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By Dr. Zahoor CARDIAC ARRHYTHMIA
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CARDIAC ARRHYTHMIA First we will have quick look at the physiology
SA Node is the pace maker of the heart and is under control of ANS (Sympathetic and Parasympathetic) Heart has its conductive tissue SA Node – Internodal fibers – AV Node – Bundle of HIS – Bundle branches (RBB and LBB) – Purkinje fibers
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CONDUCTIVE TISSUE OF HEART
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CARDIAC ARRHYTHMIA If the sinus rate (SA Node) becomes unduly slow then lower center may assume the role of pacemaker, this is known as ESCAPE RHYTHM Impulse may arise from - AV Node (Nodal Rhythm) or HIS bundle (Junctional Rhythm) or Ventricles (Idioventricular Rhythm)
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CARDIAC ARRHYTHMIA What is CARDIAC ARRHYTHMIA?
It is the disturbance of electrical rhythm of the heart. Why Arrhythmia occur? They are often due to structural heart disease, but may also occur due to abnormal conduction
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CARDIAC ARRHYTHMIA Normal heart rate (HR) 60-100/min
HR > 100/min is called Tachycardia HR < 60/min is called Bradycardia
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CARDIAC ARRHYTHMIA Arrhythmia may be 1. Supraventricular
i- Sinus (SA Node) ii- Atrial iii- Atrioventricular nodal re-entrant tachycardia (AVNRT) 2. Ventricular
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CARDIAC ARRHYTHMIA Important
Supraventricular rhythm produces narrow QRS complex. Why? Because ventricles are depolarized through AV Node and Bundle of His. Ventricular rhythm produce wide, bizarre QRS complex because ventricles are depolarized in an abnormal sequence
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SUPRAVENTRICULAR ARRHYTHMIA
i. SA NODE Sinus Arrhythmia Heart rate increases during inspiration and slows during expiration, it is called sinus arrhythmia. More commonly seen in children. It is physiological. Sinus Bradycardia Sinus rate < 60/min, may occur in healthy people at rest, athlete or it may be pathological e.g. hypothyroidism, increased intracranial pressure
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CAUSES OF SINUS BRADYCARDIA
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SUPRAVENTRICULAR ARRHYTHMIA
Sinus Tachycardia - Physiological Sinus rate > 100/min usually due to increased sympathetic activity associated with emotion, exercise, pregnancy OR It may be pathological e.g. hyperthyroidism, heart failure
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CAUSES OF SINUS TACHYCARDIA
- Some pathological causes
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ii. ATRIAL TACHYARRHYTHMIA
Atrial Tachyarrhythmia may be 1. Atrial extra systole/premature beat/ectopic beat 2. Atrial Tachycardia 3. Atrial flutter 4. Atrial fibrillation
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ATRIAL TACHYARRHYTHMIA
1. Atrial extra systole When there is atrial extra systole, it usually causes no symptoms, but can give the sensation of miss beat or abnormally strong beat Atrial Ectopic Beats – 3rd 4th and 6th complexes
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ATRIAL TACHYARRHYTHMIA
1. Atrial extra systole ECG shows premature beat, P wave has different morphology. Why? Because atria are activated from an abnormal site ( but QRS is normal) Effect – usually no consequence but very frequent atrial ectopic beat may lead to AF Treatment – beta blockers can be used
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ATRIAL TACHYARRHYTHMIA
2. Atrial tachycardia Heart rate is /min, it is due to atrial automaticity, digoxin toxicity ECG produces narrow complex tachycardia (QRS is narrow) with abnormal P wave
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ATRIAL TACHYARRHYTHMIA
2. Atrial Tachycardia Treatment Beta blockers – they reduce automaticity If ventricular response is rapid, A..V node blocking drugs (calcium blockers e.g. verapamil) Cathetor ablation to target the ectopic site in case of recurrent atrial tachycardia
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ATRIAL TACHYARRHYTHMIA
3. Atrial Flutter Atrial rate is approximately 300/min and usually associated with 2:1, 3:1 or 4:1 A.V block (with heart rate of 150, 100, or 75/min) ECG shows saw – toothed flutter waves. It is narrow complex tachycardia
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ATRIAL TACHYARRHYTHMIA
3. Atrial Flutter Management Beta blocker, verapamil, digoxin can be used to control the ventricular rate To restore sinus rhythm, we use direct current, DC cardio version or Amiodarone IV Catheter ablation – 90% chance of complete cure
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation (AF) It is due to abnormal automatic firing in the atria In AF – atria beat rapidly Atrial rate 350 to 500/min but in uncoordinated and ineffective manner The ventricles are activated irregularly at a rate determined by conduction through the AV Node. This produces irregularly irregular pulse
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation ECG shows no P-wave but fibrillation waves. QRS complex is normal but coming at irregular interval
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation It may be 1. Paroxysmal (intermittent, self terminating episode) 2. Persistent (prolonged episode) 3. Permanent AF causes are – coronary artery disease, valvular heart disease, hypertension, hyperthyroidism, alcohol, idiopathic (lone AF)
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation Causes
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation Do ECG, echo cardiogram, thyroid function test Management 1. Paroxysmal AF Paroxysmal AF may not require treatment. Beta blockers are used Other drugs used are digoxin, verapamil to limit the heart rate by blocking AV node Ablation is used for ectopic focus
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ATRIAL TACHYARRHYTHMIA
Management 2. Persistent AF and 3. Permanent AF There are two ways to treat i). Rhythm control – to restore and maintain sinus rhythm by DC cardioversion (after the administration of anti coagulants) Indication – when AF is present < 3months, patient is young, no structural heart disease
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ATRIAL TACHYARRHYTHMIA
Management ( cont ) 2. Persistent and Permanent AF (cont) ii). Rate control using treatment to control ventricular rate and prevent embolic complication Drugs used are digoxin, beta blocker, calcium antagonist e.g. verapamil or diltiazem (they act by increasing AV node delay)
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ATRIAL TACHYARRHYTHMIA
Prevention of thromboembolism in AF Loss of atrial contraction and left atrial dilatation causes stasis of blood in left atrium and may lead to thrombus formation. It predisposes the patient to the stroke. Treatment advised - Warfarin – it decreases the risk by 62% - Aspirin – it decreases the risk by 22%
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SUPRAVENTRICULAR TACHYCARDIA (SVT)
iii. Atrioventricular nodal re-entrant tachycardia (AVNRT)- Junctional-arryhythmias These tachycardia are due to re-entry in a circuit involving AV node. It produces regular tachycardia with a rate of /min. Episode may last from few seconds to many hours
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SUPRAVENTRICULAR TACHYCARDIA (SVT)
Management Carotid sinus pressure – it increases vagal tone IV adenosine or verapamil will restore sinus rhythm in most cases Beta blockers DC cardio version if SVT with hemodynamic compromise Catheter abalation HR 180/min
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WOLFF – PARKINSON WHITE SYNDROME (WPW Syndrome)
In WPW Syndrome, there is abnormal band of conductive tissue which connects atria to the ventricles. It is like Purkinje tissue that conducts very rapidly and is called accessory pathway
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WOLFF – PARKINSON WHITE SYNDROME (WPW Syndrome)
ECG shows short PR and slurring of QRS complex called Delta wave Treatment Carotid sinus pressure IV adenosine Catheter abalation in symptomatic patient For prophylaxis - Amiodarone, flecainide (they slow the conduction in the accessory pathway)
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VENTRICULAR TACHYARRYTHMIA
They are 1. Ventricular ectopic beats 2. Ventricular Tachycardia (VT) 3. Ventricular Fibrillation (VF)
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VENTRICULAR TACHYARRYTHMIA
1. Ventricular ectopic beat (extra systole, premature beat) In ventricular ectopic beat, QRS is broad and bizarre because ventricles are activated by abnormal focus QRS may be unifocal (identical), when they arise from single ectopic focus or QRS may be multi focal (varying morphology) as they arise from multiple foci
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VENTRICULAR TACHYARRYTHMIA
Ventricular ectopic beat (extra systole, premature beat) QRS Complex (arrows) are broad, bizarre with no preceding P wave
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VENTRICULAR TACHYARRYTHMIA
Ventricle ectopic beat may occur in Healthy subject – more prominent at rest and disappear at exercise Treatment in symptomatic patient - beta blocker Ventricular ectopic beat in Heart Disease Occur during acute MI Heart failure Digoxin toxicity Mitral valve prolapse
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2. VENTRICULAR TACHYCARDIA (VT)
ECG shows tachycardia with broad, abnormal QRS complex with a rate of > 120/min
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VENTRICULAR TACHYCARDIA (VT)
Common causes of VT Acute MI Cardiomyopathy Chronic IHD with poor LV function
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VENTRICULAR TACHYCARDIA (VT)
Treatment of VT Synchronized DC cardio version shock, if systolic BP < 90mmHg If VT is well tolerated then - IV Amiodarone as bolus and then continuous infusion - IV lidocaine Note – Correct hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia
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TORSADES DEPOINTES (VENTRICULAR TACHYCARDIA)
This type of VT occurs in patients who have prolonged QT interval (hypocalcaemia, hypomagnesaemia, hypokalaemia) ECG shows bradycardia with long QT interval followed by VT, rapid, irregular QRS complex
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3. Ventricular Fibrillation (VF)
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3. Ventricular Fibrillation (VF)
It is life threatening, medical emergency There is very rapid, irregular ventricular activation with no pumping of blood Patient is pulseless, becomes rapidly unconscious and respiration ceases (Cardiac arrest) Can lead to death in minutes Treatment 1- Defibrillation 2- CPR
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Prolonged PR interval 0.26 second
HEART BLOCKS First degree AV Block In first degree heart block, AV conduction is delayed. PR interval is prolonged > 0.2 second It rarely causes symptoms First Degree AV Block Prolonged PR interval 0.26 second
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HEART BLOCKS Second degree AV Block
In this condition, some impulse from atria to ventricle fail to conduct, therefore, drop beat occur. There are two types 1. Wenchebach’s Phenomenon or Mobitz type I 2. Mobitz type II
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1. Wenckebach’s phenomenon or Mobitz type I Here PR interval progressively increases, until P wave is not followed by QRS (drop beat) Wenchebach’s Phenomenon or Mobitz type I
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2. Mobitz type II – second degree AV block
Here PR interval remains constant but some P wave are not conducted
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HEART BLOCKS Third degree (complete) AV block
There is no conduction taking place through AV node, therefore atria and ventricle beat independently Atrial rate may be 80/min, ventricular rate 38/min
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AV BLOCK Treatment For second and third degree AV block
Atropine 0.6mg IV, repeated as necessary If it fails – temporary pacemaker Permanent pacemaker is indicated in patients with chronic Mobitz type II second degree heart block and third degree AV block because of risk of asystole and sudden death
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Thank you
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