Download LO2 – Ionic currents that generate cardiac action potentials

ID639 - Cardiac Muscle action potentials and
heart excitation
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LO1. Contrast the typical action potential in a ventricular muscle and a pacemaker cell.
LO2. Explain how ionic currents contribute to the five phases of the cardiac action
potential. Apply this information to explain differences in shapes of the action potentials
of different cardiac cells.
LO3. Explain what accounts for the long duration of the cardiac action potential and the
resultant long refractory period and what is the advantage of the long plateau of the
cardiac action potential and the long refractory period.
LO4. Explain the ionic mechanism of pacemaker automaticity, and identify cardiac
cells that have pacemaker potential and their spontaneous rate. Identify neural and
humoral factors that influence their rate.
LO5. Describe the normal sequence of cardiac activation (depolarization) and the role
played by specialized cells.
LO6. Explain why the AV node is the only normal electrical pathway between the atria
and the ventricles; describe the functional significance of slow conduction through the
AV node.
LO1 – Cardiac action potentials
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B.
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D.
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F.
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SA-node
Atrial myocytes
AV-node
Ventrcicular myocytes
Purkynje fibers
Injured myocytes
dV/dt: speed of depolarization
Vm: membrane potential
Ampl: action potential amplitude
LO2 – Ionic currents that generate cardiac action
potentials
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LO3 – Absolute and relative refractory periods
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5
No AP could be generated
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Deformed AP are generated
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4
Mechanism:
Inactivation of
fast Na-channels
Why is recovery
of fast Na-channels delayed?
Long depolarization (plateau)-opening of Ca-channels
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LO3 – Long duration of cardiac AP prevents contraction
before relaxation (i.e. tetanisation) and a new myocardial
depolarization with the same AP (reentry)
reentry
LO4 – The rate (slope) of phase 4 depolarization sets
the heart rate (chronotropic effects)
Sympathetic stimulation opens
more HCN-channels and L-type
calcium channels what makes
phase 4 more steeper - HR
increases
Parasympathetic stimulation
reduces IHCN and ICa what
makes phase 4 less steeper HR declines. Moreover,
opening of the acetylcholine
regulated potassium channels
hyperpolarizes the SA-node
cells. Thus, more time is
needed to reach the threshold.
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LO5 – Excitatory and conduction system of the heart
Internodal tracts
SA-node
Ectopic
pacemakers
AV-node
Ventricular escape beat (rhythm)
Cardiac activation from the
ventricular ectopic focus after a
long pause in ventricular rhythm
(protection from sudden death)
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LO6 – Electrophysiological properties of the AV node
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1. Conduction is very slow (0.02-0.05 m/sec) in the AV-node
because APs are slow and the nodal cells have small diameter.
This makes this area especially vulnerable to conduction
block (AV block).
2. AV-node delays activation of ventricles. This ensures that the
ventricles are relaxed at the time of atrial contraction and
permits optimal ventricular filling during atrial contraction.
3. Relative refractory period is long in the AV-node. Therefore,
AV-node controls the number of atrial impulses that can
activate the ventricles. This protects ventricles against too
frequent activation during atrial tachyarrhythmias that would
cause too short diastole, too short filling and too low stroke
volume.
4. AV-node can serve as a pacemaker (secondary) when the SA
node fails to function (AV-nodal rhythm is 40-55 beats/min).
LO6 – Regulation of conduction in the AV- node
Conduction velocity is called dromotropy.
Positive dromotropic intervention increases speed of
conduction; negative dromotropic interventions
decreases speed of conduction
Positive dromotropic intervention:
•sympathetic stimulation
Negative dromotropic intervention:
•parasympathetic stimulation
•ischemia
•hyperkalemia
•calcium blockers
•cardiac glycosides
•adenosine
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