ECG and Arrhythmia

ECG and Arrhythmia (Ref. Hari. 18th ed., pg -1831)

1. Rate: To calculate the rate, divide 1500 Q by
the number of small squares per R-R interval.
2. Rhythm

Af has no discernible P waves Q and the QRS

complexes are irregularly irregular. Q
Atrial flutter has a 'sawtooth' Q baseline of
atrial depolarization and regular QRS

complexes.
3. P wave:
a. Absent P wave: Af Q
b. P mitrale: wide P wave (>2.5mm),
indicates left atrial enlargement
Q

(AIIMS May 2014)

c. P pulmonale: peaked P wave (> 2.5

mm), indicates right atrial
enlargement Q.
Important point.
1. P wave is due to: Atrial depolarization
2. QRS complex indicates:Ventricular
depolarization
4. P-R interval:

a. Normal range: 0.12

- 0.20 Sec. Q
b. A prolonged P-R interval (> 0.20 Sec) =
1st degree heart block Q.
c. A short P-R interval (< 0.12 Sec) =
WPWQ syndrome.
5. Ventricular hypertrophy:
a. LVH sum of S wave in V1 and R wave in
V6 is >35mm (SV1 + RV6 > 35) Q.
b. Pathological Q waves : acute MI: Q , LV
aneurysm Q
6. QT Interval
a. Normal QT': 0.36-0.44s. Q
b. QT interval: It varies with rate. Calculate
corrected QT interval (QTc) (By using
BAZZETTS Formula Q)
c. Prolonged QT interval Q: Congenital,
Electrolyte imbalance (Hypokalemia,
HypocalcemiaQ, Hypomagnesemia Q),
Class 1A anti arrhythmic drugs (quinidine
Q

), bradycardia, head injury, hypothermia,

sotalol Q, antihistamines, macrolides Q (eg

erythromycin), amiodarone Q,
Phenothiazine Q, Tricyclic Q, Torse De
Pointes cerebrovascular accident.
d. Short QT interval: Hypercalcemia,
Hypermagnesemia, Class 1 B anti
arrhythmic drugs, Digoxin, Acute MI.
Extra Edge:
Congenital prolong QT is associated with neonatal
bradycardia.


Extra Edge:
In case of Sub arachnoid hemorrhage increase QT
interval with wide T wave inversion occurs This is
known as CVA T wave pattern
7. ST segment:
a. ST elevation: Acute MI, Prinzmetal's
angina, acute pericarditis (saddleshaped), left ventricular aneurysm.
b. ST depression: digoxin, angina, acute
posterior MI.
8. T wave:
a. Peaked in hyperkalemia Q and Hyperacute
phase of acute MI.
b. Flattened in hypokalemia Q.
9. Hyperkalemia:
a. Tall, tented T wave Q,
b. Prolong PR
c. P-Wave disappear (atrial arrest)

d. Wide QRS ('sine wave' appearance).

e. The terminal event is either ventricular
fibrillation or Asystole.
10. Hypokalemia: T waves become smaller and then
disappear, prominent U waves Q, prolong PR, ST
segment sagging.
11. Hypercalcemia: Short QT interval Q
12. Hypocalcaemia: Long QT interval Q.
13. Digoxin effect: ST depression in V5-6 (Hockey
Q

stick sign) Q.
14. In digoxin toxicity, any arrhythmia or block may
occur (ventricular ectopics and nodal bradycardia
are common) bigeminy Q is also common. Nonparoxysmal atrial tachycardia with variable block
is characteristic.Q
Extra Edge:
In digoxin toxicity all types of arrhythmias and blocks
can happened but atrial flutter, type II B block do not
occurQ.
15. Bundle branch block Delayed conduction is
evidenced by prolongation of QRS >0.11s (LQ
2012).
a. In RBBB, the following pattern is seen:
QRS >0.11s, 'RSR' pattern in V1 dominant
R in V1, inverted T waves in V1-V4, deep
wide S wave in V6.

Causes: normal variant Q (isolated RBBB),

pulmonary embolism, cor pulmonale, MI,
ASD, Ashman syndrome (AIIMS May
2013)
b. In LBBB, the following pattern is seen:
QRS >0.11s, W pattern in V1, 'M' pattern
in V5 V6, no septal Q waves, inverted T
waves in I, aVL, V5-V6.

Causes: IHD, hypertension,

cardiomyopathy, idiopathic fibrosis.
16. Bifascicular block is the combination of RBBB
and left bundle hemiblock Q Either left anterior
fascicular blockor left posterior fascicular block
17. Trifascicular block include:
a. Prolongation of the PR interval (first

degree AV block)
b. Right Bundle Branch Block
c. Either left anterior fascicular block or left
posterior fascicular block
Important Points:
Trifascicular block also is said to occur in cases of
alternating RBBB with LBBB (Ref. Hari. 18th ed., pg
-1835)
18. Pulmonary embolism: Sinus tachycardia Q is
the commonest. There may be RAD, RBBB,

Characteristic feature: the S1 QIII TIII pattern

occurs Q: i.e deep S waves in I, pathological Q
waves in III, inverted T waves in III.
19. Axis: The mean frontal axis is the sum of all
the ventricular forces during ventricular
depolarization. The axis lies at 90 to the
isoelectric complex (ie the one in which
positive and negative deflections are equal).

Normal axis is between -30 and +100 (LQ

2012) (Ref. Hari. 18th ed., pg -1832).As a
simple rule of thumb, if the complexes in leads
I and II are both 'positive', the axis is normal.
a. Left axis deviation (LAD) is -30' to -90
Q.

Causes:
i. left anterior hemiblock Q,
ii. Inferior MI.
iii. Right pneumothorax
iv. LVH
v. ASD (septum primum)(LQ
2012)

b. Right axis deviation (RAD) is +100 to +

180. Q

Causes Q:
i. RVH,
ii. PE,
iii. Anterolateral MI,
iv. Left posterior hemiblock,
v. Left pneumothorax.
vi. ASD (Septum secundum)
20. Causes of low voltage QRS complex Q: (QRS
<5mm in all limb leads)
a. Hypothyroidism
b. Emphysema
c. Pericardial effusion
21. Hypothermia :
a. Bradycardia,
b. Osborn (J) wave
22. Electrical alternans : It is seen in cardiac
tamponade due to changes in the ventricular
electrical axis due to fluid in the pericardium.
23. Athletes = ECG finding seen are
a. Bradycardia,
b. Ist degree
c. A degree heart block,
d. Increase QRS voltage,
e. T inversion. (In athletes on
auscultation S3 is heard normally)

24. MI:
a. Within minutes, the T wave may
become peaked Q (Earliest features)
Q.
b. With in 2-3 hrs, ST segments may
begin to rise (Pardees sign) Q
c. Within 8-12 hrs, the T wave inverts
Q

d. Within 24 48 hrs, pathological Q

waves Q begin to form. Q waves
usually persist in old MI Q.
Extra Edge:
Tall T is the earliest manifestation of acute MI. (FAQ)

Extra Edge:
Causes of ST elevation in ECG (LQ 2012)
1. Acute MI
2. Prinzmetal angina
3. LV aneurysm
4. Acute pericarditis

Site of MI

1. The leads affected reflect the site of the infarct:

a. Inferior (II, III, aVF) Q,
b. Anteroseptal (V1-V3) Q,
c. Anterolateral (V4- V6, I, aVL) Q,
d. Posterior (tall R and ST depression in V1
V ). Q
2

2. 'Non-Q wave infarcts' (formerly called

subendocardial infarcts) have changes without Q
waves.
There is symmetrical T wave inversion. Q

Exercise ECG testing

The patient undergoes a graduated, treadmill exercise

test, with continuous 12-
lead ECG and blood pressure
monitoring. There are numerous treadmill protocols' the
'Bruce protocol' is the most widely used.'
Stress echocardiography is used to evaluate ventricular
function, ejection fraction, myocardial thickening, and
regional wall motion pre- and post-exercise

Extra Edge:
Dobutamine Qor dipyridamole Qmay be used if the
patient cannot exercise:

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