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Cough provides an essential protective function for human airways and lungs. Without an effective cough reflex, we are at risk for retained airway secretions and aspirated material, predisposing to infection, atelectasis, and respiratory compromise. At the other extreme, excessive coughing can be exhausting; can be complicated by emesis, syncope, muscular pain, or rib fractures; and can aggravate abdominal or inguinal hernias and urinary incontinence. Cough is often a clue to the presence of respiratory disease. In many instances, cough is an expected and accepted manifestation of disease, such as during an acute respiratory tract infection. However, persistent cough in the absence of other respiratory symptoms commonly causes patients to seek medical attention, accounting for as many as 10–30% of referrals to pulmonary specialists.

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Cough Mechanism

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Spontaneous cough is triggered by stimulation of sensory nerve endings that are thought to be primarily rapidly adapting receptors and C-fibers. Both chemical (e.g., capsaicin) and mechanical (e.g., particulates in air pollution) stimuli may initiate the cough reflex. A cationic ion channel, called the type-1 vanilloid receptor, is found on rapidly adapting receptors and C-fibers; it is the receptor for capsaicin, and its expression is increased in patients with chronic cough. Afferent nerve endings richly innervate the pharynx, larynx, and airways to the level of terminal bronchioles and into the lung parenchyma. They may also be found in the external auditory meatus (the auricular branch of the vagus nerve, called the Arnold nerve) and in the esophagus. Sensory signals travel via the vagus and superior laryngeal nerves to a region of the brainstem in the nucleus tractus solitarius, vaguely identified as the “cough center.” Mechanical stimulation of bronchial mucosa in a transplanted lung (in which the vagus nerve has been severed) does not produce cough.

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The cough reflex involves a highly orchestrated series of involuntary muscular actions, with the potential for input from cortical pathways as well. The vocal cords adduct, leading to transient upper-airway occlusion. Expiratory muscles contract, generating positive intrathoracic pressures as high as 300 mm Hg. With sudden release of the laryngeal contraction, rapid expiratory flows are generated, exceeding the normal “envelope” of maximal expiratory flow seen on the flow-volume curve (Fig. 34-1). Bronchial smooth muscle contraction together with dynamic compression of airways narrows airway lumens and maximizes the velocity of exhalation (as fast as 50 miles per hour). The kinetic energy available to dislodge mucus from the inside of airway walls is directly proportional to the square of the velocity of expiratory airflow. A deep breath preceding a cough optimizes the function of the expiratory muscles; a series of repetitive coughs at successively lower lung volumes sweeps the point of maximal expiratory velocity progressively further into the lung periphery.

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Figure 34-1
Graphic Jump Location

Flow-Volume Loop. Flow-volume curve with spikes of high expiratory flow achieved with cough.

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Impaired Cough

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