Left axis deviation:
Causes:
Left anterior fascicular block
Left bundle branch block
Left ventricular hypertrophy
Inferior MI
Ventricular ectopy
Paced rhythm
Wolff-Parkinson White syndrome
Left anterior fascicular block:
Diagnostic features:
Left axis deviation (usually between -45 and -90 degrees)
Small Q waves with tall R waves (= qR complexes) in leads I and aVL
Small R waves with deep S waves (= rS complexes) in leads II, III, aVF
QRS duration normal or slightly prolonged (80-110 ms)
Prolonged R wave peak time in aVL > 45 ms
Increased QRS voltage in the limb leads
Note:
bifascicular block: RBBB + LAFB (most commonly)
Incomplete trifascicular block
Bifascicular block + 1st degree AV block (most common)
Bifascicular block + 2nd degree AV block
RBBB + alternating LAFB / LPFB
Complete trifascicular block
Bifascicular block + 3rd degree AV block
LBBB:
Diagnostic features:
QRS duration of > 120 ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL)
Prolonged R wave peak time > 60ms in left precordial leads (V5-6)
Causes:
Aortic stenosis
Ischaemic heart disease
Hypertension
Dilated cardiomyopathy
Anterior MI
Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease)
Hyperkalaemia
Digoxin toxicity
Inferior STEMI: majority due to RCA occlusion or left circumflex artery in some cases
ST elevation in leads II, III and aVF
Progressive development of Q waves in II, III and aVF
Reciprocal ST depression in aVL ( lead I)
RCA occlusion is suggested by:
ST elevation in lead III > lead II
Presence of reciprocal ST depression in lead I
Signs of right ventricular infarction: STE in V1 and V4R
Circumflex occlusion is suggested by:
ST elevation in lead II = lead III
Absence of reciprocal ST depression in lead I
Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6
Anterior STEMI: due to left anterior descending artery occlusion
ST segment elevation with Q wave formation in the precordial leads (V1-6) the high lateral leads (I
and aVL).
Reciprocal ST depression in the inferior leads (mainly III and aVF).
Wellens syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical
proximal LAD stenosis (a warning sign of imminent anterior infarction)
Patients may be pain free by the time the ECG is taken and have normally or minimally elevated
cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within
the next few days to weeks.
Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
Type B = Deeply and symmetrically inverted (75% of cases)
Ddx of Wellens syndrome:
Pulmonary embolism
Right bundle branch block
Right ventricular hypertrophy
Left ventricular hypertrophy
Hypertrophic cardiomyopathy
Raised intracranial pressure
Normal paediatric ECG
Persistent juvenile T wave pattern
Brugada syndrome
Hypokalaemia
First degree heart block: (PR interval > 200 ms)
Causes:
Increased vagal tone
Athletic training
Inferior MI
Mitral valve surgery
Myocarditis (e.g. Lyme disease)
Electrolyte disturbances (e.g. Hyperkalaemia)
AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)
May be a normal variant
AV block (2nd degree, Mobitz I):
Progressive prolongation of the PR interval culminating in a non-conducted P wave
The PR interval is longest immediately before the dropped beat
Causes:
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
Increased vagal tone (e.g. athletes)
Inferior MI
Myocarditis
Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
Clinical significance:
Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk
of progression to third degree heart block.
Asymptomatic patients do not require treatment.
Symptomatic patients usually respond to atropine.
Permanent pacing is rarely required.
Note: Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible
ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction,
fibrosis, necrosis).
AV block (2nd degree, Mobitz II): due to failure of conduction at the level of the His-Purkinje system (i.e.
below the AV node).
Intermittent non-conducted P waves without progressive prolongation of the PR interval.
The PR interval in the conducted beats remains constant.
Causes:
Anterior MI (due to septal infarction with necrosis of the bundle branches).
Idiopathic fibrosis of the conducting system (Lenegres or Levs disease).
Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).
Autoimmune (SLE, systemic sclerosis).
Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).
Hyperkalaemia.
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.
Clinical significance:
Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise,
severe bradycardia and progression to 3rd degree heart block.
Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-
Adams attacks) or sudden cardiac death.
The risk of asystole is around 35% per year.
Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and
ultimately insertion of a permanent pacemaker.
AV block (3rd degree, complete heart block)
Complete absence of AV conduction none of the supraventricular impulses are conducted to the
ventricles.
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm.
Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e.
AV dissociation.
Clinical significance:
Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac
death.
They require urgent admission for cardiac monitoring, backup temporary pacing and usually
insertion of a permanent pacemaker.
Ventricular fibrillation
Ventricular fibrillation (VF) is the the most important shockable cardiac arrest rhythm.
The ventricles suddenly attempt to contract at rates of up to 500 bpm.
This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised
manner, resulting in immediate loss of cardiac output.
Cardiac
o Myocardial ischemia / infarction
o Cardiomyopathy (dilated, hypertrophic, restrictive)
o Channelopathies e.g. Long QT (acquired / congenital) causing TdP > VF and Brugada
syndrome
o Aortic stenosis
o Aortic dissection
o Myocarditis
o Cardiac tamponade
o Blunt trauma (Commotio Cordis)
Respiratory
o Tension pneumothorax
o Pulmonary embolism
o Primary pulmonary hypertension
o Sleep apnoea
o Bronchospasm
o Aspiration
Toxic and metabolic causes
o Drugs (e.g. verapamil in patients with AF+WPW)
o Drug-induced QT prolongation with torsades de pointes
Environmental
o Electrical shocks, drowning, hypothermia
o Sepsis
Neurological
o Seizure
o CVA
Right axis deviation
Causes:
Left posterior fascicular block
Lateral myocardial infarction
Right ventricular hypertrophy
Acute lung disease (e.g. PE)
Chronic lung disease (e.g. COPD)
Ventricular ectopy
Hyperkalaemia
Sodium-channel blocker toxicity
WPW syndrome
