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In healthy individuals, respiratory and circulatory functions are linked to tissue metabolic activity by a responsive regulatory system that translates biochemical and neural signals from the tissues into adjustments in cardiac output, vascular tone, and minute ventilation. The purpose of this system is to assure that all the cells in the organism receive a supply of O2 commensurate with their metabolic needs without accumulating excessive amounts of CO2. The system relies both on local circulatory reflexes, which alter the caliber of the supplying blood vessels in accordance with tissue metabolic activity, and on central circulatory and respiratory reflexes, which adjust the pumping function of the heart and the intensity of the respiratory effort in response to changes in the concentration of the respiratory gases in the blood.1

Chemoreceptor reflexes play a singularly important role in the genesis of the manifestations of respiratory disease (Fig. 102-1). Alterations in the blood’s PO2, PCO2, and pH are sensed by specialized chemo-sensitive cells located in the carotid bodies (peripheral chemoreceptors, PO2) and reticular nuclei of the medulla oblongata (central chemoreceptors, PCO2 and pH). These cells relay the information to a medullary neuronal network of premotoneurons, which also receives inputs from mechanical and chemical sensors distributed throughout the lungs, airways, and chest wall. Chemical and mechanical inputs are integrated to define the amount of ventilation needed to sustain adequate gas exchange and the manner in which the respiratory muscles are applied to achieve this ventilation most efficiently. The physiologic basis of respiration is reviewed in more detail in Chapter 503.

Figure 102-1.

Genesis of the signs of respiratory distress. Changes in blood-gas tensions are sensed by chemoreceptor cells in the carotid bodies (O2) and in the reticular formation of the medulla oblongata (CO2). The nerve signals originating in the chemoreceptors are integrated and processed by a complex medullary neuronal network that also receives inputs from mechanoreceptors in the lungs and chest wall and from other areas of the brain. Increases in arterial Pco2 and, if sufficiently large, decreases in arterial Po2 sensed by the chemoreceptors activate neural programs that result in the progressive recruitment of a variety of respiratory muscles, as shown in the bottom of the figure. Nasal flaring (from contraction of the dilators of the alae nasae), increased vocal cord abduction, and dilation of the pharyngeal passages during inspiration may not be apparent to the observer. However, alterations in the breathing frequency (usually tachypnea) or intercostal and subcostal retractions (from the subatmospheric pleural pressures generated by the forceful contractions of the diaphragm) are prominent in almost every child with acute respiratory disease.

A variety of developmental factors render the infant, and especially the newborn at increased risk for difficulties with respiration. These include immaturity of the neural control of ...

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