Cardiac Output

Quantity of blood pumped into aorta each minute by the heart.

C.O approx.= Venous Return.

C.O = H. Rate x  Stroke Vol.

= (70/min) x  (80 ml/beat)

Cardiac output is also called ‘minute volume’.

Normal range of C.O = 5-7 L/min

Stroke vol: (S.V)

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.

Cardiac Index:

C.O per minute per square meter body surface area.

C.I = C.O/S.A = 5.0/1.7

C.I = 3.2 L/min/m2

Stroke Vol Index:

S.V per square meter body surface area.

S.V.I = 47 ml/m2

Preload and Afterload

Preload:

 Vol of blood in the ventricle at the end of diastole (E.D.V)

 Degree of tension on the muscle when it begins to contract is called

preload.

 Preload is also the degree of filling of ventricle and depends on the

venous return.

Factors affecting preload:

 Posture

 Bl.vol

 MSFP

 Atrial contraction

 Muscular activity

 Intrapleural pr.

 Intrapericardial pr.

Frank Starling Law:

Force of contraction is proportional to the initial length of

cardiac muscle fiber (i-e preload or E.D.V).

Increased Preload or E.D.V leads to

1)Increased Force of contraction  by Frank Starling Law

2)Increased Heart Rate (Approx. 75%) by

a)direct stretch on S.A Node (10-15%)

b) by Bainbridge Reflex or Cardioaccelerator Reflex (40-60%)

After load:

Arterial pressure against which ventricle contracts

i.e.

Systolic pressure, Peripheral resistance or Impedance or resistance.

Thus; increased Afterload = decreased Cardiac output

I. Increased:

Eating (30%)

Anxiety/Excitement (50-100%)

Exercise (up to 700% i-e 5-7 fold)

High environmental temp.

Pregnancy

Epinephrine, Histamin

Anemia

Metabolic Alkalosis, Low PO2 or High PCO2.

Age up to puberty

II. Decreased:

Sitting or standing from supine position (20-30%)

Rapid arrhythmias

Heart diseases (Hypo effective Heart)

III. No Change:

During sleep

Moderate change in environmental temp.

Metabolic acidosis

Menstruation

However, C.O is regulated throughout life directly in

proportion to the metabolic activity.

High Cardiac Output:

Always caused by decreased Total peripheral resistance.

1. Beri Beri

2. A-V fistula/shunt

3. Hyperthyroidism (increased Metabolism, increased Vasodilator subs= decreased T.P.R)

4. Anemia. (decreased Bood Viscosity, Hypoxia leads to decreased T.P.R)

Low Cardiac Output:

1. Decreased pumping effectiveness of heart:

Severe myocardial infarction

Severe valvular heart disease

Myocarditis

Cardiac temponade.

2. Decreased Venous Return (decreased EDV):

 Blood Volume

Acute venous dilatation (Sudden inactivity of

sympathetic system).

Obstruction to large veins (Rare)

Measurement of Cardiac Output:

1) Direct Method:

In animals

By direct cannulation of Aorta or Pul. Artery

and by flowmeters.

2) Indirect Method:

In Human beings, No surgery required.

i. Fick ‘s Method  O2 Fick Method

ii. Dye Dilution Method

iii. Flowmeters (Ultrasonic or Electromagnetic)

iv. Doppler Method.

O2 Fick Method:

Fick Principle:

Amount of substance taken up by an organ (or by whole

body) per unit time is equal to the arterial level of substance

minus the venous level (AV difference) times the blood flow.

In O2 Fick method; C.O is measured by determining the

amount of O2 consumed by the body in a period of time and

dividing this value by A-V difference across lungs.