CARDIAC OUTPUT

Cardiac Output, Venous

Return and their Regulation

Cardiac output is controlled to

maintain the proper amount of
flow to tissues and to prevent
undue stress on the heart.

Cardiac Output

Generally proportional to body surface

area.

Cardiac Index (CI): Approximately 3

liters/min/m2 of body surface area.

CI varies with age, peaking at around 8

years.

Frank-Starling Law

What goes into the heart comes out.

Increased heart volume stretches muscles

and causes stronger contraction.

Stretch increases heart rate as well.

Direct effect on sino-atrial node
Bainbridge reflex (through the brain)

Cardiac Output

Depends on venous return, which, in turn,

depends on the rate of flow to the tissues.

Rate of flow to tissues depends on tissue

needs (i.e. it depends on Total Peripheral
Resistance). Therefore, cardiac output is
proportional to the energy requirements
of the tissues.

Limit of Cardiac Output

Normal CO 5 L/min
Plateau 13 L/min
Hypereffective heart plateau 20
L/min
Hypoeffective heart plateau 5 L/min

Hypereffective Heart

1.
2.

Effected by:
Nervous excitation.
Cardiac Hypertrophy

Exercise Marathon runners may get

30 to 40 L/min
Aortic Valve Stenosis

Hypoeffective Heart

Valvular disease
Increased output pressure
Congential heart disease
Myocarditis
Cardiac anoxia
Toxicity

Autonomic Nervous System

Causes increased cardiac output

when vessels become dilated
(dinitrophenol).

Causes venous constriction during

exercise.

Disease States Lowering Total

Peripheral Resistance

Beriberi: insufficient thiamine tissues

starve because they cannot use nutrients.
AV fistula: e.g. for dialysis.
Hyperthyroidism: Reduced resistance
caused by increased metabolism
Anemia (lack of RBCs): effects viscosity
and transport of O2 to the tissues.

Disease States Lowering

Cardiac Output

Heart attack, valvular disease,

myocarditis, cardiac tamponade, shock.
Shock: Nutritional deficiency of tissues.
Decreased venous return caused by:

Reduced blood volume

Venous dilitation (increased circulatory
volume)
Venous obstruction

Changes in Intrapleural
Pressure
Heart

Pericardial
Sac

tamponade
15 L/min
CO

Generally shift the cardiac

output curve in proportion
to pressure change
(breathing, Valsalva
maneuver).
Cardiac Tamponade (filling
of pericardial sac with fluid)
lowers rate of change of CO
with right atrial pressure

Rt. Atrial Pressure

Determinants of Venous
Return
Mean
systemic
filling
pressure

Resistance to Flow
Pressure change is
slight. Thus, small
increase in RA
Pressure causes
dramatic reduction
in venous return.
(mean systemic
filling pressure).

Right
Atrial
Pressure

Normal Venous Return

Curve
Plateau: collapse of large veins
( => increased resistance)
Working Cardiac Output
5 L/min
VR
(CO)

Venous return with

heart and lung
removed.

Cardiac Output
Curve

-4

Rt. Atrial Pressure (mm Hg)

Mean systemic filling

pressure ~ 7 mm Hg

Filling Pressure

Mean Circulatory: The pressure within

the circulatory system when all flow is
stopped (e.g. by stopping the heart).

Mean Systemic: Pressure when flow is

stopped by clamping large veins.

The two are close numerically.

Venous Return & Cardiac

Output

Cardiac output increases with atrial

pressure.
Normal atrial pressure is about 0 mm Hg.
Venous return (with heart and lungs
removed) decreases with atrial pressure.
Working cardiac output is where venous
return curve meets cardiac output curve.

Compensation for Increased

Blood Volume
1.

2.
3.

4.

Increased CO increases capillary

pressure, sending more fluid to
tissues.
Vein volume increases
Pooling of blood in the liver and
spleen
Increased peripheral resistance
reduces cardiac output.

Effects of Sympathetic
Stimulation

Increases contractility of the heart.

Decreases volume by contracting the
veins.
Increases filling pressure
Increases resistance

Effects of Sympathetic
Inhibition

Shifts CO to the
right
Shifts venous
return down and to
5 L/min
the left

Venous
return
with heart
and lung
removed.

VR
(CO)

- Reduced CO
-4

Rt. Atrial Pressure (mm Hg)

Effects of AV Fistula
1.
2.

3.
4.
5.
6.

7.

Decreased VR resistance.
Slight increased CO because of reduced
peripheral resistance.
After restoration of pressure (sympathetic)
Further CO increase.
Increased filling pressure.
Decreased kidney output (leads to higher
fluid volume and more increase in CO).
Cardiac hypertrophy (caused by increased
workload).

Measurement of CO

Electromagnetic/ultrasonic (transit time)

flow meter.
Oxygen Fick method:
CO = (Rate of O2 absorbed by lungs)
[O2]la - [O2]rv
Indicator dilution method:
Inject cold saline (or dye) into RA, measure
temperature (or concentration) in aorta.