38. Small Group: Respiratory Failure Flashcards
If resp failure were due to CNS depression what would we expect in terms of ventilation, PC02, and A-a difference?
hypoventilation, high PC02, and normal A-a difference
if we give 100% 02 to a patient with low P02 and it does not improve, what is the dx?
shunt.
if a patient’s low P02 and Aa difference are due to VQ mismatch, what will supp 02 do to the P02?
raise it.
what would be differences in clinical sx between CHF and ARDS?
might be the same: CXR, resp mechanics, and gas exchange qualities.
different: edema fluid would be more proteinaceous with ARDS (due to cap damage rather than hydrostatic pressure)
also with CHF, tx with a diuretic would help.
what does a high plateau pressure indicate?
either the compliance is low or we are at very high tidal volume (where it is hard to continue to stretch)
what are 3 causes of loss of compliance in ARDS?
loss of surfactant, interstitial edema, distribution of entire tidal volume to a small # of alveolar units.
how to decrease plateau pressure?
incr lung compliance (good luck), reduce tidal volume so you don’t get to the fully-distended point.
what is represented by the difference between peak airway pressure and the plateau pressure (on ventilation)?
the pressure needed to overcome flow resistance.
how do I calc minute ventilation?
resp rate x tidal volume
can we assess the adequacy of gas exchange simply by looking at the p02 or PC02 values?
NO, because we may be able to maintain a patient with normal P02 and PC02 values, but if we need to triple minute ventilation to achieve this then there is a problem.
a normal PC02 that can only be achieved by high minute ventilation may indicate what?
a high % dead space
can we compensate for high PC02 due to increased dead space by incr ventilation? why?
yes because the relationship between PC02 and C02 content is linear (as opposed to oxygen, which is sigmoidal)
in the setting of ARDS, the loss of surfactant and presence of interstitial and alveolar edema cause what?
tendency of lungs to collapse, so that many lung units are poorly ventilated or not at all.
how does PEEP help with ventilation?
maintains alveoli open that might otherwise have a tendency to collapse upon expiration.
why is NO best delivered via inhalation? what might happen if it were delivered IV?
via inh because it will then have the greatest effect in areas that are well-ventilated already. if given IV, will cause a general vasodilation which might actually cause further mismatch (if we vasodilate areas that are not now perfused)
