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Arrhythmias (Ref. Hari. 18th ed., Pg-1867)

  1. Sinus tachycardia: Rate> 100
    1. Anaemia,
    2. Exercise,
    3. Hypovolemia,
    4. Heart failure,
    5. Pulmonary embolism,
    6. Pregnancy, thyrotoxicosis.
  2. Sinus bradycardia: Rate <60.
    1. Physiologic:- Athletes, elderly person, during sleep, 
    2. Pathologic:-  Vasovagal attacks, sick sinus syndrome, acute MI (esp. inferior) Q, drugs Q (Beta-blockers, digoxin, amiodarone, verapamil), hypothyroidism Q, hypothermia Q,  increase intracranial pressure, Deep jaundice.

      1. If asymptomatic and rate <60b/mt, no treatment is required Q.
      2. If rate <60bpm & patient is symptomatic, give atropine Q 0.6-1.2mg IV (up to maximum of 3mg).
      3. If no response start an isoprenaline Q  infusion or use temporary cardiac pacing Q. 
  3. Heart block
    1. 1st degree heart block = Prolong PR interval i.e. PR interval > 0.20 second.
    2. 2nd degree heart block = Mobitz Type I (Wenckebach phenomena)
      1. Mobitz I heart block is characterized by progressive prolongation of the PR interval on ECG on consecutive beats followed by a blocked P wave (i.e., a 'dropped' QRS complex). After the dropped QRS complex, the PR interval resets and the cycle repeats.
        Causes: Normal variant, athletes, sick sinus syndrome, IHD, acute carditis,.
      2. Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening.
    3. 3rd degree complete heart block:
      Causes: Idiopathic (fibrosis), congenital Q, IHD, aortic valve calcification, cardiac surgery/trauma, digoxin toxicity Q, infiltration (abscesses, granulomas, tumours, parasites).
  4. Sick sinus syndrome: Sinus node dysfunction causes bradycardia Q sinus arrest Q sinoatrial block Q or SVT alternating with bradycardia/asystole (tachy-brady syndrome Q). Af and thromboembolism may occur. Pace if symptomatic.
  5. SVT
    1. SVT. Narrow complex tachycardia (rate> l00bpm, QRS width <120ms),
    2. Acute management: Vagotonic maneuvers followed by IV adenosine, esmolol or verapamil (if not on B-blocker); DC shock if hemodynamically compromised.
    3. Maintenance therapy: B-blockers or verapamil.
  6. Atrial flutter
    ECG: continuous atrial depolarization (eg -300/min, but very variable) produces a sawtooth appearance 2: 1 AV block Q.
    Carotid sinus massage Q and IV adenosine Q transiently block the AV node and may unmask flutter waves.
    Treatment of Atrial flutter
    1. Control ventricular rate with digoxin Q
    2. Alternatives: Verapamil, Beta-blocker, or amiodarone Flecainide Q
    3. DC shock Q if hemodynamically compromised.
    4. Finally, permanent pacing Q may be used to overdrive tachyarrhythmias, to treat
​​Atrial flutter with 2:1 AV bradyarrhythmias, or prophylactically in conduction disturbances
Implanted automatic defibrillators can save lives.
  1. WPW syndrome (Wolff-Parkinson-White) (LQ 2012)
    1. WPW syndrome is more common in males.
    2. It can occur in a normal heart. It is seen in MVP, cardiomyopathy, Ebstein anomaly.
    3. It is caused by bundle of Kent which is a congenital abnormal extra or accessory conduction pathway between the atria and ventricles.
    4. This pathway may communicate between the left atrium and the left ventricle, in which case it is termed a "type A pre-excitation", or between the right atrium and the right ventricle, in which case it is termed a "type B pre-excitation". 
    5. Problems arise when this pathway creates an electrical circuit that bypasses the AV node. The AV node is capable of slowing the rate of conduction of electrical impulses to the ventricles, whereas the bundle of Kent lacks this capability.
    6. When an aberrant electrical connection is made via the bundle of Kent, tachydysrhythmias results.
    7. Resting ECG shows short P-R interval Q and wide QRS complex Q due to slurred upstroke or delta wave Q
    8. Patients present with Supra Ventricular Tachycardia.
Diagnoses of WPW syndrome: His bundle study (Electrophysiology)

Treatment of WPW syndrome
  1. Vagal stimulation
  2. Injection adenosine
  3. Calcium channel blocker            
  4. Procainamide
  5. Beta blocker   
  6. IA or IC antiarrhythmic drug such as quinidine, flecainide, or propafenone are used in AF with fast ventricular rate because these drugs slow conduction & increase refractoriness in the WPW syndrome. (Ref. Hari. 18th ed., pg -1891)(LQ 2012)  
Ablation of the abnormal pathway is the most Definite therapy. 
  1. Best treatment is ablation of accessory pathway is the best treatment.
    NB. Digoxin is absolutely CI in the treatment of WPW syndrome)


A characteristic delta wave (arrow marked) seen in a person with WPW syndrome. Note the short PR interval.


Extra Edge:

There are only two conditions where digoxin is absolutely contraindicated. The first one WPW syndrome and other is HOCM!!! (LQ 2012)

  1. Atrial fibrillation (Af) (Ref. Hari. 18th ed., pg -1881)
    Important Points:
    1. Af is a chaotic, irregular atrial discharge ratio is at 450-600 bpm; the AV node responds intermittently,hence an irregular ventricular rate.
    2. Cardiac output drops by 20% -30%.
    3. Af is common in the elderly.
    4. The main risk is embolic stroke Q.
    5. Warfarin reduces this.
    6. Causes
      There are 4 main causes:
      1. 1. CAD
      2. 2. HT
      3. 3. RHD
      4. 4. Hyperthyroid
​​​​Others: CHF, ASD, alcohol, Tea, Coffee, Congenital

Symptoms May be asymptomatic or cause chest pain, palpitations Q, dyspnoea, or faintness Q.


Signs: Irregularly irregular pulse Q, the apical pulse rate is greater than the radial rate Q and the heart sound is of variable intensity Q .


Tests ECG shows absent P waves Q, irregular QRS complexes Q.




For acute control of Af:

  1. Injection verapamil                  
  2. Beta blocker
  3. Injection IBUTILIDE                  
  4. Synchronize DC shock of 50 to 100 Joules. 

Treatment of chronic Af

  1. Beta-blocker.
  2. If fails and no LV dysfunction used sotalol Q.
  3. Alternative if LV dysfunction used amiodarone Q
  4. Digoxin in RHD
  5. Use anticoagulant till INR more than 1.8.
  6. Surgical treatment of Af = MAZE procedure.
  1. Ventricular extrasystoles (ectopic) are the commonest Q post-MI arrhythmia.
    1. They are also seen in healthy people
    2. Post-MI they suggest electric instability, and there is a risk of VF if the R on T pattern (ie no gap before the T wave) is seen.
    3. If frequent (> 10/min), give amiodarone. 
  2. VT:
    VT Broad complex tachycardia (rate >100 bpm, QRS duration >0.12 s Q)
    Acute management IV lidocaine Q (= Lignocaine), or amiodarone Q  IV, if no response than give DC shock Q.
    1. Amiodarone Q 300mg IV over 20-60min, then 900mg over 24hr or
    2. Lidocaine Q 50mg over 2min repeated every 5min to 200mg max.
    3. If this fails, or if cardiac arrest, use DC shock Q.
    4. After correction of VT, establish the cause from history/investigations.
      1. If VT occurs >24h after MI, give IV lidocaine infusion Q and start oral antiarrhythmic: eg amiodarone Q.
      2. Prevention of recurrent VT: Surgical isolation of the arrhythmogenic area or implantation of tiny automatic defibrillators may help.
  3. Ventricular fibrillation (VF): Use asynchronized DC shock Q
  4. Broad complex tachycardia
    1. ECG shows rate of > 100 and QRS complexes> 120ms
    2. If no clear QRS complexes, it is VF or asystole.
      Differential diagnosis
      1. VT
      2. PSVT with aberrant conduction, eg AF, atrial flutter
  1. Identification of the underlying rhythm ECG findings in favors of VT:
  2. Positive QRS concordance Q in chest leads
  3. Marked left axis deviation
  4. AV dissociation (occurs in 25%) or 2:1 or 3:1 AV block
  5. Fusion beats Q or capture beats Q
  6. RSR complex in V1 (with positive QRS in V1)
  7. QS complex in V 6 (with negative QRS in V6)

Important Points:

  1. Concordance means QRS complexes are all +ve or -ve.
  2. A fusion beat is when an 'normal beat' fuses with a VT complex to create an unusual complex,
  3. Capture beat is a normal QRS between abnormal beats.
  1. Torsades de pointes:
    1. It refers to VT characterized by polymorphic QRS complexes that change in amplitude and cycle length, giving the appearance of oscillations around the baseline. (“Twisting Of The Points”; polymorphic VT associated with long QT intervals) 
    2. It may result from –
      1. Electrolyte disturbances (particularly hypokalemia and hypomagnesemia),
      2. Use of a variety of antiarrhythmic drugs (especially quinidine),
      3. Phenothiazine
      4. Tricyclic antidepressants,
      5. Bradyarrhythmias, particularly third-degree AV block.
      6. May occur as a congenital anomaly that most often presents with torsades de pointes (syncope or sudden death) at a young age.
    3. The ECG hallmark is polymorphic VT preceded by marked QT prolongation, often in excess of 0.60 s.
    4. These patients often have multiple episodes of nonsustained polymorphic VT associated with recurrent syncope, but they may also develop VF and sudden cardiac death.
  1. Treatment of congenital long QT syndrome.
    1. Best treatment is implantable cardioverter/defibrillator (ICD) device. (LQ 2012)
  2. Treatment of acquire long QT syndrome.
    1. Magnesium sulphate
    2. Potassium
  1. Accelerated Idioventricular Rhythm (AIVR)  (Ref. Hari. 18th ed., pg - 1891)
    1. AIVR refers to a ventricular rhythm that is characterized by three or more complexes at a rate >40 beats/min and <120 beats/min. Mechanism is due to abnormal automaticity.
    2. AIVR has a characteristic gradual onset and offset and more variability in cycle length. It is typically a brief, self-limiting arrhythmia.
    3. AIVR can be seen in
      1. Acute myocardial infarction,
      2. Cocaine intoxication,
      3. Acute myocarditis,
      4. Digoxin intoxication,
      5. Postoperative cardiac surgery.
    4. In the setting of sustained AIVR, hemodynamic compromise can occur because of the loss of AV synchrony.

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