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transportation of oxygen in the body
diffuses from alveoli to blood
primarily bound to hemoglobin
transportation of carbon dioxide
produced through metabolism
diffuses out of cells and into alveoli
partial pressure drives
movement of gases across cell membranes
hypoxic hypoxia
low arterial PO2
histotoxic hypoxia
failure to use O2 and metabolic poisons
anemic hypoxia
decreased Hb-O2 and blood loss
Ischemic hypoxia
reduced blood flow, heart failure, shock, and blood clot
factors influencing alveolar gas exchange
alveolar PO2 levels, Alveolar ventilation, Altered O2 levels, and diffusion of oxygen
Alveolar PO2 levels
adequate O2 has to reach alveoli and composition of inspired air
Alveolar ventilation
decreased compliance, increased resistance, and CNS depression
Diffusion of oxygen between alveoli and blood
respiratory membrane, surface area, partial gradients, permeability, and distance
respiratory membrane
Type I pneumocytes and capillary endothelium
gas solubility
how easily gas moves from air to liquid phase
O2 solubility
low
CO2 solubility
high
Emphysema
destruction of alveoli leading to less surface area for gas exchange, and PO2 normal or low
Pulmonary Edema
fluid in interstitial space increases diffusion distance causing higher solubility of CO2 in water and normal arterial PO2
fibrotic lung disease
thickened alveolar membrane slows gas exchange and loss of lung compliance causes decrease in alveolar pressure
asthma
increased airway resistance decreases alveolar ventilation
oxyhemoglobin
hemoglobin binds to 4 O2 molecules
Hb saturation
amount of O2 bound to Hb
Normal arterial PO2 saturation
98%
resting cell PO2 saturation
75%
exercising muscle PO2 saturation
35%
how pH affects hemoglobin-oxygen binding
decreased pH facilitates unloading of oxygen
transport of CO2 in blood
CO2 diffuses out of cells into systemic capillaries
7% of CO2 remains dissolved in plasma
¼ of CO2 binds to hemoglobin
70% of CO2 load is converted to bicarbonate and H+
HCO-3 enters plasma in exchange for Cl-
at lungs dissolved CO2 diffuses out of plasma
CO2 unbinds from hemoglobin and diffuses out of RBC
carbonic acid reverses pulling bicarbonate back into RBC and converting back to CO2
peripheral chemoreceptors
carotid and aortic bodies and glomus cells activated by low PO2 levels
Glomus cells activation
close O2 sensitive K+ channels
cell depolarizes
open v-g Ca2+ channels
causes exocytosis
NT diffuses to sensory neuron
action potential
Central chemoreceptors
in medulla and control centers monitoring CO2 levels
a decrease in CO2 levels
slows ventilation
and increase in CO2
speeds up ventilation