REGULATION OF CARDIAC OUTPUT

By- AFTAB KHAN

 Objectives

• Describe intrinsic and extrinsic regulation of cardiac output

 Cardiac output

• Cardiac output is the quantity of blood pumped into the

aorta each minute by the heart.
• This is also the quantity of blood that flows through the
circulation.

• CO = SV x HR
 Normal values for cardiac output at rest and during activity
Cardiac output varies widely with the level of activity of the
body.
The following factors, among others, directly affect cardiac
output:
(1) The basic level of body metabolism,
(2) Whether the person is exercising,
(3) The person's age, and
(4) Size of the body
 Normal values cont...

For young, healthy men, resting cardiac output averages about

5.6 L/min.

For women, this value is about 4.9 L/min.

 Regulation of cardiac out put
• Under most normal unstressful conditions, the
cardiac output is controlled almost entirely by
peripheral factors that determine venous
return.

• If the returning blood does become more than

the heart can pump, then the heart becomes the
limiting factor that determines cardiac output
 Regulation cont....

• Heart is not the primary controller of cardiac output.

• Instead, factors of the peripheral circulation affecting

venous return, are the primary controllers.

• The main reason peripheral factors are usually more

important than the heart itself in controlling cardiac
output is that the heart has a built-in mechanism that
normally allows it to pump automatically whatever
amount of blood that flows into the right atrium from the
veins.
 Venous Return

• The greater the difference between the mean systemic filling

pressure and the right atrial pressure, the greater becomes
the venous return.
• Therefore, the difference between these two pressures is
called the pressure gradient for venous return.
 Factors aiding venous return
• Venous return is aided by
the:
Valve (open)
—Respiratory “pump” —
pressure changes
Co n t ract e d
created during skeletal
muscle
breathing suck blood
toward the heart by
squeezing local veins Valve {closed)

—Muscular “pump” —
contraction of skeletal
Vein
muscles “milk” blood
toward the heart
• Valves prevent backflow
during venous return 9
 Body position

b l o o d evenly dis t r ibut ed i n veins

increased
central venous pressure

b lo o d pools i nc re a sed
end-<giastolic vo l u m e

increased increased
stroke v o u m e pulse pressure

40
Factors resisting venous return

• Right atrial pressure

• Resistance to blood flow
• Venous return can be calculated by the following formula:
VR— Psf—PRA/ RVR
in which VR is venous return, Psf is mean systemic filling
pressure, PRA is right atrial pressure, and RVR is resistance to
venous return

12
 Regulation cont....

• A combination of factors together determine cardiac

output.
• These include preload, afterload, contractility and heart
rate
• Intrinsic:
filling pressure(preload)
Arterial pressure (afterload)

• Extrinsic :
Parasympathetic, sympathetic effects and hormonal
 Determinants of cardiac output

• Preload = initial stretching of the cardiac myocytes prior to

contraction (related to sarcomere length)

• Afterload = “load” that the heart must eject blood against

(related to aortic pressure)

• Contractility (inotropy) = inherent ability of myocardial cells

to develop force at given muscle lengths (related to
calcium)

• Heart rate autonomic nervous system

16
Cardiac Output Regulation— 2 Categories :

What can stretch the atria or ventricli

a} Homeometric
INCREA D PRELOAD
- stretch atria I E»< '
- irritability of SA Node

Heart Rat

- stretch ventricles
force of conYaction
 Cardiac output is controlled by venous return
• Increased venous return causes increased stretch of cardiac muscle
fibers. (Intrinsic effects)
—increased cross-bridge formation
—increased calcium influx
• both increases force of contraction
—increased stretch on SA node
• increases heart rate

48
 Increase in preload

, mo re sh a r t e n i n g

1 20
6țj‹zI zl 'eJnSsaJg A1

8O -
mrs re
stro ke vOlum e
4O
Iarg e r
v e n t rictJIar
pre Ioad
.
OO 19
L V volume, mL
Increased after load

20
 Factors Affecting End-diastolic Volume

Ventricular performance
Total blood Body Intrathoracic
V O lume positio pr e S sure
n
Atrial Intrapericardial
contrib. to STRETCHING OF MYOCARDIUM pressure
vent. filling ventricular
compliance
Pumping action Venous tone
to skeletal muscle
 Preload vs Afterload

Venules / veins Arterioles

Capacitance Resistance
vessels vessels
Affect preload Affect afterload

2J
 us Nerve R h7agus Nem•e

AV Node SA Node
Atrial muicle fibers .AYial mua:le fibei s

Rate at which K+
Heart Rate by
progressive9 declines
Rate at which K+ Intracelluhr Ca++
permeab?ity progressively within the venYieular
dec¥nes mua:le fibers

Heart Rate Force of Contraction

26
 Regulation of heart rate

mV -
25

-50

-75

• Sympathetic nervous system

• sympathetic nerves release norepinephrine
• plus circulating epinephrine from adrenal medulla
• both act on ß-receptors on sinoatrial node
• increases slope of the pacemaker potential
• increases heart rate = tachycardia
 Regulation of heart rate

mV -
25

-50

-75

• Parasympathetic nervous system

• vagus releases ACh
• acts on muscarinic receptors on sinoatrial node
• hyperpolarizes cells and decreases slope of pacemaker
potential
• decreases heart rate = bradycardia
28
 29
D
¥
o
0°
'0
 of a.trial”
c c • n . t x t Łc n

c r eæ sæ
venou. s return.

30
 Effect of Bainbridge and Baroreceptor
Reflex on HR

Increased Bainbridg
Intravenou Stimulate
s infusion right e reflex
i l t rial
atrial
receptors
pressure
Heart
rate

Increased Increased Barorecept

cardiac arterial or reflex
output pressure
 C. Humoral regulation

THYROID
GLUCAGON

POTENTIATION
CARDIAC FACTORS COUPLING FACTORS

HEART RATE PRELOAD

CARDIAC
OUTPUT

MYOCARDIAL
AFTERLOAD
CONTRACTILITY
Summary of Factors COntrOlling Cardiac 0utpUt
THANK YOU!!!