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Resorption of gas trapped in body cavities: comparison of alveolar and pleural space with inner ear and paranasal sinuses
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     Abstract

    This paper describes our attempt to devise a short text aimed at improving students' understanding of gas resorption in body cavities. Students are expected to understand the mechanisms behind paranasal sinusitis, otitis media, closed pneumothorax, and atelectasis of collapsed lung tissue, all used as examples. On the basis of the interpretation that during pneumothorax resorption, gas diffuses down pressure gradients into the blood, students are encouraged to calculate tables of pressure gradients for the above-mentioned pathological conditions. After answering a few questions, students need to analyze and eventually accept the following conclusion: in cases of air trapping in collapsible body cavities, all gases will be fully reabsorbed without pain. Air trapping in bone cavities leads only to partial reabsorption of gases and results in subatmospheric intracavity pressure. Partial vacuum causes painful mucosal edema and free fluid secretion.

    Key words: paranasal sinusitis; otitis media; closed pneumothorax; atelectasis; air trapping

    Introduction

    THIS PAPER DESCRIBES our attempt to devise a short text aimed at improving students' understanding of gas resorption in body cavities. The following text is given to medical students as reading material for a discussion that is usually scheduled for the next week. The students can use their textbooks (1, 2) or other references (3). In most cases, this is the Croatian edition of Medical Physiology by Guyton and Hall (2), used for seminars.

    During preparation of this text in English, to omit possible differences among American (pressures in mmHg) and Croatian editions (pressures in kPa), all cited figures are taken from the last international edition of textbook by Ganong (1).

    Students are expected to understand the mechanisms behind paranasal sinusitis, otitis media, closed pneumothorax, and atelectasis of collapsed lung tissue, all used as examples. In case of any doubt, they are encouraged to ask questions during seminars.

    On the basis of the interpretation that during pneumothorax resorption, gases diffuse down pressure gradients into the blood, students are encouraged to calculate tables of pressure gradients (shaded columns of Tables 1–6) for the above-mentioned pathological conditions.

    After finishing the tables, students should understand that due to tissue metabolism, venous blood is poor in oxygen and rich in CO2, making the total pressure of all gases reduced (in tables, 706 mmHg). In collapsible cavities (pleural cavity, lung tissue, etc.), there is no subatmospheric pressure and almost no pain, because the surrounding pressure reduces cavity volume and thus makes intracavitary pressure to be 760 mmHg. This compression increases partial pressures in the cavity above pressures in the venous blood. Reabsorption of gases continues until no gas is left in the collapsible cavity. In closed bone cavities, subatmospheric pressure develops due to partial resorption of oxygen by venous blood. Blood is forced to enter mucosa by the subatmospheric pressure that sucks it inside. Mucosal interstitial hydrostatic pressure is also more negative than normal, and a painful mucosal edema develops. An added volume of interstitial water in mucosal tissue together with secretion of free fluid from the edematous mucosa into the cavity reduces the negativity of the intracavitary pressure. Further absorption of trapped gas will stop when the balance of partial pressures with mucosal blood is once reached.

    We can conclude that low total gas pressure in venous blood, mainly due to tissue clearance of oxygen, is important in resorption of entrapped air in body cavities.

    TEXT FOR STUDENTS

    Resorption of Gas Trapped in Body Cavities: How Does the Body Get Rid of It?

    Please use your textbooks and other sources.

    Pneumatized body cavities can cause serious health problems if their connection with external air is somehow closed. A few conditions may be familiar.

    Paranasal sinusitis.

    In cases of paranasal sinusitis, the swollen mucosa can close the sinus opening, and soon pain develops, which can be relieved by forced allowance of some air to enter the closed cavity. In most cases, a large portion of the cavity is filled with fluid.

    Otitis media.

    Middle ear infections, particularly in small children, often close the Eustachian tube. Resorption of entrapped air reduces the pressure of gases in the middle ear to subatmospheric levels and causes pain. Air pressure from outside pushes the tympanic membrane inward.

    Closed pneumothorax.

    In cases of pneumothorax, when some air is allowed to enter the pleural space, the lung on the affected side collapses, but when the hole is closed, the entrapped air will be fully reabsorbed in following days. In the first half of the twentieth century, a common practice in Europe was to repeatedly inject air in the pleural space of patients with pulmonary tuberculosis over weeks and months. The condition of deliberately sustained lung collapse due to iatrogenic pneumothorax helped scarring of the diseased lung tissue.

    Atelectasis.

    In cases of bronchial cancer, the primary tumor can seal the involved bronchus. The entrapped air is fully reabsorbed, and the condition of the collapsed lung tissue is called atelectasis (see the computerized tomography scan of the collapsed lung in Fig. 1).

    The usual interpretation of the closed pneumothorax disappearance is as follows: "since gas is at atmospheric pressure, its total pressure, PO2 and [partical pressure of nitrogen] PN2 are greater than the corresponding values in venous blood (compare values for air and venous blood). Gas diffuses down these gradients into the blood, and after 1–2 weeks all of the gas disappears." (2)

    We will try to test this interpretation on air trapped in an unventilated lung portion that will soon become atelectatic (as seen in Fig.1). Partial gas pressures in alveolar air and venous blood are compared in Table 1.

    Try to complete Table 1. Values for alveolar gas and venous gas are taken from Ref. 2. Which gas(es) is trying to leave alveoli and which is trying to leave blood? How do you explain the subatmospheric total of only 706 mmHg for all gases in venous blood? Is it important for the transport of gases? YES or NO.

    Why should we expect that all air is going to be reabsorbed, according to the above-cited explanation? Discuss this with your colleagues.

    Because partial pressures of gases in the venous blood are stable, soon the air in the closed lobule equals pressures in the venous blood around the unventilated lobule.

    Try to complete Table 2. Values are again taken from Ref. 2.

    No gradient exists. Why should we still expect that all air is going to be reabsorbed? Discuss this with your colleagues.

    As shown in Fig. 1, the atelectatic lobule is surrounded by normal lung tissue filled with alveolar air that comes through normal airways. In them, pressure is near the outside pressure of 760 mmHg. The sealed lobule is, because of that, compressed with surrounding ventilated lung tissue, and it collapses. Its inside pressure now equals pressures in the surrounding tissue (760 instead of 706 mmHg). We can correct partial pressures by multiplying them with the ratio 760/706. Why?

    Try to complete Table 3. The uncorrected values are again taken from Ref. 2.

    Which gas(es) is trying to leave alveoli and which is trying to leave blood?

    Do you find the subatmospheric total of only 706 mmHg for all gases in venous blood important for the transport of gases? YES or NO and WHY?

    Now complete Tables 4 and 5 for the closed pneumothorax caused by instillation of outside air in the pleural cavity. As mentioned before, it was used 50 years ago as a physical measure that helped in the treatment of lung tuberculosis.

    Air trapped in the pleural space (pneumothorax gas in our tables) is compressed with atmospheric pressure coming from the collapsed lung because it is still connected with outside air through the unobstructed bronchial tree. The actual pressure transferred from the collapsed lung is reduced by the force of lung tissue elastic recoils. So, in the closed pneumothorax, total pressure in the pleural cavity is <760 but more than 706 mmHg.

    The pneumothorax can be filled with external air as well with alveolar gas. Which one is supposed to be reabsorbed faster? Look for the inspired air values in Ref. 2. They equal outside air pressures.

    Now complete Table 6, which describes gas dynamic during paranasal sinusitis, or otitis media. In both cases, inflamation seals the entrance of air to the bone cavity. Values are again taken from Ref. 2. Intracavitary gas in the open cavity equals inspired air.

    Bone cavities are incompressible, so, theoretically, after a balance of pressures with venous blood is achieved, the total pressure of gases in them can be 54 mmHg less than the outside air pressure. This never happens because the subatmospheric pressure alters Starling forces in the mucosa that cover cavity surfaces. Blood is forced to enter the mucosa by the subatmospheric pressure that sucks it inside. Mucosal interstitial hydrostatic pressure is also more negative than normal, and painful mucosal edema develops. The added volume of interstitial water in mucosal tissue together with secretion of free fluid from the edematous mucosa into the cavity reduces the negativity of the intracavitary pressure. Further absorption of trapped gas will stop when the balance of partial pressures with mucosal blood is once reached.

    Does this make sense to you? YES or NO.

    If YES, can you accept the following conclusion:

    In cases of air trapping in collapsible body cavities, all gases will be fully reabsorbed without pain. Air trapping in bone cavities leads only to partial reabsorption of gases and results in subatmospheric intracavitary pressure. Partial vacuum causes painful mucosal edema and free fluid secretion.

    REFERENCES

    Ganong WF. Review of Medical Physiology (21th ed.). Stamford, CT: Appleton & Lange, 2005.

    Guyton AC and Hall JE. Medical Physiology. Philadelphia, PA: Saunders, 2000, p. 660.

    Richardson DR, Randall DC, and Dexter DF. Cardiopulmonary System. Madison, CT: Fence Creek, 1998.

    Osijek Medical Faculty, University of Osijek, Osijek, Croatia(Zdravko Ivezi, Sven Kurbe)