respiration Flashcards
4 variables for respiratory physiology
volume, pressure, temperature, motion
what is boyle’s law
P is inversely proportional to 1/V
what is the partial pressure of saturated water vapour at 37ºc
47mmHg
what does it mean when you say inspired air is saturated with water vapor
water vapor is diluting the gases
Pressure and % of O2 in inspired gas
21kPa, 21%
partial pressure of O2 when it reaches the alveoli
19.9kPa
what is Daltons law of partial pressure
pressure exerted by each gas in a mixture of gases is independent of the other gases present
what is the PO2 in arterial blood
13.3kPa
what is the PCO2 in arterial blood
5.3kPa
what is the PO2 in the alveoli
13.3 kPa
what is the PCO2 in the alveoli
5.3kPa
what is the PO2 in venous blood
5.3kPa
what is the PCO2 in venous blood
6.0kPa
what happens during inspiration
- ribcage expands
- lungs stretch
- diaphragm moves downwards
- alveolar pressure reduced
- air drawn in
what happens during in expiration
- rib cage contracts
- lungs contract
- diaphragm moves up
- alveolar pressure increased
- air pushed out
what is PVR
pulmonary ventilation rate
PVR equation
respiration rate x tidal vol
what is the average PVR during rest
6l/min
what is the average PVR during exercise
120l/min
what does AVR mean
alveolar ventilation rate
what is AVR
the actual amount of air reaching the alveoli, to calculate it you need to allow for the ‘wasted’ ventilation of dead spaces
what is perfusion (Q)
deoxygenated blood passes through the lungs and becomes re-oxygenated
what is the ventilation perfusion ratio (VA/Q)
a ratio of alveolar ventilation to blood flow
ventilation-perfusion ratio in dead space
1.normal ventilation but no perfusion
2. no capacity to carry O2 away or bring CO2 to alveoli
3. No gas exchange between the alveoli and the blood so alveoli equilibrates with atmosphere
ventilation-perfusion ratio in shunt
- no ventilation, normal perfusion
- No new O2 in system
- alveoli equilibrates with venous blood
what is lung compliance like at high pressure
low as lung is stiffer
what part of lung is more compliant, base or apex
base
what ensues compliance
elastic recoil
how much lung compliance is healthy
high
what is tidal volume (TV)
vol of air entering and leaving w each normal breath
what is inspiratory reserve volume (IRV)
extra volume inspired w force over TV
what is expiratory reserve volume (ERV)
extra volume expired with force over TV
what is the vital capacity (VC)
TV + IRV + ERV
what volumes are measured using spirometry
TV, IRV, ERV
what is residual volume (RV)
volume of air in lungs after the most forceful expiration
what is functional residual capacity (FRC)
air remaining in lungs after normal expiration
what is total lung capacity (TLC)
maximum volume of air the lungs can hold
FRC equation (V2)
V1 x (C1-C2)/C2
what is altered if lung expansion is compromised
alterations in lung parenchyma
what is the effect of pulmonary fibrosis/ scoliosis on FVC and FEV
FVC reduced, FEV1.0 is relatively normal
effect of obstructive deficit on lungs
- airway obstruction
- narrowed airways
- resistance increased in expiration
examples of 2 disorders causing obstructive deficit
Asthma, Chronic obstructive pulmonary disease
how is carbon dioxide transported
- carbaminohaemoglobin
- bicarbonate
carbon dioxide transport via carbaminohaemoglobin
- CO2 binds to globin
- reduced Hb has greater affinity for CO2 than oxygenated Hb
- O2 unloading allows for CO2 pick up
- Hb-CO2 bond is very weak so CO2 easily released to alveoli
carbon dioxide transport via bicarbonate
- CO2 more soluble in H2O than O2 is
- reaction leads to acid base balance
CO2 reaction in RBCs
- reacts w H2O to form HCO3- and H+
- H+ removed by binding to Hb (HHb)
what happens with plasma bicarbonate (CHLORIDE SHIFT)
bicarbonate ions diffuse into plasma. Cl- ions diffuse into cell to maintain electrical neutrality (CHLORIDE SHIFT)
what causes respiratory acidosis
hypoventilation (decrease in respiratory stimuli)
what happens in lungs when there is respiratory acidosis
- decrease in pH
- increase in [H+]
- increase in CO2
how are the effects of respiratory acidosis countered in the kidney
- increase [H+]
- increase HCO3- reabsorption
what causes respiratory alkalosis
hyperventilation
what happens in lungs when there is respiratory alkalosis
- increase in pH
- decrease in [H+]
- decrease in CO2
how are the effects of respiratory alkalosis countered in the kidney
- increase [H+]
- increase HCO3- excretion
what forms in metabolic acidosis
ketone bodies -> in uncontrolled diabetes
what happens as a result of metabolic acidosis
- decreased ability of kidneys to excrete H+ and reabsorb HCO3-
- decreased pH
- decreased HCO3-
what compensation happens as a result of metabolic acidosis
- increased ventilation
- increased H+ excretion
- increased HCO3- reabsorption
what causes metabolic alkalosis
nausea, vomiting, diarrhoea, ingestion of a base
what happens as a result of metabolic alkalosis
- decreased acid
- increased base
- increased pH
- increased HCO3-
what compensation happens as a result of metabolic alkalosis
- decreased ventilation
- increased H+ reabsorption
- increased HCO3- excretion
how is ventilation controlled chemically
via central chemoreceptors (CCRs) and peripheral chemoreceptors (PCRs)
CCRs
found in medulla and sensitive to change in [H+] and pCO2
PCRs
found in carotid arteries and aortic arch, sensitive to changes in arterial pO2 and pH
pCO2 levels impact on CCRs
directly impact CCRs and activate them causing hyper or hypoventilation
what do PCRs detect
changes in pO2, decreased arterial O2 leads to hyperventilation (when pO2 is below 13.3 mmHg)
what does the medulla have which control ventilation
Dorsal respiratory group (DRG) and Venrtal respiratory group (VRG)
what is the DRG
- fibres innervate diaphragm and external intercostal muscles
- neurons switch on for 2s and off for 3 to causes rhythmic pattern
what is the VRG
- fibres innervate abdominal muscles and internal intercostal muscles
- activity plays role in forced expiration
what does the pneumotaxic centre (PONS) do
- transmits signals to DRG
- limits inspiration (inhibitory impulses to DRG)
- prevents overinflation of lungs
what is the apneustic centre responsible for and what does it stimulate
prolonged respiratory gasps, prolongs DRG stimulation
vagus nerve role in ventilation
sends afferent info from lungs to DRG, switches off inspiration
cerebral cortex role in ventilation
- stimulates motor neurone of inspiratory muscles
- bypasses medullary centres when consciously controlling breathing
- limited ability to breathhold
effects of high altitude
- hypoxia
- loss of appetite
- change in mental performance
- insomnia
adaptations to mild hypoxia
increased ventilation, decrease pCO2. This increases CSF pH, increase in HCO3-
how do choroid plexus cells correct CSF pH
export HCO3- from it