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Bay Four

          Patterns, pearls and practical medicine

ECG essentials

The basics

  • Six key questions
      • Is there electrical activity?
      • What the ventricular rate?
      • Is the QRS regular, cyclically irregular or totally irregular?
      • Is QRS normal or prolonged?
      • Is atrial activity present?
      • Is atrial activity related to ventricular, and how?
  • Always check the paper speed
      • Standard is 25mm/s (in which case a big square = 0.2 secs, small = 0.04 secs)
      • Can be set at 12.5mm/s or 50mm/s (lengthens ECG and can help with analysing the fine detail) – this can lead to error in diagnosis and management if not recognised (for instance atropine being given for a patient with an apparent HR of 40 when the paper speed was set at 50mm/s)
  • Check the calibration
      • The vertical scale (if it differs between ECGs you can get apparent ST elevation when comparing two ECGs)
  • You can use a low pass filter (eg 40 Hz) to reduce muscle tremor noise (usually an option when viewing ECGs on screen)

Components

  • P waves
      • Upright in II and AVF. If inverted – non-sinus origin. Rhythm could be junctional (short PR) or ventricular in origin. If normal PR, atrial ectopic rhythm
      • Should be negative in aVR (providing originates from SAN)
      • In lead II:
        • P-pulmonale – bigger Ps due to RA enlargement
        • P-mitrale – bifed Ps, due to LA enlargement
      • Variable morphology in multifocal atrial rhythms
  • PR interval
      • Measure from start of P to start of QRS
      • Normal = 0.12 to 0.20 seconds (3-5 small squares on standard ECG)
      • Short PR in WPW, Lown-Ganong Levine syndrome, junctional rhythms, enhanced sympathetic tone, storage diseases eg Pompe’s, normal variant
      • Long PR is 1st degree AV block. May be due to drugs (betablockers, CCBs, digoxin, amiodarone), physical fitness, advanced age, IHD, infiltrative conditions, electrolyte/hormonal issues
      • Depressed in pericarditis
  • The QRS
      • Normal QRS < 0.12 (3 small squares)
      • Prolonged in VT, bundle branch block, WPW, paced rhythms, hyperkalaemia, hypermagnesemia, sodium channel blocking drugs or TCAs, cardiac ischaemia
  • The QTC
      • Printed QTC on ECG may be inaccurate, esp if U waves present
      • Short QT
        • <330 in men / < 340 in women if asymptomatic, <360 / 370 if symptomatic
        •  Causes
            • Hypercalcaemia
            • Digoxin tx
            • Rarely inherited (AD)
        • Long QT
            • Should be < 450 in men and < 470 in women. > 500 = higher risk of death.
            • Causes:
                • Low K+, low Mg2+, low Ca2+, low temp
                • Myocarditis
                • Ischaemia
                • Long QT syndrome (inherited AD or AR)
                • Drugs – lots!
            • Often treated by stopping drugs or giving a betablocker
        • Drug causes of long QT – Think the eight ‘antis’
            • Antibiotics – erythromycin, clarithromycin
            • Antifungals – fluconazole, ketoconazole
            • Antiarrhythmics – amiodarone, flecainide, sotalol
            • Antipsychotics – haloperidol, risperidone, quetiapine, clozapine, chlorpromazine
            • Antidepressants – citalopram, amitriptyline, dosulepin
            • Antiemetics – domperidone, ondansetron
            • Antimalarials
            • Antiretrovirals
  • T waves
      • Can be bifed in ETOH, LVH and ischaemia (can be confused for Mobitz 2:1 block)
      • Tall in hyperkalaemia, early MI (hyperacute Ts), LVH, LBBB, athletes, pericarditis, CVA, early repolarisation
      • Small in hypokalaemia, hypomagnesaemia, hypocalcaemia, ischaemia, hypothyroidism, drugs, normal variant
      • Inverted in ischaemia, ventricular hypertrophy, cardiomyopathies eg ARVC, bundle branch block, following an arrythmia, non-cardiac causes (PE, CVA or SAH, raised ICP, hypokalaemia, medications).
      • Can be normally inverted in aVR, III and V1
  • U waves
      • A small deflection after T wave. Can be normal.
      • Can be mistaken for P waves
      • Should be 1-2mm or < 25% T wave
      • Prominent in bradycardia, severe low K+, low Ca2+, low Mg2+, low temp, raised ICP, LVH, digoxin, anti-arrhythmic tx.
      • A negative U wave is highly specific for the presence of heart disease and if there’s chest pain, it’s specific for ACS

The Axis (normal, left axis deviation, right axis deviation)

  • Normal axis
      • QRS POSITIVE in I, very POSITIVE in II and about equal in III
  • LAD
      • QRS is POSITIVE (dominant R wave) in Lead I
      • QRS is NEGATIVE (dominant S wave) in leads II, III and aV
      • Causes
          • LVH, LBBB, inferior MI, ventricular pacing
  • RAD
      • QRS is POSITIVE (dominant R wave) in Lead II, Lead III and aVF
      • QRS is NEGATIVE (dominant S wave) in Lead I
      • Causes
          • RVH, RV strain/PE, lateral STEMI, COPD, hyperkalaemia, TCA overdose, dextrocardia
  • AVR = sinus node lead. Usually negative. If positive, rhythm is not supraventricular, or leads reversed

ECG screw ups and pitfalls

  • Artefact
      • Esp if tremor (or concurrent use of an electric toothbrush on telemetry!)
      • Can sometimes mean a trace appears to be AF or flutter, when it’s SR.
      • Can even look like VT or VF on telemetry – look for QRS complexes marching through the artefact
      • Don’t rely on one lead/monitor to diagnose rhythms. Artefact can look for obvious on a 12 lead ECG
  • Limb lead reversal
      • Correct lead position
          • Right arm aVR
          • Left arm aVL
          • Left leg aVF
          • Lead 1 is essentially a combination of aVL and aVR
          • Lead 2 a combination of aVR and aVF
          • Lead 3 a combination of aVL and aVF
      • Left arm and right arm lead reversal
          • Inverted p and inverted QRS in I (mimic is focal atrial tachycardias when p wave inverted in I, but maybe also in aVL, and QRS upright in I)
          • aVR will look like aVL and vica versa
      • Left arm and left leg reversal
          • Inverted III, and aVF and aVL swapped
      • Right arm and left leg reversal
          • aVR positive and an upright p wave in aVR.
          • Often inverted T waves in I and AvL
          • Complexes might all be downgoing in limb leads
      • Issues
          • Lead reversal causes a different pattern of TWI, and also changes the interpretation of the axis
          • Can lead to misdiagnosis of ischaemia as ECGs appear dynamic
      • If lead reversal suspected
          • Do another ECG and check lead positions
          • Also check the connector (often 2 ports, and if these are switched, can cause lead reversal)
          • If two ECGs very different – also check they are from the same patient

Important patterns

  • Benign Early Repolarisation (High Take Off)
      • Rare if aged > 70
      • Widespread concave (‘smiley-shaped’) ST elevation, < 2mm, esp V2-V5
      • Notching at the J point (fishhook pattern) esp in V4
      • Prominent Ts
      • No reciprocal ST depression
      • No evolution
      • Perhaps not entirely benign – there may be a very small increase in risk of SCD
      • STEMI more often has convex elevation (‘frowny-face’)
      • Pericarditis also has concave elevation but ST elevation is often more than 25% of T wave height in V6, there is PR depression, more likely to include inferior leads, no fish hook pattern and ECGs evolve
  • Heart block
      • First degree HB
          • Prolonged PR (>0.2s, or 5 small squares)
          • < 2% requires intervention due to symptomatic 1st degree HB
          • Common in aortic valve disease / post aortic valve surgery
          • Clinically v significant if suspected aortic valve IE – get ECGs daily to check progression of PR interval
          • Common drug causes – betablockers, antipsychotics
      • Mobitz Type 1 second degree heart block (‘Wenckebach’)
          • Variable (not necessarily progressive) changing of PR interval until a complex is dropped
          • Can occur in normal athletes, but often pathological (eg inferior MI)
          • Assess risk of asystole and effect of symptoms on patient. If asymptomatic, doesn’t need immediate treatment
          • Common esp nocturnally. Common if vagal
      • Mobitz Type 2 second degree HB
          • No change in PR interval, then beat dropped
          • More worrying. Increased risk of complete heart block and asystole
          • Indication for PPM unless reversible causes
          • Always due to disease distal to AV node
      • 2:1 block
          • Alternate p waves followed by QRS
          • Can be due to Mobitz 1 or 2 (if BBB present, its Mobitz 2)
      • 3:1 block and 4:1 block
          • Due to Mobitz type 2
      • Complete (3rd degree) heart block
          • Needs PPM and urgent intervention
          • Usually regular (if irregular, consider slow AF)
          • If new ‘pacemaker’ is in AV node or bundle of His, rate is 40-50 and QRS can be narrow (less dangerous)
          • If new ‘pacemaker’ is in ventricular myocardium, rate is 30-40, QRS wide and higher risk of asystole
          • Patients can be very hypertensive as they will vasoconstrict
          • If escape rhythm has wide QRS, its originating quite far from the SAN, therefore atropine is less likely to be work (and may just give them a dry mouth and confusion)
          • Make a plan in case of deterioration – can anyone put in a temporary pacing wire? See emergency pacing
          • Isoprenaline is good for stabilisation esp if delay with pacing wire – contraindicated if ongoing ischaemia
          • Very few patients are asymptomatic (unless congenital CHB and a very reliable narrow escape rhythm with heart rate in the 50s)
  • Left bundle branch block (LBBB)
      • QRS duration > 120ms (WILLIAM pattern)
      • Dominant S wave in V1
      • Absence of Q waves in lateral leads
      • Prolonged R wave peak time
      • Often LAD and poor R wave progression
      • Lateral leads with tall, broad R waves will often have associated ST-segment depression and T-wave inversion, and those with deep S waves can have an allowable amount of ST elevation that does not indicate ischaemia (generally viewed as < 25% of the size of the preceding S wave)
      • Multiple causes, ensure not hyperkalemic
      • Acute and with chest pain – possible MI. Use Smith-Modified Sgarbossa Criteria – check if ST segment changes are concordant (in same direction) as dominant R wave (ischaemia) or discordant (normal LBBB)
  • Left ventricular hypertrophy (LVH)
      • Could be due to HCM, AS, HTN
      • S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm
      • ST depression and TWI in I, AVL and V5-6
      • ST elevation V1-V3
      • LAD
      • Also – dagger Qs (deep, narrow) in lateral/inferior leads
      • p-mitrale (bifed P waves)
      • May be signs of WPW (overlap)
  • Paced rhythms – rhythm depends on
      • Whether VVI, dual chamber or biventricular
          • If just pacing R ventricle, you get a LBBB morphology
          • Biventricular PPMs give a RBBB morphology
          • If atrial and ventricular pacing spikes = dual chambered PPM. LBBB pattern
          • If just ventricular spikes = still probably a dual chamber PPM but atrial lead not being needed right now
          • CRT PPM – QRS complexes are a bit narrower but still RBBB pattern
          • RBBB pattern might be a concern after PPM insertion, esp if there are spikes too – could be that the lead went into artery and the LV or there is a perforated septum and the lead went into the LV from the RV (although it could be that the patient has RBBB at baseline and the PPM is not pacing)
      • Why it’s been inserted
          • PPM will probably pace all the time in CHB or if inserted for HF, whereas if SAN disease it might pace intermittently when the rate drops
      • Unipolar or bipolar setting
          • Large pacing spikes if unipolar, small pacing spikes (which can be missed) if bipolar (which is the majority now)
      • The base rate
          • A PPM will usually allow the HR to drop a bit below the base rate (usually 10 bpm) before pacing (known as hysteresis). If kicks in, it will pace at the base rate. So PPM may still be working if HR is just below base rate. This is to minimise ventricular pacing which can cause cardiomyopathy in the long term
      • The max tracking rate
          • Max track rate usually 130
  • Pericardial effusion
      • Low QRS voltage (refers to QRS complex amplitude)
          • < 5 mm (0.5 mV) in the limb leads
          • < 10 mm (1 mV) in the precordial leads
      • Tachycardia
      • Electrical alternans
  • Raised intracranial pressure
      • Widespread, giant T wave inversions
      • Grossly prolonged QT interval
      • Bradycardia (Cushing’s reflex)
      • Prominent U waves
      • ST segment changes mimicking ischaemia
  • Right Bundle Branch Block (RBBB)
      • QRS > 120 (MARROW pattern)
      • “M-shaped” QRS complex V1-V3
      • Appropriate discordance with ST depression and/or T-wave inversion in right precordial leads (V1-3).
      • Lots of causes but make sure no PE
  • Tri-fascicular block
      • Combination of
          • RBBB
          • 1-degree HB
          • and either LAD or RAD
      • Pacing is required if syncope occurs in this setting
  • Ventricular ectopics
      • One of the commonest cause of palpitations. Usually benign.
      • Can be both the cause of HF (if high burden) and a symptom of it (chicken or egg), or can be related to a third condition like ARVC
      • If reduced LV function – trial betablocker (can also help with symptoms)
      • If normal echo, don’t worry too much
      • Can do cardiac MRI if concerned re coronary disease
      • If > 10% are VEs, repeat echo to exclude a future ectopic-induced cardiomyopathy
      • Ablation can improve ejection fraction and symptoms
      • Ablation may be indicated in:
          • > 10% burden and either symptoms or reduced EF
          • > 5% with symptoms
          • If < 5% burden but reduced EF and symptoms
      • If burden < 5%, no symptoms and normal LV function – nothing to be done
      • See palpitations, ectopics and channelopathies

 

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