EKG

Basics

Set-up

• Name, date, time, paperspeed (25mm/s), scale (10mm/mV)

  • Small square = 0.04 seconds (40ms)

  • Large square (5mm) = 0.2 seconds (200ms)

• Look for Lead placement errors

  • Lead V1 and V2 at 4th ICS, V4 at 5th ICS mid-clav, V6 mid axillary line

    • Look for RS pattern in V1 changing progressively to QR pattern in V6

  • aVF (left leg = Red), aVL (left arm = black), avR (right arm = white)

    • Check aVR for flipped P, QRS, T waves

    • aVL and aVR should generally be mirror images

• Clinical context (age, time, patient symptoms)

• Compare with previous

Rate (60-100)

• R-R 

  • 1 large square = 300/minute (5 large squares per second) 

  • 2 = 150 | 3 = 100 | 4 = 75 | 5 = 60 | 6 = 50 |7 = 40

• Or calculate 10*QRS complexes in 15cm (= 6 seconds x 25mm/s)

Rhythm

• Sinus (P followed by QRS)

• Narrow QRS tachycardia (SVT): 

  • Sinus tachycardia

  • A fib

  • A flutter (often 300/min with 2:1, 3:1, 4:1 block)

  • AVNRT (regular 180-250/min)

• Wide complex tachychardia (QRS>120ms)

  • If VERY wide (QRS>200ms) think TOX or METABOLIC

    • Try Calcium (hyperK) and Bicarb (acidosis) first!

  • V tachycardia

  • SVT with aberrancy

  • V fib

• Bradycardia

  • 1st degree AV block (PR>200ms)

  • 2nd degree AV block type I (Wenkebach)

    • PR prolongation until block

  • 3rd degree AV block (complete block /AV dissociation)

  • Ventricular escape rhythm (wide complex <40/min)

Conduction intervals

• PR interval (ie. PQ) normally 120-200ms (3-4 small squares)

  • PR >200ms = AV node delay

  • PR <120ms =  pre-excitation (LGL) or AV nodal (junctional) rhythm

  • PR <120ms + delta-wave = WPW (risk of AVRT)

• QRS complex normally < 120ms (3 small squares)

• QT interval varies with heart rate 

  • Prolonged >450ms in electrolyte abnormalties (hypokalemia) or drugs

    • QTc > 500ms Risk of V fib

Axis

• Quadrant/Three Lead Method

  • Lead 1 Positive, Lead aVF Positive = Normal Axis

  • Lead 1 Positive, Lead aVF  Negative

    • Lead II equiphasic = Physiological LAD

    • Lead II Negative = Pathological LAD

      • LVH, LBBB, Inferior MI, WPW

  • Lead 1 Negative, Lead aVF Positive = RAD

    • eg. RVH. RV strain (PE), Lateral MI, WPW

  • Lead 1 Negative, Lead aVF Negative = Extreme Axis

    • eg. Ventricular rhythm, hyperkalemia, severe RVH

Morphology

• P wave (look at lead II)

  • Normally positive in I and II, bifasic in V1, similar shape in every beat

    • Otherwise, consider ectopic atrial rhythm

• QRS

  • Pathologic Q-wave (MI, cardiomyopathy, WPW, LBBBB, COPD, PE, lead placement)

    • Q width >1mm (1 small box) OR 1/3 QRS amplitude OR any in V1-V3

  • RBBB

    • rR' or rSR' in V1

    • Large S wave in V6

  • LBBB

    • QS or RS in V1

    • Large R wave in V6

  • LAFB

    • Q1S3

  • LPFB

    • S1Q3

  • RVH

    • R>S in V1

    • S wave in V6

  • LVH

    • S in V1 + [R in V5 or V6 ] ≥35mm (7 large boxes)

    • R in aVL≥11mm

• ST

  • Elevation

    • Ischemia, percarditis, LVH, benign

  • Depression

    • Reciprocal in ischemia, LVH strain, digoxin

  • Negative T wave (opposite QRS complex)

    • Consider subendocardial ischemia, LVH

• U wave (small wave after T wave best seen V2-V3)

  • Prominent U wave if >1-2mm or 25% height of T wave

    • Bradycardia

    • Severe hypokalemia

    • Other electrolyte abnormalities (hypercalcemia), thyrotoxicosis, drug

  • Inverted U wave

    • Specific sign of MI

Do NOT Miss!

Need for PCI

• STEMI (or equivalent need for urgent repurfusion)

  • ST segment elevations at J point in 2 contiguous leads

    • Men <40yo, ≥2.5 mm in V2 and V3 and 1 mm in all other leads

    • Men >40yo, ≥2 mm in leads V2 and V3 and 1 mm in all other leads

    • Women, ≥ 1.5 mm ST elevation in V2 and V3 and 1 mm in all other leads

  • Left bundle branch block and presentation consistent with ACS

    • Unstable patient (hypotensive, acute pulmonary edema, electrical instability, unwell)

    • Modified Sgarbossa criteria can help if LBBB or paced, at least one of the following

      • ≥ 1 lead with ≥1 mm of concordant ST elevation

      • ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression

      • ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ST/S ratio ≥ 25% of the depth of the preceding S-wave.

  • New Right Bundle Branch Block with Left Anterior Fascicular Block (RBBB+LAFB)

    • Look for ST elevations, but can be difficult to discern (must identify end of QRS)

  • Inferior Wall MI

    • Elevation (even < 1mm) in two contiguous leads (II, III, aVF) with any amount of ST segment depression in aVL 

      • If there are well developed QS-waves, it is likely to be old MI with persistent ST elevation.

      • LV aneurysm, LVH, WPW, and LBBB all have repolarization abnormalities that produce reciprocal ST depression in aVL. 

      • If these are not present, ST depression in aVL is highly sensitive and specific for acute inferior MI. 

  • RV MI

    • RV MI usually has ST elevation in V1 UNLESS there is concomitant ST depression in V2 (posterior MI which attenuates the STE in V1)

    • Consider V3R and V4R elevation ≥ 0.5 mm increases specificity 

  • Posterior MI

    • Precordial ST-depression ≥ 1 mm maximal in leads V1-V4. 

      • Tall R and  upright T

    • Consider V8 and V9 elevations ≥ 0.5 mm increases specificity, but not sensitive

  • High Lateral Wall MI

    • Any degree of ST elevation in aVL with ST depressions in lead III (with or without II and aVF)

  • de Winter ST/T-wave complex (hyperacute T-wave with depressed ST takeoff)

    • ST depression >1mm upsloping at the J-point in V1-V6 

    • Tall T-waves and Normal QRS duration (consider hyperkalemia if wide QRS)

  • Diffuse ST Depressions with aVR Elevation (left-main or LAD or multivessel disease)

    • May want to avoid dual-antiplatelet therapy if expecting multivessel disease and need for CABG

    • Note: PE, aortic dissection can cause aVR elevation

• Non-STEMI 

  • ST segment depressions or deep T wave inversions without Q waves or possibly no ECG changes

• High risk of STEMI

  • Wellens/LMCA syndrome (classically pain free,  low/normal trop)

    • Pattern A is biphasic T-wave (Up and then Down) 

    • Pattern B is deeply inverted T-waves

  • Transient STEMI

• Unstable Angina

  • No EKG changes

• FALSE positive ST elevation

  • LVH (most common STEMI mimic)

    • Diagnose LVH using one of many criteria

      • Sokolow-Lyon criteria: If the sum of the amplitude of the S in V1 + R in V5/6 >35 mm

      • Semeans’ Sign (presence of QRS complexes touching or overlapping in two contiguous precordial leads) 

    • Signs of occlusion MI in patients with LVH include: 

      • New Q waves, loss of R waves

      • Disproportionate and dynamic ST elevation, eg. ST/S > 15% (or ST depression from posterior MI),

      • Hyperacute T waves

  • Rightward axis in "STEMI", consider large PE or hyperkalemia

Early reciprocal changes, suspect ACS

• New tall upright T wave  or biphasic T wave in V1

  • T wave V1>V6 (except in LVH, LBBB)

• Lone T wave inversion in aVL (except in LVH, LBBB), predict inferior MI

Other

Brugada's Syndrome

• Common in men from Southeast Asia

• Prominent J-wave with downsloping ST elevation in leads V1-3 (Saddle-back vs Coved appearance)

Long QT Syndrome

• Risk of torsade de pointes and ventricular fibrillation if QTc >500ms

• QTc = QTm / √ [R-R]

• Treatment

  • Avoid QT-prolonging drugs, high-intensity sports

  • Cardiology referral

  • B-blocker as prophylaxis

Wolff-Parkinson-White (WPW) syndrome

• PR<120ms

• Delta wave (slurring of initial QRS)

• QRS>110ms

• May present in very fast atrial fibrillation with irregular QRS

Hyperkalemia

• Tall T waves, wide QRS, flat P waves

• Bradyarrhythmia (sinus bradycardia, slow AF, AV block)

• Sine wave (pre-terminal rhythm)

Sodium Channel Blockade (TCA, cocaine, local anesthetics, propanolol)

• QRS >100ms (or 2.5 small squares)

• Terminal or secondary R wave (R') in aVR >3mm

• R'/S ratio in aVR >0.7

Digoxin Toxicity

• Increased atrial automaticity (atrial tachycardia, ectopics, AF, flutter)

• Increased ventricular automaticity (VEB, bigeminy, polymorphic VT)

• AV blocks

Hypertrophic Cardiomyopathy (HCM)

• High amplitude QRS

  • Deep, narrow (dagger) Q waves in lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads

• Suspect clinically 

  • Exertional syncope/pre-syncope

  • Pulmonary congestion (orthopnea, PND)

  • Chest pain, palpitations

• Management

  • Send for doppler echo

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

• Epsilon wave, T wave inversions, Prolonged S-wave upstroke

• QRS widening V1-V3

• Paroxysmal V tach with LBBB morphology