Anatomic and Physiologic Aspects of Neural, Muscular, and Chest Wall Interactions with the Lungs

17


Anatomic and Physiologic Aspects of Neural, Muscular, and Chest Wall Interactions with the Lungs



Movement of gas into and out of the lungs requires the action of a pump capable of creating negative intrathoracic pressure, expanding the lungs, and initiating airflow with each inspiration. This pumplike action is provided by the respiratory muscles, including the diaphragm, working in conjunction with the chest wall. However, the muscles themselves have no intrinsic rhythmic activity in the way cardiac muscle does; they must be driven by rhythmic impulses provided by a “controller.”


This chapter focuses on the anatomic and physiologic features of the controlling system and the respiratory muscles to provide background for the discussion in Chapters 18 and 19. Those chapters discuss disorders affecting respiratory control, respiratory musculature, and the chest wall. Although much of the physiology and many of the clinical problems discussed here and in the next two chapters do not directly involve the lungs, they are so closely intertwined with respiratory function and dysfunction that they are appropriately considered in a textbook of pulmonary disease.



Respiratory Control


Although the process of breathing is a normal rhythmic activity that occurs without conscious effort, it involves an intricate controlling mechanism at the level of the central nervous system (CNS). The CNS transmits signals to the respiratory muscles, initiating inspiration approximately 12 to 20 times per minute. Remarkably, this controlling system is normally able to respond to varied needs of the individual, appropriately increasing ventilation during exercise and maintaining arterial blood gases within a narrow range.


This section begins with a description of the structural organization of neural control of ventilation and proceeds to a consideration of how various stimuli may interact with and adjust the output of the respiratory controller. The ways the output of the controller can be quantified and how these techniques have proved useful in evaluating patients with a variety of clinical disorders are briefly discussed.



Organization of Respiratory Control


The basic organization of the respiratory control system is shown in Figure 17-1. Crucial to this system is the CNS “generator.” Signals that originate from the generator travel down the spinal cord to the various respiratory muscles. The inspiratory muscles, the most important of which is the diaphragm, respond to the signals by contracting and initiating inspiration. This process is described later in more detail under Respiratory Muscles.



As a result of inspiratory muscular contraction, the diaphragm descends, the chest wall expands, and air flows down a pressure gradient from the mouth through the tracheobronchial tree to the alveolar spaces. Gas exchange in the distal parenchyma allows movement of O2 into the blood and release of CO2 from the blood into gas within the alveoli.


Although this sequence of events sounds relatively straightforward, it is complicated by an intricate feedback system that adjusts the output of the generator to achieve the desired effect. If the response of the respiratory muscles to the generator’s signal is inadequate, as judged by a variety of respiratory “reflexes,” the generator increases its output to compensate for the lack of expected effect. If the arterial blood gases deviate from the desired level, chemosensors for O2 and CO2 alter their input to the respiratory generator, ultimately affecting its output. In addition, input from other regions of the CNS, particularly the cerebral cortex and pons, can adjust the generator’s net output.



The Respiratory Generator


Considering the importance of the respiratory generator in this scheme of respiratory control, its anatomy and mode of action are described here. Much of the work clarifying the location of the respiratory generator involved animal experiments with transections at various levels of the CNS and assessment of the effects on ventilation. Because transection between the brain and brainstem does not significantly alter ventilation, the generator apparently resides somewhere at the level of the brainstem or lower and does not require interaction with higher cortical centers. When transections are made at various points within the brainstem, the breathing pattern is substantially altered, but ventilation is not eliminated. Only when a transection is made between the medulla and the spinal cord does ventilation cease, indicating that the respiratory generator resides within the medulla.



A central respiratory generator within the medulla controls activity of the respiratory muscles.


Although the respiratory center (or generator) has been referred to as a single region, it appears that more than one network of neurons within the medulla is involved in initiating and coordinating respiratory activity. According to a popular model, one group of neurons is responsible for initiating inspiration and regulating its speed as a result of the intensity of neuronal activity; another group of neurons controls “switching off” inspiration and hence determines the onset of expiration.


Therefore, there are two aspects of ventilatory control: (1) the degree of inspiratory drive or central inspiratory activity (which regulates the inspiratory flow rate), and (2) the timing mechanism (which controls the termination of inspiration). These two determining factors act in concert to set the respiratory rate and tidal volume and thus the minute ventilation and specific pattern of breathing.



Input from Other Regions of the Central Nervous System


Even though the medullary respiratory center does not require additional input to drive ventilation, it does receive other information that contributes to a regular pattern of breathing and more precise ventilatory control. For example, input from the pons appears to be necessary for a normal, coordinated breathing pattern. When the influence of the pons is lost, irregularities in the breathing pattern ensue.


In addition to pathways involved in the “automatic” or involuntary control of ventilation, the cerebral cortex exerts a conscious or voluntary control over ventilation. Cortical overriding of automatic control can be seen with either voluntary breath holding or hyperventilation. Its usefulness is readily apparent in a person’s need for voluntary control of breathing during such activities as speaking, eating, and swimming. Interestingly, the automatic control of ventilation may be disturbed while conscious control remains intact. In these cases, during wakefulness the cerebral cortex exerts sufficient voluntary control over ventilation to maintain normal arterial blood gas values. During periods when the patient is dependent on automatic ventilatory control (e.g., during sleep), marked hypoventilation or apnea may occur. This rare condition, called congenital central hypoventilation syndrome, has also been known as Ondine’s curse, after a mythologic tale in which the suitor of Neptune’s daughter was cursed to lose automatic control over all bodily functions when he fell asleep. Defects in the PHOX2b gene mapped to chromosome 4p12 have been identified in most cases. PHOX2b encodes a highly conserved domain for transcription factors important in neural development. Further research into the pathogenesis of this condition undoubtedly will lead to better understanding of the mechanisms of normal ventilatory control.



Chemoreceptors


Maintenance of arterial blood gases is the ultimate goal of ventilatory control, and an important feedback loop adjusts respiratory center output if blood gases are not maintained at the appropriate level (see Fig. 17-1). Elevation of PCO2 (hypercapnia) and depression of PO2 (hypoxemia) both are capable of stimulating ventilation. In each case, one or more chemoreceptors detect alterations in PCO2 or PO2 and accordingly vary their input to the medullary respiratory center.



Changes in PCO2 are sensed primarily at a central chemoreceptor in the medulla.


The primary sensor for CO2 is located near the ventrolateral surface of the medulla and is called the central chemoreceptor. Even though it is located in the medulla, the central chemoreceptor is clearly separate from the medullary respiratory center and should not be confused with it. The central chemoreceptor does not appear to respond directly to blood PCO2 but rather to the pH of the extracellular fluid (ECF) surrounding the chemoreceptor. The pH level, in turn, is determined by the level of hydrogen (H+) and bicarbonate (HCO3−) ions as well as PCO2 (see Appendix C for further discussion). The blood-brain barrier, the permeability properties of which influence the composition of cerebrospinal fluid (CSF) and brain ECF, prevents free movement of either H+ or HCO3− from blood to brain ECF, whereas CO2 passes freely. The feedback loop for changes in PCO2 can be summarized as follows:



image

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

Related posts:

  1. Lung Defense Mechanisms
  2. Diffuse Parenchymal Lung Diseases Associated with Known Etiologic Agents
  3. Arterial Blood Gases: Guidelines for Interpretation and Sample Problems
  4. Sample Problems Using Respiratory Equations

Stay updated, free articles. Join our Telegram channel
Tags:
Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Anatomic and Physiologic Aspects of Neural, Muscular, and Chest Wall Interactions with the Lungs

Full access? Get Clinical Tree
Get Clinical Tree app for offline access