Clinical ECG(John R Hampton)

* If timing early/late for depolarization/repolarization, THINK affected wave should be accompanied

by changes/absence in the culprit wave.

*Think if dilated ventricle = pressure from input vessel; hypertrophic ventricle = pressure from
output vessel

Classical MI progression:

Acute Hours (+) Day 1-2 Days Weeks

ST elevation Reduced R wave T wave inversion ST normalizes Only deep Q
Start Q wave Q wave deepen persist

AVRT & AVNRT

For AVRT: need normal AV node and accessory pathway (+MUST BE triggered by premature/extra
beat which could overcome refractory period of accessory pathway hence completing the loop)

For AVNRT (most common type of SVT): only need normal AV node (+MUST BE triggered by
premature/extra beat which overcome refractory period of its fast pathway which has a longer
refractory period)
NORMAL

1. Sinus arrhythmia = Increased heart rate during inspiration in young people, less in elderly
and diabetic autonomic neuropathy
May mimic atrial arrhythmia when marked but PQRST complex normal with only interval
between complex changes
2. Sinus bradycardia = rule out athletes, vasovagal attacks, sick sinus syndrome, AMI esp. inf,
hypothyroid, hypothermia, obstructive jaundice, raised ICP, drugs (beta blocker, verapamil,
digoxin)
3. Supraventricular (Junctional/AV nodal or atrial) and ventricular extrasystole are common in
normal people

P wave

4. P wave always upright except aVR and aVL (aVL if QRS of lead predominantly downward)
5. Dextrocardia flip picture of leads: esp Inverted P wave in Lead 1, almost/no QRS complex in
leads V5-V6
6. Notched/Bifid = L atrial hypertrophy ; Peaked = R atrial hypertrophy (? Maybe cause SA node
more to R atrium) BUT both may be seen in normal
7. Bifid P waves with peaked T waves and U waves in V2-V3 normal variants
8. Ectopic atrial rhythm (normal variant) – sometimes p wave may be inverted in many leads
esp. in upward QRS leads
9. Notched P wave in V5 often normal

PR interval

10. Athletes PR interval may be slightly longer than normal eg. 240ms (6 small boxes)

QRS complex (WiLLiaM/MaRRoW)

11. Lead 1-3 QRS upright: tallest in 2, R and S may be equal in 1

12. If downward in Lead 1 = RAD (axis deviation)
13. If upward in Lead 1 but downward in 2 then LAD
14. Minor RAD in tall people
15. Dominant R wave in V1 usu. R ventricular hypertrophy OR true posterior infarction but can
be also normal in atheletes. R wave dominance may shift towards V5, V6, V7 or further in
chronic lung disease or mediastinal shift due to sternal depression (abnormal chest shape)
16. Limits of normality (no strictly): R wave V5/V6 & S wave V1/V2 <2.5cm (> in thin fit young)
 R wave (V5/V6) + S wave V1/V2 <3.5cm/7BB
QRS width < 0.12s/3 sb

17. Broaden QRS = ventricular rhythm OR abnormal ventricular conduction (more common due
to BBB)
18. RBBB with RSR pattern (has traversed baseline) but normal QRS width is normal variant. May
also show RSRS pattern or notched S wave in right sided leads
19. Normal rhythm may be replaced by accelerated idioventricular rhythm (temporary run of
regular ventricular extrasystoles (wide QRS)

Q waves (L to R septal depolarization)

20. Normal range: < 0.3 x 0.1 cm, may disappear on deep inspiration
21. Normal variation: septal Q waves in lead 3, aVL, V5-V6

ST segment

22. Should be isoelectric but in chest leads may slope upwards OR V2-V5 elevated after S wave
“high take-off” OR anterior leads early repolarization causes arched ST segment appears
raised
23. Elevation = usu. MI/hyperK; depression (esp. if horizontal and doesn’t slope back up) = usu.
ischemia/digoxin
24. ST depression compares TP baseline and 60-80ms after J point (when S wave ends to a
baseline)
25. Minor ST depression can be normal and called “nonspecific” BUT <0.2cm depression
26. DDx ST elevation = normal variants (high take-off and early repolarization), LBBB, acute
pericarditis/myocarditis, hyperK, Brugada syndrome, Arrhythmogenic R ventricular
cardiomyopathy, PE

T wave (most variable part)

27. ALWAYS inverted in aVR and often in V1 whereas others usu. upright, Lead 3 often inverted
but not aVF (reversed on deep inspiration).
28. aVL T wave inversion may be normal esp. if it’s P wave also inverted
29. Causes of T wave inversion: Normal variant (V1-3 in black ppl, *25, *26), ventricular
extrasystoles & other ventricular rhythms, RBBB/LBBB, MI, R/L ventricular hypertrophy,
Wolf-Parkinson-White syndrome
30. If T wave notched, QT interval measured from start of Q to the point of intersection
between maximum down slope line of 2nd notch and isoelectric line
31. General T wave flattening with normal QT interval in asymptomatic patients = “non-specific”
BUT if symptomatic = further Ix
32. Peaked T wave = hyperK/hyperacute MI
33. May be inverted in some leads simply by hyperventilation associated with anxiety.

U wave (only important if it follows a flat T wave)

34. HypoK OR normal in anterior chest leads (repolarization of papillary muscles)

QT interval

35. Varies with heart rate, gender and time of day hence corrected for heart rate (usu. Bazett’s
formula):
 QTc = QT/ √(RR interval) , upper limit longer in woman and elderly, <0.45s for men <0.47s for
women

Atheletes

Variation in rhythm Variation in ECG pattern

Sinus bradycardia Tall P waves
Marked sinus arrhythmia Prominent septal Q waves
Junctional rhythm Tall R waves and deep S waves
“Wandering” atrial pacemaker/ accelerated Counterclockwise rotation (in regards to
idionodal rhythm (short and varying PR axis)
interval where sinus node slower than AV Slight ST segment elevation
hence AV controls heart rate) Tall symmetrical T waves
1st degree block T wave inversion (esp. in lateral leads)
Wenckebach phenomenon Biphasic T waves
2nd degree block Prominent U waves

Pregnancy
36. Possible normal features: sinus tachycardia, supraventricular and ventricular extrasystoles
(latter universal), nonspecific ST segment (upward slopping depression)/ T wave changes

Children
37. Until 1yo = 140-160 bpm, puberty = 80 bpm, sinus arrhythmia usu. marked
38. Apparent R ventricular hypertrophy possible in <2yo BUT if present after then true; if normal
adult pattern in <1yo = L ventricular hypertrophy
39. T waves inversion initially V1-V4 then by 1yo V1-V2 then by 10yo normal adult pattern

Prognosis of Abnormal ECG patients: Further Ix and Tx of asymptomatic

40. 1st degree block has little effect on prognosis, 2nd and 3rd worse; congenital complete block
better than acquired block in adults
41. L ant. hemiblock and RBBB has good prognosis but LBBB without Sx increased 30% risk of
death if +Sx double that risk; Bifascicular block ALWAYS heart disease and poorest prognosis.
42. Frequent or multiform ventricular extrasystoles increased risk of death (subclinical heart
disease) but no proof Tx improves outcome
43. Atrial fib poor prognosis: 1/3 no heart disease but even within these ppl risk of death
increased 3/4x, risk of stroke 10x
44. Echocardiogram justified for: LBBB (eg. dilated cardiomyopathy, unsuspected aortic
stenosis), RBBB (seldom but may have ASD, pulm hypertension), T wave inversion (ischemia,
ventricular hypertrophy, cardiomyopathy), ventricular extrasystole if high clinical suspicion
plus check Hb(cardiomyopathy), atrial fibrillation plus check TFT,LFT (heart structure and LV
function), suspicion of rheumatic heart disease
45. Complete heart block indicated for permanent pacing but not other blocks
46. Don’t Tx in view of pro-arrhythmic effects of anti-arrhythmic drugs: atrial fib if ventricular
rate is reasonable but need anticoagulant for valvular disease eg. warfarin; ventricular
extrasystoles

PALPITATIONS AND SYNCOPE: BETWEEN ATTACKS

Palpitations
1. 3 different types experienced: extrasystoles (supraV/V), sinus tachycardia, paroxysmal
tachycardia (latter 2 diff by below)

Sinus Tachycardia Paroxysmal tachycardia

Began recently Long Hx
Slow build up Sudden onset
Stop by relaxation By breath holding/Valsalva’s manoeuvre
Sx: paraesthesia by hyperventilation Sx: Chest pain, breathlessness, dizziness,
syncope

Syncope
2. Cardiovascular causes
Obstructed blood flow heart/lungs Aortic stenosis
Pulm embolus
Pulm HPT
HOCM
Pericardial tamponade
Atrial myxoma
Arrhythmias Tachycardia
Bradycardia (pt unaware symptoms) eg.
Stokes-Adams attack in pt with complete
heart block – initially pale flushes red on
recovery
Postural hypotension Autonomic: Diabetes, Shy-drager
syndrome, amyloid neuropathy
Drugs: anti-HPTs
Neurally-mediated reflex syncopal Vasovagal/neurocardiogenic – simple faints
syndromes Situational eg. after, coughing, sneezing,
constipation, post-micturition
Carotid sinus hypersensitivity

3. S&S + dDx
Family Hx of sudden death Long QT syndrome, Brugada syndrome,
HOCM
Caused by unpleasant stimuli, prolonged Vasovagal syncope
standing, hot places (situational syncope)
Within secs/mins to standing Orthostatic hypotension
Temporal relation to medication Orthostatic hypotension
On exertion Blood flow obstruction eg. PE, aortic
stenosis
On head rotation/pressure on neck Carotid sinus hypersensitivity
Confusion >5mins afterwards Seizure
Automatism, tonic-clonic movements Seizure
Frequent attacks, usu. unobserved, with Psychiatric illness
somatic Sx
S&S of cardiac disease Cardiac disease

4. Assymptomatic ECG can rule out arrhythmic or non-arrhythmic cause of cardiac disease,
leaving neurological causes and others.
 Normal
Cardiac disease
Intermittent tachyarrhythmia
Intermittent bradyarrhythmia
Anxiety, epilepsy, atrial myxoma, carotid
sinus hypersensitivity
LBBB/L ventricular hypertrophy – aortic
stenosis
R ventricular hypertrophy – pulmonary
hypertension
Anterior T wave inversion – hypertrophic
cardiomyopathy (blockes LV output OR
arrhythmias)
L atrial hypertrophy – mitral stenosis +/-
atrial fib
Pre-excitation syndromes
Long QT syndrome
Flat T waves suggest hypokalaemia
Digoxin effect -?digoxin toxicity
2nd degree block
1st degree block + BBB
Digoxin effect

Tachycardia
5. Mitral stenosis causes atrial fib but may only have paroxysmal atrial fib before that.
Hence, L atrial hypertrophy suggests paroxysmal atrial fib.
6. Pre-exitation syndromes (additional pathway/multiple pathways of conduction
bypassing AV node) – combination of AV node + His bundle + accessory pathway may
cause “re-entry” tachycardia
7. Wolf-Parkinson-White syndrome (+bundle of Kent – LA to LV or RA to RV; 1:3000 and
only ½ have symptoms) – QRS complex normal/narrow (concealed) as at times
conduction is through normal His bundle pathway and at times in same forward
direction as His bundle and AV node. BUT faster ventricular conduction caused causes
shorten PR interval and slurred upstroke to QRS complex (delta wave) causing a wide
QRS complex. Also, inverted T waves in leads 2,3, aVF, V1-V4. Possibly, arrhythmia
(narrow OR wide complex), if wide-irregular complex suggests WPW with atrial fib.
 L-sided = dominant R wave in V1 (Type A pattern) compared to R ventricular
hypertrophy there’s presence of short PR interval
 R-sided = dominant S wave in V1 (Type B pattern) +/- anterior T wave inversion
8. Long-Ganong-Levine syndrome (+accessory pathway atria to bundle of His) – short PR
interval but QRS complex normal, dDx accelerated idionodal rhythm (PR interval varies)
9. Long QT syndrome – possibly paroxysmal ventricular tachycardia potentially causing
collapse/sudden death “torsade de pointes” usu. occurring during increased
sympathetic nervous system activity. Torsades rare when QT/ QTc interval <0.5s
 Familial prolonged QT = fainting attacks/ sudden death
 Pharmacological (most common)
Congenital Antiarrhythmic Other drugs Electrolyte
drugs imbalance
Jervell-Lange- Quinidine Tricyclic
Nielson Procainamide antidepressants
syndrome Disopyramide Erhythromycin
Romano-Ward Amiodarone
syndrome Sotalol
10. Brugada syndrome

Bradycardia

Ambulatory ECG

TACHYCARDIA

BRADYCARDIA

CHEST PAIN

BREATHLESSNESS

OTHER CONDITIONS EFFECT ON ECG

4 STEPS OPTIMIZE ECG USE

NON-ECG FACTS
1. Fondaparinux lower bleeding risk than enoxaparin but cannot be used in renal failure
patients.
2. Proximal coronary artery stenosis <60% compensatory vasodilatation sufficient, >70%
not sufficient hence at exertion Sx, >90% at rest
3. Vessel narrowing has 2 factors: thrombus size and endothelial dysfunction; endothelial
dysfunction reducing antithrombotic effects and also reduced NO for vasodilatation to
oppose natural catecholamine during stress
4. Myocardium states after ischemia: Stunned/hibernating/infarcted myocardium =
transient reversible dysfunction/chronic ischemic dysfunction reversible with
revascularization/ dead. To differentiate latter two to decide for revascularization =
positron emission tomography or dobutamine echocardiography
5. Atrial myxoma is most common primary heart tumour (benign) usu. on atrial septum
(mimics cardiac failure and infective endocarditis and if on L mimics mitral stenosis). Sx
associated with body position.
6. Important to decide if heart failure predominantly R (venous/feet retention Sx but if
cause if cor pulmonale then has long-standing lung Sx) or L (lung retention Sx) for Tx
 considerations. Usu. R-sided is a result of chronic L-sided failure otherwise cor
pulmonale. R-sided can conversely cause L-sided failure 2° to decreased preload. IN
BOTH lung Sx exist for some time before leg Sx hence diff by Hx of lung disease risk
factors, examination and further Ix.
7. R-sided MI (eg. inferior) don’t give NO as it aggravates preload decline.
8. Warfarin induced skin necrosis develop within 3-5 days upon initiation esp. if started at
high doses. Paradoxical effect is caused by high doses aggravating the initial warfarin
effect of inhibiting protein C and factor 7 more than the other factors. First appears red
and painful – sharp border and petechial – bloody bullae – slow-healing eschar. Tx is
cease warfarin temporarily, Vitamin K, FFP/activated protein C