Cardiac output &

venous return
 CARDIAC OUTPUT &
VENOUS RETURN
CARDIAC OUTPUT: Quantity of blood pumped into the
aorta each minute by the heart. In a resting supine man,
it is 5L/min
C.O = ARTERIAL PRESSURE (Ohm’s Law)
TPR
C.O = STROKE VOLUME X HEART RATE
C.O = 70ml x 72 beats/min = 5000ml = 5 L (approx)
 CARDIAC INDEX
It is the correlation between resting C.O &
body surface area.
C.I = C.O / min / m2 of body surface
70kg man has body surface area = 1.7 m 2
So C.I = 5L/min = 3L / min / m2 (approx)
1.7m2
 CO=V.R X H.R
VENOUS RETURN is the quantity of blood
flowing from the veins into the right atrium each
minute.

Normally V.R = C.O (Frank starling law)

STROKE VOLUME is the difference between

EDV & ESV = 120 – 50 = 70ml.

S.V is the amount of blood pumped out by each

ventricle during each beat. When heart rate is
normal (72/min), it is 70ml (60-80ml).
EJECTION FRACTION: is the fraction of
EDV that is ejected out by each ventricle.
Normally it is 60-65%.

MINUTE VOLUME: is the amount of blood

pumped out by each ventricle in one minute.

M.V = S.V (stroke vol.) X H.R (heart rate)

M.V = 5L /ventricle / minute
 CARDIAC RESERVE:
is the maximum amount of blood that can be
pumped out by the heart above normal value.

SIGNIFICANCE: It can increase C.O during

stress like exercise.
C.R = 300-400% (in young adult)
C.R = 200-250% (in old age)
C.R = 500-600% (in athletes)
C.R = 0% approx (in cardiac diseases)
FACTORS AFFECTING C.O:
PHYSIOLOGICAL FACTORS

PATHOLOGICAL FACTORS
 PHYSIOLOGICAL FACTORS:
1. AGE:

CHILDREN = less C.O (due to low B.Vol)

& C.I of children >C.I of adults (due to
less body surface area).

OLD AGE = less C.O (due to low

metabolic activity).
2. SEX:

In FEMALES: C.O = less,

C.I = more (due to less
surface area)

In MALES: C.O = more,

C.I = less (due to more body
surface area)
3. BODY BUILD:

C.O is more if body build is greater

4. DIURNAL VARIATION:

C.O = low in morning (due to low BMR)

C.O = more in day time (due to high

BMR,vasodilatation when more

oxygen is required.)
5. TEMPERATURE:

C.O = increases if temp increases above

30°C.
Mechanism:Vasodilatstion of skin bd vs to
loose heat, dereased PR, increased CO.
6. EMOTIONAL CONDITIONS:
C.O = increases by 50-100% in Anxiety
& excitement.

Mechanism: Release of CATS 

increased H.Rate & Force of contraction.
7. AFTER MEALS:

C.O = increased during 1st hour after

meal.
8. EXERCISE:

C.O = increased (depending on severity

of exercise).

MECHANISM: Increased oxygen

consumption by tissues. Increase in H.
Rate & Force of contraction.
9. HIGH ALTITUDE:

C.O = increased

MECHANISM: Due to hypoxia 

secretion of adrenaline.
10. POSTURE:

C.O = decreases when recumbent 

upright position.

MECHANISM: Pooling of blood  in

lower limbs, when we stand up from lying
position.
11. PREGNANCY:

C.O = increased by 45-60% in later

months of pregnancy due to
increased bd volume.
12. SLEEP:
C.O = reduced / unchanged during sleep.
 PATHOLOGICAL FACTORS:
1. PYREXIA / FEVER:
C.O = increased (rapid metabolism),
Direct effect on SA node to increase heart
rate.
2. ANEMIA:
C.O = increased
In anemia, two peripheral effects greatly
A -decrease the total peripheral resistance.
reduced viscosity of the blood, resulting from
the decreased concentration of red blood cells.
B - diminished delivery of oxygen to
the tissues, which causes local vasodilatation.
3. ABNORMAL THYROID FUNCTION:

HYPERTHYROIDISM: C.O increases

(due to increased BMR).

HYPOTHYROIDISM: C.O decreases

(due to decreased BMR).
4. ABNORMAL HEART CONDITIONS:

ATRIAL FIBRILLATION: C.O is decreased (due

to incomplete filling).

INCOMPLETE HEART BLOCK with coronary

sclerosis or myocardial degeneration: C.O is
decreased (due to defective pumping).

CCF: C.O is less (due to weak contraction of

heart).
AV FISTULA
severe coronary blood vessel
blockage and consequent myocardial
infarction,
severe valvular heart disease, myocarditus,
cardiac tamponade(External pressure on
heart) ,
cardiac metabolic derangements
 5. ABNORMAL CIRCULATORY
CONDITIONS:
1. Decreased blood volume
HEMORRHAGE : C.O = less (due to low
blood volume :
SHOCK: C.O = less (due to poor pumping
& deficient circulation).
2. Acute venous dilation: sudden loss of
sympathetic nervous system inactivity,
which causes the peripheral capacitative
vessels, especially the veins, to dilate
markedly. the blood “pools” in the vessels
and does not return to the heart.
3. Obstruction of the large veins. =no return
to heart=low C.O
4. Decreased tissue mass, especially
decreased skeletal muscle mass .With
normal aging or with prolonged
periods of physical inactivity, there is usually
a reduction in the size of the skeletal
muscles.less oxygen demand,less bld
flow=lowC.O
 DISTRIBUTION OF C.O:
BLOOD  LEFT VENT.  SYSTEMIC
CIRCULATION:
LIVER = 1500ml = 30%
KIDNEYS = 1300ml = 26%
SKELETAL MUSCLES = 900ml = 18%
BRAIN = 800ml = 16%
SKIN+BONE+GIT = 300ml = 6%
HEART = 200ml = 4%
(charagh talay undhaira)
TOTAL = 5000ml = 100%
 Abnormal cardiac output
Abnormal regulatory factors:
A- Abnormal heart rate.
B-Abnormal stroke volume (contractility of
myocardium, end diastolic and end systolic
vol.)
C. Abnormal PR. Increased PR decreases CO.
Abnormal CO due to abnormal
PR
 FACTORS REGULATING C.O:

C.O = STROKE VOL. X HEART RATE

C.O REGULATING FACTORS INCLUDE:

1. FACTORS REGULATING S.V (EDV-

ESV)

2. FACTORS REGULATING HEART

RATE
EDV AFFECTING FACTORS:
1. V.R (most important factor)
2. M.S.F.P
3. B.P
4. SYMPATHETIC STIMULATION
5. SKELETAL MUSCLE PUMP
6. GRAVITY
7. RESPIRATORY PUMP

8. FILLING TIME
9. DURATION OF DIASTOLE
10. DISTENSIBILITY OF VENTRICLE
11. ATRIAL CONTRACTION
ESV AFFECTING FACTORS:
1. FORCE OF HEART CONTRACTION
(FRANK STARLING LAW)

2. AFTER LOAD

3. SYMPATHETIC / VAGUS NERVES

4. CONDITION OF MYOCARDIUM

5. HORMONES / DRUGS WHICH INCREASE

CONTRACTILITY OF HEART

6. FACTORS WHICH DECREASE C.O.

 FACTORS AFFECTING EDV:
1. VENOUS RETURN:
Most important factor.
Amount of blood which returns to heart/min.
Basic factors affecting V.R:

V.R = ARTERIAL B.P

TPR

V.R = MEAN SYSTEMIC FILLING Pr – Rt. At. Pr

RESISTANCE TO V.R

V.R = MSFP-RAP
RVR
2. MSFP:
Mean Systemic Filling Pressure is average pressure in
systemic blood vessels which tends to push the blood
towards the heart, when there is no active circulation.
It indicates the degree of filling of blood vessels.
MSFP depends on:
A) how much vessel is filled
B) if the vessel is compressed from
outside
Normal MSFP = 7mmHg
MSFP is affected by blood volume, symp. Stim. &
contraction of skeletal muscles. (Directly proportional)
More B.V  more pr.  more V.R (in blood loss 
low B.V  low V.R)
Symp. Stim.  V.C  more V.R
Skeletal muscle contraction  more pr.  more V.R
RIGHT ATRIAL PRESSURE = C.V.P = 0 in
most of Cardiac Cycle.
RVR (RESISTANCE TO V.R) is resistance
offered by veins against the return of blood
= 1.4mmHg/L
So V.R = MSFP-RAP
RVR
V.R = 7-0 = 5L
1.4
 Effect of hormones & drugs
which increase C.O: (by increaseing contraction of
heart)
Cats
Thyroxine
Glucagon
Increased temperature
Caffeine
Theophylline
Digitalis
Calcium ions
Factors which decrease C.O

Heart failure
Hypoxia
Acidosis
Barbiturates
Beta adrenergic blockers
 FLOW CHART OF C.O:
C.O

H.RATE STROKE
FILLING TIME VOLUME
TEMP P.SYM INHIB
SYMP ST ATRIAL CONTR EDV ESV
DIST OF VENT
PRELOAD AFTER LOAD
IMPULSES FROM STARLING LAW ART. Pr
CVS RECEPTORS VR
& BRAIN CENTERS CARDIAC CONTRACTILITY

ART BP & TPR MSFP

THOR. NERVOUS STIM. CARDIAC NUTR
MOVE& DRUGS & MET
I.Th.Pr B.VOL SYMP ST SK MUS CONTR
FACTORS AFFECTING HEART
RATE COMPONENT OF C.O:
RELATION BETWEEN H.R & C.O:
Generally when H.R increases  C.O
increases. (but the limit is 150/min)
Between 150-180 beats/min, there is no
increase in C.O.
Beyond 180-190 beats/min, C.O
decreases, with increasing heart rate.
WHY???
*THIS DECREASE IN C.O, WITH H.R
BEYOND 180-190/MIN IS BECAUSE OF
TOO SHORT DIASTOLE. (FRANK
STARLING LAW).
NERVOUS CONTROL OF HEART
RATE:
Heart beat is autonomous but is modified
by nervous mechanisms:
1) Autonomic nerves supplying the heart:
Sympathetic
Parasympathetic
2) Vasomotor centre (effected by impulses

from different parts of the body).

SYMPATHETIC NERVE SUPPLY
TO HEART:
Pre-ganglionic sympathetic nerve fibers
from upper thoracic segments of spinal
cord (T1-T5) supply the heart.
These will go through sympathetic chain to
cervical ganglia & from here post-
ganglionic fibers supply the heart (through
superior, middle & inferior nerves).
 EFFECTS OF SYMPATHETIC
STIMULATION:
1) +CHRONOTROPIC EFFECT:
Increase in heart rate.
Due to release of nor-epinephrine from
post-ganglionic nerve endings.
Nor-epinephrine  decreased permeability
for K ion (at SA node)
But  increased permeability for Na & Ca
ions (at SA node)
RESULT: increase in H.R.
2) + IONOTROPIC EFFECT:
Increased force of contraction.
Due to increased permeability for Ca ion
 more Ca ions inside the sarcoplasm.
3) + DROMOTROPIC EFFECT:
INCREASED CONDUCTIVITY IN HEART.
Due to AV nodal delay.
4) + BATHMOTROPIC EFFECT:
INCREASED EXCITABILITY OF HEART.
Sympathetic stimulation can cause 
extrasystoles by increased excitability.
 EFFECT OF SYMPATHETIC STIMULATION ON
CORONARY BLOOD FLOW:

SYPATHETIC STIMULATION has

DIRECT EFFECT (coronary V.C)
& INDIRECT EFFECT* (coronary V.D
with increased coronary blood flow)
* INDIRECT EFFECT IS MORE
IMPORTANT.
Main factor which regulates coronary
blood flow is LOCAL METABOLISM of
myocardium, here important factor is
OXYGEN CONSUMPTION & DEMAND.

Coronary blood flow is autoregulated

according to oxygen consumption &
demand. More oxygen consumption 
increased blood flow.
INDIRECT EFFECT:
Symp. Stimulation  increased force &
.contraction  increased oxygen consumption
 decreased partial pressure of oxygen in
myocardium  release of V.Ds in myocardium:
(Adenosine is most important & others are CO2,
K ion, H ion, PGs, Bradykinin, Pyruvate &
Lactate)  dilatation of coronaries  coronary
blood flow increased
PARASYMPATHETIC N.SUPPLY:
THROUGH VAGI.

RIGHT VAGUS: Supplies SA node

LEFT VAGUS: Supplies AV node

Vagi contain pre-ganglionic parasympathetic fibers,

which arise from dorsal nucleus of vagus.

Vagal nerve fibers supply SA node, AV node, Atrial

muscle & AV bundle BUT NOT THE VENTRICULAR
MUSCLE.
 EFFECTS OF VAGAL
STIMULATION:
1) – CHRONOTROPIC EFFECT:
SLOWING OF H.R.

On vagal stimulation  Acetyl Choline

(from vagal nerve endings)  increased
permeability of SA nodal fiber Mm for K
ion  hyperpolarization & slowing of H.R.
2) SLIGHT – IONOTROPIC EFFECT:
Only slight effect because vagal fibers do
not supply ventricular muscle.
3) – DROMOTROPIC EFFECT:
Slowing of conduction in heart & AV nodal
delay is prolonged.
4) – BATHMOTROPIC EFFECT:
DECREASED EXCITABILITY OF HEART.
5) EFFECT ON CORONARY BLOOD
FLOW:
DIRECT (coronary V.D)?
INDIRECT * (coronary V.C which
decreases coronary blood flow).
* INDIRECT EFFECT IS MORE
IMPORTANT.
With vagal stimulation  decreased H.R &
decreased force of contraction 
decreased myocardial oxygen
consumption  decreased release of V.Ds
 V.C  decreased coronary blood flow
& vagal stimulation.
 VAGAL ESCAPE:
When there is strong vagal stimulation, the heart stops
beating, but when this strong stimulation of vagi is
continued, after sometime, heart starts beating again.
MECHANISM:
1) Due to continuous vagal stimulation, the stores of
A.Ch in vagal nerve ending are exhausted.
2) Idio-ventricular rhythm:
Because of vagal stimulation, when impulses are not
produced by SA node, ventricles develop their own
rhythm called IDIO-VENTRICULAR RHYTHM.
There is continuous effect of vagi on heart or there is
continuous inhibitory or breaking effect of vagi on heart,
called VAGAL TONE.
If we cut one vagus N, heart rate increases. If
we cut other vagus, further increase in H.R.
Sympathetics also have tonic effect on heart, but
not as strong as vagal tone.
Normally vagal tone is more predominant than
sympathetic tone, specially in ATHLETES.
If heart is taken out of body, H.R becomes
90/min. (tachycardia) . WHY???
IT IS DUE TO NO MORE EFFECT OF
VAGAL TONE.
 Effect of Sympathetic
Inhibition on Cardiac Output.
The sympathetic nervous system can be
blocked by inducing
total spinal anesthesia or by using some
drug, such as hexamethonium, that blocks
transmission of nerve signals through the
autonomic ganglia.
The lowermostcurves in Figure 20–15 show
the effect of sympathetic inhibition caused by
total spinal anesthesia, demonstrating that
(1) the mean systemic filling pressure falls
to about 4 mm Hg and
(2) the effectiveness of the heart
as a pump decreases to about 80 per cent
of normal.
The cardiac output falls from point A to
point B, which is a decrease to about 60
per cent of normal.