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INTRODUCTION

The respiratory control system is made up of three main components: (1) the central neural respiratory generator, (2) the sensory input system, and (3) the neuromuscular effector system.1 These three systems work in unison for the purpose of carbon dioxide (CO2) elimination and oxygen (O2) uptake. By incorporating sensory and chemosensory input, a ventilatory response to physiologic or neuromuscular stress arises, the goal of which is to produce steady alveolar ventilation, while expending minimal energy to meet a person’s metabolic needs.

The alveolar–capillary CO2 gradient is small. Effective elimination of CO2 requires an active pump mechanism that preserves this diffusion gradient. This is physiologically achieved by the respiratory system but often requires extrinsic mechanical support in disease states. A large diffusion gradient for O2 makes O2 transport simpler and explains why supplemental oxygen administration without pump support is often sufficient.

Disease states that affect neuronal stimulation of the muscles of respiration (e.g., congenital central hypoventilation), muscular function (e.g., neuromuscular disease), respiratory mechanics (e.g., kyphoscoliosis, morbid obesity), or dead space ventilation and respiratory pump efficiency (e.g., chronic obstructive pulmonary disease [COPD]) potentially decrease alveolar ventilation and, correspondingly, impair CO2 elimination. As a compensatory mechanism in disease states, the body may turn to maladaptive respiratory mechanics or breathing patterns which are inefficient and nonsustainable, ultimately resulting in chronic hypercapnic respiratory failure.

Chronic hypercapnic respiratory failure is defined as a steady state partial arterial CO2 pressure (PaCO2) larger than >45 mm Hg during wakefulness. This value is arbitrary, but it is useful in clinical practice, as it allows for standardization of clinical outcomes. In most patients, rather marked abnormalities in the respiratory control system are required before chronic hypercapnic respiratory failure ensues.

Oftentimes hypercapnia first transiently appears during rapid eye movement (REM) sleep, heralding the forthcoming development of chronic hypercapnic respiratory failure and daytime hypercarbia. Mechanical ventilatory support during sleep, both invasive and noninvasive, may delay and, often, reverse this process by enhancing ventilation, achieving eucapnia, and by unloading respiratory muscles during sleep, leading to increased diurnal ventilatory reserve.

This chapter deals with the pathogenic mechanisms at work in the development of CO2 retention in diseases characterized by increased pulmonary dead space, neuromuscular derangements, or restrictive processes of the lung and chest wall. The compensatory or adaptive mechanisms that help preserve ventilation (e.g., respiratory chemosensitivity, motor responses to alterations in the mechanics of breathing, intrinsic changes in respiratory muscle strength and endurance) and the decompensating, maladaptive responses that predispose to CO2 retention (e.g., respiratory muscle wasting and fatigue, a rapid, shallow pattern of breathing) will be discussed, as will the concepts involved and technologies utilized in managing chronic hypercapnia.

PATHOPHYSIOLOGY AND MECHANICS OF VENTILATION

In considering hypercapnic respiratory failure, an understanding of respiratory control mechanisms ...

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