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Anatomy & Physiology of the Pulmonary Circulatory System

Pulmonary Vessels: The pulmonary artery extends only 5 centimeters beyond the apex of the right ventricle and then divides into right and left main branches that supply blood to the two respective lungs. The pulmonary veins, like the pulmonary arteries, are also short. Bronchial Vessels: Blood also flows to the lungs through small bronchial arteries that originate from the systemic circulation, amounting to about 1 - 2% of the total cardiac output. This bronchial arterial blood is oxygenated blood, in contrast to the partially deoxygenated blood in the pulmonary arteries. It supplies the supporting tissues of the lungs. Lymphatics: Lymph vessels are present in all the supportive tissues of the lung, beginning in the connective tissue spaces that surround the terminal bronchioles, coursing to the hilum of the lung, and thence mainly into the right thoracic lymph duct.

Pressures in the Pulmonary System Pressures in the Pulmonary Artery: During systole, the pressure in the pulmonary artery is essentially equal to the pressure in the right ventricle. In the normal human being, the pulmonary arterial pressures are: § The systolic pulmonary arterial pressure averages about 25 mm Hg. § The diastolic pulmonary arterial pressure is about 8 mm Hg. § The mean pulmonary arterial pressure is 15 mm Hg.

Pulmonary Capillary Pressure: The mean pulmonary capillary pressure is about 7 mm Hg. Left Atrial and Pulmonary Venous Pressures: The mean pressure in the left atrium and the major pulmonary veins averages about 2 mm Hg in the recumbent (lying down) human being, varying from as low as 1 mm Hg to as high as 5 mm Hg.

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Blood Volume of the Lungs: The blood volume of the lungs is about 450 milliliters, about 9% of the total blood volume of the entire circulatory system. Approximately 70 milliliters of this pulmonary blood volume is in the pulmonary capillaries, and the remainder is divided about equally between the pulmonary arteries (190 ml) & the veins (190 ml).

Automatic Control of Pulmonary Blood Flow Distribution Effect of Diminished Alveolar Oxygen on Local Alveolar Blood Flow: When the concentration of oxygen in the air of the alveoli decreases below normal, especially when it falls below 70% of normal (below 73 mm Hg PO2), the adjacent blood vessels constrict, with the vascular resistance increasing more than fivefold at extremely low oxygen levels. Effect of Increased Cardiac Output on Pulmonary Blood Flow & Pulmonary Arterial Pressure: During heavy exercise, blood flow through the lungs increases fourfold to sevenfold. This extra flow is accommodated in the lungs in three ways:

1. By increasing the number of open capillaries, sometimes as much as threefold.

2. By distending all the capillaries and increasing the rate of flow through each capillary more than twofold.

3. By increasing the pulmonary arterial pressure.

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Pulmonary Capillary Dynamics It is important for us to note that the alveolar walls are lined with so many capillaries that, in most places, the capillaries almost touch one another side by side. Therefore, it is often said that the capillary blood flows in the alveolar walls as a “sheet of flow,” rather than in individual capillaries. Capillary Exchange of Fluid in the Lungs, & Pulmonary Interstitial Fluid Dynamics: The dynamics of fluid exchange across the lung capillary membranes are qualitatively the same as for peripheral tissues. However, quantitatively, there are important differences, as follows:

1. The pulmonary capillary pressure is low, about 7 mm Hg, in comparison with a considerably higher functional capillary pressure in the peripheral tissues of about 17 mm Hg.

2. The interstitial fluid pressure in the lung is slightly more negative than that in the peripheral subcutaneous tissue. This has been measured in two ways: § By a micropipette inserted into the pulmonary interstitium, giving a

value of about –5 mm Hg. § By measuring the absorption pressure of fluid from the alveoli, giving

a value of about –8 mm Hg. 3. The pulmonary capillaries are relatively leaky to protein molecules, so

that the colloid osmotic pressure of the pulmonary interstitial fluid is about 14 mm Hg, in comparison with less than half this value in the peripheral tissues.

4. The alveolar walls are extremely thin, and the alveolar epithelium covering the alveolar surfaces is so weak that it can be ruptured by any positive pressure in the interstitial spaces greater than alveolar air pressure (greater than 0 mm Hg), which allows dumping of fluid from the interstitial spaces into the alveoli.

Negative Pulmonary Interstitial Pressure & the Mechanism for Keeping the Alveoli “Dry”: One of the most important problems in lung function is to understand why the alveoli do not normally fill with fluid. One’s first inclination is to think that the alveolar epithelium is strong enough and continuous enough to keep fluid from leaking out of the interstitial spaces into the alveoli. This is not true, because experiments have shown that there are always openings between the alveolar epithelial cells through which even

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large protein molecules, as well as water and electrolytes, can pass. However, if one remembers that the pulmonary capillaries and the pulmonary lymphatic system normally maintain a slight negative pressure in the interstitial spaces, it is clear that whenever extra fluid appears in the alveoli, it will simply be sucked mechanically into the lung interstitium through the small openings between the alveolar epithelial cells. Then the excess fluid is either carried away through the pulmonary lymphatics or absorbed into the pulmonary capillaries. Thus, under normal conditions, the alveoli are kept “dry”, except for a small amount of fluid that seeps from the epithelium onto the lining surfaces of the alveoli to keep them moist.

Pulmonary Edema The most common causes of pulmonary edema are as follows:

1. Left-sided heart failure or mitral valve disease, with consequent great increases in pulmonary venous pressure and pulmonary capillary pressure and flooding of the interstitial spaces and alveoli.

2. Damage to the pulmonary blood capillary membranes caused by infections such as pneumonia or by breathing noxious substances such as chlorine gas (Cl2) or sulfur dioxide gas (SO2).

Each of these causes rapid leakage of both plasma proteins and fluid out of the capillaries and into both the lung interstitial spaces and the alveoli. Fluid in the Pleural Cavity: When the lungs expand and contract during normal breathing, they slide back and forth within the pleural cavity. To facilitate this, a thin layer of mucoid fluid lies between the parietal and visceral pleurae. The total amount of fluid in each pleural cavity is normally slight, only a few milliliters. Whenever the quantity becomes more than barely enough to begin flowing in the pleural cavity, the excess fluid is pumped away by lymphatic vessels opening directly from the pleural cavity into:

1. The mediastinum. 2. The superior surface of the diaphragm. 3. The lateral surfaces of the parietal pleura.

Therefore, the pleural space, the space between the parietal and visceral pleurae, is called a potential space because it normally is so narrow that it is not obviously a physical space.

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“Negative Pressure” in Pleural Fluid: A negative force is always required on the outside of the lungs to keep the lungs expanded. This is provided by negative pressure in the normal pleural space. The basic cause of this negative pressure is pumping of fluid from the space by the lymphatics.

Pleural Effusion Pleural effusion means the collection of large amounts of free fluid in the pleural space. The causes of the effusion are including:

1. Blockage of lymphatic drainage from the pleural cavity. 2. Cardiac failure, which causes excessively high peripheral & pulmonary

capillary pressures, leading to excessive transudation of fluid into the pleural cavity.

3. Greatly reduced plasma colloid osmotic pressure, thus allowing excessive transudation of fluid.

4. Infection or any other cause of inflammation of the surfaces of the pleural cavity, which breaks down the capillary membranes and allows rapid dumping of both plasma proteins and fluid into the cavity.

Edited By Noor Al-Deen M. Al-Khanati