Transcript cardiac output and regulation of stroke volume during exercise

BY : DR FARIHA RIZWAN

Quantity of blood ejected by ventricle per
minute.

Quantity of blood ejected by left ventricle into
aorta and from Rt.ventricle in pulmonary
arteries is same.
It is equal to venous return i.e, the amount of
blood enters the right atrium per min.
 C.O= S.V x H.R
=70 x 72 =5.5 L/min
 So the C.O is 5.5 L/min in male adults
 it is 10-20% less in young females.

1) Emotional state (anxiety, excitement)
2) Exercise ( In trained atheletes, it increases
to 35 L/min).
3) Intake of meals.
4) Exposure to high environmental temp.
5) Pregnancy in later months.
6) Hyperthyroidism: Increase metabolic
activity, increase oxygen consumption.
7) Anaemia
8) Injection of epinephrine
 Postural
change: Sitting & standing from
lying position.
 Myocardial diseases.
 Atrial fibrillation
 Complete heart block
 Cardiac failure
 CARDIAC
OUTPUT
 Cardiac output (0) is the product of the heart
rate (HR) and the stroke volume (SV)
(amount of blood pumped per beat)
CO=HR x SV
 Thus cardiac output can be increased due to
a rise in either heart rate or stroke volume.
 During exercise in the upright position (e .g.,
running, cycling, etc. ),the increase in
cardiac output is due to an increase in both
heart rate and stroke volume.
 Regulation
of Heart Rate
 During exercise, the quantity of blood
pumped by the heart must change in
accordance with the elevated skeletal
muscle oxygen demand.
 Because the SA node controls heart rate,
changes in heart rate often involve factors
that influence the SA node.
 The two most prominent factors that
influence heart rate are the parasympathetic
and sympathetic nervous systems
The parasympathetic fibers that supply the heart
arise from neurons in the cardiovascular control
center in the medulla oblongata and make up a
portion of the vagus nerve.
 Upon reaching the heart,these fibers make
contact with both the SA node and the AV node.
 When stimulated, these nerve endings release
acetylcholine.
 It increases the permeability of K ions causes a
decrease in the activity of both the SA and AV
nodes due to hyperpolarization.
 The end result is a reduction of heart rate.
Therefore the parasympathetic nervous system
acts to slow down the heart rate.

 Studies
have shown that the initial increase
in heart rate during exercise, up to
approximately 100 beats per minute, is due
to a withdrawal of parasympathetic tone
 At higher work rates , stimulation of the SA
and AV nodes by the sympathetic nervous
system is responsible for increases in heart
rate.
 Sympathetic
fibers reach the heart by means
of the cardiac accelerator nerves,
 which innervate both the SA node and the
ventricles .
 Endings of these fibers release
norepinephrine upon stimulation, which act
on beta receptors in the heart and cause an
increase in both heart rate and the force of
myocardial contraction.
 At
rest. a normal balance between
parasympathetic tone and sympathetic
activity to the heart is maintained by the
cardiovascular control center in the medulla
oblongata.
 For
example, an increase in resting blood
pressure above normal stimulates pressure
receptors in the carotid arteries and the arch
of the aorta, which in turn send impulses to
the cardiovascular control center.
 In response, the cardiovascular control
center increases parasympathetic activity to
the heart to slow the heart rate and reduce
cardiac output . This reduction in cardiac
output causes blood pressure to decline back
toward normal.
 Another
regulatory reflex involves pressure
receptors located in the right atrium.
 In this case, an increase in right atrial
pressure signals the cardiovascular control
center that an increase in venous return has
occurred; hence, to prevent a backup of
blood in the systemic venous system.
 The
cardiovascular control center responds
by sending sympathetic accelerator nerve
impulses to the heart which increase heart
rate and cardiac output.
 The end result is that the increase in cardiac
output lowers right atrial pressure back to
normal, and venous blood pressure is
reduced.
 Finally,
a change in body temperature can
influence heart rate.
 An increase in body temperature above
normal results in an increase in heart rate,
 whereas lowering of body temperature below
normal causes a reduction in heart rate.
 Stroke
volume, at rest or during exercise, is
regulated by three variables
( I) the end-diastolic volume (EDV),
which is the volume of blood in the
ventricles at the end of diastole
(2) the average aortic blood pressure;
(3) the strength of ventricular contraction.
 EDV
is often referred to as "preload," and it
influences stroke volume in the following
way
 Two physiologists, Frank and Starling,
demonstrated that the strength of
ventricular contraction increased with an
enlargement of EDV (i.e , stretch of the
ventricles)
 This relationship has become known as the
FrankStarling law of the heart
 The
increase in EDV results in a lengthening
of cardiac fibers which improves the force of
contraction in a manner similar to that seen
in skeletal muscle.
 the influence of fiber length on cardiac
contractility is that an increase in the length
of cardiac fibers increases the number of
myosin cross-bridge interactions with actin
resulting in increased force production .
A rise in cardiac contractility results in an
increase in the amount of blood pumped per
beat
 The principal variable that influences EDV is the
rate of venous return to the heart.
An increase in venous return results in a rise in
EDV and therefore an increase in stroke volume.
Increased venous return and the resulting
increase in EDV play a key role in the increase in
stroke volume observed during upright exercise.
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A second variable that affects stroke volume is the
aortic pressure (mean arterial pressure) .
In order to eject blood, the pressure generated by
the left ventricle must exceed the pressure in the
aorta.
Therefore, aortic pressure or mean arterial pressure
(called afterload) represents a barrier to the
ejection of blood from the ventricles.
Stroke volume is thus inversely proportional to the
afterload; that is, an increase in aortic pressure
produces a decrease in stroke volume.
However, it is noteworthy that afterload is
minimized during exercise due to arteriole dilation.
This arteriole dilation in the working muscles reduces
afterload and makes it easier for the heart to pump a
large volume of blood .
 The
final factor that influences stroke
volume is the effect of circulating
epinephrine norepinephrine and direct
sympathetic stimulation of the heart by
cardiac accelerator nerves
 Both of these mechanisms increase cardiac
contractiIity by increasing the amount of
calcium available to the myocardial cell
 In particular, epinephrine and norepinephrine
both increase in entry of extracellular
calcium into the cardiac muscle fiber.
 There
are three principal mechanisms
1. VENOCONSTRICTION
2. MUSCLE PUMP
pumping action of contracting skeletal
muscle
3.RESPIRATORY PUMP
(pumping action of the respiratory system)
 I.
Venoconstriction increases venous return
by reducing the volume capacity of the veins
to store blood .
 The end result of a reduced volume capacity
in veins is to move blood back toward the
heart.
 Venoconstriction occurs via a reflex
sympathetic constriction of smooth muscle in
veins which is controlled by the
cardiovascular control center
 2.
Muscle pump.
 is a result of the mechanical action of
rhythmic skeletal muscle contractions.
 As muscles contracts they compress veins
and push blood back toward the heart
 Between contractions, blood refills the veins
and the process is repeated .
 Blood is prevented from flowing away from
the heart between contractions by one-way
valves located in large veins
 3.
Respiratory pump. The rhythmic
pattern of breathing also provides a
mechanical pump by which venous
return is promoted
During inspiration, pressure within the thorax
(chest) decreases and abdominal pressure
increases.
 This creates a flow of venous blood from the
abdominal region into the thorax and therefore
promotes venous return .
 the role of the respiratory pump is enhanced
during exercise due to the greater respiratory
rate
 recent evidence indicates that the respiratory
pump is the predominant factor that promotes
venous return to the heart during upright
exercise.
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•Cardiac output is the product of heart rate and
stroke volume (0 = HR X SV)
The pacemaker of the heart is the SA node. SA node activity is
modified by the parasympathetic nervous system (slows HR) and
the sympathetic nervous system (increases HR).
Heart rate increases at the beginning of exercise due to a
withdrawal of parasympathetic tone. At higher work rates , the
increase in heart rate is achieved via an increased sympathetic
outflow to the SA nodes.
Stroke volume is regulated via
(I) end-diastolic volume
(2) aortic blood pressure
(3) the strength of ventricular contraction.
Venous return increases during exercise due to
(I) venoconstriction,
(2) the muscle pump
(3) the respiratory pump.