There is little argument that the urge to breathe is the most compelling drive that humans face, one they must satisfy every minute of life. Our dependence on aerobic metabolism to perform life’s complex functions requires coordinated interaction among multiple organ systems to deliver sufficient O₂ for those demands (Fig. 1.1). Although only the upper elements of this O₂ transport cascade are the formal purview of this book, physicians need to appreciate each aspect since failure at any step can become an O₂ transport bottleneck with catastrophic consequences for their patients.

From this perspective, respiration really consists of two sequential processes within the lung, ventilation and diffusion. Each will require several chapters to describe their constituent parts and boundary conditions. As an obvious example, ventilation is the algebraic product of respiratory frequency, f, multiplied by the amount of air moved per breath, termed the tidal volume (V_T). Less obvious is the fact that only a portion of each V_T enters the alveolar volume (V_A) where diffusion can occur, while the remaining portion of V_T is confined to anatomical regions unsuitable for diffusion, collectively called the dead space volume (V_D). Thus, one goal of this text is to provide the intellectual tools both to determine the fraction of V_A in each V_T, and to identify possible treatments for patients whose V_A/V_T is not optimal. As will be seen, the work of breathing and the calories required are substantial to inhale the 8,000-12,000 L of air per day just to support basal oxygen consumption. Clinicians must be able to distinguish if a patient’s work of breathing is excessive, and if so, whether due to altered recoil properties of the lungs and chest wall, or to reduced airway diameters which increase dynamic resistance. Such functional distinctions, and the structural changes that underlie them, form the central framework for sorting lung disorders into the so-called restrictive lung diseases and obstructive airway diseases. Later subsections of this book are devoted to providing a detailed introduction to both disease categories.

Even when the physical forces that regulate ventilation are ideal, the inhaled O₂ must still diffuse through the delicate membrane sandwich that separates alveolar airspace from blood within the underlying pulmonary capillaries (Fig. 1.2). The resistance that the septal barrier poses to diffusion is related to its thickness and total surface area, which are modified in diseases like interstitial fibrosis and emphysema, respectively. Alveolar diffusion may be enhanced by interventions like increasing the fraction of inspired O₂ in the ambient air, thereby increasing the pressure gradient for oxygen between the airspace and blood that is the driving force for diffusion. Much importance will be placed in the following chapters on training the clinician to determine when such supplemental O₂ will probably improve tissue oxygenation versus when that tactic alone will fail.

Numerous terms and phrases pertaining to respiratory biology and pulmonary medicine will be introduced in this book. Among the most fundamental are abbreviations and acronyms that succinctly describe the origin and contents of a gas or fluid sample. With such shorthand, the phrase carbon dioxide partial pressure of alveolar gas usefully compresses to just P_Aco₂, with its most common units of mm Hg implied. Likewise, the phrase fractional concentration of oxygen in the inspired gas mixture reduces to F_Io₂. The proper labeling of respiratory gases begins with the notation of F (fractional concentration, as a decimal from 0.0-1.0), or P (for pressure in mm Hg, torr, kilopascals, etc). The second letter (often subscripted) states the source or location of the gas, if known, including: A = alveolar; AW = airway; a = arterial; B = ambient barometric; c = capillary; ć = end-capillary; E = expired or expiratory; Ē = mean expiratory; É = end-expiratory (sometimes called end-tidal); I = inspired; IP = intrapleural; IT = intratracheal; v = venous; and v̄ = mixed or mean venous. Note that conventional usage may specify upper versus lower case lettering to distinguish locations. The final designation is to the gas species: O₂, N₂, CO₂, H₂O, etc. Thus, the phrases F_Ēco₂ = 0.08 and P_ćo₂ = 105 mm Hg indicate respectively that the average fractional CO₂ concentration in a sample of expired air is 8%, and that the partial pressure of O₂ in blood exiting an alveolar capillary to enter a pulmonary venule is 105 mm Hg.