULAR RHYTHM NO P WAVES RRPWST HR: 180 bpm CAUSES Rhythm: irregularly irregular P: absent IHD, HTN, valve disease W: narrow complex Acute infections Hypokalemia, 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 NARROW COMPLEX TACHYCARDIA (QRS < 120 bpm) DDX REGULAR/IDENTIFIABLE RHYTHM? NO YES NO ATRIAL FIBRILLATION VISIBLE P ATRIAL TACHYCARDIA/ FLUTTER WITH WAVES? VARIABLE AV CONDUCTION YES VENTRICULAR RATE? YES NO ANALYSE R-P ATRIAL FLUTTER INTERVAL ATRIAL TACHYCARDIA SHORT RP LONG RP RP < 70 ms RP > 70 ms AVRT AVNRT ATRIAL TACHYCARDIA AVNRT NARROW COMPLEX TACHYCARDIA REGULAR RHYTHMAVES RRPWST HR: 150 bpm Rhythm: sinus CAUSES P: absent W: narrow complex TYPICALLY PAROXYSMAL (<120ms) May occur spontaneously or ST: isoelectric provoked by caffeine, alcohol, beta-agonists or sympathomimetics WOLFF-PARKINSON-WHITE PATTERN SHORT PR INTERVAL ECG DELTA WAVE (SECONDARY TO PRE-EXCITATION) ORTHODROMIC PATTERN RRPWST CAUSES Congenital Bundle of Kent HR: 110 bpm pathway, causing ventricular Rhythm: Sinus pre-excitation P: present W: broad, delta wave Associated with AVRT, AF ST: isoelectric MONOMORPHIC VT UNIFORM QRS COMPLEXES WITHIN EACH LEAD (EAHC QRS IS IDENTICAL) RRPWST HR: 300 bpm CAUSES Rhythm: regular IHD P: absent Dilated cardiomyopathy W: broad, monomorphic Hypertrophic cardiomyopathy pattern Chaga’s disease ST: loss of isoelectric baseline 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 diseasesVENTRICULAR FIBRILLATION CHAOTIC IRREGULAR DEFLECTIONS OF VARYING AMPLITUDE NO IDENTIFIABLE P WAVES, QRS COMPLEXES OR T WAVES RATE 150-500 bpmLET’S HAVE A BREATHER! NEXT: ischaemia & electrolyte abnormalities… ANTERIOR NON-ST ELEVATION MYOCARDIAL INFARCTION RRPWST Rhythm: Sinus P: present W: normal QT: normal ST: isoelectric T waves inverted in V3, V4 and biphasic in V2 & V5 RRPWST HR: 110bpm ANTEROLATERAL MYOCARDIAC Rhythm: Sinus W: normalt INFARCTION & LEFT ANTERIOR Q waves in aVL, V2, v3 QT: normal HEMIBLOCK ST: elevated in I, aVL, V2-V5 Left axis deviation (dominant S waves in II & III) RRPWST HR: 70 bpm Rhythm: Sinus P: present W: normal Q waves in aVL, V2, v3 QT: normal ST: isoelectric Dominant R waves in leads V1 POSTERIOR MYOCARDIAL Can be easily mistaken for RVH INFARCTION ACUTE PERICARDITIS RRPWST HR: 75 bpm Rhythm: Sinus P: present , PR depression V2-V6 & I,II, aVL and aVF W: normal QT: normal ST: elevated in V2-V6 and I, II, aVL and aVF Reciprocral ST depression and PR elevation in aVR HYPERKALAEMIA PEAKED T WAVES P WAVW WIDENDING PR PROLONGATION RRPWST BRADYARRHYTHMIAS HR: 100 bpm CONDUCTION BLOCKS Rhythm: Sinus QRS WIDENING WITH BIZARRE MORPHOLOGY P: present , widened and merged with QRS W: broad, bizarre merging with preceding P wave and subsequent T wave Peaked T waves HYPOKALAEMIA HYPERKALAEMIA PEAKED T WAVES INCREASED P WAVE AMPLTIDUE P WAVW WIDENDING PROLONGED PR PR PROLONGATION WIDESPREAD ST DEPRESSION BRADYARRHYTHMIAS T WAVE FLATTENING/INVERSION CONDUCTION BLOCKS PROMINENT U WAVES QRS WIDENING WITH BIZARRE MORPHOLOGY THANKS FOR WATCHING Please fill in the feedback form!