Cardiac OutputBy

Dr. Sumaira Iqbal

Learning Objectives

By the end of lecture, student should be able to

Define cardiac output

Define cardiac index

Enumerate factors affecting cardiac output

Explain the regulation of cardiac output

Comment on hypoeffective and hypereffective heart

Outline te causes of low and high cardiac output states

State the methods of measurement of cardiac output

Explain the oxygen fick’s method.

Definition

Cardiac output is the quantity of blood

pumped into the aorta each minute by the

heart. This is also the quantity of blood that

flows through the circulation.

Also known as minute volume

CO = SV x HR

Cardiac Index

Cardiac output per square meter of body surface area.

Average cardiac index for adults is about 3 L/min/m2 of body surface area.

Effect of Age on Cardiac Output

Cardiac Index

Stroke Volume

Amount of blood pumped out of each

ventricle per beat; also called ‘Systolic

discharge’.

S.V = E.D.V - E.S.V

= 140 ml - 60 ml

S.V = 80 ml/beat in resting man.

Factors Determining Cardiac Output

PRELOAD = Initial stretching of the cardiac myocytes prior to contraction (related to sarcomere length)

AFTERLOAD = “load” that the heart must eject blood against (related to aortic pressure)

CONTRACTILITY (INOTROPY) = Inherent ability of myocardial cells to develop force at given muscle lengths (related to Calcium)

HEART RATE autonomic nervous system

Physiological variations of cardiac output

Age: Cardiac output is more in adults than in children

because blood volume is more.

Gender: cardiac output is more in male than females.

Altitude: cardiac output increases at high altitude

places.

Pregnancy: cardiac output increases during pregnancy

Exercise: cardiac output increases during exercise

Emotions: cardiac output increases during emotional

expressions.

Cardiac Output

REGULATION OF STROKE VOLUME-- Regulated by three variables:

a. End diastolic volume (EDV): volume of blood in the ventricles at

the end of diastole.

Sometimes called preload

Stroke volume increases with increased EDV.

b. Total peripheral resistance: Frictional resistance in the arteries.

Inversely related to stroke volume

Called after load

c. Contractility: strength of ventricular contraction

Cardiac Output

1. Stroke volume increases with contractility.

Ejection fraction (EF) – percentage of the EDV

that is ejected per cardiac cycle.

Stroke volume = EDV – ESV

EF% = (SV / EDV) x 100

Normal ejection fraction is about 50-65%.

RELATIONSHIP WITH BLOOD PRESSURE

As Cardiac output is made up of heart rate and stroke

volume - at rest these are relatively constant.

With exercise the heart beats faster – more blood is pumped out with each beat contributing to a rise in

BP.

Changes in the volume of blood within the

cardiovascular system will also affect blood pressure

BP= CO X TPR

BP= SV X HR X TPR

Regulation

Cardiac output is regulated by:

1. Frank Starling Mechanism

2.Stretch on SA node

3.Bainbridge Reflex

MECHANISM OF REGULATION

1. By venous return:

Force of

contraction of a

muscle fibre is

proportional to its

initial length .It is

known as

Starling’s law of

muscle

contraction

MECHANISM OF REGULATION

2. By nervous system:

Autonomic nervous system takes a major role in the regulation of

cardiac output.

Whenever sympathetic nervous activity increases e.g. ; during

emotions, exercise etc, it will stimulate both SA node as well as

ventricular myocardium.

This will increase both heart rate as well as force of contraction of

muscles or stroke volume .This will inturn increase cardiac output.

If parasympathetic activity increases as during sleep, it will inhibit

SA node, it will decrease heart rate, this will inturn decrease

cardiac output.

MECHANISM OF REGULATION

3. Hormonal regulation of cardiac output:

Whenever adrenaline level in the blood

increases it will stimulate SA node and

ventricular myocardium. This will increase both

heart rate and stroke volume.

This will inturn increase cardiac output

VENOUS RETURN

End diastolic volume is controlled by factors that affect venous

return:

a. Total blood volume

b. Venous pressure (driving force for blood return)

Veins have high compliance – stretch more at a given pressure

than arteries (veins have thinner walls).

Veins are capacitance vessels – 2/3 of the total blood volume is

in veins.

They hold more blood than arteries but maintain lower pressure.

Controlling Factors

Primary controller

Peripheral factors

Venous return

TPR

If the returning blood does become more than the heart can pump, then the heart becomes the limiting factor that determines the cardiac output

Considering Ohms Law

Flow=Pressure/Resistance

Cardiac Output=Arterial Pressure/Total

Peripheral Resistance

High Cardiac Output: Always caused

by decreased T.P.R.

1.Beri Beri— Vitamin B1 deficiency

2.A-V fistula/shunt

3.Hyperthyroidism (increased Metabolism,

increased Vasodilator substances– decreased

T.P.R)

4.Anemia. (increased Blood Viscosity & Hypoxia

Leads to decreased T.P.R)

Low Cardiac Output

1. Reduced Pumping effectiveness of heart:

Severe myocardial infarction

Severe valvular heart disease

Myocarditis

Cardiac temponade.

2. Decreased Venous Return (decreased EDV):

Decreased blood Volume

Acute venous dilatation (Sudden inactivity of

sympathetic system)

Obstruction to large veins (Rare)

• Limits to the pumping ability of the heart ( plateau)

– CO increases---plateau at 13L/min (2.5 times normal)

max limit under normal conditions

Hypereffective heart

Nervous stimulation

Sympathetic stimulation

Parasympathetic inhibition

Increase the heart rate

Increase the strength of force of contraction

Hypertrophy of the heart muscle

Marathon runners

Nervous stimulation + hypertrophy

Plateau at 30- 40 L/min ( 2½ times normal)

Hypoeffective heart

Factors that decreases the heart's ability to pump blood

Coronary artery blockage, causing a "heart attack"

Inhibition of nervous excitation of the heart

Pathological factors that cause abnormal heart rhythm or rate of heartbeat

Valvular heart disease

Increased arterial pressure against which the heart must pump, such as in hypertension

Congenital heart disease

Myocarditis

Cardiac hypoxia

Cardiac output curvesEffect of external pressure

Normal external pressure = normal intrapleural

pressure = - 4 mm Hg

Rise causes the shift of the curve to the right

Cyclical changes of intra pleural pressure during

respiration

±2mm Hg during normal breathing

Breathing against a –ve pressure

Positive pressure breathing

Opening the thoracic cage (0 mm Hg)

Cardiac tamponade

Cardiac output

Equilibrium point

Venous return = cardiac output

Electromagnetic flow meter

Oxygen Fick Method

CO = (O2 consumption / (A-V O2 difference)

Indicator dilution (dye such as cardiogreen)

Thermal dilution

Measurement of Cardiac Output

Measurement of Cardiac Output

Oxygen Fick Principle

Measurement of Cardiac Output

Indicator dilution method

Thank you