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-criteriae for normal sinus rhythm (benda nie beza2, so myb different
bw different sources)
1. heart rate of 60-100 bpm
2. regular rhythm
3. P wave must present for every QRS complex in ratio of 1:1
4. PR interval is bw 0.12 sec to 0.2 sec (3-5 small sq)
5. QRS should be less than 0.12 sec (3 small sq)
-lead v1/v2 look at RV, lead v3/v4 look at IV septum, lead v5/v6 look at
-description of ECG step by step
1. rhythm & rate
4. cardiac axis
2. PR interval
5. T waves, ST segments, etc
3. QRS complex duration

origin of
-P waves - atrial contraction
-QRS - ventricular depolarization
-T - ventricular repolarization
-U - repolarization of papillary ms

first degree heart block

-signs of CAD, acute rheumatic carditis, digoxin toxicity, or electrolyte
-PR interval prolonged (normal 3-5 small sq)

-1 small square 0.04 sec (40 millisec)

-1 large sq 0.2 sec (200 ms)
-5 large sq 1 sec
-to calculate heart rate - 300 divide by how many large boxes bw R-R
-normal PR interval - 3-5 small squares
-normal QRS complex - less than 3 small squares
-normal QT interval - less than 2.5 large sq (<450 millisec). if >450 may
leads to VT
-right leg - earth lead
-cardiac rhythm - identify from whichever lead shows P wave most
clearly, usually lead 2
-to determine cardiac axis, look at lead 1 and 2, in which one the S
wave taller than R wave? [1R 2L]
1. if in lead 1 then it is right axis deviation (+90 to -90) - means RV
2. if in lead 2 then it is left axis deviation (-30 to -90) - means LV
3. if both lead 1 and lead 2 S is shorter than R, then normal cardiac axis
(N cardiac axis -30 to +90)

second degree heart block

-there are 3 variations
1. wenckebach or mobitz type 1
-one nonconducted P wave followed by progressively longer
conducted waves
-in mobitz type 1 next conducted beat has longer PR interval than
preceeding conducted beats

2. mobitz type 2
-one P wave not followed by QRS complex
-PR interval of conducted beats is constant
right axis deviation

left axis deviation

ECG axis

3. 2:1, 3:1 or 4:1 conduction AV block

-2:1 means 2 P waves per QRS complex. same for 3:1 and 4:1
-the jarak bw P is constant regardless ada QRS or not

-the cause of 1st degree heart block is delay somewhere along the
conduction pathway
-for 2nd degree heart block the excitation completely fails to pass
through AV node or bundle of His. the underlying causes are still the
same as 1st degree heart block
-wenckebach is usually benign but mobitz type 2, 2:1, 3:1, and 4:1 may
precedes complete or 3rd degree heart block
third degree heart block / complete heart block
-occur when atrial contraction normal but no beats conducted to the
-may occur as acute phenomenon in pt with MI (usually transient), or it
myb chronic, usually dt fibrosis around bundle of His. may also be
caused by block of both bundle branches
-possible patterns
1. PR interval at all leads no consistency
3. abN shaped QRS
2. no relationship bw P & QRS

pathways of depolarization
-conduction problems in :1. AV/BoH 2. LBB/RBB - results in bundle branch block

with its large muscle mass

6. if RBBB + LAH - ECG shows RBBB + left axis deviation - also called as
bifascicular block
-bifascicular block indicates widespread damage to the conducting
complete heart block
-RBBB can be further divided into 2, complete and incomplete RBBB.
incomplete RBBB are those with QRS <120 millisec whereas complete
RBBB are those with QRS >120 millisec
-causes of RBBB - normal heart, ASD & other congenital heart dz, PE

bundle branch blocks

-wide QRS complex - indicates bundle branch block
-RBBB - often indicates problems in right side of heart. but RBBB
patterns with QRS complex of normal duration (incomplete RBBB) are
quite common in healthy people
-LBBB however, always an indication of heart dz, usually of LV
-RBBB pattern 1. 2nd R wave (RSR') in lead v1
2. wide & deep S wave, and consequently a wide QRS complex in lead
-LBBB pattern 1. M pattern, best seen in lead v6
2. W pattern in lead v1, often not fully developed
3. associated with T inversion in lateral leads (1, aVL, v5-v6), though
not necessarily in all these


practical issues
1-first degree block
-often seen in normal people. but always think of AMI & ARF
-no specific action needed
2- second degree block
-usually indicates heart dz. often seen in AMI
-mobitz type 2 & wenckebach block do not need specific tx
-2:1, 3:1, or 4:1 block may indicate need for temporary of permanent
pacing, esp if ventricular rate is slow

4) accelerated idioventricular rhythm

-often ass with AMI
-although appearance of ECG similar to VT, AIR is benign & should not
be treated
-VT should not be diagnosed unless HR > 120/min
-pattern - ventricle escape, wide QRS, abN T

3- third degree block / complete heart block

-always indicates conducting tissue dz - more often fibrosis than
-consider temporary or permanent pacemaker
-think about ASD. no specific tx
-think about aortic stenosis & ischemic dz
-if pt asx no action needed
-if pt recently had severe chest pain, LBBB may indicate an AMI, and
intervention should be considered
6- left axis deviation
-think about LV hypertrophy and its causes. no action needed
7- bifascicular block
-indicates severe conducting tissue d/o. no specific tx needed
-pacemaker required if pt has sx suggestive of intermittent complete

*extrasystole - a premature cardiac contraction that is independent of

the normal rhythm and arises in response to an impulse outside the
5)supraventricular extrasystole. 2 forms
a- atrial extrasystole - appears as early and abN P wave, followed by
normal QRS complex
b- junctional extrasystole - no P wave, normal QRS

---here begins the little bit more complex part of ECG--1)atrial escape
-atrium takes over as focus of depolarization
-abN P with normal QRS
-if widespread called as ectopic atrial rhythm

junctional extrasystole
2) junctional escape
-AV node takes over as focus of depolarization
-no P, normal QRS

3) ventricular escape
-no P, abN QRS (& wide), abN T

6) ventricular extrasystole
-common, but usually of no importance. but when they occur early in T
wave of preceding beat they may induce VF
-early beat, wide QRS, abN T

ventricular extrasystole occur at peak of T waves of preceeding sinus

-R on T phenomenon

torsades de pointes VT
-broad complex tachycardia in which QRS initially upright but then
changed to become downward pointing
-its either self-limiting or progress to VF

7) atrial flutter
-atrial rate of >250/min & no flat baseline bw P waves (sawtooth
-atrial flutter usually with AV block eg atrial flutter with 2:1 block, atrial
flutter with 3:1 block

8) supraventricular tachycardia
a- atrial tachycardia -P waves superimposed on T waves of preceding
beats. normal QRS
b- junctional tachycardia - no P waves, QRS complexes completely
regular, narrow QRS, normal T waves

10) atrial fibrillation

-irregularly irregular rhythm
-no P waves, irregular baseline, QRS complexes mb irregular or normal
-some waves may resembles atrial flutter (common in AF)

11) ventricular fibrillation

-ECG totally disorganized, no QRS complex can be identified, pt loss of

atrial tachycardia

12) Wolff-Parkinson-White (WPW) syndrome

-short PR interval, QRS complex shows early slurred upstroke called
delta wave
junctional tachycardia
9) ventricular tachycardia
-also called broad complex tachycardia. theres wide QRS, T waves
difficult to identify, no P wave

13) Lown-Ganong-Levine (LGL) syndrome

-short PR with normal QRS

WPW syndrome

LGL syndrome


abN of P wave
1)RA hypertrophy - causes - tricuspid valve stenosis, pulmonary HPT
-P wave peaked
-only significant if features of RVH present
2)LA hypertrophy -causes - usually dt mitral stenosis
-broad & bifid P wave

subendocardial ischemia (exercise induced or during angina atk)

RA hypertrophy

LA hypertrophy

abN of QRS complex

-normal QRS 1. duration <3 small sq
2. V1, S>R
3. in V5-V6, height of R <25 mm
4. V5-V6 may show Q waves dt septal depolarization, but less than
2 mm deep & <1 small sq
1)abN of the width
-abN wide in BBB, or when ventricular ms takes over as focus of
depolarization, or in WPW syndrome
2)height of QRS compex
a-RV hypertrophy
-in V1, R>S
-deep S waves in V6 (clockwise rotation)
-rt axis deviation, peaked P waves,
-in severe cases, inversion of T in V1 & V2, sometimes in V3 & V4
b-pulmonary embolism
-ECG may shows features of RV hypertrophy
-when PE suspected, look for any of following :
-peaked P waves -inverted T in V1 spreading across V2-V3
-rt axis deviation -clockwise rotation
-tall R in V1
-Q wave in lead III resembling inf infarction
c-LV hypertrophy
-tall R in V5-V6, deep S in V1-V2 (but in practical are unhelpful to dx
LV enlargement)
-with significant hypertrophy inverted T in I, aVL, V5, V6,
sometimes V4, there mb left axis deviation
-diffcult to dx minor degrees of LVH
d-MI (tgk nota ACS)
abN of ST segment
-normal - isoelectric - same lvl as part bw T & next P
-elevation - indication of acute myocardial injury, usually dt either to
recent infarction or pericarditis
-horizontal depression ass with upright T wave usualy sn of ischemia as
opposed to infarction eg exercise induced angina
-digoxin downward sloping ST (reversed tick)

abN of T wave
-T wave inversion is seen in the following :
1. normal - leads aVR, V1, sometimes leads III & V2
2. MI/ischemia
4. BBB
3. ventricular hypertrophy 5. digoxin
-biphasic T waves seen in leads adjacent to those
showing inverted T waves
electrolyte abN
-hypoK - T wave flattening + appearance of a hump on end of T wave
called as U wave
-hyperK -peaked T waves with disappearance of ST segment
-QRS complex mb widened
-effects of abN Mg lvl are similar
-hypoCa - prolongation of QT interval
-hyperCa - shortens QT interval
-hypo/hyperNa - no effect on ECG
prolonged QT (>450 ms or 11 small sq)
-causes - Romano-Ward syndrome
-antiarrhythmic drugs (mc) eg amiodarone, procainamide,
disopyramide, sotalol
-other drugs - TCA, erythromycin
-low K, low Mg, low Ca
-sick sinus syndrome - sinus bradycardia + junctional escape (or could
be others eg atrial extrasystole etc)
-pt often asx, but may complain dizziness,
syncope, or sx suggesting paroxysmal tachycardia