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Approach to the ECG Shannon McCarter PGY2 FM Civic 99 Topics General Approach to ECG 1. 2. 3. 4. 5. 6. Rate Rhythm Axis Rotation Waves, Segments, Intervals Hypertrophy 1. RATE Regular rhythms: Paper speed: 25mm/sec – 300/# large square between R-R – 1500/# small squares between R-R – Countdown sequence 300-150-100-75-60 -50 Irregular rhythms: – # of complexes on ECG (10seconds) x 6 2. Rhythm Step 1: Is the QRS regular or irregular – ?regularly irregular or irregularly irregular Step 2: Assess the QRS ?wide or narrow complex Step 3: P waves present? Step 4: Relationship of P wave with QRS 3. Axis Look at Lead I and AVF (other methods involve Lead II) Lead I AVF Axis + + Normal (-30 to 90) + - Possible LAD - + RAD - - Extreme axis deviation 3. Axis Another method: – Examine isoelectric limb lead – Most of electrical current moving perpendicular to isoelectric lead Lead Grouping II, III, AVF – inferior leads V1, V2 – antero-septal leads V3, V4 – anterior leads V5,V6, I, aVL – lateral leads 4. Rotation Looking at the heart in the transverse axis General rule: – Heart rotates to hypertrophy and away from infarct Clockwise rotation: isoelectric QRS in V5, V6 Counter-clockwise: isoelectric in V1, V2 5.Waves, Intervals, and Segments PR interval: – 0.12-0.20 seconds QRS complex: – 0.06-0.11 seconds QT interval – N < 440msec men,<460 women – Varies with HR. In General should be <1/2R-R – Ventricular depolarization + repolarization Waves: assess morphology, voltage (P, Q, R, S, T) Segments assess for elevation or depression (PR, ST) 6. Hypertrophy Left Ventricular Hypertrophy S wave of V1/ V2 + R wave of V5/V6 > 35mm R wave in aVL >11 mm May also see LAE and LAD Right Ventricular Hypertrophy RAD +/- RAE R wave in V1 > 7mm or R/S ratio >1 Jeopardy Life In The Fast Lane Took Me Right Off My Feet Achy, Breaky Heart Ah, Ah, Ah, Ah…Staying alive Medication Master $100 $100 $100 $100 $100 $200 $200 $200 $200 $200 $300 $300 $300 $300 $300 $400 $400 $400 $FREE $FREE Final Jeopardy 1 - $100 This rhythm is the most common sustained arrhythmia. What is atrial fibrillation? Atrial fibrillation Most common sustained arrhythmia Complications: cardiomyopathy, embolic events, CHF Etiology: HTN, IHD, Valvular heart disease, infection, electrolytes (hypoK, hypoMg), pulmonary (PE), pericardial disease, drugs, endocrine (thyrotoxicosis, pheo), acid-base disturbance, cardiomyopathies, preexcitation syndromes ECG: irregularly irregular rhythm, no P waves, QRS normally < 120msec Atrial Fibrillation Classification: first episode, recurrent (>2), paroxysmal (< 7 days), persistent (>7 days), permanent (> 1 year) Management: – Anti-coagulant: CHADS2 – Rate control – Rhythm Control – Cardioversion – **Treat underlying** See Canadian Cardiovascular Guidelines for Management of Atrial Fibrillation (2014) 1 - $200 This supraventricular tachycardia has a characteristic saw-tooth pattern. What is atrial flutter? Atrial Flutter Rate approximately 300bpm Etiology: re-entrant circuit Look for conduction 2:1, 3:1, 4:1 Saw tooth waves best seen in inferior leads Mngt: – Ablation – Similar management to atrial fibrillation 1 - $300 Unless ACLS and shock is rapidly instituted, this rhythm is invariably fatal What is Ventricular fibrillation? 1 - $400 This mnemonic is instrumental in ACLS and helpful for remembering the causes of cardiac arrest. What is 5 H’s and 5 T’s? 5 H’s and 5 T’s – 5 H’s: Hypoxia Hypovolemia HyperK+ Hydrogen ion Hypothermia – 5 T’s: Tension pneumothorax Tamponade Toxins Thrombosis – heart Thrombosis - lung 2 - $100 This heart block often is benign and does not require treatment. What is: AV block: 2nd degree, Mobitz Type I – Aka Wenckebach Heart Blocks 1st degree: PR > 200ms – Usually benign. No treatment required. 2nd degree – Mobitz I (Wenckebach): progressive PR prolongation until QRS dropped Rarely progresses to Type II, CHB Rx: asymptomatic do not require rx. Usually responds to atropine – Mobitz II: PR interval stable with occasional dropped QRS High risk of syncope or CHB Requires temp pacing/ permanent pacemaker Etiology: high vagal tone, age related, infectious, infarct, drugs, electrolyte abN, post-cardiac surgery Heart Blocks 3rd degree – Complete Heart Block – Complete AV dissociation – P waves not conducted – Etiology: inferior MI, progression of Mobitz Type I/ II, AV nodal blockers – Require temporary pacing and permanent pacemaker 2 - $200 What drugs should you avoid with a patient with this condition? What are AV blockers? Pre-excitation syndrome: WPW • Congenital accessory pathway (Bundle of Kent) • Can cause AVRT (atrioventricular reentry tachycardia) • ECG findings: PR < 120msec, delta wave, prolongation QRS, ST segment and T wave discordant changes (opposite direction of QRS complex) • Treatment with AV nodal blockers VT or VF • Unstable: cardioversion • Stable: procainamide 2 - $300 This syndrome is caused by a sodium channelopathy. What is Brugada? Brugada Brugada Syndrome • Epidemiology: often Asian males, middle age • ECG changes can be transient and unmasked by fever, drugs, ischemia, hypothermia, hypoK • Diagnosis requires: ECG changes + 1 clinical criteria • ECG: Type I: Brugada sign: coved ST segments >2mm in >1 of V1-V3 followed by negative T wave • Type II: nondx - > 2mm of saddleback ST elevation in V1-V3 • Clinical criteria: family history of SD < 45, Vfib/ polymorphic VT, Coved ECG changes in family, syncope, inducible VT with electrical stimulation, nocturnal agonal respirations • Management: ICD • No treatment SD age 40s 2 - $400 What is the name of this condition? Bonus marks: what is the clinical significance What is Wellen’s Syndrome? It indicates critical stenosis of the LAD. Wellen’s Syndrome Deep, symmetric or biphasic T wave inversion in anterior precordial leads (V2, V3) Indicates significant proximal LAD stenosis Patients may be pain free initially but at high risk of extensive anterior wall infarct in the upcoming days/weeks No ST segment changes. No Q waves. Pathophysiology: sudden occlusion of LAD transient anterior STEMI reperfusion biphasic T waves deep inverted T waves 3 - $100 This condition produces a characteristic chest pain that is pleuritic in nature, worse with lying flat, relieved with sitting forward and often is associated with a viral infection. What is pericarditis? Pericarditis ECG changes: – – – – – Diffuse concave ST segment elevation Diffuse PR depression Sinus tachycardia Reciprocal changes in AVR Progresses N ST segments + flat T waves T waves inverted (3+ weeks) ECG normal Etiology: infectious (viral –coxsackie), immunological (SLE), uremia, post-MI, trauma, post-cardiac surgery, drug related, post radiotherapy, paraneoplastic syndromes Management: treat underlying – NSAID + colchicine – Glucocorticoids if refractory, autoimmune, connective tissue d/o, uremia not responding to dialysis, contraindications to NSAIDs – If associated effusion +/- drainage 3 - $200 This ECG belong to an individual with retro sternal chest pressure, SOB and a history of smoking. What is anterior STEMI? 3 - $300 These drugs should be used with caution in patients presenting with inferior STEMI. What is drugs that affect preload e.g. nitrates, morphine? Inferior STEMI More favorable prognosis than anterior STEMIs 40% have right ventricular infarction GET right sided leads – Concern about posterior STEMI in ALL inferior and lateral STEMIs OBTAIN 15 lead ECG 20% associated with bradyarrhythymias Most common etiology RCA (80%), left circumflex (20%) ECG: ST elevation in II, III and AVF, reciprocal changes in aVL DO NOT MISS! ST elevation in aVR with diffuse ST depression indicates left main disease, triple vessel disease or proximal LAD occlusion STEMI Management ABCs, cardiac monitoring Oxygen if O2 sats < 90% Reperfusion – PCI: <90 minutes – Fibrinolytics Anti-platelet: – ASA – Clopidogrel (if fibrinolytic candidate) – Ticagrelor (if PCI) Anti-coagulant: Heparin Nitrates: 3 SL then IV. Caution if preload dependent Morphine: caution as can increase mortality B-blockers: caution in heart failure, low CO, high risk of cardiogenic shock, bradycardia, reactive airway disease Statins: as early as possible 3 - $400 These criteria are useful in differentiating a LBBB from an acute myocardial infarction. What are the sgarbossa criteria? 4 - $100 This is the textbook ECG finding for pulmonary embolism even though the most common finding is sinus tachycardia. What is S1, Q3, T3 pattern? Pulmonary embolism Findings on ECG not sensitive, non-specific DDX: any cause of acute/chronic cor pulmonale: – Acute: pneumonia, COPDAE, pneumothorax, recent pneumonectomy – Chronic: COPD, CF, ILD, OSA, recurrent small PEs ECG findings: – #1 sinus tachycardia – RBBB – Right ventricular strain pattern, RAD – Right atrial enlargement – S1Q3T3 – T wave inversions in inferior leads 4 - $200 The phenomenon of electrical alternans produced by the heart swinging (QRS height varies from beat to beat) and low voltage on an ECG can be indicative of this condition that may require a tap? What is severe pericardial effusion and cardiac tamponade? 4 - $300 A patient presents with the following rhythm strip to the ED after being prescribed levofloxacin. Translated this conditions means twisting of the spikes. What is Torsades de pointes? (Secondary to Prolonged QT) Prolonged QT Symptoms: – Most episodes revert spontaneously to sinus rhythm – Palpitations, dizziness, syncope, sudden cardiac death Pathophysiology: prolonged repolarization gives rise to early after depolarizations PVCs If PVC occurs in preceding T wave = R on T phenomenon Torsade's de Pointes VF Etiology: – – – – Drugs: anti-psychotics, tramadol, abx, type I anti-arrhythmic Metabolic (low Mg, Low K, low Ca) Congenital prolonged QT syndromes Increased ICP Management: – – – – Treat underlying + stop offending agent Replace electrolytes MgS04 +/- antiarrhythmic drugs Overdrive pacing, defibrillation 5 - $100 This ECG demonstrates a common pattern that is useful for DDX VT versus SVT with aberrancy. What is fusion beat? VT versus SVT with aberrancy – Features that suggest VT Absence of RBBB/LBBB Extreme axis deviation Broad complexes >160ms Capture beats Fusion beats RSR’ complex with taller left rabbit ear AV dissociation – Clinical history that increases likelihood of VT Age >35 Structural heart disease IHD Previous MI CHF Family history of sudden death 5 - $200 This medication can be used as an antidote to treat most beta-blocker overdoses. What is glucagon *? Beta-Blocker Overdose **Propranolol causes sodium channel blockage QRS widens Give NaHCO3 **Sotalol causes K efflux blockage Long QT TdP S/S: heart failure, bronchospasm, hyperK, hypoglycemia, coma, seizure ECG findings: bradycardia, heart block, Management: – Fluid, B-agonists, Vasopressors – Atropine, Pacing – Antidotes: Glucagon High dose insulin Intralipid if refractory 5 - $300 This ECG strip has a characteristic T wave pattern of an acute metabolic disturbance. Bonus: What are the treatment options? What is treatment of hyperkalemia? Hyperkalemia Pathophysiology: high K+ > 5.5 levels decrease myocardial excitability Etiology: – renal failure, dialysis, – Drugs: ACEI, K sparing diuretics, K+ supplements, NSAIDS, digoxin toxicity, succinylcholine – Release from cells (Rhabdo, burns, hemolysis, shifts – acidosis/low insulin/bblockers ECG findings: peaked T waves (symmetrical), – P wave widens, PR segment lengthens P waves eventually disappear – QRS prolonged, sinus bradycardia, conduction blocks – Sine wave (LATE) Treatment: – Calcium gluconate – Temporary Measures Insulin, Salbutamol – Elimination Hemodialysis, Kayexalate, Loop diuretics Final Jeopardy This traditional Newfoundland musical instrument (featured in the picture) is fashioned out of household and toolshed items. What is the ugly stick?