The ECG VAQ
Description
 Rate
o Tachycardia vs. bradycardia – state severity
 Rhythm – sinus/ventricular/junctional/ectopic
 Axis – LAD or RAD or normal
 PR segment
o PR > I large square (0.2s) → 1st HB
o Progressive prolongation of PR → type 1 2nd degree Wenkebach’s → stable
o Absence of prolongation/ missed beats → type 2 2nd degree Mobitz’s → unstable
o No relationship between P and QRS → 3rd degree complete HB → check stability of escape
rhythm
 P waves
o P-mitrale or p-pulmonale → m shaped or peaked appearance
o Ectopic atrial rhythms
 QRS complexes
o Narrow complex vs. broad complex
o QRS duration
Pathology
Left anterior
hemiblock
Left posterior
hemiblock
RBBB (QRS>0.12s)
LBBB (QRS>0.12s)
Nonspecific IV
conduction delay
LVH
RVH
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Features
LAD, Q waves in I/aVL, small R in III
Causes
RAD, small R in I, small Q in III
Terminal R’ wave in V1 (rSR’), terminal S
waves in I, aVL, V6, terminal R wave in aVR
Terminal S wave in V1, terminal R waves in
aVL, V6; poor R wave progression in V1-3
QRS >0.10s, no criteria for LBBB or RBBB
May be normal
Ischemia, age-related
Ventricular hypertrophy, AMI, drugs
class IA and IC, hyperkalemia
Tall R waves in LV leads, deep S waves in RV
leads
S in V1 + R in V5 or 6 ≥ 35mm
RAD, tall R waves in RV leads, deep S waves in
LV leads
R in V1 + S in V5 or 6 >10mm
T-waves and U-waves
Pathology
T wave inversion
Peaked T-waves
Upright U-waves
Inverted U-waves
Causes
Q wave and non-Q wave MI, ischemia, pericarditis
(old), myocarditis, contusion, CNS disease, digoxin
effect, RVH/LVH strain
Hyperkalemia, LAD occlusion, early repolarization
Sinus bradycardia, hypokalemia, quinidine, CNS
disease with prolonged QT
LAD disease, ischemia during EST, Prinzmetal’s angina
The Ischemic ECG
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State the leads with primary changes and leads with reciprocal changes
State the territory you think it involves
Look for complications → arrhythmias/blocks/ associations e.g. anterior MI with blocks/VPC
Is there features of cardiogenic shock
Is the history fishy → drug use, diffuse changes, wrong age group, wrong symptoms
Can this be something else → aortic dissection/ ventricular aneurysm
Does the patient need right sided or posterior leads done?
Wall affected
Anterior
Leads
V2, V3, V4
Anterolateral
I, aVL, V3,
V4, V5, V6
Anteroseptal
V1, V2, V3,
V4
II, III, aVF
Inferior
Lateral
Posterior
Right
ventricular
Wellen’s
abnormality
I, aVL, V5,
V6
V8, V9
V4R, V5R,
V6R
V2-4
Sgarbossa
criteria
LMCA
Artery involved
Left coronary artery,
left anterior
descending (LAD)
LAD and diagonal
branches, circumflex
and marginal branches
LAD
Reciprocal changes
II, III, aVF
Right coronary artery
(RCA)
Circumflex branch of
left coronary artery
RCA or circumflex
I, aVL
RCA
Proximal critical LAD
stenosis
LBBB with AMI
aVR – with
many
other leads
Promimal LMCA
occlusion
II, III, aVF
None
II, III, aVF
V1, V2, V3, V4 (R greater than S in V1 and V2, STsegment depression, elevated T wave)
None
Symmetrical deeply inverted T waves in V2-3 or
Biphasic in V2-3 with minimal ST elevation.
Changes occur in pain free state and normalise
when pain
ST elevation >1mm concordant with QRS complex
(5pts), ST depression >1mm in V1-3 (3pts), ST
elevation >5mm discordant with QRS 2 points. >3
points consistent with MI
Widespread changes may be seen but presence of
ST↑ in aVR essentially predicts LMCA involvement
by 94.3%sens and 89.5% specificity
The Electrolyte ECG
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Is it life threatening, if so state it
What are the complications and immediate risks
Always include a differential diagnosis and if asked for a quick management plan
ECG effects of electrolyte imbalances
Imbalance
Hypercalcemia
Key finding
Shortened
QT interval
Hypocalcemia
Prolonged
QT interval
Tall, peaked
T waves
(sinus arrest and slow
repolarization with
increased automaticity)
Hyperkalemia
Hypokalemia
Flat T wave;
U wave appears
Other possible findings
• Prolonged PR interval
• Prolonged QRS complex
• Depressed T wave
• Flat or inverted T wave
• Prolonged ST segment
• Low amplitude P wave (mild hyperkalemia)
• Wide, flattened P wave (moderate hyperkalemia)
• Indiscernible P wave (severe hyperkalemia)
• Widened QRS complex
• Shortened QT interval
• Intraventricular conduction disturbances
• Elevated ST segment (severe hyperkalemia)
• Peaked P wave (severe hypokalemia)
• Prolonged QRS complex (severe hypokalemia)
• Depressed ST segment
The Toxic ECG
The most common drugs associated with cardiac toxicity and ECG changes include:
 Antiarrhythmic drugs
 Antimalarial drugs – chloroquine and quinine
 Antipsychotic drugs – especially thioridazine
 Anticonvulsants – especially carbamazepine and phenytoin
 Beta-blockers – especially propranolol and sotalol
 Calcium channel blocker – particularly diltiazem and verapamil
 Dextropropoxyphene
 Digoxin
 Lithium
 Tricyclic antidepressants
Mechanism
Fast sodium channel
blockade
Changes
Widened QRS, RAD,
bradycardia/tachycardia,
VT/VF
Potassium efflux
blockade during
repolarization
Prolonged QT interval,
torsades des pointes
Na-K-ATPase pump
blockade
Calcium channel
blockade
↑IC Ca level, ↑ automaticity,
↓ AV node conduction → HB
Sinus bradycardia, ↓AV
conduction, IV conduction
defects
Bradycardia, ↓AV conduction
→ AV block
ST-depression/elevation,
conduction abnormalities
Peaked T waves, conduction
abnormalities
QT prolongation
QRS>100ms, terminal R wave
in aVR>3mm, R/S ratio >0.7 in
aVR
β – adrenergic blockade
Myocardial ischemia
Hyperkalemia
Hypocalcemia
TCA classical
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Causes
TCA, class 1A (quinidine), class 1C (flecainide),
local anesthetics (cocaine, bupivacaine),
phenothiazines, anti-histamines, propranolol,
dextropropoxyphene, chloroquine,
diltiazem/verapamil
Antipsychotic agents – phenothiazines, atypical
antipsychotics, halo/dro-peridol
Class 1A, Class 1C, Class III – sotalol, TCA, other
antidepressants –
citalopram/venlafaxine/moclobemide/bupropion
Antihistamines –
diphenhydramine/astemizole/terfenadine
Chloroquine/quinine/erythromycin
Cardiac glycosides – digoxin, digitalis, yellow
oleander
Especially diltiazem and verapamil
Propranolol and sotalol, metoprolol less likely
Cocaine
Digoxin, diuretics
Hydrofluoride
Risk stratification for TCA – QRS duration >100ms risk for seizures, >160ms risk for VT/VF
QT prolongation >450 ms in previously normal ECG → ↑risk for torsades
The Arrhythmia ECG
Arrhythmia Determination
Step One: Determine the heart rate
Step Two: Determine the ventricular rhythm
Step Three: Identify and analyze the P, P′, F, or f waves
1. Identify the P, P′, F, or f waves
2. Determine the atrial rate and rhythm
3. Note the association of the P, P′, F, or f waves to the QRS complexes
Step Four: Determine the PR or RP′ intervals and AV conduction ratio
1. Determine the PR intervals
2. Assess the equality of the PR intervals
3. Determine the AV conduction ratio
Step Five: Identify and analyze the QRS complexes
1. Identify the QRS complexes
2. Note the duration and shape of the QRS complexes
3. Assess the equality of the QRS complexes
Step Six: Determine the site of origin of the arrhythmia
Step Seven: Identify the arrhythmia
Step Eight: Evaluate the significance of the arrhythmia
Sinus arrhythmias
Type
Characteristic
Sinus
HR – 60-100, p waves before
arrhythmia
each complex, irregularity
Sinus
HR <60bpm, normal PR interval,
bradycardia
usually regular, upright P in lead
II
Sinus
Normal SR followed by dropped
arrest/pause
P wave
Sinus
HR >100, upright P in lead II,
tachycardia
usually regular
Cause
Respiratory changes, common in young and old
Pathological – AMI (inferior), digoxin, morphine
Increased vagal tone, drugs – BB/CCB/digoxin, sick sinus
syndrome, AMI, hypothyroidism, hypothermia, hypoxia,
athletes
As above and myocarditis/fibrosis
Stimulants, catecholamine excess, CCF, PE, MI, fever,
thyrotoxicosis, hypovolemia, hypoxia
Atrial arrhythmias
Type
Characteristic
Wandering
Irregular HR, changing P wave
atrial
size/shape/direction, varying PR intervals
pacemaker
Premature
Irregular HR, may be single site PAC or multiple
atrial
site. Ectopic P wave close to preceding
contractions
complex, compensatory or non-compensatory
pause, isolated/grouped beats/repetitive beats
(atrial bigeminy), QRS complexes
normal/narrow unless BBB
Atrial
HR 160-240, ventricular rate similar unless AV
tachycardia
block, >3PAC by definition, regular. Abnormal P
(ectopic and
wave morphology (upright if site close to SA,
multifocal)
inverted if close to AV)
Atrial flutter
Atrial rate 240-360, ventricular rate usually 150
Cause/significance
May be normal in young/old and digoxin
administration
Increased catecholamine states,
stimulants, digoxin toxicity, ischemia,
CCF, dilated atria from valvular HD or ASD
→ risk for SVT/PSVT/AF in abnormal
hearts
Digoxin toxicity, acute alcohol abuse,
electrolyte disturbances, hypoxia, CAL,
IHD, rheumatic HD. AV block usually seen
with digoxin.
May cause ↓CO → dizziness/syncope,
ischemia, hypotension or cardiogenic
shock in susceptible patients.
Advanced RHD, VHD, CAD
(2:1AVB), usually regular unless variable AVB.
Sawtooth appearance F waves
Atrial
fibrillation
Atrial rate >350, ventricular rate usually 160180 in uncontrolled cases. Considered fast if
ventricular rate >100. Irregularly irregular. ‘f’
waves maybe seen as fine 1mm spikes.
Junctional arrhythmias
Type
Characteristic
Premature
Irregular HR, P waves absent with PJC, may be
Junctional
isolated/grouped/repetitive. QRS similar to
contractions
usual complexes bt no P waves seen. P’ waves
of abnormal morphology close to/on QRS may
be seen
Junctional
escape rhythm
HR 40-60, regular, P waves +/-, no correlation
with QRS, AV dissociation. Inverted reverse P
waves may be seen following QRS.
Accelerated
Junctional
tachycardia
HR>60 as AV node rate <60, regular rhythm.
Rest as above.
Paroxysmal
SVT
HR 160-240, regular, may be AVRT or AVNRT,
QRS normal unless aberrancy
Cardiomyopathy/ atrial dilation,
thyrotoxicosis, hypoxia, cor pulmonale,
CCF, pericarditis/myocarditis, alcoholism
→ loss of atrial kick → incomplete filling
→ signs of ↓CO
As above → reduction of cardiac output
by 25-30%
Cause/significance
Digoxin toxicity (commonest cause),
enhanced automaticity of AVN, increased
vagal tone, class IA drugs or
sympathomimetics, CCF/CAD. >6/min
increased risk for AVNRT, early sign of
digoxin toxicity.
Severe sinus bradycardia(arrest), third
degree AV block → signs of severe
bradycardia → need for pacing if clinically
indicated
Digoxin toxicity, catecholamine excess,
damage to AVN (MI), hypoxia →
significant digoxin toxicity, need for
treatment, symptoms of AF
Increased catechoamine, stimulants,
electrolyte/acid-base abnormalities,
hyperventilation, stress→SOB/syncope
Ventricular arrhythmias
Type
Characteristic
Premature
HR of underlying rhythm, irregular. May be from single
ventricular
ectopic site or multifocal. P wave unrelated and
contraction
retrograde P waves may occur. Bizarre wide QRS
complexes. Full compensatory pause + P wave
superimposed on premature beat make positive
diagnosis
Ventricular
tachycardia
HR >100 (110-250). >3 consecutive PVC. >30 sec
sustained. May be
monmorphic/polymorphic/bidirectional/torsades.
QRS>120ms, QS>0.1s in any lead, concordance in V
leads, AV dissociation, fusion /capture beats, absent
RS complexes in precordial leads.
Clinical criteria Age>35, h/o CAD, chest pain.
Ventricular
fibrillation
No coordinated ventricular beats, HR300-500 may
slow late, irregular. Pacemaker usually multiple
Cause/significance
Suggestive or increased ventricular
automaticity. Increased
sympathetic tone, stimulants, CCF,
ischemia, digoxin, hypoxia,
acidosis.
Hypokalemia/hypomagnesemia.
>3 consecutive PVC constitue VT,
bigeminy, trigeminy may occur.
>6PVC/min, R-on-T phenomenon
and incomplete pauses suggest
unstable rhythm.
Significant cardiac disease – CAD,
Cmyopathy, valvular HD, LVH/CCF,
drug toxicity, hypokalemia, CNS
diseases.
Stable/unstable depending on
underlying cardiac status. Lifethreatening in most cases. Very
important to diagnose SVT with
aberrancy
End-point of most cardiac diseases,
drug toxicities, electrolyte
ectopic sites in Purkinje network and myocardium.
Wide no QRS morphology. Coarse or fine of no
Accelerated
idioventricular
rhythm
Idoventricular
rhythm
HR 40-100, usually regular. Pacemaker in Prukinje
network or myocardium. P waves if present,
independent of QRS. QRS>0.12s, bizarre features of VT
present but rate essentially slower.
HR<40. Rest same as above
imbalances, electrical
abnormalities. Life-threatening
requiring immediate defibrillation.
Acute MI, SA node arrest or CHB.
Digoxin toxicity. If in AMI, no
treatment usually necessary. If
symptomatic treat as VT.
As above. Need for transcutaneous
pacing.
Specific other situations
Wolff-Parkinson-White pre-excitation patterns
Mechanism
Pre-excitation of ventricles by atrio-ventricular
bypass tracts
Site of bypass tract –
Left lateral (type C) 60% →
Right lateral type (type B) 10% →
Others 30% →
Arrhythmias with WPW
Mechanism
Orthodromic – from normal
pathway return through accessory
pathway
Antidromic – through accessory
pathway return from normal
pathway
Other important ECG findings
Mechanism
Brugada syndrome - Sodium
channelopathy
40% familial (AD)
Takostubo cardiomyopathy –
Octopus pot heart. Significant
emotional/physical stressor.
Long QT syndromes
Romano-ward and Lange-NeilsonJerville → inherited defect in Na
and corrective K channel.
Pulmonary embolism
Effects
Widened QRS due to slurred upstroke but shortened
PR interval <0.12s. notching of QRS waves →delta
waves.
+ve V1 V2 (LLV+V)
-ve V1 V2 (RLV-V)
+ve or –ve V1 and V2 combinations
Effect
95% cases, SVT with accessory
pathway, delta waves may be
seen, regular
5% cases of tachyarrhythmia with
WPW, 0.1% may lead to VT/VF.
Rates >180-200 may point toward
diagnosis. P waves may be seen
embedded. ECG may look like
irregular VT due to fusion beats
Significance
NO AV NODAL AGENTS → risk VT
Procainamide/ Flecainide useful
Effect
RBBB with ST elevation in V1-3 and
concave ST-segments, biphasic T
waves
Severe LV hypokinesis. Raised
troponin/BNP/catecholamines.
Widespread ST-elevation and TWI.
Long QT, T wave alternans, R-on-T
phenomenon → Torsades
Deafness in LNJ type
Significance
Risk for sudden death → ICD
placement advised
Sinus tachycardia most common.
RBBB may occur s/o RV dilatation.
S1Q3T3 in 20-30% cases s/o Cor
pulmonale
Adenosine may be tried according
to new guidelines but better stay
away. NO AV NODAL AGENTS
Flecainide drug of choice.
Normal angiogram, supportive
management.
Risk for torsades and VT,
electrolyte control and ICD
required. Syncope and palpitations
indications for intervention.
ECG non-significant to rule out PE