From Guyton
Readings required or recommended: Guyton and Hall (9th edition). Chap. 41; Ganong (19th edition). Chap. 36
CONTROL OF VENTILATION – The discussion of terms is related to normal respiratory function unless otherwise indicated. The nervous system regulates respiration. It adjusts the rate of alveolar ventilation almost exactly to the demands of the body so that the PaO2 & PaCO2 are hardly altered even during moderate to strenuous exercise and most other types of respiratory stress. The intensity of the respiratory signals up to and from the respitory center match the needs of the body. The goal of respiration is to maintain proper concentrations of oxygen, CO2, and Hydrogen ions in the tissues, and respiratory activity is highly responsive to changes in these levels.
medullary respiratory center: Is composed of several groups of neurons located bilaterally in the medulla oblongata and pons, see figure below. Its divided into 3 major collections of neurons.
From Guyton
dorsal respiratory group: one of the three major collections of neurons which are located in the dorsal portion of the medulla, which mainly causes inspiration. This group plays the most fundamental role in the control of respiration. The dorsal respiratory group (DRG) of neurons extends most of the length of the medulla. All or most of its neurons are located with in the nucleus of the tractus solitarios. The basic rhythm of respiration is generated mainly in the DRG. Respiratory neurons in this area still emit repititive bursts of inspiratory action potentials, despite disruption of peripheral neurons entering this area.
ventral respiratory group (VRG): One of the three major collections of neurons which is located in the ventrolateral part of the medulla, which can cause either expiration or inspiration, depending on which neurons in the group are stimulated.
The neurons in the VRG remain almost inactive during normal quiet respiration. There is no evidence that VRG participates in the basic rhythmical oscillation that controls respiration.
When the respiratory drive for increased pulmonary ventilation becomes > than normal, respiratory signals spill over into VRG from the basic oscillatory mechanisms of the DRG area. Then the VRG does contribute to the respiratory drive.
VRG area is very important in providing powerful expiratory signals to abdominal muscles during expiration. The VRG area operates as an overdrive mechanism when high levels of pulmonary ventilation are required.
nucleus tractus solitarius: the area where all or most of the dorsal respiratory group neurons are located in the medulla. This area also is the sensory termination of both the vagal and glossopharyngeal cranial nerves which transmit sensory signals into the respiratory center from the peripheral chaemoreceptors, the baroreceptors, and several types of receptors in the lung. All signals from this area help in the control of respiration
nucleus ambiguus: area where the ventral respiratory group of neurons reside rostrally
nucleus retroambigualis: the area where the ventral respiratory group of neurons resides caudally
pneumotaxic center: one of the 3 major collections of neurons which is located dorsally in the superior portion of the pons, which helps control the rate and pattern of breathing. ( the pontine center seems to fine tune respiratory rate and rhythm). Neurons from this area transmit signals to the inspiratory area. These neurons control the switch off of the inspiratory ramp, thus controlling the duration of the filling phase of the lung cycle.
Pneumotaxic signals – if weak, inspiration may last a long time
If strong, inspiration may last a short time
The function of the pneumotaxic center is to limit inspiration secondary to effect of increased respiratory rate limiting inspiration à shorter Expiration, thus shorter I&E.
nucleus parabrachialis medialis:
apneustic center: located in the lower part of the pons- its function is demonstrated when the ventral neurons and other neurons connecting to the pneumotaxic center have been blocked. Then the apneustic center of the lower pons sends signals to the DRG of neurons that prevent or retard the switch off inspiratory ramp signalà the lungs fill with air , followed by short expiratory gasps. Its function is misunderstodbut may operate with the pneumotaxic center to control depth of inspiration.
central chemoreceptor area: The chemosensative area of neuronal tissur located just below the ventral surface of the medulla. Its sensitive to changes in the CO2 or H ion conc and it in turn excites the other portions of the CSF.
carotid body: the corotid body is a peripheral chemoreceptor which transmits appropriate nervous signals to the respiratory center for control of respirations in rt oxygen content. Mikhail says that the corotid bodies are the principal peripheral chemoreceptors in humans an dare sensitive to changes in PaO2 & PaCO2, pH, and arterial perfusion pressure
aortic bodies: chemoreceptors in the aortic arch which are involved in respiratory control. Their afferenrt nerves pass thru the vagi to the DRG area. These bodies receive arterial blood supply at a high rate. An alteration in the O2 content changes the rate of nerve impulse transmission.
apnea: cessation of breathing – 3 kinds: 1. Central – no central drive to respiration, no diaghratimic mvt and no airflow- usually in infants < 40 wks. 2. Obstructive – there is respiratory effort but no airflow because of upper airway obstruction. 3. Mixed apnea is a central apnea that is immediately followed by an obstructive event. Central is caused by some pathology in the brains respiratory control center.
dyspnea: labored or difficult breathing. A symptom of a variety of disorders and is primarily indicative of inadequate ventilation or insufficient amount of O2 in circulating blood.
respiratory arrest: cessation of respiratory function
respiratory failure: failure of pulmonary system to maintain oxygenation and/or CO2 homeostasis. Impairment of normal gas exchange severe enough to require acute therapeutic intervention. Diagnostics: A-aDo2 on 100%= >450, ratio Vd:TV = >.5. intrapulmonary shunt fraction Qs:Qt = > 20%, compliance < 20ml/cmH2o, Po2<60, RR< or = to 5 or > 49, PaCO2 >= 55mmHg, arterial-alveolar oxygen tension difference >=350mmHg.
hyperventilation: abnormally prolonged and deep breathing. It can cause transient respiratory alkolosis. More prolonged hyperventalition may be caused by disorders of the CNS or drugs like ASA that increase the sensitivity of the respiratory center. Prolonged hyperventilation attacks may à tetany with muscle spasm of the hands, feet, and periorbital numbness.
hypoventilation: reduction in the amount of air entering the pulmonary alveoli, which causes an increase in PaCO2.
inspiratory ramp: anervous signal that is transmitted the primary inspiratory muscles like the diaphram. Its not an Action potential. It works by nervouw emmission of weak impulses which steadily increase in a ramp manner for about 2 seconds. It abruptly ceases for 3 seconds afterwards, which turns off the excitation of the diaphram and allows for elastic recoil of the chest wall and lungs to cause expiration. Expiration occurs in between the inspiratory ramp signals. This ramp allows for steady increase in volume entering lungs rather than inspiratory gasps. The ramping controls respiratory rate. The shorter the rampà the shorter the duration of inspirationà this shortens the expiratory duration as well.
pulmonary stretch receptors: located in the muscular portion of the walls of the bronchi and bronchioles. These reflex nerve signals are transmitted thru the vagi into the DRG when the lungs become over stretched, which causes a negative feedback response which switches off the inspiratory rampà stops further inspiration. This is called the Hering-Breuer inflation reflex. This reflex increases respiratory rate the same as the pneumotaxic signals. This reflex is probably activated once tidal volume reaches 1.5L. Its probably a protective mechanism.
pulmonary irritant receptors: The epithelium of the trachea, bronchi, and bronchioles is supplied with sensory nerve endings which are stimulated by some irritants entering the respiratory system. They cause coughing and sneezing and possibly bronchial constriction in asthma and emphysema.
pulmonary "j" receptors: these are sensory receptors in alveolar walls in
"j" uxtaposition to the pulmonary capillaries. They are stimulated by especially when the pulmonary capillaries become engorged with blood or when pulmonary edema occurs in some conditions as CHF. Their function is unknown but it maybe that their excitation may cause the feeling of dyspnea.
Information about chemoreceptors. Which area is affected by the CO2 . quickly and why?The CSF changes occur quicker than the brain because the subarachnoid blood brings CO2 and there is not as many protein buffers in CSF to buffer the acids with in seconds.
The brains, H ion concentration in response to CO2 occurs in about a minute; the delay is because of the protein buffers present in the brain.
The kidneys increase blood HCO3 in response to increased H, in about 2-3 days, in response to chronic elevated cO2, therefore the respiratory drive is not as strong as in an acute increase of O2. Acute increases in CO2 cause strong effects on respiratory drive.
Are O2 changes on peripheral receptors direct or indirect? The heme oxy buffer system delivers normal amounts of O2 even when pulmonary o2 changes are between 60-1000mmHg. VERSES CO2 where blood and tissue Co2 change inversely with the rate of pulmonary ventilation.
Chemoreceptors 1. Dec o2 à chemoreceptors strongly stimulated to inc RR and are > sensitive in the 30-60mmHg range, via unknown mechanisms. One hypothesis is that inc Co2 or H excites chemoreceptors à inc resp activity. But the direct effects of CO2 & H are much > powerful than their effects mediated by chemoreceptors.
Peripheral chemoreceptors respond to CO2 > quickly than central chemoreceptors do.
describe using a graph of minute ventilation (ordinate) and partial pressure (abscissa) the RESPONSES OF THE VENTILATORY SYSTEM to changes in the arterial partial pressures of carbon dioxide and of oxygen:
From Guyton
From Guyton
Figure 41-7 above shows an effect of different levels of PaO2 on alveolar ventilation. Figure 41-8 above shows the interrelated effects of PCO2, PO2, & Ph on alveolar ventilation. At a pH of 7.3 and a CO2 of 40, as the Pco2 increases, the alveolar ventilation increases. The body is truing to blow off CO2.
At a pH of 7.4 a higher CO2 is required to drive an increase in alveolar minute volume
At the lower pH and the lower the PO2, the higher the minute volume. At the higher pH the low PO2 did not affect the minute volume in the same manner as the lower pH combined with the PO2 did. The Pco2 s were higher in the 7.4 pH group and the minute volume remained @ 50 or more L/Min in a PO2 range of 40-100mmHg.
describe in words or diagrams the anatomical locations and central connections of the PERIPHERAL AND CENTRAL CHEMORECEPTOR AREAS: See figure 41-4 below. The aortic bodies are located in the aortic arch and connect to the vagus nerve bilaterallyà go to the medulla. The corotid bodies are located in the bifurcation of the internal and external cootids and connect into the glossopharyngeal nerveà the medulla.
From Guyton
compare and contrast using a table, chart, or flow diagram the ROLES OF THE PERIPHERAL AND CENTRAL CHEMORECEPTORS in the ventilatory response to each of the following:
Changes in alveolar ventilation rosponsible for pulmonary conpensation of PaCO2 are mediated by chemoreceptors with in the brainstem. These receptors respond to changes in the CSF fluid pH. Minute ventilation increases 1-4L/Min for every 1mmHg inc in PaCO2. Decreases in arterial blood pH stimulate meduallary respiratory centers. The increase in alveolar ventilation lowers paCo2 and tends to restore arterial pH towards normal. The pulmonary response to lower PaCo2 pccirs rapidly but a steady state may not be reached until 12-24 hrs.
explain in words or using diagrams the role of readjustments in CEREBROSPINAL FLUID HYDROGEN ION CONCENTRATION in the VENTILATORY RESPONSE TO CHRONIC HYPERCAPNIA: In contrast to HCO3 & H, CO2 diffuses easily across the blood and CSF, enabling the Pco2 of CSF to adjust quickly to acute changes on PaCo2 of blood. Since changes in pH if caused by o2 (resp pH changes) can only be buffered by the non bicarbonate buffers (NBBs) whose conc in CSF is low, acute fluctuations in Pco2 of CSF lead to relatively large changes in its pH. These are registered by the central chemo receptors and result in appropriate changes in the respiratory activity.
CHRONIC changes of Co2 – the medullary center becomes insensitive to changes in PCO2 so the Po2 becomes the chief respiratory drive. ALSO in response to chronic inc PO @ the blood is well supplied with NBBs so thata decreases in pH secondary to CO2 can be effectively buffered. Consequently, the actual HCO# conc in blood rises to higher values than in CSF, and the HCO# diffuses slowly into the CSF. This brings a ise in pH of CSF via chemoreceptors. A reduction in the stimulus to respirations - the process is enhanced by renal compensationà Inc pH à adaptation.
All of these events are followed 1st by buffering of the excess H ions. Any loss of HCO3 by kidneys or intestine is equivilent to an increase in H ions.
Bicarbonate buffers (BBs) and NBBs contribute to buffering in a ratio of BB=2:3 & NBB= 1:3. CO2 arising from HCO3 leaves via lungs then via buffer base.
The 2nd step is compensation of metabolic acidosos. The dec pH value leads( via central chemoreceptors) to a rise in resp rate, which dec ACO2 & aCO2. This respiratory conpensation restores the ratio [HCO3] : [CO2] to near values of 20:1, but also due to an inc in pH reconverts NBBs –H to NBB(no H). this consumes HCO3 à compensation along with inc resp rate elimination of CO2. If the reason for acidosis persists, then respiratory compensation is inadequate and an inc in H excretion by kidneys is necessary.
name and locate on a diagram of the brain stem the various areas within the medulla and pons that are thought to be responsible for the GENERATION OF A RHYTHMIC PATTERN OF BREATHING and in the CONTROL OF MINUTE VENTILATION:
pneumotaxic center- one of the 3 major collections of neurons which is located dorsally in the superior portion of the pons, which helps control the rate and pattern of breathing. ( the pontine center seems to fine tune respiratory rate and rhythm). Neurons from this area transmit signals to the inspiratory area. These neurons control the switch off of the inspiratory ramp, thus controlling the duration of the filling phase of the lung cycle.
Pneumotaxic signals – if weak, inspiration may last a long time
If strong, inspiration may last a short time
The function of the pneumotaxic center is to limit inspiration secondary to effect of increased respiratory rate limiting inspiration à shorter Expiration, thus shorter I&E.
dorsal respiratory group- one of the three major collections of neurons which are located in the dorsal portion of the medulla, which mainly causes inspiration. This group plays the most fundamental role in the control of respiration. The dorsal respiratory group (DRG) of neurons extends most of the length of the medulla. All or most of its neurons are located with in the nucleus of the tractus solitarios. The basic rhythm of respiration is generated mainly in the DRG. Respiratory neurons in this area still emit repititive bursts of inspiratory action potentials, despite disruption of peripheral neurons entering this area.
ventral respiratory group (VRG)- One of the three major collections of neurons which is located in the ventrolateral part of the medulla, which can cause either expiration or
inspiration, depending on which neurons in the group are stimulated.
The neurons in the VRG remain almost inactive during normal quiet respiration. There is no evidence that VRG participates in the basic rhythmical oscillation that controls respiration.
When the respiratory drive for increased pulmonary ventilation becomes > than normal, respiratory signals spill over into VRG from the basic oscillatory mechanisms of the DRG area. Then the VRG does contribute to the respiratory drive.
VRG area is very important in providing powerful expiratory signals to abdominal muscles during expiration. The VRG area operates as an overdrive mechanism when high levels of pulmonary ventilation are required.
compare and contrast the ROLES OF OXYGEN AND CARBON DIOXIDE IN THE REGULATION OF VENTILATION in a normal human subject and in a patient with long-standing chronic obstructive pulmonary disease: Total body oxygen consumption and CO32 production are matched by immediate adjustmants in rate and depth of breathing to maintain ABGs and pH at stable physiologically acceptable levels. This ventilatory response is entirely dependent on nervous system control.
Dec or inc Co2 results in cooresponding H concentrations changes. OCO2 above 40mmHg à inc CSF H concà central respiratiory ocntrol mechanisms to fire signals to the respiratory muscles at increased frequency à hyperventilation à dec Pco2 and Pcsf CO2.
The peripheral nervous system chemoreceptors transmit excitatory signals to central respiratory center in brainstem in response to dec Pao2 (most noted range is 30-60mmHg) . The peripheral chemoreceptors also respond weakly to inc PaCO@, low perfusion states, metabolic or respiratory acidosos, anemia, and /or dec hbg conc or sat.
Overall, central chemo receptors are most influenced by and primarily regulated by PaCO2. The peripheral chemoreceptors are primarily affected by blood o2 content and thereby maintain ventilatory effects on blood oxygen.
COPD
O2 and CO2 regulate ventilatory response in COPD. Poorly ventilated alveoli either fail to be efficient gas sxchanging units à ventilation perfusion MM or shunts. COPDers have varying degrees of V/Q mm, intrapulmonary shunting, and significant blood gas abnormalaties all the time. Hypoxemia, hypercarbia, and respiratory acidosis with compensatory metabolic acidosos are of the patients steady state.
In patients with a chronic inc PCO2, O2 may worsen hypercarbia. Due to the chronically inc PaCO2à chemoreceptors become insensitive to CO2 and hypoxemia becomes the primary drive to breathe, therefore corrections of the hypoxemia with supplemental o2 eliminates the only constant stimulus to breathe. Hypoventalation à inc PCO2à CNS depressionà CO2 narcosis. PaSo2 about 90% is usually a good value in chronically hypercarbic patients.
REFERENCES ARE GUYTON, DAROVIC, THEIME, MIKHAIL
Last Updated 09/06/01 08:53:24 PM
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