9. Pacemaker Activity (automaticity)
Absence of fast Na+ current in SA & AV node
Ca++ current initiates action potential.
Long action potential (Plateau) & Refractory period
Influx of Ca+ during Plateau
13. During Cardiac Cycle:
Ions ( Na+, K+, Ca+ & Cl- ) moves across cell
membranes in response to their concentration
gradients only when their channels open.
Ionic movement produces currents responsible
for the cardiac action potential.
15. m (activation) gate: their opening for Na+ ions leads to depolarization
from threshold to action potential voltage.
h (inactvation) gate: closure occurs after this brief opening of m gates
16. - 85
influx
eflux
Absolute
Refractory
Period
Relative R.P.
E
after
depolarization
D
Threshold
Phase 0:
Depolarization; Rapid Sodium Influx;
Resting voltage has become positive.
Phase 1:
Early Repolarization; brief K+ & Cl- eflux
Phase 2:
Plateu phase; Ca++ influx
Phase 3:
Rapid repolarization; K+ & Cl- eflux
Phase 4 ( automaticity ):
Ratio of Na+/K+ permeability; cellular
electrolyte balance is slowly restored.
Slow Diastolic Depolarization;
Until the threshold potential is reached.
Early & Delayed - after depolarization may
occur during relative refractory period
before the phase 4, due to myocardial damage,
so leading to arrhythmias.
Early & Delayed depolarizations
interrupt Phase 3
18. Myocardial Action Potential
I b = background
inward sodium current,
If = ‘funny current’,
I cat= transient or ‘T’ type
calcium current,
opening of channels
leads to threshold
I cal = slow responding
‘ L’ type calcium channels,
I k = delayed rectifier
potassium current,
Threshold
Ical
Slow Responding Fibers; Ca++ role; as at -55 mV Na+ channels close
SA Node & AV Node or Damaged fibers
19. I k1= inward rectifier current,
I Na= Fast responding
inward sodium current,
( Na channels closes at -55 to -70 mv
at which however Ca channel opens )
so in ischemic damage,
fast responding fibers are changed
into slow responding fibers
I to = transient outward
potassium current,
I cal = ‘L’ type calcium channel,
I k = delayed rectifier
potassium current,
Upstroke
-85 resting potential
O -
Fast Responding Fibers; Na+ Role
20. the only conduction pathway
Body Surface Manifestations
of the Depolarization and
Repolarization Waves
of the heart.
The only conduction pathway
delay of
0.15 sec.
at
to allow blood
to enter from atria
to Ventricles
AV node
23. The Main Factors affecting Heart Rate
Gender
ANS activity ( Sympathetic/Parasympathetic)
Age
Circulating Hormones ( Adrenaline, Thyroxin)
Physical Activity
Temperature
Baroreceptors Reflex
Emotional States
25. Cardiac Arrhythmia is an abnormality
in:
Rate,
Rhythm,
Site of origin &
the conduction of
cardiac impulse.
26. Arrhythmias occur in:
Myocardial Infarction ( >80% )
Anesthetized Patients ( Up To 50% )
Digitalized Patients ( Up To 25% )
(All Antiarrythmics are Arrhythmogenic )
27. Arrhythmias are caused by:
• abnormal pacemaker activity or
• abnormal impulse propagation & conduction
• Shift of pacemaker function from SA to other part of
the Heart
• Block transmission in the Heart
• Abnormal pathway in the heart
• Spontaneous generation of Impulses in the heart
There is a normal relationship between
“refractory period and conduction velocity”.
Any change in this relationship may lead to arrhythmias
31. • A). Disturbances of Impulse Formation:
1. Changes in Automaticity:
2. Triggered Activity:
• B). Disturbances of Impulse Conduction;
1. Abnormal Regulation of the Heart Beat by
sympathetic, vagal activity or re-entry
• C). Molecular & Genetic Basis of Arrhythmias
32. A). Disturbances of Impulse Formation:
a). Increase or decrease in pacemaker rate:
due to increased or decreased depolarization of Pace Maker Cells;
slope 4: if decreased i.e., more negative leads to slow normal
pace maker rate,
e.g., Vagal discharge, β-receptor Blockers
b). Latent Pace Makers: ( Some Purkinje Fibers;
Quiescent Atrial & Ventricular Cells )
they show normally slow phase 4 depolarization and are more
prone to acceleration thus may show repetitive pace maker
activity esp. in hypokalemia
D
1. Changes in Automaticity:
34. Early After Depolarization's:
are usually produced & exacerbated at slow heart rates and contribute
to the development of long QT – related arrhythmias.
Delayed After Depolarization's:
occur when intracellular calcium is increased and are exacerbated by
fast heart rates and usually responsible for arrhythmias related to
digitalis / catecholamine & to myocardial ischemia
35. a. Increased slope of phase 4
depolarization as in
hypokalemia, β stimulation, etc.
leads to early completion of
diastolic depolarization,
↑Pace Making
b. Reduced Threshold Potential
--- early completion of
diastolic depolarization.
“Triggered Activity”:
stimulating during relative
refractory period so getting
action potential earlier than
normal.
E. Early after depolarization,
arises almost from the
plateau.
D. Delayed after depolarization,
arises from the resting
potential.
a b
accelerated automaticity e.g.,
in sympathetic stimulation
Threshold
Normal or
Reduced
Pace Maker Depolarization=
Durations of Action Potential &
Diastolic Interval )
36. Four Basic Mechanisms CAUSING
Disturbed rhythm
• Delayed after Depolarization
• Re-Entry
• Ectopic pace maker
• Heart Block
37. B). Disturbances of Impulse Conduction;
Abnormal Regulation of the Heart Beat
1). In A / B: Effects of sympathetic stimulation &
Nor epinephrine.
Sympathetic stimulation increases the heart rate
by increasing the slope of the pacemaker potential
38. 2). In C / D: depressed conduction due to increased
vagal activity (AV nodal block, bundle branch block)
C D
Vagal stimulation decreases the atrial force of contraction
by marked shortening of action potential;
also increased K+ permeability & reduced Ca++ current
both contribute to block AV conduction
39. 3). Re - entry (circus movement tachycardia):
if an ectopic beat finds one limb refractory
Impulse
passes down
both limbs at equal
speed
Retrograde Impulse will pass
When: the refractory period is
shorter
than
the conduction time
or on recovery
it passes if the other side is slowly
excited
esp. at
AV node,
Atrial or
Ventricular
Walls
Normal Damaged
40. C). Molecular & Genetic Basis of
Arrhythmias
as in several congenital & acquired cardiac
arrhythmias;
there is either increased inward current
or
decreased outward current during
the plateau,
46. Sinus Bradycardia
may be due to: hypothermia, hypothyroidism,
cholestatic jaundice, raised intracranial pressure, β-blockers,
digitalis etc., IHDs,
sick sinus syndrome- fibrosis of the atrium & sinus node.
Heart Block
• conduction block at any level in the conducting system;
Prolongation of PR interval > 0.22 s & then gradually
P waves don’t conduct.
( 1st – 3rd degree block )
• block lower than the Bundle of His produces Bundle Branch
Block;
widening of QRS complex up to 0.11 s ( N: < 0.10 s) .
47. Sick Sinus Syndrome
sinus arrest & junctional escape beats (J).
P waves are inverted in the cavity leads
48. Complete Heart Block
Congenital Complete Heart Block: QRS complex is narrow
with rate 52 beats/min.
Acquired Complete Heart Block: QRS complex is broad with
rate 38 beats/min.
49. Tachy-arrhythmias:
( rate >100 beats/min.),
may be due to
Exercise, Emotion, Pain, Fever, Infection,
Acute Myocardial Infarction, Acute Heart Failure,
Acute Pulmonary Embolism, Hypovolemia,
Pregnancy, Anemia, Hyperthyroidism,
Pheochromocytoma, Excess Sympathetic or
Reduced Parasympathetic Stimulation, etc.
50. Tachycardias are more symptomatic if the
arrhythmia is fast & sustained
Supraventricular Tachycardia:
Sinus Tachycardia,
Atrial Fibrillation, Atrial Flutter,
Ventricular Tachyarrhythmias:
Ventricular Tachycardia,
Ventricular Fibrillation,
The Brugada syndrome,
Torsades de pointes,
Ventricular Premature Beats.
52. Supra-Ventricular Tachycardia
at atrium or AV junction e.g.,
Atrial Premature Beats conducts to the ventricles
with a slightly prolonged PR interval
Premature P waves are different from the sinus P waves
54. P waves= Atrial rate is 150/min.
R-waves=Ventricular rate is 75/min.
Atrial Tachycardia
with IInd Degree AV. Block
55. F= flutter waves; flutter rate= 240/min.
Every fourth F wave is transmitted to the ventricles;
Ventricular rate= 60/min.
Atrial Flutter
56. Atrial Fibrillation
( Irregular Rhythm Atrial Rate 300 To 600 /Min.)
Ventricular Rate Depends On
Atrial Regularity At Av Node Entry
57. Atrioventricular Junctional Tachycardia
AV Nodal re-entry Tachycardia
QRS complex are narrow & P waves not
visible
Atrioventricular re-entry
Tachycardia
After narrow QRS complexes the
tachycardia P waves are clearly seen.
During sinus rhythm of WPW
Syndrome
short PR interval & δ waves ( arrow )
Atrial Fibrillation in the WPW
Syndrome.
Tachycardia with broad QRS complexes
with fast & irregular ventricular rate
58. Familial Atrial Fibrillation:
there is increased inward current of
potassium
mutation of the gene for subunits of the
slow delayed rectifier potassium current,
59. Ventricular Ectopics
Ventricular Ectopics of
different morphology
A pair of PVCs
Frequent PVCs
Following PVCs, non -
sustained, a brief run of
Ventricular Tachycardia
61. Torsade de pointes
( which is associated with syncope and
sudden death )
decreased outward current of Potassium
due to:
mutation in gene of potassium channels
leading to decreased repolarization &
long QT subtypes 1, 2, 5 & 6.
62. Torsade de pointes
( a short lived atypical ventricular tachycardia which arises when
ventricular repolarization is greatly prolonged - long QT syndrome:
may be due to decreased K+, Mg+, Ca++ or drugs )
may be dangerous if resulting in ventricular fibrillation.
a brief period of idioventricular rhythm
63. The Brugada Syndrome:
( which is characterized by
ventricular fibrillation & sudden death )
increased outward current of Sodium
due to:
mutation in gene of sodium channels
leading to congenital
long QT subtype 3 syndrome
64. The Brugada
Syndrome
( an inheritable condition )
Idiopathic Spontaneous
Ventricular Fibrillation
with ST - Elevation in V1 – V3
Right Bundle Branch Block
68. Why arrhythmias should be treated?
Arrhythmias may cause:
Sudden Death,
Stroke ( emboli )
Syncope,
Heart Failure,
Dizziness,
Palpitation, or
Asymptomatic at all.
because
70. Treatment of arrhythmias
is needed only
if
• cardiac output is reduced,
or if
• some arrhythmias can precipitate
serious / lethal rhythm disturbances
e.g., ventricular fibrillations.
71. Cardiac Output is decreased
due to:
Increased rate of contraction
Decreased rate of contraction
Asynchronised rate of contraction
72. The major anti-arrhythmic mechanisms
1. Sodium Channel Blockade
2. Sympathetic Blockade at heart
3. Prolongation of Effective Refractory Period
4. Calcium Channel Blockade
83. Aim of the Treatment is
to make the depolarized tissues silent
84. - 85
influx
eflux
Absolute
Refractory
Period
Relative R.P.
E
after
depolarization
D
Threshold
Phase 0:
Depolarization; Rapid Sodium Influx;
Resting voltage has become positive.
Phase 1:
Early Repolarization; brief K+ & Cl- eflux
Phase 2:
Plateu phase; Ca++ influx
Phase 3:
Rapid repolarization; K+ & Cl- eflux
Phase 4 ( automaticity ):
Ratio of Na+/K+ permeability; cellular
electrolyte balance is slowly restored.
Slow Diastolic Depolarization;
Until the threshold potential is reached.
Early & Delayed - after depolarization may
occur during relative refractory period
before the phase 4, due to myocardial damage,
so leading to arrhythmias.
Early & Delayed depolarizations
interrupt Phase 3
85.
86. The anti-arrhythmic drugs:
a). Decrease: automaticity, Conduction,& Ecitability
The automaticity
of ectopic sites more than at SA Node
by
1) reducing the ratio of sodium & potassium
permeability so the membrane-potential
during phase 4
stabilizes closer to potassium equilibrium
at which K+ movement is stopped
2) or by
increasing the threshold
( making more positive ),
87. ii). the conduction & excitability of depolarized tissues
by reducing:
excitatory currents to a level below for
propagation,
due to decreased available ‘un blocked channels’
88. b). Increase:
the refractory period more at
depolarized tissues than in normally polarized tissues
by prolongation of recovery time of the channels
which are still able to reach the rested state thus
extra-systoles are unable to propagate at all;
later impulses propagate more slowly
and
are subject to bidirectional block in re-entry arrhythmias.
101. Pacemaker Activity Depressed
(SA node/ Ectopic Sites):
Ia (except Disopyramide),
Ib, Ic, II, III (except Ibutilide),
IV, Adenosine (No effect)
Action Potential (Prolonged duration):
Ia, III
102. Refractory period
Atrial / Ventricular
(prolonged): Ia, Ib, II, III
(except Bretylium)
(some): Ic, IV
AV Node (Prolonged): II, III, IV, Adenosine,
AV Node (some): Ib, Ic, Bretylium,
Ibutilide
PR-Interval (Prolonged): II, III
(except Bretylium, Ibutilide)
107. USES:
1. To relieve symptoms due to:
• AV node re-entry tachycardia,
• WPW syndrome,
• Atrial fibrillation or flutter or
• tachycardia.
( Class Ic or Class III ; Anticoagulants if needed, Catheter
Ablation )
108. 2. To prevent sudden death in:
• Life-threatening ventricular tachyarrhythmias,
• Congenital long QT,
• Ventricular Tachycardia.
( Beta-blockers +/- pacemaker, Calcium Channel
Blockers, Catheter Ablation, or ICD )
109. 3. Supra-ventricular (Only or mainly):
IV, I, Adenosine (Some)
4. Ventricular (Only or Mainly):
I, II, Bretylium
5. Both (equally):
III (except Bretylium)
112. Contra Indications
CCF: Disopyramide, Flecainide, Beta blockers
SA Node/AV node Dysfunction:
Beta blockers,
Ca Channel blockers,
Digoxin
Myocardial Infarction:
Flecainide
Prolonged QT Interval:
Quinidine, Procainamide,
Disopyramide, Sotalol,
Bretylium, Amiodarone,Ibutilide
113. 2. Catheter Ablation
Three or four electrode - catheters are placed into the
heart chambers to record and pace from various sites.
Radio – frequency catheter ablation is frequently
employed for symptomatic tachy – arrhythmias like:
AV re-entry tachycardia or with WPW syndrome:
first line therapy to avoid the risk of sudden death .
Ventricular & Atrial Tachycardia ( in normal hearts ):
easily cured by catheter ablation.
114. Atrial flutter:
If not easily managed medically; 90 – 95 % effective.
Atrial fibrillation:
After AV node ablation & pacemaker implantation a
marked symptomatic improvement occurs but
anticoagulants are still required. ( successful in 60 – 80 %
cases )
Complications:
Pulmonary vein stenosis, thrombosis, stroke.
115. X-Ray of a dual-chamber Implantable Cardioverter-defibrillator( IUD )
in a left pectoral position with atrial & ventricular leads
3.CARDIOVERTER
DEFIBRILLATOR
116. Termination of ventricular fibrillation
by the direct current shock after detecting it correctly
Electrogram recorded internally from the ventricular lead of an ICD
shows chaotic ventricular activity consistent with ventricular fibrillation
The ICD recognizes ventricular tachycardia or fibrillation and
automatically delivers pacing or a shock to the heart to cause
cardioversion to sinus rhythm
117.
118.
119. ECG – Body manifestation
of
Depolarization and Repolarization Waves
of the Heart
120. Β - agonists
Pacemaker
potential
(Phase 4)
Rapid
depolarization
(Phase 0)
Plateau
(Phase 2)
Repolarisation
(Phase 3)
Class II
Class I
Class IV
Class III
(and Ia)
123. PR Interval: Conduction Time From Atria
to Ventricles
QRS Duration: Ventricular Conduction Time
QT Interval: Duration of Ventricular Action
Potential
QRS Complex: Ventricular Depolarization
P – Wave:
Atrial Depolarization
T – Wave: Ventricular Repolarization
127. Cardiac Vectors:
a). The hexaxial Reference
System
e.g., lead l is O0,
lead ll is 600,
lead lll is + 1200.
b). Direction of the vector:
e.g., in lead lll positive &
negative deflections
are equal, so the mean
QRS vector is perpendicula
to lead lll
