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Control of ventilation

Reading: Sherwood Chapter 13 Control of respiration 8th ed. 491-501 7th ed. 498-507 6th ed. 487-496

Be prepared to answer or discuss: (i.e. dont just sit there with the questions and wait to be told the answers!) How are the rhythmic muscle contractions that produce breathing generated? o Where is the pacemaker? Pacemaker activity that establishes breathing rhythm widely belived to reside in Pre-Btzinger Complex, located near upper end of medullary respiratory center. o Where do the impulses to the respiratory muscles originate? o Impulses to respiratory muscles originate from medullary respiratory center. What do the centres in the pons do? Pneumotaxic center and apneustic center in the pons influence output from medullary respiratory center to produce normal and smooth inspiration and expiration. Pneumotaxic center sends impulse to dorsal respiratory group (DRG) in medullary respiratory center to help switch off inspiratory neurons, limiting inspiration duration. Apneustic center prevents inspiratory neurons from being switched off. o Pneumotaxic center dominates over apneustic center, helping halt inspiration and letting expiration occer normally. What is the Hering-Breuer reflex Hering-Breuer reflex is a reflax triggered to prevent over inflation of lungs. Pulmonary stretch receptors within smooth muscle layers

of airways respond to excessive stretching of lung during large inspirations. What chemical factors in the blood influence respiration? PO2, PCO2, H+ Where are the chemoreceptors for these? Arterial PO2 monitored by peripheral chemoreceptors know as carotid bodies and aortic bodies. Central chemoreceptors, located in medulla near respiratory center. (dont monitor CO2 but sensitive to changes in CO2-induced H+ concentration in brain ECF.) Which is the dominant chemical factor under most circumstances? PCO2, plays key role in regulating respiration How and where is this sensed? PCO2 sensed by central chemoreceptors. Any increase in PCO2 causes similar rise in brain-ECF PCO2 as CO2 diffuses down its pressure gradient from cerebral blood vessels into brain ECF. Increased PCO2 in brain ECF raises concentration of H+ according to law of mass action. Why is PO2 not a stimulus to respiration until it falls to ~ 60 mm Hg? Decrease in PO2 not stimulus until below 60 mm HG as safety margin in % Hb saturated afforded by plateau portion of O2-Hb curve. Haemoglobin still 90% saturated at arterial PO2 of 60mm HG, but drops precipitously when falls below this level. Peripheral chemoreceptors are directly sensitive to [H+] o What would H+ but not PCO2? Addition of non-carbonic acid from the body would increase arterial H+ but no PCO2. i.e. Arterial H+ concentration increase during diabetes mellitus because excess H+-generating keto acids are abnormally produced and added to the blood.

Why is increased ventilation an appropriate response to H+?

What other factors influence respiratory rhythm? Respiratory rhythm can be influenced by the following: 1) Exercise 2) Sneezing and coughing 3) Inhalation of particularly noxious agents triggering immediate cessation of ventilation 4) Pain originating anywhere in the body 5) Involuntary modification of breathing occurring during expression of emotional states 6) Swallowing