Cardiac Output: Meaning and Measurement | Cardiovascular System | Biology

In this article we will discuss about:- 1. Meaning of Cardiac Output 2. Alterations in Cardiac Output 3. Factors 4. Measurement.

Meaning of Cardiac Output:

Cardiac output is the volume of blood pumped by the heart per minute. Cardiac output is a function of heart rate and stroke volume. The heart rate is simply the number of heart-beats per minute, 70 beats/minute. The stroke volume is the volume of blood, in milliliters (ml), pumped out of the heart with each beat, 70 ml/beat. Increasing either heart rate or stroke volume increases cardiac output.

Cardiac output in ml/min = Heart rate (beats/min) × Stroke volume (ml/beat)

Cardiac output = 70 (beats/min) × 70 (ml/beat) = 4900 ml/minute.

The total volume of blood in the circulatory system of an average person is about 5 liters (5000 ml). According to our calculations, the entire volume of blood within the circulatory system is pumped by the heart each minute (at rest). The output per minute is also called as minute volume.

End-diastolic volume (EDV) is the amount of blood in the ventricle at the end of diastole. Normal value is about 120 ml.

Ejection fraction (EE) is the portion of end-diastolic volume that is pumped out during one systole, EF = SV/EDV.

Cardiac Index:

It is defined as cardiac output divided by body surface area. An average surface area is 1.73 square meters (m²). Therefore, a person with an average cardiac output of 5 liter/min would have a cardiac index of―5 liter/min ÷ 1.73 m² = 2.89 1/min/m². The normal range for cardiac index is approximately 2.6 – 4.2. A cardiac index less than 2.5 may indicate mild left heart failure. Shock is suggested by a cardiac index less than 1.8.

Stroke volume index is stroke volume divided by body surface area.

Cardiac Reserve:

It is the maximum percentage increase in cardiac output above normal that can be achieved. During vigorous exercise, the cardiac output can increase up to 20-25 liter/min (300-400%) while a trained athlete can increase up to 30-35 liters/min (500-600%).

Alterations in Cardiac Output:

Physiological:

i. Exercise:

Increased skeletal muscle metabolism increases the total O₂ demands. Increased blood flow to muscle decreases peripheral resistance to flow. This along with the muscle pumping action and respiratory pump action, increases venous return and cardiac output. Cardiac output can increase 4 to 6-fold in exercise.

In spite of the reduced peripheral resistance, arterial pressure does not decrease in exercise because of the baroreceptor reflex.

ii. Emotional States:

In anxiety and fear cardiac output is increased.

iii. Posture:

Standing, after sitting or lying, decreases cardiac output by as much as 20% due to pooling of blood in the veins of the legs with a resultant reduction of venous return.

iv. Pregnancy:

Cardiac output increases by as much as 10% during pregnancy, partially due to the increased body mass and blood volume, but also due to the low resistance of the placental and uterine vasculature producing a shunt of blood from arterial to venous sides. Cardiac output is reflexly increased to maintain arterial pressure.

v. Digestion:

About 1-3 hrs after a meal, cardiac output is increased.

vi. Temperature:

Cardiac output is increased in high environmental temperature.

Pathological:

i. Anemia:

Two factors increase cardiac output. Anemia lowers blood viscosity which marginally reduces resistance to blood flow. More importantly, anemia reduces O₂ content of blood. Delivering more blood per minute to transport the same quantity of O₂ must compensate this.

ii. Hemorrhage:

Decrease blood volume (decreased circulatory filling pressure) reduces venous return.

iii. Metabolic:

Hyperthyroidism, like fever and exercise, increases tissue metabolic activity and O₂ demand.

iv. Cardiac Failure:

Includes syndromes in which myocardial cells fail to contract normally.

Factors Determining Cardiac Output:

The cardiac output is affected by four important factors:

I. Venous return

II. Force of contraction

III. Heart rate

IV. Preipheral resistance.

I. Venous Return:

Venous return is the amount of blood entering the right atrium via the veins in one minute. Over a period of time, the cardiac output is equal to the venous return. The resting venous return is 5 liter/min, but increases up to 35 liter/min during exercise. The venous return is extremely important as it determines the cardiac output and also the filling of the heart, the end diastolic volume, the preload, and the fiber length.

Determinants of Venous Return:

a. Respiratory Pump:

During inspiration the intrathoracic pressure becomes more negative and increases the intrathoracic volume, which by distending the thoracic veins increases the return of blood to the heart. Also the descent of diaphragm during inspiration increases the intra­abdominal pressure and squeezes the blood out of the splanchnic veins into the thorax. The effect of negative intrathoracic pressure is referred to as ‘vis a fronte’ which means force from the front.

If the intrathoracic pressure becomes positive, venous return decreases (positive pressure breathing or valsalva maneuver).

b. Muscle Pump:

When skeletal muscle contract, they squeeze the veins in the muscles and drive the blood towards the heart and increases the venous return.

c. Venous Tone:

The pressure in the veins helps to propel blood towards the heart. Increase in venous tone and vasoconstriction increases intrathoracic blood volume and in turn venous return. This is called ‘vis a tergo’ means force from behind. Distension of the veins has the opposite effect.

d. Gravity:

In the erect posture, as there is pooling of blood in the dependent parts, venous return decreases.

e. Blood Volume:

Blood volume and venous return are directly propor­tional to each other.

II. Force of Contraction:

Increase in force of contraction increases stroke volume and cardiac output.

The force of contraction depends upon the following factors:

i. Initial length of cardiac muscle fiber

ii. Autonomic nerve activity

iii. Ions.

i. Initial Length of Cardiac Muscle Fiber:

The initial length of the cardiac muscle fiber is determined by the EDV which is the preload. The greater is the initial length of the cardiac muscle fiber, the greater is the force of contraction within physio­logical limits. This is known as the Frank-Starling’s law of the heart.

If the venous return increases, the diastolic filling increases and thus EDV (preload). This stretches the cardiac muscle and increases the muscle length and force of contraction. The regulation of cardiac force by alteration in the length of muscle fiber is called as heterometric regulation.

ii. Autonomic Nerve Activity:

The sympathetic stimulation increases and parasym­pathetic stimulation decreases the force of contraction. This neural regulation without change in fiber length is referred to as homometric regulation.

iii. Ions:

Optimal ionic concentrations are essential for heart’s action. Na is necessary for excitability and Ca for contraction while K favours diastole.

III. Heart Rate:

Increase in heart rate increases cardiac output, if venous filling is maintained or is not much reduced. In rapidly beating heart, the diastolic phase is much reduced and hence initial fiber length is smaller, and thus stroke volume and cardiac output are reduced. If the heart is beating slowly, the diastolic phase is longer, and hence venous filling and end-diastolic volume are increased and thus stroke volume and cardiac output are increased. In muscular exercise however, a great increase in heart rate is associated with moderate increase in stroke volume as well so that the cardiac output is considerably increased.

IV. Peripheral Resistance (Afterload):

If the resistance to flow against which the ventricle has to pump is increased, the amount of blood pum­ped out by the ventricle is reduced. Aortic pressure (and/or aortic valve diameter) is the major deter­minant of afterload on the left heart.

The effects of venous return, distension of the heart and cardiac muscle length, and peripheral resistance have been studied in the heart, lung preparation in dogs. The heart and lungs are cannula ted so that blood flows from the aorta to the right atrium via a system of tubes and reservoir, back to the aorta through the heart and lungs. The heart is functioning but the nerves of the heart are not functioning. Venous return is increased by raising the reservoir thereby increasing the venous pressure. The peripheral resistance is increased by reducing the caliber of the outflow tube.

Measurement of Cardiac Output:

Determination of cardiac output is based on two principles:

1. Fick principle

2. Indicator dilution technique.

1. The Fick Principle:

The Fick principle relies on the observation that the total uptake of (or release of) a substance by the peripheral tissues is equal to the product of the blood flow to the peripheral tissues and the arterial-venous concentration difference (gradient) of the substance.

The essence of the Fick principle is that blood flow to an organ can be calculated using a marker substance if the following information is known:

i. Amount of marker substance taken up by the organ per unit time.

ii. Concentration of marker substance in arterial blood supplying the organ.

iii. Concentration of marker substance in venous blood leaving the organ.

a. Direct Fick Principle:

In the determination of cardiac output, the substance most commonly measured is the oxygen content of blood, and the flow calculated is the flow across the pulmonary system. This gives a simple way to calculate the cardiac output. The O₂ uptake can be measured by rebreathing through a spirometer filled with O₂ and by analyzing the spirometer gas samples before and after re-breathing. Arterial and venous O₂ concentrations can be measured by withdrawing and analyzing blood from both vessels. Arterial O₂ content is measured from femoral or brachial artery. Venous blood from pulmonary artery, i.e. by cardiac catheteri­zation.

Therefore:

Cardiac output = Oxygen consumption/Arterial – venous oxygen gradient x 100

If the minute O₂ consumption is 250 ml and O₂ content of 1 liter of arterial and venous blood are 190 and 140 ml respectively, then

Cardiac output = 250 ÷ (190 – 140) = 5 liter/min.

b. Indirect Fick Method:

Here arterial and venous CO₂ concentrations were calculated from the analysis of an alveolar air before and after breathing gas in mixtures containing different CO₂ %. This method is not in use nowadays.

2. Indicator Dilution Technique:

A known quantity of a dye is injected into the right atrium via catheter. Small amounts of blood are continuously withdrawn from the arterial system with an indwelling catheter and passed through a photo­sensitive device that measures dye concentration. The concentration of the dye rises rapidly, reaches peak and then declines, but again rises due to recirculation.

The downslope is extrapolated to time scale, and this gives the time taken for the first passage of the dye through the circulation. The area under the dye- dilution curve can be calculated and approximates the average concentration of dye over time. Knowing the quantity of dye injected, the cardiac output can be determined by ―

Cardiac output = Quantity of dye injected ÷ Area under the curve

It is critical that the dye must be well mixed in the blood, should not be lost from the circulation, must not be toxic, or has any cardiac effects of its own.

Another variation on this theme is the thermo-dilution technique in which a bolus of cold dextrose solution substitutes for the dye. The procedure is the same, but blood temperature is measured instead of dye color. The thermodilution technique uses a special thermistor-tipped catheter (Swan-Ganz catheter) that is inserted from a peripheral vein into the pulmonary artery. A cold saline solution of known temperature and volume is injected into the right atrium from a proximal catheter port.

The injectant mixes with the blood as it passes through the ventricle and into the pulmonary artery, thus cooling the blood. The blood temperature is measured by a thermistor at the catheter tip, which lies within the pulmonary artery, and a computer is used to acquire the thermo-dilution profile, that is, the computer quantifies the change in blood temperature as it flows over the thermistor surface. The computer then calculates flow (cardiac output from the right ventricle) using the blood temperature information, and the temperature and volume of the injectant.

Indicator injected – (I) 5.0 mg

Mean dye conc. (C) – 1.6 mg/I

Duration of 1st circulation (T) – 39 sec

CO = I ÷ (C × T) = 5.0 mg ÷ (1.6 mg/I × 39/80)

Echocardiography techniques and radionuclide imaging techniques can be used to estimate real-time changes in ventricular dimensions, thus computing stroke volume, which when multiplied by heart rate, gives cardiac output.

Ballistocardiography:

It is based on Newton’s Third Law, that every action has equal and opposite reaction. Thus the forward thrust of the heart during systole is balanced by the recoil of the body. By measuring the small thrust and the recoil and applying the formula developed, the stroke volume was calculated. This is an old age method and is not in use nowadays.

Distribution of Cardiac Output:

Liver (splanchnic) ― 1400 ml/min

Kidney ― 100 ml/min

Skeletal muscle ― 800 ml/min

Brain ― 750 ml/min

Heart ― 250 ml/min

Skin ― 300ml/min

Others ― 600 ml/min

Liver is the organ which receives highest amount of blood flow per minute (1400 ml/min).

Kidney is the organ which receives highest amount of blood flow per 100 gm of tissue per minute (350- 400 ml/100 gm/min).