Cardiac Control (Myogenic hearts) summary

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7 Mar 2011
Myogenic Hearts
The spontaneous rhythmic beating of the heart is the result of electrical activity that originates
from a pacemaker. This electrical activity spreads throughout the heart causing it to contract. In
vertebrates, the pacemaker cells are located in the sinoatrial (SA) node in the upper region of the
right atria. The pacemaker cells spontaneously depolarise and generate action potentials (AP)
that then spread throughout the heart. Although the activity of the pacemaker can be influenced
by nervous input, it does not need any input in order to depolarise. A myogenic heart is one in
which the pacemaker cells are specialised muscle cells.
The electrical activity (action potential) generated in the SA node spreads in an orderly fashion
throughout the heart. First, the wave of depolarisation (action potentials) spreads throughout both
atria. The cells in the atria are large and therefore have a low resistance to the flow of electrical
current. This allows the wave of depolarisation to pass very quickly throughout the atria. A
fibrous septum between the atria and the ventricles prevents the spread of electrical activity from
the atria to the ventricles at all but one location – the atrioventricular (AV) node).
The wave of depolarisation that swept through the atria converges at the AV node. Conduction
through the AV node is slow due to the fact that the cells in the AV node are quite small and have
a large resistance to the flow of current. This slow transition through the AV node is important
because it allows time for the atria to fully contract before the wave of depolarisation hits the
ventricles causing them to contract. Since contraction of the atria is (in part) involved in the
filling of the ventricles with blood, it is important to allow the atria to completely contract and
eject blood into the ventricles before the ventricles pump it out through the aorta or the
pulmonary artery.
From the AV node, the wave of depolarisation moves down the Bundle of His and into the right
and left branch bundles. The Bundle of His and the branch bundles are located in a fibrous
septum that separates the right and left ventricle. As the electrical activity spreads down the
branch bundles there is no depolarisation (or contraction) of the cardiac muscle itself. The
electrical activity remains in the branch bundles within the fibrous septum.
The wave of depolarisation leaves the branch bundles and enters Purkinjie fibres. The Purkinjie
fibres move upward into the cardiac muscle. The wave of depolarisation passes from the
Purkinjie fibres into the muscle causing the muscle cells to depolarise and the ventricles to
contract. Since the wave of depolarisation moves from the bottom (apex) of the heart upward,
contraction of the ventricles occurs from the bottom to the top of the ventricles. This is important
because the vessels leaving the ventricles (aorta and pulmonary artery) are at the top of the
ventricles. This pattern of contraction means that blood is being forced upward in the ventricles
toward the blood vessels.
The cells in the heart are electrically joined (or coupled) together by gap junctions. Within the
gap junction there is a channel that connects one cell to the next cell. This means that electrical
activity can directly pass from one cell to the next without the need of a neurotransmitter. This
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has the advantage of allowing for rapid movement of the wave of depolarisation throughout the
muscle and helps to ensure a smooth contraction. Within the gap junction collections of protein
fibres called a desmosomes help to keep cells held together when the heart muscle stretches
during the filling of the atria and ventricles with blood. This is important because stretching of
the heart can lead to a reduced ability to pump blood.
The Neuronal Action Potential (AP)
The neuronal action potential begins from a starting point at which the membrane potential is at
the resting level. A stimulus causes a small depolarisation which increases the membrane
potential slightly. Once the membrane potential reaches the threshold for firing (threshold
potential), an action potential occurs in which membrane potential rapidly increases (cell
depolarises) and then decrease (repolarises). It ends with a slight overshoot of the repolarisation
(i.e., membrane potential goes below the resting potential for a brief period) before membrane
potential once again stabilises at the resting potential. For another AP to occur, the cell must be
stimulated again so that membrane potential rises to the threshold for firing.
The depolarisation phase of the neuronal action potential occurs due to an increase in Na+
permeability (opening of voltage-gated Na+ channels) and the influx of Na+ (with its positive
charge) into the cell. At the top of the AP, Na+ permeability begins to decrease. This helps
contribute to the repolarisation. At the same time, the K+ permeability is beginning to increase
(K+ channels open) and potassium moves out of the cell. This is the delayed rectifier K+ current
(delayed because it does not start until the middle of the AP and rectifier because it helps return
membrane potential to rest). The undershoot (hyperpolarisation below rest) results from the
increase in potassium permeability and the delayed closure of the K+ channels.
Following the AP, membrane potential remains at the resting level until a stimulus triggers
another AP.
The Pacemaker Potential
Pacemaker cells within the sinoatrial (SA) node do not have a resting membrane potential. As
soon as one AP has finished, the membrane begins to spontaneously depolarise until it reaches
threshold and an AP is generated. This spontaneous depolarisation is referred to as the
pacemaker potential.
The pacemaker potential can be divided into two parts, the first and second part. In the first part,
the depolarisation is the result of opening of “funny channels that allow Na+ to move into the
cell. However, the funny channels do not stay open very long. They close when the membrane
potential is about half way to depolarisation (i.e., around -55mV). At this point, T-type Ca++
channels open and Ca++ enters the cell. This Ca++ current carries the membrane potential to
threshold at which point an AP is generated.
Autonomic Regulation of Heart Rate
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