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Outline the effects of the sympathetic nerves on the heart

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					Outline the effects of the sympathetic nerves on the heart?
Sympathetic nerves act as part of the reaction to the ‘fight, fright or flight’
scenario. The nerves are distributed not only to the sinoatrial and
atrioventricular nodes but also to the cardiac muscle of both ventricles and
atria. The effects of sympathetic innervation can be broken down into
increasing the heart’s rate of pumping and also increasing the heart’s
strength of contraction. The sympathetic nerves release noradrenaline at
their junctions. Sympathetic activity also causes adrenaline to be released
from the adrenal medulla. Both these neurotransmitters bind to β 1
adrenoreceptors in the SA node. This process increases cAMP levels in the
cell and results in a faster increase in sodium and calcium permeability
during the pacemaker stage of the potential and thus producing early action
potentials. Hence more action potentials can occur in a set time and the rate
of firing of the SA node determines the rate of contraction in the heart and so
this increases as well. Sympathetic fibers also innervate the atria, AV node,
Purkinje fibers and ventricular muscle. Their effect here is mostly to
increase the speed of conduction. The AV node delay is decreased and the
action potential duration itself is shortened. This shorter cycle is caused by
sarcolemmal increases in permeability to potassium and calcium ions and a
more rapid uptake of calcium ions in to the sarcoplasmic reticulum. The
other effect of the sympathetic innervation in increasing contractile strength
and ejection velocity is explained by the increased permeability to calcium
ions which are essential for the contraction process. In this way cardiac
output can be increased by up to 100%. Under normal conditions the
sympathetic stimulation has the heart pumping at about 30% of a higher rate
than it would do without stimulation.

Explain the effects of parasympathetic nerve activity on heart rate.
The parasympathetic nerve system is associated with energy conservation
and the normal activity of the body. Parasympathetic activity decreases the
heart rate. Both sympathetic and parasympathetic systems are tonically
active in the heart but the latter is more active in humans at rest and reduces
the rate from about 100 to 70 beats per minute. Since the vagus transmits the
parasympathetic fibers, the heart is described as having vagotonic tone. The
vagus has fibers distributed to the AV and SA nodes as well as the atria. The
system releases acetylcholine at its junctions and this acts on muscarinic
cholinoceptors in the SA node to hyperpolarize and slow the rate of
pacemaker potential depolarization. The hyperpolarization is achieved by a
decrease in cAMP activity which is triggered by the muscarinic receptors
which inhibit adenylate cyclase via the G protein. This decrease in cAMP
causes additional potassium channels to open, and reductions in the
permeability to calcium and sodium ions reduces the slope of the pacemaker
potential. This response is faster to occur than sympathetic stimulation.
Parasympathetic fibers also innervate the atria and the AV node where it
increases the AV node delay. The action potential duration itself is
lengthened by parasympathetic activity. Although parasympathetic
innervation via the muscarinic receptors decreases atrial contractility it does
not affect ventricular contractility. This reinforces the notion that the main
effect of parasympathetic innervation is to reduce heart rate and hence
cardiac output.

Discuss the mechanisms used by the body to increase cardiac output.
Cardiac output is the volume of blood pumped per minute by each ventricle.
It is the product of stroke volume and heart rate. Thus to increase the cardiac
output, one must increase either of these two elements. To increase, heart
rate, sympathetic stimulation can increase the rate of firing in the SA node
and also the rate of conduction of action potentials in the heart’s conducting
system and this increases the heart rate. On the other hand, stroke volume is
subject to intrinsic and extrinsic control. Intrinsic control causes the heart to
respond with a greater force of contraction, ejecting a larger stroke volume
when end diastolic volume increases according to Starling’s law of the heart.
EDV can be altered by events in the chest and changes in blood volume or
venous capacity. More negative intrathoracic pressure than normal such as
occurs on large inspirations will increase EDV. An increased venous return
when one changes from standing to reclining will do the same. A moderate
increase in heart rate increases end-diastolic volume due to an increase in
atrial contractility. Very high heart rates are more complicated. A very high
heart rate reduces the time available for filling and so end diastolic volume
has a tendency to fall. The increase in myocardial contractility increases the
rate of ventricular relaxation and this increases the rapid phase of ventricular
filling. On balance the end diastolic volume remains about the same and so
cardiac output increases. Increased volumes in the ventricle produce stronger
contractions as the cardiac muscle fibers are normally at a less than optimal
state before contractions. Increased volumes bring the fibers closer to the
optimal position and thus contractile strength increases. This control is
limited as the ventricle can only stretch to a limit before one exceeds the
optimal position. Extrinsic control is dependent on sympathetic controlled
calcium entry into muscle fibers which enhances myocardial contractility
and ejection velocity.
Draw an ECG trace and briefly explain the origin of each wave.
The first wave in an ECG is the P wave. This is caused by atrial
depolarization. The SA node produces action potentials which spread
throughout the atrial muscle which then depolarizes as a synctium. The
action potential causes the opening of fast sodium channels and slower
calcium channels with a decrease in permeability to potassium ions which
depolarizes the membrane. The inside of the cell thus becomes positive and
the outside is also reversed to become negative. The P wave is soon
followed by atrial contraction. The next wave is the QRS complex. This is
the product of depolarization of the ventricles. The complex hides the
repolarization of the atrium which happens almost simultaneously. Thus
while the atria are relaxing the ventricles start to contract. The Q and S parts
are negative because their vectors are directed to the right. The S wave is
directed upwards and to the right because the last part of the myocardium to
be depolarized is the base. The T wave then corresponds to the ventricular
repolarization due to the action of slow acting potassium channels which
leak potassium ions out of the cell and cause it to repolarize. The PQ interval
is the time taken for excitation to spread through the atria, AV node and
bundle of His. The QT and PS intervals are measurements of the duration of
ventricular and atrial action potentials. The reason for the dip before the
spike in the QRS complex is because as ventricular depolarization begins at
the IV septum which depolarizes from left to right, it gives a vector directed
downwards to the right.

How do myocardial autorhythmic cells generate spontaneous
depolarizations?
The resting membrane potential of the cells of the SA node is between -55 to
-60 mV which is less than normal. The lower negativity is caused by the
leaky nature of the membrane of there cells which allow sodium and calcium
ions to enter and thus reduce the negativity of the cell interior. Although
most of the fast sodium channels are closed, the leaky membrane and the
high sodium concentration outside the cell causes further sodium entry and
when the membrane depolarizes to about -40mV, the sodium-calcium
channels open. Thus the depolarization process quickens up until potassium
channels open and cause repolarization as positive potassium ions leave the
cell. At the same time as the opening of the potassium channels the sodium-
calcium channels close. Thus a state of hyperpolarization is obtained but the
potassium channels gradually close and the leaky membrane lets the sodium
and calcium ions in again until the threshold is again reached and another
action potential is released. The rate of action potentials in the SA node is
higher than in the other autorythmic cells and so it is referred to as the
pacemaker of the heart.

Explain how heart sounds are generated during a cardiac cycle.
Heart sounds are caused by the closure of valves in the heart. The first heart
sounds are caused by the closure of the AV valves, the bicuspid or mitral
and tricuspid valves respectively. These are opened by the pressure building
in the atria as they fill with blood to allow filling of the ventricle. When the
ventricle is filled, however, the ventricular muscle begins to contract and an
effect of the rising pressure in the ventricle is the closure of the AV valves.
This produces the first heart sound. After this blood is ejected through a
second set of valves, the semilunar valves of the pulmonary trunk and aorta.
However when the blood is ejected, the pressure in the ventricle begins to
fall rapidly as the muscle relaxes. For a moment, the pressure in the aorta
and pulmonary trunk is higher than that in the respective ventricle and thus a
reflux of blood occurs in the direction of the heart. This causes the semilunar
valves to collect the blood into their sinuses and they close. This causes the
second heart sound, which is shorter due to the more rapid closure.

Describe the responses of the cardiovascular and respiratory systems to
exercise.

What property of the sino-atrial node makes it the normal pacemaker of
the heart?
The slope of the pacemaker potential in the SA node is steeper than in the
AV node. Therefore the SA node triggers its action potential first and is the
pacemaker from which the heart beat originates. The action potential arrives
in the AV node well before the pacemaker in the AV node has reached its
threshold and thus is triggered to activation by the AV’s rate of pulsation.

With the aid of a diagram, clearly indicate the pressure changes that occur
in the right side of the heart during a cardiac cycle.
The right atrium has a negative pressure at the end of its ejection of slightly
below zero. This allows a pressure difference for venous blood return from
the capillaries and veins which drain the tissues. It rises to about 2mmHg due
to blood from the veins accumulating behind a closed AV valve. This is
signified by the v wave on the diagram. When right ventricular pressure
drops to below this, the AV valve opens and the blood enters the ventricle.
This corresponds to the y descent in the graph. Atrial contraction in response
to depolarization occurs in late diastole and this contributes the final 20% to
ventricular filling. This is signified by the a wave in the graph. Soon after
this the ventricle starts to contract. When it reaches a greater pressure than
the right atrium, the tricuspid valve is forced to close. The bulging of the AV
valve back into the atrium causes its pressure to rise to about 5mmHg,
known as the c wave. Then, after the isovolumetric contraction period, when
ventricular pressure exceeds pulmonary pressure the pulmonary valve opens
and blood is ejected. The pressure recorded in the pulmonary trunk is
8mmHg in diastole and 25mmHg in systole. The AV fibrous rings are pulled
down during this ejection and this leads to the x descent in the atria. The
ventricles soon relax again and pressure drops leading to the closure of the
pulmonary valve and the opening of the AV valve again.

Explain the changes that occur in each of the following when sympathetic
nerves to the heart are activated:
(a) R-R interval This refers to the time taken for one full cycle in the ECG
to occur. The interval is reduced as the rate of firing in the SA node
increases due to noradrenaline activating a cAMP second messenger system
in the cells which increases the cells permeability of sodium and calcium
ions. Thus a higher firing rate increases the number of ECGs recorded in a
set time. The length of the ECGs themselves also decreases due to the
increased conduction speeds and shorter action potentials in the electrical
conduction system of the heart, in the AV node and purkinje fibers etc. Thus
the interval between two R waves is reduced by both these effects.
(b) P-R interval This refers to the time taken for depolarization to spread
from the atria to the ventricles. This time is shortened because the
conduction speeds of the atria and the AV nodes as well as the purkinje
fibers and the ventricles are all increased under the influence of sympathetic
innervation. The action potential time itself and the AV node delay are both
reduced and so the time between atrial and ventricular depolarizations is
reduced.
(c) duration of systole Systole refers to the contraction of the ventricles and
their emptying of blood into the aorta and pulmonary vessels. The length of
contraction is dependent on the time between ventricular depolarization and
repolarization. This time interval would decrease because of the increased
permeability to potassium and calcium in the sarcolemma.

Outline the changes that occur in the cardiovascular system when one
changes from a supine to an upright position.
When this change occurs, the blood pools in the legs and so venous return is
reduced to the heart. Venous return determines end diastolic volume and this
in turn determines stroke volume. Hence if blood pools in the legs, cardiac
output via stroke volume is reduced.

Discuss the factors that can aid venous return to the heart.
Firstly, 70% of the body’s blood is beneath the level of the heart when
standing. Thus the blood must flow uphill to reach the heart from the veins.
One way of increasing the venous return to the heart is to lie down. In a
supine position blood can flow readily and does not have to oppose the force
of gravity.
Another factor is the work of the muscle pump which pushes blood through
the veins when the muscles around them contract. This muscle pump thus
increases in activity when a person is moving for example when walking the
leg muscles contract and cause blood to flow more rapidly towards the
thorax. This muscle pump when active increases the venous return to the
heart.
Obviously to avoid the reflux of blood back down to the feet after its
movement towards the thorax, valves are an essential factor. Although they
do not actively increase venous return through activation or inactivation, the
venous return of some one whose valves are incompetent will be a lot less
than some one whose valves are functional.
The respiratory pump is also a factor. Flow in the venae cavae increases
during inspiration and falls on expiration. This effect is enhanced when
someone breathes deeply. The intrathoracic pressure is as low as -5mmHg at
the end of respiration and this causes dilation of intrathoracic veins during
inspiration. The descent of the diaphragm increases abdominal pressure and
compresses its veins. The decreased resistance to flow towards the thorax
thus can increase venous return.
There is also a suction effect of the heart’s right atrium found during the x
and y descents. These occur when the AV ring moves downwards and the
AV valve opens respectively. Both these events, temporarily increase venous
return and this effect is greatest during greater cardiac activity.
The primary factor which regulates the venous return is the right atrial filling
pressure. This is the pressure difference between the mean right atrial
pressure and the mean systemic filling pressure. MSFP is usually about
7mmHg and is otherwise known as circulatory pressure. MSFP increases
when blood volume is expanded (when venous capacity is decreased). Thus
when the venous blood is compressed by venoconstriction, the MSFP rises.
Mean right atrial pressure is about 1mmHg and so the difference determines
the rate of venous flow into the heart.
Describe the reflex responses that occur when blood pressure is elevated
above normal levels.
Baroreceptors are located in the wall of the aortic arch and also in the carotid
sinus. An increase in transmural pressure stretches the arterial wall and
stimulates the baroreceptors. This causes the frequency of their action
potentials to increase and the recruitment of more afferent fibers. An
increase in arterial pressure will cause the following changes-
There is an increase in parasympathetic and a decrease in sympathetic
discharge to the SA node causing a fall in heart rate.
There is a decrease in sympathetic discharge to ventricular muscle and the
subsequent decrease in contractility means a reduction in stroke volume.
There is a decrease in sympathetic discharge to the veins which causes
increased compliance and capacity, reducing end diastolic volume.
There is a decrease in sympathetic discharge to the arterioles causing a
decrease in total peripheral pressure. This will result in a greater capillary
pressure, more ultrafiltration across the capillary wall and thus a reduction in
blood volume.

Draw a diagram which shows clearly the magnitude and time course of a
ventricular action potential. Show diagrammatically the conductance
changes which are responsible for this potential change.




The action potential in the ventricles has a magnitude of about 110 mV. The
resting membrane potential is about -90mV and this rises as high as +20mV.
After the initial spike, the membrane remains depolarized for about 0.2
seconds which gives ventricular muscle a contraction 15 times longer than
skeletal muscle. Then about 0.3 seconds into the action potential the
membrane becomes repolarized and the action potential ends.
The above diagram shows the conductance changes in the membrane of a
ventricular muscle fiber during an action potential. The yellow line shows
the opening of the fast acting sodium channels which causes a spike in the
action potential and a dramatic depolarization once the membrane potential
reaches threshold. The red line then shows the increase in permeability to
calcium ions, the opening of the so called slow calcium channels. This is
responsible for the plateau in the action potential. Finally in blue is the
conductance change for potassium ions which is originally reduced by the
membrane depolarization but slowly the effects wear off and more
potassium channels reopen and repolarize the membrane and lead to the fall
in the action potential.

Describe the effects on left ventricular stroke work of:
(a) increased mean arterial pressure;
(b) decreased venous return.
(c) increased heart rate;

Describe the role of the Purkinje system in the heart.
The purkinje fiber system is a part of the conducting system of the heart
which allows the spread of electrical excitation arising rhythmically from the
SA node in the right atrium. The purkinje fibers travel from the AV node in
the IV septum in two bundles of fibers towards the apex of the heart. They
allow for fast conduction of the action potentials so that all parts of the
ventricles contract at roughly the same time. Thus they are large fibers (the
greater the diameter of the fiber the faster the velocity) which allow
conduction speeds of up to 2-4m/s. This speed allow for almost
instantaneous transmission of the excitation throughout the ventricles. The
high speeds of conduction are accounted for also by the high level of
permeability in the gap junctions between successive fibers. The fibers also
have very few myofibrils which means little contraction during the course of
the conduction of the impulse.
A man has a heart rate of 40 beats/min. His ECG has no P waves but has
normal QRS complexes. What is the likely explanation?
This is a slow heart rate. It should be as high as 70 beats/min which is
roughly the rate set by the SA node. The fact that the ECG has no p waves
implies that there is no atrial depolarization. Both these facts lead to the
conclusion that the SA node is not discharging at its normal pacemaker level
and so an ectopic pacemaker, perhaps in the AV node is now controlling the
heart rate.

Use a diagram to show the immediate effects of a sudden, severe decrease
in cardiac pumping ability on cardiac output and right atrial pressure.
A sudden decrease in cardiac pumping ability would lead to a fall in stroke
volume; that is the volume of blood pumped by the heart would decrease. As
cardiac output is dependent on stroke volume by heart rate, then this would
also fall. Mean arterial pressure would also be reduced due to the reduced
blood output. The end diastolic volume in the heart before the next
contraction would then greatly increase as would the atrial pressure as blood
will accumulate here also.
The graphical effect of this decrease in pumping ability can be seen on pg.
397 of lecture notes on human physiology.

Account for the changes in each of the following when impulse frequency
in baroreceptors nerves is increased:
(a) heart rate; The impulse rate in the baroreceptor nerves controls the level
of sympathetic and parasympathetic stimulation in the body. An increase in
MABP will increase the impulse frequency of the baroreceptors. The reflex
change is a decrease in sympathetic activity to the SA node and an increase
in the parasympathetic innervation leading to bradycardia. This will reduce
the cardiac output and thus the MABP.
(b) venous tone; There is a decrease in sympathetic innervation of the veins.
This leads to an increased venous compliance and capacity. The end
diastolic volume of the heart is thus reduced as the relaxation of the veins
reduces venous return and the end result of this is to reduce cardiac output
via stroke volume. This will reduce the MABP.
(c) splanchnic blood flow. The baroreceptor reflex decreases sympathetic
activity to the arterioles and this leads to a decrease in the TPR. This
vasodilation is greatest in the Splanchnic area. There is great potential for
blood reservoir usage here and so diverting blood flow in this direction will
lessen the amount of blood flow in the skeletal circulation etc. Thus sending
blood more easily towards the Splanchnic area can reduce blood volume and
hence lower MABP.

Discuss the factors which determine blood flow through skeletal muscle .
Skeletal muscle receives at rest about 20% of the cardiac output through a
highly resistant vascular bed, the tone of which is controlled by sympathetic
innervation and also by myogenic autoregulation. The veins in skeletal
muscle are almost devoid of sympathetic nerve endings and so their venous
capacity cannot be altered and they cannot act as a blood reservoir. During
exercise, vasodilation occurs in skeletal blood flow. This vasodilation is
mainly controlled by metabolites being released from the energy consuming
muscle fibers. Decreases in pO2, increases in pCO2 pH, potassium ions,
osmolality and adenosine all cause vasodilation. It is impossible to say
which has the strongest effect as the removal of one metabolite leads to
compensation from the others. The contraction of the muscle itself has the
effect of compressing the blood vessels and reducing blood flow into the
muscle. If the contraction is phasic, the blood flow is then seen to be
intermittent and the compensation occurs during relaxations. In maintained
contractions, the metabolites build up but the compression of the blood
vessels is the governing factor. When contraction ends, the metabolites have
an extremely powerful compensatory effect to replenish the oxygen debt. In
skeletal muscle blood vessels, both α and β receptors are present, where
activation of the former causes constriction and the latter causes dilation.
Noradrenaline released from sympathetic fibers causes constriction and
adrenaline, which is present in the circulatory system during exercise, causes
vasodilation. When exercise is ongoing, strange sympathetic fibers are
activated and these release acetylcholine at the nerve endings. The
acetylcholine leads to vasodilation which is paradoxical as one would expect
it to cause smooth muscle to contract. It acts on endothelial cells to
synthesize nitric oxide which diffuses out of the cell and causes smooth
muscle relaxation. Another effect of exercise is to open more muscle
capillaries to allow for greater blood flow through the tissue.

Discuss the factors that determine blood flow through:
(a) brain (see cerebral blood flow)
(b) skin
Cutaneous circulation has two main functions. It provides nutrition to the
tissues and supports metabolic activity and also acts to transfer heat from the
core of the body to the surface. There is a high level of tonic sympathetic
activity in the skin. These release noradrenaline which causes constriction of
the blood vessels and reduces blood flow. This is an important regulatory
step in defense against hemorrhage. Cutaneous tissue can tolerate low blood
flow levels by reducing its oxygen consumption proportionately. Metabolic
regulation is thus deemed to be poor unless the blood flow has been reduced
for some time in which case reactive hyperemia can occur. Large numbers of
arteriovenous anastomoses can also occur in the skin. These have smooth
muscle walls which remain contracted under sympathetic stimulation. When
body temperature increases, the sympathetic levels decrease and these
pathways open. No exchange of nutrients occurs along these anastomoses
but heat is dissipated in the skin surface. Metabolic regulation can over-ride
sympathetic control when the body is exposed to the cold to cause
vasodilation. A triple response is also described to when pressure is applied
to the skin from the outside. Firstly the area of contact is seen to go pale, the
mechanical pressure initiating local contraction of venules or precapillary
sphincters. Greater pressure then causes the skin to become red, followed by
a flare and then a local swelling. This is the triple response. The red reaction
probably results form damaged cells releasing histamine which is a potent
vasodilator. The flare results form mechanical stimulation of nocireceptors
which release substance P (dilating local arterioles and causing mast cells to
release more histamine) and the wheal results from the increase in capillary
permeability induced by histamine and substance P with a consequent rise in
interstitial fluid. Finally adrenaline as is released from the adrenal medulla
due to sympathetic stimulation also causes intense vasoconstriction. This
explains why people go white when they get a fright.

Explain why contractions in cardiac muscle cannot sum or exhibit
tetanus.
This principle is explained with the refractory period of the heart in mind.
During the absolute refractory period of the action potential the cardiac cell
is inexcitable and during the further relative refractory period the heart
gradually recovers excitability. A second action potential cannot be elicited
during the ARP but a very strong stimulus can cause an action potential in
the RRP. This is caused by the closure of the inactivation gates of the
sodium channels shortly after the action potential opens the activation gates.
These channels require the membrane to undergo repolarization before they
will revert to their original conformation and then they can be reopened. The
mechanical and electrical events of the cardiac muscle overlap quite an
amount in time. All of the contraction has taken place by the time the
absolute refractory period is over and cardiac muscle has begun to relax,
which it continues to do so during the relative refractory period. Thus high
frequency stimulation which is necessary to cause summation and tetanus in
skeletal muscle is impossible in cardiac muscle where the action potential is
much longer.

				
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