Test 2: 22+23 Flashcards
pressure in lungs at inspiration vs expiration
inhale: -5
exhale +5
why do alveoli change size
to control ventilation/perfusion: V/Q
lung areas more dorsal and caudal have larger aveoli- ribs in that area are more flexible and diaphragm curved= moves more
vs
lung areas ventral and cranial are smaller, ribs sturdier and diaphragm moves less
how do alveolar size and blood flow allow for V/Q matching in lungs
dorsal alveoli are bigger and get more blood
while ventral alveoli are smaller and only a small amount of blood is brought there
how does alveoli stretching effect blood flow
inhale causes vessels to contract leading to RBC getting stuck/staying still
exhale- capillaries open and blood is pulled in
pumping mechanism
Hypoxic Pulmonary Vasoconstriction (HPV)
small pulmonary arteries constrict in the presence of alveolar hypoxia (low oxygen levels). By redirecting blood flow from poorly-ventilated lung regions to well-ventilated lung regions, HPV is thought to be the primary mechanism underlying ventilation/perfusion matching
Hypoxic Pulmonary Vasoconstriction (HPV) is controlled by — channels
voltage dependent Calicum
active mechanism
less O2 to area causes increased Ca into the cell that cause vasoconstriction
more blood to high O2 areas, less blood to low O2 area → VQ matching
what happens to alveoli when in dorsal recumbancy
weight of horse cause dorsal alveoli to collapse
ventral lung areas still not that great
central part of the lung now does most of the work (central shifting)
Hypoxic Pulmonary Vasoconstriction (HPV) does not work during anesthesia (drugs prevent Ca channel from working) →VQ mixmatch
how does increasing FiO2 fix VQ mixmatch
normal air 21% O2 →normal PaO2= 110mmHg
when you increase O2 to 100% → PaO2 = 670 mmHg
can overcome hypoxia
be careful of oxygen toxicity and resportion atelectasis
The problems with increasing the FiO2 to 100% are
oxygen toxicity and resorption atelectasis
explain resorption atelectasis on 100% FiO2
normally O2 and Nitrogen inhaled- O2 is absorbed into blood but Nitrogen stay in alveoli and keep them open
if you increase FiO2 - then only O2 is inhaled and then all the O2 moves into the blood and alveoli collapse cause they are empty
two drugs to improve pulmonary perfusion during anesthesia in dorsal recumbancy
acepromazine- cause vasodilation: Because of the impaired perfusion in non-dependent, upper lung areas the effect of acepromazine on these lung areas is stronger leading to a relative shift of blood to these lung areas.
positive inotropic drug like dobutamine to increase cardiac output, therefore general perfusion and therefore pulmonary perfusion. Again, the effect might be on all lung areas but the strongest on poor perfused areas.
how does inhalation of nitric oxide effect ventilation
local vasodilation
By inhaling NO, the NO reaches only ventilated lung areas (because its inhaled!!!) and crosses the alveolar barrier. Therefore, is causes only vasodilation at ventilated lung areas leading to a blood shift to these lung areas.
effect lasts 20-25 secs
$$ and need special machines
three ways to improve V/Q mixmatch
increase FiO2
improve bloodflow- acepromazine, dobutamine, NO, albuterol
improve ventilation-
why not useinhalation of β2-mimetic drugs like albuterol/salbutamol to improve perfusion
works but lasts longer in body and can cause systemic vasodilation
— is a simple way to improve ventilation
reverse trendelenburg/ recumbency
reduce the amount of pressure on lung field= better ventilation
This way the pressure from the abdominal organs on the thorax and lungs is reduced and the likelihood of atelectasis formation reduced.
