gas exchange Flashcards
composition of the air we breathe
78 percent nitrogen
21 percent oxygen
0.033 percent carbon dioxide
dalton’s law
the total pressure exerted by a mixture of gases is the sum of pressures exerted by all individual gases
the pressure exerted by an individual gas is called the partial pressure of that gas
total air pressure equation
Patm = PN2+PO2+PCO2
total air pressure equation in humid air
Patm=PN2+PO2+PCO2+PH20
total partial pressure in dry air equation
Pgas= Patm x % of gas in atmosphere
total partial pressure in humid air equation
Pgas= (Patm-PH2O)x % of gas in atmosphere
gas composition in the atmosphere of O2 and CO2
PO2= 160 mm Hg
PCO2= 0.25 mm HG
alveolar partial pressures during normal quiet breathing
PO2= 100 mm Hg
PCO2 = 40 mmHg
as alveolar ventilation increases alveolar PO2 _______ and PCO2 ______
increases, decreases
explain pulmonary gas exchange and transport
- Oxygen enters the blood at alveolar-capillary interface
- oxygen is transported in blood dissolved plasma or bound to hemoglobin inside RBCS
- oxygen diffuses into cells, cellular respiration determines metabolic CO2 production
- CO2 diffuses out of the cells
- CO2 is transported, dissolved, bound to hemoglobin or as HCO3-
- CO2 enters alveoli at alveolar-capillary interface
what is the rate of diffusion directly proportional to
concentration (partial pressure) gradient
AxDx (delta Pgas)/ T^2
partial pressures in venous blood
O2: 40 mm Hg
CO2: 46 mm Hg
partial pressures in arterial blood
O2: 100 mm Hg
CO2: 40m HG
partial pressures in cells
O2<= 40 mm Hg
CO2> = 46 mm Hg
what is alveolar gas exchange influenced by
oxygen reaching alveoli: composition of inspired air; alveolar ventilation - rate and depth of breathing, airway resistance, lung compliance
gas diffusion between alveoli and blood: SA, diffusion distance - barrier thickness and amount of fluid
adequate perfusion of alveoli
factors that decrease the amount of oxygen in the blood
insufficient exchange
hypoxia
low oxygen in the atmosphere
low alveolar ventilation: decreased lung compliance (how easily they can expand), increased air resistance, CNS depression: drugs, alcohol overdose
emphysema
affects elastance (lose it)
destruction of alveoli means less SA for gas exchange
oxygen is normal or low (Po2 low)
affects SA and partial pressure gradient in ficks law
ie/ from smoking
astma
increased histamine
increased airway resistance, decreases alveolar ventilation
bronchioles constricted
increased resistance, decreased airflow
affects partial pressure gradient
fibrotic lung disease
thickened alveolar membrane shows gas exchange. loss of lung compliance may decrease alveolar ventilation
PO2 low
build up of scar tissue around alveoli by particulate irritants ie/ asbestos
affects distance (scar tissue build up) and partial pressure gradient (decreased in compliance)
pulmonary edema
fluid in interstitial space increases diffusion distance. Arterial PCO2 may be normal due to higher CO2 solubility in water
increase in interstitial fluid is often a result of heart failure
affects distance in fick’s law
name the four pathological conditions that cause hypoxia
emphysema
astma
fibrotic lung disease
pulmonary edema
what happens at equilibrium to partial pressures
they are equal
what is more soluble O2 or CO2
CO2
what happens to concentrations at equilibrium
they are unlikely to be equal
Hemoglobin
found in rbs
reversibly binds to O2 - unbuckling when o2 is low and loads up when high
each hb molecule has the ability to bind to 4 o2 molecules
total O2 in blood equation
amount dissolved in plasma + amount bound to hemoglobin
Po2 value at the resting cell
40 mm Hg (unloads at tissure)
Po2 value at alveoli
100 mm Hg (loads at lungs)
why does the O2-Hb dissociation curve plateau
all hemoglobin will all eventually be bound to O2
what would happen if oxygen binding to hemoglobin was not cooperative
hemoglobin would just hang onto oxygen
curve would be hyperbolic
what happens to affinity when pH is low
reduces oxygens carrying capacity of Hb
oxygen dissociates more at the tissues
what happens when PCO2 is increased
oxygen dissociates more at tissues
O2 transport in blood
98 percent bound to hemoglobin - then will transport to cells, HbO2->Hb+O2, oxygen then dissolved in plasma and then used in cellular respiration
2 percent dissolved in tissues - will just stay dissolved in plasma
In lungs: PO2 is high, drives oxygen exchange into plasma, high plasma PO2 drives oxygen binding to Hb. forward reaction dominates
In tissues: PO2 is low, drives oxygen exchange out of plasma, low plasma PO2 drives O2 release from hemoglobin, reverse rxn dominates
CO2 transport in blood
7% dissolved gas in plasma
23% as HbCO2, not binding just hitches a ride, gets transported to the lungs then CO2 diffuses out to the plasma and then alveolus
70% as bicarbonate dissolved in plasma
CO2 + H2O <—> H2CO3(carbonic acid) <—>H+ + HCO3-
carbonic anhydrase enzyme
H+ buffered by Hb in rbcs
respiratory acidosis
excess H+ present
central chemoreceptors
located in medulla
increased activity in response to increase PCO2
resulting in increased rate and depth of respiration
peripheral chemoreceptors
located in carotid sinuses and aortic arch
increased activity in response to increased PCO2 and H+ concentration or decreased PCO2
afferent signals back to respiratory control center of medulla oblongaae, resulting in increased rate and depth of respiration
