Beachey: Respiratory Care Anatomy and Physiology, 3rd Edition Chapter 11: Control of Ventilation Answers to Workbook Questions Key Terms and Definitions
Medulla oblongata—Portion of the brainstem from which rhythmic, cyclical breathing impulses originate.
Pons—Located above the medulla oblongata, portion of the brainstem that is responsible for regulating the output of the medulla. The two groups of neurons found in the pons are the apneustic and pneumotaxic centers, known collectively as the “pontine centers.”
Apneustic center—Pontine center thought to be responsible for apneustic breathing.
Pneumotaxic center—Pontine center responsible for controlling the length of inspiration.
Hering-Breuer reflex—Reflex generated by stretch receptors located in smooth muscle of large and small airways that inhibits further inspiratory efforts when large tidal volumes are reached.
Head’s reflex—Paradoxical reflex to Hering-Breuer reflex that causes increased inspiratory effort in response to hyperinflation, thought to be helpful in maintaining large tidal volumes during exercise.
Chemoreceptors—Specialized nerve structures that, when stimulated, transmit impulses to respiratory centers in the medulla.
Central chemoreceptors—Specialized nerve cells located in the medulla that are stimulated by hydrogen ions in cerebral spinal fluid.
Peripheral chemoreceptors—Highly vascular tissue also referred to as carotid bodies (located in the bifurcation of carotid arteries) and aortic bodies (located in the aortic arch). Peripheral chemoreceptors respond to increased arterial [H+] regardless of origin.
Apneustic breathing—Abnormal breathing pattern characterized by prolonged inspiratory gasps with occasional expirations.
Biot’s breathing—Abnormal breathing pattern characterized by abnormal respiratory rates with intermittent periods of apnea. May be associated with lesions of the pons.
Cheyne-Stokes breathing—Abnormal breathing pattern characterized by progressively deeper and faster breathing, followed by decreasing rates and volumes that result in periods of apnea. May be seen in association with brain lesions, or in congestive heart failure as a result of delayed blood transit time between lungs and brain.
The rhythmic spontaneous breathing pattern is caused by nerve impulses originating in the medulla oblongata. The nerve group containing mainly inspiratory neurons is known as the dorsal respiratory group while the nerve group containing both inspiratory and expiratory neurons is known as the ventral respiratory group.
The Botzinger complex and the pre-Botzinger complex are thought to be responsible for the basic, rhythmic pattern of breathing. Two theories are presented to explain rhythm generation: the pacemaker hypothesis and the network hypothesis. The pacemaker hypothesis suggests that certain medullary cells have intrinsic pacemaker capabilities, and that these cells drive other medullary neurons. The network hypothesis suggests that there is a pattern of interconnections between neurons located throughout the rostral ventral respiratory group, the pre-Botzinger complex, and the Botzinger complex, and that these inspiratory and expiratory neurons inhibit one another.
After expiration ceases, the inspiratory impulses coming from dorsal and ventral neurons gradually increase their firing rate, creating a smooth, increasing “ramp” signal that causes progressively stronger inspiratory muscle contractions, rather than abrupt inspiratory “gasps.”
The pneumotaxic center of the pons and pulmonary stretch receptors are responsible for controlling the “off switch” of the dorsal respiratory group’s inspiratory ramp signal, thus inhibiting inspiration. As inspiratory impulses get stronger, inhibitory neurons also begin to fire with increasing frequency until they stop, or “switch off,” the inspiratory signal and expiration occurs. A weak signal from the pneumotaxic center will result in longer inspiratory times and larger tidal volumes.
The apneustic center, if not restrained by the pneumotaxic center, will produce apneusis, a breathing pattern characterized by prolonged inspiratory gasps. This type of breathing pattern is generated by severing the connection between the pneumotaxic and apneustic centers, and also by severing the vagus nerves.
Stretch receptors in the smooth muscle of large and small airways are responsible for the Hering-Breuer reflex, which, like the pneumotaxic center, generates impulses that act to inhibit inspiration. The difference between them, however, is that the Hering Breuer reflex is activated only at large tidal volumes. The pneumotaxic center, then, is responsible for inhibition of inspiration during quiet breathing, while the Hering-Breuer reflex is more important in regulating rate and depth of breathing during exercise.
A. Vagovagal reflexes result in laryngospasm, bronchospasm, coughing, and bradycardia. These receptors are found in the epithelium of large airways.
B. J-receptor reflexes are found in the lung parenchyma near pulmonary capillaries and are stimulated by inflammation (pneumonia), pulmonary vascular congestion (congestive heart failure), and edema fluid. J-receptors cause rapid, shallow breathing and a sensation of dyspnea. They are also responsible for the glottic narrowing that causes expiratory grunting associated with dyspnea.
The central chemoreceptors are located the medulla and respond directly to hydrogen ions. Because the blood-brain barrier is impermeable to hydrogen ions but permeable to CO2, elevated arterial CO2 levels will cause CO2 to diffuse rapidly through the blood-brain barrier into the cerebral spinal fluid (CSF). In the CSF, CO2 reacts with water to form [H+] and HCO3–. The CSF contains no buffers, so the generation of [H+] stimulates the chemoreceptors to increase ventilation within seconds.
The peripheral chemoreceptors are responsive to hypoxemia, but unlike elevated CO2 levels (see Question 8) hypoxemia indirectly increases the drive to breathe. Peripheral chemoreceptors consist of two areas of vascular tissues known as the carotid and aortic bodies, which are found, respectively, in the bifurcations of the carotid arteries, and in the arch of the aorta. Hypoxemia causes peripheral chemoreceptors in the carotid bodies to become more sensitive to [H+]. When Pao2 is low, carotid body sensitivity to [H+] increases, stimulating the peripheral chemoreceptors to fire more rapidly, resulting in increased ventilation. Peripheral chemoreceptors are also sensitive to arterial CO2 levels.
The explanation as to why oxygen administration causes hypercapnic, hypoxemic patients to hypoventilate is unclear. The traditionally accepted explanation is that administration of higher oxygen concentrations negates hypoxemia’s stimulatory effect on the peripheral chemoreceptors. Other investigators believe that oxygen administration worsens ventilation/perfusion relationships in the lung (due to pulmonary vasodilation and absorption atelectasis), resulting in elevated blood Pco2. Finally, some investigators believe that oxygen-induced hypercapnia is due to a combination of the effects described above.
Mechanical hyperventilation of the head injury patient will lower Paco2, causing cerebral vasoconstriction, which will decrease cerebral blood flow and intracranial pressure. The problem with the approach is that the reduction in cerebral blood flow may cause cerebral ischemia and exacerbate the injury to the brain. The effect of hyperventilation on cerebral blood flow will diminish after 24 to 48 hours due to the kidney’s compensatory response to hyperventilation (renal elimination of bicarbonate). A 2005 review of mechanical hyperventilation of the head injury patient concluded that long-term clinical outcomes were not improved with the use of hyperventilation therapy. The authors also concluded that hyperventilation therapy should be considered only in patients with high ICPs, advising against Paco2 levels less than 30 mm Hg because of the risk of cerebral ischemia.
The patient may or may not be using excessive pain medication, but the arterial blood gas report reflects normal baseline values for a patient with chronic hypercapnia. Although there is a slight upward trend in Po2, Pco2, and [H+], the values represent a ventilatory status almost identical to the pre-operative state. Po2 and Sao2 values indicate that the hypoxic drive is probably active. A normally functioning central nervous system is confirmed by the patient’s alert mental status, normal breathing frequency, and normal arterial pH.
Decreases in mental awareness and breathing frequency indicate that the patient’s Pco2 (and CSF [H+]) has probably risen substantially above his baseline. Oxygen is flowing at more than twice the rate normally required by the patient and is suppressing ventilation. The chronically hypercapnic patient is no longer being driven to breathe by hypoxia, since the Spo2 is now 95% (Pao2 > 60 mm Hg, within the oximeter’s margin of error) Reducing the oxygen flow rate to the patient’s normal requirements will allow Po2 to decrease below 60 mm Hg, stimulating the carotid bodies to drive ventilation. Pco2 will decrease to the patient’s “normal” level” when alveolar ventilation increases. As CSF Pco2 decreases because of diffusion along the CSF-arterial gradient, CSF [H+] will decrease and negate the cause of the central nervous system depression.
Key Concept Questions
C. The pontine center of the brain serves to fine-tune neural respiratory impulses originating from the medulla. A spinal cord injury between the pons and medulla results in an irregular breathing pattern.
D. Central and peripheral chemoreceptors are stimulated in response to increased [H+], which occurs in hypercapnia and acidosis. Hypoxemia stimulates the carotid bodies in the peripheral chemoreceptors by making them more sensitive to [H+]. Alkalemia results in decreased [H+], and therefore would not stimulate ventilation.
C. Hypoventilation results in elevated blood CO2 levels, which increase [H+], dilate cerebral blood vessels, and may increase intracranial pressure, causing cerebral ischemia.
A. Peripheral proprioceptors located in muscles, tendons, and joints send impulses to the medullary centers to increase inspiratory activity in response to painful stimuli and movement of the limbs.