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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:
    1. Absent P wave: Af Q
    2. P mitrale: wide P wave (>2.5mm), indicates left atrial enlargement Q (AIIMS May 2014)
    3. 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
  1. P-R interval:
    1. Normal range: 0.12­ - 0.20 Sec. Q
    2. A prolonged P-R interval (> 0.20 Sec) = 1st degree heart block Q.
    3. A short P-R interval (< 0.12 Sec) = WPW Q syndrome.
  2. Ventricular hypertrophy:
    1. LVH sum of S wave in V1 and R wave in V6 is >35mm (SV1 + RV6 > 35) Q.
    2. Pathological Q waves : acute MI: Q , LV aneurysm Q
  3. QT Interval
    1. Normal QT': 0.36-0.44s. Q
    2. QT interval: It varies with rate. Calculate corrected QT interval (QTc) (By using BAZZETT’S Formula Q)
    3. 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.
    4. 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

  1. ST segment:
    1. ST elevation: Acute MI, Prinzmetal's angina, acute pericarditis (saddle-shaped), left ventricular aneurysm.
    2. ST depression: digoxin, angina, acute posterior MI.
  2. T wave: 
    1. Peaked in hyperkalemia Q and Hyperacute phase of acute MI.
    2. Flattened in hypokalemia Q.
  3. Hyperkalemia:
    1. Tall, tented T wave Q,                            
    2. Prolong PR
    3. P-Wave disappear (atrial arrest)                        
    4. Wide QRS ('sine wave' appearance).
    5. The terminal event is either ventricular fibrillation or Asystole. 
  4. Hypokalemia: T waves become smaller and then disappear, prominent U waves Q, prolong PR, ST segment sagging.
  5. Hypercalcemia: Short QT interval Q
  6. Hypocalcaemia: Long QT interval Q.
  7. Digoxin effect: ST depression in V5-6 (Hockey stick sign) Q.
  8. In digoxin toxicity, any arrhythmia or block may occur (ventricular ectopics and nodal bradycardia are common) bigeminy Q is also common. Non-paroxysmal 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 occur Q.

  1. Bundle branch block Delayed conduction is evidenced by prolongation of QRS >0.11s (LQ 2012).  
    1. 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)
    2. 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.
  2. Bifascicular block is the combination of RBBB and left bundle hemiblock Q Either left anterior fascicular block or left posterior fascicular block
  3. Trifascicular block include:
    1. Prolongation of the PR interval (first degree AV block)
    2. Right Bundle Branch Block
    3. 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)

  1. 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.
  2. 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.
    1. Left axis deviation (LAD) is -30' to -90° Q
      1. left anterior hemiblock Q,
      2. Inferior MI.
      3. Right pneumothorax
      4. LVH
      5. ASD (septum primum) (LQ 2012)
    2. Right axis deviation (RAD) is +100 to + 180°. Q
      Causes Q:
      1. RVH,
      2. PE,
      3. Anterolateral MI,
      4. Left posterior hemiblock,
      5. Left pneumothorax.
      6. ASD (Septum secundum)
  3. Causes of low voltage QRS complex Q: (QRS <5mm in all limb leads)
    1. Hypothyroidism
    2. Emphysema
    3. Pericardial effusion
  4. Hypothermia :
    1. Bradycardia,
    2. Osborn (J) wave
  5. Electrical alternans : It is seen in cardiac tamponade due to changes in the ventricular electrical axis due to fluid in the pericardium.
  6. Athletes = ECG finding seen are
    1. Bradycardia,
    2. Ist degree
    3. A degree heart block,
    4. Increase QRS voltage,
    5. T inversion. (In athletes on auscultation S3 is heard normally)
  7. MI:
    1. Within minutes, the T wave may become peaked Q (Earliest features) Q.
    2. With in 2-3 hrs, ST segments may begin to rise (Pardees sign) Q
    3. Within 8-12 hrs, the T wave inverts Q
    4. 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:
    1. Inferior (II, III, aVF) Q,                       
    2. Anteroseptal (V1-V3) Q,
    3. Anterolateral (V4- V6, I, aVL) Q,        
    4. Posterior (tall R and ST depression in V1 – V2). Q
  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 Q or dipyridamole Q may be used if the patient cannot exercise:

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