Respiration begins in the nervous system by means of centers located in the brain stem (which automatically command every inhalation–exhalation cycle) but is influenced by voluntary cortical control.
Most of the time, respiration is under the control of the automatic respiratory center, which can alter respiration to meet the metabolic demand, activating the respiratory system in a highly sensitive manner by a system of negative feedback in response to the partial pressures of oxygen and carbon dioxide (PaO2 and PaCO2) and the pH. The ventilatory response to hypoxemia emerges when PaO2 values reach 50–60 mmHg, when the afferent influence of peripheral chemoreceptors (especially carotid bodies) on the regulatory center increases. The ventilatory response increases significantly when there is a slight concomitant increase in PaCO2 values (42–48 mmHg) and follows a logarithmic curve as PaO2 decreases. The ventilatory response to hypercapnia is determined by a rapid response at the central level, where the PaCO2 of the cerebrospinal liquid, which is in balance with the blood because of its capacity to easily diffuse through the blood–brain barrier, stimulates the central chemoreceptors linearly (Fig. 19.1). Parallel to this, ventilation increases along with a rise in the concentration of hydrogen ions of between 20 and 60 nEq/L, whether they are of respiratory or metabolic origin. If the respiratory system is in a condition to respond to the stimuli of hypoxemia and hypercarbia, the increase in alveolar ventilation improves PaCO2 levels, which significantly decreases the afferent influence of carotid chemoreceptors in the respiration process (Fig. 19.2).
Fig. 19.1
Respiratory response to partial pressure of O2 (PaO2)
Fig. 19.2
Respiratory response to partial pressure of CO2 (PaCO2)
The respiratory cycle is influenced by afferent receptors of diverse voluntary and involuntary respiratory control mechanisms, such as the reflexes of the lungs and respiratory tract, the cardiovascular system, and the reflexes of stretched muscles and articulations. Moreover, the respiratory cycle is influenced by higher centers such as the hypothalamus and areas of the cerebral cortex that take control over the automatic system when we speak, cry, or laugh.
Etiology
Assessment of persistent tachypnea requires adequate knowledge of the possible causes. Identification of the probable etiology is necessary to appropriately deal with and manage the condition. Once the influences of fever, crying, and pain on the respiratory rate have been assessed, it is important to determine the respiratory and nonrespiratory causes of tachypnea in infants (Table 19.2).
Table 19.2
Organic causes of tachypnea
Only gold members can continue reading. Log In or Register to continue
