Heart Rate of Humans: Mechanism and Factors (With Diagram) | Biology

In this article we will discuss about:- 1. Normal Values of Heart Rate 2. Regulation of Heart Rate 3. Mechanism 4. Factors Affecting.

Normal Values of Heart Rate:

In adult males – 72 per minute, the range is from 70 – 80 per minute. In adult females-the rate is slightly higher than in males.

Cause may be due to:

(a) Lower blood pressure, and

(b) More sympathetic tone.

Apart from sex, heart rate depends on the following factors:

i. Age:

Roughly the heart rate is inversely proportional to age. Heart rate during various stages of life is listed in Table 7.6.

At younger ages the cause may lie in the higher basal metabolic rate (B.M.R.). In old age the rate is slightly higher-probably due to compensatory circulatory adjustment against gradual circulatory failure with the aging process.

ii. Metabolic Rate:

Heart rate is directly proportional to the metabolic rate. They always run parallel. Anything that increases the basal metabolic rate, viz., exercise, excitement, etc., will also increase the heart rate. Similarly, factors which reduce basal metabolic rate diminish the heart rate.

iii. Respiration:

Heart and respiration run parallel. Stimulation or depression of one will always cause paral­lel changes in the other under normal conditions.

iv. Size of the Animals:

It is seen that under normal conditions heart rate has an inverse relation with the size of the animal. Smaller the size, greater the heart rate. For instance, heart rate of canary is about 1,000 per minute, that of an elephant, only 25 per minute.

Regulation of Heart Rate:

Heart rate can be adjusted according to the metabolic needs. In exercise the rate increases; during sleep it falls. The purpose of this regulation is to maintain an optimum blood pressure and an optimum rate of blood supply to the tissues.

Mechanism of Heart Rate:

The mechanism involves two factors:

i. The Local Mechanism:

This includes the S.A. node and the junctional tissues. Any factor, which by its local action on the S.A. node can alter its rhythmicity, will also alter the heart rate.

ii. The Nervous Mechanism:

It includes:

a. Cardio-inhibitory centre connected with the vagus.

b. Cardio-accelerator centre connected with the sympathetic. Stimulation of the vagus depresses and that of the sympathetic increases the heart rate.

c. Of the two nerves, the vagus exerts a stronger action. Atropine prevents action of acetylcholine to the cardiac muscle and increases the heart rate even up to 150 per minute. This proves that the vagus exerts a tonic inhibitory control over heart rate. This vagal tone is reflexly produced through the Sino-aortic nerves. The sympathetic also exerts a tonic accelerating effect but to a lesser extent.

The variations of heart rate, under normal physiological conditions, are mainly brought about by alteration of vagal tone. It is only in extreme cases that sympathetic stimulation comes into play.

Thus alterations of heart rate may be brought about in two ways:

(a) By affecting the local mechanism, i.e., the S.A. node and the junctional tissues, or

(b) By acting through the nervous mechanism.

The cardiac centres, again, may be influenced in two ways—directly or reflexly. There is evidence to show that the two cardiac centres are in reciprocal relation. Stimulation of one will depress the other and vice versa.

Factors Affecting Heart Rate:

i. Impulses from the Higher Centres:

Excitement generally quickens the heart rate but sudden shock may slow or even stop the heart rate. These changes are due to the influence of frontal lobes (area 13) of the cerebral cortex and the hypothalamus.

ii. Respiration:

During inspiration heart rate increases; during expiration it falls. This phenomenon is known as sinus arrhythmia. It is very often found in healthy children. In adults, it becomes prominent after deep voluntary respiration. It is abolished by atropine, showing that the vagus is involved.

Three explanations are advanced:

a. Afferent impulses arise from the lungs during inspiration and reflexly inhibit the vagal tone.

b. During inspiration venous return increases, causing congestion of the right atrium and great veins, and thus mobilising Bainbridge reflex (mentioned below).

c. Central Irradiation:

During inspiration, motor impulses irradiate from the respiratory centre to the neighbouring cardiac centre and inhibit the vagal tone. Experimental evidence shows that this is likely to be the chief cause.

iii. Reflexes:

Factors influencing the cardiac centre have been presented in Fig. 7.80. Heart rate can be altered by various reflexes.

For instance:

(a) Cardio-inhibitory reflexes,

(b) Cardio-accelerator reflexes, and

(c) Reflexes from other parts of the body.

(a) Cardio-Inhibitory Reflexes (Sino-Aortic or Marey’s Reflex):

There are stretch receptors in the carotid sinus and aortic arch. When blood pressure rises, these nerve endings become stimulated due to stretching; sensory impulses pass up through the Sino-aortic nerves and increase the vagal tone, so that heart rate falls. When blood pressure falls, no inhibitory impulse passes up and heart rate rises. Thus heart rate and blood pressure have an inverse relation. This is known as Marey’s law.

This Sino-aortic effect is best seen when the initial blood pressure remains near about the normal range. A fall of pressure from 125 to 100 mm of Hg or a rise from 125 mm to 150 mm of Hg causes more quickening or slowing respectively, than changes of same magnitude that alter the heart rate in subjects whose initial blood pressures are already higher or lower.

Since the Sino-aortic nerves help to maintain blood pressure variations through a limited range by regulating the heart rate, these nerves are called the buffer nerves of heart. [The inverse relation between heart rate and blood pressure does not hold good in all conditions. For instance, exercise, emotion, anoxia, etc., increase both heart rate and blood pressure.]

(b) Cardio-Accelerator Reflexes:

Venous engorgement of the right atrium and the great veins reflexly increases the heart rate. The afferent fibres, arising from the roots of the great veins and right atria, pass along the trunk of the vagus to the cardiac centre. Engorgements of these parts stimulate the nerve endings, reflexly inhibit the vagal tone and also stimulate the sympathetic to some extent.

Thus heart rate rises. This reflex is called Bainbridge reflex (more appropriately venous reflex). This happens in muscular exercise and in deep inspiration when venous return increases. This is also a cause of increased heart rate during congestive cardiac failure.

(c) Reflexes from other Parts of the Body:

Sensory stimuli from other parts of the body may alter the heart rate in either direction. Moderately painful stimuli generally quicken the heart rate. Stimulation of the central end of the fifth nerves or of the splanchnic nerve slows the heart rate. A sudden blow on the abdomen may stop the heart rate.

iv. Anoxia:

It increases the heart rate which is directly proportional to the degree of anoxia. The effect is due partly to its action on the cardiac centre and partly to reflex stimulation through the chemoreceptors in the carotid and aortic bodies. This is one cause of rapid pulse in heart failure, anaemia, haemorrhage, high altitude, CO poisoning, etc.

v. CO₂ Excess:

In moderate amounts it increases the heart rate, partly by its direct action and partly reflex. But in larger amounts it produces heart block and reduces heart rate. [It should be noted that circulation is more sensitive to O₂ lack but respiration is more sensitive to CO₂ excess]

vi. Body Temperature:

Rise of body temperature (muscular exercise, fever, hyperthyroidism, etc.) increases the heart rate:

(a) By acting on the S.A. node, and

(b) By stimulating the cardio-accelerator centre.

vii. Increased Intracranial Pressure:

It slows the heart rate by directly stimulating the vagus.

viii. Adrenaline:

Since it acts like the sympathetic, it should accelerate the heart rate, but in intact animals the rate is often reflexly reduced. Because, by causing vasoconstriction, adrenaline raises blood pressure and thus mobilises the Sino-aortic reflex, so that heart rate may be reduced. But the force of contraction invariably rises.

ix. Thyroxine:

It quickens the heart rate:

(a) By directly stimulating the metabolic rate of the Sino-atrial node,

(b) By increasing the basal metabolic rate of the body, and

(c) By a probable stimulating effect on the sym­pathetic.

x. Muscular Exercise:

It increases the heart rate. Because most of the factors concerned with acceleration, are operating during exercise. For instance, increased venous return initially mobilises Bainbridge reflex. Increased respiration, excitement, anoxia, CO₂ excess, adrenaline secretion, etc., all come in and increase the heart rate.