respiratory physiology Flashcards
anatomic dead space begins in the mouth and ends in the
terminal bronchioles (also called the conducting zone)
gas exchange occurs across the _______________ (type of cell) in the respiratory zone by _______________
flat epithelium (type 1 pneumocytes)
by diffusion
pneumonic for exhalation and muscles utilized:
I let the air out of my TIRES
Transverse abdominis
Internal oblique
Rectus Abdominis
External Oblique
where are the two parts of the airway where you will find cartilage
trachea and bronchi (NOT the bronchioles)
does the conducting zone participate in gas exchange
no because it is anatomic dead space
TPP (trans pleural pressure) =
alveolar pressure - intrapleural pressure
transpulmonary pressure is always
positive
intrapleural pressure is always
negative
alveolar ventilation =
(tidal volume - dead space) x RR
in a healthy adult, the normal dead space is
2mg/kg (or 150mL for 70kg)
how does atropine increase anatomic dead space
it is a bronchodilator so it increases the volume of the conducting zone
dead space is reduced by anything that does these 2 things (and 3 examples)
reduces conducting volume or increases pulmonary blood flow
ex) LMA, ETT, neck flexion
anatomic dead space definition and example
air confined to the conducting airways
example: nose and mouth to terminal bronchioles
alveolar dead space definition and example
alveoli that are ventilated but not perfused
example: decreased pulmonary BF
physiologic dead space definition and example
anatomic Vd and alveolar Vd
ex: variable
apparatus dead space definition and example
Vd added by equipment
ex: face mask, heat and moisture exchanger
Vd/Vt ratio definition
the fraction of Vt that contributes to Vd
in the circle system, dead space begins at the
y piece
the bohr equation compares
partial pressure of CO2 in the blood versus partial pressure of CO2 in exhaled gas
the bohr equation itself
Vd/Vt = (PaCO2 - PeCO2) /PaCO2
in the textbook patient, ventilation is ___L/min and perfusion is ___L/min
ventilation is 4L/min
perfusion is 5L/min
ventilation is greatest at the lung base due to
high alveolar compliance
perfusion is greatest at the lung base due to
gravity
what does HPV minimize
shunt aka zone 3 (not dead space)
Law of laplace
P=2T/R
pressure, tension, radius
with no surfactant, there is an increase in ___________ and likelihood that alveoli will collapse
surface tension
does each alveolus contain the same amount of surfactant?
yes, the concentration just varies
zone 1
dead space
PA>Pa>Pv
zone 2
waterfall (V/Q =1)
Pa>PA>Pv
-BF is directly proportional to the difference in Pa-PA
zone 3
shunt (V/Q=0)
Pa>Pv>PA
zone 4
pulmonary edema
Pa>Pis>Pv>PA
alveolar gas equation
FiO2 x (Pb-PH2O)-(PaCO2/RQ)
FiO2 x (760-47)-(____/.8)
how respiratory quotient (RQ) is calculated
= CO2 production / O2 consumption
= 200mL/250mL
=.8
hypoxemia is when PaO2 is technically <
<80
what is the A-a gradient of a healthy patient breathing room air?
105-95=10mmHg
things that increase A-a gradient include (4)
aging (closing capacity increases relative to FRC)
vasodilators (decreased HPV)
right to left shunt (atelectasis, PNA, intubation, intracardiac defect)
diffusion limitation (alveocapillary thickening)
shunt increases by what percent for every 20mmHg of A-a gradient
1%
ex) If Aa gradient is 218mmHg, then 218/20 ~11% shunt
normal IRV
3,000
normal ERV
1100
normal RV
1200
norrmal Closing volume
~30% TLC by age 20
~50% TLC by age 70
normal TLC and what its comprised of
5.8L
IRV + TV + ERV + RV
normal VC and what its comprised of
4.5L
IRV + TV + ERV
normal IC and what its comprised of
3.5L
IRV + TV
normal FRC and what its comprised of
2.3L
RV + ERV
normal closing capacity composition
RV + CV
VC = _______ mL/kg
65-75
FRC can be measured indirectly by (3)
nitrogen washout
helium wash in
body plesmythography
normal FRC mL/kg
35
time until patient desaturates equation
FRC/VO2 (O2 consumption)
when FRC is reduced, which west zone increases
west zone 3 (shunt)
factors that increase closing volume
CLOSE-P
COPD
Left ventricular failure
Obesity
Surgery
Extremes of age
Pregnancy
oxygen content equation (CaO2)
(1.34 x HGB x SaO2) + (PaO2 x .003)
oxygen delivery equation (DO2)
CaO2 x CO x 10 OR
CaO2 x (HR x SV) x 10
after oxygen diffuses through the capillary membrane, it is transported in the blood in 2 ways
- reversibly binds with HGB (97%)
- Dissolved in plasma (3%)
each gram of HGB molecule can carry how many molecular mL of O2?
1.39 (but since all HGB carry some metHGB or carboxyHGB, thats why you see 1.34)
VO2 (O2 consumption) equation
=CO x (CaO2 - CvO2) x 10
VO2 = _______ mL/kg/min or ______ mL/min (assumes 70kg male)
3.5mL/kg/min
250mL/min
decreased P50 = shift to the
left on the oxygHGB curve
ex)HgbF
increased P50 = shift to the
right on the oxyHGB curve
when PaO2 is >100mmHg, what happens to the O2 in the body
no additional O2 will bind to HGB but it will continue to dissolve in blood
define bohr effect
Bohr effect happens in BLOOD
CO2 and H+ cause conformational change in HGB to facilitate O2 release of O2.
AKA increased partial pressure of CO2 and decreased pH causes HGB to release O2
O2 OFFLOADING
what happens to 2,3 DPG in banked blood
concentration falls and shifts O2/HGB dissociation curve to the left and reduces amount of O2 available at tissue level
when is 2,3 DPG produced
during RBC glycolysis
does HgbF respond to 2,3 DPG?
no, which explains why it has a left shift (p=19mmHg)
what happens during glycolysis
glucose –> pyruvic acid
1. 1 glucose molecule becomes 2 pyruvic acid molecules. (in the presence of O2, pyruvic acid is transported to mitochrondria. without O2 available, pyruvic acid becomes lactate in the cytoplasm)
2. the 2 pyruvic acid are converted to 2 acetyl coenzyme A
-2,3 DPG is produced about half way through glycolysis which is why increased glycolysis means increased 2,3 DPG
what is the ATP net gain during glycolysis and the krebs cycle
2 ATP
krebs cycle (citric acid cycle)
- oxaloacetic acid and acetyl coenzyme A react to produce citric acid in matrix of mitochondria.
- reaction ends with production of oxaloacetic acid, NADH, and CO2
- goal is to produce large quantity of H+ in form of NADH because its used for electron transport
oxidative phosphorylation (and net gain)
- NADH is split into NAD, H+ and 2 electrons
- a gradient is generated which causes ATP synthesis with the help of ATP synthase
- O2 serves as final electron acceptor
- end product is 34 ATP and H2O
primary byproduct of aerobic metabolism
CO2
how is CO2 transported in the blood? (3)
- as bicarbonate (70%)
- bound to HGB as carbamino compounds (23%)
- dissolved in plasma (7%)
describe Haldane effect
CO2 loading on HGB. O2 causes erythrocyte to release CO2
what is the reaction for carbonic acid buffer r/t bicarbonate
H2O + CO2 <-> H2CO3 <-> H+ + HCO3-
what is needed to facilitate the carbonic acid buffer
carbonic anhydrase (facilitates creation of carbonic acid)
when talking about the solubility of CO2 relative to O2, which law is being referenced
henrys law (solubility)
deoxygenated HGB causes CO2 dissociation curve to shift to the
left
when referencing CO2 dissociation curve, explain the left shift
blood has increased affinity for CO2. we are referencing deoxygenated HGB.
- lower PO2 means more CO2 is carried
when referencing CO2 dissociation curve, explain the right shift
blood has a decreased affinity for CO2. we are referencing oxygenated HGB.
-higher PO2 means less CO2 is carried.
where in the body is the CO2 dissociation curve right shfited
lungs
where in the body is the CO2 dissociation curve left shifted
capillaries
PaCO2=
CO2 production / alveolar ventilation
hypercapnia and K
activates H/K pump
buffers CO2 in exchange for releasing K into the plasma
primary internal monitor of PaCO2
central chemoreceptors in medulla
secondary monitors of PaCO2
peripheral chemoreceptors in aortic bodies and transverse aortic arch
MV increases with PaCO2 in a linear fashion when PaCO2 is between
20-80mmHg
a left shift in the CO2 ventilatory response curve implies that the apneic threshold has
decreased
a right shift in the CO2 ventilatory response curve implies that the apneic threshold has
increased
what is the respiratory pacemaker
dorsal respiratory center (in NTS of medulla)
where does neural control of ventilation take place
medulla
function of, location of pneumotaxic center
inhibits DRG, located in upper pons
triggers end of inspiration by inhibiting DRG
function and location of ventral respiratory group
located in the medulla
primarily active during expiration, has pre botzinger complex
function and location of apneustic center
in lower pons
stimulates DRG (stimulates pacemaker), causes inspiration.
action is inhibited by pulmonary stretch receptors (J receptors)
what can and cant diffuse through BBB
CO2 can, H+ and HCO3- cannot
primary stimulus at central chemoreceptor
H+
if H+ cant pass through BBB, how can is stimulate central chemoreceptor
CO2 + H2O combine to become H+ and HCO3-
what does the carotid body monitor for
hypoxemia (PaO2 < 60mmHg)
(secondary responsibilities include monitoring for PaCO2, H+ and perfusion pressure)
hypoxic ventilatory response to hypoxemia
- PaCO2 <60mmHg closes oxygen sensitive K channels in type 1 gloms cells
- raises RMP, opens Ca2+ channels, increases neurotransmitter release (Ach and ATP)
- AP propagated among herrings nerve (CN9)
- afferent pathway terminates in inspiratory center in medulla)
- MV increases to restore PaO2
which reflex prevents alveolar over distention
hering breuer INFLATION reflex
which reflex is initiated when lung volumes are too small
Hering breuer DEFLATION reflex
HPV occurs due to a reduction in
alveolar oxygen tension (NOT arterial PO2)
drugs that can inhibit HPV
gases
vasodilators
PDE inhibitors
dobutamine
CCB’s
vasoconstrictive agents (neo, epi, dopa), may constrict well oxygenated vessels and increase shunt flow
which conditions decrease O2 carrying capacity but do not initiate HPV response
anemia
carbon monoxide poisoning
what does this graph tell us
towards the apex: V>Q
towards the base: V < Q
label this graph
what does increased Vd do to the PaCO2 EtCO2 gradient and CO2
widens gradient, increases CO2 retention
VA is inversely proportional to
PaCO2. higher CO2 creates faster and deeper breathing thereby increasing VA (alveolar ventilation aka MV without dead space)
CV v CC
CV: when dynamic compression of aw begins (CLOSE-P)
closing capacity: CV+RV. Volume of gas contained in lungs when airways begin to collapse
which principle calculates O2 consumption
Ficks (VO2 is the difference between the amount of O2 that leaves the lungs and the amount of O2 that returns to the lungs)
VO2= CO x (CaO2-CvO2) x 10
what happens to 2,3 DPG in banked blood and what does it do to the oxyhgb curve
decrease in 2,3 DPG and curve shifts to the left
what is the energy currency in the body
ATP
a more acidic environment and Bohr v Haldane
bohr enhances O2 offloading from Hgb (Bohr effect) and co2 loading onto Hgb (haldane)
solubility is a function of which law (and example)
henrys
solubility of CO2 is 0.067
CO2 ventilatory response curve describes relationship between
PaCO2 and MV
what is the primary monitor of PaCO2
central chemoreceptor in medulla
MV increases with PaCO2 in a linear fashion when it’s between
20-80mmHg
left shift and increased slope in CO2 ventilatory response curve creates what
respiratory alkalosis
right shift and decreased slope in CO2 ventilatory response curve creates what
resp acidosis
a left shift in the CO2 ventilatory response curve implies that the apneic threshold has
decreased (things that make you breathe a lot to create that resp alkalosis on the left side)
a right shift in the CO2 ventilatory response curve implies that the apneic threshold has
increased (things that make you breathe less to cause that resp acidosis on the right side)
5 causes of hypoxemia and how A-a gradient is affected
normal A-a
- reduced FiO2 (hypoxic mixture)
-hypoventilation (opioid OD)
increased A-a
-diffusion limitation (p.fibrosis)
-V/Q mismatch (COPD)
-shunt (R-L, intracardiac)
