Pulmonary Blood Flow, Ventilation and Perfusion -Karius Flashcards
normal CO
3.5 L/min - 5.0 L/min
Hypoxia response of the pulmonary circulation
vasoconstriction
Hypoxia response of the systemic circulation
vasodilation
PvO2
PvCO2
PvO2 : 40mmHg
PvCO2: 45mmHg
PaO2
PaCO2
PaO2 : 100mmHg
PaCO2 : 40mmHg
what causes vasoconstriction in pulmonary circulation during hypoxia
SM of pulmonary tissues do it themselves to direct blood to areas of good gas exchange
steps in vasoconstriction of the pulmonary vessels
- low O2
- K + leak channels open
- depolarization
- opens Ca+2 LCAT channels
- more depolarization to SM contractions
- vasoconstriction
where do alveoli get blood from and then they go where
the RV —-> LA
where do bronchial (extra-alveolar) capillaries get their blood from
and then they go where
LV * to supply the lung tissues that are far from the alveolar capillaries
—-> 1. Azygous V (–> RA), 2. LV = venous admixture
how to calculate pulmonary BP
CO x PVR(pulmonary vascular Resistance)
= 25/15mmHg (lower then systemic TPR)
BP and capillaries that are open relationship
the more capillaries that are open the lower the PVR
PVR during exercise
decreases due to more capillaries that are open
PVR relationship with lung volume
at very high lung volumes (a lot of air) + at very long lung volumes (Chest wall pushes in)
= Resistance increases because the capillaries get compressed when tissues are stretched or pushed in
main cause of pulmonary HTN
vasoconstriction
(in COPD/emphysema) you also see low SA and capillaries and alveoli die = also increases gas volume inside = increases resistance
what brings blood back up to the heart when knees are not locked
skeletal muscle pump pumping blood back up to the heart and prevents decrease in venous return
3 zones of the lung ZONE 1 alveoli size BF BP and Ps
Zone 1 : apex (biggest avloli, least amount of BF, smallest BP
PA > Pa > Pv
*Pa is close to 140mmHg
3 zones of the lung ZONE 2 alveoli size BF BP and Ps
Zone 2 : middle
medium sized alveoli, normal BF, normal BP equal to BP at level of the heart
Pa> PA > Pv
*Pa is close to 100mmHg
3 zones of the lung ZONE 3 alveoli size BF BP and Ps
Zone 3: base smallest alveoli highest BF highest BP Pa > Pv > PA *Pa is close to 40mmHg
NO function
Para—-> vasodilate
SM relaxation
PULMONARY FLOW, decreases PVR
Endothelin 1 funciton
made in lung
vasoconstrictor , usually under not normal conditions or disease
Thromboxane A2 function
vasoconstrictor not normal conditions
usually during inflammation
reason you would want to prone a patient
patient has a hard time getting O2 to all parts of the body
prone the Pt and gravity will push chest in = increase PVR = increases BF and BP in pulmonary circulation (more O2 is picked up)
pneumonia and pulmonary edema do what to O2 to cross the wall
the fluid build up in the capillary and prevents the O2 to cross since it doesn’t dissolve in fluid
water leakage from capillaries to alveoli
should not happen , stopped by starling forces and lymphatics
biggest starling force in the lung
Pc (hydrostatic capillary)
Ptissue
tissue hydrostatic P pushing water from alveoli to the capillary
= -5mmHg (fluid goes into alv), *since Pil is -5
which starling forces make fluid go to the alv
Pc
Ptissue (-5mmHg)
pi tissue
with net filtration of water into alv in lungs , how is O2 able to cross the alveolar wall and do gas exchange
LYMPHATICS , get rid of fluid in the interstitium so it doesnt go into the alv
ACE has 2 roles
- converts angiotensin 1 –> angiotensin 2 (increase aldosterone and BP)
- inhibit bradykinin production
those who are placed on ACE inhibitors can develop what
what would be an ideal drug to take if this happens
- lowered BP AND
cough up excess bradykinin made - angiotensin 2 inhibitor (only lowers BP) =ARB
how are immune cells and products from inflammation removed from our circulation
PGE, leukotriens, Thromboxane A2 are removed by lungs
LUNGS METABOLIZE ARACHIDONIC ACID
what is PIo2
inpired o2 pressure accounting for water vapor also
PIo2 = (760mmHg - 47mmHg) x %o2
normal percent o2
normal water vapor P
21%
47mmHg
normal R value
0.8
= V(dot)aCO2 / V(dot)O2 = (200ml/min) / (250ml/min)
** How to calculate PAo2 (amount of O2 partial pressure in alveoli)**
= alveolar gas equation
reason this is important
PAo2 = PIo2 - (PaCO2 / R)
important to see if alv is damaged (if PAo2-Pao2 is greater then 20 = damage, diffusion impairment)
normal A-a O2 gradient
difference between the Pa and PA shoudl be less then 20mmHg
LUNG ZONES (zone 1) Pip PaO2 PaCO2 V/Q ratio
Pip = -10mmHg (due to less intrapleural fluid)
PaO2 = 130mmHg
PaCO2 = 28mmHg
V/Q ratio = high (3.0)
LUNG ZONES (zone 1) Pip PaO2 PaCO2 V/Q ratio
Pip = -5mmHg
PaO2 = 100mmHg
PaCO2 = 40mHg
V/Q ratio = 0.8
LUNG ZONES (zone 1) Pip PaO2 PaCO2 V/Q ratio
Pip = -2 to -3mmHg (due to more intrapleural fluid)
PaO2 = 89mmHg
PaCO2 = 42mmHg
V/Q ratio = low (0.6)
apex of the lung : how does the Pip change with inhalation
the Pip is already very negative and the alv is big
= when inhaling only small amount of air can enter
base of the lung : how does the Pip change with inhalation
the Pip is more positive and alv are smaller in size
= when inhaling the alveoli can get a lot bigger
what is a normal V/Q ratio and how was it calculated
V= 4L/min (ventilation) Q = 5L/min (perfusion = also cardiac output) normal = 0.8
what does it mean if you have a high V/Q
low V/Q
high V/Q = more air then blood
low V/Q = more blood then air
what are the PaO2 and PaCO2 and PAo2 and PAco2 when V/Q = 0.8
PaO2 = 100mmHg (equilibrilize) PaCO2 = 40mmHg (equilibrilize) PAo2 = 100mmHg PAco2 = 40mmHg
what are the PaO2 and PaCO2 and PAo2 and PAco2 when V/Q = high due to very little blood coming to the alveoli
PaO2 = 150mmHg (only very little blood) PaCO2 = 1mmHg (only very little blood) PAo2 = increase 150mmHg PAco2 = decrease 1mmHg
what are the PaO2 and PaCO2 and PAo2 and PAco2 when V/Q = low, due to V=0 blockage in airway
ORIGINALLY
*blood keeps coming to deliver CO2 and take O2 from the alv PaO2 = 80mmHg (equilibrilize) PaCO2 = 42mmHg (equilibrilize) PAo2 = decrease to 80mmHg PAco2 = increase to 42mmHg
what are the PaO2 and PaCO2 and PAo2 and PAco2 when V/Q = low, due to V=0 blockage in airway
AFTER A WHILE OF THIS
*blood keeps coming to deliver CO2 and take O2 from the alv, however there is not mich more to take and deliver since everything is at equilibrium PaO2 = 40mmHg (equilibrilize) PaCO2 = 45mmHg (equilibrilize) PAo2 = decrease to 40mmHg PAco2 = increase to 45mmHg
after a while of having blockage in airway what does that represent to the blood
like a shunt bypassing lungs since its not able to pick up O2 or drop of any CO2 to the alv
when V/Q = high due to very little blood coming to the alveoli
what happens to OVERALL BODY PaO2 and PaCO2 and then the PAo2 and PAco2
* done by majority of blood passing lungs and not reaching any alv = LOW V/Q PaO2 = 80mmHg (equilibrilize) PaCO2 = 42mmHg (equilibrilize) PAo2 = decrease 80mmHg PAco2 = increase 42mmHg
how does the V/Q change during COPD/emphysema
more air trapping due to many alv walls broken down and capillaries that have died = less blood in these dead areas
V/Q = INCREASED in areas that are dead (no BF)
MOST BLOOD floods areas that are not dead = CAUSING OVERALL LOW V/Q (most of lung is having low V/Q)
=lowered gas exchange
how to minimize the difference in V/Q in different areas of the lung in a patient with COPD/emphysema
Hypoxic vasoconstriction
redirect blood from areas that are hypoxic in the lung (for improved O2 exchange)