Pulmonary 9: Extreme Conditions Flashcards
What would a water bottle look like at high altitude vs low?
Altitude Andes mountains (4938 m)
Pacific ocean - 0 feet
full/condensation of water at high altitude
collapses on self w cap on at low altitude
slide 4
How do barometric pressure and inspired PO2 change with altitude?
barometric pressure and inspired PO2 decrease with altitude
Slide 5
The barometric pressure is 255mmHg at Mt Everest. Calculate PO2 and PiO2.
PO2 = .21 x 255 mmHg = 54mmHg
PiO2: .21 (255-47mmHg) =44mmHg
Find PAO2 assuming PCO2 = 40mmHg, respiratory ratio = 1.
barometric pressure is 255mmHg
How does this value change with acclimatization? (Also, how does one acclimatize?)
4mmHg
acclimatization occurs through hyperventilation (5 fold increase)
PAO2 = 44 -8 = 35mmHg
unacclimatized persons are unconscious in 45 sec and dead in 4-6 min
Describe the lung under extreme conditions.
How do permanent residents at 4600 m adapt?
When are chemoreceptors stimulated? By what? (What type of chemoreceptor?)
Typical PaCO2 in permanent residents at 4600m is about 33mmHg
hypoxic stimulation of peripheral chemoreceptors
How does someone adapt when they first arrive at high altitude?
initial respiratory alkalosis (low PaCO2 and high pH) inhibits increase in ventilation but is compensated within 2-3 days, thus further increasing ventilation
The barometric pressure in Denver is about 600mmHg. What happens when you first arrive?
Calculate PIO2 and PAO2.
How do you accommodate?
abrupt decrease in PIO2 when first arrive in mountains.
(PIO2= [600-47] x .21= 116mmHg)
and alveolar and arterial O2 decrease
(PAO2= 116 - [40/.8] = 66mmHg; PaO2=61mmHg (assuming AaDO2 is 5mmHg/hasn’t changed)
the decrease in arterial O2 stimulates the peripheral chemoreceptors and thereby increases ventilation
this increase in ventilation decreases arterial PCO2 and elevates arterial pH… result of this increase in ventilation is to minimize the hypoxemia by increasing PAO2.
(if PACO2 decreases to 30mmHg then [(600-47) x .21] - [30/8] = 78mmHg
decrease in arterial PCO2 also decreases PCO2 of CSF… (Bc HCO3- is unchanged, pH of CSF increases… this increase in pH of CSF attenuates the rate of discharge of central chemoreceptors and decreases their contribution to ventilatory drive)
over next 12-36 hours, HCO3- in CSF decreases as acid-base transporter proteins in blood reduce HCO3-
What is polycythemia? What effect will it have?
- increase in RBC concentration
- erythropoietin from kidney
- increases Hb/O2 carrying capacity
- normalizes O2 concentration
Describe/draw a graph showing PO2 values from inspired air- alveolar gas- arterial blood- mixed venous blood at sea level and at 4600m.
Slide 9
At moderate and high altitude how does does the O2 binding curve shift? (why)?
moderate- rightward shift of O2 binding curve due to 2/3 DPG (develops bc of respiratory alkalosis) …assists in unloading O2 in venous blood
-at higher altitudes leftward shift (alkalosis) …this assists in loading of O2 in the pulmonary capillaries
Is air more or less dense at high altitude? Will maximal breathing capacity increase or decrease?
maximal breathing capacity increases as air is less dense
What does alveolar hypoxia result in?
alveolar hypoxia results in pulmonary vasoconstriction
-right heart hypertrophy and pulmonary edema
(hypertension is exaggerated by polycythemia, which raises the viscosity of the blood
The probable mechanism is that the arteriolar vasoconstriction is uneven, and leakage occurs in unprotected, damaged capillaries. The edema
fluid has a high protein concentration, indicating that the permeability of the
capillaries is increased.
Describe acute mountain sickness and chronic mountain disease.
acute mountain sickness: headache, fatigue, dizziness, nausea…can progress to high altitude pulmonary edema, high altitude cerebral edema
chronic mountain disease: polycythemia, fatigue, reduced exercise tolerance, hypoxemia
In diving, how do pressures change as you descend deeper?
pressure doubles with every 10m/33ft below water.
So at 0 depth pressure is 1 atm
at 33’ pressure is 2 atm
See slide 11
Describe the diving response.
How is it induced?
Will the body respond with peripheral vasoconstriction or dilation? Due to parasympathetic or sympathetic activity?
Initial hypotension or hypertension?
Bradycardia or tachycardia?
Reduction or increase of CO?
Hb changes?
- detectable in all air breathing vertebrates
- induced by apnea
- peripheral vasoconstriction due to sympathetic activity
- initial hypertension
- vagally induced bradycardia and reduction of the cardiac output
- enhancement of hemoglobin concentration of circulating blood by splenic contraction
When does hypoxic loss of consciousness occur? At what PO2?
LOC at PO2: 20-25mmHg
How does hyperventilation affect divers?
- reduces CO2 drive to breathe
- loss of consciousness without forewarning bc the weak respiratory stimulus from hypoxia is voluntarily overridden
Breath holders die every year due to preventable
pathophysiological mechanisms
Describe ascent blackout (hypoxia of ascent).
What is pressure at a depth of 40m?
What is PiO2 and PO2 in the lungs?
(Fraction of oxygen is reduced from .21 to .016)
Breath holders die every year due to preventable
pathophysiological mechanisms
-reduction of water pressure and gas pressure
For example, at a depth of 40m under water, pressure is 5x the pressure at sea level (5 x 760mmHg=3800mmHg) and PO2 in the lungs is 749mmHg.
PiO2= (760x5)-47 x .21 =788mmHg
PO2 of 60mmHg when PAO2 reduced to 1.5%
PO2 is still 60 mmHg when the fraction of O2 in the lung has been reduced from 21% to 1.6%.
What happens when the diver ascents to 10m of water? (What is PO2 then?) What may result?
When the diver ascents to 10m under water, PO2 will be 23mmHg, which may result in LOC.
at 10m:
PO2= (760 x 2)-47 mmHg x 0.01 =23mmHg =LOC
Hyperventilation and ascent blackout can result in deaths in divers. What else?
carbohydrate depletion (less CO2 production)
Discuss diving-barotrauma of descent before the dive. Explain/draw the components of diagram A on slide 20
Does the manometer show overpressure or equilibrium/why?
Before dive: inhalation to TLC before submersion;
vital capacity (VC) represents the portion of TLC that can be used for pressure equilibration. The manometer indicates overpressure in lung air relative to the ambient atmosphere due to inward recoil of chest and lungs
RV represents the “noncollapsable” fraction of TLC
the normal intrathoracic blood volume (ITBV) in the vascular bed and heart) is modest in size; the extrathoracic blood volume is ETBV
Describe beginning of descent (equilibrium, etc) (diagram B slide 20)
beginning of descent with pressure equilibrium relative to ambient water maintained as indiciated by manometer, by compression of chest and some translocation of blood from ETBV to ITBV
Describe diagram C slide 20.
at greater depth the limits of mechanical compression of chest wall and stretching of diaphragm have been reached, but further compression of lung air and maintenance of pressure equilibrium is achieved by redistribution of large volume of blood from ETBV to ITBV
Describe diagram D slide 20.
with further descent, the dispensibility limit of blood containing structures in the chest wall may be reached, an underpressure develops in the lung relative to the ambient water and therefore to the ITBV with possible extravasation of fluid (pulmonary edema) and bleeding due to capillary rupture
