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Control of Respiration. Dr Shihab Khogali Ninewells Hospital & Medical School, University of Dundee. What is This Lecture About?. What makes the inspiratory muscles contract and relax rhythmically? How could the respiratory activity be modified ?
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Control of Respiration Dr Shihab Khogali Ninewells Hospital & Medical School, University of Dundee
What is This Lecture About? • What makes the inspiratory musclescontract and relax rhythmically? • How could the respiratory activity be modified? • How could the expiratory muscles be called on during active expiration? • How could the arterial PO2and PCO2 be maintained within narrow limits? • What is the role of the respiratory system in regulating blood H+ concentration? See blackboard for detailed learning objectives
To answer these questions we need to understand: The Neural & Chemical Control of Respiration
Neural control of Respiration anterior The Rhythm: inspiration followed by expiration Fairly normal ventilation retained if section above medulla Ventilation ceases if section below medulla medulla is major rhythm generator
It is now generally believed that the breathing rhythm is generated by a network of neurons called the Pre-Brotzinger complex. These neurons display pacemaker activity. They are located near the upper end of the medullary respiratory centre Neural control of Respiration Until recently, it was thought the Dorsal respiratory group of neurons generate the basic rhythm of breathing
What gives rise to inspiration? Dorsal respiratory group neurones (inspiratory) PONS Fire in bursts Firing leads to contraction of inspiratory muscles - inspiration MEDULLA SPINAL CORD When firing stops, passive expiration
What about “active” expiration during hyperventilation? Increased firing of dorsal neurones excites a second group: In normal quiet breathing, ventral neurones do not activate expiratory muscles Ventral respiratory group neurones Excite internal intercostals, abdominals etc Forceful expiration
The rhythm generated in the medulla can be modified by neurones in the pons: “pneumotaxic centre” (PC) + Without PC, breathing is prolonged inspiratory gasps with brief expiration - APNEUSIS Stimulation terminates inspiration - PC stimulatedwhendorsal respiratory neuronesfire Inspiration inhibited
The “apneustic centre” Apneustic centre Conclusion? Impulses from these neurones excite inspiratory area of medulla Rhythmgenerated in medulla Rhythm can be modified by inputs from pons Prolong inspiration
Reflex modification of breathing Pulmonary stretch receptors Activated during inspiration, afferent discharge inhibitsinspiration - Hering-Breuer reflex Do they switch off inspiration during normal respiratory cycle? Unlikely - only activated at large >>1litre tidal volumes Maybe important in new born babies May prevent over-inflation lungs during hard exercise?
Joint receptors • Impulses from moving limbs reflexly increase breathing • Probably contribute to the increased ventilation during exercise
Factors That May Increase Ventilation During Exercise • Reflexes originating from body movement • Increase in body temperature • Adrenaline release • Impulses from the cerebral cortex • Later: accumulation of CO2 and H+ generated by active muscles
Chemical Control of Respiration • An example of a negative feedback control system • The controlled variables are the blood gas tensions, especially carbon dioxide • Chemoreceptors sense the values of the gas tensions
Peripheral Chemoreceptors Carotid bodies Aortic bodies Sense tension of oxygen and carbon dioxide; and [H+] in the blood
Central Chemoreceptors • Situated near the surface of the medulla of the brainstem • Respond to the [H+] of the cerebrospinal fluid (CSF) • CSF is separated from the blood by the blood-brain barrier • Relatively impermeable to H+ and HCO3- • CO2 diffuses readily • CSF contains less protein than blood and hence is less buffered than blood CO2 + H2O H2CO3 H+ + HCO3-
Hypercapnia and Ventilation 40 The system is very responsive to PCO2 30 Ventilation (l/min) 20 CO2 generated H+ through the central chemoreceptors 10 20 40 60 80 10.6 8 5.3 2.7 Pco2 (kP) (mmHg)
% Haemoglobin Saturation O2 concentration ml/100 ml 13.3 8.0 5.3 Blood PO2 (kPa) Hypoxia and Ventilation Neuron depressed when hypoxia so severe 50 40 Peripheral Chemoreceptors Stimulated 30 Ventilation (l/min) 20 10 0 8.0 13.3 0 Arterial Po2 (kPa)
Hypoxic Drive of Respiration • The effect is all via theperipheral chemoreceptors • Stimulated only when arterial PO2 falls to low levels (<8.0 kPa) • Isnot importantinnormal respiration • May become important in patients with chronic CO2 retention (e.g. patients with COPD) • It isimportant at high altitudes
The H+ Drive of Respiration • The effect is via theperipheral chemoreceptors • H+ doesn’t readily cross the blood brain barrier (CO2 does!) • The peripheral chemoreceptors play a major role in adjusting for acidosis caused by the addition of non-carbonic acid H+ to the blood (e.g. lactic acid during exercise; and diabetic ketoacidosis) • Their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body (remember CO2can generate H+, so its increased elimination help reduce the load of H+ in the body) • This is important in acid-base balance
