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122 Cards in this Set

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what cannot be measured by spirometry?
residual volume (RV)
minute ventilation
MV = TV x breaths/min
alveolar ventilation
AV = (Tidal volume - Dead space) x Breaths/min
define inspiratory capacity
sum of TV and IRV
define FEV1
forced expiratory volume
- the amount of air that you can blow out in the first second of forced maximal expiration
what is the normal value for FEV1?
80% of the FVC (forced vital capacity)
FEV1/FEV = 0.8
what happens in obstructive lung disease? (FEV1)
e.g. asthma
- FEV1 is decreased more than FVC, so FEV1/FVC is decreased
what happens in restrictive lung disease? (FEV1)
e.g. fibrosis
- both FEV1 and FVC are reduced.
- FEV1/FVC is either normal or increased
muscles of inspiration
1. diaphragm
2. external intercostals and accessory muscles:
- only used during exercise and during respiratory distress
muscles of expiration
- normally passive
- during exercise or during obstructive lung disease, you will use
1. abdominal muscles
2. internal intercostal muscles
compliance of respiratory system
C = V/P

C= compliance (mL/mm Hg)
V = volume (mL)
P = pressure (mm Hg)
what is compliance of the respiratory system?
- describes the distensibility of the lungs and chest wall
- the slope of the pressure-volume curve
- change in volume for a given change in pressure
what is the transmural pressure?
alveolar pressure - intrapleural pressure
what happens when the intrapleural pressure is negative?
lung expands
what does it mean when the inflation of lungs follows a different PV curve than expiration
what happens to compliance during emphysema?
increased compliance. Tendency of the lungs to collapse is decreased
- the tendency for the chest wall to expand overwhelms the tendency for the lungs to collapse --> you'll raise your FRC and patients present barrel chested
what happens to compliance during fibrosis?
decreased lung compliance. Tendency for lungs to collapse overwhelms tendency for chest to expand --> lowered FRC
surface tension of alveoli
- derives from the atractive forces between liquid molecules lining the alveoli
- creats a collapsing pressure that is directly proportional to surface tension
- inverse prop. to radius
eqn for the collapsing pressure on alveolus
P = 2T/r

T = surface tension (dynes/cm)
do large alveoli have small or large collapsing pressures?
small. easy to keep open
do small alveoli have small or large collapsing pressures?
large. hard to keep open.
in the absence of surfactant --> atelectasis
what is collapse of alveoli called?
how do surfactants work?
decrease the attractive intramolecular forces --> decrease the collapsing pressure and increases compliance
where is lung surfactant made?
made by type II alveolar cells.
- consists primarily of DPPC (dipalmitoyl phophatidylcholine)
when is surfactant present in the fetus?
generally by wk 34 (sometimes even by week 24)
how do you detect whether a fetus has mature surfactant?
if the lecithin: sphingomyelin ratio is greater than 2:1 in amniotic fluid
eqn for airflow
Q = delta P/R
eqn for resistance
R = 8nl/(pi*r^4)

n = viscosity of gas
l = length of airway
where is the site of main airway resistance?
medium sized bronchi
- not the smallest bronchi, since they're arranged in parallel
what does parasympathetic stimulation do to airway resistance?
constrict airways
what does sympathetic stimulation and symapthetic agonists do to airway resistance?
dilate airways via B2 receptors
B2 agonist. dilates airways
how does lung volume affect airway resistance?
high lung volumes decrease resistance b/c there is traction from lung tissue pulling outwards on the airways.
how does the viscosity or density of gas change airway resistance?
- during deep sea dive, air density and reistance to flow are both increased
- low density gas reduces airflow resistance
Breathing cycle:
At rest (before inspiration begins)
1. alveolar pressure equals atm pressure = 0
2. intrapleural pressure is neg (chest wall pulling out, alveoli pulling in)
3. lung volume is at FRC
how do you measure intrapleurla pressures?
by inserting a balloon catheter in the esophagus
Breathing cycle:
during inspiration
1. inspiratory muscles contract. Alveolar pressure is less than atm --> inflow of air
2. intrapleural pressure becomes more neg b/c the elastic recoil strength of the lungs increase as the lung vol increases
3. lung vol increases by one TD. Total lung vol = FRC + TV
how do you measure dynamic compliance?
changes in intrapleural pressure during inspiration
Breathing cycle:
during expiration
1. alveolar pressure is greater than atm pressure --> air flows out
2. intrapleural pressure returns to at rest values (passive expiration)
3. lung volume returns to FRC
what happens during forced expiration?
intrapleural pressures become positive and can cause airway compression --> makes expiration more difficult
why do COPD patients learn to breath out with pursed lips?
slow expiration during forced expiration can help prevent airway collapse.
- obstructive --> impaired expiration
- decreased FVC and FEV1 --> DECREASED FEV1/FVC
- not all the air is expelled --> air trapping --> increased FRC
- combination of chronic bronchitis and emphysema
- obstructive, with increased compliance
- decreased FVC and FEV1 --> DECREASED FEV1/FVC
- not all air is expelled (impaired expiration) --> increased FRC
- pink puffers and blue bloaters
chronic bronchitis
increased compliance
Pink puffers
- part of COPD
- mainly emphysema
- mild hypoxemia
- maintain alveolar ventilation --> normocapnia
Blue Bloaters
- part of COPD
- mainly chronic bronchitis
- severe hypoxemia
- unable to ventilate alveoli --> hypercapnea
- restrictive
- decreased lung compliance
- decrease in all lung volumes
- FEV1 is decreased less than FVC --> FEV1/FVC increased (sometimes normal)
partial pressure
total pressure x fractional gas constant
Partial pressure of O2 in dry inspired air
fractinal concentration = 0.21
PO2 = 760mmHg x 0.21 = 160mmHg
Partial pressure of O2 in humidified tracheal air
correct for partial pressure of H20, which is 47mm Hg
P_total = 760-47 = 713
713 x 0.21 = 150mmHg
what is the physiologic shunt?
approx 2% opf the systemic CO bypasses the pulmonary circulation
- as a result, the admixture of venous blood of venous blood (slight) with oxygenated blood makes the PO2 slighlty lower than alveolar air
dissolved gasses
dissolve [O2] = PO2 x Solubility of O2 in blood
= 100mmHg x 0.03mL O2/L/mmHg
= 0.3ml O2/100mL blood
partial pressures of O2 in:
- dry inspired air
- humidified air
- alveolar air
- systemic arterial blood
- mixed venous blood
- dry inspired air: 160
- humidified air: 150
- alveolar air: 100
- systemic arterial blood: 100
- mixed venous blood: 40
partial pressures of CO2 in:
- dry inspired air
- humidified air
- alveolar air
- systemic arterial blood
- mixed venous blood
- dry inspired air: 0
- humidified air: 0
- alveolar air: 40
- systemc arterial blood: 40
- mixed venous blood: 46
Perfusion limited exchange
- gas equilibrates early along the lenght of the pulmonary capillary
- partial pressure of the gas in arterial bloo becomes equal to the parital pressures in alveolar iar
how do you increase gas diffusion in a perfusion-limited exchange?
increase blood flow
Diffusion-limited exchange
- in firboris, the diffusion of O2 is restricted b/c of thickening of the alveolar membrane
- in emphysema, diffusion is limited b/c the surface area is decreased
what is hemoglobin's role?
to increase the O2 carrying capacity of blood by 70-fold
iron in the ferric state (Fe3)
- does not bind O2
fetal Hb
the b chains are replaced by gamma chains --> a2g2
why does fetal Hb have greater O2 affinity than adult Hb?
2,3 diphosphoglycerate (DPG) binds less avidly to fetal Hb
- DPG binds to deoxygenated hemoglobin in RBCs. In doing so, it allosterically upregulates the ability of RBCs to release oxygen near tissues that need it most.
O2 binding capacity of blood
- the max amount of O2 that can be bound to Hb in the blood
- depends on the Hb concentration
O2 content in blood
- total O2 carried in blood, including bound and dissolved O2

= (O2 binding capacity x % saturation) + Dissolved O2

% saturation: % of heme groups bound to O2
Hb-O2 dissociation curve
- plot of % saturation of Hb as a function PO2
Hb % sat at PO2 of:
- 100mmHg
- 40mmHg
- 25mmH
-100 mmHg: 100% sat. all four heme groups are bound
- 40 mmHg: 75% sat. about 3 out of 4 heme groups are bound
- 25 mmHg: 50% sat. about 2 out of 4 heme groups are bound.
positive cooperativity
change in affinity of Hb as each successive O2 molecule binds to the heme site
affinity for which O2 is the highest?
4th O2
- change in affinity faciliates loading of O2 in the lungs (flat on curve) and the unloading at the tissues (steep part on curve)
where is the Hb-O2 dissociation curve almost flat?
between 60 -100mmHg
- humans can tolerate changes in atm presure without compromising the O2 carrying capacity of Hb
what does it mean for a right shift in the Hb-O2 dissociation curve?
- affinity for O2 is decreased
- P50 is increased
what causes a right shift in the Hb-O2 dissociation curve?
1. increase in PCO2 or decrease in pH
- Bohr effect
2. increase in temp (e.g during exercise)
3. increase in 2,3 DPG concentration
- DPG binds to b changes of deoxyhemoglobin and facilitates unloading
adaptation to chronic hypoxemia
living at high altitudes- can cause increased synthesis of 2,3 DPG
what does it mean for a left shift on the Hb-O2 dissociation curve?
- affinity of Hb for O2 is increased
- P50 is decreased
what causes a left shift in the Hb-O2 dissociation curve?
1. decreased CO2, increased pH
2. decreased temp
3. decreased 2,3 DPG
4. fetal Hb
5. CO poisoning
- competes for O2 binding site. Has 200x higher affinity for Hb
A-a gradient
A-a gradient = PAO2 - PaO2

PAO2 = alveolar PO2 (gotten from alveolar gas eqn)
PaO2 = arterial PO2 (measured in arterial blood)
how do you get PAO2?
alveolar gas eqn

PAO2 = alveolar PO2
PIO2 = inspired PO2
PACO2 = alveolar PCO2 = arterial PCO2 (measured in arterial blood)
R = respiratory exchange ratio (CO2 production/O2 consumption, normally 0.8)
what is the normal A-a gradient?
< 10 mmHg
anything above 10mmHg indicates that O2 is not equilibrating, due to:
- diffusion defect
- V/Q defect
- right to left shunt
eqn for O2 delivery
O2 delivery = CO x O2 content of blood
dependent on:
- O2 binding capacity of Hb
- % sat of Hb by O2
- % sat itself depends on the PO2
How is CO2 carried in the blood?
1. Dissolved CO2 (small amount)
2. Carbaminohemoglobin (small amount)
3. HCO3-
- hydration of CO2 in the RBCs
- 90%
what is the chloride shift?
- HCO3- leaves the RBCs in exchange for Cl-
how is H+ buffered inside the RBCs?
by deoxyhemoglobin, which is better than oxyhemoglobin
- so, it's best that Hb be deoxygenated by the time the blood reaches the venous end of the capillaries
what is the normal:
- pulmonary arterial pressure?
- aortic pressure?
- 15mmHg
- 100mmHg
describe Zone 1 of the lung
- lowest blood flow when person is standing
- alveolar pressure > arterial pressure > venous pressure
- high alveolar pressure may compress capillaries and reduced blood flow. Can occur if:
1. arterial pressure is reduced b/c of hemorrhage
2. alveolar pressure is increased b/c of positive pressure ventilation
describe Zone 2 of the lung
- flow is medium when standing
- arterial pressure > alveolar pressure > venous pressure
- as you move down the lung, arterial pressure increases b/c of gravitational effects
describe Zone 3 in the lung
- highest flow while standing
- artieral pressure > venous pressure > alveolar pressure
- blood flow is driven by diff btw arteiral and venous pressures
what happens during hypoxia in the lungs?
vasoconstriction (not vasodilation as in other organs!)
- vasoconstriction redirects blood away from poorly ventilated regions
fetal pulmoanry vascular resistance
- in fetuses, pulmonary vascular resistance is high b/c of generalized hypoxemia (--> vasoconstriction)
- with first breath, alveoli are oxygenated, and vascular resistance decreases
Right to left shunts
- physiologic shunting: 2% of CO bypasses the lungs
- seen in tetralogy of Fallot
- always decreases arterail PO2 b/c of admixture of venous blood
how do you measure maginitude of L-R shunting?
- have patient breath 100% O2 and measure the degree of dilution of the oxygenated arteiral blood by shunted blood
Tetralogy of Fallot
1. Pulmonary stenosis (obstructs flow from the R ventricle to the PA)
2. Ventricular septal defect (defect in the ventricular septum)
3. Overriding aorta (aortic valve is enlarged and appears to arise from both the left and right ventricles)
4. Right ventricular hypertrophy
Left to right shunts
- more common than R--> L shunts b/c pressures are higher on the L side
- caused by congenital abnormalities (patent ductus arteriosus)
- do not cause decrease in arterial PO2
V/Q ratio
- ratio of alveolar ventiation to pulmonary flow
- normal: 0.8 --> arterial PO2 of 100mmHg, and arterial PCO2 of 40mmHg
how is the V/Q ratio distributed across the lung zones?
- higherst at the apex and lowest at the base
- at apex- PO2 is highest and PCO2 is lowest
- at base: PO2 is lowest and PCO2 is highest (less exchange)
what are the regional differences for ventilation?
- lower at the apex and higher at the base
V/Q ratio in airway obstruction
- if airways are completely blocked --> V/Q is zero (aka shunt)
- PO2 and PCO2 of pulmonary capillary blood will approch values of mixed venous blood
- increase in A-a gradient
V/Q ratio in pulmonary embolism
- V/Q is infinate (aka dead space)
- PO2 and PCO2 of alveolar gas will approach levels of inspired air
where is breathing coordinated?
brain stem
- sensory info: PCO2, lung stretch, irritants, muscle spindles, tendons, and joints
Medullary respiratory center
- found in the reticular formation
- Dorsal respiratory group
- ventral respiratory group
which 4 centers control breathing?
1. medullary respiratory center
2. Apneustic center
3. Pneumotaxic center
4. Cerebral cortex
Dorsal respiratory group
- responsible for inspiration and generation of rhythm
- input: input comes from the vagus (info from chemoreceptors and mechanoreceptors in the lung) and glossopharyngeal (info from chemoreceptors)
- output: the dorsal respiratory group travels, via the phrenic nerve, to the diaphragm
Ventral respiratory group
- primarily responsible for expiration
- not active during normal breathing, when expiration is passive
- activated during exercise, when expiration is active
Apneustic Center
- located in the lower pons
- stimulates inspiration- producing a depp and prolonged inspiratory gasp (apneusis)
define apneusis
breathing irregularity: a form of breathing, caused by brain damage, in which each full inhalation is held for a prolonged period
Pneumotaxic center
- located in upper pons
- inhibits inspiration and therefore regulates inspiratory volume and respiratory rate
Cerebral cortex
- breathing can be under voluntary control
Central chemoreceptors in the medulla
- sensitive to pH in CSF. Low pH causes hyperventilation
- H+ does not cross the BBB as well as CO2 (remember, it's the H+ that comes from the action of CA that the medulla senses, not the H+ in the arterial blood)
how does CO2 cross the BBB?
- diffuses from arterial blood to CSF b/c CO2 is lipid-soluble
- changes in H+ will either stimulate or decrease breathing rate
Peripheral chemoreceptors in the carotid and aortic bodies
- decreases in arterial _PO2_ stimulate chemoreceptors to cause increase in breathing rate
- PO2 must go below 60mmHg before breathing is stimulated
- increases in arterial _PCO2_ increase breathing rate
- response of peripheral chmoreceptors to CO2 is less important than central chemoreceptors
- increase in arterial H+ stimulate carotid bodies directly, independent of PCO2
where are carotid bodies found?
at the bifurcation of the common carotid arteries
where are the aortic bodies found?
below the aortic arch
what stimulates hyperventilation in metabolic acidosis?
- increase in arterial H+
- NOT, the increase in CO2
Lung stretch receptors
- found in smooth m. of airways
- Hering-Breuer reflex
what is the Hering- Breuer reflex?
- when lung stretch receptors are stimulated by lung distention, they decerease breathing frequency
Irritant receptors
- found between the airway epithelial cells
- stimulated by noxious susbtances (dust, pollen)
J (juxtacapillay receptors)
- found in alveolar walls, close to the capillaries
- engorgement of pulmonary capillaries (e.g. left heart failure) stimulates the J receptors and causes shallow breathing
joint and muscle receptors
- activated during limb movement
- early stimlulation of breathing during exercise
what happens to the arterial PO2 and PCO2 levels during exercise?
arterial pH does not change, but may decrease during strenuous exercise b/c of lactic acidosis
what happens to venous PCO2 during exercise?
increases be/c excess CO2 is produced by muscles
what changes about the distribution of V/Q ratios during exercise?
the ratio is more even and there is a resulting decrease in the physiologic dead space
adaptation to high altitude
- alveolar PO2 decreases --> arterial PO2 decreases
- hypoxemia stimulates peripheral chemoreceptors --> hyperventilation --> respiratory alkalosis --> stimulates renal production of erythropoietin --> increased [Hb] --> increased O2 content of blood
- 2,3-DPG elevated
- pulmonary vasoconstriction --> higher pulmonary resistance --> RV hypertrophy
how do you treat respiratory alkalosis?
Acetazolamide, sold under the trade name Diamox®, is a carbonic anhydrase inhibitor that is used to treat glaucoma, epileptic seizures, benign intracranial hypertension, _altitude sickness_, cystinuria, and dural ectasia. Acetazolamide is available as a generic drug and is also used as a diuretic.