1.
Cardiac output
Dr. Amruta Nitin Kumbhar
Assistant Professor
Dept. Of Physiology

2.
SLOs
1. Definition of cardiac output and related terms
2. Measurement of cardiac output
3. Variations in cardiac output
4. Regulation of cardiac output
5. Cardiac output control mechanisms
6. Role of heart rate in control of cardiac output
7. Integrated control of cardiac output
8. Heart–lung preparation

3.
CARDIAC OUTPUT
 Cardiac output is defined as amount of blood pumped out of each ventricle
per minute.
 Cardiac output is expressed in two forms,
 1)stroke volume
 2) minute volume Unit – liter (ml) / min

4.
 CO = SV x HR
 cardiac output = stroke volume X heart rate (ml/minute) (ml/beat)
(beats/min)
 a.Average heart rate = 70 bpm
 b.Average stroke volume = 70−80 ml/beat
 c.Average cardiac output = 5000 ml/minute
 Cardiac output varies widely with the level of activity of the body.
 CO = SV x HR
 Cardiac index is the cardiac output expressed in relation to the
body surface area.
 The normal cardiac index is about 3.2 L/min/m2.

5.
Distribution of the cardiac output
 Of the total cardiac output, about 75% is distributed to the vital organs of the
body and rest of 25% to the skeletal muscle, other organs of the body and
skin.

6.
Regulation of cardiac output
1. Control of HR or Extrinsic autoregulation
2. Control of SV or Intrinsic autoregulation
All the conditions that affect either heart rate or stroke volume or both will produce
variations in the cardiac output

7.
Stretching of myocardium (i.e. extent of preload)
determines

8.
Stretching of myocardium(i.e. extent of
preload)
Increased by Decreased by
1. Increase in total blood volume Decrease in total blood volume
2. Atrial contraction (aid ventricular filling) Increase in intrapericardial pressure
3. Increase pumping action of skeletal
muscle
Decrease in ventricular compliance
4. Increase venous tone Body position
5. Decrease in intra thoracic pressure
(during inspiration)
increase in intra thoracic pressure
(during expiration)

9.
Interaction between the factors that regulate
cardiac output and arterial pressure

10.
Control of heart rate or extrinsic
autoregulation
 Primarily govern by cardiac innervation
 Cardiac centres located in medulla (vasomotor centre, VMC and cardiac vagal
centre, CVC)

11.
Control of stroke volume or intrinsic
autoregulation
1. Heterometric regulation
2. Homometric regulation

12.
Heterometric regulation
 Force of contraction of myocardium is dependent upon its
pre-load and afterload
 Pre-load : is the degree to which the myocardium is
stretched before it contracts
 After- load is the resistance against which the ventricles
pump the blood

13.
Heterometric regulation Homometric regulation
1.Hetero means different; metric means
measure. Therefore, here change in
myocardial contractility varies with initial
length of cardiac muscle fibers.
Thus within physiological limits, force of
ventricular contraction is directly
proportional to the initial length of muscle
fibres
1.Homo means same; therefore here change
in myocardial contractility is independent of
the resting length of cardiac muscle fibers
2. This effect is independent of cardiac
innervation
2. This effect is dependent on cardiac
innervation. Eg.
i. Sympathetic stimulation increases and
ii. Parasympathetic stimulation decreases
myocardial contractility

14.
 The relationship between extent of pre-load and the total
tension developed in cardiac muscle is given by length-
tension relationship (Frank – Starling law)
 Extent of pre-load is directly proportional to the End-
diastolic Volume(EDV) i.e. amount of blood remaining in
ventricles at the end of diastole.
 Any factor which increases venous return (VR) i.e. volume of
blood returning to heart will increase ‘EDV’
 More is ‘EDV’, more will be stretching of the myocardium, i.e
initial length of cardiac muscle fiber ; and more will be the
force of contraction of myocardium

15.
Factors affecting venous return
1. Thoracic pump or respiratory pump
2. Cardiac pump
3. Muscle pump
4. Total blood volume
5. Capacity of venous system
6. Body position
7. Ventricular compliance (distensibility)

16.
Thoracic pump or respiratory pump
 Normal intrathoracic pressure at the end of expiration is
subatmospheric, (-2 mm Hg)
 During inspiration:
i. Intra- thoracic pressure decreases to -5mm Hg causing less
pressure over larger veins and arteries;
ii. Descent of diaphragm, increases intra-abdominal pressure
to squeeze blood out of the abdomen

17.
Cardiac pump
i. Vis-a-tergo i.e force from behind which drives the blood forward
‘VR’ depends on vis-a-tergo i.e. forward push from behind i.e propelling
force which is imparted by:
a) The contraction of heart to the blood during its passage through the
heart
b) Elastic recoil of arterial wall, blood enters the venules with an
appreciable pressure higher than that of right atrium(RA). The flow of
blood in the veins is therefore towards the heart
ii. Vis-a-fronte i.e. force acting from the front to attract blood in the veins
towards the heart. It is exerted by contraction of the ventricles and has 2
components –
a) Ventricular systolic suction-
b) Ventricular diastolic suction-

18.
Muscle pump
 Rhythmic contraction of skeletal muscles, venous segments are squeezed and the
rise of pressure forces the blood towards the heart
 Venous valves prevents back flow
 As soon as muscle relax the depleted segments are promptly refilled from the
more peripheral channels and also from superficial veins vai their valved
communicating channels

19.
Total blood volume
 Increase in total blood volume increases , while decrease in
total volume decreases VR

20.
Capacity of venous system
 Veins are capacitance vessels
 Increase sympathetic activity , increases venous tone, thus
increase VR

21.
Body position
 In standing position , peripheral pooling occurs and VR
decreases

22.
Ventricular compliance
 Following MI ventricular compliance decreases thus
decreases VR

23.
Homometric regulation
 Here, myocardial contractility increases without an increase
in initial length of cardiac muscle fiber
 Increase myocardial contractility :
1. Ventricles able to do more work per stroke at a given EDP
2. Venrticles develop tension more rapidly
3. Myocardial fibers shorten quickly
4. Ejection of blood is faster
5. Duration of myocardial contraction is brief
6. Rate of ventricular relaxation is faster

24.
Factors affecting myocardial contractility
Increased Decreased
Catecholamines MI
Sympathetic stimulation Parasympathetic activity
Digitalis, glucagon, caffeine,
theophylline
Intrinsic myocardial depression
Hypoxia, hypercapnia,acidosis
barbiturates, overdose of
anaesthetic agents,

25.
INTEGRATED CONTROL OF CARDIAC OUTPUT

26.
ROLE OF HEART RATE IN CONTROL OF
CARDIAC OUTPUT

27.
Clinical significance of Frank–Starling
mechanism
 For small, momentary adjustments necessary for keeping the outputs of two
ventricles equal
 Maintenance of constant stroke volume when the peripheral resistance is
increased is carried out by intrinsic mechanism
 Intrinsic control mechanism serves as a life-saving device in a cardiac failure.

28.
MEASUREMENT OF CARDIAC OUTPUT
1. Methods based on Fick’s principle
2. Indicator or dye dilution method
3. Thermodilution method
4. Method employing inhalation of inert gases
5. Physical methods such as –
 Doppler technique echocardiography –
 Ballistocardiography

29.
METHODS BASED ON FICK’S PRINCIPLE
 Fick’s principle
 The Fick’s principle states that the amount of a substance taken up by an organ (or by the whole
body) per unit of time is equal to the arterial level of the substance (A) minus the venous level (V)
times the blood flow (F), i.e.
Q = (A − V) F
or F = Q
(A − V)
 This principle can be of course, only in situations in which the arterial blood is the sole source of
the substance taken up.
 In this method ,cardiac output is determined by measuring the pulmonary blood flow.
 Pulmonary blood flow/min = right ventricular output.
 Right ventricular output = left ventricular output (cardiac output).

30.
Measurement of pulmonary blood flow
 by measuring the amount of O2 taken by the blood from the lungs,
 O2 concentration of the venous blood from pulmonary artery (PAO2)
and
 O2 concentration of the arterial blood from the pulmonary vein
(PVO2).
 Amount of O2 uptake/min is determined with the help of a
spirometer,
 PAO2 is measured from the venous blood sample taken from the
pulmonary artery directly with the help of a cardiac catheter.
 PVO2, because of practical difficulty in taking sample from pulmonary
vein, is measured from the arterial blood sample taken from any
peripheral artery,
 e.g. brachial artery (the O2 content of all the major arteries is same
as that of pulmonary veins).

31.
 Amount of O2 taken by the lungs/min
Pulmonary blood flow =
PVO2 − PAO2
O2 taken up by the lungs/min
 Cardiac output =
PVO2 − PAO2

32.
 If O2 uptake is 250 mL/min. PVO2 is 19 mL/ 100 mL and
PAO2 is 14 mL/100 mL, then calculate cardiac output

33.
Disadvantages of Fick’s principle
1. It is an invasive technique, so there are risks of infection and
haemorrhage.
2. The cardiac output estimated may be somewhat higher than
normal as the patient becomes conscious of the whole
technique.
3. A fatal complication like ventricular fibrillation may occur if
the indwelling catheter irritates the ventricular walls,
especially when the cardiac output is being measured during
heavy exercise.

34.
INDICATOR OR DYE DILUTION METHOD
 In this method, a known amount of the dye is injected into a large vein or
preferably into the right atrium by cardiac catheterization.
 By its passage through heart and pulmonary circulation it will be evenly
distributed in the blood stream.
 Its mean concentration during the first passage through an artery can be
determined from the successive samples of blood taken from the artery.
 The blood flow in litres/min (F) is given by the following formula:
Q
 F =
Ct
F = Blood flow in litres/min,
Q = Quantity of the dye injected,
C = Mean concentration of dye and
t = Time duration in second of the first passage of dye through the artery.

35.
Prerequisites for an ideal indicator
1. It should be non-toxic.
2. It must mix evenly in the blood.
3. It should be relatively easy to measure its concentration.
4. It should not alter the cardiac output or haemodynamics of blood
flow.
5. Either it must not be changed by the body during mixing period or
the amount changed must be known.
6. The dye commonly used in humans for determining the cardiac
output is Evans blue (T-1824) or radioactive isotopes.

36.
 Calculation of cardiac output-
 Q
 Cardiac output=
 ct
 Q= 5mg
 C=1.5mg/L
 t=40sec 5x60
 Cardiac output=
 1.5 x 40

37.
THERMODILUTION METHOD
 Principle: It is also an indicator dilution technique in which instead
of a dye, ‘cold saline’ is used as an indicator.
 The cardiac output is measured by determining the resultant
change in the blood temperature in the pulmonary artery.
1. A known volume of sterile cold saline is then injected into the
inferior vena cava.
2. Temperature of the blood entering the heart from the inferior
vena cava and that of the blood leaving the heart via pulmonary
artery is determined by the thermistors.
3. The cardiac output is then measured from the values of
temperature by applying the principle of indicator dilution
technique.

38.
PHYSICAL METHODS
Echocardiography
 Echocardiography refers to the ultrasonic evaluation of cardiac functions.
 It is a noninvasive technique that does not involve injections or insertion of a
catheter.
 It involves B-scan ultrasound at a frequency of 2.25 MHz using a transducer
which also acts as a receiver of the reflected waves.
 The recording of the echoes displayed against time on an oscilloscope provides a
record of:
1. The movement of the ventricular wall and septum, and valves during the cardiac
cycle.
2. When combined with the Doppler techniques, echocardiography can be used to
measure velocity and volume of flow through the valves.
3. It is particularly useful in evaluating end-diastolic volume (EDV), end-systolic
volume, CO and valvular defects.

39.
VARIATIONS IN CARDIAC OUTPUT
 PHYSIOLOGICAL CAUSES OF VARIATIONS IN CARDIAC OUTPUT
1. Age- Because of less body surface area the children have more
cardiac index than adults.
2. Sex- Since the body surface area is less in females so they have
more cardiac index than the males.
3. Diurnal variation- In the early morning cardiac output is low
which increases in the day time depending upon the basal
condition of the individual.
4. Environmental temperature- Moderate change in the
environmental temperature does not cause any change in
cardiac output. A high environmental temperature is associated
with an increase in the cardiac output.
5. Anxiety and excitement are reported to increase the cardiac
output by 50–100%.

40.
PHYSIOLOGICAL CAUSES OF VARIATIONS IN
CARDIAC OUTPUT
6. Eating is associated with an increase in cardiac output
approximately by 30%.
7. Exercise may increase the cardiac output up to 700% depending
upon the vigorousness of exercise.
8. Pregnancy- An increase in cardiac output to the tune of 45–60%
is reported during the later months of the pregnancy.
9. High altitude- The cardiac output is increased at a high altitude
due to release of adrenaline as a consequence to hypoxia.
10. Posture change - Sitting or standing from lying down position
may decrease the cardiac output by 20–30% because of pooling of
blood in the lower limbs.

41.
PATHOLOGICAL CAUSES OF VARIATIONS IN
CARDIAC OUTPUT
 Increase in cardiac output :
1. Fever, due to increased oxidative processes
2. Anaemia, due to hypoxia
3. Hyperthyroidism, due to increased metabolism

42.
Decrease in cardiac output
1. Rapid arrhythmias,
2. Congestive cardiac failure,
3. Cardiac shock,
4. Incomplete heart block,
5. Haemorrhage and
6. Hypothyroidism

43.
References
1. Text book of medical physiology Indu Khurana
2. Text book of Physiology, Gyuton 2nd south Asian Edition
3. Text book of Physiology, Ganong
4. Comprehensive Text book of Physiology, G.K.Pal vol.I
5. Internet source