Cardiac Muscle I

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Cardiac Muscle I
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Essential Features of Vertebrate Cardiac Muscle

• Striated
• Cells connected by gap junctions
• Dually innervated by ANS
• Spontaneously active, either normally or in
  disease states, depending on the cell type.
• In mammals highly dependent on oxidative
  metabolism

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Differentiation of Functional Cell Types in the
Heart

• Nodal fibers- spontaneously active pacemakers
  that can initiate heartbeat
• Conducting fibers - rapidly carry excitation from
  one part of the heart to another
• Myocardial fibers - compose most of the mass of
  the heart and provide essentially all of the
  force.

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Nodal and conducting fibers in the heart
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Sequence of electromechanical events in a
heartbeat

• Spontaneous AP in SA nodal pacemakers
• Excitation spreads throughout atria, followed by
  atrial contraction
• Excitation reaches AV node, enters bundle of His,
  is conducted into both ventricles by branch
  bundles, and is rapidly spread throughout the
  ventricular myocardium by Purkinjie fibers -
  followed by ventricular contraction or systole.

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Agenda of topics to consider

• Nature of pacemaker action potentials
• Control of heart rate by the ANS
• Nature of myocardial action potentials
• Relationship between myocardial action potentials
  and the electrocardiogram
• Myocardial excitation-contraction coupling
• Control of myocardial contractile force by
  stretch and by autonomic inputs

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Action potentials recorded from the ventricular
myocardium, SA node and atrial myocardium. The
total time in each window is about 300 msec for
the myocardial cells and about 150 msec for the
SA nodal cell.
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Pacemaker potentials

• Nodal cells (pacemakers) do not have stable
  resting potentials.
• Instead, the cells undergo a spontaneous, slow
  depolarization (prepotential) until threshold is
  reached.
• The upstroke of the AP is slow compared to nerve
  and skeletal muscle.
• Each action potential leads to a temporary
  afterhyperpolarization that leads into the next
  prepotential.

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If inward
K
T Ca
L Ca
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The rate of pacemaker potentials is modulated by
the autonomic NS

• In the absence of any autonomic input, the
  natural rate of pacemaker potentials is about
  100/min in human heart.
• Cholinergic input slows the heart rate by slowing
  depolarization during the prepotential
  adrenergic input increases the heart rate by
  increasing the rate of depolarization.

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This slide shows the effects of isoproterenol (a
beta agonist A), stimulation of the vagus nerve
(B), and two concentrations of Ach. Before and
after traces are overlain c indicates control
beats and experimental beats.
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How beta1 receptors increase heart rate

• Second messenger cAMP (slow), but directly by Gs
  (rapid)
• Channel effects
• 1. shift activation of L channels to more
  negative voltages, causing threshold to be
  reached sooner increase current carried by L
  channels.
• 2. Increase If, causing hypolarization at
  beginning of prepotential to be smaller.

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How muscarinic receptors slow the heart

• Second messengers Gi-mediated inhibition of
  adenylyl cyclase (slow) but direct effect of Gi
  on K channels (rapid).
• Channel effects
• 1. Open Ach-sensitive K channels
• 2. Shift L channel activation to more positive
  voltage values and decrease channel conductance.
• 3. Decrease If, causing a greater
  hyperpolarization at the beginning of the
  prepotential.

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Key features of the myocardial action potential

• Rapid upstroke
• LONG plateau
• Potential relatively stable during the interbeat
  interval, except in disease.

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Channels involved in the myocardial AP
fast Na channels
L Ca channels
K channels (several types)
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The electrocardiogram is an extracellular
recording of the myocardial AP

• Voltage is measured at several spots on the body
  surface - because body fluid is a conductor of
  electricity, these spots could be thought of as
  wires connected directly to the heart surface.
• A voltage difference will exist only when some
  parts of the heart are depolarized while others
  are not. During the interbeat interval, OR when
  the ventricle is all depolarized, the EKG trace
  will return to baseline.

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If we measure the voltage difference between the
right arm and left leg over a heart cycle, we
will watch excitation start in the atria, spread
through the ventricles, and end with ventricular
repolarization
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Relationship between atrial and ventricular AP s
and EKG waves
Atrial
Ventricular