Chapter 22 – Control of Ventilation




Abstract




Sensors – the central and peripheral chemoreceptors, pulmonary stretch receptors, J-receptors, irritant receptors and joint proprioceptors.





Chapter 22 Control of Ventilation




Which anatomical sites are involved in the control of ventilation?


Ventilation is controlled by means of neuronal feedback loops. All feedback loops involve sensors, effectors and a control centre. For ventilation, these are:




  • Sensors – the central and peripheral chemoreceptors, pulmonary stretch receptors, J-receptors, irritant receptors and joint proprioceptors.



  • Control centre – the respiratory nuclei in the brainstem.



  • Effectors – the muscles of respiration.



How does the respiratory centre control ventilation?


The respiratory centre has four main anatomical areas, each with a different function:




  • The dorsal respiratory group (DRG) of neurons primarily controls the diaphragm and thus is responsible for normal tidal inspiration.



  • The ventral respiratory group (VRG) of neurons controls the intercostal muscles; its function is to initiate forced expiration and to increase the force of inspiration. Additionally, the VRG contains the pre-Bötzinger complex, a cluster of neurons thought to be the respiratory pacemaker.1



  • The apneustic centre modifies the activity of DRG neurons to prevent overexpansion of the lungs.



  • The pneumotaxic centre modifies DRG impulses to reduce the depth of inspiration, acting to fine-tune the respiratory pattern. The pneumotaxic centre can also increase the respiratory rate (RR).



What are the inputs to the respiratory centre?


The major inputs to the respiratory centre are the peripheral chemoreceptors, central chemoreceptors, mechanoreceptors and bronchial irritant receptors.




  • Peripheral chemoreceptors. These are located in the:




    1. Carotid bodies at the bifurcation of the carotid artery. Their afferent nervous impulses are carried by the glossopharyngeal nerve. The carotid bodies are the most important peripheral chemoreceptors for respiratory responses.



    2. Aortic bodies on the aortic arch. Their afferent nervous impulses are carried by the vagus nerve. They play a more important role in cardiovascular responses.

    The peripheral chemoreceptors have a very high blood flow in relation to their weight. They are stimulated by:


    1. Low PaO2. The aortic and carotid bodies are the only chemoreceptors in the body that respond to hypoxaemia. Note: the peripheral chemoreceptors are stimulated by low arterial O2 tension, not low O2 content – anaemia and carbon monoxide poisoning do not stimulate the chemoreceptors.



    2. High PaCO2. The peripheral chemoreceptors are only responsible for 20% of the body’s response to hypercapnoea, with the central chemoreceptors responsible for the remainder. However, the peripheral chemoreceptors respond the most rapidly, within the order of 1–3 s.



    3. Acidaemia (pH < 7.35). Only the carotid bodies are stimulated by acidaemia.



    4. Hypotension. Reduced perfusion of the carotid and aortic bodies increases their neuronal output. This is why an increased RR is seen during the development of septic shock, even when there may not be any impairment of gas exchange.




  • Central chemoreceptors. These are located on the ventral surface of the medulla close to, but separate from, the VRG neurons. In contrast to the peripheral chemoreceptors, central chemoreceptors are solely stimulated by a fall in cerebrospinal fluid (CSF) pH. However, because H+ and HCO3‾ ions cannot cross the blood–brain barrier (BBB), changes in plasma pH do not directly affect ventilation. Instead, the course of events is as follows:




    1. CO2 freely diffuses from the blood into the CSF, and then from the CSF into the extracellular fluid (ECF) surrounding the central chemoreceptors.



    2. The reaction between CO2 and water results in the formation of H2CO3. H2CO3 then dissociates into H+ and HCO3‾.



    3. H+ diffuses into the chemoreceptor tissue, directly stimulating the chemoreceptors to activate the respiratory centre. The pH of the chemoreceptor ECF therefore provides an indirect measure of arterial PaCO2.



    4. Therefore, as PaCO2 increases, the central chemoreceptors are stimulated and E increases.

    There are a few important points to make about the central chemoreceptors:


    1. The CSF protein concentration is much lower than that of plasma and thus minimal buffering of CO2 occurs. This makes the CSF more sensitive to small changes in PCO2 than plasma.



    2. Respiratory acidosis stimulates the central chemoreceptors more than metabolic acidosis: CO2 can diffuse across the BBB, whereas H+ ions cannot. However, in profound metabolic acidosis, as exemplified by diabetic ketoacidosis, ventilation is stimulated via the carotid bodies, resulting in Kussmaul breathing.



    3. The cerebral vasodilatation that accompanies hypercapnoea enhances the central chemoreceptor mechanism by increasing the blood flow to the medulla.



    4. If hypercapnoea becomes chronic, as occurs in a subset of chronic obstructive pulmonary disease (COPD) patients, the increase in E cannot be sustained and returns to near normal. The underlying mechanism is as follows:




      1. HCO3‾ ions are actively secreted into the CSF to buffer the change in pH.



      2. CSF pH returns to normal and the central chemoreceptors are no longer stimulated: the activity of the respiratory centre is reduced.



      3. The kidneys also reabsorb more HCO3‾, which normalises arterial pH, thus reducing the stimulation of the respiratory centre by the carotid bodies.

      These compensatory mechanisms result in a loss of sensitivity to CO2, causing these patients to rely on hypoxaemic drive alone. Care must be taken when administering O2 to COPD patients with chronic hypercapnoea as there is a theoretical risk that these patients will stop breathing.



    5. Unlike the peripheral chemoreceptors, the central chemoreceptors are not stimulated by hypoxaemia. In fact, in the absence of the peripheral chemoreceptors, hypoxaemia depresses the respiratory centre.

    The inputs of the peripheral and central chemoreceptors are synergistic. For example, if hypoxaemia is sensed by the peripheral chemoreceptors and hypercapnoea by the central chemoreceptors, the resulting ventilatory response is greater than the sum of the two effects.



  • Mechanoreceptors. The contribution that mechanoreceptors make to the stimulation of ventilation is controversial.2 Mechanoreceptors that possibly affect the respiratory centre are:




    1. Lung stretch receptors, located in bronchial smooth muscle. Overinflation of the lung stimulates these stretch receptors, whose impulses are conveyed to the apneustic centre by the vagus nerve, causing a reduction in the depth of inspiration. This is called the Hering–Breuer reflex. During normal physiological breathing, it is unlikely that sufficient stretch will occur to trigger the Hering–Breuer reflex. However, stretch responses may be important in neonates and ventilated patients.



    2. Muscle spindles. The ventilatory response to exercise is thought to be initiated by muscle spindle activity.




  • Other factors. The respiratory centre also receives other inputs from the peripheral and central nervous systems:




    1. Juxtacapillary receptors (J-receptors). These are non-myelinated C-fibres in the alveolar walls. Activation causes an increase in ventilation, a feeling of dyspnoea, bradycardia and hypotension. It is thought that J-receptors are stimulated by pulmonary oedema and pulmonary emboli.



    2. Irritant receptors. Located in the airway epithelium, these cause bronchoconstriction and stimulate ventilation in the presence of noxious gases.



    3. Pain receptors. Activation of pain receptors stimulates ventilation.



    4. Thalamus. An increase in core body temperature stimulates ventilation.



    5. Limbic system. Extreme emotional states stimulate the respiratory centre, resulting in hyperventilation.



    6. Cerebral cortex. All of the other inputs to the respiratory centre can be transiently overridden by voluntary thought. However, one cannot breath-hold indefinitely; after a short period of apnoea, chemoreceptor stimulation by hypoxaemia or hypercapnoea overrides voluntary control, known as the ‘break point’.


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Sep 27, 2020 | Posted by in ANESTHESIA | Comments Off on Chapter 22 – Control of Ventilation
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