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Cardiac output, venous return

and
Arterial blood pressure
Cardiac function curve
(Frank-Starling relationship)
Venous return (VR)
Venous return is the amount of blood received by the
right atrium per minute
In normal person, it is same as cardiac output (5 L/min)
The pressure gradient between the right atrium and
the peripheral veins is the driving force for VR
Higher the gradient, greater will be the venous return;
Lower the gradient, less will be the venous return
Factors that increase this gradient improve VR
Factors that increase venous return are:
Negative intrathoracic pressure
Increase in total blood volume (preload)
Contraction of skeletal muscles
The vascular function curve
V
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o
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s

r
e
t
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n

(
L
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i
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)

Right atrial pressure (mm Hg)
It is the plot between the venous return and right atrial pressure
Normal
point
An inverse relationship exists
between RAP and VR in the
range 0 to 7 mm Hg of RAP
No further increase in VR
occurs when RAP < 0 mm Hg
as veins collapse at negative
pressures
Mean circulatory filling
pressure

The effect of changing total blood volume on
vascular function curve
N
N = Normal blood volume
Low blood volume:
Curve shifts downward
& to the LEFT
Mean circulatory
pressure falls
Increased blood volume:
Curve moves upward & to RIGHT
Mean circulatory pressure rises
Combining cardiac function curve and
vascular function curve
Cardiac output and venous return are dependent
on each other
Interaction between them is best understood by combining
the two function curves because RAP is common in both
The point at which the two curves intersect is called the
steady state (CO=VR)
Combining the two curves helps us to predict the changes
in cardiac output under various conditions
In every condition, a new steady state is reached
The new steady state depends on which curve is primarily
changing due to the disturbance
Combining cardiac function curve and
vascular function curve
Steady state
The factors that change the cardiac and
vascular function curves
Factor Curve that gets
altered

Change in myocardial Cardiac
contractility function curve

Change in blood volume Vascular
function curve

Effect of increasing myocardial contractility
on combined curves:
Positive inotropic agents
E.g.: Sympathetic nerves,
digitalis
Normal
N
N
Increase in contractility

Increase in cardiac output

Decrease in RAP

Increase in venous return

Steady state point moves
upward & to the left
Effect of increasing total blood volume
on combined curves:
Increased blood volume:
E.g.: Infusion of IV fluids
Normal
N
N
Increase in blood volume

Increase in venous return

Increase in RAP

Increase in cardiac output

Steady state point moves
upward & to the right
Progressive changes in cardiac function curves
in Heart Failure (failure of contractility)
See next graph
Immediate effect of reduced contractility: (Point B)
There is a reduction in CO; This soon changes due to
the compensatory changes
Compensated failure: (Point C)
Blood volume expansion has partially restored the
CO by Starlings mechanism; This gradually progresses
to massive volume expansion
Decompensated failure: (Point D)
As failure progresses, there is severe reduction in
contractility despite extreme increase in preload, due
to overstretching of ventricle.
At this point, increase in preload is harmful to heart!
Progressive changes in Heart Failure
A
B
C
D
SYSTEMIC ARTERIAL BLOOD PRESSURE (BP)
Blood pressure is the lateral pressure exerted by the
flowing blood on the vessel wall
Arterial blood pressure is of two types:
Systolic pressure (SP) and diastolic pressure (DP)
Normal expression of arterial blood pressure:
BP = SP/DP in mm Hg
BP apparatus:
Sphygmomanometer
Normal BP in adults:
120/80 mm Hg
SYSTEMIC ARTERIAL BLOOD PRESSURE (BP)
Mean arterial pressure (MAP):
Is the average arterial pressure during a single cardiac cycle
It is calculated by formula:
MAP = Diastolic pressure + 1/3 Pulse pressure
Normal MAP = 80+(1/3x40) = 93.33 mm Hg
(approximated to 100 mm Hg)
It is the driving force for blood flow to the organs
The relationship between MAP, cardiac output (CO) and
total peripheral resistance (TPR):
MAP = CO x TPR
Note: Since CO and TPR are not independent factors, doubling TPR
will not double MAP in the body; same with changes in CO!
Regulation of systemic arterial blood pressure (BP)

Normal MAP is maintained at a value of about 100 mm Hg
This constant value is called set point value of MAP
The set point value is determined by the BP regulatory
centers in the brain stem
Any disturbance that tries to change the BP from this
set point value is strongly resisted by the BP regulatory
systems in the body
The responses offered by the BP regulatory systems
bring MAP back to the set point value. This is called
arterial pressure regulation
Two major BP regulatory systems exist in human:
a. Baroreceptor reflex mechanism short term control
b. Renin-angiotensin-aldosterone system long term
Baroreceptor reflex mechanism of regulation
of arterial blood pressure (BP)
It is a rapid, short term BP regulatory mechanism
It is a reflex mechanism mediated through nervous system
Components of baroreceptor reflex:
Stimulus: Changes in mean arterial pressure
Receptors (sensors): Baroreceptors (stretch receptors)
in carotid sinus and aortic arch
Afferent (input) path: Sinus nerve (IX N), vagus nerve (X N)
Integrating center: Brain stem BP regulatory centers
Efferent (output) path: Sympathetic nerves to heart & blood
vessels; Parasympathetic nerves to heart (via X N)
Effector organs: Heart, arterioles, veins
Response (effect): Changes in cardiac output and TPR
Purpose: To maintain MAP at set point value
Baroreceptor are mechanoreceptors
that detect arterial blood pressure (BP)
Increase in MAP

Stretching of carotid sinus
and aortic arch

Increased firing rate of
baroreceptors

Action potentials travel
via IX N and X N

Cardiovascular regulatory
centers in brain stem
Baroreceptor response to increase in BP
Decrease in sympathetic nerve activity
& increase in parasympathetic nerve
activity to the heart
Decrease in sympathetic nerve
activity to veins and arterioles
Decrease in heart rate and
decrease in contractility
Decrease in
venous return
Dilatation of
arterioles
Decrease in cardiac output
(CO = HR x SV)
Decrease in
TPR
Decrease in arterial BP
(MAP = CO x TPR)
Increase in baroreceptor impulses to cardiovascular regulatory centers
Baroreceptor response to decrease in BP
Increase in sympathetic nerve activity
& decrease in parasympathetic nerve
activity to the heart
Increase in sympathetic nerve
activity to veins and arterioles
Increase in heart rate and
increase in contractility
Increase in
venous return
Vasoconstriction
of arterioles
Increase in cardiac output
(CO = HR x SV)
Increase in
TPR
Increase in arterial BP
(MAP = CO x TPR)
Example : Hemorrhage Fall in arterial BP
Decrease in baroreceptor impulses to cardiovasc. regulatory centers
Regulation of BP by Renin-angiotensin-
aldosterone mechanism
This is a long term mechanism of regulation of BP since
the system takes hours to days to become effective
The mechanism is mediated by hormones
The mechanism regulates BP by regulating blood volume
The activation of the system in response to a low BP
produces a series of responses to increase blood volume
Blood
volume
Cardiac
output
Arterial
BP
Blood volume is altered by altering salt and water in body
Regulation of BP by Renin-angiotensin-
aldosterone mechanism
Decrease in blood volume
Decrease in arterial blood pressure
Decrease in blood flow to the kidneys
Sensed by juxtaglomerular cells of afferent arterioles and
they secrete enzyme, renin into circulation
Renin converts angiotensinogen to angiotensin I in plasma
Angiotensin I is converted to angiotensin II as blood flows through
lungs and kidneys by enzyme, angiotensin converting enzyme
Continued to the next slide..
Regulation of BP by Renin-angiotensin-
aldosterone mechanism
Angiotensin II acts on zona
glomerulosa of adrenal cortex
Hormone, Angiotensin II
Angiotensin II acts on the
hypothalamus
Secretion of hormone,
Aldosterone by adrenal cortex
Secretion of hormone,
antidiuretic hormone (ADH)
Aldosterone increases
sodium reabsorption in kidneys
ADH increases water
reabsorption in kidneys
Retention of salt and water in the body increases blood volume
Increase in arterial blood pressure
Regulation of arterial BP by
Renin-angiotensin-aldosterone mechanism
Retention of Salt and
Water increases plasma
volume, Cardiac output
and Blood Pressure
Increase in TPR and
Blood Pressure
Pathophysiological basis for hypertension

Hypertension: Is a sustained elevation of the systemic
arterial pressure
Basis: There is either an increase in blood volume
or increase in TPR or increase in both
Any disease that increases these factors will produce
elevation of arterial pressure
Salt and water retention increases blood volume
and increases blood pressure
Examples:
Renal diseases: Activation of renin-angiotensin-
aldosterone system as in renal artery stenosis
Endocrine diseases: Adrenal cortical tumors producing
large amount of aldosterone or mineralocorticoids as
in Conns syndrome, Cushings syndrome