2. cardiac output

CARDIAC OUTPUT
PHYSIOLOGY: CARDIOVASCULAR

CONTROL OF HEART RATE
OVERVIEW
‣ The heart rate is established by the Sinoatrial Node (SAN) – the pacemaker of the
cardiac muscle
‣ In the absence of any influences the SAN pacing rate would be 100 bpm, however
heart rate and cardiac output must be able to vary in response to the needs of the
body
‣ By influencing the cells in the SAN, nerve impulses and hormones can affect the
speed at which the SAN generates electrical impulse
‣ This affects the heart rate (or chronotrophy), which in turn affects the cardiac
output
Learning Goal
‣ To discuss how hormones and nerve impulses work to control the rate of the heart

THE AUTONOMIC NERVOUS SYSTEM
‣ The ANS is responsible for controlling many physiological
functions:
‣ the force of contraction of the heart
‣ peripheral resistance of blood vessels
‣ heart rate
‣ The ANS has both sympathetic and parasympathetic
divisions that work together to maintain balance

PARASYMPATHETIC
‣ The parasympathetic input into the heart is via the vagus
nerve (CN X)
‣ The vagus nerve forms synapses with postganglionic cells
in SAN and AVN
‣ When stimulated, acetylcholine which binds on to M₂
receptors, which acts to decrease the slope of the
pacemaker potential, leading to a decrease in heart rate (a
negative chronotropic effect)

SYMPATHETIC
‣ The sympathetic input into the heart is via the postganglionic fibres from
the sympathetic trunk which innervate the SAN and AVN
‣ The post ganglionic fibres release noradrenaline, which acts on B₁
adrenoreceptors to increase the slope of the pace maker potential, thereby
increasing the heart rate (a positive chronotropic effect), as well as increasing
the force of contraction (positive inotropic effect)
‣ The parasympathetic input on the SAN dominates at rest, to give a normal
resting heart rate of around 60bpm
‣ Any initial increases in heart rate are brought about by a reduction in
parasympathetic outflow, and increasing the heart rate over 100bpm is via
an increase in sympathetic outflow

http://droualb.faculty.mjc.edu/Course%20Materials/Physiology%20101/Chapter%20Notes/Fall%202007/
chapter_13%20Fall%202007%20Phy%20101.htm

BARORECEPTOR REFLEX
‣ Baroreceptors are mechanoreceptors located in both
the carotid sinus and the aortic arch, which are sensitive to
stretch
‣ Their function is to detect changes in arterial pressure and
communicate this to the medulla oblongata in the brainstem
‣ The medullary centres in the brain are responsible for the
overall output of the autonomic nervous system, and use the
information fed back from baroreceptors to coordinate a
response.

BARORECEPTOR REFLEX
‣ If an increased arterial pressure is detected:
‣ the parasympathetic pathway is activated to reduce heart rate
‣ this, along with increasing vasodilation of vessels, acts to reduce
the arterial pressure
‣ If a decrease in arterial pressure is detected:
‣ the sympathetic pathway is activated to increase the heart rate and
the force of contraction of the heart
‣ this, along with increasing vasoconstriction of vessels, acts to
increase the arterial pressure

https://teachmephysiology.com/cardiovascular-system/cardiac-output/control-heart-rate/

HORMONAL CONTROL
‣ Hormones also have the ability to affect the heart rate
‣ One example would be adrenaline, which is released from
the medulla of adrenal glands
‣ This hormone can be released into the blood stream at a
time when a person encounters a stressful situation
‣ The release of this hormone can result in a number of
effects one of which is increasing of the heart rate

REVIEW QUESTIONS
‣ Which of these is normally the natural pacemaker of
cardiac muscle?
‣ Sino-atrial node (SAN)
‣ Atrio-ventricular node (AVN)
‣ Ventricular myocytes
‣ Purkinje fibres

REVIEW QUESTIONS - RATIONALE
‣ While all of these are natural pacemakers, the heart will
follow the rhythm of the fastest pacemaker.
‣ This is normally the SAN which would naturally fire at a
rate of approximately 100 action potentials per minute.
‣ It actually fires 70 times a minute due to parasympathetic
influences.
‣ However, this may not always be the case as in disease
states the SAN may not be the fastest pacemaker.

REVIEW QUESTIONS
‣ Which of these terms refers to the rate at which the heart
beats?
‣ Inotropy
‣ Inopulsy
‣ Chronotropy
‣ Chronopulsy

REVIEW QUESTIONS
‣ Which of these terms refers to the rate at which the heart beats?
‣ Inotropy
‣ Inopulsy
‣ Chronotropy
‣ Chronopulsy
(Chronotropy refers to the rate at which the heart beats. You can
remember this as chrono- refers to time (as in chronology). Conversely
inotropy refers to the force of the heartbeat. Inopulsy and chronopulsy
do not exist.)

REVIEW QUESTIONS
‣ Through which receptor does the parasympathetic system
act to influence the heart?
‣ M1-AchR
‣ M2-AchR
‣ M3-AchR
‣ M4-AchR

REVIEW QUESTIONS
‣ Through which receptor does the parasympathetic system act
to influence the heart?
‣ M1-AchR
‣ M2-AchR
‣ M3-AchR
‣ M4-AchR
(The parasympathetic system acts on the heart via the M2
acetylcholine receptor.)

REVIEW QUESTIONS
‣ Which of these is NOT an action of the sympathetic
nervous system (SNS) on the heart?
‣ Reduce the AV delay
‣ Increase heart rate (positive chronotropy)
‣ Increase force of contraction (positive inotropy)
‣ Activate beta-1 adrenoceptors

REVIEW QUESTIONS
‣ Which of these is NOT an action of the sympathetic nervous system
(SNS) on the heart?
‣ Reduce the AV delay
‣ Increase heart rate (positive chronotropy)
‣ Increase force of contraction (positive inotropy)
‣ Activate beta-1 adrenoceptors
(The SNS does not affect the AV delay. It is only parasympathetic nervous
system that affects it, increasing this delay. The SNS increases the rate
and force of contraction via its activation of beta-1 adrenoceptors.)

REVIEW QUESTIONS
‣ What is the correct chronological order of the baroreceptor reflex?
Increased blood pressure,…
‣ ..increased baroreceptor firing, changes in medullary centre firing,
blood pressure falls, reduced cardiac output
‣ ..changes in medullary centre firing, increased baroreceptor firing,
reduced cardiac output, blood pressure falls
‣ ..reduced cardiac output, increased baroreceptor firing, blood
pressure falls, changes in medullary centre firing

REVIEW QUESTIONS
‣ What is the correct chronological order of the baroreceptor reflex?
Increased blood pressure,…
blood pressure falls, reduced cardiac output
‣ ..changes in medullary centre firing, increased baroreceptor firing,
‣ ..increased baroreceptor firing, changes in medullary centre
firing, reduced cardiac output, blood pressure falls
‣ ..reduced cardiac output, increased baroreceptor firing, blood
pressure falls, changes in medullary centre firing

‣ Changes in blood pressure are detected by baroreceptor
pressure sensors located in the walls of blood vessels.
‣ This change in firing is relayed to the central medullary
centres which can co-ordinate the response.
‣ These responses will include changes in cardiac output as
well as vasodilation/vasoconstriction.
‣ This will oppose the original changes in blood pressure,
restoring homeostasis.

REVIEW QUESTIONS
‣ Which of these is NOT a cause of tachycardia at rest?
‣ Infection
‣ Hypovolemia
‣ Hypothyroidism
‣ Hypoglycaemia

REVIEW QUESTIONS
‣ Which of these is NOT a cause of tachycardia at rest?
‣ Infection
‣ Hypovolemia
‣ Hypothyroidism
‣ Hypoglycaemia
(Hyperthyroidism, rather than hypothyroidism, is a cause
of tachycardia at rest.)

REVIEW QUESTIONS
‣ Which of these is a type of wide complex tachycardias?
‣ Wolff-Parkinson-White syndrome
‣ Atrial flutter
‣ Sinus tachycardia
‣ Atrial fibrillation

‣ Wolff-Parkinson-White sysndrome is the only condition
listed that produces a tachycardia with a wide QRS
complex.
‣ Another example could have been ventricular
tachycardias.
‣ Atrial flutters, sinus tachycardias and atrial fibrillation are
all narrow complex tachycardias as the produce narrow
QRS complexes on an ECG.

CONTROL OF STROKE VOLUME
OVERVIEW
‣ Cardiac output is defined as stroke volume multiplied by heart rate
‣ This is therefore affected by stroke volume and sympathetic/
parasympathetic output to the heart
‣ Stroke volume is affected by how much the heart fills in diastole and
how easy it is for blood to be expelled in systole
Learning Outcome
‣ To consider components of stroke volume, Starling’s law, its
regulation and clinical conditions that may occur when it is
inadequate to meet the body’s needs

STROKE VOLUME
‣ Stroke volume is defined as
‣ the difference between the volumes of blood in the heart at the end of
diastole (maximum filling) and the volume remaining in the heart at the end of systole
‣ i.e. the volume of blood that is expelled with each beat
‣ Control of stroke volume is therefore directly related to the amount the heart fills and the
heart’s ability to pump blood into the arteries
‣ Central venous pressure changes result in a change to the diastolic filling pressure
‣ Total peripheral resistance/arterial resistance dictates how easy it is for the heart to expel
blood
‣ Total peripheral resistance increases with vasoconstriction -> increasing arterial blood
pressure -> making it harder for the heart to expel blood into the arteries -> thus reducing
stroke volume

https://teachmephysiology.com/cardiovascular-system/cardiac-output/control-stroke-volume/

STARLING’S LAW
‣ Central venous pressure increases if the volume of blood in the venous system
increases
‣ This increases the diastolic filling pressure therefore increases the volume of
blood that is available to be pumped out (this is explained by Starling’s law of
the heart)
‣ Starling’s law states that the more the heart fills the harder it will contract
therefore the bigger the stroke volume (up to a point)
‣ This is based on the principle that the force developed in a muscle fibre
depends on the degree to which the fibre is stretched
‣ Therefore a rise in central venous pressure will result in an increased stroke
volume automatically

STARLING’S LAW
‣ The Starling curve relates stroke volume to venous pressure and the slope defines the contractility of the ventricles
‣ The preload of the heart is the volume of venous blood that stretches the resting cardiac muscle
‣ The filling of the left ventricle during ventricular diastole results in the end-diastolic volume
https://teachmephysiology.com/cardiovascular-system/cardiac-output/control-stroke-volume/

AUTONOMIC REGULATION
‣ Contractility is also controlled by the autonomic nervous system
‣ It has both sympathetic and parasympathetic (vagal) innervation that act to
increase or decrease heart rate and contractility
‣ Sympathetic stimulation has a positive inotropic effect (increases contractility)
acting via beta-1 adrenoceptors
‣ Vagal stimulation has a (very mild) negative inotropic effect (decreases
contractility) acting via muscarinic (M2) receptors
‣ Autonomic control is regulated by the medulla oblongata in the brainstem
which receives sensory input from peripheral and central baroreceptors and
chemoreceptors located in the carotid sinus, arch of the aorta and carotid body

REVIEW QUESTIONS
‣ What is the definition of cardiac output?
‣ 5L/min
‣ The volume of blood that leaves the heart every
second
‣ Stroke volume multiplied by heart rate
‣ Volume of blood pumped by the heart every minute
divided by the body surface area in square meters

REVIEW QUESTIONS
‣ Cardiac output is the volume of blood leaving the heart in a
given time. Conventionally we use the units L/min. This can be
calculated by using the volume of blood that leaves that heart
during each ventricular contraction (stroke volume) and the
number of times the heart beats in a single minute (heart rate).
Just multiply them together! This is normally around 5L/min,
however this is not the definition of the term cardiac output. If
you divide the cardiac output by the body surface are in
square meters, you will get the cardiac index. This is also a
very useful measure but not what the question was asking for!

REVIEW QUESTIONS
‣ Which of the following will cause an increase in stroke volume?
‣ An increase in total peripheral resistance (TPR) such as from
an increase in sympathetic tone
‣ An increase in venous return such as from increase skeletal
muscle pump action during running
‣ Use of verapamil hydrochloride (a calcium channel blocker)
such as to treat angina
‣ Hyperkalemia

REVIEW QUESTIONS
‣ Which of the following will cause an increase in stroke volume?
‣ An increase in total peripheral resistance (TPR) such as from
an increase in sympathetic tone
‣ An increase in venous return such as from increase
skeletal muscle pump action during running
‣ Use of verapamil hydrochloride (a calcium channel blocker)
such as to treat angina
‣ Hyperkalemia

REVIEW QUESTIONS
‣ Increasing venous return increases the force with which the
heart fills (increased preload), causing it to fill and stretch more.
The increased stretch causes it to contract with more force,
ejecting more blood (and increasing SV) via the Frank Starling
mechanism. Increasing TPR increased the forces opposing
ejection of blood from the heart (increased afterload). This
makes it harder for the heart to empty, reducing SV. Verapamil
hydrochloride reduces the force with which the heart contracts
(reduced contractility) which lead to less blood leaving the
heart (reduced SV). Hyperkalemia also reduces contractility,
causing a decrease in SV.

REVIEW QUESTIONS
‣ Which of the following is not true? The more the heart
fills…
‣ ..the greater the force generated in maximum
contraction, up to a point
‣ ..the more actin-myosin cross bridges form, up to a point
‣ ..the greater the muscle stretches
‣ ..the less energy is needed to empty it

REVIEW QUESTIONS
‣ As the heart fills it requires more energy to empty. This
question is based on Frank Starling's Law, which states that
as the heart fills, the muscle stretches more, creating more
regions of overlap for actin-myosin cross bridges to form,
allowing a greater force of contraction to be generated
during systole. However, as there are more cross-bridges,
there will be more cross-bridge cycling occurring which
uses more ATP and more energy.

REVIEW QUESTIONS
‣ Which of the following does not affect contractility?
‣ Direct stimulation of the sino-atrial node (SAN)
‣ Use of dobutamine (a beta-1 adrenoceptor agonist)
such as for treatment of cardiomyopathies
‣ Increased parasympathetic stimulation
‣ Activation of peripheral and central baroreceptors

REVIEW QUESTIONS
‣ Stimulating the SAN will increase the heart rate, rather than
contractility. Sympathetic and parasympathetic stimulation
of the heart has positive and negative effects, respectively,
on its contractility. Though, the parasympathetic effect is
much lower in the ventricles. Dobutamine activates the
sympathetic receptors in the heart and so increases
contractility. Physiologically, peripheral and central
baroreceptors can increase parasympathetic tone on
detection of high blood pressure. Thus, the activation of
these baroreceptors can also cause changes in contractility.

REVIEW QUESTIONS
‣ Which of these is not a type of shock?
‣ Toxic shock
‣ Acute stress shock
‣ Cardiogenic shock
‣ Mechanical shock

REVIEW QUESTIONS
‣ While shock can be caused by acute stressors, it is not a
classification of shock. Toxic shock is related to
widespread vasodilation such as that caused by bacterial
toxins. Cardiogenic shock is that caused by a failing heart.
Mechanical shock is where filling of the heart is physically
restricted, such as in cardiac tamponade.

REVIEW QUESTIONS
‣ Which of these is not a sign of shock?
‣ Low blood pressure
‣ Rapid and shallow breathing
‣ Acute memory loss
‣ Tachycardia

REVIEW QUESTIONS
‣ While acute memory loss may be seen in psychological
shock, it is not generally associated with the physiological
shock discussed in this article. Low blood pressure, rapid
and shallow breathing and a fast heart rate are typically
seen in shock.

References
These slide reflect a summary of the contents of
TeachMePhysiology.com and are to be used for
educational purposes only in compliance with the terms of
use policy.
Specific portions referenced in this summary are as follows:
‣ https://teachmephysiology.com/cardiovascular-system/cardiac-output/control-
heart-rate/
‣ https://teachmephysiology.com/cardiovascular-system/cardiac-output/control-
stroke-volume/
Additional sources are referenced on the slide containing
that specific content.

2. cardiac output

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