Integrated Control of the Cardiovascular
 Points A & B = venous P at CO 1 & 5L/min
System
LPU-SC College of Medicine 2019
Factors Influencing Vascular Function Curve
 Four factors affecting cardiac output:
- 2 Cardiac: HR & Contractility
- 2 Coupling: Preload & Afterload
*Preload and afterload called coupling
factors = mutually dependent on fxn of heart
and vasculature (fxnal coupling bet heart
and BV)
Central Venous P – P in thoracic vena cava near RA
Vascular Fxn Curve – defines changes in CVP caused by
changes in cardiac output
- Dependent variable (Y) – CVP
- Independent var (X) – CO
 Variables opposite those of cardiac fxn curve
 CVP and CO have and inverse relationship
 ↓cardiac output, ↓rate at w/c heart pumps
blood from veins to arteries, ↑rate at w/c blood
flows from arteries to veins thru capillaries, ↑
net vol of blood in veins, ↓ arterial pressure, ↑
venous pressure
 Pmc = equilibrium P throughout CVS when CO=0
respectively
1. CO = ↓CO, ↓arterial P, ↑venous P
2. Blood Volume = @ 0 CO, Pmc depends only on
blood volume and total vascular compliance
 ↑BVol, ↑Pmc
 @ CO=0, Pmc (hemorrhage) = 5
 @ CO=0, Pmc (transfusion) = 9
 ↑BVol, ↑CVP
 CVP @ w/c veins collapse (sharp
change in slope) unaffected by
change in blood volume
3. Venomotor Tone = pressure w/in vascular
system as a result of ↑smooth muscle tension
(hemorrhage:↓tone::transfusion:↑tone)
 ↑tone,↑Pmc
 Change in peripheral resistance, no change
in Pmc
4. Blood Reservoirs = vascular beds that undergo
significant venous constriction
 Evoked largely by blood loss (diversion
of blood away from less needy organs to
save blood for perfusion through more
vital organs) (gives pale skin color during
hemorrhage)
 Include vascular beds of liver, lungs,
spleen
5. Peripheral resistance = changes in arteriolar
tone

 Changes in contractile state of arterioles
do not significantly alter Pmc (arterioles
contain only 3% of total BVol)
 CVP varies inversely w/ TPR (when all
other factors remain constant)
 If CO=constant, ↑TPR  ↑arteriolar
BVol  ↓venous BVol  ↓venous P
Starling’s Law of the Heart - CO depends closely on right
atrial pressure (CVP).
Cardiac Fxn Curve – graph of cardiac output as a fxn of
CVP
 Cardiac Fxn Curve: Frank Starling Mechanism, a
rise in CVP will result to a rise in CO
 Vascular Fxn Curve: a rise in CO diminishes CVP
 Equilibrium point: intersection of both curves
 Coordinates of equi. pt. represent values of CO
and CVP at w/c the system tends to operate
 Description of how equilibrium is attained after
an increase in CO:
- ↑CVP (may be due to injection of blood
in venous side during ventricular systole)
 ↑CO during nxt vent. systole (A to B)
 transfer of net amt of blood from
venous to arterial side of circuit  small
↓CVP during 1 heartbeat (B to C) 
↓CO during very nxt beat (C to D) 
(while D is still above intersection)
heart will pump blood from veins to
arteries @ a rate greater that that @ w/c
blood will flow across the peripheral
resistance from arteries to veins  CVP
continues to fall until equilibrium is
reached.
Myocardial Contractility
 During the control state the equilibrium point is
designated by point A
 Cardiac sympathetic nerve stimulation abruptly
raises cardiac output to point B because of the
enhanced myocardial contractility.
 However, the vascular function curve is
unaffected, because it only affects the heart.
 And a new equilibrium point is reached (Point
D)
↑ CO, but the CVP (Pv) remained the same
Blood Volume
 Changes in blood volume do not directly affect
myocardial contractility, but they do influence
the vascular function curve.
 After a blood transfusion, the vascular
function curve is shifted to the right.
 Both cardiac output and venous pressure are
increased, as denoted by translocation of the
equilibrium point from point A to point B.
***In cases of Hemorrhage the effect is opposite the
change in ventricular filling pressure (Pv) evoked by a
given change in blood volume alters cardiac output by
changing the sensitivity of the contractile proteins to the
prevailing concentration of intracellular Ca++
Peripheral Resistance
 It affects both the cardiac and vascular
function curves
 Vascular function curve is rotated
counterclockwise, but it converges on the
same Pv axis intercept as the control curve
does.
 Cardiac function curve is also shifted
downward because at any given Pv, the
heart is able to pump less blood against the
greater cardiac afterload imposed by the
increased peripheral resistance.
↑PR = ↓CO
Two-Pump System
 LV- Systemic Vasculature (Rs)
 RV - Pulmonary Vasculature (Rp)
What if the Right Ventricle stops pumping?
 stoppage of right ventricular pumping
markedly curtails cardiac output, systemic
arterial pressure, and pulmonary venous
pressure and raises systemic venous
pressure mode.
***Right ventricle prevents the development of extreme
edema in dependent region of the body.
Role of the Heart Rate in Control of Cardiac Output
 Cardiac output is the product of stroke
volume and heart rate.
 Change in Heart rate alters the:
1. Preload
2. Afterload
3. Myocardial Contractility
***Cardiac Output is Stable

Exercise

 Neural Factors Cardiac output and blood flow to active muscle

 Central command increases as the intensity of exercise increases.
-Brain
Arterioles
-Cerebrocortical activation of the Potassium relaxes 15-20-
sympathetic nervous system fold
 Reflexes that originate in the contracting Adenosine
Increase in
muscle Decrease in pH Blood flow
-Stimulation of mechanoreceptors
 Baroreceptor reflex
 Total Peripheral Resistance
-Pressure  Afterload
 Local Factors  Cardiac output
 Adenosine  Capillary Recruitment
 Potassium
 Hydrostatic pressure in the capillaries
 pH
 H2O and solutes move into the muscle
Mild to Moderate Exercise tissue
 Lymph flow
In humans or trained animals, anticipation of
physical activity inhibits vagal nerve impulses to the Lymph flow is increased as a result of the rise in
heart and increases sympathetic discharge. capillary hydrostatic pressure and the massaging
effect of the contracting muscles on the valve-
Heart rate
containing lymphatic vessels.
Myocardial contractility Cardiac output

Peripheral resistance
 Sympathetic nervous system – mediated
vasoconstriction increases vascular
resistance
 Blood away from the skin, kidneys,
splanchnic regions and inactive muscles.
Sympathetic drive
Parasympathetic drive inhibition of sinoatrial
node
This will lead to Tachycardia
- HR increases until a plateau of 180bpm
In contrast to the large increase in HR the Increase
in SV (stroke volume) 10-35%
Well trained runners’ cardiac output can reach 6-7x
resting value and a stroke volume of 2x the resting
value.
Venous Return HEMORRHAGE
Constriction of capacitance vessels (sympathetic
response)

Increase in Venous return

Blood volume initially decreases during exercise

which results to:
Increase in H2O externally
- Sweating
- Enhanced ventilation
- Fluid movement into the contracting muscle
Coupling Between Heart and Vasculature
Increase in Cardiac Output
Increase in HR, SV, Contractility
Decrease in TPR, Increase in MCP
Arterial Pressure
The increase in Cardiac Output is proportionally
greater than the decrease in TPR
Severe Exercise
Limits of exercise performance
1. Rate of O2 use by muscles
2. O2 supply to muscles
Inability to increase cardiac output beyond
critical level
-limited pumping capacity of the heart
Physical training and conditioning
To increase the capacity to deliver O2
Highly trained athletes
- Decrease Resting HR
- Increase Stroke Volume
- Decrease Peripheral Resistance
Resting HR: Higher vagal tone and lower
sympathetic tone
CO: Stays the same.