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Lecture 9

KINE 3012 Lecture Notes - Lecture 9: Parasympathetic Nervous System, Stroke Volume, Cardiac Muscle


Department
Kinesiology & Health Science
Course Code
KINE 3012
Professor
Tanya Da Sylva
Lecture
9

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The amplitude of the QRS wave is much larger because there are more muscle fibres in the
ventricles. In ventricular depolarization, the atria are actually repolarization. You do not detect
the atria repolarization in the ECG because the ventricles send out a stronger signal and mask
it.
As soon as the ventricles begin to contract, their pressure is higher than the atria which closes
the AV valve. The blood needs to go out the arteries but for a little while it cannot do that
because the pressure in the ventricles need to exceed the arteries. The ventricles must contract
a little bit more after the closing of the AV valve for the blood to go out to the arteries.
Cardiac Output
CO is how much the blood is putting out into circulation. EDV is how much volume of the blood
is in the ventricles after atrial contraction. ESV is the total volume of blood that remains after
ejection. We never eject out the whole volume, there is a little bit left. We can modify both hear
rate and stroke volume to meet the demands of exercise.
Regulation of Heart Rate
Depending on the balance of autonomic nervous system inputs we can control heart rate. We
can speed it up or slow it down through these inputs. Normally at rest parasympathetic
stimulation dominates, so without predominance off parasympathetic stimulation we get 100
beats per minute at rest. Under normal the heart rate is about 70 beats per minute. Normally at
rest parasympathetic stimulation dominates.
Parasympathetic stimulation releases acetylcholine, sympathetic stimulation releases
epinephrine and norepinephrineadrenaline
Slide 54
Increasing heart rate shortens diastolic time, shortening filling time. Because the whole time that
the ventricles are contracting, the atria have been filling up with blood, so even though we have
shortened ventricular filling time, we do not significantly impact the volume coming in. Most of
the volume comes in almost immediately after that rapid filling.
Slide 55
We can increase venous return, the heart is timed so that the more volume comes in the more
comes out. We can also intrinsically increase the force of contraction. We can intrinsically and
extrinsically increase SV. The heart is tied such that the more volume that comes in the more
that goes out. Intrinsic is inside the system, extrinsic is hormonal and neuronal control. The
intrinsic control is coming from the heart’s ability to inherently control stroke volume.
Frank-Starling mechanism
Cardiac muscle contraction is not determined by bone but heart position its self unlike skeletal
muscle. At rest your cardiac muscle is not at tits optimal length, as we fill the heart with more
and more blood, it approaches optimal length. Under normal operating condition, the heart
muscle fibres never stretch beyond optimal length. The more blood coming in, the more we
eject out. It is the intrinsic nature of contractile fibres themselves.
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Extrinsic control of SV
CA that couple electrical stimulation and contraction. Mainly going to be the autonomic nervous
system, in this case mainly sympathetic and epinephrine.
61
When we increase stroke volume though sympathetic innervation more blood comes back to the
heart and the end diastolic volume increases as well.
62
Frank-Starling mechanism and sympathetic innervation work together. Sympathetic stimulation
can actually increase the contraction force.
Ejection Fraction
Around 40% of blood consistently remains in the ventricles
The overall goal is to equal cardiac output to metabolic levels. We need ways to both increase
and decrease cardiac output. Sympathetic activity can increase the heart rate and strength of
heart contraction. Parasympathetic activity can affect the Auto rhythmic tissue of the SA node
and affect HR.
If a heart begins to weaken and fail we can no longer match cardiac output with the body’s
demands. For a while we cannot notice that the heart is beginning to fail because our body can
increase sympathetic stimulation to somewhat compensate to increase EDV, contraction and
heart rate. Especially on end diastolic volume. As we continue to demand more from the heart
we cannot keep up. Muscle tissue over time can become numb to epinephrine and
norepinephrine. Eventually the muscles become unresponsive. The kidneys begin to retain
more water to compensate for less blood reaching the tissues. Less blood means lower stroke
volume, the retaining of water increases fluid volume. As we retain more water, increasing blood
volume, we are increasing end diastolic volume. Now what can happen is that we’ve gone over
optimal lengths. If we’ve stretched the heart muscle too far as the body tries to compensate, we
actually end up pumping out less blood. Congestive heart failure is also called forward failure.
Backwards failure is when the blood pools in the venous system. Slide 69 is very important
Diastolic dysfunction
Chambers need to go in a cycle, if the ventricle cannot properly relax then it does not fill
adequately. Unfortunately no drugs can make the heart reliably relax.
Systolic dysfunction
There are ways we can treat this unlike the aforementioned.
Nourishment of the heart muscle
Needs nutrients and gases and waste removal. The heart receives most of its blood supply
during diastole. During systole, the coronary blood flow is actually decreased significantly
because the muscles compress the coronary arteries.
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