Respiratory adaptions DSA Flashcards
what will the RQ be in a diabetic/hypoglycemic patient?
0.7- relying solely on FFA
what is the normal RQ?
0.8
what is the RQ of a patient on IV glucose solution?
1.0
what happens when the V/Q ratio decreases?
perfusion (adding CO2 to alveoli and removing O2) is happening quicker than ventilation
this decrease in O2 in the alveoli leads to an decrease in arterial O2 (PaO2) along with an increase in arterial CO2
ventilation is not keep up with metabolic needs
what happens when there is an increase in V/Q?
increase in ventilation and a decrease in perfusion
increase in PAO2 and therefore an increase in PaO2
decrease in PACO2 and PaCO2
ventilation is in excess of metabolic needs
what is V/Q in pulmonary embolism and what are the effects?
V/Q becomes very low or essentially 0
the blood will be very oxygenated, however very little of it and leads to low blood volume
wasted energy by giving blood to this dead alveolar space
** I think it starts out high V/Q and then compensatiion happens (discussed in other lecture) leads to low V/Q
what is V/Q in choking or an allergic reaction and what effects does it have?
V/Q is low or close to zero
blood coming to lungs but cant get oxygenated so it looks like venous blood
wasted energy getting blood to the non funcitoning lungs–> physiological shunt (anatomic is when blood physically cannot get to lungs)
what is V/Q in COPD or emphysema?
some areas of body get hight V/Q and others low
some alveoli are large and arent near blood vessels (less O2 leaving blood) but some alveoli are getting too much blood, along with the destruction of capillaries (less CO2 being put into lungs)
V/Q mismatches contribute to hpoxia and hypercapnia
what is respiratory quotient?
relationship between O2 and CO2 in tissues where this exchange occurs
RQ= VdotCO2/ VdotCO2
**Vdot= volume per unit time
How is alveolar PO2 calculated and each of the equations individual components?
PAO2= inspired oxygen- oxygen consumed
** difference between amount of O2 in alveoli and amount of O2 consumed by tissues
inspired oxygen= difference between atmospheric pressure (780 mm Hg) and water vapor added by airways before reaching alveoli (about 47 mm Hg) multiplied by percent oxygen in atmosphere (21%)
oxygen consumed= measured by amount of CO2 produced (40 mm Hg) and RQ –> PaCO2/RQ
should be a little under 100 mm Hg
how does body compensate in low V/Q?
hypoxic conditions–> vasocontricts (decrease blood flow/perfusion to hypoxic regions)
how does body compensate in high V/Q?
bronchocontstricts to decrease ventilation in areas of alveolar dead space (not receiving blood)
what is hyppoxic hypoxia?
PaO2 is low because of low PAO2 or blood cant form an equilibrium with air because of a diffusion impairment (emphysema or fibrosis or low environment oxygen)
what is anemic hypoxia? what causes it?
lungs work fine but the blood loses O2 carrying capacity
can be caused by anemia or carbon monoxide poisoning which leads to build up of CO2 that has much higher affinity for Hb
what is circulatory hypoxia? what causes it?
lungs and blood capacity are just fine but the heart is unable to deliver blood to tissues
could be due to clot or sickle cell anemia
what is histotoxic hypoxia? what can cause it?
lungs, blood capacity, and heart working just fine. there is oxygen there but the tissues are unable to use it becuase of poison
cyanide can cause this
what is direct stimulus to increase firing rate of central chemoreceptors?
what happens when they are stimulated?
H+ ions in CSF
carbonic anhydrase produces both HCO3 and H+ ions which then the choroid will separate (HCO3 goes to CSF to reset pH and H+ go to blood to be excreted—> raises the pH of CSF)
once pH has been adjusted, firing rate returns to normal levels
in the early stages of COPD, when PaO2 and PaCO2 are low, will ventilation increase or decrease?
will his H+ concentration be lower or higher?
increase to keep oxygen levels up
lower (less CO2 means less H+)–> will increase pH
when ventilation increases, futhering the decrease in PaCO2 (resulting in hypocapnia), how do the chemoreceptors reset to bring PaCO2 back up? why do they need to do this?
make CSF more acidic (to get back to normal value) due to the choriod plexus putting more H+ ions into blood (or less HCO3)
works thru carbonic anhydrase
CO2 and O2 are low which has counter effects… need to increase O2 levels overrides that of CO2
how do the central chemoreceptors compensate in chronic hypercapnia?
choroid plexus adds more bicarbonate to CSF (while H+ ions excreted from kidney)
what are the 3 steps that are in response to acute hypoxia (min-hrs) (n regards to both COPD and increase in altitude?
- increase in ventilation due to increase of peripheral chemoreceptors firing (they detect low PaO2)
- PaO2 increases and PaCO2 decreases
- decrease PaCO2 decreases firing of central chemoreceptors
what are the three events that take place in acclimization (chronic hypoxia/hypocapnia)?
**due to the immediate effects of hypoxia, ventilation has been increased which has in turn decreased PaCO2
- choroid plexus will reset CSF to produce more H+ ions and less HCO3, which will in turn allow the body to continue increasing ventilation
- kidney releases more erthyropoientin–>stimulates bone marrow to produce more RBC’s–> increases hematocrit–> increases O2 carrying capacity in blood
- cells increase their number of mitochondria which allows for more anaerobic glycolysis
how does cerebral vasculature respond to altitude sickness?
dilate the vessels with local factors—> increase perfusion therefore increases filtration—> produces cerebral edema (especially if autoregulation/downstream vasocontriciton not working)
how are the lungs impacted by altitude sickness?
increased pulmonary vascular permeability—> pulmonary edema
also pulmonary hypertension due to local hypoxic vasoconstriction which causes more work for right ventricle
