Regulation of Breathing

Regulation of Breathing

Will Beachey

Breathing, similar to the heartbeat, is an automatic activity requiring no conscious awareness. In contrast to the heartbeat, breathing patterns can be consciously changed, although powerful neural control mechanisms overwhelm conscious control soon after one willfully stops breathing. The normal unconscious cycle of breathing is regulated by complex mechanisms that continue to elude complete understanding. The rhythmic cycle of breathing originates in the brainstem, mainly from neurons located in the medulla. Higher brain centers and many systemic receptors and reflexes modify the output of the medulla. These different structures function in an integrated manner, precisely controlling ventilatory rate and depth to accommodate the gas exchange needs of the body. This chapter helps the clinician understand basic physiologic mechanisms that regulate breathing; with this knowledge, the clinician can anticipate the effects that various therapeutic interventions and disease processes have on ventilation.

Medullary Respiratory Center

Animal experiments show that transecting the brainstem just below the medulla (Figure 14-1, level IV) stops all ventilatory activity. However, breathing continues rhythmically after the brainstem is transected just above the pons (see Figure 14-1, level I). Until more recently, physiologists thought that separate inspiratory and expiratory neuron “centers” in the medulla were responsible for the cyclic pattern of breathing. Researchers believed that inspiratory and expiratory neurons fired by self-excitation and that they mutually inhibited one another. More recent evidence shows that inspiratory and expiratory neurons are anatomically intermingled and do not inhibit one another.1 No clearly separate inspiratory and expiratory centers exist. Instead, the medulla contains several widely dispersed respiratory-related neurons, as shown in Figure 14-1. The dorsal respiratory groups (DRGs) contain mainly inspiratory neurons, whereas the ventral respiratory groups (VRGs) contain both inspiratory and expiratory neurons.

Dorsal Respiratory Groups

As shown in Figure 14-1, DRG neurons are mainly inspiratory neurons located bilaterally in the medulla. These neurons send impulses to the motor nerves of the diaphragm and external intercostal muscles, providing the main inspiratory stimulus.1 Many DRG nerves extend into the VRGs, but few VRG fibers extend into the DRGs. Reciprocal inhibition is an unlikely explanation for rhythmic, spontaneous breathing.1

The vagus and glossopharyngeal nerves transmit many sensory impulses to the DRGs from the lungs, airways, peripheral chemoreceptors, and joint proprioceptors. These impulses modify the basic breathing pattern generated in the medulla.

Ventral Respiratory Groups

VRG neurons are located bilaterally in the medulla in two different nuclei and contain inspiratory and expiratory neurons (see Figure 14-1). Some inspiratory VRG neurons send motor impulses through the vagus nerve to the laryngeal and pharyngeal muscles, abducting the vocal cords and increasing the diameter of the glottis. Other VRG inspiratory neurons transmit impulses to the diaphragm and external intercostal muscles. Still other VRG neurons have mostly expiratory discharge patterns and send impulses to the internal intercostal and abdominal expiratory muscles.

The exact origin of the basic rhythmic pattern of ventilation is unknown. No single group of pacemaker cells has been identified. Two predominant theories of rhythm generation are the pacemaker hypothesis and the network hypothesis.2 The pacemaker hypothesis holds that certain medullary cells have intrinsic pacemaker properties (i.e., rhythmic self-exciting characteristics) and that these cells drive other medullary neurons. The network hypothesis suggests that rhythmic breathing is the result of a particular pattern of interconnections between neurons dispersed throughout the rostral VRG, the pre-Bötzinger complex, and the Bötzinger complex. This hypothesis assumes that certain populations of inspiratory and expiratory neurons inhibit one another and that one of the neuron types fires in a self-limiting way, such that it becomes less responsive the longer it fires. There is no definitive proof of either hypothesis; the precise origin of respiratory rhythm generation remains elusive.2

Inspiratory Ramp Signal

The inspiratory muscles do not receive an instantaneous burst of signals from the dorsal and ventral inspiratory neurons. Rather, the firing rate of DRG and VRG inspiratory neurons increases gradually at the end of the expiratory phase, creating a ramp signal (Figure 14-2). The inspiratory muscles contract steadily and smoothly, gradually expanding the lungs rather than filling them in an abrupt inspiratory gasp. During exercise, various reflexes and receptors influence the medullary neurons, steepening the ramp signal and filling the lungs more rapidly.

During quiet breathing, inspiratory neurons fire with increasing frequency for approximately 2 seconds and then abruptly switch off, allowing expiration to proceed for approximately 3 seconds.3 At the start of expiration, inspiratory neurons again fire briefly, retarding the early phase of expiration (see Figure 14-2). The inhibitory neurons that switch off the inspiratory ramp signal are controlled by the pneumotaxic center and pulmonary stretch receptors, which are discussed later in this chapter.

Pontine Respiratory Centers

If the brainstem is transected above the medulla (see Figure 14-1, level III), spontaneous respiration continues, although in a more irregular pattern. The pons does not promote rhythmic breathing; rather, it modifies the output of the medullary centers. Figure 14-1 shows two groups of neurons in the pons: (1) the apneustic center and (2) the pneumotaxic center.

Pneumotaxic Center

The pneumotaxic center is a bilateral group of neurons located in the upper pons (see Figure 14-1). The pneumotaxic center controls the “switch-off” point of the inspiratory ramp, controlling inspiratory time. Strong pneumotaxic signals increase the respiratory rate, and weak signals prolong inspiration and increase tidal volumes. The exact nature of the interaction between the pneumotaxic and apneustic centers is poorly understood. They apparently work together to control the depth of inspiration.3

Reflex Control Of Breathing

Hering-Breuer Inflation Reflex

The Hering-Breuer inflation reflex, described by Hering and Breuer in 1868, is generated by stretch receptors located in the smooth muscle of both large and small airways. When lung inflation stretches these receptors, they send inhibitory impulses through the vagus nerve to the DRG neurons, stopping further inspiration. In this way, the Hering-Breuer reflex has an effect similar to that of the pneumotaxic center. In adults, the Hering-Breuer reflex is activated only at large tidal volumes (≥800 to 1000 ml) and apparently is not an important control mechanism in quiet breathing.2 This reflex is important, however, in regulating respiratory rate and depth during moderate to strenuous exercise.

Muscle Spindles

Muscle spindles in the diaphragm and intercostal muscles are part of a reflex arc that helps the muscles adjust to an increased load. Muscle spindles are sensing elements located on intrafusal muscle fibers, arranged parallel to the main extrafusal muscle fibers (Figure 14-3). The extrafusal fibers that elevate the ribs are innervated by different motor fibers (alpha fibers) than the fibers that innervate the intrafusal spindle fibers (gamma fibers). When the main extrafusal muscle fiber and the intrafusal fibers contract simultaneously, the sensing element (spindle) of the intrafusal muscle fiber stretches and sends impulses over spindle afferent nerves directly to the spinal cord (see Figure 14-3

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Regulation of Breathing

Full access? Get Clinical Tree

Get Clinical Tree app for offline access