Topic 13 Flashcards
3 processes involved in exchange of air
- pulmonary ventilation
- external respiration
- internal respiration
Pulmonary ventilation
result of pressure gradients caused by changed in thoracic cavity volume.
Boyles Law
gas volume is inversely proportional to pressure. as volume increase pressure decrease (vice versa) for the same number of molecules of air (gas amount is constant)
3 pressures involved in pulmonary ventilation
- P atm: atmospheric (760 mmHg) sea level
- P pul: intrapulmonary: air pressure inside lungs (= P atm between breaths)
- P ip: intrapleural: fluid pressure in pleural cavity
Intrapleural pressure is ..
- always < P pul
- usually < P atm (just slightly, 756 mmHg)
- throacic wall recoils, out lungs recoil in but fluid holds them together so P ip decreases slightly
Quiet inspiration
active process (muscles contract). at start P atm =P pul (760 mmHg). no air moves then..
- diaphragm, ext intercostals contract (active) , ⇑ vol. of thoracic cavity
- lungs resist expansion ∴ Pip ⇓ (756⇒754 mmHg)
- higher pressure difference between Ppul and Pip pushes lungs out ⇒ lungs expand ∴ Ppul ⇓ (760 ⇒ 758 mmHg)
- air moves in down P gradient (until Ppul = Patm)
Forced inspiration
active process.diaphragm, external intercostals + sternocleidomastoids, pectoralis minors, scalenes contract (∴ active).⇑⇑ vol. of thoracic cavity ∴ pressure gradient ⇑, and
more air moves in
Quiet expiration
- relax diaphragm, ext. intercostals ⇒ lungs to resting size ∴ ⇓ thoracic cavity size (passive process)
- vol ⇓, Pip ⇑ (754 ⇒756 mmHg) ∴ Ppul ⇑ (760⇒762 mmHg) ⇒ air moves out down pressure gradient
Forced expiration
- laboured or impeded (e.g. asthma) breathing
- relax diaphragm, ext. intercostals + contract internal intercostals, abdominals (active process)
- Pip ⇑ ⇒ lung volume ⇓ ∴ Ppul ⇑ and air moves out
Stretch in lungs determined by either..
- compliance
- recoil
Compliance
effort needed to stretch lungs; low = much effort
Recoil
ability to return to resting size after stretch
Both compliance and recoil =
result of elastic CT + surfactant
Lungs collapse prevented by..
- P ip is always below P pul
- Presence of surfactant
Pneumothorax
air in pleural cavity. Patm = Pip = Ppul so lungs collapse, thoracic wall expands
Surfactant= Lipoprotein / phospholipid mixture
- in watery film coating alveoli (decrease surface tension)
- allows easier stretch of lungs (increase compliance)
- prevents alveolar collapse
Respiratory distress syndrome
newborns to 7 months gestation. inadequate surfactant so alveoli tend to collapse (love compliance) so effort is high which leds to death
Air flow and airway resistance equation
F= air flow P= Patm - Ppul R= airway resistance
Airway resistance determined by diameter of bronchi and bronchioles so..
-inspiratory mechanics open airways/ expiratory close always.
SNS dilates..
bronchiolar smooth muscle
PSNS
contracts it (bronchocontriction)
Asthma, bronchitis, emphysema increase airway resistance so..
more difficult to expire than to inspire
Respiratory volumes used measuring..
spirometer
1 respiration =
1 inspiration + 1 expiration
Tidal volume (TV)
inspired or expired air during quiet respiration (500 ml)
Inspiratory reserve volume (IRV)
excess air over TV take in on a max inspiration (3000 ml)
Expiratory reserve volume (ERV)
excess air over TV pushed out on max expiration (1200 ml)
Residual volume (RV)
volume of air in lungs after maximal expiration (1200 ml)
Minute respiratory volume
TV x respiratory rate (ex: 500 ml x 12 breaths/min = 6L/ min)
Forced expiratory volume in 1 second (FEV1)
volume expired in 1 sec with max effort, following max inspiration
Lung capacity
2 or more volumes
Inspiratory capacity (IC)
= IC + IRV
Vital capacity (VC)
= TV + IRV + ERV (largest volume in and out of lungs)
Total lung capacity (TLC)
= TV + IRV + ERV + RV (= VC + RV) ** max amount of air lungs can hold
FEV1 measured while..
measuring VC and expressed as %VC (allows correction for body size) usually FEV1 = 80% VC
Measurements of lung capacity allows for diagnoses of..
- obstructive disorders
- restrictive disorders
Obstructive disorders
hard to expire = high R. therefore RV high, VC low, and FEV1 < 80% VC. (ex: emphysema, asthma, cystic fibrosis)
Restrictive disorders
restrict lung expansion, hard to inspire. therefore IC low, VC low, FEV1 low (but FEV1 = 80% VC) (ex: scoliosis, pneumothorax)
External respiration
O2 from alveoli to blood and CO2 from blood to alveoli
External respiration aided by..
- thin respiratory membrane (2 cells + basement membrane)
- large surface area: capillaries, alveoli and rbc single file in capillaries ∴ max rbc exposure to gases
- blood velocity slow compared to gas diffusion (rbc have time to pick up/release gases)
Internal respiration
O2 from blood to cells and CO2 from cells to blood
Partial pressure of gases =
the pressure exerted by a single gas in a mixture of gases (ex: O2 = 21% of air). written as P o2, P co2, P n2, etc. pressure gradients promote gas movements from high to low pressure
Partial P =
0.21 x 760 mm Hg = 160 mmHg
O2 carried in 2 ways either.
- dissolved in plasma (1.5%) (=Po2)
- bound to hemoglobin (98.5)
O2 dissolved in plasma at lung capillaries (external)
O2 moves from high pressure (105 mmHg in the lungs/alveoli) to low pressure (40 mmHg in the capillary)
O2 dissolved in plasma at tissue capillaries
arterial Po2 = mmHg. resting venous + ISF P o2 = 40 mmHg. ICF Po2 < 40 mmHg. O2 diffuses: capillary to ISF to cell (down P gradient)
O2 dissolved bound to hemoglobin
each hemoglobin (Hb) can bind to 4 O2 molecules (1 O2/Fe)
Plateau on the O2 Hb dissociation curve (between 60 and 100 mmHg Po2)
= range of PO2 in lung at which Hb picks up O2 (Hb 97% saturated)
- if alveolar PO2 ⇓ a little below normal ⇒ little change in Hb saturation
- e.g. at high altitude ⇒ if alveolar PO2 above 60 mm Hg ⇒ Hb carries normal amount of O2
Steep portion on the O2 Hb dissociation curve at rest
- range of PO2 in tissues - O2 unloaded from Hb
- ISF PO2 = 40 mm Hg ⇒ Hb = 75% saturated (97-75 = 22% unloaded to cells)
- allows holding of breath
Steep portion on the O2 Hb dissociation curve at high metabolism
(e.g. exercise): ISF PO2 = 20 mm Hg ⇒ Hb = 40% saturated (97% - 40% = 57% of O2 unloaded): or more
Shift to the right on the O2 Hb dissociation curve
for a given PO2, get less Hb saturation i.e. O2 unloads more easily/loads less easily
Shift to the right on the O2 Hb dissociation curve occurs when..
– ⇑ PCO2
– ⇓ pH (related to ⇑ CO2, also lactic acid) = decreased ability of O2 to bind to Hb when H+ is bound to globin (= Bohr effect)
– ⇑ temp.
§ All occur when ⇑ cell metabolism e.g. exercise - Hb releases more O2
Shift to the left on the O2 Hb dissociation curve
For a given PO2, get more Hb saturation i.e. O2 loads more easily/unloads less easily
Shift to the left on the O2 Hb dissociation curve occurs when..
– ⇓ PCO2
– higher pH
– ⇓ temp.
§ = conditions at lung (⇓ temp. due to evaporative cooling)
CO2 carried in 3 ways
- dissolved in plasma = 8%
- bound to hemoglobin = 20%
- as bicarbonate ions = 72%
CO2 dissolved in plasma at the lungs (external)
- alveolar PCO2 = 40 mmHg
- resting venous PCO2 = 45 mmHg
- arterial PCO2 = 40 mmHg
§ CO2 diffuses: capillary → alveolus
CO2 dissolved in the plasma at the tissue (internal)
- arterial PCO2 = 40 mmHg
- ICF PCO2 > 45 mmHg
- ISF PCO2 = 45 mmHg
- resting venous PCO2 = 45 mmHg
§ CO2 diffuses: cell → ISF → capillary
CO2 bound to hemoglobin
=carbamino Hb (CO2 on global) .CO2 binds to deoxyHb better than to oxyHb ∴ Hb binds CO2 readily at the tissues
CO2 carried as a bicarbonate can be either..
- inside RBC at tissues (high CO2)
- inside RBC at lungs
Respiratory centres in medulla
set rate ad depth of breathing
2 groups of neurons in the respiratoy centre of medulla
- ventral (VRG)
- dorsal (DRG)
VRG
generates rate, expiratory and inspiratory neurons
DRG
receives chemoreceptor input and modifies VRG output
Inspiratory neurons
impulses down spinal cord to the phrenic nerve (innervates diaphragm) or the thoracic nerves (innervate intercostals_
Expiratory neurons
fire to inhibit insp. neurons and expiration occurs passively
Quiet breathing VRG
- Insp. neurons active ∼ 2 sec = insp.
- expir. neurons inhibit inspir. neurons’ output ∼3 sec = expir.
- VRG also active for forced insp. and expir., to recruit the additional muscles
- respiration may cease if VRG damaged or suppressed e.g. by alcohol, morphine
Pontine respiratory centres
work w medullary centres to make breathing smooth, even. damage can cause gasping or irregular
Lung stretch receptors
in smooth muscle of bronchi and bronchioles. the Hering Breuer reflex
Voluntary control of respiration
- 1⁰ motor cortex to skeletal muscle (corticospinal pathway) and bypass medulla
- if medulla damaged, must remember to breathe
- hold breath - ⇑ PCO2 - medulla overrides voluntary control ⇒ breathe
Peripheral chemoreceptors
carotid and aortic bodies. not sensitive to P co2. very sensitive to H+, If blood H+ ⇑ (⇓ pH) ⇒ vent rate ⇑ (+ vice versa). PO2 - stimulates receptors when PO2 reaches ∼ 50-60 mmHg (end of plateau of Hb-O2 curve), emergency situation. PO2 ⇓ due to lung disease, low atm PO2
Central chemoreceptors- medullae oblongata (dominant control)
respond indirectly to arterial P co2. resting arterial P co2 = 40 mmHg. (set point 37-43) CO2 crosses blood brain barrier easily (H, HCO3 don’t). CSF poorly buffered, small change is stim response
Hyperventilation
⇓ arterial PCO2 ⇒ cerebral vasocon (intrinsic metabolic response) ∴ ⇓ PO2 to brain ⇒ dizziness
Hypoventilation
⇑ arterial PCO2, ⇑ H+ = acidosis ⇒ CNS confusion
CO poisoning
CO binds 210x more strongly to Fe than O2 – forms carboxyHb (HbCO), result: ⇓ total O2. no change in PO2 or PCO2 (dissolved gases) ∴ ventilation rate doesn’t change
CO in environment
incomplete burning of gas (cars, furnaces), coal, wood, cigarettes