Cardiac Electrophysiology

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Cardiac Electrophysiology

• Part I
• Lecture 3

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Direction of cardiac muscle depolarization
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Electrical system of the heart
3 possible Pacemakers Primary Sinoatrial
node, Secondary Atrioventricular node Tertiary
Purkinje fibers
Sinoatrial node
Bundle of His
Purkinje fibers
Atrioventricular node
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Pacemaker activity

• Spontaneous time-dependent depolarization leading
  to action potentials
• Pacemaker with highest frequency sets the heart
  rate.
• SA node 60 b/min smallest electrical region
  in the heart, sum of 3 ion channels produces
  pacemaker (ca, k, f)
• AV node 40 b/min can take over for SA node,
  pacemaker determined by same three channels as SA
  node.
• Purkinje fibers slow 20 b/min unreliable
  pacemaker, but great conducting system, pacemaker
  determined by f channels only.

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Generic action potential
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IK
ICa
INa
(activated during depolarization)
MAJOR MYOCYTE ION CHANNELS
repolarizing (all myocytes)
rapid depolarizing (non-nodal)
depolarizing (nodal AP and myocyte contraction)
Read- Table 20-1
Na/K
funny channel or HCN Pacemaker
current (activated during hyperpolarization) Hyper
polarization activated Cyclic Nucleotide gated
channel
Which channel is absent in SA and AV node? Absent
in ventricular myocytes?
If
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Intra and extracellular ion concentrations
Resting membrane potential -(60-80) mV
Na 10 mM
Na 145 mM
K 120mM
K 4.5 mM
Ca .0001 mM
Ca 1.0 mM
Cl- 116 mM
Cl- 20 mM
A- protein 4 mM
A- protein 0 mM
intracellular
extracellular (interstitial fluid)
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Ventricular action potential
5 Phases
0 upstroke of AP Ica slow Ica/Ina - fast
1 rapid repolarization Ik
activation Ica/Ina - inactivation
2 plateau phase Ica/Ina - activated
3 repolarization Ik
4 diastolic potential Ik Ica If Produce
pacemaker activity SA/AV node, purkinje use If
Phase 1 and 2 not present in SA/AV node
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Comparison of slow nodal and fast non-nodal
cardiac action potentials
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Another comparison of slow nodal and fast
non-nodal cardiac action potentials
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Effective and relative refractory periods
ERP
RRP
ERP due to inactivated Na and Ca channels, once
they begin to recover the RRP begins.
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Velocity of electrical conduction
Functionally, how might the speeds be important?
(0.05 m/s)
(1 m/s)
Sinoatrial node
(1 m/s)
Bundle of His
(4 m/s)
Purkinje fibers
Atrioventricular node
(0.05 m/s)
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Mechanisms for altering heart rate or rate of
nodal depolarization
Parasympathetic vagal release of acetylcholine

• Decrease RATE
• of depolarization
• (more time to reach threshold)

Decrease in If activity
2. Decrease maximum diastolic potential. (more
time to reach threshold)
Increase in Ik activity
3. Increase threshold potential. (more time to
reach threshold)
Decrease in Ica activity
Read about catecholamines p. 493
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Pharmacological manipulation of ion channels and
heart rate and conduction velocity activity.
Potassium channel blockers Increase AP duration
and ERF (phase 3) Calcium channel blockers
L-type Ca, slows rate in SA and AV node Sodium
channel blockers Reduce phase 0 and slope of
depolarization
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Calcium channel blockers
Used for Angina Hypertension Arrhythmias
Dihydropyridine class and Verapamil
Decrease entry of calcium and delay the
depolarization of SA and AV nodal cells.
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Potassium channel blockers
-Slow repolarization and therefore extends the
Effective Refractory Period. -Extends the Q-T
interval on the electrocardiogram (lecture Part
II) -Helpful in preventing tachyarrhythmias from
re-entry mechanisms (lecture Part II).
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Sodium channel blockers
-Slow the rate and magnitude of depolarization in
non-nodal cells -Used to treat tachycardia -Extend
s the Effective Refractory Period
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Beta blockers
-Prevent calcium entry into the cell -Decrease
HR, conduction velocity, strength of contraction.
-Used to treat many CVS conditions -Hypertens
ion (inhibit renin) -Angina/myocardial
infarction -Arrhythmias (slows rate of depol.)