Cardiac Output: Meaning, Determination and Regulation

In this article we will discuss about:- 1. Definition of Cardiac Output 2. Determination of Cardiac Output 3. Regulation.

Definition of Cardiac Output:

Cardiac output is defined as volume of blood pumped out per ventricle per minute (Table 3.9). Right ventricle pumps blood into pulmonary circulation and during the same time an identical volume of blood is also pumped out from the left ventricle into systemic circulation.

Right ventricular = Left ventricular output = 5L/min output

i. The normal cardiac output is about 5 liters/ventricle/minute

ii. Cardiac output is a product of stroke volume and heart rate.

iii. Stroke volume (SV) is volume of blood pumped out per ventricle per beat, which is normally about 70 ml.

iv. The normal heart rate (HR) can be considered as about 70 per minute. In which case

Cardiac output = HR x SV

= 70 x 70 = 4900 ml

Cardiac output has direct relationship with body surface area. Hence expression of the absolute value of cardiac output is not very appropriate. It is better to express as cardiac index.

Cardiac Index:

i. Expression of cardiac output in relation to body surface area

ii. Normally, it is expressed as L/Sq m Body surface area (BSA)/min

iii. To calculate cardiac index, cardiac output must be divided by body surface area.

Cardiac index = Cardiac output (L/min)/BSA (m²)

Assuming that cardiac output is 5 L/min, BSA is 1.7 m²

Cardiac index will be 5/1.7 = about 3 L/min/m² BSA

Determination of Cardiac Output:

It can be done by many methods.

Some of the common methods employed are (Table 3.10):

1. Using Fick’s principle.

2. Dye method.

3. Thermodilution method.

Fick’s Principle:

It states that the quantity of a substance taken up by an organ or given out by an organ is equal to concentration difference of the substance in arterial and venous blood multiplied by blood flow through the organ per minute. Hence, Fick’s principle can also be used for determination of blood flow through organs, like brain, coronary, renal, etc.

According to this principle:

Q = (C_a – C_v)/Blood flow through the organ/min

Q is quantity of substance taken up or given out by the organ per minute

C_a concentration of the substance in arterial blood

C_v concentration of the substance in venous blood.

While determining cardiac output by this method, the quantity of substance taken up or given out by the organ per minute and arteriovenous concentration of the substance must be known. Hence, the volume of blood flow through the ventricle per minute (which is nothing but cardiac output) has to be calculated.

So the formula has to be rewritten:

(C_a – C_v)/Blood flow through the organ (CO)/min = Q

So cardiac output will be:

CO = Q/(C_a – C_v)/min

For determination of cardiac output by applying this principle, either oxygen or carbon dioxide content of blood can be used. More often, it is the oxygen content of blood that is used.

While determining cardiac output by using oxygen, the following data are required:

1. Volume of oxygen used up by the body per minute (Q). This can be estimated by making the person to breathe from a bag containing 100% oxygen.

2. The arterial oxygen content can be estimated by taking a sample of arterial blood (C_a).

3. The venous blood oxygen is estimated by taking a sample of mixed venous blood. Mixed venous blood sample can be obtained from pulmonary artery by cardiac catheterization (C_v).

Assuming the data as follows:

1. Q = 250 ml/min

2. C_a = 20 ml/100 ml

3. C_v = 15 ml/100 ml

So cardiac output = Q/(C_a – C_v) = 250/5 x 100

= 5000 ml/min

Dye Method:

The dye that is normally used is T₁₈₂₄,which is also known as Evan’s blue.

Any dye which is used should possess the following criteria:

i. Should get diluted properly in plasma.

ii. Should be non-toxic.

iii. Should not alter hemodynamics.

iv. Should not alter blood volume.

v. Concentration of the dye can be easily estimated.

Procedure:

i. Dye has to be dissolved in an isotonic fluid.

ii. A known quantity of dye has to be injected into a peripheral vein.

iii. A series of blood samples have to be collected from an artery at regular intervals (may be every 3 sec).

iv. Concentration of the dye in the sample of blood is determined.

v. The data has to be plotted on a semi-log paper (Fig. 3.30).

vi. In the graph, there will be a gradual increase in the concentration of dye till it reaches maximum. After this, the concentration of dye goes on decreasing till a point wherein there will be again a slight increase in concentration of dye. The slight increase in the concentration of dye is because of recirculation of blood.

vii. Wherever the concentration of dye starts increasing for the second time, the rising point will be taken as mean concentration of dye.

viii. From the lowest concentration point, line is extrapolated to cut the X axis. This will indicate the time required for one circulation.

ix. Calculation of cardiac output has to be done based on the above available data.

For example:

1. Quantity of dye injected is 3 mg in 1 ml of isotonic fluid.

2. Concentration of dye in it is about 1.5 mg/ml

3. Time for one circulation is 30 sec.

Thermodilution Method:

i. Equipment used is thermister.

ii. A double lumen catheter is introduced into the heart.

iii. Through one of the lumens of the catheter, cold saline of known temperature and volume is introduced into right atrium.

iv. This saline from right atrium enters right ventricle from where it is pumped into pulmonary artery. The change in the temperature of the saline that was introduced is measured by the devise in the pulmonary artery.

v. The extent to which a change in the temperature has taken place depends on the right ventricular output.

vi. This is said to be more advantageous because:

a. Since the indicator used is cold saline, in cases where cardiac output has to be determined repeatedly it can be done easily.

b. Since blood is pumped out into systemic circulation, whatever changes that have occurred with respect to temperature can be minimized further by the tissues as blood flows through the tissues. Because of this, the temperature of venous blood will not be altered much.

There are many conditions in which cardiac output is altered.

Some of the conditions in which cardiac output will be more than normal are:

1. Muscular exercise in which it can be as much as 35 L/min that is about 7-fold increase.

2. Sympathetic stimulations, like anxiety, anger, fear, etc., will also increase cardiac output.

3. In pregnancy, anemia, hyperthyroidism also

4. More in the recumbent posture when compared to erect posture

Conditions in which cardiac output decreases will be:

1. Hemorrhage

2. Arrhythmias

3. Left ventricular failure

4. Sleep

5. Hypothyroidism

Regulation of Cardiac Output:

i. Determinants of cardiac output are heart rate and stroke volume.

ii. Hence any factor, which affects either the heart rate, or stroke volume, or both will alter the cardiac output.

iii. Peripheral resistance also affects cardiac output by altering the stroke volume. This is brought about because of after-load effect.

iv. In addition to this, some of the other factors, which try to regulate cardiac output, will be distensability of cardiac chambers.

Hence regulation of the cardiac output can be discussed under the following headings (Fig. 3.31 and Table 3.11):

1. Factors which are going to affect the heart rate

2. Factors that are going to affect the stroke volume

Heart rate alterations can be brought about by:

1. Neural mechanism

2. Hormonal mechanism

Neural Mechanism:

Stimulation of parasympathetic nerve (vagus) is going to have negative chronotropic effect. Hence it is going to decrease the heart rate and decreases cardiac output.

But a moderate decrease of heart rate is not going to alter the cardiac output for the reason that when there is decrease of heart rate, the ventricular filling time is increased and thereby the end diastolic volume increases, increases stroke volume based on Starling’s law and hence the stroke volume will increase.

Stimulation of sympathetic nerve will increase the heart rate by exerting positive chronotropic effect and hence increases the heart rate and cardiac output. An increase in the heart rate up to a certain extent increases the cardiac output.

But on further increase in the heart rate, the cardiac output starts decreasing. When the heart rate increases beyond a certain range, the ventricular filling time decreases. This decreases the end diastolic volume, stroke volume and, therefore, cardiac output.

Hormonal Mechanism:

i. Thyroxin is going to increase the sensitivity of beta- receptors in the heart for catecholamine action. In addition, it also increases the number of beta- receptors in cardiac muscle. Because of this, in hyperthyroidism, there will be increase of heart rate and cardiac output.

ii. Catecholamines (adrenaline and noradrenaline) due to their action on the cardiac muscle through beta-receptors will also increase the heart rate. This action is similar to the action that is brought about the sympathetic stimulation. Sympathetic stimulation increases not only the heart rate but also the force of contraction. This brings about a marked increase in cardiac output.

Stroke volume is altered by many of the factors. Stroke volume is difference between end diastolic volume (EDV) and end systolic volume (ESV).

iii. End diastolic volume is volume of blood present in the ventricle at the end of diastole, which is normally about 140 ml.

iv. End systolic volume is volume of blood present in the ventricle at the end of systole, which is normally about 70 ml.

v. Ejection fraction (SV/EDV): It is the fraction of EDV that has been ejected out during ventricular systole, which in this case will be about 0.5 or 50%.

vi. Either by altering the EDV or ejection fraction, stroke volume can be affected.

vii. There are many factors, which can alter either the EDV or ejection fraction.

They are:

a. Preload effect (venous return)

b. After-load effect (peripheral resistance)

c. Myocardial contractility

Preload Effect:

i. Preload means load acting on the muscle before it starts contracting.

ii. In the case of cardiac muscle, preload is exerted by the extent of venous return. Therefore, the end diastolic volume and preload effect have direct relationship.

iii. When venous return increases, more blood is brought to ventricle.

iv. This brings about distension of the chambers.

v. Stretching of the ventricular muscle fibers.

vi. Hence as per Starling’s law, force of contraction gets increased (Starling’s law states that force of contraction is directly proportional to initial length of muscle fibers within physiological limits).

vii. Hence any factor which affects venous return will alter stroke volume and cardiac output.

After-load Effect:

i. After-load means it is load acting on the muscle after the muscle has started contracting.

ii. In the case of ventricle, for blood to get pumped out, there should be opening of the semilunar valves present at the origin of aorta.

iii. The semilunar valves normally open at a particular pressure (when the ventricular pressure exceeds that of the diastolic blood pressure).

iv. So the ventricles are able to experience the resistance offered by the semilunar valves only after the ventricle has started contracting and because of this, it is termed as after-load effect.

v. When the after-load effect is more, the volume of blood pumped out by the ventricle decreases because lot of the exertion of the ventricle will be spent to overcome the resistance offered by the semilunar valves.

vi. It is for this reason, in condition of severe hyper­tension especially that of diastolic hypertension person may tend to go into left ventricular failure.

vii. In hypertension, since the ejection fraction decreases and the end systolic volume increase. In the mean-time, the volume of blood (venous return) returning to the heart will continue to be as usual. This will increase the further distension of the ventricles. So abnormal stretching of the ventricle may occur beyond a limit and the ventricle may fail to contract.

viii. It is for this reason, whenever a patient is suffering from diastolic hypertension, due attention has to be paid to reduce the blood pressure in order to reduce the stress on the left ventricle exerted because of the after-load effect and prevent consequent cardiac failure.

Myocardial Contractility:

Keeping the preload and after-load effects constant, there are many factors which can just affect the myocardial contractility and hence the stroke volume and cardiac output.

Myocardial contractility is affected by factors, like (Fig. 3.32):

1. Effect of sympathetic and parasympathetic stimulation because of their inotropic effects. The increase in the force of contraction when sympathetic nerve is stimulated will increase the stroke volume at the expense of end systolic volume.

Normally, the end systolic volume will be about 70 ml. When there is sympathetic nerve stimulation, for the same end diastolic volume, the force of contraction gets increased because of positive inotropic effect. This increases the ejection fraction.

2. Hypoxia, hypercapnia and acidosis of myocardium, which occurs when there is decrease in blood flow through coronary vessels. When the coronary blood flow decreases, due to the above changes, there will be decrease in force of contraction of the ventricle.

3. Death of myocardium as it occurs in myocardial infarction will decrease the muscle mass and hence decreases the stroke volume.

4. Functional depression of myocardium will reduce the force of contraction.

5. Inotropic agents action: Positive inotropic agents, like digitalis, facilitate the force of contraction, whereas verapamil, diltiazem, etc., by reducing the calcium conductance into ICF, will decrease the force of contraction.

6. Catecholamines are going to imitate the sympathetic stimulation action and hence bring about a positive inotropic effect and increase the force of contraction.

Distensability of the cardiac muscle is decreased in pericardial effusion, hemopericardium and when the patient has recovered from myocardial infarction. When distensability is decreased the stroke volume and cardiac output also decreases.

The influence of various factors in the regulation of cardiac output can be studied with the help of heart- lung preparation.

Cardiac Catheterization:

Cardiac catheterization is an invasive technique in which a thin tube is (catheter) is introduced into the peripheral blood vessel and guided to reach the different parts of heart. It was first performed by Frossmann in the year 1929. Later on he won the Nobel prize for this path breaking technique which he had first performed on himself.

To reach the right side of heart, the catheter has to be introduced into a peripheral vein. This type of catheterization is called as anterograde catheterization.

To reach the left side of heart, the catheter has to be introduced into a peripheral artery. This type of catheterization is known as retrograde catheterization.

Advantages of cardiac catheterization:

i. Measure pressure changes in different chambers of heart.

ii. Measure volume changes in ventricles (EDV and ESV).

iii. Obtain a sample of mixed venous blood.

iv. Study septal defects.

v. Introduce drugs directly into heart.

vi. Stimulate pacemaker region.

vii. ECG can be recorded directly from heart.

Disadvantage of cardiac catheterization:

Catheteri­zation may induce fibrillations in ventricular muscle.