45 - Anterior Transthoracic Approaches to the Spine

Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.

Title: General Thoracic Surgery, 6th Edition

Copyright 2005 Lippincott Williams & Wilkins

> Table of Contents > Volume I - The Lung, Pleura, Diaphragm, and Chest Wall > Section XI - The Pleura > Chapter 55 - Resorption of Gases from the Pleural Space

Chapter 55

Resorption of Gases from the Pleural Space

Yvon Cormier

Under normal circumstances, there are no free gases in the pleural space. A variety of conditions, however, can lead to the accumulation of gases in this cavity. Because the virtual space between the parietal and visceral pleura is under negative pressure, any communication with the surrounding structures (bronchi, alveoli, extrathoracic communication through the chest wall) immediately causes gases to enter the pleural space (i.e., to produce a pneumothorax). The pressure in the pleural space is negative in relation to the atmosphere because of the elastic properties of the lungs, which tend to collapse, and of the chest wall, which, at volumes below 75% of the total lung capacity, tends to expand. In normal individuals, at functional residual capacity when respiratory muscles of the thoracic wall are in the relaxed state, this pressure is approximately 5 cm H₂O lower than that of the surrounding atmosphere. This pressure further decreases during inspiration, especially in the presence of airway obstruction. During a M ller maneuver (i.e., maximal inspiratory efforts against a closed glottis), pleural pressure can transiently become negative, to lower than 100 cm H₂O.

When gases enter the pleural space, pressure gradients and the physical laws of gases favor their eventual resorption.

FACTORS DETERMINING GAS RESORPTION

Gas resorption from the pleural space is achieved by a simple diffusion from the pleural space into the venous blood. This diffusion, which can occur in both directions, is possible because the pleura and capillary walls are permeable to gases and because the partial pressures of gases in the pleural space and those in the venous blood can differ. For example, a positive pressure gradient between the gases in the pneumothorax and those dissolved in the venous blood would favor the passage of those gases from the pneumothorax into the venous blood. No active transport mechanisms for gas resorption exist; the only driving forces that determine gas resorption are pressure gradients.

The rate of gas resorption depends on four variables: the diffusion properties of the gases present in the pleural space, the pressure gradients for the gases in the pleural space in relation to the venous blood, the area of contact between the pleural gas and the pleura, and the permeability of the pleural surface (e.g., a thickened fibrotic pleura absorbs less than a normal pleura).

Because the solubility and diffusion properties of different gases vary considerably, the speed of resorption depends on the type of gas involved. For example, oxygen is resorbed 62 times faster than nitrogen (N₂). Water vapor (H₂O) and carbon dioxide (CO₂) equilibrate almost instantaneously, CO₂ being 23 times more soluble than O₂.

Depending on the clinical situation, a pneumothorax can initially contain room air (i.e., a leak from the outside) or alveolar air (i.e., a leak through the lungs). The alveolar air contains different proportions of CO₂, O₂, or N₂, depending on the ventilation of the patient and the presence of supplemental O₂ given to the patient at the time of the leak into the pleural space. If a patient is receiving 100% O₂, the pleural gases will be composed mostly of this gas and contain no N₂, the slowest gas to be resorbed. Initial gas compositions in a pneumothorax when the air entry is from room air or from alveolar air with the patient breathing room air or 100% O₂ are presented in Fig. 55-1.

PARTIAL PRESSURE OF GASES IN VENOUS BLOOD

Because the pressure gradients that favor gas resorption are those between the pneumothorax and the venous blood, it is also important to consider the venous blood partial gas pressures. Under normal circumstances, the total gas pressure in a pneumothorax is within a few millimeters of mercury of that of the atmosphere (760 mm Hg), whereas that in the venous blood is 702 mm Hg, 58 mm Hg lower. This positive pressure gradient between the pneumothorax and the venous blood constitutes the driving force responsible for gas resorption from a pneumothorax.

Fig. 55-1. Gas partial pressures initially present in a pneumothorax when air entry comes from room air (A); alveoli, subject breathing room air (RA) (B); and alveoli, subject breathing 100% O₂ (C). After equilibration (phase 1), the resulting gas partial pressures become identical regardless of the initial gas composition. Note that the volume change of the pneumothorax during phase 1 was least when the pneumothorax was initially constituted from room air; intermediate when from alveolar air, with the patient breathing room air; and much greater when the patient was breathing 100% O₂.

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MECHANISMS OF GAS PRESSURE GRADIENTS BETWEEN THE PNEUMOTHORAX AND THE VENOUS BLOOD

A schematic approach is used here to explain the gas composition in venous blood. Dry room air contains, for all practical purposes, 80% N₂ and 20% O₂. Other gases (e.g., CO₂, argon) are present in minute quantities. The normal atmospheric pressure is 760 mm Hg (1,031 cm H₂O); therefore, the partial pressure of N₂ in dry room air is 608 mm Hg, whereas that of O₂ is 152 mm Hg. When room air enters the alveoli, it gains H₂O vapor and CO₂ and loses O₂; the resulting gas composition is N₂=571 mm Hg, O₂=102 mm Hg, H₂O=47 mm Hg, and CO₂=40 mm Hg. Because the alveoli are in close communication with the atmosphere, the total gas pressure at this level must equal 760 mm Hg. This alveolar gas composition is in contact with the blood at the alveolar capillary level, and gas exchange occurs. The resulting normal arterial gas composition is Pao₂=97 mm Hg, Paco₂=40 mm Hg, and Pan₂=569 mm Hg, with water vapor remaining constant at 47 mm Hg; the total arterial gas pressure is 753 mm Hg. Note that a 7-mm Hg pressure gradient exists between the alveolar gas pressure and that of the arterial blood.

Our cells consume O₂ and produce CO₂, consuming 300 mL of O₂ for 240 mL of CO₂ produced, a respiratory quotient of 0.8. Despite this small difference between the quantity of O₂ consumed compared with that of CO₂ produced, the metabolic changes increase the Paco₂ by 6 mm Hg and decrease that of oxygen by 57 mm Hg in the gases' passage through the capillaries from the arterial to the venous system. This large difference in the changes in O₂ and CO₂ partial pressures is caused by the difference in the solubility and transport capacity of the blood for these two gases. N₂ is not metabolized and therefore remains unchanged between the arterial and venous blood. Water vapor also remains constant at 47 mm Hg. The resulting venous gas pressure is therefore P

o₂=40 mm Hg, P

co₂=46 mm Hg, P

n₂=569 mm Hg, and P

H₂O=47 mm Hg, for a total gas pressure of 702 mm Hg (i.e., 51 mm Hg less than that in the arterial blood and 58 mm Hg less than that of alveolar or room air total gas pressures).

A schematic summary of gas pressures from room air to the venous blood is given in Fig. 55-2. A pneumothorax results because of a communication between the pleural cavity and the atmosphere, either via the thoracic wall or the lung. Because of this communication, the initial gas pressure in a pneumothorax equals that of the atmosphere at 760 mm Hg, thus creating a 58-mm Hg gradient between the two.

PHASES OF GAS RESORPTION

Gas resorption from the pleural space occurs in two phases: equilibration of gases' partial pressures, and constant resorption.

Phase 1: Equilibration

The first phase represents the equilibration of gases initially placed into the pleural cavity with those of venous blood. Its

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duration and the amount of gas resorbed during this phase depend on the composition of the initial gases in the pneumothorax. The second phase is the constant resorption rate that follows once the equilibration has occurred.

Fig. 55-2. The total and partial gas pressures in room air (RA), alveolar air (AA), arterial blood (AB), and venous blood (VB). The total pressure for RA and AA is the same, whereas a small total pressure decrease occurs between AA and AB (7 mm Hg), and a further, more significant decrease is seen between AB and VB (51 mm Hg). The difference between RA and VB therefore equals 58 mm Hg.

Regardless of the quality of gases initially in the pneumothorax, the first phase results in an equilibrating period, after which the composition of the remaining gases in the pneumothorax is similar in all situations. It follows, therefore, that gases can enter or leave the pleural cavity as this equilibration takes place. If the initial pneumothorax contained 100% O₂, the N₂ partial pressure would be greater in the venous blood than in the pleural cavity; in this condition the N₂ gradient favors N₂ to leave the venous blood and enter the pleural space. However, because O₂ is more soluble, more O₂ leaves the pleural cavity than N₂ will enter. Therefore, the total quantity of gases in the pleural cavity decreases, despite ingoing N₂. If one filled a pleural cavity with 100% N₂, the initial phase of equilibration would produce an increase in the quantity of gases in the pneumothorax because more O₂ and CO₂ would enter the cavity than N₂ would leave.

The gas composition at equilibration is determined by the partial pressures of gases in the venous blood. At this time, the gas composition in the remaining pneumothorax is the same, regardless of the composition of the initial gas. The volume resorbed during the equilibrating phase can be different (see Fig. 55-1): The greater the quantity of the more soluble gases and the greater the gradient between the pleural space and the venous blood, the faster the resorption. The high solubility and resorption rate of CO₂ is the reason this gas is infused into the abdominal cavity for laparoscopy.

If a patient receives supplemental O₂ for more than 2 or 3 minutes, the Pn₂ in the alveoli and in the blood decrease proportionally. For example, if a subject received 50% O₂, the partial pressure of N₂ would decrease in the alveolar air, and subsequently in the venous blood, from 569 mm Hg to approximately 350 mm Hg. Because the P

o₂ does not increase significantly with an increase of inspired O₂, the pressure gradient between a pneumothorax would be greatly increased in such a situation, from 58 mm Hg to 277 mm Hg in this case.

Phase 2: Constant Resorption

If all gases in the pleural space were at equilibrium with the venous gas pressure, the intrapleural total gas pressure would be O₂+CO₂+H₂O+N₂=702 mm Hg, or 58 mm Hg less than atmosphere. Such a negative pleural pressure (58 mm Hg) is impossible on a long-term basis.

CLINICAL TYPES OF PNEUMOTHORACES

Three potential types of pneumothoraces result in different behavior of gas resorption from the pleural cavity. The pneumothorax can behave as a closed rigid cavity, a closed collapsible cavity, or an open cavity. Clinical conditions and mechanisms of gas resorption under these three conditions are discussed separately.

Closed Rigid Cavity

In theory, a closed rigid pneumothorax (e.g., non-reexpandable lung) could remain air filled. As gases are resorbed along each gas partial pressure as previously described, the pressure inside the pleural space would progressively decrease until it stabilized at a pressure of 58 mm Hg lower than the atmosphere. At this negative pressure, no pressure gradient remains to ensure continued resorption. Although such a negative pleural pressure is possible on a short-term basis, if this negative pressure is maintained, fluid eventually seeps into the pleural cavity and gradually fills it with liquid, which subsequently solidifies and fibroses. Permanent residual pneumothorax equals a persistent opening, as, for example, a bronchopleural fistula.

Closed Collapsible Cavity

A closed collapsible cavity is by far the most frequent form of pneumothorax. This condition occurs when gases enter the pleural space, the opening responsible for the pneumothorax becomes occluded, and the lungs are freely reexpandable. As gases are resorbed, no new gases enter the pleural space, and the reexpansion of the lungs compensates for the volume of resorbed gases, therefore preventing the appearance of negative intrapleural pressure. All gases eventually are resorbed, and the lungs take their normal place, leaving no physical pleural cavity.

As the intrapleural gas pressure tends to decrease as a result of gas resorption, the lung reexpands, and the amount of air in the pleural cavity progressively decreases until it is all resorbed. At the so-called equilibrium, therefore, O₂, CO₂, and H₂O partial pressures are similar in the venous blood and in the pleural cavity. The slower N₂, however, is 58 mm Hg higher in the pleural cavity, which is at or close to atmospheric pressure, than in the venous blood, which is 58 mm Hg subatmospheric. The decreasing volume of the pneumothorax prevents large intrapleural negative pressures and ensures the persistence of this positive partial pressure gradient between gases in the pleural cavity and the venous blood. The intrapleural pressure is not allowed to decrease to -58 mm Hg, as in a closed rigid cavity, where such a gradient would no longer exist and all gas resorption would cease. The time required to absorb all gases in a pneumothorax is quite variable and depends on previously described characteristics. It has been estimated that 6% of a pneumothorax is absorbed in 24 hours.

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Open Cavity

As long as the communication between the pleural cavity and the lung or through the thoracic wall persists, the lung does not reexpand because all absorbed gases are replenished from the outside. In this condition, gases in the pleural space are resorbed as for the closed cavity; however, the gases resorbed are determined by what is returned into the pleural cavity. Because the composition of pleural gases remains constant, what comes in is what is resorbed. For example, if the pleural cavity is opened to the outside, O₂ and N₂ are resorbed at a proportion of 20:80, corresponding to the gas composition of dry room air.

EFFECTS OF BAROMETRIC PRESSURE ON PLEURAL GASES

People living at different altitudes live in different barometric pressures (e.g., the barometric pressure at 11,000 feet above sea level is 500 mm Hg, compared with 760 mm Hg at sea level). However, the gas fractions in the atmosphere always remain the same, regardless of the altitude. For an atmospheric pressure of 500 mm Hg, the Pn₂ in the atmosphere would be 400 mm Hg and the Po₂ would be 100 mm Hg, dry air. Changes in these gas pressures from room air to the venous blood would follow the same principle as when the atmospheric pressure is 760 mm Hg. At 11,000 feet, the arterial pressure of O₂ would be approximately 60 mm Hg and that of venous blood not significantly different from that at sea level (40 mm Hg), giving an arterial to venous oxygen pressure decrease of only 20 mm Hg, compared with 51 mm Hg at sea level. Because the O₂ decrease between arterial and venous blood is the major cause of the lower total gas pressure in the venous blood and the eventual N₂ gradient between the venous blood and gases in a pneumothorax at equilibrium, this N₂ gradient would therefore be much smaller at this high altitude. Such differences in pressure gradients would decrease the rate of N₂ resorption.

Although the proportions of different gases do not change with changing barometric pressures, the volume occupied by a given quantity of gases does. For example, a pneumothorax of 1 L volume would increase by 33% if the patient were transported in an airplane pressurized at 8,000 feet, which is common practice. If a pneumothorax developed in a deep sea diver at 30 feet below the surface, the volume of the pneumothorax would double as the diver resurfaces, even when no new gases enter the pleural space.

THERAPEUTIC CONSIDERATIONS

The dynamics of gas resorption from the pleural space can be used clinically. A potential application is to give 100% O₂ to a patient during a maneuver that is at risk of creating a pneumothorax. A typical example of when this is useful is transthoracic lung biopsy. When 100% O₂ is given during the procedure, any resulting pneumothorax resorbs much faster for two reasons: (a) The pneumothorax is filled with the more soluble O₂, and (b) the pressure gradient between the pneumothorax and the venous blood is larger, because giving 100% O₂ washes out N₂ from the alveoli and eventually the venous blood. Giving 100% O₂ to a patient when the pneumothorax is already in place also increases the rate of gas resorption by decreasing P

N₂ and therefore increasing the pressure gradient for this gas between the pneumothorax and the venous blood. This beneficial effect, however, is relatively small and probably not clinically useful.

Reading References

Cormier Y, Laviolette M, Tardif A: Prevention of pneumothorax in needle lung biopsy by breathing 100% oxygen. Thorax 35:37, 1980.

Dale WA, Rahn H: Rate of gas absorption during atelectasis. Am J Physiol 170:606, 1952.

Kircher LT, Swartzel RL: Spontaneous pneumothorax and its treatment. JAMA 155:24, 1954.

Loring SH, Butler JP: Gas exchange in body cavities. In Fishman AP, Farhi LE, Tenney MR (eds): Handbook of Physiology. Section 3. The Respiratory System. Washington, DC: American Physiological Society, 1987, p. 238.

Piiper J: Physiological equilibria of gas cavities in the body. In Fenn NO, Rahn H (eds): Handbook of Physiology. Vol. 2. Respiration. Washington, DC: American Physiological Society, 1965, p. 1205.