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Topic: Let’s learn common ECG interpretation to diagnose both cardiac arrythmia and ischaemia along with relevant management. Speakers: Dr Hiramoti (Medical Registrar) Dr Mgbeoma K. K. (Medical Registrar) Learning Objectives electrocardiogram (ECG) readings related to cardiac arrhythmias and ischaemia. To diagnose different types of cardiac arrhythmias and ischemia accurately using ECG readings. To learn about the latest management strategies for cardiac arrhythmias and ischaemia. To engage in clinical case discussions for enhancing practical understanding and decision-making skills in managing cardiac arrhythmias and ischemia. To gain knowledge on how to apply ECG effective patient management.clinical settings for • How to do Basic ECG interpretation? • Common practical challenges while interpret ECG. Presentatio • Acute Coronary Syndrome evaluation and management. n outline • Heart block and conduction abnormalities • Common Bradyarrythmia and tachyarrythmia evaluation and management. • Will have a short break (10 min) What is ECG? Electrocardiogram (ECG) is the test to check heart’s electrical activity. ECG is a non-invasive easily available test to diagnose and monitor heart conditions specifically arrhythmia and ischaemia. Misinterpretation can delay care or provide inappropriate treatment and can have lifethreatening consequences for the patients. • Waveforms are labelled as P , Q, R, S, T, and U Components of • But keep in mind Isoelectric line (flat, horizontal line when there is no ECG electrical activity) and J point (is the located on isoelectric line) segment,Normal ECG ECG reading steps 2. what is the 3. is the QRS rhythm 1. Is there any ventricular rate (HR) regular or electrical activity? (QRS)/HR?——Rate irregular?——-Rhythm 4. is the QRS 5. is atrial activity (?P 6. is atrial activity (?P complex duration wave) present?——P wave) related to normal or prolonged? wave ventricular activity ——QRS complex and if so how? Common practical problems which you might face in daily practice 1. Lead 2. Benign early Misdisplacemen repolarisation/ t. high take-off/J- point elevation. • Quick guide to spotting: Lead • Think about Detrocardia • Lead I is completely inverted (P wave, QRS Misdisplaceme complex and T wave). • Lead aVR often becomes positive. nt • There may be marked right axis deviationAfter Correcting Leads placement Benign early repolarisation (BER) • Also known as “high take-off” or “J-point elevation”, it may mimic pericarditis or acute MI. • Usually benign ECG pattern producing widespread ST segment elevation that is commonly seen in young people considered a normal variant and a marker of good health. • Uhave BER on their ECG, making it a common diagnosticn will challenge for clinicians. ECG features in BER • Generalised concave ST elevation in precordial (V2-6) and limb leads (I, II, III, aVF): smiley-shaped” ST elevation • Notching or slurring at the J point in the prominent in V4(II, III and aVF), sometimes more • that are concordant with the QRS complex • ST elevation : T wave height ratio in V6 < 0.25 • Occlusion MI. ST depression to suggestHow do you differentiat e BER and Pericarditis ECG picture Chest pain in urgent GP Real patient ECG: BER clinicManagement of BER There is a link between Global BER pattern and future risk of idiopathic ventricular fibrillation (VF). ICD for the patients who have developed cardiac arrest and VF. Avoid diagnosing BER in patients over the age of 50, especially those with risk factors for ischaemic heart disease. Do troponin, repeat ECG to see any involutional changes and ask expert opinion if patient symptomatic and troponin high. There are three Acute traditional types of ACS Coronary Syndrome •1. S-elevation MI (STEMI) (ACS) •2. Non-ST-elevation myocardial infarction (NSTEMI) •3. unstable angina EVALUATION of ACS History: characterisation of symptoms– Onset: exertional or not, any ongoing symptoms (eg, recurrence), change in symptoms (eg, improvement with nitrates). PMHx: Details Cardiovascular disease history– any cardiovascular risk factors, and any recent acute coronary syndrome or revascularization procedure (eg, coronary artery bypass grafting, percutaneous coronary intervention). Other co-morbidities, performance status to assess suitability of PCI. Physical examination: The physical examination and vital signs are used to identify the presence of cardiogenic shock and other high-risk features. Risk score: the preferred risk models are the Global Registry of Acute Coronary Events (GRACE) risk score calculator for six-month risk of death. The Thrombolysis in Myocardial Infarction (TIMI) risk score (calculator 1) for two-week risk of death or MI The role of these scores in the approach to revascularization. Risk factors for ACS • Older age • High blood pressure or cholesterol • Smoking • Lack of physical activity • Unhealthy diet or obesity, or overweight • Diabetes • Family history Investigations • ECG and troponin • Blood test: FBC, CRP, coagulation, U&Es to assess the safety of angiography, anticoagulation, and antiplatelet therapies. • CXR • Echo to see any RWMAs if suspected NSTEMI • Persistent ST-segment elevation (> or equal 1mm/1 small square elevated from isoelectric line except V2-V3 (> or equal 2mm/2 small square elevated) in at least ECG 2 anatomically contiguous ECG leads. features • Reciprocal ST depressions and T - wave inversions. in STEMI • Pathological Q-waves. • New Left bundle branch block (LBBB) • ST depression in V1 to V3 indicates Post MICoronary artery anatomy and ECG leads Causes of ST elevation • Acute myocardial infarction • Coronary vasospasm (Printzmetal’s angina) • Pericarditis • Benign early repolarization • Left bundle branch block • Left ventricular hypertrophy • Ventricular aneurysm • Brugada syndrome • Ventricular paced rhythm • Raised intracranial pressure • Takotsubo CardiomyopathyInferior MIHigh Lateral MIPosterior MIReal patient Ant MI: with Chest pain with no significant PMHxEvaluation and management of suspected ACS Treatment of acute MI: 1. Loading dose aspirin 300mg and Ticagrelor 160mg 2. PCI (transfer patient to primary PCI centre within 2h) 3. Keep patient in cardiac monitor bed 4. Symptomatic treatment: analgesia morphine preferable ?why Morphine is also thought to decrease the amount of oxygen the heart needs by reducing sympathetic nervous system activation., anti-emetic Treatment of NSTEMI • Start Medical management ASAP- Loading dose aspirin 2.5mg S/C Ticagrelor 160mg along with Fondaparinux • myocardial dysfunction likely caused by infarction or who have signs or symptoms of persistent infarction or ischemia despite medical therapy require immediate angiography and appropriate revascularization. • Invasive angiography with appropriate PCI is typically performed within 48 hours of presentation. However, it is reasonable to perform angiography within 24 hours in high-risk patients, including those with multiple risk factors for MI (eg, diabetes, known coronary artery month mortality >140 points. GRACE score for six- Treatment of Unstable Angina • Start Medical management • If ongoing S/S of ishaemia or infarction, then IP Invasive angiography. • If no signs of NSTEMI (infarction/ischaemia) after appropriate monitoring about 12h, can be discharged with OP Investigation (stress echo and CT coronary angio) and cardiology hot clinic F/U. • If patients with indeterminate findings (eg, T-wave inversions) or significant risk factors for ischemia may undergo stress or anatomic imaging prior to discharge. Recent PCI/cardiac Bypass • Patients with recent NSTEACS, STEMI, PCI, or coronary artery bypass grafting who now present with symptoms of ACS, please use a low threshold to obtain invasive coronary angiography and thus, involve cardiologist early. • and relieved by GTN.sually exertional Tips and • Don’t forget atypical chest pain: SOB, epigastric burning sensation like pain. tricks about • Don’t forget to look for any ST elevation along with any reciprocal ST depression, diagnosing new LBBB, and ST depression in V1 to cardiac which requires urgent intervention.I • Always compare ECG with the previous ischaemia by ECG. • Only Troponin can help to differentiate S/S and ECG NSTEMI and Unstable angina as ECG interpretatio could be normal in both cases. • Troponin can be elevated for so many n reasons. • Ask for help if any confusion.Difficulties still can arise: No previous ECG to compare?how do I know this is new LBBB—do troponin urgently if high then treat as STEMI. Confusing ST elevation such as high take off (BER)/hyperacute T wave then speak to your senior or if you are a senior then speak to the cardiologist and simultaneously do troponin. No one will blame you if you give loading dose dual anti platelet medication in confusing ST elevation while awaiting for troponin or expert opinion. Heart block and conduction abnormalities • 1 degree block- Prolongation of PR interval >0.2ms • nd 2 degree block- - Mobitz type 1 (Wenckebach): progressive lengthening of PR interval with eventual dropped ventricular conduction - Mobitz type 2 (Hay): intermittent dropping of ventricular conduction - Fixed ratio blocks • 3 degree block (Complete heart block): complete dissociation between atria and ventricule Heart block and conduction abnormalitie s: ECG Findings 1 Degree Heart block There is delay, 1 degree block- without ‘Marked’ first PR interval >200ms interruption, in degree heart block (5 small squares) conduction from is present if PR atria to ventricles interval > 300ms- Marked first degree heart block - PR interval > 300 ms, P waves are buried in the preceding T wave - Sinus bradycardia with 1st degree AVblock - PR interval > 300 ms• Normal sinus rhythm with 1st degree AV block • PR interval 260 ms 2 degree AV • Progressive prolongation of the PR interval culminating in a non-conducted block- Mobitz P wave: type 1 • PR interval is longest immediately before dropped beat • PR interval is shortest immediately after dropped beat • Progressive prolongation of PR interval, with a subsequent non-conducted P wave 2 degree AV • Relatively constant P-P interval despite irregularity of QRS complexes block- Mobitz • The first clue to the presence of Mobitz I AV block on this ECG is the way the QRS complexes cluster type 1 into groups, separated by short pauses. 2 degree AV • QRS complexes clustered in groups, separated by non-conducted P waves. block- Mobitz • Note the difference in PR interval between the type 1 first and last QRS complex of each group. nd • A form of 2nd degree AV block in 2 degree AV which there is intermittent non- block- Mobitz conducted P waves without progressive prolongation of the PR type 2 interval nd 2 degree AV block- Mobitz type 2 Fixed ratio AV blocks Second degree heart Fixed ratio blocks can block with a fixed ratio be the result of either of P waves: QRS Mobitz I or Mobitz II complexes (e.g. 2:1, conduction. 3:1, 4:1). • 2:1 block: - The atrial rate is approximately 75 bpm. Fixed ratio AV - The ventricular rate is approximately 38 bpm. blocks - Non-conducted P waves are superimposed on the end of each T wave.2:1 block • 3:1 block: - The atrial rate (arrows) is approximately Fixed ratio 90 bpm. - The ventricular rate is approximately 30 AV blocks bpm. - Note how every third P wave is almost entirely concealed within the T wave. Fixed ratio AV blocks 4:1 block: High-grade AVblock (4:1 conduction ratio) Atrial rate is approximately 140 bpm. Ventricular rate is approximately 35 bpm. Method 1 (Quadrant method): Axis• Method 2: Three Lead analysis – (Lead I, Lead II and aVF)• Normal AxisRight axis deviationLeft Axis Deviation (Physiologic)Extreme axis deviation. Left Anterior Fascicular Block - Left axis deviation (usually -45 to -90 degrees) - qR complexes in leads I, aVL - rS complexes in leads II, III, aVF - L > 45msd R wave peak time in aV• rS complexes in leads II, III, aVF, with small R waves and deep S waves • qR complexes in leads I, aVL, with small Q waves and tall R waves • Left Axis Deviation (LAD): Leads II, III and aVF are NEGATIVE; Leads I and aVL are POSITIVE• qR complexes in lateral limb leads, and rS complexes in inferior leads + Left Axis DeviationProlonged R-wave peak time •Left axis deviation LAFB •qR complexes in I, aVL •rS complexes in II, III, aVF •Prolonged R wave peak time in aVL Rdeviation rS (RAD) (> complexes Left +90 in leads I degrees) and aVL Posterior Fascicula qR Prolonged r Block complexes R wave III and aVF, pein aVFe• rS complexes in leads I and aVL, with small R waves and deep S waves • qR complexes in leads II, III and aVF, with small Q waves and tall R waves • Right Axis Deviation (RAD): Leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE + prolonged R wave peak time in aVF Right bundle branch block QRS duration > 120ms RSR’ pattern in V1-3 Wide, slurred S wave in (“M-complex)QRS lateral le-6) (I, aVL, V5RBBB: Right Bundle Branch Block • V1: RSR’ pattern in V1, with (appropriate) changesant T wave • V6: Widened, slurred S wave in V6Typical RSR’ pattern (‘M’-shaped QRS) in V1 Wide slurred S wave in lead IIsolated RBBB. • RSR’ pattern in V1-3 •Lateral S wave changed are not evident here •Note normal axis in isolated RBBBIsolated RBBB. • Typical RSR’ pattern in V1-2 •Widened S waves again demonstrated in lateral leads, especially V4-6 •Appropriate discordance in leads V1-2 QRS duration ≥ 120ms Left Dominant S wave in V1 bundle Broad monophasic R wave in branch lateral leads (I, aVL, V5-6) Absence of Q waves in lateral block leads Prolonged R wave peak time > 60ms in leads V5-6LBBB: Left Bundle Branch • V1: Dominant S wave Block V6: broad, notched (‘M’-shaped) R wave • QRS Morphology in the Lateral Leads LBBB: Left • The R wave in the lateral leads may be either “M-shaped”, notched, monophasic, or an RS Bundle complex Branch BlockLBBB • 1) rS complex in V1 (tiny R wave, deep S wave) 2) Characteristic lateral lead morphology in V5-6Broad notched R waves are best appreciated in leads aVL and I here. There is absence of Qwaves in leads V5-6.LBBB with AF. Note deep S waves in leads V1-3 and tall broad R waves laterally.Incomplete LBBB is diagnosed when typical LBBB morphology is associated with a QRS duration <120ms. Bifascicular block • anterior fascicular block (LAFB), manifested as left axis deviation (LAD)- Common • RBBB and left posterior fascicular block (LPFB), manifested as right axis deviation (RAD) in the absence of other causesTypical bifascicular block pattern: RBBB combined with LAFB (manifested as LAD)RBBB with LAFB: • RBBB pattern in RSR’ complex in V1-2h • Prominent LAD indicating LAFBRBBB with LPFB: - RBBB with wide QRS, slurred S wave in lead I and slurred R in V1. - Right axis deviation (dominant negative deflection in leads I and aVl) with dominant positive deflection in aVf along with rS pattern in lead I and qR pattern leads III and aVf, suggesting left posterior fascicular block. Truetrifascicular block refersto thepresenceof conduction delay in allthreefasciclesbelow theAV node(RBBB, LAFB, LPFB), manifesting asbifascicular block and 3rd degreeAV block. Oneof two ECG patternsispresent: Trifascicula r block 3rd degreeAV block + RBBB + LAFB or; 3rd degreeAV block + RBBB + LPFB • True Trifascicular Block: • Right bundle branch block Trifascicular • Left axis deviation (Left anterior fascicular block) block • Third degree heart blockBifascicular block + first degree AVblock (Incomplete trifascicular block) Right bundle branch block Left axis deviation (= left anterior fascicular block) First degree AVblock Management. nothing unless 1st degree: sother causes of symptoms excluded nothing unless symptomatic and 2nd degree other causes of (Mobitz type I): symptoms excluded 2nd degree (Mobitz type II): Pacemaker Management: • 3rd degree: - Pacemaker • Branch blocks: - nothing unless progresses or symptomatic -> pacemaker - if sympatomatic -> pacemaker - trifascicular block -> pacemaker • May need temporary pacing wire or external pacing • Also if rates too slow and unresponsive to drugs -> pace. Emergency Mx of Bradycardia Atropine 500mcg IV repeat every 3-5 mins Isoprenaline Check blood pressure to maximum of 3mg 5mcg/min IV or Glycopyrrolate. Alternative drugs: Aminophylline, Temporary pacing – Adrenaline 2 Dopamine, Glucagon tranthoracic, -10mcg/min IV (if beta blocker or transoesophageal, CCB overdose) transvenous Commonest Narrow complex tachycardias Sinus Atrial fibrillation Atrial flutter tachycardia • Irregularly irregular rhythm Atrial • No P waves fibrillation • Absence of an isoelectric baseline • Variable ventricular rate • QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction • Fibrillatory waves may be present and or coarse (amplitude > 0.5mm)< 0.5mm) • Fibrillatory waves may mimic P waves leading to misdiagnosisAtrial fibrillation: - Irregular ventricular response - Coarse fibrillatory waves are visible in V1 - “Sagging”ST segment depression is visible in V6, II, III and aVF, suggestive of digoxin effect• AF with rapid ventricular response • Irregular narrow-complex tachycardia at ~135 bpm • Coarse fibrillatory waves in V1• AF with slow ventricular response • Irregular heart ratewith no evidenceof organised atrial activity • Finefibrillatory wavesin V1 • STdepression / Twave inversion in thelateralleads could represent ischaemia or digoxin effect • Theslow ventricular rate suggeststhat thepatient is being treated with an AV- nodalblocking drug (e.g. beta- blocker, digoxin). Another causeof slow AF is hypothermia Narrow complex tachycardia Regular atrial activity at ~300 bpm Loss of the isoelectric baseline Atrial “Saw-tooth” pattern of inverted flutter flutter waves in leads II, III, aVF Upright flutter waves in V1 that may resemble P waves Ventricular rate depends on AV conduction ratioAtrial flutter with 2:1 block • Inverted flutter waves in II, III + aVF at a rate of 300 bpm (one per big square) • Upright flutter waves in V1 simulating P waves • 2:1 AVblock resulting in a ventricular rate of 150 bpm • Note the occasional irregularity, with a 3:1 cycle seen in V1-3Atrial flutter with variable block • Inverted flutter waves in II, III + aVF with atrial rate ~ 300 bpm • Positive flutter waves in V1 resembling P waves • The degree of AVblock varies from 2:1 to 4:1Atrial flutter with 4:1 block • There are inverted flutter waves in II, III + aVF at a rate of 260 bpm • There are upright flutter waves in V1-2 (= anticlockwise circuit) • There is 4:1 block, resulting in a ventricular rate of 65 bpm • The relatively slow ventricular response suggests treatment with an AVnodal blocking agentAtrial flutter with high grade AVblock • There is anticlockwise flutter with marked AVblock (varying from 5:1 up to 8:1) • The very low ventricular rate suggests treatment with AVnodal blocking drugs (e.g. digoxin, beta-blockers) • Other possibilities could include intrinsic conducting system disease (true “AVblock ”) or electrolyte abnormality (e.g. hyperkalaemia) Ventricular Wide complex tachycardia tachycardi (VT) a Ventricular fibrillation (VF) Regular, broad complex tachycardia Monomorphic VT (commonest) Uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats)Monomorphic VT - Classic monomorphic VT with uniform QRS complexes - Indeterminate axis - Very broad QRS (~200 ms) - Notching near the nadir of the S wave in lead III = Josephson’s sign Ventricular fibrillation Chaotic irregular No identifiable P deflections of waves, QRS varying amplitude complexes, or T waves Amplitude Rate 150 to 500 per decreases with minute duration (coarse VF –> fine VF)Ventricular fibrillation (rhythm strip): Chaotic irregular deflections without identifiable P-QRS-T wavesConclusion Keep in mind the reason of doing ECG. Don’t miss the diagnosis of STEMI and life threatening Bradyarrythmia CHB/ tachyarrythmia Fast AF/SVT/VT. Look for any acute MI features: 3 things—any ST elevation in any lead, new LBBB, ST depression in V1 to V3. Any confusion please ask for help. Study materials  150 ECG problems by John R Hampton  Life in the fast lane: EKG Library LITFL ECG Library Basics