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Physio post midterm > Pulmonary facts > Flashcards

Pulmonary facts Flashcards

1
Q

Partial Pressure of water vapor is dependent on what?

A

Core body temp

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2
Q

what happens when you half the alveolar ventilation?

A

the CO2 is going to be DOUBLED!

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3
Q

If you double the bicarb concentration then what is the acid-base situation

A

no change
remember that pH is determined by the ratio of HCO3: dissolved CO2
so you double both values overall same ratio

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4
Q

Calculate of Alveolar ventilation if you have TV or Vt same thing=750mL, dead space= 150mL, RR=10bpm. What happens if you decrease TV=500ml but increase rate to 20bpm

A

Va=(Vt - Vd) F
Va = (750ml - 150ml)(10) = 6,000ml/min or 6L/min
Va= (500ml-150ml)(20) = 7,000ml/min or 7L/min
increase in alveolar ventilation by 1L/min

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5
Q

what are causes of hypoxemia?

A

reduced PAO2
Diffusion Impairment
Ventilation/Perfusion Inequality (think of this first)
R–>L shunting (not corrected on 100% O2)

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6
Q

what does not cause hypoxemia (low oxygen tension in the blood, PaO2)?

A

L–>R shunting

Hypoventilation (increased PaCO2 and Increased PaO2 and decreased alveolar ventilation)

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7
Q

Drop in O2 pressure from 150-140mmHg –> causes big ventilation drive. Removal of what extinguishes this response?

A 
Removal of carotid arch 
peripheral chemoreceptors ( increases the carotid/aortic bodies) located at carotid sinus-> senses O2 (hypoxia) then H+ and CO2 levels
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8
Q

Alveolar Ventilation, what are the different formulas?

A

Va= Ve (minute ventilation) - Vd (wasted ventilation)
Va=FeCO2/PaCO2
Va= (Vt-Vd) RR or F

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9
Q

what happens to the V/Q when there is a pulmonary embolus?

A

perfusion stops but ventilation is unaffected so the V/Q ratio will be infinity
then the gas in the affected alveolus will eventually equilibrate with atmospheric gases (since no gas is entering the blood stream) and alveolar gas tensions will be 150mmHg PO2 and 0mmHg PCO2 (alveolar dead space)
Increases A-a gradient (due to increase in alveolar gas tension (PAO2))

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10
Q

why is there an A-a gradient??

A

A-a gradient= PAO2- Pa02 –> equilibration between atmospheric 150mmHg and Alveolar 100mmHg –> 100mgHg Arterial PaO2 but this decreases as O2 is used up metabolically as you move through the system circulation so by the time it returns the P02 is 40mmHg
Other equation is PAO2=PIO2-(PACO2/R)

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11
Q

If you are breathing a partial pressure of 50% then this means you have inhaled 50% O2 instead of the normal 21% so what happens?

A

760mm Hg - 47= 713 x .50 = 356.5
760 mm Hg - 47= 713 x .21 = 149.73
these would be your inspired PIO2 values
.50 or .21 would be your FIO2 values, fractional concentration of O2
plug these into the PAO2= PIO2 - (PACO2/R (0.8)) equation

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12
Q

what is the reason that PH2O is always constant?

A

temperature dependent variable not pressure dependent so since core body temp is pretty constant we assume 47mmHg

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13
Q

In pulmonary fibrosis (restrictive disease), what happens to the FEV, FVC and lung volume

A 
FEV decreases 
FVC decreases 
Lung volume declines 
compliance declines 
elastase increases
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14
Q

what do central and peripheral chemoreceptors respond to?

A

Peripheral –> Hypoxia sensors (low PaO2), low arterial pH (high H) and increased PaCO2
Central –> PCO2 levels detect via pH of CSF (detects respiratory acidosis)(located in the medulla)

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15
Q

Emphysema will the EPP go proximal or distal?

A

EPP will go distal (more resistance because the lungs are much more compliant)
called dynamic compression

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16
Q

In a pressure-volume compliance curve what will emphysema look like compared to fibrosis

A

Emphysema–> increase compliance of lung–> shift of the pressure-volume curve to the left, increasing the gradient
Fibrosis–> decreased compliance of lung–> shift of the pressure volume curve down to the right (below FRC)

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17
Q

what are the causes of pulmonary edema?

A

Increased hydrostatic pressure (accumulation of fluid in the interstitum)
Decreased oncotic pressure = lack of absorption and favoring of filtration
Decreased lympathetic drainage
Increased Alveolar Tension

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18
Q

what is the equation for physiological dead space?

A

PCO2= PeCO2/PCO2
Alveolar Ventilation = (Vt-Vd) x F
Vd= Vt x (PaCO2-PeCO2)/PaCO2
(arterial PCO2 is always equal to alveolar PCO2)
Vd= anatomic dead space + alveolar dead space (normal person this value is 0)

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19
Q

How do you increase alveolar minute ventilation?

A

increase breaths per minute or tidal volume

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20
Q

Why is lung easier to collapse with saline than with water??

A

Saline washes out the surfactant and therefore there is no surface tension

21
Q

Increase in lung volume is an increase in radial traction. The amount of air you take in does have an effect on airflow. If you decrease the volume coming in what happens?

A

increase in resistance?? not sure though

22
Q

why is the systemic arterial blood partial pressure of oxygen 90mmHg vs 100mmHg in alveoli?

A

because of physiological shunting, right to left shunt mixes venous and arterial blood, lowering the partial pressure of oxygen

23
Q

How do you increase minute or alveolar ventilation the best?

A

80% NO and 20% O2, causes vasodilation and increased the O2 of blood the best

24
Q

When blood stays in a blood bank for a long time it has decreased 2,3-BPG, so what happens when you transfuse it into someone?

A

So when transfused into someone they will have a left shift (lower P50) or a decrease in the ability to unload their O2

25
Q

If you increase the deoxyhemoglobin state (bind H+ or 2,3bpg) what happens?

A

increase offloading of O2 at lower P02 decreased (lower P50).

26
Q

Where in the 3 levels of the lung is blood flow and ventilation the highest?

A

the bottom zone 3

high perfusion, ventilation

27
Q

If a patient presents to your office and has a tumor and part of his lung is dysfunctional then what physiologically is going on with the patient?

A

Hypoxic vasoconstriction
decreased blow flow to that part of the lung, the tumor is essentially closing up the alveoli. So if you run blood past that area you will get deoxygenation of that blood.

28
Q

A patient has decreased Pa02 and you give the patient 100% oxygen however the partial pressure of O2 in not increased, what is a possible reason for this finding?

A 
Anatomical Shunt (no bloodflow past alveoli so no gas exchange is possible) 
aka R --> L shunt
29
Q

If a patient presents to the ER with a head injury and his respiration rate is resulting in hyperventilation, taking deep breaths. then what will happen to the PCO2 and pH?

A

Hyperventilation = decreased PaCO2 and increased pH

30
Q

When you begin to exercise, what happens?

A

Increased O2 consumption
Increased Ventilation Rate (respiratory rate)(joint/muscle receptors that stimulate respiration rate)
Increased venous PC02
Increased blowing off CO2
Decreased venous P02
Collateral impulses from higher brain centers

31
Q

What parameters remain constant when you exercise?

A

Arterial P02, PCO2 and pH

32
Q

what parameters cause a right shift in the oxygen dissociation curve?

A 
Increased Temp
decreased pH (increased H+)
increased CO2
Increased 2,3BPG
(working muscle is an example)
33
Q

If a patient has a normal A-a gradient, then what does this mean?

A

If the PAO2 is different from the PaO2 then there is an A-a gradient.
For some reason arterial blood gases are less than alveolar gas partial pressure.
In a healthy individual there is some A-a gradient, so the PaO2 is usually 5-15mmHg less than the PA02.
This gets worse with age for each year beyond 20 yo get an A-a increase of 0.4mmHg per year

34
Q

If you have an elevated PaCO2 and yet an A-a gradient of 5-20mmHg still, what is this indicative of?

A

Hypoventilation

35
Q

what are the steps in alveolar gas exchange from alveolus to plasma to RBC?

A

In the lungs PO2 is high and PCO2 is low
O2 combines with deoxy-Hb, driving H+ ions off of Hb
H+ combines with HCO3- to form H2CO3- which dissociates to CO2 and water
Carbamino-Hb releases the CO2
CO2 moves down its PCO2 gradient to the alveoli
Blood can carry less CO2 when PO2 increases for all of the above reasons-this shift in CO2 carrying capacity is termed the Haldane effect.

36
Q

what are the steps in alveolar gas exchange from the tissue to the plasma to the RBC?

A

In the tissues the PO2 is low and the PCO2 is high
CO2 dissolves into the plasma and diffuses to the RBC cytosol
Some remains dissolved, some forms carbamino Hb and H+ and some forms HCO3- and H+ from CA activity
Since PO2 is low –> there are large amounts of deoxy-Hb
Deoxy-Hb is a good proton acceptor and binds the H+ ions from step 3 –> encouraging the formation of more HCO3- and carbamino compounds
In addition the H+ ions generated in step 3 drive any Oxy-Hb to deoxy-Hb (drive O2 unloading)

37
Q

TLC-RV=

A

VC

38
Q

RV + ERV=

A

FRC

39
Q

TLC-(RV+ERV)

A

IC

40
Q

IRV+Vt+ERV =

A

FVC

41
Q

what happens in carbon monoxide poisoning?

A

CO binds Hb with very high affinity. So very low concentration of CO can compete with O2 to bind to Hb
So 50% CO-Hb means a loss of 50% capacity for O2 binding
The high affinity of Hb for CO means that Hb is locked in its relaxed state- which means it has a high affinity for O2
Therefore O2 can bind with the Hb sites that are not occupied by CO however once they are bound they remain bound.
Oxygen is unable to offload and the tissues get hypoxic.

42
Q

What would the curve for carbon monoxide poisoning look like then?

A

CO decreases the P50 meaning that O2 loading is enhanced but that offloading is reduced/stopped
So the curve is left shifted (because the offload is so low)
Low O2 content but still 100% saturation

43
Q

what are the parameters for COPD (obstructive disease)

A 
FEV decreases (hard time expiring because lung volume is huge)
FEV:FVC ratio is low (below 0.8)
FVC remains the same 
Increased compliance 
Decreased elastase 
decreased vascular cross sectional area (bv are destroyed) 
Increased hydrostatic presure 
dynamic airway compression
44
Q

Bicarb is mostly found where?

A

in venous plasma

45
Q

If you have a COPD patient what is happening chronically a and acutely in terms of PCO2 and PO2 levels?

A

patient loses hypoxic drive
Chronic compensation of arterial and CSF pH inhibits hypercapnic ventilatory drive
In short term: decreased PaO2, Increased PaCO2, decreased pH arterial and decreased pH CSF
Chronically: decreased PaO2, Increased PaCO2, normal pH arterial and normal pH CSF
PCO2 ventilatory drive from central chemoreceptors and arterial peripheral receptors are lost–> since pH is compensated–> leaving only the PO2 drive from peripheral receptors.

46
Q

If you give a COPD patient more then 2L/min of O2, what happens?

A

Patient needs O2 therapy but giving O2 will severely reduce their ventilatory drive.
Therefore O2 must be given but at a lower fractional O2 concentration to prevent ventilatory depression

47
Q

What happens with increased and decreased surfactant concentration?

A

Increased SA= decreased surfactant concentration = increased surface tension
Decreased SA= increased surfactant concentration= decreased surface tension
Surfactant prevents small alveoli from completely collapsing (Atelectasis) and acts as a brake to prevent large alveoli from expanding further.

48
Q

what will decrease the volume of gas from crossing a barrier?

A

Vgas= AxD/T (P1-P2) (Ficks law–> volume of gas crossing a surface)
decrease SA, increase thickness, decrease PO2 and increase PCO2

49
Q

If a patient has a positive pressure ventilation what does this mean?

A

A patient with increased airway compression or resistance
COPD or asthma ( compressed airway on forced expiration –> moves the EPP closer to alveoli)
Decreased PA and PIP still same therefore these two values become equal much sooner (distal)

Physio post midterm (4 decks)

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