5. Conduction System of the Heart
• SA node: sinoatrial node. The pacemaker.
– Specialized cardiac muscle cells.
– Generate spontaneous action potentials (autorhythmic tissue).
– Action potentials pass to atrial muscle cells and to the AV node
• AV node: atrioventricular node.
– Action potentials conducted more slowly here than in any other part of
system.
– Ensures ventricles receive signal to contract after atria have contracted
• AV bundle: passes through hole in cardiac skeleton to reach
interventricular septum
• Right and left bundle branches: extend beneath endocardium to
apices of right and left ventricles
• Purkinje fibers:
– Large diameter cardiac muscle cells with few myofibrils.
– Many gap junctions.
– Conduct action potential to ventricular muscle cells (myocardium)
5
8. ACTION POTENTIAL
Duration – 200- 400 msec
Regulated by activity of time & voltage
dependent ionic currents
Ionic currents maintained by
Ionic channels –passively conduct ions along
electrochemical gradient
Pumps, transporters – transport ions against
gradients
Exchangers- electrgenically exchange species
AP are regionally distinct
8
9. Electrical Properties of Myocardial
Fibers
1. Rising phase of action potential
• Due to opening of fast Na+ channels
2. Plateau phase
• Closure of sodium channels
• Opening of calcium channels
• Slight increase in K+ permeability
• Prevents summation and thus tetanus of cardiac
muscle
3. Repolarization phase
• Calcium channels closed
• Increased K+ permeability 9
13. Heart Physiology: Intrinsic
Conduction System
• Autorhythmic cells:
– Initiate action potentials
– Have unstable resting potentials called
pacemaker potentials
– Use calcium influx (rather than sodium)
for rising phase of the action potential
13
14. DEPOLARIZATION OF SA NODE
SA node - no stable resting membrane potential
Pacemaker potential
gradual depolarization from -60 mV, slow influx of Na+
Action potential
occurs at threshold of -40 mV
depolarizing phase to 0 mV
fast Ca2+ channels open, (Ca2+ in)
repolarizing phase
K+ channels open, (K+ out)
at -60 mV K+ channels close, pacemaker potential starts over
Each depolarization creates one heartbeat
SA node at rest fires at 0.8 sec, about 75 bpm
14
17. ELECTROCARDIOGRAM
P wave
Depolarization of atria
Followed by contraction
QRS complex
3 waves (Q, R, & S)
Depolarization of
ventricles
Followed by contraction
T wave
Repolarization of
ventricles
17
19. ELECTROCARDIOGRAM
Intervals show timing of cardiac cycle
P-P = one cardiac cycle
P-Q = time for atrial depolarization
Q-T = time for ventricular depolarization
T-P = time for relaxation
19
20. MECHANISMS OF
ARRYTHMOGENESIS
Some tacyarythmias start by one mechanism &
gets perpetuated by another mechanism
Some caused by one mechanism can precipitate
another episode caused by different mechanism
Mechanisms are
Disorders of impulse formation
Disorders of impulse conduction
both
20
21. DISORDERS OF IMPULSE FORMATION
Characterised by
Inappropriate discharge rate of normal pacemaker
Inappropriate discharge of ectopic pacemaker
21
22. Abnormal automaticity
Arise from cells that have reduced maximum
diastolic potentials
Don’t need prior stimulation
Triggered activity
Initiated by after depolarisations
Induced by one or more preceding action
potentials
22
23. After depolarisations are of two types
Early after depolarisation- occurs during
phase 2 & phase 3
Delayed after depolarisation- occurs during
phase 4
All depolariations doesn’t reach threshold
potential but if they reach they trigger another
after depolarisation & thus perpetuate
23
25. DAD’S
Result from activation of calcium sensitive
inward current due to increase in intra cellular
ca concentrations
Acquired or inherited abnormalities in
Sarcoplasmic reticulum properties
CA release channels
SR calcium binding proteins
25
27. EAD’S
AP prolongation may increase ca influx through
l-type ca channels during cardiac cycle , causing
excessive ca accumulation in SR & spontaneous
SR ca release
Increased intracellular ca cause depolarisation by
activation of ca dependent cl currents ,NA +/CA +
exchanger provoking EAD,S
27
28. Re-entry
Two types
Anatomical re-entry
Functional reentry
ANATOMICAL REENTRY
Characters
-2 or more pathways with different
electropohysiological properties
-impulse blocked in one pathway
-impulse conducts slowly in alternate pathway
&returns in pathway initially blocked in reversed
direction to re exite tissue proximal to site of block 28
30. For re entry to occur anatomical length of circuit
should be greater than reentrant wave length
Conditions that depress conduction velocity &
refractory period promote development of re
entry[λ = c.v x rp]
Sustained reentry occurs due to excitable gap
between activating head & recovery tail.
30
31. Fuctional reentry
Occur in fibres that exhibit functionally different
EP properties caused by local differences in
transmembrane AP
functional heterogenities can be fixed or change
dynamically
31
32. Mechanisms of termination are
When conduction & recovery characters of circuit
change
When activating head of wave collides with tail
32
34. DETERMINANTS OF AMPLITUDES OF
AFTER DEPOLARISATIONS
intervention Effect on
amplitude of EAD’S
Effect on
amplitude of
DAD’S
Long cycles ↑ ↓
Long AP duration ↑ ↑
Reduced membrane
potential
↑ ↓
Na channel blockers No effect ↓
Ca channel blockers ↓ ↓
catecholamines ↑ ↑
34
35. APPROACH TO TACHYARRYTHMIAS
HISTORY
•Mode of onset
•Mode of
termination
•Drug history
•Dietary
history
•H/o systemic
illness
•Family
history
PHYSICAL
EXAMINATION
•Symptoms
•Signs
NON INVASIVE
INVESTIGATIONS
• 12 lead ECG
• Holter monitor
• Patient
activated event
monitor
• Implanted loop
ECG monitor
• HUT
• Exercise ECG
• 2D ECHO
INVASIVE
INVESTIGATIONS
•Electrophysio
logical
studies
35
36. HISTORY
MODE OF ONSET
Occuring in the setting of exercise and stress – caused by catecholamine
sensitive automatic or triggered activity
At rest – may be caused by vagal initiation (AF)
Lightheadedness, syncope in setting of tightly fitting collar, turning head-
suggests carotid hypersensitivity
• MODE OF TERMINATION
•If terminated by vagal manevoure – suggests AV node as integral part of
tachyarrythmias
May help determine diagnosis or further guide to diagnostic tests
• DRUG HISTORY
•nasal decongestants
•Beta blockers
•Drugs prolonging QT interval. 36
37. DIETARY HISTORY
Alcoholic intake
Food containing Ephedrine
H/O SYSTEMIC ILLNESS
COPD
Thyrotoxicosis
Pericarditis
Congestive heart failure
FAMILY HISTORY
HOCM
Long QT syndromes
Myotonic dystrophies
37
38. PHYSICAL EXAMINATION
MORE HELPFUL IF DONE DURING SYMPTOMATIC PERIOD
HR
>100
Regularly irregular
Irregularly irregular
JVP
Increased JVP
Cannon waves
Heart sounds
Variable heart sounds
murmurs
BP -- Variable
Physical manoeveurs– Can have diagnostic and therapeutic value.
Valsalva/Carotid sinus massage - terminate or slow tachyarrythmias that depend
on AV node. 38
39. 12 LEAD ECG
Primary tool in arrhythmia analysis
3 steps in diagnosing tachyarrythmia.
Step 1 – determine if QRS complex is narrow or wide.
Step 2 – determine if QRS complex is regular or irregular.
Step 3 -- look for p waves and relation to QRS complex.
Major branch point in DD is QRS duration.
QRS < .12 – always almost SVT
QRS >.12 – often VT
39
40. 24 hr Holter monitoring - for patients with daily symptoms
Patient activated event monitor – for patients with
intermittent symptoms
Implanted loop ECG monitor – for patients with infrequent
severe symptoms
Exercise ECG - to determine myocardial ischemia
-For analysis of morphology of QT interval.
HUT – used in patients with recurrent syncope
Syncope with injuries in absence of heart disease
2D ECHO – for cardiac chamber size and function.
To rule out valvular diseases.
40
41. ELECTROPHYSIOLOGICAL STUDIES
For diagnostic purposes
For therapeutic purposes
COMPONENTS OF TEST
Measuement of conduction under resting , stress conditions
and maneuvers
41
42. SITE OF ORIGIN
Atrial
SA node
Atrial muscle
Junctional
AV node
His bundle
Kent bundle
Bundle branches
Purkinje fibres
Ventricular muscle
SUPRAVENTRICULAR VENTRICULAR
42
48. WIDE QRS TACHY CARDIA
Ventricular
tachycardia
SVT with BBB
Antidromic AV re –
entry tachycardia
Torsades de – pointes
LBBB with AF or
Atrial flutter with
variable block
WPW with AF or AFL
with variable block
WITH REGULAR
RHYTHM
WITH IRREGULAR
RHYTHM
48
49. DIFFERENTIAL DIAGNOSIS OF WIDE QRS
TACHYCARDIA
Initiation with premature P
wave
Changes in P-P interval
precedes R – R interval
changes
Slowing or termination by
vagal maneuvers
Initiation with premature QRS
complex
Changes in R – R interval
precedes P – P interval
AV – dissociation
Fusion ,capture beats
QRS duration-
RBBB type V1 morphology - >140
ms
LBBB type V1 - > 160 ms
Delayed activation –
LBBB - R- wave > 40 ms
RBBB- onset of R- wave to nadir
of S – wave > 100 ms
Concordance of QRS complexes in
all precordial leads
SVT VT
49
50. ANTIARRYHTHMIC DRUGS
Class IA.
This includes drugs that reduce V.max (rate of rise of action
potential upstroke [phase 0]) and prolong action potential
duration
Eg-quinidine, procainamide, disopyramide.
Class IB.
This class of drugs does not reduce V.max and shortens
action potential duration—
Eg-mexiletine, phenytoin, and lidocaine.
Class IC.
This class of drugs can reduce V.max, primarily slow
conduction, and prolong refractoriness minimall
Eg-flecainide, propafenone, and moricizine. 50
51. Class II.
These drugs block beta-adrenergic receptors.
Eg- propranolol, timolol, and metoprolol.
Class III.
This class of drugs predominantly blocks
potassium channels (such as IKr) and prolongs
repolarization.
Eg-sotalol, amiodarone, and bretylium.
Class IV.
This class of drugs predominantly blocks the slow
calcium channel (ICa.L)—
Eg-verapamil, diltiazem, nifedipine,
51
58. FOCAL ATRIAL TACHYCARDIAS
Can not be initaiated
by programmed atrial
stimulation
First P wave same as
othr P waves
Response to adenosine
–AV block seen
-- slow or terminate
Initiated by
programmed
stimulation
First P wave different
from others
Response to adenosine
-AV block seen
-cant slow or terminate
Automatic AT Focal reenterant AT
58
59. ECG –
P wave distinct from sinus P wave
PR interval shorter than RP interval
TREATMENT
Rate control
Rhytm control
Anticoagulation if LA diameter > 5cm
Catheter ablative theraphy
DC version
59
63. ECG
Atrial deflections are irregular and chaotic – ragged baseline
Ventricular rate is irregular
In longstanding cases, baseline almost straight with minimal undulation
.
63
64. TREATMENT
Control ventricular rate
Betablockers
Ca channel blockers
Digoxin
Anticoagulation
When AF >12hrs and risk
factors for stroke present.
Maintain INR – 2 to 3
Warfarin
DC cardioversion – 200 J
Pharmacological
To terminate - Amiodarone , Procainamide iv
To maintain restored sinus rhytm – beta
blockers ,class Ic drugs.
Emergency
If AF >24 - 48hrs
TEE done to r/o atrial thrombus
Heparin given with warfarin until INR > 1.8
Anticoagulate for 1 month after restoration of
sinus rythm
Elective
Anticoagulate for atleast 3 weeks before
cardioversion.
RATE CONTROL TERMINATION OF AF
ACUTE
64
65. CHRONIC
Beta blockers
Ca channel blockers
Digoxin
His bundle / AV junction
ablation with implantation of
activity sensor pacemaker
Anti coagulation
Surgical ablation of left atrial
appendage
Catheter ablation – of atrial
muscle sleeves entering
pulmonary veins
Surgical ablation – COX –
MAZE procedure
RATE CONTROL TERMINATION OF AF
SURVIVAL OUTCOME
Restoration of sinus rhytm not superior to rate control with anticogulation as
evidenced by AFFIRM and RACE trials
65
66. ATRIAL FLUTTER
atrial rate = 250-350 cycles/min
Ventricle rate is closer to 150, 100 or 75
beats/min
2:1, 3:1 and 4:1
F waves
“sawtooth” shape
68. ATRIAL FLUTTER
Treatment
DC – version 50 – 100 j
Anticoagulation
If asymptomatic –
- rate control
-rhythm control
- catheter ablation
69. AV NOAL RE ENTERANT TACHYCARDIA –
Most common
Mostly in women
Repetitive activation down slow pathway & up
fast pathway results in tachycardia
ECG –
Rate – 120 – 150
P waves negative
Narrow QRS complexes
P wave not visible or distorts QRS complex 69
73. WPW SYNDROME
ECG
Short PR interval.
Short or long RP
interval.
Delta waves
Narrow QRS
complex.
SITES OF BYPASS
TRACTS
Left lateral
Right lateral
Posteroseptal
Anteroseptal
73
83. COMPLICATIONS
Reciprocating tachycardia
Orthodromic – AV reentry – conduction to ventricle via AV
node and reentry via AP.
Antidromic - conduction to ventricle via AP and reentry
via His purkinje system – mimics VT
Atrial fibrillation
50% predisposed
-fast ventricular rate results in hemodynamic compromise.
83
89. PREMATURE VENTRICULAR
COMLEXES
Broad QRS > 120ms
T wave is large ,opposite in direction to QRS
No preceding p waves
Compensatory or noncompensatory pause
Fixed or variable coupling interval.
91. Incidence >60% of healthy males during 24hr
Holter
>80% post MI
Benign ectopics disappear on exercise
Pts –normal life span.
92. CLINICAL SIGNIFICANCE
LOWNs grading system of VPCs
Determines prognostic significance after MI
As grade advances, there is increased risk of SCD
92
GRADES VPCs
0 none
1 <30/hr
2 >30/hr
3 multiform
4A 2 consecutive
4B >3 consecutive
5 R on T phenomenon
93.
94.
95. MANAGEMENT
In Normal heart
Asym- No treatment
Sym - betablockers
Structural heart disease
betablockers
Class IA, III drugs
96.
97.
98.
99.
100. VENTRICULAR TACHYCARDIA
VT consists of at least three or more
consecutive VPCs at a rate of 100bpm.
Types-
-Nonsustained <30s
-sustained > 30s
Rhythm- Regular / slightly irregular
Rate 70 to 250 / min
101. ECG DIAGNOSIS
QRS duration
RBBB > 140 ms
LBBB > 160 ms
Wellens et al
QRS >140ms good indicator of VT
QRS 120- 140 ms only 50% have VT
107. FUSION & CAPTURE BEATS
33 % cases of VT
Diagnosis of VT is certain
Seen in VT of lower rates(< 160)
Capture beat- sinus beat
Fusion beat- hybrid beat due to both atrial &
ventricular activation.
109. VT IN PATIENTS WITH CORONARY
ARTERY DISEASE
Non-sustained VT (NSVT) -67%
Sustained VT 3.5% VF – 4.1%
VT + VF – 2.7 %
Mortality
VT - 18.6%
VT + VF – 44%
1 yr mortality 7%
Without VT is 3 %
110. CLINICAL PRESENTATION
Symptoms are variable
Depend upon rate of VT & degree of LV
dysfunction
Syncope / presyncope / dizziness
Palpitations
Sudden death
111. TREATMENT OF VT
HEMODYNAMIC COMPROMISE --
DC – version
asynchronously 200j ,
repeat with ↑energy if
no response
IV lidocaine,
amiodarone
DC –version
synchronously with R
wave
IV lidocaine ,
procainamide ,
amiodarone
Polymorphic VT Monomorphic VT
111
112.
113. NO HEMODYNAMIC COMPROMISE
Correction of k+ & mg
Removal of offending
drug
B – blocker iv
Treat acute ischemia
Pacing
Catheter ablation
Quinidine,procainami
de for BRUGADA
syndrome
Lidocaine ,
procainamide ,
amiodarone
Catheter ablation
Polymorphic VT Monomorphic VT
113
115. SPECIFIC TYPES OF VT
ARRHYTHMOGENIC RT
VENTRICULAR DYSPLASIA(0.4%)
LBBB contour with right axis deviation
during VT
ICRBBB ,T waves inverted over the right
precordial leads
Type of Cardiomyopathy, possibly familial,
with hypokinetic thin walled RV
Abnormality in Chr 1 & Chr 10 -apoptosis
116. Imp cause of VT in children & young adults
with normal hearts
Rt heart failure or asymptomatic rt
ventricular enlargement can be present
with normal pulmonary vasculature
Males predominate
Pathology- Fatty & fibrofatty infiltration
OR myocardial atrophy
117. Preferentially affects rt ventricular inflow &
outflow tracts & the apex
ECG- T wave inversion in V1 to V3, Terminal
notch in QRS called “epsilon” wave can be
present due to slowed intra ventricular
conduction
ICDs are preferable to pharmacological
Radio frequency catheter ablation is often not
successful
118.
119. LEFT SEPTAL VT
Arises in the left posterior septum, often
preceded by a fascicular potential.
It is sometimes called Fascicular tachycardia
Cause – Re-entry
Mgm – Verapamil or Diltiazem
Oral verapamil is less effective than iv
verapamil
120. LEFT SEPTAL VT(FASCICULAR VT)
Seen in normal heart.
70% males ,15-40 yrs
Resting ECG normal
VT – RBBB pattern with left superior axis
QRS < 140 ms
121. Left septal ventricular tachycardia. This tachycardia is
characterized by a right bundle branch block contour. the axis
is rightward.
122. C/F – palpitations, syncope
Not associated with sudden death
Treatment-
Verapamil .
RF ablation 85-100%
Prognosis – good
123. CATECHOLAMINERGIC
POLYMORPHIC VT
Uncommon form of inherited VT
Occurs in children & adolescents without
any overt structural heart disease
Adenosine sensitive
Pts present with syncope or aborted sudden
death with highly reproducible stress
induced VT that is often bidirectional
QT interval – Normal
Family history present in 30%
124. During exercise typical responses, initial
sinus tachycardia & ventricular extrasystoles
followed by monomorphic or bidirectional VT,
which eventually leads to polymorphic VT as
exercise continues
Mgm – Beta blockers & ICDs
Lt cervicothoraic sympathetic ganglionectomy
125.
126. BRUGADA SYNDROME
30-40% of idiopathic VF
AD, M:F 8:1
2-4th decade
Distinct form of idiopathic VT,V fib
RBBB & ST segment elevation in anterior
precordial leads
No evidence of structural heart disease
Mutation in gene responsible for sodium
channel
127. Acceleration of Na channel recovery or
nonfunctional channels
Common in apparently healthy south east
Asians – 40-60%
Precise mechanism is not known
Can be reproduced by sodium channel
blockers
ICDs are the only effective treatment to
prevent sudden deaths
128.
129. LONG QT SYNDROMES
Normal QT males - 440 ms females – 470ms
Congenital
Jervell Lange-Neilsen syndrome- AR with
deafness
Ramano-Ward syndrome - AD with normal
hearing
Defect in Na, K channels.
136. CARDIOMYOPATHIES
DILATED CARDIOMYOPATHY
Focus basal septum
Mutiple macrorentry
ICDs -life threatening ventricular
arrhythmias
Comparing amiodarone v/s ICD, improved
survival was found with ICD
In case bundle branch re-entry is the basis,
ablate the RBB
137. HYPERTROPHIC CARDIOMYOPATHY
Risk of sudden death is increased by presence
of syncope, family h/o, sudden death in 1st
degree relative, septal thickness >3cms or
presence of non sustained VT in 24 hr
recordings
Infrequent episodes of non sustained VT have
low mortality
Amiodarone – Useful symptomatic non
sustained VT but not in improving survival
138. MITRAL VALVE PROLAPSE
VT in MVP has good prognosis although sudden
death can occur
Treated with betablockers.
139. CHD
Can occur in pts some years after repair
Sustained VT can be caused by re entry at the
site of surgery
Mgm- resection or catheter ablation of the area
140. VENTRICULAR FLUTTER
Severe derangement of heart beat
Macro-reentrant
Sine wave appearance, with large regular
oscillations (150-300 Bpm)
Distinct QRS ,ST T are absent
Difficult to distinguish between rapid VT
& V.flutter
141.
142. VENTRICULAR FIBRILLATION
Grossly irregular ,undulation of varying
amplitudes, contours with rates >300 /min
Starts with VT
Distinct QRS ,ST T are absent
Multiple wavelets of reentry
75% of sudden death after MI have VF.
145. TORSADES DE POINTES
VT characterized by
QRS complexes of changing amplitude that
appear to twist around the isoelectric line &
occur at rates of 200 to 250 /min
Prolonged ventricular repolarization with QT
intervals generally exceeding 500 msec
U wave can also become prominent& merge
with T wave
146.
147. Torsades de Pointes can terminate with
progressive prolongation in cycle length with
distinctly formed QRS complexes &
culminate into basal rhythm, ventricular
standstill, or VFib
148. Common causes
Potassium depletion
Congenital LQTS
Antiarrhythmic drugs IA,IC,III
c/f
Palpitations, syncope, death
Women are at a greater risk
149. Management
IV magnesium
Temporary ventricular or atrial pacing+ ICD
Lidocaine, mexiletine or phenytoin can be
tried
K channel activating drugs pinacidil,
cromakalim
Cause of long QT should be treated
150. REFERENCES
BRAUNWALD ‘S HEART DISEASE 8 th ed
HARRISONS INTERNAL MEDICINE 17 th ed
HURST ‘S HEART DISEASES
SHAMMROTH ECG
MARRIOTS ECG
MEDICINE UPDATE
150
