Gas Exchange Flashcards
anatomy of the pulmonary interface
- THIN endothelial cytoplasm of the T1P
- THIN basal lamina (connective tissue between the cells)
- THIN endothelial cytoplasm of the capillary
physiology of the pulmonary interface
propertities of diffusion
gas exchange is a passive process of diffusion
gas goes from high to low concentrations
diffusion is proportional to
- pressure gradient
- cross-section involved
- soluable gas
diffusion is inversely proportional to
- the distance in which it must travel
explain how the partial pressures of gases change depending on their location during ventilation
atmosphere: PPO2 = 21% (160)
alveoli: immediately will equilibriate with the arterial pressure (as it passes by in the capillary)
brings oxygen to the tissues and takes the co2
venous PP will be higher in CO2 and lower in O2 and deliver the CO2 out
what is aedquacy of ventilation
how does the breathing (respirations) match up to the metabolic need for gases
** defined in terms of CO2**
define hypoventilation & hyperventilation
hypoventiliation: increase in CO2 production in which the alveolar ventilation cannot keep up –> PaCO2 increased
hyperventilation: alveolar ventilation is increased in comparison to the CO2 production –> PaCO2 decreased
** carbon dioxide diffuses at a much faster rate than oxygen does **
what is diffusion capactiy and how is it influenced
the ability of the pulmonary interface to exchange gases over a set amount of time
** this value can change depending on demand for gas exchange**
influenced by…
- ventilation changes
- thickness of the membrane where diffusion occurs
- changes in circulatory renewal (cant get RBC there –> cannot diffuse gases)
clinical examples of…
- changes in ventilation that will effect diffusion capacity
-environmental pressure (sea level vs. Vail)
- obstruction in the airway (FB)
- bronchoconstriction (asthma)
clinical examples of…
- changes in membrane thickness that will effect diffusion capacity
- added secretions in the alveolar surface (pneumonia, pulmonary edema)
- reductions in the overall respiratory surface (emphysema, TB)
clinical examples of…
- changes in circulatory renewal that will effect diffusion capacity
- circulatory failure (HF)
- pulmonary emboli (blocks the flow)
define the ventilation/perfusion ratio
Va/Q
the relationship between the rate that the alveoli is ventilating gas in relation to the flow of the blood through the lungs
– better match = better perfusion and exchange of gas to the blood
what is often the probelm with ventilation/perfusion ratios
** not poor oxygen**
a mismatch between the perfusion of blood and the ventilation of gas from the alveoli
- poor ventilation: a lack of the air getting to the pulmonary interface –> the PERFUSION is okay (blood still got there) but no gas exhcange could occur –> results in shunting of blood ( deO2 blood) to the heart
** cannot be fixed by increasing O2** - poor perfusion: a lack of blood flow getting to the alveoli –> the VENTILATION is okay but there is no blood to exchange the gas with
** can be fixed by increasing O2 because it will flow to other areas and oxygenate the blood**
approximate values for Va/Q
(vary by lung region?)
Va/Q varies by region of the lung
- average: ventilation 4.5L/min & perfusion 5L/min == Va/Q = .9
why might the Va/Q be low?
- poor ventilation (most commonly)
- ** ex. (3.0/5 =.6 instead of .9)**
- excessive blood flow
what is shunting
movement of unoxygenated blood through the capillaries back to the heart
happens when there is a LOW Va/Q because there is improper ventliation –> cannot exchange gas to the blood
leads to a hypoxemic state
why might the Va/Q be high?
what is the result or possible negative outcome?
- high ventilation
- poor perfusion (most common)
** blood not getting to the interface**
results in….
- increases oxygen tension in the alveoli (no one to pass the O2 to!)
- can create environment for infections to occur (TB, bacterial infections, etc.)
factors of the circulation that can impact transport of oxygen
- circulatory renewal –> how fast the blood is passing through the capillary
- hemoglobin affity of oxygen
how long is RBC in capillary? how long does it take for gas to diffuse?
RBC in capillary for .8-.9 seconds
takes O2 .3 seconds to diffuse
** overlap leads to ensuring that the gas is exchanged –> think of exercise**
how does oxygen travel through the blood?
- small % in the plasma dissolved in solution
- majority bound to Hgb
** when taking a PaO2 = getting the plasma amount of O2 which estimates amount in Hgb**
hemogobin strucutre, function and relationship with oxygen
4 heme complexes
each heme = 1 O2 to bind
4 o2 per 1 Hgb
2 polypeptide alpha chains
2 polypeptide beta chains
oxyhemoglobin: Hgb with O2
deoxy-hemoglobin : not fully saturated with O2
approx. 20.1 mL of O2 in 3 oz. of saturated RBC Hgb
what is the relationship between PaO2 and Hgb saturation with O2
the amount of O2 in the liquid plasma drive the amount of O2 bound to Hgb
- high amounts of O2 in the plasma –> increase Hgb O2 (increased affinity for O2)
- low amounts of O2 in the plasma –> decrease Hgb O2 (decreases affinity for O2)
** this relationship is sigmoid –> in that if we dont have a lot of O2 in the plasma – we dont what to hoard it in the hgb –> we want to dump it and give it to the tissues who are needing it **
explain the oxygen-Hgb dissociation curve
- normal arterial oxygen: 98% O2 sat & 104 mmHg ppO2
- normal venous oxygen: 75% O2 sat & 40 mmHg ppO2
- as arterial blood leaves the lungs it drops off the oxygen to the tissues and then venous blood has less
- blood gives approx. 25% of O2 from the Hgb to the tissues
- a small decrease in the partial pressure of O2 will significantly decrease the % sat. of Hgb
how does the Oxygen-Hgb curve chnage with increase metabolic activity
- greater demand for O2
- blood still has approx. 98% Hgb sat.
- Hgb might give up more than the typical 25% of O2 to the tissue
- if it gives up more O2 –> the partical pressure of O2 in the venous blood will be less than normal 40
- then it will recover and repeat itself
how does the oxygen-hgb curve change with increase (H+) acidity
increased acidity will shift the curve to the RIGHT
- Hgb will dump its O2 sooner than normal to attempt to combat the acidity of the blood
** because the Hgb will bind to the free H+ and decrease the acidity**
how does the oxygen-hgb curve change with carbon dioxide
increased Co2 – increases acidity –> shift curve right & O2 will dump off Hgb sooner
decrease Co2 –> shift curve left & Hgb will take up more O2 (since theres a lot)
how does the oxygen-hgb curve change with temperature
increased temp: shift curve to the right –> dump O2 sooner
** sepsis, fever, etc.**
decreased temp: shift curve to the left –> take up more O2 sooner
how does the oxygen-hgb curve change with 2,3 DPG
2,3 DPG: enzyme in the RBC which is released during hypoxic conditions
- when hypoxic , 2,3 DPG released –> triggers a shift of the curve to the right –> influences the Hgb to dump O2 sooner to release it to the tissues
** made in RBCs, triggers a decreased affinity for O2 in Hgb (binds irreversibly)
abnormalities of Hgb and its role in O2
anemias, thalassemias, sickle cell & polycythemia impact the Hgb ability to bind and impact oxygen carrying capacity
anemias & thalassemias : decreases carrying capacity (becuse decreased Hgb, or wrong Hgb with less affinity, or hemolysis of Hgb/RBC)
carboxyhemoglobin
- carbon monoxide has a HIGH affinity for Hgb (more than O2)
- binds to same site as O2 –> kicks off O2 & impossible to get it off
how is carbon dioxide transported thorugh blood
how does Hgb play a role?
- some in solution
- some as carbonic acid (H2CO3)
- some on Hgb
- MOST: as bicarbonate (HCO3-)
becomes bicarb. via carbonica anhydrase enzyme which drives the process of creating CO2 –> HCO3-
- the H+ that is a result of creating HCO3- is bound to Hgb to buffer the blood and avoid the build up of H+ to make acidic
