Pulmonary Circulation: Anatomy and Peculiarities | Humans | Biology

Anatomy of Circulation:

Blood enters lungs through two sources; pulmonary artery and bronchial arteries. The cross-sectional area of the pulmonary artery is same as that of the aorta, but it is more elastic and distensible. Through the pulmonary artery venous blood of the right ventricle goes to the lungs for oxygenation. It also carries nutrition to the pulmonary tissues. Bronchial arteries, originating from the aorta, carry oxygenated blood for the nutrition of bronchi and bronchioles (Fig. 7.104).

The pulmonary artery breaks up into wide arterioles and capillaries which form a rich network surrounding the alveoli where gaseous exchange takes place. The bronchial artery also breaks up into capillaries which partly join the alveolar network but is mostly returned through bronchial veins and partly through azygos vein.

The branches of the bronchial artery are also distributed to the bronchial glands and walls of the bronchioles as well as respiratory bronchioles and thus form capillary plexuses which drain blood into the pulmonary venules (Fig. 7.105). The oxygen supply to the pulmonary tissues comes from the deoxygenated blood as well as from the oxygenated blood.

Method of Recording Pulmonary Arterial Pressure:

With the help of the cardiac catheter—it is inserted through the systemic vein into the right atrium and then into the right ventricle and then into the pulmonary artery from where the pulmonary arterial pressure can be recorded.

Vasomotor Supply:

The sympathetic supply is from upper thoracic segments and the parasympathetic supply from the vagus. Results of stimulation of nerves are variable. Stimulation of the chemoreceptors of the carotid body causes diminution of the pulmonary vascular resistance which disappears after section of the vagus and the sympa­thetic. So pulmonary circulation is under reflex control.

Normal Values of Pulmonary Circulation:

i. Minute Blood Flow:

It is the sum total of right ventricular output and blood flow through the bronchial arteries. Hence a little over 4-5 litres.

ii. Blood Pressure:

The systolic pressure in the human pulmonary artery is about 22 mm of Hg (right ventricle—about 22 mm of Hg). The diastolic pressure is about 10 mm of Hg (right ventricle 0 to 1 mm of Hg). With each heart beat the pressure rises in the pulmonary artery and thus causes pulsation in these vessels. The pulmonary capillary pressure is about 8 mm of Hg. The pulmonary venous pressure is about 5 mm of Hg (left atrium—approximately 4 mm of Hg).

iii. Circulation Time:

3-9 Seconds (Ether).

Functions of Pulmonary Circulation:

i. Gas Exchange:

It is the main function of the pulmonary circulation. Through circulation the mixed deoxygenated blood is passed through alveolar capillaries and thus gaseous exchange in between the alveolar air and alveolar capillaries takes place. Due to gaseous exchange, blood that passes through alveolar capillaries gets proper amount of O₂, and gets rid of proper amount of CO₂.

ii. Filter:

The fine pulmonary blood vessels act as a filter. It traps the emboli that pass through the pulmonary capillaries. Thus filter prevents from reaching and blocking the vessels in the brain and heart.

iii. Nutrition:

Pulmonary circulation maintains the nutrition of the lung tissue.

iv. Fluid Exchange:

Pulmonary capillary pressure is very low which tends to pull fluid from the alveoli and thus any fluid accumulation in the alveoli is speedily absorbed into the blood. This phenomenon has been observed by Cohn (1873). He introduced 25 litres of water through the trachea slowly and observed no discomfort in the Animals. Of course, rapid absorption of water in the blood may cause haemolysis and at the same time may increase the work load of the heart due to increase of plasma volume.

v. Reservoir for Left Ventricle:

Left ventricular output is fully dependent upon the return of blood from the pulmonary bed to the left atrium. So any alteration of the pulmonary haemodynamics will alter the left ventricular function.

Control of Pulmonary Circulation:

The amount of blood passing through lungs follows the same general principles as elsewhere.

It depends upon the following factors:

i. Output of the Right Ventricle (Mechanical Factor):

It depends upon the force and frequency of contraction and the degree of venous return. Cardiac output may increase 3 or 4 times but the pulmonary arterial pressure does not rise appreciably.

ii. Resistance of the Pulmonary Bed: It depends upon the following factor-  (a) Lumen of the pulmonary vessels- Hypoxia produces pulmonary vasoconstriction. Increased CO₂ tension in the blood constricts the pulmonary blood vessels. It has been observed that if one lung is ventilated with a mixture of CO₂ and O₂, and the other lung with air then most of the blood is shifted to the normally ventilated lung so as to protect the body from hypercapnoic effect. This is auto-regulation of pulmonary blood flow.

Adrenaline and noradrenaline also produce vasoconstriction. Acetyl-choline also dilates the pulmonary blood vessels but the degree of vasodialtion is mostly dependent upon pre-existing tone of the smooth muscle of the pulmonary blood vessel. Serotonin, a humoral substance originating from disintegrating platelets or by secretory products of chromaffin tissues also constricts the pulmonary blood vessels. Recently it has been observed that the emboli in the pulmonary capillaries produce reflex vasoconstriction of the pulmonary arterioles.

This, according to some physiologist, is due to – (a) Stimulation of the vagal receptor lying near these small vessels. The receptors respond to 5-hydroxytryptamine (serotonin) released from the platelets near the emboli. (b) Condition of the lungs—Fibrosis, emphysema (overstretching), pneumonia, etc., increase the resistance, (c) Condition of the heart—Mitral stenosis of left heart failure retards venous out-flow from the lung and increases the pulmonary resistance, and (d) Respiration.

iii. Role of Respiration:

During inspiration, the pulmonary bed enlarges, capillary pressure falls to about —2 mm of Hg and therefore more blood enters the lungs. This is caused by elongation of the capillaries due to stretching and their dilatation due to negative pressure and probably vasomotor effect. Thus during inspiration, lungs can hold about 10% of total blood volume.

During expiration, reverse changes take place, pressure rises to about 4 mm of Hg and lungs can hold only about 6% of the blood volume. But total pulmonary vascular resistance increases during both maximal inflation and forced deflation of the lungs. Measurement of vital capacity acts as a guide. A fall shows pulmonary congestion.

iv. Nervous Control:

The pulmonary blood vessels have got both parasympathetic and sympathetic nerve supply. But there is still doubt that these nerve supplies have got any major physiological role in main­tenance of normal circulation. Gracia Ramos and Rudomin (1957) have claimed the presence of active nervous control of the pulmonary blood vessels as they have observed reduction in O₂, saturation of arterial blood following stimulation of the sympathetic nerve. Electrical stimulation of caudal end of cut cervical vago-sympathetic nerve also causes vasodilatation which is observed following administration of atropine.

v. Reflex Control:

The pulmonary circulation is also modified through reflexes originated due to stimulation of baroreceptors and present in the Sino-aortic areas. Stimulation of baro-receptors in the carotid sinus and aortic arch produces reflex vasodilatation in the pulmonary vascular bed, whereas stimulation of chemoreceptors in the aortic bodies or carotid bodies produces pulmonary vasoconstriction.

Peculiarities of Pulmonary Circulation:

i. Pulmonary artery carries deoxygenated blood and pulmonary veins carry oxygenated blood.

ii. Filtration of fluid in systemic capillaries filtration of fluid takes place into the tissue space, but, nothing such happens in the lungs. The purpose is obvious. Filtration would cause collection of liquid in the alveoli and retard oxygenation of blood. The mechanism is also obvious.

In the pulmonary capillaries the colloidal osmotic pressure (25 mm of Hg) is much higher than the blood pressure. In the systemic capillaries it is just the reverse. Hence, no filtration in the lungs. Pulmonary congestion, from any cause, will increase the local blood pressure leading to filtration and causing oedema of lungs.

iii. Filtration of emboli the fine pulmonary capillary acts as a filter that traps emboli from reaching and blocking the blood vessels of heart, brain or other organs.

iv. Blood enters lungs through pulmonary and bronchial arteries. Blood is returned from the lungs through similar two channels; the pulmonary veins (oxygenated blood) and bronchial veins (reduced blood). One may think that the reduced blood instead of being returned through the bronchial veins could have easily joined the alveolar capillaries, become oxygenated and be returned through the pulmonary veins to the left heart.

But in that case the venous return to the left heart would be more than the output of the right heart. This discrepancy may lead to heart failure. Only that amount of blood which was expelled by the right heart will return to the left heart, so that the output of the two ventricles may remain same. Thus blood flow through the two systems—pulmonary and systemic, are equal.

v. The pulmonary vascular bed is a low, resistance circuit, whereas the systemic one is a high resistance circuit.

vi. Pulmonary vascular bed has to supply blood to one type of tissue, whereas the systemic one has to supply blood to different types of tissues.

vii. Pulmonary vascular bed is relatively short distensible with large calibre and can accommodate a large volume of blood (blood reservoir).

viii. As the pulmonary vascular bed is exposed to sub-atmospheric pressure, the pulmonary pressure and flow are altered during inspiration and expiration.

ix. As the pulmonary vascular bed is short and distensible, blood flow is not fully dependent upon neurogenic control; and mechanical factor of the right heart plays an important role in maintenance of normal blood flow.

x. Local actions of CO₂ and low O₂ on the pulmonary vascular bed are of vasoconstrictions which are just the reverse in case of the systemic one.

xi. Though the pulmonary vascular bed has got both sympathetic and parasympathetic innervations, yet its role in the maintenance of circulation is less important than the systemic one.

Effect of Respiration on the Systemic Blood Pressure:

Generally systemic blood pressure falls during inspiration and rises during expiration. This is due to increased capacity of the pulmonary vascular bed during inspiration holding a larger volume of blood and thus momentarily reducing the return of blood to the left heart. Because during inspiration, pulmonary vascular resistance is greatly reduced as the intrathoracic pressure is below the atmospheric pressure.

So at the first phase of inspiration, aortic pressure is decreased and at the last phase of inspiration as well as with the onset of expiration the systemic pressure is increased. Because venous returns to the left heart is gradually increased at the later phase of inspiration and towards the early phase of expiration.

1. Pulmonary Vascular Reflex:

There are baroreceptor areas in the pulmonary arch of aorta and when these receptors are stimulated, reflexly alter the systemic blood pressure, heart rate and capacity of the peripheral blood vessels. An increase in the pulmonary arterial pressure produces reflex bradycardia, hypotension and increase of blood flow in the splanchnic bed.

These responses are abolished following divisions of the vagus nerves:

i. Reflexes from the pulmonary vascular bed may participate in the regulation of blood volume. Increased blood volume in the thoracic cavity reflexly produces diuresis through the inhibition of the antidiuretic hormone (ADH) secretion.

ii. Intravenous injection of starch grain, multiple emboli may produce rapid shallow breathing. This reflex respiratory response is due to the stimulation of receptors in the pulmonary vascular bed and can be abolished following section of the vagi.

2. Pulmonary Depressor Chemoreflex:

Intravenous injection of phenyl diguanide induces bradycardia and hypotension. It has been claimed that these reflex effects are initiated through the stimulation of pulmonary deflation receptors. Likewise serotonin, starch grain, multiple emboli stimulate these deflation receptors and induce pulmonary depressor chemoreflex.

Circulatory Status in Different Cardiopulmonary Diseases:

1. Mitral Stenosis:

It is the condition when the orifice of the valve is narrowed by fusion of the cusp margins. The cusps become rigid and thickened. The chordae tendineae hold the valve in a fixed position and the opening becomes narrowed. The whole ring looks like a narrow rigid funnel. Due to narrowing of the opening, a resistance is offered for blood flow from the left atrium to the left ventricle. The left atrium is dilated and thickened due to accumulation of blood within itself.

Furthermore the great problem that arises due to this is the occurrence of pulmonary hypertension. With the obstruction of blood flow from the left atrium to the left ventricle, the left atrial pressure is tremendously increased causing decrease in pulmonary driving force. So the consequence is the decrease in pulmonary flow, right ventricular hypertrophy or cor pulmonale ultimately leading to right heart failure.

2. Emphysema:

It is the condition in which there is enlargement of the air spaces distal to the terminal bronchiole. Obstruction to expiration due to oedema, inflammatory changes or mucus in the bronchi may cause emphysema. In emphysema, pulmonary vascular resistance is greatly enhanced causing obstruction to blood flow.

Ultimately, the pulmonary hypertension and then right heart failure may occur. The increase of pulmonary vascular resistance is the consequence of destruction of blood vessels. Poor exchange of air in the emphysematous alveoli may also cause increase of vascular resistance by accumulated CO₂ in the blood.

3. Pulmonary Embolism:

In pulmonary embolism either massive or diffuse, the blood flow is greatly affected due to blockade of pulmonary blood vessels by free-moving clot (embolus).

4. Atelectasis:

It is the condition when a lung or a part of a lung remains in a collapsed state. In pneumothorax that is when the chest cavity is opened to atmospheric pressure. In such condition, the pulmonary vascular resistance is greatly increased causing the decrease of pulmonary blood flow.

In natural atelectasis, the alveoli not only constrict, blood vessels lining the alveoli are also constricted causing vascular detachment with the rest of the lung. This is a safety mechanism of the lung so that the ill-ventilated lung is prevented from supplying major quantities of blood.

5. Removal of Lung:

In case of pneumectomy or lobectomy, pulmonary haemodynamics remain unaltered so long the subject maintains a sedentary life. But if the subject performs heavy work then due to increase of cardiac output, the pulmonary pressure may be increased drastically because in such subject the pulmonary reserve is very low.

6. Diffuse Sclerosis of Lung Vessels:

In sclerosis of the pulmonary blood vessels the elasticity as well as the distensibility of the lung vessels is decreased. Pulmonary vascular capacity is also affected greatly. In such case if subjects do not have such heavy or even mild work so that the cardiac output is increased, then there should have no trouble. In late or extreme stages of sclerosis, the pulmonary blood flow is greatly decreased and pulmonary hypertension along with the right heart hypertrophy may be happened.

7. Pulmonary Fibrosis:

It is the cause of formation of fibrous tissue during healing of the wound. The generalised fibrosis happens in lung tissue following recovery from tuberculosis, bronchopneumonia, pneumoconiosis, gas poisoning, etc. Under such condition the pulmonary vascular resistance is increased. Thus obstruction to blood flow may be offered causing pulmonary hypertension in late stage.