The breath of life

Abstract

I 'N THE PRE-Listerian era, fever and general . debility after surgery were accepted as no special complication. In 1843, Chevers reported that of 134 deaths after injury and surgery in London hospitals, 86 were to chest diseases. He wrote that this was due to vitiated atmosphere, irritable nervous system and congestion of the posterior part of the lungs. In 1844, Mendelsohn demonstrated that bronchial blockade with lead shot, gum acacia, and other foreign matter resuited in atelectasis. In 1908, Pasteur gave the classical lecture on massive collapse of the describing lower lobe atelectasis, and suggested it was to lack of motion of the diaphragm. In 1930, Coryllos demonstrated that after bronchial obstruction, alveolar gases were absorbed subject to normal diffusion and solubility laws. For example, CO2 disappeared in 4 minutes, 02 in 15 minutes, and N2 in 16 hours. This presumed a normal alveolar blood supply. The respiratory membrane is the most extensive of all tissues in the body, interfacing directly between humans and their environment. Each day a surface as large as a tennis court is exposed to a volume of air, including contaminants, that would fill a swimming pool. The infectious agents, chemical toxins, mineral dusts, and immunogenic particles contained in that pool , which penetrate to the depths of the lung, encounter a variety of pulmonary defense mechanisms preventing their contact with vulnerable tissues. The extent to which these lung defenses are breached by inhaled foreign materials will determine the appearance of acute or chronic respiratory disease. Smog bronchitis, smoker's emphysema, silicosis, tuberculosis, and allergic asthma represent failures of pulmonary defense mechanisms to deal effectively with inhaled foreign materials. If surgery and anesthesia are used in a patient with these conditions, a respiratory emergency may ensue. The lung contains 300 million alveoli; these are not simply air sacs, but are surrounded by an extensive capillary network. This relationship between the venous capillaries, alveolar membrane, and arterial capillaries determines the degree to which oxygen reaches blood and carbon dioxide is excreted. An air-liquid interface, the largest in the body, lies between the alveoli and capillaries. The lung as an organ is intimately involved with both left and right chambers of the heart. It is remarkable that the amount of blood entering each chamber of the heart is roughly equivalent to the amount of blood in the lungs, and also that the lungs are not a cesspool of constant suppuration, carbon dioxide build-up, or acute lowering of the oxygen tension. Normally, the work of breathing is performed economically, leaving a large reserve of energy to be used for other body requirements (muscular movement, heart beating, etc). If, however, breathing is inefficient, the work of breathing becomes costly. The conscious patient now chooses between enduring the uncomfortable sensation of dyspnea or curtailing normal physical activities; at the end of this spectrum, because of hypoxemia, the patient may lose consciousness. In a normal patient at rest, the oxygen cost of breathing is approximately 0.5/mL O2/L ventilation or 2% of the resting oxygen consumption. During a hypothetical hyperventilation of 60 to 90 L/min, the oxygen requirement jumps to 10 to 15 mL O2/L ventilation. With disease and impaired breathing efficiency, the resting cost of breathing is considerably increased, explaining why most victims of a respiratory emergency require such a large amount of oxygen at rest. A respiratory emergency may be defined as an event (or a series of events) that results in inadequate oxygenation and/or ventilation of the patient; if not promptly treated, it may result in