Control of breathng Flashcards
(24 cards)
What is partial pressure of a gas?
Mixture is the pressure which that gas contributes to total pressure
Barometric pressure decreases as altitude increases
What does amount of gas dissolved in liquid (e.g. blood) depend on?
Solubility of gas in blood e.g. around alveolus - constant
PP of gas in alveolar air is variable
So amount of dissolved gas proportional to alveolar Pco2 and Po2
What are partial pressure gradients?
Gas will always diffuse down a partial pressure gradient
If po2 alveoli is greater than po2 of blood in pulmonary capillaries then o2 diffuses into blood until po2 alveolar = po2 blood
If pco2 alevoli < pco2 blood in pulmonary capillaries then co2 diffuses out of blood until equal in blood and alveoli
How does alevolar po2 differ from atmospheric po2?
a) It becomes saturated with water vapour
b) Remember that because of dead space not all air is fresh after every breath
po2 remains fairly constant during resp cycle because:
- Only quite small change in alveolar air/breath
- Oxygen being removed by passive diffusion into blood
Why does alveolar pco2 differ from atmospheric pco2?
Tissues produce CO2 but pco2 remains quite constant because:
- CO2 removed from blood - alveoli by passive diffusion
- CO2 leaves alveoli in expiration
Why control breathing?
PCO2, Po2 and H+ must be controlled within narrow limits
Alveolar Pgas change -> Pgas change in pulmonary capillaries -> Pgas change in systemic arterial blood
This is achieved by varying pulmonary ventilation - Ve
Ve = TV x RF
Rate and depth of breathing can be altered by changing the discharge of the motor neurones supplying the respiratory muscles
What does increased and decreased Ve achieve?
Ve is pulmonary ventilation
Increased Ve - CO2 gets flushed out of body so alveolar Pco2 decreases - alveolar po2 increases and approaches atmospheric po2
What are the key elements in respiratory control system?
Sensors - receptors (e.g. chemo), gather info and feed to…
Central controller - pons, medulla (co-ordinate info and send impulses to effectors)
Effectors - respiratory muscles and cause ventilation
How is basic respiratory rhythm generated?
Fairly normal ventilation retained if section above medulla
Ventilation ceases if section below medulla
Medulla is major rhythm generator
What gives rise to inspiration?
Pre-Botzinger complex drives dorsal respiratory group neurones (inspiratory)
Fire in bursts. Firing leads to contraction of respiratory muscles - inspiration
When firing stops, passive expiration
What is basic resting rhythm?
Inspiratory area
Active in 2 secs - diaphragm contracts (and ext intercostals) giving normal quiet inspiration
Inactive in 3 secs - diaphragm relaxes followed by elastic recoil of chest wall and lungs, normal quiet expiration
Active expiration during hyperventilation?
Increased firing of dorsal neurones excites a second group - ventral respiratory group hormones
Excite internal intercostals, abdominals etc giving forceful expiration
In normal quiet breathing ventral neurones do not activate expiratory muscles
How can rhythm generated in medulla be modified?
Can be modified by neurones in pons Pneumotaxic centre (PC) Stimulation terminates inspiration. Pc stimulated when dorsal respiratory neurone fire so inspiration inhibited
Without PC breathing is prolonged inspiratory gasps with brief expiration - apneusis
What is the apneustic centre?
Impulses from these neurones excite inspiratory area of medulla
Prolong inspiration
Basic rhythm generated in medulla (in pre-Botzinger complex which drives DRG)
Respiratory centres in pons (pneumotaxic and apneustic centres) modify the basic rhythm
Normal control of ventilation
Resp control centres receive afferent info about what is happening in body, entilation adjusted in proportion to inputs
ventilation has wide range - 6L/min to 100L/min according to needs of body
Inputs to medullary control centres from cerebral cortex - voluntary control
Voluntary control achieved by bypassing the resp centres in brainstem. Instead, control is via cerbral cortex which sends signals directly to motor neurones in spinal cord that supply the resp muscles
If we hyper or hypo ventilate to extremes this will trigger resp centre and voluntary input will be overridden. Voluntary control required e.g. for speaking, singing
Inputs to medullary centre controls by reflex modification of breathing (1 and 2)
1) Inputs from pulmonary stretch receptors - activated during inspiration at large tidal volumes, not used in normal cycle - important in new borns and potentially prevents over-inflation of lungs during hard exercise
2) Inputs from irritant receptors - free nerve endings between airway epithelial cells. Stimulated by smoke, dust, noxious gases etc. Initiate reflex bronchial and laryngeal constriction, mucus production. Implicated in asthmatic and allergic bronchoconstriction
Inputs to medullary centre controls by reflex modification of breathing (3 and 4)
3) Inputs from J receptors (juxta-capillary receptors)
These receptors are believed to be in alveolar walls close to capillaries. Impulses pass up vagus nerve in slowly conducting myelinated fibres and can result in rapid, shallow breathing although intense stimulation will cause apnoea.
4) Inputs from upper airway receptors - nose, pharynx, larynx
Stimulated by various mechanical (dust, pollen) and chemical stimuli. Initiate deep inspiration, closure of glottis. Pressure builds up to give a high pressure blast of expired air to expel irritant. Sneezing and coughing. No role in normal breathing control
Cough reflex
Various parts of resp apparatus sensitive to various stimuli. Receptors trigger afferent impulses via vagus nerves to medulla response:
- Up to 2.5L air rapidly inspired
- Epiglottis and vocal cords close, trapping air in lungs
- Abs contract, push up against diaphragm, expiratory acccessory muscles contract, pressure in lungs increases, epiglottis and vocal cords open suddenly releasing air, force is enough to collapse bronchi and trachea, air ejected through narrow slits, irritanr ejected
What are the other inputs?
- Inputs from joint and muscle receptors - impulses from moving limbs reflexly increase breathing believed to contribute to increased ventilation during exercise
- Inputs from Gamma system - intercostals and diaphragm contain muscle spindles that sense muscle elongation which can control contraction strength
- Inputs from arterial baroreceptors - increase in ABP can cause reflex hypoventilation of apnea through stimulation of aortic and carotid sinus baroreceptors
- Inputs from pain and temp control receptors both likely to cause hyperventilation
What 3 things change to increase ventilation rate?
Increased arterial pco2 and H+
decreased arterial po2
Inspiratory centres automatically triggered
Arterial po2 decrease changes
Monitored by carotid bodies and aortic bodies - peripheral chemoreceptors
Located on right and left of carotid arteries and arch of aorta
Receptors respond to chem changes in arterial blood. Not usually involved in quiet resp - used in disease or dec atmospheric pressure/oxygen availability
Sensitive to po2 dec but don’t initially cause a response, po2 must fall below 60mmHg. Receptors then send afferent impulse to medullary inspiration neurones to inc ventilation - important at altitude
Arterial pco2 rise changes
Most important magnitude regulator in quiet ventilation
Aortic body peripheral receptors not responsive to chnage in pco2. Carotid may respons to change in pH and pco2 but not usually at sea level in health. Central chemoreceptors monitor changes in CO2 induced H+ in brainstem ECF
In brainstem inc H+ stimulates central chemoreceptors, inc ventilation, inc co2 blown off, pco2 dec, H+ dec
If Pco2 and H+ decrease below normal levels, chemoreceptors trigger dec in vent
Effect of hypercapnia (inc co2) on ventilation
Body very responsive to raised pco2
Small inc in pco2 giveslarge inc in ventilation
