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CVPR Pulmonary > Pulmonary Principles > Flashcards

Pulmonary Principles Flashcards

1
Q

How many times doe the lung airways branch? We do they stop being solely conduction airways?

A

23 total

At 17th branch they become respiratory zones

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2
Q

From what embryonic tissue layer is the lung derived from?

A

Mesoderm

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3
Q

Describe ‘Embryonic’ stage of lung development

A

4-7 weeks, 3 rounds of branching forms 5 lobes of lung

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4
Q

Describe what happens in weeks 4,5,6,7

A

Week 4 - single bud from Laryngotracheal groove
Week 5 - single bud branches into right and left lungs
Week 6 - pleural-peritoneal membrane separates spaces
Week 7 - lung growth runs into liver

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5
Q

Describe ‘Pseudoglandular’ stage of lung development

A

6-17 weeks, 14 rounds of branching giving terminal bronchioles

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6
Q

Describe ‘Canalicular’ stage of lung development

A

16-26 weeks, terminal bronchioles branch into respiratory bronchioles. At the end of this stage surfactant production begins!

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7
Q

When does surfactant production begin

A

6 months (24 weeks) at the end of the canalicular stage

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8
Q

Describe ‘Saccular’ stage of lung development

A

26-36 weeks, respiratory bronchioles become terminal sacs

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9
Q

Describe ‘Alveolar’ stage of lung development

A

36-3 years old. The majority of this occurs after birth! Lungs grow, alveoli mature, gas exchange unit established.

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10
Q

Which aortic arch do pulmonary arteries come from

A

6th

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11
Q

Which aortic arch do pulmonary veins come from

A

Trick question! They don’t, develop off of left atrium

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12
Q

List the timing breakdown for 5 stages of lung development

A 
Embryonic 4-8 weeks
Pseudoglandular 6-17 weeks
Canalicular 16-26 weeks
Saccular 26-36 weeks
Alveolar Birth-3yo
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13
Q

Define intrapleural pressure (P-IP)

A

Pressure in-between visceral pleura on lungs and parietal pleura on chest wall. 2 forces working on pressure. Intrinsic volume of lungs is shrinking (elastic recoil), intrinsic volume of chest wall is expanding.

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14
Q

Define elastic recoil pressure

A

Lungs intrinsically want to shrink. It is this tendency that creates a positive pressure in lungs to force air out during expiration (doesn’t require activation of muscles)

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15
Q

Which phase of breathing does decreased compliance affect

A

Inspiration, conversely increased compliance leads to expiratory problems (usually due to air trapping)

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16
Q

Define hysteresis

A

Tendency for it to take more work to stretch a material than letting the material return to its original length. Lung displays hysteresis with it taking more work to inspire than expire due to elastic and surface tension forces. Shows a right shift in inspiration curve for PV graph

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17
Q

Define transpulmonary pressure (P-TP)

A

Difference between the pressure in the lung versus the intrapleural pressure (P-Lung - P-pleura). Thus if P-TP is greater than lung pressure, lung expands.

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18
Q

How does decrease in compliance in lung versus in chest differ on the P-V graph.

A

In chest wall the slope of the line doesn’t change but entire curve will get shifted down. In lung compliance both slope and height on graph can change significantly.

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19
Q

What does surface tension do to the lung

A

Decreased compliance
Water enters lung
Small alveoli collapse
(All three of these factors are working to decrease the surface area of the air-water interface)

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20
Q

Why do small alveoli collapse when surface tension is high

A

Because of equation (P need to keep alveoli open = 2 * Surface tension/radius) Thus if radius is small you need even more pressure to keep alveoli open

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21
Q

What happens when you fill lung with saline solution

A

You have removed the air-water interface, thus surface tension is no longer an issue. Thus compliance increases and hysteresis decreases.

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22
Q

What happens to surfactant when alveolar radius decreases

A

Its concentration at the air-water interface increases which works to further decrease surface tension forces and keep the alveoli open (away from collapse)

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23
Q

What is the difference in calculation between laminar and turbulent flow

A

Laminar flow increases directly with change in pressure and to the fourth power of radius. Turbulent flow is proportional to the square root of the change in pressure.

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24
Q

What factors can increase airway resistance (4)

A
  • Chemical (bronchoconstrictors)
  • Decreased lung volumes
  • Increased mucous production
  • Dynamic airway collapse (resistance equal infinity)
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25
Q

What happens when we expire below our functional residual capacity (FRC)

A

FRC is our equilibrium point, made up of expiratory reserve volume and residual volume. When we expire below FRC it requires recruitment of expiratory muscles (when expiration is usually a passive process). This increases intrapleural pressure and causes dynamic airway collapse. This is largely what accounts for effort independent portion of flow rate during expiration.

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26
Q

Describe inter-relation between emphysema and dynamic airway collapse (3)

A
  • Lung has less elastic recoil, leading to greater chance of positive intrapleural pressures (P-IP)
  • Reduced elastic recoil has also conditioned patients to use expiratory muscles also getting positive (PIP)
  • Dysfunction in connective tissue also adds to collapse of the airways
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27
Q

What is difference between minute ventilation and alveolar ventilation

A

Minute ventilation is total volume of air moved by lungs (tidal volume x RR). Alveolar is only the volume that passes the alveoli and is necessarily smaller than minute because of dead space in conducting airways

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28
Q

What are typical values for minute ventilation and alveolar ventilation

A

6 L and 4.2 L

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29
Q

How does gravity affect ventilation

A

Causes regional variation. Weight of lungs pulls down on its apex increasing upper intrapleural pressure. This expands the apex volume which decreases compliance since it is higher up on PV curve in a flatter section. Ultimately accounts for 2.5x decrease in ventilation compared to lower lobes

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30
Q

Relate tidal volume and respiratory rate to WORK done during breathing

A

The forces in play during WORK of breathing are resistance forces and elastic forces. Elastic forces are related to tidal volume (such as restrictive diseases). Resistance forces are related to respiratory rate (such as obstructive diseases).

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31
Q

How are tidal volume and respiratory rate affected when elastic forces increase

A

Elastic forces are related to tidal volume (restrictive disease). We want the minimal work for optimal ventilation. Increased elastic forces makes use want to decrease tidal volume to make it less of a component of work. To maintain ventilation respiratory rate increases. TV decreases, RR increases.

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32
Q

How are tidal volume and respiratory rate affects when resistive forces increase

A

Resistive forces are related to respiratory rate (obstructive disease). We want to minimize this increases affect on our work. Thus respiratory rate decreases and tidal volume increases (to maintain proper ventilation)

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33
Q

Define deadspace

A

Area that does NOT take part in gas exchange

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34
Q

Define anatomic deadspace

A

Area of your conducting airways, accounts for 30% of lung volume, is reason for minute ventilation > alveolar vent

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35
Q

Define alveolar deadspace

A

Area of alveoli that ARE well ventilated, but NOT well perfused, thus no gas exchange occurs

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36
Q

Define physiologic deadspace

A

Combination of anatomic and alveolar deadspace. This is usually extremely close to the value of anatomic deadspace unless there is severe disease (making alveolar deadspace bigger)

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37
Q

In Pulmonary Fibrosis what happens to

  • Residual volume
  • Functional reserve capacity
  • Total lung capacity
  • Vital capacity
  • FEV1/VC
A

This is a restrictive disease defined by decreased lung volumes. Thus RV, FRC, TLC, and VC will all be decreased. FEV1/VC thought will actually be normal or increased since VC decreased (increasing the ratio). As well increased elasticity of lung could maintain FEV1.

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38
Q

In Bronchitis what happens to

  • Residual volume
  • Functional reserve capacity
  • Total lung capacity
  • Vital capacity
  • FEV1/VC
A

This is an obstructive disease thus TLC is unaffected. However patients breath at higher volumes thus FRC and RV are increased, since VC = TLC - RV, vital capacity decreases. Even though VC decreased the increased airway resistance of the disease greatly lowers FEV1 and thus gives lowered FEV1/VC (hallmark of obstructive disease)

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39
Q

In Emphysema what happens to

  • Residual volume
  • Functional reserve capacity
  • Total lung capacity
  • Vital capacity
  • FEV1/VC
A

Although this is an obstructive disease TLC is increased because elastic recoil has been destroyed so patients can reach super high volumes. Just like obstructive disease patients breath at higher volumes thus FRC and RV are increased. Since TLC was also increased VC is preserved. Dynamic airway collapse and decreased elastic recoil gives decreased FEV1/VC (this is why emphysema is an obstructive disease).

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40
Q

What is barometric pressure at sea level? Denver?

A

760 Torr

620 Torr

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41
Q

How do you calculate partial pressure of oxygen in inspired air (P-IO2)

A

P-IO2 = (Barometric pressure - 47) * Fraction of oxygen
Atmospheric is 21%

This is Dalton’s Law

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42
Q

Why is the partial pressure of oxygen different between inspired air and alveolar air

A

Because you have residual gases, particularly CO2 left in the alveoli

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43
Q

What is the respiratory exchange ratio

A

When new air enters the lungs it can NOT just be mixed with the residual gases and CO2 since lung volume needs to be maintained, thus O2 and CO2 are exchanged. The rate of exchange is based off our cellular metabolism (i.e. diet)

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44
Q

What are the respiratory exchange ratio values for carbohydrates, fats, proteins, and normal average

A

Carbohydrates 1.0
Proteins 0.8
Fats 0.7
Average 0.8

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45
Q

What do you need to remember to change in your equations when you have a patient on 100% O2

A

Change FiO2 to 100%
ALSO change respiratory exchange ratio to 1.0 because the discrepancy in exchange ratio is allowed by Nitrogen in air, if no Nitrogen then they have to be traded 1:1

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46
Q

How do you calculate alveolar O2 partial pressure

A

P-AO2 = (Barometric pressure - 47)*FiO2 - (Partial pressure of CO2/respiratory exchange ratio)

This is alveolar gas equation

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47
Q

Is diffusion or ventilation rate limiting for CO2 removal

A

CO2 is a nonpolar molecule with very fast diffusion across alveolar membrane, thus ventilation is rate limiting

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48
Q

How do we calculate alveolar ventilation

A

Using equation V-A = (Amount of CO2 exhaled) / (CO2 in the blood).

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49
Q

What is the alveolar gas equation

A

P-AO2 = (Barometric pressure - 47)*FiO2 - (Partial pressure of CO2/respiratory exchange ratio)

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50
Q

What is dalton’s law

A

P-IO2 = (Barometric pressure - 47) * Fraction of oxygen

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51
Q

What is the alveolar ventilation equation

A

Alveolar CO2 (P-ACO2) = Volume of CO2 produced per minute / Alveolar ventilation

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52
Q

What does alveolar ventilation equation help tell us

A

Alveolar CO2 (P-ACO2) = Volume of CO2 produced per minute / Alveolar ventilation

That if we double alveolar ventilation we can halve alveolar CO2 (which because of fast diffuse is equal to arterial CO2)

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53
Q

What is normal arterial CO2 at sea level? Denver?

A

40 - sea level

36 - denver

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54
Q

Define hypoventilation

A

Ventilation rate that increases arterial CO2 (not necessarily respiratory rate below 22/min)

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55
Q

Define hyperventilation

A

Ventilation rate that decreases arterial CO2 (not necessarily respiratory rate above 22/min)

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56
Q

Define hyperpnea

A

Ventilation rate that occurs during exercise to maintain arterial CO2 during time of increased CO2 production

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57
Q

What is the solubility coefficient for CO2 and O2

A

O2 - 0.0013 mM/Torr

CO2 - 0.0300 mM/Torr

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58
Q

What is difference between C-aO2 and P-aO2

A

P-aO2 is the free oxygen in the blood
C-aO2 is the total oxygen in the blood including that bound to hemoglobin, granted free oxygen directly correlates to hemoglobin saturation (outside of disease)

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59
Q

What factors affect O2 diffusion from alveoli to blood (3)

A
  • Difference in O2 pressure between alveoli and blood (freely dissociated, which is kept high since O2 gets grabbed up by Hb so fast)
  • Thickness of membrane
  • Surface area for diffusion
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60
Q

Which is more starkly affected during disease? Oxygen or CO2 diffusion

A

Oxygen by far, CO2 diffusion is RARELY affected during disease because if its fast diffusion rate and ability to dissolve in plasma much better than O2

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61
Q

What does emphysema do to O2 diffusion

A

Decreases because surface area to diffuse is decreased

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62
Q

What does interstitial lung disease do to O2 diffusion

A

Decreases because thickness of alveolar membrane increased

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63
Q

What is typical perfusion to lungs at rest

A

6L

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64
Q

What factors affect perfusion in lungs (5)

A
  • Chemicals (thromboxane constrict, prostacyclin dilates)
  • Capillary recruitment (open up other vessel beds)
  • Oxygen tension (hypoxia vasoconstricts)
  • Blockage (embolism)
  • Gravity (regional differences, more at bottom)
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65
Q

Describe effects of gravity on lung perfusion

A

Arteries come into the middle of lung, half has to travel up against gravity and other gets aided by gravity. Lower arteries will get 6x more blood than upper (much greater than 2.5x difference in ventilation)

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66
Q

How does ventilation stay normal overall with V/Q mismatch

A

Because body is SUPER sensitivity to changes in CO2 (to maintain pH), one area of decreased ventilation will stimulate increase in ventilation elsewhere

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67
Q

Describe physiologic V/Q mismatch

A

It is when overall perfusion and ventilation are normal. However there is a decrease in arterial O2 due to regions of high V/Q being unable to properly balance out regions of low V/Q since hemoglobin is already saturated at 98% in high V/Q regions

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68
Q

What happens to arterial CO2 during physiologic V/Q mismatch

A

It does NOT change, stays the same because body is so proactive in increasing ventilation to maintain CO2, as well CO2 transport is NOT limited by a protein saturation curve like O2 with Hb

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69
Q

What is V/Q of apex of lung compared to lower lung

A

Apex V/Q is 2.4 times higher than lower lung. This is because ventilation was 2.5x greater in lower lung but perfusion was 6x greater in lower lung. 6/2.5 = 2.4

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70
Q

Describe the drops in oxygen partial pressure from inhaled air to alveolar air to arterial O2 (at sea level)

A

Inhaled air 150
Drops to 100 in alveoli because of O2-CO2 exchange
Drops to 90 in arteries because of V/Q mismatch

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71
Q

How does dead space impact V/Q

A

Dead space is where there is no gas exchange, thus perfusion is zero. V/Q goes to infinity

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72
Q

How does shunt impact V/Q

A

Shunt is when blood completely bypasses areas of ventilation (think R to L shunt in heart bypassing lungs). V/Q goes to zero

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73
Q

How does body work to combat V/Q mismatch (2)

A
  • If CO2 rises then ventilation increases
  • In areas of low ventilation there is hypoxemia, low arterial O2, this causes hyperemic vasoconstriction which limits the amount of blood that is essentially traveling through a shunt (in most extreme case). Works to limit the decrease in arterial O2.
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74
Q

What are four factors that increase Oxygen off-loading of hemoglobin

A

Decreased pH, increased temperature, increased CO2 concentration, increased 2,3-DPG

Called the Bohr effect, right shifts the Hb dissociation curve

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75
Q

What is oxygen coefficient in mL of O2/100 mL/Torr

A

0.003 (as opposed to 0.0013 mM/Torr)

This gives you the 0.3 mL of free oxygen in blood at sea level

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76
Q

How much oxygen do we normally deliver to the tissues and how much do we normally consume (sea level)

A

Deliver 1000 mL = Cardiac output (5L) x arterial oxygen content (20.7)
We consume 240 mL = Cardiac output (5L) x difference in oxygen saturation in arteries from veins (98-75) x hemoglobin concentration (15) x constant (1.39)

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77
Q

Compare hypoxia and hypoxemia

A

Hypoxia is low oxygen at TISSUES

Hypoxemia is low arterial O2 partial pressure (<65 Torr in Denver)

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78
Q

What is definition of hypoxemia

A

Arterial Oxygen partial pressure (P-aO2) of <65 Torr in Denver

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79
Q

Compare hypoxemia and desaturation

A

They are NOT the same there, while in our tables they both decrease together, there are cases where either one can be normal and the other abnormal

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80
Q

What are the causes of hypoxemia (5)

A
  • Low inspired oxygen pressure (altitude)
  • Low alveolar oxygen pressure
  • Diffusion problems
  • V/Q mismatch
  • Shunt
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81
Q 
During Low P-IO2 what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

This is what occurs at altitude
P-aO2, S-aO2, and P-aCO2 are all decreased due to the drop in barometric pressure
A-a gradient stays normal

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82
Q 
During Low P-AO2 what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

This is a case of hypoventilation
P-aO2 and S-aO2 are both decreased
However due to definition of hypoventilation P-aCO2 increases
A-a gradient stays normal

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83
Q

How can the tell the difference in cause of hypoxemia between low inspired O2 and low alveolar O2

A

Inspired O2 is altitude, alveolar O2 is hypoventilation
Both have normal A-a gradients
The big difference is P-aCO2 is increased in hypoventilation

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84
Q 
During Diffusion problems what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

This is case of interstitial lung disease
P-aO2 and S-aO2 are both decreased
Remembering that CO2 diffusion is extremely resilient compared to O2, P-aCO2 is normal
A-a gradient however is extremely increased, there is far more oxygen in Alveoli than in arteries (>10)

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85
Q 
During V/Q mismatch what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

This could present in a case of moderate COPD
P-aO2 and S-aO2 are both decreased
Remembering that body is super sensitive to CO2 changes, ventilation has been compensated to have normal P-aCO2
A-a gradient is high because there are areas where there is inadequate ventilation from obstruction leading to hypoxemia

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86
Q 
During Shunt what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

This could be a case of severe pneumonia where alveoli have filled up
P-aO2 and S-aO2 both decreased
P-aCO2 is normal
A-a gradient is very big as there are full vessels that do not get ventilated leading to overall hypoxemia in comparison to alveoli that are getting ventilated

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87
Q

What is the first big branch point in determining the cause of hypoxemia

A

Is the A-a gradient normal or enlarged
Normal = altitude or hypoventilation
Enlarged - Diffusion problem, V/Q, shunt

88
Q

How do you differentiate a hypoxemia with an enlarged A-a

A

You do a CO breath test to check for diffusion problem. If normal then give patient 100% oxygen, if A-a gradient corrects then it was V/Q mismatch (even though ventilation was poor there was some). If it does not correct it means it was a full shunt and oxygen didn’t get close to blood in problem area

89
Q 
During low hemoglobin concentrations what happens to:
P-aO2
S-aO2
P-aCO2
A-a gradient
A

They ALL remain NORMAL, the better way to figure out if patient has low Hb concentration is to directly blood test. C-aO2 however would low in this situation

90
Q

How do we calculate the A-a gradient

A

Get P-aO2 and P-aCO2 from blood test
Equate P-aCO2 to P-ACO2 and use alveolar gas equation
P-AO2 = (P-Barr - 47)*FiO2 - (P-ACO2/R)
Once you’ve calculated P-AO2, subtract P-aO2

91
Q

How is CO2 carried in blood (3)

A
  • Freely dissolved (1.2 mM)
  • Carbamino compound (bound to Hb) (1.2 mM)
  • Bicarbonate (24 mM)
92
Q

What is Haldane effect

A

When O2 concentration increases Hb affinity for CO2 decreases

93
Q

Compare Bohr and Haldane effects

A

They are essentially opposites
Bohr - when CO2 increases Hb affinity to O2 decreases
Haldane - when O2 increases Hb affinity for CO2 decreases

94
Q

What are the big intra and extracellular buffers

A

Intracellular - hemoglobin

Extracellular - bicarbonate

95
Q

What is Henderson Hasselbalch Equation

A

pH = pK + log [A-]/[HA]

96
Q

What is H-H Equation for CO2

A

pH = 6.1 + log [HCO3-]/[CO2]

at sea level with normal bicarbonate = 24 and carbon dioxide = 40, ph = 7.4 (normal physiologic level)

97
Q

What makes bicarbonate such a good buffer (3)

A
  • There is a TON of it in our blood
  • Its pKa is close to our pH of 7.4
  • Its conjugate acid CO2 can be tightly controlled since it can be ventilated away
98
Q

Why is pH in your veins only slightly lower than arterial despite all the extra CO2

A

Because deoxyhemoglobin is an excellent buffer, gets CO2 transformed into bicarbonate and buffers the protons the bicarb releases

99
Q

What ways do we compensate for pH (2)

A

-Ventilate off CO2
-Kidneys retain/conserve bicarbonate
(these two can go either way)

100
Q

What are normal values for pH, P-aCO2, and Bicarbonate at sea level

A

pH - 7.4
P-aCO2 - 40 Torr
Bicarbonate - 24 mM

101
Q

Will compensation completely correct initial acid-base disorders?

A

NO!! NEVER!

102
Q

Will initial acid-base disorder ever be completely compensated

A

NO!!

103
Q

Describe respiratory acidosis

A

Increased P-aCO2 giving a decreased pH. This is mainly hypoventilation leading to the increased CO2

104
Q

What are the compensation rules for respiratory acidosis

A

Acute - 10 Torr increase in CO2 gives 0.08 decrease in pH

Chronic - 1 Torr increase in CO2 gives 0.4 mEq increase in Bicarbonate

105
Q

Describe compensation

A

Does NOT mean pH has been brought back to normal, it means the body is acting at maximal capacity to bring pH back to normal

106
Q

What are some acute causes of respiratory acidosis (2)

A
  • Drugs (opiates, benzos, EtOH)

- Muscle fatigue

107
Q

What are some chronic causes of respiratory acidosis (5)

A
  • Central obesity hypoventilation
  • Neuromuscular disorders (ALS)
  • Chronic lung disease (COPD, emphysema, bronchitis)
  • Hypothyroidism
  • Bronchiectasis
108
Q

Describe respiratory alkalosis

A

Decreased P-aCO2 giving increased pH, largely due to hyperventilation

109
Q

What are the compensation rules for respiratory alkalosis

A

Acute - 10 Torr decrease in CO2 gives 0.08 increase in pH

Chronic - 1 Torr decrease in CO2 gives 0.4 mEq decrease in Bicarbonate

110
Q

How do compensation rules for respiratory alkalosis and acidosis differ

A

They don’t! They are exactly the same except the increase and decrease are switched

111
Q

What are some acute causes of respiratory alkalosis (4)

A
  • Pain
  • Anxiety/Panic
  • Fever
  • Mechanical ventilation (improper settings)
112
Q

What are some chronic causes of respiratory alkalosis (4)

A
  • High altitude (excessive respiratory drive from hypoxia)
  • Brain injury (disabled inhibitory input)
  • Pregnancy
  • Salicylate toxicity (Aspirin)
113
Q

Describe metabolic acidosis

A

Increased acid from a source OTHER than CO2 leading to decreased HCO3-

114
Q

What are the compensation rules for metabolic acidosis

A

Winter’s formula: P-aCO2 = 1.5 * [HCO3-] + 8 (+ or - 2)
If values match then compensation is complete
If they don’t then there is also a component of respiratory acidosis

115
Q

What is Winter’s Formula

A

Compensation rules for metabolic acidosis

P-aCO2 = 1.5 * [HCO3-] + 8 (+ or - 2)

116
Q

What is the anion gap

A

Anion Gap = Na - (Cl + HCO3) which should = 12 + or - 2 (10-14)

117
Q

What does the anion gap tell you

A

If it is greater than 12 (+ or - 2) then there are additional acids in the blood that are not accounted for. You have a anion gap metabolic acidosis and can apply MUDPILES!

If not elevated but pH is low then you and have non-gap metabolic acidosis which could be from loss of HCO3 in diarrhea, from kidneys, or diluted form too much IV saline

118
Q

What does mudpiles stand for and what is is used for

A 
Pneumonic for causes of anion gap metabolic acidosis
Methanol
Uremia
Diabetic Ketoacidosis
Propylene glycol
Isoniazid
Lactate
Ethylene glycol
Salicylates
119
Q

What are some causes for non-anion gap metabolic acidosis (4)

A
  • Loss of bicarbonate in diarrhea
  • Loss of bicarbonate from kidneys
  • Retentions of H+ in kidneys
  • Too much IV saline diluting HCO3
120
Q

Describe metabolic alkalosis

A

Too much bicarbonate or other base (or too much decrease in acid OTHER than CO2) leading to increase in pH

Body attempts to hypo ventilate but will NOT go so low as to cause hypoxia

121
Q

Is our body better at dealing with alkalosis or acidosis

A

Acidosis by far!
Alkalosis is difficult because we will NOT hypo ventilate to the point to cause hypoxia to decrease pH

At pH of 7.7 can get fatal seizures and arrhythmias

122
Q

What are the compensation rules for metabolic alkalosis

A

1 mEq increase in [HCO3-] gives 0.7 Torr increase in CO2

123
Q

What are some causes of metabolic alkalosis (4)

A
  • Vomiting (loss of gastric acid)
  • Diuretics (loss of acid in urine)
  • Hypovolemia (causes kidneys to contract)
  • Ingesting too many antacids or HCO3
124
Q 
What are normal values for the following in Denver
pH
P-aCO2
[HCO3-]
P-aO2
A

pH - 7.4
P-aCO2 - 36
[HCO3-] - 22
P-aO2 - 80

125
Q

What happens to [HCO3-] in acute respiratory acidosis

A

Nothing, it is normal acutely, but once problem becomes chronic and kidney gets involved [HCO3-] increases

126
Q

What happens to [HCO3-] in acute respiratory alkalosis

A

Nothing, it is normal acutely, but once problem becomes chronic and kidney gets involved [HCO3-] decreases

127
Q

Where are peripheral chemoreceptors located

A

Carotid bodies at the branch point of carotid artery

128
Q

What do peripheral chemoreceptors detect (3)

A
  • Low O2 - most important
  • High CO2 - fast but only accounts for 20% of vent change
  • High [H+] - fast, only mediator of metabolic acid/base insults
129
Q

Where are central chemoreceptors located

A

Ventral surface of medulla

130
Q

What do central chemoreceptors detect

A

Changes in CO2 - slow

131
Q

Are there central chemoreceptors for oxygen

A

NO

132
Q

How can central chemoreceptors be so sensitive to changes in [H+]

A

Because there are NO buffers in the CSF

133
Q

What three areas have dual blood supply

A

Liver - hepatic portal and hepatic artery
Lung - pulmonary and bronchial artery
Anterior pituitary

134
Q

If you are coughing up blood what artery is it coming from

A

Bronchial artery (because of higher pressure), NOT pulmonary

135
Q

How does pulmonary circulation relate to electrical physics

A

Voltage = Flow * Resistance
Change in pressure = CO * Pulmonary vascular resistance
Change in pressure is (Pulmonary Artery - Left Atrium)

136
Q

What is going on if pulmonary artery pressure is far different from post capillary wedge pressure

A

If the difference in DIASTOLIC pressure is >5 Torr this means there is some pulmonary vascular resistance problem occurring. (in normal circumstances pulmonary vasculature is low pressure, low resistance, low elastance)

137
Q

Compare systemic and pulmonary vasculature (3)

A 
Pulmonary is:
-low resistance
-low pressure
-low elastance
Systemic is opposite (elastance allows for accepting high systolic pressures and evenly pushing out that kinetic energy)
138
Q

What are systolic pressures of RA, RV, LA, LV

A

Remember nickel, dime, quarter, dollar

139
Q

How do systolic pulmonary pressures differ from diastolic

A

During systole pulmonary artery is 25 but PCWP is 12. But during diastole they are both the same at 10.

140
Q

Describe physiologic lung zone 1

A

P-A > P-a > P-v
In this case alveolar pressure is greater than both vascular pressures thus there is NO blood flow in the area, there is very little of zone 1 in normal lungs

141
Q

How does blood pressure in apex compare to lower lobe

A

Blood pressure increases by about 11 Torr from Apex to middle of lung, and then by another 11 Torr to lower lobe. 22 Torr difference overall

142
Q

Describe physiologic lung zone 2

A

P-a > P-A > P-v
This is case at the apex of lung of intermittent blood flow, during systole blood flows with arterial pressure overcoming alveolar pressure, but during diastole alveolar pressure overcomes venous and collapses the vessel

143
Q

Describe physiologic lung zone 3

A

P-a > P-v > P-A

Blood flow is constant, this is where you want swan-gaz catheter

144
Q

Where do you want to place catheter when attempting to get Pulmonary Artery and PCWPressure

A

In physiologic lung zone 3, or another way of saying it is in a lower lobe of the lung

145
Q

What are the ways the lung circulation can go bad (3)

A
  • Abnormal gas exchange (hypoxemia/hypercapnea)
  • Increase in fluid in lung (cardiogenic/non-cardiogenic)
  • Increase in pulmonary vascular resistance (left heart failure)
146
Q

How does hydrostatic pressure difference in lung compare to oncotic pressure difference

A

Hydrostatic > Oncotic
This leads to slight net flow of fluid into lung but that is OK because lymphatic vessels are able to shuttle that extra fluid away

147
Q

How do lungs deal with extra fluid (3)

A
  • Lymphatic vessels shuttle away
  • Extra fluid decreases osmolarity of interstitial space which increases osmotic pressure for fluid to reenter blood
  • Hydrostatic pressure in interstitial space increases, which decreases the difference between interstitial space and vessel, slowing flow
148
Q

Describe cardiogenic edema

A

Increased pulmonary vascular pressure pushes fluid into lungs, most commonly high PCWP from left heart failure

149
Q

Describe non-cardiogenic edema

A

Increased pulmonary vascular permeability, destroys oncotic gradient (ARDS, pneumonia)

150
Q

How do you differentiate cardiogenic from non-cardiogenic edema (5)

A
  • Clinical history (CHF - cardio) (ARDS/pneumonia - NON)
  • Time course (fast minutes - cardio) (slow hours - NON)
  • CXR (central edema w/ Kerley B lines - cardio) (infiltration everywhere - NON)
  • Response to diuretics (helps - cardio)
  • PCWP above 15 (cardio)
151
Q

What is definition of pulmonary hypertension

A

Mean arterial blood pressure of pulmonary artery > 25

152
Q

What is needed for pulmonary ARTERIAL hypertension (3)

A
  • mean PAP >25 (high)

- PCWP 3 (high)

153
Q

Name the 5 WHO groups for pulmonary hypertension

A 
1- Pulmonary Arterial Hypertension
2- PH due to left heart disease
3- PH due to Lung disease or hypoxia (e.g. ILD or altitude)
4- Embolism
5- Unclear reasons
154
Q

What are subcategories for WHO group 1 (7)

A
  • Idiopathic
  • Heritable (bone morphogenic protein)
  • Drugs
  • Connective tissue disorder (scleroderma)
  • HIV
  • Schitosomiasis
  • Congenital heart disorder (Eisenmengers)
155
Q

What are ways you get ACUTE pre-capillary pulmonary hypertension (3)

A
  • Pneumonia (hypoxic vasoconstriction)
  • High altitude (hypoxic vasoconstriction)
  • Embolism
156
Q

What are ECG changes seen in Pulmonary Embolism

A

S I, Q III, T III

Also see sinus tachycardia

157
Q

What are 3 key findings in idiopathic pulmonary hypertensions

A

NORMAL pulmonary function tests, NORMAL lung sounds, decreased DLCO (you will also see JVD and peripheral edema but those are easier to intuit from a pre capillary hypertension disease)

158
Q

What pathways can you target with pharmaceuticals in patients with pulmonary arterial hypertension (4)

A
  • Endothelin (block this vasoconstrictor)
  • NO (cGMP) (with Phosphodiesterase inhibitors)
  • Prostacyclin (cAMP)
  • Calcium channel blockers (only use in acute vasodilator responders)
159
Q

What should you think about first in patient’s with pulmonary arterial hypertension before giving vasodilators (4)

A
  • Treat underlying cause
  • Hypoxia
  • Coagulation
  • Volume overload
160
Q

What are acute vasodilator responders (3)

A

During catheterization administration of NO or IV prostacyclin causes:
- 10 Torr decrease in PAP
- PAP drops below 40
- CO stays stable
This means person can be given calcium channel blockers as treatment and they have very good prognosis

161
Q

What medications would you use for NON acute vasodilator responders

A
  • Endothelin antagonists
  • Phosphodiesterase antagonists (NO pathway)
  • Prostacyclin
162
Q

How do you treat pulmonary venous hypertension

A

Do NOT give pulmonary artery dilators like in PAH or else you will totally overload lungs leading to severe injury. Treat like you would heart disease

  • Decrease preload with diuretics
  • Decrease afterload
  • Increase isotropy
  • Check for valve disease or ischemia
163
Q

What type of pulmonary edema develops in pulmonary arterial hypertension PAH

A

NONE! Impedance to blood flow occurs before the capillary bed, thus no increase in hydrostatic pressure and thus no edema

164
Q

What decreases tactile fremitus

A

Separation of the lung from the chest wall (pleural effusion or pneumothorax) or complete collapse of alveoli (atelectasis)

165
Q

What increases tactile fremitus

A

When lung is partially filled with fluid, i.e. consolidation and pulmonary edema

166
Q

When does tracheal deviation go towards pathology (3)

A
  • Part of lung removed
  • Atelectasis
  • Pulmonary fibrosis pulling it towards its side
167
Q

When does tracheal deviation go away from pathology

A

When pleura is filling with fluid or air (pleural effusion or pneumothorax)

168
Q

With a pleural effusion what do the following show
Tactile Fremitus
Tracheal Deviation
Percussion

A

Decreased
Away
Dull

169
Q

With a pneumothorax what do the following show
Tactile Fremitus
Tracheal Deviation
Percussion

A

Decreased
Away
Hyper-resonant

170
Q

With atelectasis what do the following show
Tactile Fremitus
Tracheal Deviation
Percussion

A

Decreased
Toward
Dull

171
Q

What can Crackles indicate (3)

A

-Pulmonary edema
-Pneumonia
-Interstitial lung disease
(lecturer gave example of Cystic fibrosis with crackles)

172
Q

What can Rhonci indicate

A

Narrowed airways from MUCUS

173
Q

What can Wheezes indicate (3)

A

General narrowing of conducting airways, usually expiratory

  • Asthma
  • Bronchiolitis
  • could be emphysema/COPD
174
Q

What can Egophony indicate

A

Compressed or fluid filled areas (Pneumonia)

175
Q

What can Stridor indicate

A 
Usually inspiratory (vocal chord dysfunction)
(expiratory could be tumor)
176
Q

What are some possible causes for an increased DLCO (3)

A
  • Polycythemia vera
  • Early CHF (increased PCWP slows blood for more time for diffusion)
  • Asthma (not sure why)
177
Q

What are some possibly causes for decreased DLCO (5)

A
  • Anemia
  • Late CHF (pulmonary edema develops inhibiting diffusion)
  • Pulmonary vascular disease (blood going too fast?)
  • Interstitial lung disease (thick wall)
  • Emphysema (area decreased)
178
Q

What is possibly happening when TLC and FRC are normal but RV is high

A

Dynamic airway collapse

179
Q

What constitutes a positive bronchodilator response

A

> 12% increase and >200cc absolute change in FEV-1 and/or FVC

180
Q

What constitutes a positive bronchoprovocation test

A

You are looking at what amount of methacholine do you need to get a 20% decrease in airflow (FEV-1). If it only takes 8 mg/ml then that is such a low response you suspect asthma

181
Q

How does our body compensate for high V/Q

A

Decreased CO2 leads to increase in AIRWAY resistance, this lower ventilation for high V/Q

182
Q

How does our body compensate for low V/Q

A

Decreased O2 leads to hypoxic vasoconstriction, this lowers perfusion for low V/Q

183
Q

What are normal values for P-aO2, sea level and Denver

A

Sea level - 104

Denver - 80

184
Q

What are normal values for P-aCO2, sea level and Denver

A

Sea level - 40

Denver - 35

185
Q

What are normal values O2 saturation, sea level and Denver

A

Sea level - 97.5%

Denver - 95%

186
Q

What are normal values for C-aO2, sea level and Denver

A

Sea level - 20.7

Denver - 19

187
Q

What are normal values for C-aCO2, sea level and Denver

A

Sea level - 44

Denver - 42

188
Q

How did O’Donaughy define hypoventilation

A

Breathing that is NOT sufficient for metabolic needs (production of CO2)

189
Q

How does dead space increase P-aCO2

A

P-aCO2 = V-CO2 / V-A (alveolar ventilation equation)
V-A = Respiratory Rate * (Tidal Volume - Dead Space)
Thus Dead space increases, V-A decrease, P-aCO2 increases

190
Q

What is the difference between S-pO2 and S-aO2

A

S-pO2 is percentage of hemoglobin that is bound at all. S-aO2 is percentage of hemoglobin bound to O2 specifically. Thus in case of CO poisoning pO2 would still be read as high while aO2 would be low.

191
Q

What can cause increased dead space (4)

A
  • Rapid shallow breathing (anatomic deadspace, hypoventilation)
  • Embolism (alveolar deadspace)
  • Cardiac output problems (alveolar)
  • Ventilation in excess of perfusion (from ventilators or emphysema)
192
Q

What are 5 causes of hypoxemia

A
  • Low ambient O2
  • Hypoventilation (obesity, neuromuscular, drugs)
  • V/Q mismatch
  • Shunt
  • Diffusion problems (ILD)
193
Q

What causes hypercapnea

A

Poor ventilation (Can’t breath or won’t breath)

194
Q

What are causes of a “won’t breath” hypercapnea (4)

A
  • central obesity hypoventilation
  • drugs
  • traumatic brain injury
  • seizures
195
Q

How do you determine chronicity of respiratory hypoxemia

A

medical history and clinical context from patient

196
Q

How do you determine chronicity of respiratory hypercapnea

A

Compensation equations for respiratory acidosis!
Acute
pH change = 0.008 * change in CO2
HCO3 increases 1 mEq for every 10 Torr increase in CO2
Chronic
pH change = 0.003 * change in CO2
HCO3 increases 4 mEg for every 10 Torr increase in CO2

197
Q

What is another way of calculating respiratory acidosis compensation equations

A

(Change in pH) / (Change in P-aCO2)
If it equals 0.008 then acute
If it equals 0.003 then chronic

198
Q

How is ARDS defined (4)

A
  • occurring over last week
  • bilateral diffuse infiltrates
  • no cardiac component
  • severity ratio of <200 (more severe acute lung injury, ALI)
199
Q

How do you calculate severity of ARDS

A

Divide P-aO2 by FiO2, should be 500
<200 is ARDS
(example in Denver 80/.21 = 380, still normal?)

200
Q

What are most common causes of ARDS (5)

A
  • Sepsis
  • Trauma
  • Pancreatitis
  • Aspiration
  • Transfusion
201
Q

Before increasing someone’s tidal volume on a ventilator what should you double check?

A

CXR to see if they have bilateral infiltrates and could possibly be experiencing ARDS because ONLY good treatment is LOW tidal volume ventilation, prone if more severe

202
Q

What are the effects of EtOH on immune function (4)

A
  • Changes mouth bacterial flora
  • Depresses coughing function (leads to more aspiration)
  • Depresses innate immune system
  • Depresses adaptive immune system
203
Q

What is Kartagener’s syndrome

A

Collection of symptoms from immotile cilia

  • situs inversus (visceral organs flipped)
  • chronic sinusitis
  • bronchiectasis
  • infertility in women (fallopian tube immotility)
204
Q

When you see hilar and mediastinal lymphadenopathy on CXR what should you be thinking

A

Sarcoidosis OR Non-hodgkins lymphoma

205
Q

What is the primary cell you would find in a bronchoalveolar lavage in a normal lung

A

Macrophages 90-95%

Also you would see 2:1 ratio of CD4:CD8 in lymphocytes

206
Q

What is the primary cell you would find in a bronchoalveolar lavage of a lung with sarcoidosis

A

Lymphocytes 95%

Also CD4:CD8 ratio goes from 2:1 to 15:1

207
Q

For Th1 cells:
What factor stimulated their differentiation from naive CD4
What type of pathogens does it combat
Example
What factor increases the percentage of cells

A
  • IL12
  • intracellular pathogens with cell mediated immunity
  • sarcoidosis
  • IFN-gamma (inhibits Th2 and Th17 production)
208
Q

For Th2 cells:
What factor stimulated their differentiation from naive CD4
What type of pathogens does it combat
Example
What factor increases the percentage of cells

A
  • IL4
  • helminths and allergies
  • asthma
  • IL4 (also inhibits Th1 and Th17 production)
209
Q

For Th17 cells:
What factor stimulated their differentiation from naive CD4
What type of pathogens does it combat
Example
What factor increases the percentage of cells

A
  • IL23 and IL6
  • bacteria and autoimmunity
  • rheumatoid arthritis and multiple sclerosis
  • TGF-beta (inhibits Th1 and Th2 production)
210
Q

What is difference between CD4 and CD8 memory

A

CD8 lasts longer

CD4 memory requires RE-immunization to maintain immunity

211
Q

What does activation of Toll Like Receptors accomplish

A

Bridges innate and adaptive immunity, generates an inflammatory response

212
Q

What is MyD88

A

Adapter within cell for when Toll Like Receptors are activated that helps activate NF-kB to get big changes in cell

213
Q

What are two general causes of obstructive lung disease

A
  • Narrowing of conducting airways

- Floppiness of conducting airways leading to dynamic collapse

214
Q

What are two components of work during breathing

A

Resistive - airway resistance - inspiration

Elastic - elastic recoil of lungs - expiration

215
Q

What is double whammy of obstructive lung diseases

A

Not only do you have increased airway resistance making it harder to breath, but you are breathing at large lung volumes which puts your already stressed diaphragm into a bad position

  • increased airway resistance
  • overstretched diaphragm
216
Q

What are abnormal PaO2 levels at sea level, at Denver

A

At sea level remember normal progression of PIO2 = 150, PAO2 = 100, PaO2 = 90. Abnormal values are
Sea level < 80
Denver < 65
These would mean person is hypoxemic

CVPR Pulmonary (2 decks)

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