6. Transmembrane Potentials in Heart Cells
Property Sa Nodal Cell Atrial Myocyte Av Nodal Cell His Purkinje Cell Ventricular Myocyte
Resting potential (mV) −50 to −60 −80 to −90 −60 to −70 −90 to −95 −80 to −90
Action Potential
Features
Amplitude (mV) 60–70 110–120 70–80 120 110–120
Overshoot (mV) 0–10 30 5–15 30 30
Duration (msec) 100–300 100–300 100–300 300–500 200–300
V ̇max (V/sec) 1–10 100–200 5–15 500–700 100–200
Propagation velocity
(m/sec)
<0.05 0.3–0.4 0.1 2–3 0.3–0.4
Fiber diameter (μm) 5–10 10–15 1–10 100 10–15
7.
8.
9. Bradycardia
1. The lower limit of normal resting heart rate is defined as
50 beats/min
2. Classified
1. Physiological
2. Pathological
3. Level of disturbance
1. SA node
2. AV node
3. His-Purkinje system
10. Sinus
Bradycardia
• Sinus node discharges at a rate less than 50 beats/min
• P waves have a normal contour, and are usually upright in leads I, II, and
aVF, and occur before each QRS complex, usually with a constant PR interval
longer than 120 msec
• Sinus arrhythmia often coexists
11. CAUSES AND TREATMENT
• Mostly physiological :Sleep ,athlete
• Increased vagal activity
• Decrease sympathetic activity
• Medication
• Raised intra cranial pressure
• Raised pericardial pressure
• Hypothyroid
• MI :10-15% MI
• No treatment is required
most of the times
• Atropine
• Theophylline
• Isoprenaline
12. Sinus
Arrythmia
• A phasic variation in sinus cycle length
• Maximum sinus CL minus the minimum
sinus CL > 120 msec
• Maximum sinus CL minus the minimum
sinus CL divided by the minimum sinus CL >
10%
• It is the most frequent form of arrhythmia
• Physiologically normal
•
13. Ventriculo-phasic Sinus Arrhythmia
• Occurs during complete AV block
• At slow ventricular rate
• P-P cycles that contain a QRS complex are shorter than P-P cycles
without a QRS complex
• Lengthening can be present in the P-P cycle that follows a premature
ventricular complex (PVC) with a compensatory pause
• Alterations in the P-P interval are probably caused by the influence of
the autonomic nervous system responding to changes in ventricular
stroke volume
14. Sinus Pause or Sinus Arrest
• Disease of SA node
• Impulse formation disorder
• Sinus pause [absence of p wave]
• PP interval without P not equal a multiple of the basic P-P
interval
• Can not be distinguished from sinoatrial (SA) exit block in 12
lead ECG
• Failure of sinus nodal discharge results in the absence of
atrial depolarization and can also result in ventricular asystole
if escape beats initiated by latent pacemakers do not occur.
• Acute MI, degenerative fibrotic changes, digitalis toxicity,
stroke, or excessive vagal tone can produce sinus arrest
• Transient sinus arrest (especially while sleeping) may have no
clinical significance by itself if latent pacemakers promptly
escape to prevent ventricular asystole or the genesis of other
arrhythmias precipitated by slow rates
• Sinus arrest and AV block have been demonstrated in many
patients with sleep apnea
17. Sinoatrial Exit Block
• Mechanism
• SA forms normal impulse but atria is not depolarized because of conduction disturbance does so
with delay
• TYEPS
• Type I:At the block site ,all the SA node impulses pass to depolarize atria but slowly
like PR prolongation
• Only SA node EP study detects it
• Can not be detected in the 12 lead ECG
• Type-II:
• Type-I: Gradual shortening of PP interval before the non conduction, but long PP
is less than x2 of basic PP
• Type-II :Long PP interval =2,3,4XBasic PP interval
• Type-III :No P waves and can’t distinguished from SA node arrest
18.
19. Sinus nodal exit block
• A: Type I sinoatrial (SA) nodal exit block
has the following features. The P-P
interval shortens from the first to the
second cycle in each grouping, followed
by a pause. The duration of the pause is
less than twice the shortest cycle length,
and the cycle after the pause exceeds the
cycle before the pause. The PR interval is
normal and constant. Lead V 1 is shown
• B:The P-P interval varies slightly because
of sinus arrhythmia. The two pauses in
sinus nodal activity equal twice the basic
P-P interval and are consistent with type
II SA nodal exit block. The PR interval is
normal and constant. Lead III recording is
shown.
20. Sick Sinus Syndrome
• Persistent spontaneous sinus bradycardia inappropriate for the
physiologic circumstance
• Sinus arrest or exit block
• Combinations of SA and AV conduction disturbances
• Bradycardia-tachycardia syndrome: Alternation of paroxysms of rapid
regular or irregular atrial tachyarrhythmias and periods of slow atrial
and ventricular rates
•
21. Sick sinus syndrome with bradycardia-
tachycardia
Intermittent sinus arrest is
apparent with junctional escape
beats at irregular intervals (red
circles) . Bottom, A short episode
of atrial flutter is followed by
almost 5 seconds of asystole
before a junctional escape rhythm
resumes. The patient became pre-
syncopal at this point.
22. TREATMENT OF TBS
• Tachycardia-bradycardia syndrome (TBS)
occurs when a patient has
tachyarrhythmias and bradyarrhythmias
closely associated in time. That can occur
when a tachyarrhythmia, typically atrial
fibrillation or atrial flutter terminates,
with a resultant excessive post-conversion
pause . TBS can also occur during atrial
fibrillation when periods of atrial
fibrillation with rapid ventricular rates
alternate with periods of excessive
bradycardia (due to high-grade AV block)
during atrial fibrillation. While TBS can
occur without medication, it typically
occurs as a result of treatment with beta
blockers or calcium channel blockers.
• PACEMAKER IMPLANTATION followed by
beta blocker
23. CAUSES OF SICK SINUS SYNDROME
• Total or subtotal destruction of the
sinus node, areas of nodal-atrial
discontinuity, inflammatory or
degenerative changes in the nerves
and ganglia surrounding the node,
and pathologic changes in the atrial
wall. Fibrosis and fatty infiltration
occur, and the sclerodegenerative
processes generally involve the
sinus node and the AV node or the
bundle of His and its branches or
distal subdivisions. Occlusion of the
sinus node artery can cause sinus
node dysfunction.
24. Chronotropic Incompetence
• HR does not increase appropriately in the setting of increased
physiologic demand
• Failure to obtain 80% or 85% of either maximal expected heart rate,
or of inadequate heart rate reserve (the difference between resting
heart rate and age predicted maximal heart rate
• Ventilatory expired gas analysis during exercise to calculate the
chronotropic index allows for an objective calculation of the
relationship between metabolic reserve and heart rate reserve
adjusted for age and functional capacity
