control of breathing Flashcards
What is the composition of atmospheric, dry air?
N2 = 79.04% O2 = 20.93% CO2 = coc3% others = <1%
What is the total atmospheric pressure?
760mmHg at sea level
or 101.08 kPa –> divide by 7.5
Define Partial Pressure
pressure which an individual gas in a mixture contributes to the total pressure
What happens to barometric pressure as altitude increases?
less atmospheric pressure, therefore partial pressure of oxygen is also lower (will be 21% of new total pressure)
What is meant by gas tension
partial pressure of gases in a liquid (e.g. blood)
The amount of gas dissolved in a liquid/ blood depend on what 2 factors?
1) solubility of gas in blood around alveolus - CONSTANT
2) pressure of gas (gas tension) in alveolar air - VARIABLE
*there will be a pressure gradient between alveoli and blood
What will happen to O2 if PO2 in alveoli > PO2 in pulmonary capillaries?
Diffuse into blood until PO2 alveolar = PO2 blood
What are the two reasons for why the alveolar PO2 (100mmHg) differs from atmospheric PO2 (160mmHg - remember 21% of 760mmHg)?
1) it becomes saturated with water vapour
2) because of dead space not all air is fresh with every breath
Taking into account saturation from water vapour, how would you calculate initial PO2 in alveolar air?
- Pwater at body temperature = 47mmHg
- need to factor in that the air breathed in is diluted by this
- so, PO2 = (760-47)x(21/100)
= 150mmHg
Explain the dilution factor of dead space
- PO2 is already lowered by dilution of water
- only 350/500 mL is new air
- so, alveolar PO2 = 100mmHg (of 160mmHg in atmospheric air)
- remains pretty constant
why does PO2 remains fairly constant during resp. cycle?
1) only small change in alveolar air/ breath
2) O2 being removed by passive diffusion into blood
PCO2 of alveolar differs from atmospheric PCO2, but remains quite constant in the tissues because:
1) CO2 is removed from blood to alveoli by passive diffusion
2) CO2 leave alveoli expiration
composition of dry (atmospheric) and saturated (alveolar) air
DRY Pgas: ALVEOLAR Pgas: N2 = 593 567 O2 = 160 150 -> 100 CO2 = 0.23 0.21 -> 40 H2O = 0 47 others = v.low v.low
What is the partial pressure gradient of O2 and CO2 across pulmonary capillaries?
O2:
- from alveoli to blood
- 60mmHg (100->40)
CO2:
- from blood to alveoli
- 6mmHg (46->40)
changes in PO2 from atmosphere to tissue cell
160 > 100 > 40 (mmHg)
why do we need to control breathing?
acid/base balance
PCO2, PO2 and [H+] need to be controlled within narrow limits
how do we achieve alveolar Pgas change -> Pgas change in pulmonary capillaries -> Pgas change in systemic arterial blood?
varying pulmonary ventilation
VE = TV x RF
(typically 500mL x 12bpm =6000mL/min… can range from 6L at rest to 100L/min during exercise)
how is the rate and depth of breathing altered by the CNS
changing the discharge of the motor neurons supplying the respiratory muscles
what happens if VE is increased?
CO2 is flushed out so alveolar PCO2 decreases
alveolar PO2 increases and approaches atmospheric PO2
what happens if VE is decreased?
CO2 is retained in the lungs so alveolar PCO2 is increased
PO2 in the alveoli decreases
what are the key elements of the respiratory control system?
Sensors: chemoreceptors, mechanoreceptors, cerebral cortex, hypothalamus
central controller: pons (1 resp. group with 2 areas: pneumotaxic centre and apneutic area), medulla (2 resp. groups: ventral and dorsal)
Effectors: respiratory muscles (cause ventilation)
where is our basic respiratory rhythm generated?
medulla
What neurons/ area of the brain stem generates rhythm for inspiratory breathing movements?
pre-Botzinger complex (ventral resp. group)
how does the pre-Botzinger complex drive inspiration?
fires to Dorsal respiratory group (most fundamental role in the control of resp by initiating inhalation) that then fires in bursts, leading to contraction of respiratory muscles. when firing stops, you get passive expiration
describe the basic resting respiratory rhythm
Active:
- 2 secs
- diaphragm and ext. intercostals actively contract
Passive:
- 3 secs
- diaphragm relaxes, followed by elastic recoil of chest wall and lungs
what happens in active expiration during hyperventilation?
- excitation of ventral respiratory group (inactive in normal breathing)
- excite expiratory muscles (internal intercostals, abdominals etc) that produce forceful expiration
-also get increased firing of dorsal neurons that influence inspiration
what occurs during labored breathing?
inspiratory area is active:
- diaphragm, ext. intercostals, scm, pec minor and scalene muscles contract
expiratory area is active:
-internal intercostals and abdominal muscles contract
explain how the resp group in the pons can influence the rhythm generated in the medulla
pneumatic centre:
- controls rate and pattern of breathing
- stimulates the termination of inspiration
apneustic centre:
- promotes inhalation by constant stimulation of the neurons in the medulla
- delays switch-off from pneumotaxic centre
- controls intensity of breathing
- prolong inspiration
what would happen without the pnumotaxic centre?
prolong inspiratory gasps with brief expiration = APNEUSIS
describe what happens to medullary control centres during voluntary control (required for speaking, singing etc.)
- input from cerebral cortex
- achieved by bypassing resp. centres
- signals sent directly to motor neurons in spinal cord that supply resp. muscles
- overridden by resp. centres if hypo/hyper ventilate to extremes
describe the 4 inputs to the medullary control centres during reflex modification of breathing
1) inputs from pulmonary stretch receptors:
- activated during large inspiration: 1L TV (unlikely during normal cycle)
- afferent signals to inhibit inspiration = Hering-Breuer reflex
2) input from irritant receptors
- free n.endings between airway epithelia
- stimulated by smoke, dust etc.
- stimulate reflex bronchial and laryngeal constriction and mucus production (implication for asthmatics)
3) input from J receptor (juxta-capillary)
- in alveolar walls close to pulmonary capillaries
- respond to changes in vol of fluid (cause stretch)
- role in inducing changes in breathing rhythm (rapid, shallow breathing) in L. heart failure and interstitial lung disease
4) inputs from upper airway receptors - nose, pharynx, larynx
- stimulated by mechanical and chemical stimuli
- initiate coughing and sneezing
describe the cough reflex
noxious stimulus triggers receptors in the upper airway. Vagus nerve is stimulated to give medulla response:
- up to 2.5L air rapidly inspired
- epiglottis and vocal cords close, trapping air in lungs
- abs contract, push up against diaphragm. accessory expiratory muscles contract
- pressure in lungs increases (100mmHg or more!)
- epiglottis and vocal cords open suddenly, releasing air at 75-100 mph
- force is enough to collapse bronchi and trachea, air ejected through narrow slits
- irritant is ejected
list some of the other inputs that affect ventilation
- joint and muscle receptors - impulses from moving limbs increase ventilation during exercise
- gamma system - muscle spindles sense dyspnoea and increase strength of contraction
- arterial baroreceptors - increase in arterial BP may cause reflex hypoventilation or visa versa
- pain and temperature receptors - pain often cause a period of apnoea followed by hyperventilation and excess heat leads to hyperventilation
what are the chemical drivers for increasing ventilation rate?
arterial PO2 decrease
arterial PCO2 increase
arterial [H+] increase
describe what happens if arterial PO2 decreases
- monitored by carotid and aortic bodies
- not used in quiet respiration
- PO2 must fall below 60mmHg (>40%) to cause response
- receptors send afferents to medullary inspiration neurons to increase ventilation (important in altitude)
describe what happens if PCO2 increases
- monitored by central chemoreceptors (monitor CO2 induced changes in [H+])
- responds to proton changes in brainstem ECF
- increase ventilation
- increase amount of CO2 blown off
- PCO2 and [H+] decrease
- can do opposite if PCO2 decreases
- small changes in PCO2 have big changes in ventilation
what is the most important magnitude regulator in quiet ventilation?
PCO2
