Unit 1 - Respiratory Physiology Flashcards
what is tidal volume?
the amount of gas that is inhaled and exhaled during a breath
where does Vt go when you take a breath?
- part goes to the respiratory zone, where gas exchange occurs
- remainer sits in conducting zone (dead space)
normal dead space in a healthy ~70 kg adult
~2 mL/kg or 150 mL
normal removal of gas with exhalation
- conducting zone gas removed first
- followed by exhalation of respiratory zone gas
consequence of any condition that increases dead space
makes it more difficult to eliminate expiratory gases from lungs
- widens PaCO2-EtCO2 gradient
- causes CO2 retention
what is ventilation rate
volume of air moved into and out of lungs in a given period of time
what is minute ventilation (VE)?
amount of air in a single breath (Vt) multiplied by RR
what is alveolar ventilation?
fraction of VE that is available for gas exchange
= (Vt - Vd) x RR
calculating VA in relation to PaCO2
= CO2 production / PaCO2
VA is directly proportional to:
CO2 production
- higher CO2 production stimulates body to breathe deeper and faster to eliminate more CO2
VA is inversely proportional to:
PaCO2
- faster and deeper breathing reduces PaCO2
How does Vd (dead space) affect the PaCO2-EtCO2 gradient?
any condition that increases dead space also increases the gradient
how does atropine affect the PaCO2-EtCO2 gradient
increases
- bronchodilator, so it increases anatomic dead space by increasing volume of the conducting zone
how does hypotension affect PaCo2-EtCO2 gradient
increases
- reduced pulmonary blood flow = increased alveolar dead space
how does PPV affect PaCO2-EtCO2 gradient?
increases
- increases alveolar pressure, which increases ventilation relative to perfusion (dead space increases)
examples of decreased dead space
reduced by anything that reduces the volume of the conducting zone or increases pulmonary blood flow
- ETT
- LMA
- neck flexion
what is anatomic dead space?
air confined to conducting airways
nose & mouth to terminal bronchioles
what is alveolar dead space?
examples?
alveoli that are ventilated but not perfused
decreased pulmonary blood flow
what is physiologic dead space?
anatomic Vd + alveolar Vd
what is apparatus dead space?
examples?
Vd added by equipment
facemask, HME
what is the dead space to tidal volume ratio (Vd/Vt)
fraction of Vt that contributes to dead space
Vd to Vt ratio in spontaneously ventilating 70 kg pt
Vd/Vt = 150 mL/450 mL = 0.33
why does mechanical ventilation increase the Vd/Vt ratio to 0.5 (50%)?
mechanical ventilation increases alveolar pressure, which increases ventilation relative to perfusion
most common cause of increased Vd/Vt under GA
reduced CO
r/o hypotension with acute EtCO2 decrease before considering other causes of increased dead space
what does it mean if something increases Vd?
more of the Vt is lost to dead space and alveolar ventiltion will decrease
what does it mean for something to decrease Vd
less of the Vt is lost to dead space; alveolar ventilation will increase
how does an LMA reduce Vd
it bypasses much of the anatomic Vd between the mouth and glottis (similar to ETT)
how does neck position affect Vd
- extension = increased Vd
- flexion = decreased Vd
how do surgical positions affect Vd
- sitting: increased
- supine, trendelenburg: decreased
how to maintain a constant PaCO2 with increased dead space
increase minute ventilation (RR, Vt, or both)
why do patients with chronic bronchitis retain CO2?
Vd/Vt ratio is increased
(minute ventilation must increase to 30-50 L/min to maintain a normal PaCO2 - difficult to maintain)
where does dead space begin in a circle system
at the y-piece
does increasing the length of the circuit impact dead space?
no - anything proximal to the y-piece does not influence dead space, nor does increasing the length of the circuit
when can the proximal circle circuit become dead space?
incompetent valve - the entire limb with the faulty valve becomes apparatus dead space
what is the equation used to calculate physiologic dead space?
Bohr equation
compares PaCO2 in the blood vs. PCO2 in exhaled gas (greater difference in values = greater amount of dead space)
Bohr equation
Vd/Vt = (PaCO2 - PeCO2) / PaCO2
gross estimation of dead space
difference between PaCO2 and EtCO2
ventilation and perfusion values in the textbook patient
normal V/Q ratio in this patient?
ventilation is 4 L/min
perfusion is 5 L/min
V/Q - 0.8
what is alveolar compliance
a change in alveolar volume for a given change in pressure
what part of the lungs contain the largest alveoli?
the alveoli near the apex
how does volumetric change affect alveolar ventilation
an alveolus that undergoes a greater degree of volumetric change during a breath is going to be better ventilated (aka better gas exchange) vs. smaller degree of volumetric change
compliance =
change in volume/change in pressure
in what part of the lung is ventilation the greatest
lung base d/t higher alveolar compliance
in what part of the lungs is perfusion the greatest
lung base
d/t gravity
alveoli with the poorest ventilation
alveoli in the apex bc they have the poorest compliance
alveoli with the greatest ventilation
alveoli in the base
why are there higher V/Q ratios towards the apex and lower ratios towards the base
- gravity and hydrostatic pressure affect distribution of blood flow to the lung
- when standing upright, there’s less blood flow towards apex of lung and more blood flow towards the base
how is ventilation affected in the apex of the lungs in the upright position and in the non-dependent lung in lateral position
- decreased alveolar ventilation
- decreased alveolar compliance
- decreased PACO2
- increased PAO2
how is ventilation affected in the base of the lungs in the upright position and dependent lung in lateral position
- increased alveolar ventilation
- increased alveolar compliance
- increased PACO2
- decreased PAO2
how is perfusion affected in the nondependent lung in lateral position and in the apex of the lung in upright position
- decreased blood flow
- decreased vascular pressure
- increased vascular resistance
how is perfusion affected in the dependent lung in lateral position and base of lung in upright position
- increased blood flow
- increased vascular pressure
- decreased vascular resistance
dependent and non-dependent lung regions in sitting position
dependent: base
non-dependent: apex
dependent and non-dependent lung regions in supine position
dependent: posterior
non-dependent: anterior
dependent and non-dependent lung regions in left lateral position
dependent: left lung
non-dependent: right lung
dependent and non-dependent lung regions in right lateral decubitus
dependent: right lung
non-dependent: left lung
how does V/Q mismatch normally affect the A-a gradient
usually increases
what determines the final partial pressures of oxygen and carbon dioxide in the bood
balance between ventilation and perfusion in each unit and throughout the lung
V and Q in apex and base of lungs in sitting position
apex: V > Q
base: Q > V
Q=
pulmonary blood flow or cardiac output
most common cause of hypoxemia in PACU
V/Q mismatch (specifically atelectasis)
consequences of decreased FRC with anesthesia and surgery
- less radial traction to keep airways open
- atelectasis, R-L shunt, V/Q mismatch, hypoxemia
treatment of V/Q mismatch d/t atelectasis
- humidified O2
- maneuvers to reopen airways (mobility, coughing, deep breathing, incentive spirometry)
consequences of V/Q mismatch in underventilated alveoli
blood passing through underventilated alveoli tends to retain CO2 and can’t take in enough O2
consequences of V/Q mismatch in overventilated alveoli
blood passing through tends to give off excessive amount of CO2
oxyhemoglobin dissociation curve with overventilated alveoli
- flat curve (blood can elminate a large amount of CO2 but can’t take up a proportionate amount of O2)
- once PaCO2 reaches 100 mmHg, hgb is fully saturated and any additional O2 in blood must be dissolved in blood
(alveolus can transfer much more CO2 than it can O2)
why does the PACO2-PaCO2 gradient usually remain small with V/Q mismatch
a lung with V/Q mismatch eliminates CO2 from overventilated alveoli to compensate for underventilated alveoli
why is the PAO2-PaO2 gradient usually large with V/Q mismatch
a lung with V/Q mismatch can’t absorb more oxygen from overventilated alveoli to compensate for underventilated alveoli
how does the body compensate for V/Q mismatch
- bronchioles constrict to minimize ventilation of poorly perfused alveoli
- HPV reduces pulmonary blood flow to poorly ventilated alveoli to combat shunting
what does V/Q = infinity mean
dead space
what does V/Q = 0 mean
shunt
variables in the law of Laplace
- tension
- pressure
- radius
describes the relationship between pressure, radius, and wall tension
law of Laplace
equation for tension in a cylinder
examples
pressure * radius
ex. blood vessels, cylindrical aneurysms
equation for tension of a sphere
examples
(pressure * radius) / 2
ex. alveoli, cardiac ventricles, saccular aneurysm
according to the law of Laplace, the tendency of an alveolus to collapse is directly proportional to:
surface tension
more tension = more likely to collapse
according to the law of Laplace, the tendency of an alveolus to collapse is indirectly proportional to:
alveolar radius
smaller radius = more likely to collapse
why are alveoli prone to collapse?
they’re coated with a thin layer of water, which increases surface tension and promotes collapse
function of surfactant
modulates surface tension and prevents alveolar collapse
which alveoli have more surfactant?
each alveolus has the same amount of surfactant
what variable impacts the concentration of alveolar surfactant
radius
what prevents smaller alveoli from collapsing and emptying into larger alveoli
as radius changes, so does concentration of surfactant - this keeps alveolar pressures constant
when do type 2 pneumocytes start producing surfactant
when does production peak
22-26 weeks gestation
peaks at 35-36 weeks
what determines the V/Q ratio of each alveolar unit
relative pressures between alveolus (PA), arterial capillary (Pa), venous capillary (Pv), and interstitial space (Pist)
Pa, Pv, and PA in all 4 lung zones
1: PA > Pa > Pv
2: Pa > PA > Pv
3: Pa > Pv > PA
4: Pa > Pis > Pv > PA
which lung zone usually does not occur in a normal lung
zone 1 (dead space)
ventilation without perfusion
???
what factors increase zone 1 (dead space)
- hypotension
- PE
- excessive airway pressure
compensation for zone 1 (dead space)
bronchioles of unperfused alveoli constrict to reduce dead space
in which zone does V/Q = 1
zone 2
ventilation and perfusion (V/Q = 1)
how is it possible for a zone 2 unit to transiently change to zone 1 or zone 3
because pulmonary capillary pressure and alveolar pressure change throughout the respiratory cycle
relationship between blood flow and Pa/PA
- blood flow is directly proportional to the difference in Pa - PA
- the greater the differences between Pa-PA, the greater the blood flow
why should the tip of a PAC be placed in zone 3
the pressure in the capillary is always higher than the alveolus, so the vessel is always open and blood is always moving through it
what is an anatomic shunt?
any venous blood that empties directly into the left side of the heart (bypasses lungs and never has opportunity to saturate with O2)
sites that contribute to normal anatomic shunt
- thesbian veins (drain L heart)
- bronchiolar veins (drain bronchial circulation)
- pleural veins (drain bronchial circulation)
classic example of zone 4
pulmonary edema
2 phenomena normally responsible for pulmonary edema
- fluid is pushed across capillary mebrane by significant increase in hydrostatic pressure (ex. fluid overload)
- fluid is pulled across capillary membrane by profound reduction in pleural pressure (NPPE)
purpose of alveolar gas equation
estimate the partial pressure of oxygen in the alveoli
how does supplemental oxygen affect hypoxemia and hypercarbia
- can easily reverse hypoxemia
- no effect on hypercarbia
what does the alveolar gas equation tell us about PAO2
the max PAO2 that can be achieved in a given FIO2
alveolar oxygen equation
FiO2 * (Pb - PH2O) - (PaCO2 / RQ)
- Pb = barometric pressure
- PH2O = humidity of inspired gas
- RQ = respiratory quotient
what is PH2O assumed to be
47 mmHg
what is RQ assumed to be
0.8
is FiO2 always higher or lower than partial pressure of O2 in alveoli? why?
always higher
- inspired air becomes 100% humidified as it moves towards alveoli, which dilutes O2 concentration
- inspired air mixes with expired air, which dilutes the concentration of oxygen going toward alveoli
how does supplemental oxygen affect PaO2 and PAO2
can increase both
(masks hypoventilation, doesn’t treat cause)
what does an RQ > 1 suggest
- lipogenesis
- occurs with overfeeding
what does an RQ of 0.7 suggest
lipolysis
occurs with starvation
equation for RQ
CO2 production (200 mL/min) / O2 consumption (250 mL/min) = 0.8
5 causes of hypoxemia
- hypoxic mixture
- hypoventilation
- diffusion limitation
- V/Q mismatch
- shunt
what is the A-a gradient in hypoxic mixture and hypoventilation
normal
what PaO2 defines hypoxemia
< 80 mmHg
hypoxemia vs. hypoxia
- hypoxemia = low concentration of O2 in blood
- hypoxia = state of insufficient O2 to support tissues
does supplemental O2 fix A-a gradient in hypoxemia caused by a shunt
nope
what does a large difference in PAO2 and PaO2 imply
significant degree of shunt, V/Q mismatch, or diffuse defect across alveolar-capillary membrane
5 things that increase A-a gradient
- aging
- vasodilators
- R-L shunt
- diffusion limitations
- V/Q mismatch
why does aging increase the A-a gradient
closing capacity increases relative to FRC
how do vasodilators affect A-a gradient
increase due to decreased HPV
how does R-L shunt affect A-a gradient
increases d/t atelectasis, pneumonia, bronchial intubation, intracardiac defect
how do diffusion limitations affect the A-a gradient
increase d/t alveolarcapillary membrane thickening hindering O2 diffusion
how to calculate A-a gradient
PAO2 - PaO2
how to estimate degree of shunt in relation to A-a gradient
increases by 1% for every 20mmHg of A-a gradient
normal inspiratory reserve volume in a healthy 70 kg male
3,000 mL
what is IRV?
inspiratory reserve volume - volume of gas that can be forcibly inhaled after a tidal inhalation
what is Vt? what is normal Vt in 70 kg healthy male?
volume of gas that enters and exits lungs during tidal breathing
500 mL
what is ERV?
normal in healthy 70 kg male?
expiratory reserve volume - volume of gas that can be forcibly exhaled after a tidal exhalation
1100 mL
what is closing volume?
the volume above residual volume where the small airways begin to close
variable
- ~30% at age 20
- ~55% at age 70
what is RV?
what’s normal for a healthy 70 kg man?
residual volume - volume of gas that remains in lungs after a complete exhalation
1200 mL
-
-
can residual volume be exhaled from lungs?
no
what is total lung capacity
IRV + TV + ERV + RV
5800 mL in healthy 70kg male
what is vital capacity
IRV + TV + ERV
normal: 4500 mL
what is FRC
RV + ERV
lung volume at end expiration
normal: 2300 mL
what is closing capacity?
RV + CV
- absolute volume of gas contained in lungs when small airways close
normal vital capacity
65-75 mL/kg
lungs volumes in males vs. females
~25% smaller in females
lung volumes in patients with obstructive lung disease
increased RV, CC, and TLC d/t air trapping
can spirometry measure TLC or FRC?
no, since it can’t measure RV
dynamic measurements that assess small airway closure
closing capacity
closing volume
reservoir of oxygen that prevents hypoxemia during apnea
FRC
normal FRC
35 mL/kg
what is static equilibrium
at FRC, the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall
3 ways FRC can be indirectly measured
- nitrogen washout
- helium wash-in
- body plethysmography
how can we estimate the amount of time a pt can be apneic before desaturation
FRC / VO2
VO2 = oxygen consumption
what happens to zone 3 when FRC is reduced
increases (intrapulmonary shunt)
how do ARMs and PEEP restore FRC
by reducing West zone 3
how does general anesthesia affect FRC and why
- decreases
- diaphragm shifts cephalad ~4 cm d/t decreased insp muscle tone and increased exp muscle tone
FRC in obesity
decreased d/t decreased chest wall compliance and increased airway collapsibility
FRC in pregnancy
- decreased
- diaphragm shifts cephalad as a result of gravid uterus, decreased chest wall compliance
FRC in neonates
- decreased
- less alveoli = decreased lung compliance
- cartilaginous ribcage is prone to collapse during inspiration
FRC in advanced age
- increased
- dec lung elasticity = inc air trapping = inc RV = inc FRC
FRC in lithotomy and trendelenburg
decreased
in what positions is FRC increased
- prone
- sitting
- lateral
now do NMBs affect FRC
- decreased
- diaphragm shifts cephalad and decreases lung volumes
how does light anesthesia affect FRC
decreased d/t straining and forceful expiration causing decreased lung volumes
how do excessive IV fluids affect FRC
- decreased
- fluid accumulation in dependent lung regions favor zone 3 development
how does high FiO2 affect FRC
- decreased
- absorption atelectasis = shunt
suggested FiO2 to prevent absorption atelectasis
< 80% at emergence + PEEP or CPAP
how does PEEP affect FRC
increases d/t recruitment of collapsed alveoli, partially overcoming affect of GA, and decreased venous admixture = increased PaO2
how do sigh breaths affect FRC
increase (recruits collapsed aleoli)
6 factors that increase closing volume
CLOSE-P
- COPD
- LV failure
- Obesity
- Surgery
- Extremes of age
- Pregnancy
what determines if airways collapse during tidal breathing
- relationship between FRC and closing capacity
- normally, FRC > CC and airways don’t collapse during tidal breathing
what happens when CC > FRC
- airway closure occurs during tidal breathing
- contributes to intrapulmonary shunting and hypoxemia
when does airway closure occur in a young healthy pt vs. an older patient
- young & healthy: just above residual volume
- old: pleural pressure becomes progressively higher and small airwas close sooner and at higher volumes
what happens to FRC, CC, RV, and VC with aging
- increased FRC
- increased CC
- increased RV
- decreased VC
how do anesthesia and age affect closing capacity?
- by 30, CC ~ FRC under GA
- by 44, CC ~ FRC when supine
- by 66, CC ~ FRC when standing
how does increased CC relative to FRC affect oxygenation
anything that decreases FRC relative to CC or anything that increases CC relative to FRC will convert normal V/Q units to low V/Q units or shunt units
what is CaO2?
oxygen content - measure of how much oxygen is present in 1 deciliter (100 mL) of blood
how is O2 transported by the blood
- reversibly binds with hgb (97%)
- dissolves in plasma (3%)
calculation for CaO2
(1.34 * hgb * SaO2) + (PaO2 * 0.003) = 20 mL O2 per dL
theoretical max of molecular oxygen that can be carried by each gram of hgb
1.39 mL
- often see 1.34 because hgb usually contains a small amount of methemoglobin
normal hgb and hct values for men vs. women
men: 15 g/dL and 45%
women: 13 g/dL and 39%
how is O2 that is dissolved in plasma measured
PaO2
what should a PaO2 measurement be used to determine
gas exchange in the lungs, not as a measurement of oxygen content in the blood
what gas law explains O2 dissolving in the plasma
Henry’s law
solubility coefficient for oxygen
0.003 mL/dL/mmHg
what tells us how fast a quantity of o2 is delivered to tissues
oxygen delivery (DO2)
what is the driving mechanism of DO2
cardiac output
what principle is used to calculate oxygen consumption
fick’s principle/law
what does Fick’s law assume about VO2
- that it is the difference between amount of O2 that leaves the lungs and the amount of O2 that is returned to the lungs
- difference in values is the amount of O2 consumed by the body
equation for VO2
cardiac output * (CaO2 - CvO2) * 10
normal value for VO2
- 3.5 mL/kg/min
- approx 250 mL/min in healthy 70 kg male
what does the oxyhgb curve plot
hgb saturation (SaO2) vs. oxygen tension in blood (PaO2)
what is P50?
the PaO2 where hgb is 50% saturated with oxygen
what causes a decreased P50? what does this do to oxyhgb curve?
- left shift (hgb has a stronger bond on O2)
- ex. Hgb F, hypocarbia, carboxyhemoglobin
what causes increased P50? what does this do to the oxyhgb curve?
- shift to right (hgb more willing to release O2)
- acidosis, hyperthermia, increased 2,3 DPG
what does a left shift in the oxyhgb dissociation curve mean
- increased affinity of hgb to O2
- occurs in the lungs
left = love
what does a right shift of oxyhgb dissociation curve mean
- decreased affinity for O2 (right = release)
- occurs near metabolically active tissue
how does acidosis affect oxyhgb dissociation curve
right shift
what happens to the oxyhgb curve with increased and decreased P50
lower P50 = left shift
higher P50 = right shift
when does maximal O2 loading occur
PaO2 of ~100 mmHg
will FiO2 increase binding of O2 to hgb if PaO2 is already 105 mmHg?
no - further increase in Fio2 will increase amount of oxygen dissolved in blood but won’t increase binding
examples of common hemoglobinopathies
how do they affect the oxyhgb dissociation curve
left shift
- fetal hgb
- methemoglobin
- carboxyhemoglobin
what is the Bohr effect
CO2 and hydrogen ions cause a confirmational change in the hgb molecule and facilitates the release of O2
(increased partial pressure of CO2 and decreased pH cause Hgb to release O2)
what is 2,3-DPG?
- produced during RBC glycolysis
- maintains oxyhgb curve in slightly right shift at all times
- important compensation mechanism in chronic anemia
what happens to 2,3-DPG in hypoxia
increased production - facilitates O2 offloading
2,3 DPG concentration in banked blood
decreased - shifts oxyhgb dissociation curve to left and reduces amount of O2 available at tissue level
what explains why Hgb F has a left shift
Hgb F doesn’t respond to 2,3-DPG
1 molecule of glucose converts to ____ molecules ATP
38
what produces ATP
oxidation of proteins, carbs, and fats
primary substrate for ATP synthesis
glucose
which produces more ATP - aerobic or anaerobic metabolism
aerobic
primary goal of glycolysis
convert 1 glucose to 2 pyruvic acid molecules
what happens to pyruvic acid with and without oxygen
- no oxygen available = converted to lactate in cytoplasm
- oxygen available = transported into mitochondria
net gain of glycolysis
2 ATP
how does glycolysis affect 2,3 DPG
the more glucose molecules that go through glycolysis, the more 2,3 DPG is produced
where does the Krebs cycle take place
matrix of mitochondria
when does the Krebs cycle begin and end
- begins when oxaloacetic acid and acetylCoA react to produce citric acid
- ends with production of oxaloacetic acid, NADH, and CO2
primary goal of Krebs cycle
produce a large quantity of H+ ions in form of NADH - used in electron transport
net gain from krebs cycle
2 ATP
what happens to NADH in oxidative phosphorylation
split into NAD+, H+, and 2 electrons
what drives ATP synthesis
electrons from NADH split are fed into chemiosmotic mechanism, generating a proton gradient across membrane
has help from ATP synthase
net gain from oxidative phosphorylation
34 ATP
final electron acceptor in electron transport
oxygen
what is the lactic acid pathway
provides an alternative mechanism to convert pyruvic acid to ATP (just 2 molecules)
what is the basis of altered homeostasis in setting of acidosis
body’s enzymes tend to not function properly in acidic environment
how is serum lactate primarily cleared
liver
what causes lactic acid build up
if there is no oxygen to accept electrons in electron transport, pyruvic acid isn’t used and concentration increases
lactic acid pathway converts pyruvic acid into ATP
lactic acid is a byproduct of this pathway
primary byproduct of aerobic metabolism
CO2
how is CO2 transported in blood
- as bicarbonate (70%)
- bound to hgb as carbamino compounds (23%)
- dissolved in plasma
how is CO2 transported to lungs
venous blood
PvCO2 vs. PaCO2
PvCO2 is about 5 mHg higher than PaCo2
what is the Haldane effect
increased CO2 loading on hgb in acidic environment
what is carbonic anhydrase
an enzyme that facilitates formation of carbonic acid (H2CO3) from H2O and CO2
what does carbonic acid rapidly dissociate into
H+ and HCO3-
what buffers H+
hgb and HCO3-
what is the Hamburger shift
chloride shift
Cl- is transported into erythrocyte to maintain neutrality
how does the Hamburger effect impact venous circulation
chloride shift adds osmotically active ions (Cl-) to erythrocyte in venous cirulation. erythrocyte swells and cell volume is increased relative to plasma volume
- this explains why venous hct is ~3% higher than arterial hct
solubility coefficient of dissolved Co2
0.067 mL/dL/mmHg
solubility is a function of which gas law
Henry’s
what is the Haldane effect
- at a given PaCO2, deoxygenated hgb can carry more CO2
- in the presence of deoxygenated hgb, the CO2 dissociation curve shifts to the left
Bohr effect vs. Haldane effect
- Bohr: says that CO2 and decreased pH cause erythrocyte to release O2
- Haldane: says that O2 causes erythrocyte to release CO2 (deoxygenated blood can carry more CO2)
what happens to the CO2 dissociation curve in the presence of oxygenated hgb
- shifts to the right
- blood has decreased affinity for CO2
what happens to co2 dissociation curve in presence of deoxygenated hgb
- shifts to left
- blood has increased affinity for CO2
where does increased deoxygenated hgb occur
in systemic capillaries to facilitate loading and subsequent transport of CO2
where in the body is the CO2 dissociation curve right shifted
in the lungs to facilitate unloading of CO2 so it can be excreted
..
..
how does deoxygenated hgb shift the CO2 dissociation curve
left shift (blood can hold more CO2)
what is hypercapnia
PaCO2 > 45 mmHg
how is PaCO2 calculated
CO2 production / alveolar ventilation
3 causes of hypercapnia
- increased CO2 production
- decreased CO2 elimination
- rebreathing
examples of increased co2 production that cause hypercapnia
- sepsis
- overfeeding
- MH
- intense shivering
- prolonged sz activity
- thyroid storm
- burns
examples of decreased CO2 elimination that contribute to hypercapnia
- airway obstruction
- increased dead space
- increased Vd/Vt
- ARDS
- COPD
- resp center depression
- drug overdose
- inadequate NMB reversal
3 things that can cause rebreathing
- exhausted soda lime
- incompetent unidirectional valve in circle system
- inadequate FGF with Mapelson circuit
patho of hypoxemia with hypercapnia
increased alveolar CO2 displaces alveolar O2 and causes arterial hypoxemia
how does hypercarbia affect cardiac muscle
- myocardial depressant
- also activates SNS, increases catecholamine release from adrenal medulla
- SNS stim. offsets cardiac depression and vasodilatoin unless acidosis is severe
how does hypercarbia affect cardiac rate and rhythm
- tachycardia
- dysrhythmias
- prolonged QT
CO2 is a smooth muscle dilator. what’s the exception to this?
the pulmonary vasculature - increases PVR and right heart workload
how does hypercarbia affect minute ventilation
increases - CO2 is a resp stimulant
what happens to K+ in hypercarbia
increased - hypercarbia activates H+/K+ pump, which buffers CO2 acid in exchange for releasing K+ in plasma
calcium in hypercarbia and why
- increased
- iCa competes with H+ for binding sites on plasma proteins
how does hypercarbia affect heart in presence of acidosis
plasma proteins buffer H+ and release Ca2+, increasing inotropy and offsetting acidosis-induced cardiac depression
effect of increased Ca2+ in alkalosis
plasma proteins release H+ and Ca2+, which decreases inotropy
how does hypercarbia affect ICP
- increased ICP
- CO2 freely diffuses across BBB
- dec CSF pH = dec cerebrovascular resistance = increased CBF and volume
at what point does CO2 narcosis occur
PaCO2 > 90 mmHg
how does hypercarbia affect blood pH
- resp acidosis: kidneys excrete H+ and conserve bicarb to return pH to normal
- begins with hours
- full compensation may take several days
how does PaCO2 affect pH in acute respiratory acidosis
for every 10 mmHg increase above 40 mmHg pH decreases by 0.08
how does PaCO2 affect pH in chronic respiratory acidosis
for every 10 mmHg increase above 40 mmHg, pH decreases by 0.03 due to HCO3- retention in the kidneys
what is the primary monitor of PaCO2
central chemoreceptor in medulla
what plays a secondary role in monitoring PaCo2
peripheral chemoreceptors in carotid bodies and transverse aortic arch
when PaCO2 is between ___ and ___, minute ventilation increases in a linear fashion
20-80 mmHg
what is a MAC of CO2
200 mmHg
causes of a right shift of the CO2 ventilatory response curve
- metabolic alkalosis
- CEA
- natural sleep
- volatiles
- opioids
- NMBs
causes of a left shift of the CO2 ventilatory response curve
- hypoxemia
- metabolic acidosis
- surgical stim
- CNS etiologies: inc ICP, fear, anxiety
- salicylates
- aminophylline
- doxapram
- norepinephrine
what do a left shift and increased slope of CO2 ventilatory response curve indicate
- Vm is higher than expected for a given PaCO2
- creates respiratory alkalosis
what is apneic threshold
highest PaCo2 at which a person won’t breathe
what is implied by a right vs left shift of CO2 ventilatory response curve
- left: implies apneic threshold has decreased
- right: implies apneic threshold has increased
what is the pacemaker for normal breathing?
dorsal respiratory center
new evidence: pre-Botzinger complex
primarily responsible for expiration
ventral respiratory center
where is neural control of RR and pattern
respiratory center in medulla
where is chemical control of RR and pattern
- central chemoreceptors in medulla
- peripheral chemoreceptors in carotid bodies/aortic arch
where does the resp center receive afferent input
- central and peripheral chemoreceptors
- stretch receptors in lungs
where do efferent respiratory center pathways terminate
diaphragm, intercostals, and accessory muscles
where is the respiratory center located
in RAS in medulla and pons
primary job of respiratory center
determine RR and depth
4 components of the respiratory center
- pneumotaxic center
- apneustic center
- dorsal respiratory group
- ventral respiratory group
when is the dorsal respiratory group primarily active
during inspiration
where are the pneumotaxic and apneustic centers located
pons
- pneumotaxic: upper
- apneustic: lower
what does the pneumotaxic center do
inhibits DRG ( inhibits pacemaker)
what does the apneustic center do
stimulates DRG (stimulates pacemaker)
where are central chemoreceptors located
just a few microns below surface of anterolateral aspect of medulla
function of central chemoreceptors in medulla
- respond to PaCo2 indirectly
- sends stimulatory impulses to dorsal respiratory center
CO2, H+, HCO3- and the BBB
- CO2 freely diffuses
- H+ and HCO3- do not
most important stimulus for central chemoreceptor
hydrogen ion concentration in CSF
what drives the respiratory pacemaker in the dorsal respiratory center
H+
what happens to H+ with an acute rise in PaCO2
increased H+ in CSF and increased Vm (Ve)
what happens to H+ with an acute decline in PaCO2
decreased H+ in CSF and decreased Ve
do non-volatile acids affect Ve?
- on a short term basis, no (don’t pass BBB)
- on a long term basis, yes
how long does HCO3- equilibration between blood and CSF take
begins after a few hours and peaks at ~2 days
does hyperventilation affect PaCO2?
effect limited to the time before HCO3- equilibrates between blood and CSF (~ 2 days)
what happens to pH of CSF after equilibration of HCO3-
restored to normal (7.32) as a result of active transport of HCO3- from plasma to CSF
what stimulates and depresses central chemoreceptor
- stimulated by hypercarbia and hypoxemia
- depressed by profound hypercarbia and hypoxenia
what is the primary stimulus at the central chemoreceptor?
H+
If H+ can’t pass through the BBB, how does it stimulate the central chemoreceptor?
CO2 diffuses across BBB and spontaneously combines with H2O to become H+ and HCO3-
what do the central chemoreceptors primarily respond to?
peripheral ?
central - PaCO2
peripheral - PaO2
what are type 1 glomus cells
- sensors that transduce PaO2 into an action potential
- mediate hypoxic drive
what is the afferent limb of carotid chemoreceptors
- Hering’s nerve
- glossopharyngeal nerve (CN 9)
how does CEA affect function of peripheral chemoreceptors
impairs function on operative side
chief responsibility of the carotid body
monitor for hypoxemia
(don’t respond to SaO2 or CaO2)
secondary responsibilities of carotid body
- monitoring PaCo2
- monitoring H+
- perfusion pressure
PaO2 < ____ closes oxygen-sensitive K+ channels in type 1 glomus cells
60 mmHg
steps of the hypoxic ventilatory response
- PaO2 < 60 mmHg closes O2-sensitive K channels in type 1 glomus cells
- RMP increases, Ca2+ channels open, inc release of ACh and ATP
- AP propagated along Hering’s nerve to CN 9
- afferent pathway terminates in inspiratory center in medulla
- minute ventilation increases to restore PaO2
why can’t we do bilateral CEA simultaneously or close together
CEA severs afferent limb of hypoxic respiratory response - takes the body time to recalibrate
why is postop hypoxia not always countered by reflexive increase in minute ventilation
- subanesthetic doses (0.1 MAC) of inhalation and IV anesthetics depress HPV
- volatiles impair diaphragmatic, intercostal, and upper airway muscle function
name 2 conditions that affect tissue oxygenation that do not impair HPV
anemia and carbon monoxide poisoning
how do the carotid bodies respond to oxygen
they increase minute ventilation when PaO2 < 60 mmHg
purpose of Hering-Breuer inflation reflex
prevents alveolar overdistention by stopping inflation when lung volume is too large
how do the lungs influence respiratory control
stretch receptors transduce pressure conditions in the airway and transmit this information along CN 10 to dorsal respiratory center
when does the Hering-Breuer inflation reflex “turn off” the dorsal respiratory center
when lung inflation is > 1.5 L above FRC (x3 normal Vt)
is Hering-Breuer inflation reflex active during normal inspiration
nope
what is the Hering-Breuer deflation reflex
- stimulates the patient to take a breath when lung volume is too small
- helps prevent atelectasis
function of J receptors
- activated by things that Jam traffic in pulmonary vasculature (PE or CHF)
- stimulation causes tachypnea
what is the paradoxical reflex of head
causes a newborn baby to take first breath
steps of the Hering-Breuer inflation reflex
- central respiratory activity
- phrenic nerve activity to diaphragm
- inspiration stops
- lung inflation > 1.5 L
- vagus nerve stim
- inspiratory off switch
only region in the body that responds to hypoxia with vasoconstriction
pulmonary vascular bed
function of HPV
- within seconds, selectively increases PVR in poorly ventilated areas to minimize shunt flow to these regions
- full effect in about 15 minutes
how do anesthetics affect HPV
- volatiles > 1.5 MAC reduce effectiveness
- IV anesthestics do NOT affect HPV
how do vasodilators, PDE inhibitors, dobutamine, and some calcium channel blockers affect HPV?
increase shunt flow by inhibiting HPV
how do phenylephrine, epinephrine, and dopamine affect HPV
constrict well-oxygenated vessels and increase shunt flow
how does volume status affect HPV
- hypervolemia (LAP > 25 mmHg) and elevated CO may distend constricted vessles and increase shunt flow
- hypovolemia may cause pulmonary vasoconstriction to well ventilated alveolar units
2 critical functions of ventilation
- deliver O2 to hgb to support aerobic metabolism
- eliminate CO2 from blood
muscles of expiration
TIREs
Transverse abdominis
Internal oblique
Rectus abdominis
External oblique
function of diaphragm and external intercostals during inspiration
contraction
when does exhalation become active
- when minute ventilation increases
- pts with lung disease (COPD)
vital capacity required for an effective cough
at least 15 mL/kg
which airway division is anatomic dead space
conducting zone
parts of airway in conducting zone
- trachea
- bronchi
- bronchioles
where does the conducting zone begin and end
- begins at nares
- ends with terminal bronchioles
last structures perfused by bronchial circulation
terminal bronchioles
what does the transitional zone contain
respiratory bronchioles
function of transitional zone
dual function: air conduit and gas exchange
airway zone in which gas exchange takes place
respiratory zone
where does the respiratory zone begin and end
- begins at alveolar ducts
- extends to alveolar sacs
why are bronchioles and alveolar ducts susceptible to external compression
they don’t contain cartilage
what is transpulmonary pressure
alveolar pressure - intrapleural pressure
is TPP positive or negative with airway collapse
negative
TPP during tidal breathing
always positive
TPP at FRC
+5
TTP and airflow during expiration
TTP = +7
airflow = in
TTP and airflow during end inspiration
TTP = +8
airflow = none
TTP and airflow during quiet expiration
TTP = +6
airflow = out
TTP and airflow during forced expiration
TTP = -1
airflow = out
muscles of inspiration
- diaphragm
- external intercostals
- anterior scalene
- posterior scalene
- sternocleidomastoid
normal A-a gradient breathing room air
15 mmHg
2 etiologies of hypoxemia with normal A-a gradient
low FiO2
hypoventilation
supplemental O2 can improve oxygenation in all causes of hypoxemia except
shunt
A = IRV
B = FRC
C = IC
D = VC
3 key processes involved in aerobic glucose metabolism
glycolysis
Kreb’s cycle
electronic transport
cells that mediate HPV
type 1 glomus cells
peripheral chemoreceptors in carotid body primarily respond to:
PaO2
predicted PaO2 by age
110 - (age * 0.4)
primary determinant of CO2 elimination
alveolar ventilation
A = insp reserve volume
B = FRC
C = inspiratory capacity
D = vital capacity
