Summary Guyton and Hall Chapter 10 Notes Cardiac Muscle - The Heart as a Pump and Function of the Heart Valves
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Physiology (PHYSIOIOGY)
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Cebu Doctor's University
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Guyton and Hall Textbook of Medical Physiology
This is a condensed summary of the Chapter 10 - Rhythmical Excitation of the Heart from Guyton and Hall Textbook of Medical Physiology. It contains pictures from the book as well. Use these notes to study for your upcoming exam or quiz.
the heart as a pump and function of the heart valves
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Common test bank questions and answers (85) from Guyton and Hall Textbook of Medical Physiology / 14th edition
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CHAPTER 10 At -55 mV resting potential, the fast sodium channels mainly
have become inactivated or blocked, and remain so. Therefore,
RHYTHMICAL EXCITATION OF THE HEART only slow sodium-calcium channels can open and thereby cause
the action potential.
Because of this, the atrial nodal action potential is slower to
develop than the action potential of the ventricular muscle.
Return to negative state occurs slowly as well.
Positive sodium ions from outside the fibers tend to leak to the
inward through “funny” currents. This causes a slow rise in the
resting membrane potential between heartbeats, meaning, the
resting potential becomes less negative between each two
heartbeats.
The inherent leakiness of the sinus node causes their self-
excitation.
This leakiness does not cause the sinus nodal fibers to remain
Special system for rhythmic self-excitation by a system that does depolarized all the time because:
the following:
1. L-type calcium channels become inactivated within
1. Generates electrical impulses to initiate rhythmical 100-150 ms after opening
contraction of the heart muscle 2. Greatly increased numbers of potassium channels
2. Conducts these impulses rapidly through the heart open.
3. Allows all portions of the ventricles to contract almost
Hyperpolarization – where potassium channels remain open for
simultaneously, essential for the most effective
another few tenths of a second to continue movement of positive
pressure generation in the ventricular chambers.
charges outside the cell, with resultant excess negativity inside
- This system is susceptible to damage by heart disease,
the cell. This state is not maintained forever because potassium
esp by ischemia resulting from inadequate coronary
channels also close.
blood flow.
INTERNODAL AND INTERATRIAL PATHWAYS TRANSMIT
CARDIAC IMPULSES THROUGH THE ATRIA
SPECIALIZED EXCITATORY AND CONDUCTIVE SYSTEM
Sinus nodal fiber ends connect directly with the surrounding
OF THE HEART
atrial muscle fibers, and action potentials travel outward into
SINUS (SINOATRIAL) NODE these atrial muscle fibers. This way, AP spreads through the
entire atrial muscle mass to the A-V node.
- Small, flattened, ellipsoid strip of specialized cardiac
muscle about 3mm wide, 15mm long, and 1mm thick. Velocity of conduction – 0.3m/sec
- Located in the superior posterolateral wall of the right
Conduction in several
atrium immediately below and slightly lateral to the
small bands – 1m/sec;
opening of the superior vena cava.
these bands contain
- Sinus nodal fibers connect directly with the atrial
specialized conduction
muscle fibers, so that any action potential that begins in
fibers.
the sinus node spreads immediately into the atrial
muscle wall. Anterior interatrial band –
one of the smaller atrial
Some cardiac fibers have the capability of self-excitation, a
bands; passes through the
process that can cause automatic rhythmical discharge and
anterior walls of the atria
contraction.
to the left atrium.
Self-excitation is what makes the sinus node control the beat
Anterior, middle, and
rate of the entire heart.
posterior intermodal
Mechanism of sinus nodal rhythmicity pathways – three other
small bands curve through
the anterior, lateral, and posterior atrial walls and terminate in
the A-V node.
THE ATRIOVENTRICULAR NODE DELAYS IMPULSE
CONDUCTION FROM THE ATRIA TO THE VENTRICLES
This delay allows time for the atria to empty their blood into the
ventricles before ventricular contraction begins.
It is primarily the A-V node and its adjacent conductive fibers
that delay this transmission into the ventricles. Look at fig 10-3
above.
Resting membrane potential of sinus nodal fiber is of lower
A total delay of 0.16 second happens before the excitatory
negativity at -55 to -60 millivolts. This is caused by the leaky cell
signal finally reaches the contracting muscle of the ventricles.
membranes of sinus nodes to sodium and calcium ions. The
0.13s delay in the A-V nodal and A-V bundle system, and 0.03s
positive charges of these ions neutralize some of the
from the sinus node to the A-V node.
intracellular activity.
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