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Brady Tachy Lecture 2

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Brady Tachy Lecture 2 Powered By Docstoc
					Disorders of Cardiac Rhythm
          Bernard C. Nkum
            MD FWACP
     School of Medical Sciences
   Komfo Anokye Teaching Hospital
              Objectives
• To understand basic cardiac cellular
  mechanisms of action potential
• To understand the concepts of impulse
  formation and propagation
• To become familiar with the mechanisms
  of clinical arrhythmias
• To diagnose and manage the common
  clinical arrhythmias
        Cardiac Action Potential
• The cardiac action potential has a characteristic time
  course that depends on sequential changes in
  membrane permeability which are due to activation and
  inactivation of ionic channels
• Types of Action Potential: Spectrum
   – SA and AV nodes: Contain pacemaker cells and have slow
     upstroke velocity (10-15 V/s) and very slow spontaneous
     depolarization between action potentials (pacemaker
     depolarization);
   – Ventricular: At the opposite end of the scale are ventricular
     action potentials that have a fast upstroke (200-400 V/s) and no
     spontaneous depolarization between action potentials
   – Atrial similar to vent but shorter duration
   – Conducting cells (e.g., Purkinje fibres): Similar to vent but may
     display spontaneous depolarization
Anatomy of Cardiac Conduction
           System
  Phases of the Action Potential
• 5 Phases
   –   Phase 0: Rapid Depolarization
   –   Phase 1: Early Repolarization
   –   Phase 2: Plateau Phase
   –   Phase 3: Rapid Repolarization
   –   Phase 4: Resting Phase

• Phases 1 and 2 along with the early part of Phase 3 are
  known as the absolute refractory period. A cell in these
  stages cannot receive further stimulation
• last half of Phase 3 is known as the relative refractory
  period. A cell in this stage can only respond to a stimulus
  which is larger than normal
    Phases of the Action Potential
•   Phase 0: rapid depolarization; the result of Na+ permeability (INa)
•   Phase 1: a brief phase of repolarization due to transient outward current of
    K+ (Ito)
•   Phase 2: plateau phase; the result of a delicate balance between a small K+
    outward membrane current (I K) and a slow Ca 2+ inward current (I Ca)
•   Phase 3: repolarization which is due to inactivation of the slow inward Ca2+
    current, activation of the outward-going K+ current (IKl ) and the electrogenic
    Na-K pump ( IP)
•   Phase 4: diastolic portion of the action potential

•   Nodal cells: Normal automaticity is a net result of the absence of I Kl and
    the presence of If. Spontaneous diastolic depo occurs as a result of the
    activation of the pacemaker current If .This forms the basis of automaticity.
     – Phase 0 is the result of increased Ca 2+ influx (I Ca)
     – In the nodal cells (IKl ) is not present
 Clinical Arrhythmia, Mechanisms
          and Drug Action
Impulse formation
  – Automaticity (Sinus tachycardia)
  – Triggered (Digoxin induced arrhythmia)
• Impulse conduction (Reentry)
  – Na channel depend: Long excitatory gap-
    Flutter I, WPW; Short excitatory gap- Afib,
  – Ca channel depend: AVNRT, Verapamil sens
    VT
Disorders of Impulse Formation
• Normal automaticity: Defined as spontaneous diastolic
  depolarization (phase 4) that occur in cells with intrinsic
  automatic mechanisms, normally the SA node but occ in
  specialized atrial cels, in some regions of the AV junction
  and in Purkinje fibres. Atrial and vent cells normally do
  not demonstrate automaticity.
• Intrinsic automaticity is dependent on 3 factors
   – Slope and rate of phase 4 depo which set the rate of impulse
     formation
   – The threshold potential –the potential at which an action
     potential is initiatedand
   – The maximal diastolic potential – the potential from which phase
     4 depo begins spontaneously
      Factors Affecting Phase 4
•   Autonomic mediators
•   Acid –base changes
•   Hypoxia
•   Temperature
•   Cardioactive medications
•   Tissue stretch
       Abnormal Automaticity
• Definition: Alteration of the normal automatic
  mechanisms (enhanced automaticity, in cells
  with intrinsic automatic mechanism) or an
  occurrence of abnormal automatic mechanism in
  cells that do not have automatic intrinsic
  mechanisms.
• Occurs when resting membrane potential is
  partly depo (ie in injured atrial/vent cells)
• Eg: Ectopic atrial tachy
           Triggered Activity
         (Afterdepolarizations)
• Arrhythmias originating in afterdepo, the
  genesis of which is dependent on previous
  electrical activity
  – Early afterdepo: phase 2 and phase 3
  (Torsades depointes)
  – Delayed afterdepo: after complete depo
    (phase 4)
  (digoxin toxicity, ischemia, hypokalemia,
    hypercalcemia- all these lead to increased
    intracellular calcium)
    Abnormal Impulse Conduction
             (Reentry)
3 pre-requisites
• At least 2 functionally distinct conduction
  pathways
   – Pathways may be anatomically (accessory AV) or
     functionally (dual AV nodal pathway) distinct
   – E.g.,: Fibrosis and infarction
• Unidirectional block in one pathway
• Slow conduction down the second pathway
    Basic Electrophysiology and
           Pharmacology
• Ventricular Action Potential
  – Phase 0: QRS complex
  – Phases 1 and 2: ST segment
  – Phase 3: T wave
  – Phase 4: Isoelectric baseline

  The duration of the action potential corresponds
   to the QT interval
Reentry Tachycardia Mechanism
     Cardiac Action Potential and
        Underlying Currents
Phase     SA       Atrial AV     Purkinj   Vent
          node     myocar node   fibre     myocar
Amp       50-60    2x SA   70-80 2x SA  2xSA
Vmax      1-10     100-20  5-15  500-70 100-20
Curren    Ca/Na    Na      Ca/Na Na     Na
Oversh    -        30      -     30     30
Curren    -                -
AP dur    175-25   200-25 100-17 250-40 200-30
Velocit   <0.05    0.3-0.4 0.1   2-3    0.3-0.4
Dia pot   50-60    80-90 60-70 90-95 80-90
 Vaughan William Classification
• Class I: Block sodium channels
• Class II: Block cardiac beta adrenergic
  receptors
• Class III: Characteristically prolong
  refractoriness
• Class IV: Calcium channel antagonists
• Other: Adenosine, ATP, Digoxin, Atropine
        VW Classification of Anti-
Class I       Arrhythmics
          Class II  Class III Class IV

1A           Acebutolol Amiodaron Diltiazem
Disopyrami   Atenolol    Bretylium Verapamil
Procianami   Esmolol     Sotalol
Quinidine    Sotalol
1B           Propranolol
Lidocaine
1C
Fleicanide
Propafenon
 History in Detecting the Cause of
            Palpitations
Description of            Probable Cause
Palpitations
Occ “flip flop” or        PVCs or PACs
“skipped beats”
Sudden onset, rapid and   SVT or VT
regular
Sudden onset, rapid,      PAF
irregular
Sudden onset regular      Sinus tachycardia
with exercise
Associated with drugs     Tobacco, coffee, tea, etc
Normal Sinus Rhythm
            Sinus Tachycardia
• Pathophysiology: Normal impulse formation and
  conduction
• Defining criteria and ECG:
  –   Rate > 100bpm
  –   Rhythm sinus
  –   PR < 0.20s
  –   QRS complex normal
• Clinical features: None specific. Symptoms due
  to underlying cause (fever, hypovolaemia,
  normal exercise, anxiety, hyperthyroidism)
• Rx: Underlying cause
Sinus Tachycardia Cont’d
            Tachyarrhythmias
• Classified as supraventricular or vent.
• SVT: Defined as a tachy in which either the
  atrium or the AV tissue is the source for initiation
  and maintenance.
• The term SVT is used broadly to describe any
  arrhythmia whose origin is above the vent. Since
  VT and VF are tachy of vent origin, they are
  excluded from the SVT category. All other
  tachys, however fall into this category.
      Tachyarrhythmias cont’d
• Prevalence: 2.25 per1000
• Onset can occur at any age
• Age of onset for AVNRT (4th decade) is higher than for
  accessory pathway mediated tachy (AVRT) (3rd decade).
• Classification
   – AV node dependent SVT
      • AVNRT: Reentrant circuit within the AV node
      • AVRT: Utilizes an accessory pathway for one direction of the circuit
        and an AV node for the other.
   – Non-AV node dependent SVT
      •   Sinus tachy
      •   Focal atrial tachy (uni- or multifocal)
      •   Atrial reentrant tachy (including atrial flutter)
      •   Atrial fibrillation
Atrial Flutter
                               Atrial Flutter
•   Significance: Rarely seen in normal hearts. It typically occurs in CAD. As in Afib,
    there is loss of “atrial kick” and concern that AF may contribute to a diminished CO.
    The faster the vent rate, the more chance that the CO will be compromised.
•   Causes
     –   Ischemic heart disease
     –   Valvular heart disease
     –   Cardiomyopathy
     –   Hypertensive heart disease
     –   Hypoxia
     –   Post cardiac surgery
•   Treatment
     –   Depends on clinical condition and haemodynamic stability of the patient
     –   May convert spontaneously to NSR.
     –   Control the rate
     –   Convert the rhythm
     –   Synchronized cardioversion
     –   Radio-frequency catheter ablation
     –   Rapid atrial (overdrive) pacing
     –   Provide anticoagulation
                      Atrial Flutter
• Common form of atrial reentrant tachy that involves a single rapidly
  firing reentrant circuit in the right atrium that propagates
  counterclockwise around the atrial side of the tricuspid valve.
• Caused by enhanced automaticity or reentry
• Electrical impulses are conducted through the atria so fast that
  normal P waves cannot be produced
• Instead of P waves, flutter or “F” waves are formed which which
  have a characteristic “ sawtoothed” appearance.
• Due to the fast atrial rate the AV node is not able to repolarize quick
  enough to conduct all the impulses to the ventricles
• Atrial impulse is usually blocked at the AV node in a pattern e.g., 2:1
  (for every two flutter waves one is conducted through the AV node to
  generate one QRS.
               Atrial Flutter
            ECG Characteristics
• Characterized by sawtoothed waves instead of P waves
• Rhythm: Atrial is regular. Vent may be reg or irreg
• Rate: Atrial rate varies from 220-350. The vent rate may
  vary , described in terms of the ratio of F waves to QRS
  Atrial (F) waves may be buried in QRS, ST segment or T
  waves
• P-P interval: Regular F-F interval
• P-R Interval: Cannot be assessed
• QRS: Usually narrow.
• R-R interval: May be regular or irregular
Atrial fibrillation
                   Atrial fibrillation
• Definition: Irregularly irregular rhythm – with variation in
  both interval and amplitude from R wave to R wave.
• Pathophysiology:
   – Atrial impusles faster than SA impulse
   – Mechanism of impulse formation:
       • Multiple chaotic random depolarizing pathways through the atrial
         tissue. “Multiple wavelet” hypothesis: Basis for the maze procedure.
       • Rapidly firing ectopic focus especially in structurally normal hearts::
         Pulm vein mapping or isolation and catheter ablation.
   – Some impulses are completely blocked at the AV node, others
     are conducted to the ventricles at irregular intervals
   – Atria quiver or “fibrillate” instead of contracting
   – Fibrillatory activity in the atria produces a characteristic irregular
     wavy pattern (fibrillatory waves) instead of P waves.
         Physical Examination
•   Irregularly irregular HR
•   Variable pulse volume
•   Absence of P wave of the JVP
•   Variable S1 intensity
              Atrial Fibrillation
             ECG Charateristics
• Characterized by a wavy baseline with coarse or fine
  fibrillatory waves and an irregular vent response.
  Classically described as irregularly irregular rhythm
• Rhythm: Atrial rhythm is chaotic and disorganized. Vent
  rhythm is irreg
• Rate: Atrial >350. Vent varies. (If >200 think of WPW)
• P: No identifiable P
• P-P interval: Cannot be measured
• P-R Interval: Cannot be measured
• QRS: Usually narrow. May be wide if there is a pre-
  existing conduction delay.
• R-R/R amplitude: Very irregular/Very irregular
Atrial Fibrillation
                 Atrial fibrillation
• Clinical manifestations
   Symptoms/signs are a function of vent response to fibrillatory
     waves. Rapid- DOE, SOB, acute pulm oedema. Tachycardia
     mediated CMP
   – Loss of atrial kick may lead to a drop in CO and decreased
     coronary perfusion
   – Irregular rhythm perceived as palpitations
   – Can be asymptomatic
   – Commonest cardiac arrhythmia. Prevalence increases with age
• Common aetiologies
   – HHD, VHD, Hyperthyroidism, Post cardiac surgery
   – ACS, CAD, HF
   – Hypoxia, PE, Drugs (Digoxin, Quinidine
                 Atrial fibrillation
                    Treatment
• Evaluation
  –   Patient clinically stable?
  –   Cardiac function impaired?
  –   WPW present?
  –   Duration ≤48 or >48h
• Therapy
  –   Treat unstable patients urgently
  –   Control the (vent) rate
  –   Convert the rhythm
  –   Provide anticoagulation
                  Atrial fibrillation
                 Treatment cont’d
• With pulm oedema, hypotension and ACS require
  immediate intervention
• Control Rate
   – Normal cardiac function: CCB (Verapamil/Diltiazem) or BB
     (Metoprolol)
   – Impaired cardiac function: Digoxin or Amiodarone
• Convert Rhythm
   – Impaired function
      • ≤48h- DC cardioversion or Amiodarone
      • > 48h- Anticoagulate x4wk, then DC cardiovert, then anti coagulate
        x4wk.
   – Normal function
• IV Heparin, and TEE to rule out clot; then DC
  cardioversion within 24h, then anticoagulate x4wk
        Management of SVT
• Unstable: Synchronized electrical cardioversion
• Stable (AVNRT/ AVRT): Manoeuvers such as
  Valsava or carotid sinus massage or Adenosine
  (6mg-18mg iv push)
• BB or Diltiazem/Verapamil may be necessary for
  recurrent episodes
• Vent pre-excitation: Avoid AV nodal blocks
  (Diltiazem/ Verapamil/Digoxin
• Stable acute Afib: Procainamide
Ventricular Arrhythmias: VT
Ventricular Fibrillation
   Atrioventricular Blocks (AVB)
• Conduction blocks can occur anywhere in the conduction system but
  most commonly seen in the AV junction. They may be transient or
  permanent.
• AV junction serves as an electrical bridge between the atria and
  vent. AVB occurs when there is delayed or impaired transmission of
  the electrical impulse through the AV junction.
• There are 3 degrees of AVB. 1st, 2nd and 3rd. Each is diagnosed by
  examining the relationship between the P waves and QRS
  complexes. 1st and 2nd AVB are considered “partial” blocks since
  all or some (respectively) are conducted to the ventricles. 3rd degree
  AVB is considered to be “complete” block since there is no
  conduction thru the AV junction, therefore no communication
  between the atria (P waves) and ventricles (QRS complexes)
1o AV Block
                      1o AVB
• Impulses originate at the SA node
• Impulses travel normally from the SA node through the
  atria
• Upon reaching the AV junction, the impulses slows or is
  delayed longer than normal. The delay can occur in the
  AV node or in the His bundle.
• The impulse then usually continues through the
  ventricles in a normal manner.
• PR interval (time bet the start of atrial depo and vent
  depo) is prolonged, > o.20s
• Every atrial impulse is conducted thruthe AV junction to
  activate the ventricles. Not truly a “block” but rather a
  “delay” in conduction.
               1o AVB
          ECG Characteristics
• Characterized by a prolonged PR interval
• Rhythm: Regular
• Rate: Atrial and vent rates are the same
• P wave: Normal size and configuration
• P-P Interval: Regular
• PR interval: Prolonged > 0.20s
• QRS: Usually normal and alike (may be wide if
  there is a pre-existing vent conduction delay).
• R-R Interval: Regular
              1o AVB
          ECG Characteristics
• Characterized by a prolonged PR interval
• Rhythm: Regular
• Rate: Atrial and vent rates are the same
• P wave: Normal size and configuration
• P-P Interval: Regular
• PR interval: Prolonged > 0.20s
• QRS: Usually normal and alike (may be wide if
  there is a pre-existing vent conduction delay).
• R-R Interval: Regular
                   1o AVB
• Significance: Usually tolerated well unless
  bradycardia occurs and the patient is
  symptomatic. The patient should be monitored
  for progression to 20 or 30 AVB. 10 AVB can be
  normal.
• Causes: Drugs (Procainamide, Dig, BB),
  degenerative disease of the conduction system,
  rheumatic fever, K imbalance, hypothyroidism
• Rx: Directed at underlying cause
                             2o AVB
• In 2o AVB some but not all of the atrial impulses are transmitted thru
  AV junction.
• Some P waves are not followed by QRS
• 2 types of 2o AVB: Types 1 and 2

• Mobitz Type 1 . Wenckebach
    – block occurs within the AV node
    – Impulses originate in the SA node but are delayed in the AV node
    – The delay in the AV node becomes progressively greater with each
      impulse until one impulse is not conducted to the ventricles
    – ECG shows a progressive lengthening of the PR interval with each beat
      until suddenly a P wave is not followed by a QRS
    – There is a “dropped” beat or QRS
    – After the “ dropped” beat the sequence usually repeats itself.
    – Characteristic clustering of beats (group beating) separated by a pause
                     2o AVB
                ECG Characteristics
• Characterized by clusters of beats separated by a pause, with
  progressive lengthening of the PR interval until a QRS is dropped
• 2o AVB
   – Rhythm: Atrial rate is regular. Vent rate is irreg
   – Atrial rate > vent rate. Atrial and vent rates vary
   – P wave: Normal and alike. P waves more than QRS seen. The P waves
     begin to appear earlier and earlier in the absolute refractory period, until
     a P wave is not followed by a QRS complex. The # of P waves in
     relation to the QRS is described as a ratio eg 5:4, 4:3. 3:2, 2:1
   – P-P interval is regular
   – PR interval: Becomes progressively longer with each cycle until a P
     wave is not conducted to the ventand a QRS is dropped.
   – QRS: Usu5;ally normal and alike. May be wide if there is a pre-existing
     conduction delay. A QRS is periodically dropped. Each QRS is
     associated with a P wave.
   – R-R interval: Irregular
Mobitz Type 1. Wenckebach
              2o AVB Type I
        Mobitz Type I, Wenckbach
• Significance
   – Usually due to a conduction block in the AV node. It is often
     transient and benign. And rarely progresses to 3rd degree AVB.
     The patient is usually asymptomatic but should be monitored for
     progression to a more serious degree of AVB.
• Causes
   – Same as 1o AVB
   – May be seen with acute IMI
   – Drugs (BB, CCB)
• Treatment
   – 2o Type 1 AVB does not require treatment unless the vent rate is
     slow and the patient is symptomatic e.g., hypotensive syncopal.
             2o AVB Type II
             Mobitz Type II
• More serious form of 2o AVB
• Block occurs in the His bundle below the
  AV node
• Characteristic feature is the sudden
  appearance of a non-conducted sinus P
  wave. (P wave not followed by a QRS)
• PR intervals are constant
• May occur in a pattern e.g., 2:1, 3:1, 4:1.
                2nd AVB Type II
              ECG Characteristics
• Characterized by the sudden appearance of non-
  conducted sinus P waves. PR intervals are constant
• Mobitz Tpe II
   – Rhythm: Atrial is regular. Vent is irregular.
   – Rate: Atrial rate is usually normal, varies according to the
     underlying sinus rhythm.
   – P wave: Normal and alike
   – P-P Interval: Regular
   – Remains constant until a QRS is dropped
   – QRS: Usually normal but may be wide. Periodically absent
   – R-R Interval: Irregular if isolated dropped beats occur. May be
     regular if there is a constant block ratio e.g., 2:1, 3:1, 4::1
              2o AVB Type II
• Significance: Mobitz II block is usually a sign of
  conduction system disease due to a block below
  the AV node in the His bundle. Patients often
  progress 3o AVB and require a pacemaker. The
  rhythm is usually not well tolerated.
• Causes
  – Acute AM
  – Degenerative disease of the conduction system
• Treatment
  – Atropine
  – Pacemaker
       Comparison of Mobitz
                Mobitz I         Mobitz II

Pattern of block Cycles of       Abrupt. P
                 Gradually       waves with a
                 Increasing PR   consistent PR
                 followed by a
                 nonconducted
                 P
Usual location AV node           His or bundle
of block                         branches

Occurrence      Inferior         Anterior
3O AVB
3O (Complete) AV Block
                 3o AVB
              (Complete AVB)
• Impulses may originate in the SA node but no
  impulse passes between the atria or ventricles
  (neither antegrade nor retrograde)
• A secondary pacemaker or an escape rhythm
  stimulates the ventricles
• AV dissociation with ventricular escape
  depolarization slower than atrial rate. Atria and
  ventricles beat independently, usually at their
  intrinsic rates
                          Complete AVB
• Significance: 3o AVB is serious and potentially life threatening. Clinical
  manifestations are rate related. Slow vent rates can decrease CO,
  with symptoms of SOB, chest discomfort, and impaired level of
  consciousness or syncope. Signs: hypotension, shock, CHF. With IMI,
  3o AVB is often transient and may not require Rx. With AMI, the
  prognosis is poor and requires the insertion of a pacemaker.
• Causes:
    –   Congenital
    –   Rheumatic fever
    –   Chronic degeneration
    –   MI
    –   Digoxin toxicity
    –   Mitra /aortic valve replacement

• Rx:
    – Atropine
    – Pacemaker
                Bradycardias
• Treat only symptomatic bradycardias
• Bradycardia must cause the symptoms
• Recognize bradycardias that are likely to
  deteriorate even if asymptomatic
  – Second degree AV block type II
  – Third degree AV block
• The overall Rx approach (acute):
  –   Atropine
  –   Transcutaneous pacing (TCP)
  –   Dopamine
  –   Epinephrine

				
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