Mechanism of arrhythmogenesis

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Mechanism of arrhythmogenesis

• Abnormal automaticity
• Triggered activity and afterdepolarization
• Reentrant mechanism

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Automaticity Alterations in impulse
initiation
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Abnormal Automaticity

• Causes
• Parasympathetic nervous system activation slows
  the rate of rise of phase 4 depolarization and
  vice versa
• Ischemia, infarction, hypokalemia, beta agonists
  enhance phase 4 depolarization
• Significance
• Atrial tachycardia, accelerated idioventricular
  rhythms, ventricular tachycardia

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Afterdepolarizations and Triggered activity
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Afterdepolarizations and Triggered activity

• EAD (Early AD)
• Due to increase in cytosolic Ca2
• Causes - hypokalemia, hypomagnesemia, hypoxia,
  acidosis, bradycardia, class IA and III
  antiarrhythmics, antihistaminics, phenothiazines
• Significance - torsades de pointes
• DAD (Delayed AD)
• Due to increased Ca2
• Causes- catecholamines, quinidine, caffiene
• Significance - idioventricular rhythms, digitalis
  toxicity

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Reentrant Mechanism
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Reentrant arrhythmias

• Circulation of an activation wave around an
  inexcitable obstacle
• Most common arrhythmia mechanism
• Property of a network of myocytes
• Presence of excitable gap
• In the absence of excitable gap wavefront
  propagates through partially refractory tissue
  with no anatomic obstacle- leading to circle
  re-entry( functional re entry)

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Classification of arrhythmias

• By heart rate
• Bradyarrhythmias
• Tachyarrhythmias
• Conduction blocks
• By anatomic origin
• Supraventricular
• Junctional
• Ventricular
• By type of disorder
• Disorders of impulse formation
• Disorders of impulse conduction

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Disorders of impulse formation

• Sinus rhythms
• Sinus bradycardia
• Sinus tachycardia
• Sinus arrhythmia
• Atrial rhythms
• Premature atrial complexes
• Atrial flutter
• Atrial fibrillation
• PSVT
• Junctional rhythms
• Ventricular rhythms
• Ventricular premature beats
• Ventricular tachycardia
• Ventricular fibrillation

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Disorders of impulse conduction

• Conduction blocks
• Sino atrial blocks
• Atrioventricular blocks
• First degree AV block
• Mobitz type I block
• Mobitz type II block
• Third degree AV block
• Intraventricular blocks
• Hemiblocks
• LBBB
• RBBB

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Sinus Bradycardia
Heart rate lt50 bpm with chronic ßblocker
therapy
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Sinus Bradycardia (contd.)

• Causes Vagal stimulation, increased intracranial
  pressure, hyperkalemia, digoxin, beta blocker,
  hypothyroidism, sedation, obstructive jaundice,
  glaucoma.
• Normal phenomenon in athletes and during sleep

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Sinus Bradycardia Management

• Atropine
• First drug of choice for symptomatic bradycardia
• Dose - 0.5 mg IV bolus repeated every 3-5 min up
  to a total dose of 0.04 mg/kg or 3mg
• Other drugs
• Dopamine 2-10 µg/kg/min infusion
• Epinephrine 2-10 µg/min infusion
• Ephedrine 5-25 mg IV bolus
• Isoproterenol 2-10 µg/min infusion
• Transcutaneous/transvenous pacing
• Symptomatic bradycardia with signs of poor
  perfusion

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SinusTachycardia
QRS complex- normal May be associated with ST
segment depression
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Sinus Tachycardia (contd.)

• Causes
• Pain, inadequate anaesthesia, hypovolemia, fever,
  hypoxia, hypercapnia, cardiac failure, anaemia,
  thyrotoxicosis, drug effects
• Significance
• Prolonged tachycardia increased myocardial
  work, decreased myocardial O2 supply ?can ppt MI
  or CHF in patients with heart disease
• Treatment
• Treat the underlying cause
• Beta blockers and calcium channel blockers

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Sinus Arrhythmia

• Alternate periods of slower and faster rates
• Rate increases with inspiration and decreases
  with expiration
• Common in children and young adults
• Accentuated by vagotonic procedures and
  abolished by vagolytic procedures
• No treatment required

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Atrial Premature Complexes

Rhythm- irregular with incomplete compensatory
pause QRS complex- usually normal unless
ventricular aberration present
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Atrial Premature Complexes

• PACs are of 3 types
• Premature P wave with normal QRS
• Ectopic focus with different morphology from
  sinus P wave
• Premature P wave with no QRS
• P waves occur very early
• AV node in refractory period
• Premature P wave with aberrant ventricular
  conduction
• Impulse reaches the bundle branch when only
  one has fully recovered

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Atrial Premature Complexes

• Increased incidence with age
• More common in patients with chronic rheumatic
  valvular disease, coronary artery disease, CHF,
  hyperthyroidism
• Little clinical significance
• Frequent APCs may trigger more serious
  supraventriculr arrhythmias e.g. atrial
  fibrillation, flutter, PSVT
• Treatment rarely necessary

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Atrial Flutter

• Heart rate - atrial rate 250 to 350 bpm,
  ventricular rate 150 bpm
• Rhythm - atrial rhythm regular
• P wave- saw toothed appearance (F waves),
• F waves best seen in leads II, V1 and
  oesophageal leads
• P/QRS- usually 21 (may vary between 21 and
  81)
• QRS complex- normal, T waves - lost in f waves

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Atrial Flutter (contd.)

• Mechanism
• Re entrant atrial activity (most common)
• Focal discharge
• Significance
• Can be seen in patients with CAD, mitral
  valve disease, pulmonary embolism,
  hyperthyroidism, cardiac trauma, cancer of heart,
  myocarditis

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Atrial Flutter - Management

• Initial treatment - Control of ventricular
  response rate
• ß-blockers - esmolol 1 mg/kg
• Calcium channel blockers - verapamil 5-10 mg or
  diltiazem
• Excessively rapid ventricular response/
  haemodynamic instability/ both
• DC cardioversion starting at 100J and increasing
  to 360J
• Ibutilide 1 mg in 10 ml saline/5 D over 10 min
  4-8 hrs monitoring after treatment
• Procainamide 5-10 mg/kg, no faster than 0.5
  mg/kg/min
• Amiodarone 150 mg over 10 min ? 1 mg/min for 6
  h ? 0.5 mg/min for 18 hrs

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Atrial Fibrillation

• Heart rate- atrial rate 350 to 500 bpm.
  Ventricular rate 60 to 170 bpm
• Rhythm - irregularly irregular
• P wave - absent, f waves or no obvious atrial
  activity
• P/QRS- no p waves
• QRS complex- normal

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Atrial Fibrillation (contd.)

• Most common postoperative arrhythmia with
  significant consequences on patients health
• Associated with old age, thyrotoxicosis, HTN,
  CAD, CHF, RHD, congenital heart disease
• Best seen in leads V1-2 and inferior leads
• Caused by numerous wavefronts of depolarization
  spreading throughout the atria simultaneously
  leading to absence of coordinated atrial
  contraction

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Atrial Fibrillation (contd.)

• Hemodynamic effects
• Loss of mechanical AV synchrony? impairs
  ventricular filling? decreases cardiac output
• Thromboembolism
• After 24-48 hrs
• Atrial thrombi usually arising from left atrial
  appendage
• Increased incidence of stroke(most feared
  consequence)

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Atrial Fibrillation (contd.)

• Risk Factors for development of thromboembolism

Mild risk factors Moderate risk factors High risk factors
Female gender gt75 yrs Previous stroke, TIA
65-75 yrs Hypertension, DM Prosthetic valves
CAD CHF Mitral stenosis
thyrotoxicosis EFlt35 Previous embolism
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Atrial Fibrillation Management

• Control of ventricular rate

Phases Recommended therapy
Acute phase iv diltiazem, metoprolol, esmolol, verapamil
Chronic phase Oral beta blockers digoxin Catheter ablation
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Atrial Fibrillation Management

• Antithrombotic therapy

Risk factors Recommended therapy
No risk factor Aspirin, 81325 mg daily
1 moderate risk factor Aspirin, 81325 mg daily, or warfarin (INR 2.03.0)
gt1 mod risk factor/any high risk factor Warfarin (INR 2.03.0)
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Atrial Fibrillation Management

• Cardioversion

DC approach DC approach DC approach Antiarrhythmic agents Antiarrhythmic agents
lt48 hrs gt48 hrs gt48 hrs 1week Long duration
DC without prior anti- coagulation Oral warfarin(INR 2-3)f/b cardioversion f/b continous warfarin therapy TEE and heparin f/b cardioversion f/b oral warfarin oral flecainide, dofetilide, propafenone, iv ibutilide dofetilide
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Atrial Fibrillation Management

• Post operative atrial fibrillation
• Routine use of beta blockers throughout the
  periop period
• Anticoagulation
• Maintenance of sinus rhythm
• In the absence of structural heart disease-
  flecainide, propafenone
• In the presence of significant structural heart
  disease- sotalol, amiodarone

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Paroxysmal Supraventricular Tachycardia
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Paroxysmal Supraventricular Tachycardia

• Rapid regular rhythm with narrow QRS complex and
  lacking the normal p wave
• ECG characteristics
• Rate 130-270/min
• Rhythm regular
• P/QRS 1 1 (p wave may be hidden in QRS complex
  or T wave)
• QRS complex generally normal

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PSVT - Significance

• Seen in 5 normal young adults
• Accounts for 2.5 of arrhythmias in anaesthetized
  patients
• Not a/w intrinsic heart disease or systemic
  illness
• Precipitated under anaesthesia by changes in
  autonomic nervous system tone, drug effects,
  intravascular volume shifts
• Can produce severe hemodynamic deterioration

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PSVT Management

• Vagal maneouvres applied only to one side
• DOC-iv Adenosine 6mg rapid bolus, 2nd 3rd doses
  of 12 and 18 mg if no response
• Verapamil 2.5-10 mg iv - terminates AVNRT
  successfully, provides long term relief
• Amiodarone 150 mg infusion over 10 min - recent
  addition
• Esmolol 1 mg/kg bolus ? 50-200 mg/kg/min
• Phenylephrine 100 µg- if associated hypotension

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PSVT Management (Contd.)

• Edrophonium or neostigmine iv
• Intravenous digitalization ouabain 0.25-0.5 mg
  iv or digoxin 0.5 -1.0 mg iv
• Rapid overdrive pacing
• Synchronized cardioversion
• Electrode catheter ablation with radiofrequency
  energy

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Junctional Rhythm

• AV node and sites above and below it act as
  pacemaker
• Heart rate- variable, 40 to 180 bpm
• Rhythm- regular
• P/QRS- 11
• QRS complex- usually normal

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Junctional Rhythm (contd.)

• Types
• High nodal rhythm- impulse reaches atrium before
  ventricles, P precedes QRS, short PR interval
• Mid nodal rhythm- impulse reaches atrium and
  ventricle at the same time, P lost in QRS
• Low nodal rhythm- impulse reaches ventricles
  before atrium, P follows QRS
• Common in patients under anaesthesia(20)
  especially with halogenated anaesthetic agents

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Junctional Rhythm (contd.)

• Treatment
• Usually reverts spontaneously, no treatment
  required
• If associated with hypotension poor perfusion
  t/t with atropine/ ephedrine/ isoproterenol
• Dual chamber electrical pacing

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Ventricular Premature Beats

• VPB s arise from ectopic pacemaker activity
  arising in the ventricles
• Heart rate variable, Rhythm irregular,
  Compensatory pause seen
• P/QRS- no P wave associated with VPB
• QRS complex- Wide, bizarre, gt0.12 s
• QRS and T wave point in opposite direction

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VPB - Types

• Early in the cycle - R on T phenomenon,
  dangerous in acute ischaemic situation because
  ventricles are prone to VT and VF
• After T wave
• Late in the cycle fusing with next QRS - fusion
  beats

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VPB (contd.)

• Unifocal, multifocal
• Causes hypoxia, electrolyte imbalance, blood gas
  abnormality, digitalis toxicity, CHF, MI
• Common during anaesthesia(15) especially in
  patients with pre existing cardiac disease

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VPB - Significance

• May progress to VT or VF in following situations
• Coronary artery insufficiency, MI
• Digitalis toxicity with hypokalemia
• Hypoxemia
• Multiple, multifocal or bigeminal VPB
• R on T phenomenon

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VPB Management

• Maintain adequate depth of anaesthesia
• Oxygenation and ventilation are the initial
  treatment for all kinds of ectopics
• Correct underlying abnormalities
• Treat if hemodynamic impairment or harbinger of
  worse arrhythmias
• Lidocaine(TOC) 1.5 mg/kg initial bolus f/b
  infusion_at_1-4 mg/min
• Other drugs beta blockers, procainamide ,
  calcium channel blockers, atropine, disopyramide,
  quinidine

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Ventricular Tachycardia

• Definition
• 3 or more VPB s in a row
• Types(depending on morphology)
• Monomorphic- all QRS complexes have same
  morphology
• Polymorphic- more than 1 morphology
• Torsades de pointes Polymorphic VT with long
  QTc
• Types(depending on duration)
• Non sustained- upto 30s
• Sustained- gt30s

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Ventricular Tachycardia

• Heart rate -100 to 200 bpm
• P/QRS- no fixed relationship due to AV
  dissociation
• QRS complex- wide and bizarre, gt0.12 s, similar
  to VPB

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Ventricular Tachycardia (contd.)

• Causes MI, hypoxia, electrolyte imbalance,
  myocardial trauma, digitalis toxicity
• Mechanism usually caused by re entry and most
  commonly seen in patients following MI
• Complications decreases cardiac output,
  decreases cardiac perfusion, increases cardiac
  workload, can deteriorate into VF

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VT Management

• Acute onset is life threatening and requires
  immediate treatment
• Treat the precipitating metabolic or toxic causes

Monomorphic VT Monomorphic VT Polymorphic VT Polymorphic VT
Hemodynamically stable Hemodynamically unstable Normal QT Prolonged QT
iv amiodarone 150 mg in 100ml NS over 10min f/b infusion iv procainamide 20mg/min iv lidocaine 1 mg/kg cardioversion iv amiodarone 150 mg slow cardioversion iv infusion of 1g magnesium over 2-3 min
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Torsades de pointes
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Ventricular Fibrillation

• An irregular rhythm that results from rapid
  discharge of impulses from one or more
  ventricular foci or from multiple wandering
  reentrant circuits in the ventricle
• Ventricular contractions erratic, bizarre
  patterns of various sizes and configurations
• Causes MI, hypoxia, hypothermia, electrolyte
  imbalance, electric shock, drugs
• Significance No effective CO, life must be
  sustained by artificial means

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Ventricular Fibrillation
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VF - Treatment

• CPR immediately and then asynchronous external
  defibrillation
• Manual biphasic device specific 120-200 J
• Monophasic 360 J
• AED device specific
• Epinephrine 1 mg IV every 3 to 5 min or
  Vasopressin 40U iv bolus
• Consider amiodarone, lidocaine, magnesium sulfate
  

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Conduction Blocks

• Chronic, represent underlying disease state of
  myocardium or conduction system
• Types
• Sinoatrial block
• AV block
• Incomplete- 1and 2
• Complete- 3
• IV conduction block

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Sino atrial block

• Sinus impulse is blocked within the SA junction
• No atrial or ventricular activation
• No P wave or QRS complex recorded

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Sino atrial block - Significance

• SA block rare, found in same conditions as marked
  sinus bradycardia or sinus arrhythmia
• Young vagotonic individuals, particularly
  athletes
• Digitalis administration
• Uraemia
• Hypokalemia
• May be an expression of Sick Sinus Syndrome

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First degree AV block

• PR interval gt0.20 sec all P waves conduct to
  the ventricles
• Healthy individuals, CAD, digitalis
  administration, acute rheumatic carditis, beta
  blockers
• Requires no treatment

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Mobitz Type I / Wenkebach Block

• Progressive lengthening of PR interval till an
  impulse is not conducted and the beat is dropped
• Relatively benign and often reversible
• Pacemaker not required
• Causes MI, digitalis toxicity
• Reflects disease of AV node

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Mobitz Type II Block

• Dropped beats occur without progressive
  lengthening of PR interval
• Less common, more serious
• Disease of His bundle or purkinje fibres
• Serious prognosis, frequently progresses to
  complete block
• Treatment pacemaker insertion

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Third Degree AV Block

• AV dissociation
• QRS complex may be normal or widened
• HR usually too slow to maintain adequate CO
• Treatment- transvenous endocardial or epicardial
  pacemaker(dual chamber)

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Left anterior fascicular block

• Delayed activation of antero-superior division
  of left bundle
• Left axis deviation in frontal plane, usually
  -45 to -90 degrees
• Deep S waves in leads II, III, aVF
• tall R wave in aVL
• QRS duration usually lt0.12s unless coexisting
  RBBB

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Left anterior fascicular block-Causes

• MI
• Fibrosis due to chronic coronary insufficiency,
  chronic cardiac failure
• Fibrosis in chronic cardiomyopathy
• Left ventricular hypertrophy
• Calcareous encroachment on left bundle branch
  from aortic valve or interventricular septum

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Left posterior fascicular block

• Right axis deviation
• Prominent S waves in leads I, aVL
• Tall R waves in leads II, III, aVF
• Secondary changes in T wave
• QRS duration normal

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Left Bundle Branch Block

• Prolonged QRS duration gt 120 msec
• ST-T abnormalities
• Broad notched, M shaped R waves in left sided
  leads I, aVL, V5, V6, no initial q waves
• Wide and notched QS in right sided leads
• QRS axis - variable

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LBBB - significance

• Ominous prognostic sign
• Reflects severity of underlying cardiac disease
• Obscures or simulates other patterns on ECG
• Makes diagnosis of LVH, acute ischaemia or MI
  difficult or impossible

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Right Bundle Branch Block

• Prominent notched R waves on right sided leads
• Wide S waves on left sided leads
• QRS prolongation gt120msec
• ST-T waves discordant with QRS complex

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RBBB (contd.)

• Incomplete RBBB
• Diminution of S wave in lead V2
• Slurring of upstroke of S wave in V2
• Small r deflection in V2
• Increased R amplitude in V2
• QRS complex lt 0.11 s

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RBBB - Significance

• Common in general healthy population no
  prognostic significance in this group
• In patients with organic heart disease, new onset
  of RBBB predicts higher rate of CAD, CHF and
  mortality

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Arrhythmia Management
Sinus arrhythmia No treatment required
Sinus bradycardia Atropine dopamine, epinephrine
Sinus tachycardia ß-blockers, CCB
Atrial premature beats Treatment rarely necessary
Atrial flutter Rate control, Cardioversion
Atrial fibrillation Rate control, cardioversion, antithrombotic
PSVT Carotid sinus massage, adenosine, ß-blocker
Junctional bradycardia Junctional tachycardia Atropine ß-blocker, CCB
Ventricular premature beats Lignocaine
Ventricular tachycardia Amiodarone, lignocaine, cardioversion
Ventricular fibrillation Defibrillation CPR
Torsades de pointes Magnesium
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Cardioversion

• DC discharge synchronized with peak of R wave in
  QRS complex
• Indications
• Wide or narrow QRS complex tachycardia in
  unstable patients
• Stable VT not responding to iv medications
• Hemodynamically unstable AF, Atrial flutter, SVT

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Cardioversion (contd.)

• Advantage
• Avoids delivery of a shock during cardiac
  repolarization thus avoiding precipitation of VF
• Energy requirements
• AF- 100 to 200J monophasic initially?360J or
• 75J of biphasic
• Atrial flutter and PSVT- 50J initially?100J
• VT- 50J initially?200J

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Cardioversion (contd.)

• Successful cardioversion depends on
• Adequately anaesthetized
• Shock must be synchronized with the QRS complex
• Conductive pre gelled pads to be used

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Antiarrhythmic agents
Class Action Drugs Clinical uses
Ia Na channel block (intermediate association/dissociation) Quinidine, procainamidedisopyramide Ventricular arrhythmias, prevention of paroxysmal recurrent atrial fibrillation, procainamide in WPW syndrome
Ib Na channel block (fast association/dissociation) Lidocaine, phenytoin, mexiletine Ventricular tachycardia, atrial fibrillation
Ic Na channel block (slow association/dissociation) Flecainide, propafenone, moricizine Prevention of paroxysmal atrial fibrillation, recurrent tachyarrhythmias
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Antiarrhythmic agents(contd.)
Class Action Drugs Clinical uses
II Beta blockers Propanolol, esmolol, metoprolol, atenolol Decreases MI mortality, pevent recurrence of tachyarrhythmias
III Potassium channel blockers Amiodarone, sotalol, ibutilide, dofetilide WPW syndrome, atrial fibrillation and ventricular tachycardia(sotalol), atrial flutter(ibutilide)
IV Calcium channel blockers Verapamil, diltiazem Prevent recurrence of PSVT, reduce ventricular rates in AF
Other drugs Enhances vagal activity Digoxin, Atrial fibrillation, AVNRT
Other drugs Prolonged hyperpol. adenosine PSVT
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Adverse effects
Drugs Adverse effects
Quinidine QT prolongation, Torsades de pointes, cinchonism
procainamide QT prolongation, Torsades, hypotension, LE like picture
disopyramide Urinary retention, dry mouth, constipation
lidocaine Neurologic(mc), proarrhythmic
mexiletine neurologic
flecainide proarrhythmic
moricizine Dizziness, nausea
propafenone Metallic taste
Drugs Adverse effects
Propanolol, esmolol, atenolol, metoprolol Worsening of angina, bronchoconstriction, sudden cardiac death
amiodarone Bradycardia, heart blocks, Pulmonary fibrosis, thyroid dysfunction, corneal deposits, photodermatitis, hepatitis
Dofetilide, ibutilide Prolonged QTc
Verapamil AV block, VF, peripheral edema
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References

• Millers Anaesthesia. 7th edition. Ronald D.
  Miller42
• Millers Anaesthesia. 6th edition. Ronald D.
  Miller
• Harrisons Principles of Internal Medicine. 17th
  edition221
• An introduction to electrocardiography. 7th
  edition. Leo Schamroth
• Meek S, Morris F. ABC of clinical
  electrocardiography. BMJ 2002324470-473

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