Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

2021-02-08 12:00 AM

Pulmonary oedema occurs in the same way that oedema occurs elsewhere in the body. Any factor that increases the filtration of fluid out of the pulmonary capillaries or interferes with pulmonary lymphatic function and causes an increase in interstitial pulmonary filtration pressure from negative to positive.

The lungs have two circulations, a high pressure, low flow rate and one low pressure, high flow rate. High pressure, low circulatory flow provides arterial blood circulation to the trachea, bronchial tree (including the terminal bronchi), the supporting tissues of the lungs and the outer (outer) lining of the artery. and pulmonary veins. The bronchial artery is the branch of the thoracic aorta, supplying blood to most of these artery systems at a pressure that is only slightly lower than the aortic pressure. Low pressure, high circulating flow supplies venous blood from all parts of the body to the alveolar capillaries where oxygen (O2) is added and carbon dioxide (CO2) is removed. The pulmonary artery (which receives blood from the right ventricle) and its artery branches carry blood to the alveolar capillaries for gas exchange,

Exchange air between the alveolar air and the pulmonary capillary blood, it is important to note here that the alveolar wall is lined with a lot of pulmonary capillaries, in most places the capillaries almost touch one edge different side by side. Therefore, it is often said that the capillary blood flows in the alveolar wall as "sheet of flow", not individual capillaries.

Pulmonary capillary pressure

No direct measurements of pulmonary capillary pressure have been performed. However, “is gravimetric” measuring pulmonary capillary pressure, using a technique described in Chapter 16, gave a value equal to 7 mmHg. This measurement is probably approximate because the mean left atrial pressure is about 2 mmHg and the mean pulmonary artery pressure is only 15 mmHg, so the mean pulmonary capillary pressure should be between these two values.

The length of time the blood remains in the pulmonary capillaries. From histological study on the total cross-sectional area of ​​all pulmonary capillaries, it can be calculated that with normal cardiac output, the blood passes through the pulmonary capillaries in about 0.8 s. As cardiac output increases, this time can be shortened to 0.3 seconds. The shortening would be much greater without the fact that additional capillaries, which are often collapsed, open to accommodate increased blood flow. Thus, in just a fraction of a second, the blood passing through the alveolar capillaries becomes oxidized and leaves an excess of CO2.

Pulmonary capillary fluid exchange and interstitial fluid dynamics

The dynamics of fluid exchange across the pulmonary capillary membrane are characteristic of the peripheral tissue. However, the quantity has the following important differences:

  1. Pulmonary capillary pressure is low, about 7 mmHg, and is significantly higher than the functional pulmonary capillary pressure in peripheral tissue about 17 mmHg.
  2. The negative interstitial fluid pressure in the lung is more negative than in the peripheral subcutaneous tissues (this pressure has been measured in two ways: by inserting a micropipette into the interstitial lung, creating a value of about -5 mmHg, and by Measure the absorbance pressure of the fluid from the alveoli, giving values ​​about -8 mmHg).
  3. The colloid osmotic pressure of interstitial fluid is about 14 mmHg, less than half of this value in peripheral tissue.
  4. The alveolar walls are so thin and the alveolar epithelium covering the alveolar surface is so weak that it can rupture by any positive pressure in the interstitial space greater than the alveoli (0 mmHg), allowing fluid coming from the interstitial spaces into the alveoli. Let us now see how the different quantities affect the lung dynamics.


Figure. Hydrostatic and osmotic pressure in mmHg at the capillaries (left) and the alveolar membrane (right) of the lung. Also shown are the ends of a lymphatic (central) vessel that pumps fluid from the interstitial lung spaces.

Correlation between fluid pressure and another lung pressure

The figure shows a pulmonary capillary, a pulmonary alveolus, and a duct that drains the lymphatic capillaries into the interstitial space between the capillary and the alveoli. Note that the pressure balance in the capillary membrane is as follows:

Minimum pressure to induce displacement from the capillaries out and into the interstitial lung:

Capillary pressure: 7 mmHg.

Interstitial colloid osmolality: 14 mmHg.

Interstitial fluid negative pressure: 8 mmHg.

Total outside pressure: 29 mmHg.

Minimum pressure to induce capillary uptake of fluid:

Plasma colloidal osmolality: 28 mmHg.

Total pressure inside: 28 mmHg.

Consequently, the normal external pressures are slightly greater than the internal pressure, creating an average filtration pressure in the pulmonary capillary membrane, which can be calculated as follows:

Total outside pressure: +29 mmHg.

Total pressure inside: -28 mmHg.

Average filtration pressure: +1 mmHg.

This filtration pressure causes a weak, constant outflow from the pulmonary capillaries into the interstitial spaces, except for a small amount now slightly in the alveoli, which is pumped back into circulation through the pulmonary lymphatic system.

Interstitial negative pressure and the mechanism that keeps the alveoli dry

What keeps the fluid-filled alveoli under normal conditions? If only the pulmonary capillaries and the normal pulmonary lymphatic system maintain a slight negative pressure in the interstitial space, it will only be mechanically absorbed into the interstitial lung through the pores between the epithelial cells. alveoli. The excess fluid is then carried through the pulmonary lymphatic system. Therefore, under normal conditions, the alveoli are kept "dry" except for a small amount that seeps from the epithelium onto the mucous surface of the alveoli to keep them moist.

Pulmonary oedema

Pulmonary edema occurs the same way that oedema occurs elsewhere in the body. Any factor that increases the filtration of fluid from the pulmonary capillaries or interferes with pulmonary lymphatic function and causes an increase in interstitial pulmonary filtration pressure from negative to positive will cause rapid interstitial filling and waste nag with large amounts of fluid. free.

The most common causes of pulmonary edema are:

  1. Left-heart failure or mitral valve disease results in an increase in pulmonary venous pressure and pulmonary capillary pressure and alveolar fluid retention.
  2. Damage to blood capillary membranes due to infections such as pneumonia or by inhaling toxic substances such as chlorine gas or sulfur dioxide. Each mechanism leads to the rapid leakage of both plasma protein and fluid from the capillaries and into both the interstitial and alveolar spaces.

Figure. The rate of fluid entering the lung tissues when left atrial pressure (and pulmonary capillary pressure) increases.

Safe pulmonary oedema factor

Animal experiments have shown that the pulmonary capillary pressure must often rise to a value that is at least equal to the plasma colloid pressure in the first capillaries, suggesting pulmonary edema will occur. To give an example, the figure shows different degrees of left atrial pressure accelerating the formation of pulmonary edema in dogs. Remember that each time the left atrial pressure rises to a high value, the pulmonary capillary pressure increases by one to two mm Hg more than the left atrial pressure. In these experiments, as soon as the left atrial pressure increased above 23 mm Hg (due to the pulmonary capillary pressure increased above 25 mmHg), fluid began to accumulate in the lungs. This increased fluid accumulates even more rapidly with increasing capillary pressure. The plasma colloid pressure throughout this experiment is equal to the critical pressure of 25 mmHg. Therefore, in the normal human, the plasma colloid pressure is 28 mmHg,

Safety factor in chronic condition

When the pulmonary capillary pressure is consistently high (at least 2 weeks), the lungs counteract pulmonary edema due to the greatly enlarged lymph vessels, increasing the ability to carry fluid away from the interstitial space by about 10 times. Therefore, in patients with mitral stenosis, pulmonary capillary pressures of 40-45 mmHg have been measured without progression of lethal pulmonary edema.

Rapid death in acute pulmonary edema

When pulmonary capillary pressure rises slightly above the safety factor, lethal pulmonary edema can occur within hours or even 20-30 minutes if capillary pressure rises above the safety factor. 25-30 mmHg. Thus, acute left-heart failure, in which pulmonary capillary pressure sometimes rises to 50 mmHg, death can ensue in less than 30 minutes as a result of acute pulmonary edema.


Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Prothrombin activation: initiates blood clotting

Graphical analysis of high-volume heart failure

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Estimated renal plasma flow: PAH clearance

Nephron: The functional unit of the kidney

Reduced sodium chloride, dilates arterioles, increases Renin release.

Ammonia buffering system: excretes excess H + and creates new HCO3

Red blood cells: differentiation and synthesis

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Origin of lymphocytes: the body's resistance to infection

The endocrine regulates tubular reabsorption

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Physiological anatomy of the kidneys and urinary system

Self-regulation of glomerular filtration rate and renal blood flow

Pathophysiology of fever

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure

Iron metabolism: haemoglobin synthesis