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adv princip II exam 2 (6/13) > anesth 4 thoracic surg 1/3 (pgs 1-28) > Flashcards

anesth 4 thoracic surg 1/3 (pgs 1-28) Flashcards

0
Q

section 1: anatomy of respiration

what is pao2 at the lips?

A

160mmhg (.21 x 760)

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1
Q

section 1: anatomy of respiration

  1. what is the moisture content of air in the nasopharynx?
  2. what is it by the time it reaches the carina
A
  1. 70-80% relative humidity

2. 100% humidified by the time it reaches the carina

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2
Q

section 1: anatomy of respiration

what is pao2 by the time it leaves the nasal turbinates?

A

150 (760-40=720… 720 x .21=150)

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3
Q

section 1: anatomy of respiration

how much of the Dead space anatomy does the upper airway constitute?

A

30-50% of VD anat.

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4
Q

section 1: anatomy of respiration

  1. what can a NT tube block/ cause?
  2. how long might it take for symptoms to emerge?
A

1a) eustachian tube
b) frontal and maxillary sinuses (causing sinusitis)
c) otitis media
d) mastoiditis
2. may occur several days later

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5
Q

section 1: anatomy of respiration
lower airway:
what are bronchi and bronchioles sometines called?

A
  1. bronchi= central or large airways

2. bronchioles= peripheral or small airways

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6
Q

section 1: anatomy of respiration

what type of respiration is the lower airway responsible for?

A

external respiration (the transfer of gasses from and to the atmosphere)

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7
Q

section 1: anatomy of respiration

  1. what generation is the trachea?
  2. what is its length and diameter?
  3. what vertebral level is the carina at?
  4. what forms the trachea?
  5. where are the cords?
A
  1. trachea is generation “0”
  2. length is 10-13 cm; diameter is 1.5-2.5 cm
  3. carina is at level of T4-T6
  4. formed by 16-20 “C” shaped cartilaginous rings
  5. cords at C4-5
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8
Q

section 1: anatomy of respiration

  1. what generation is mainstem bronchi?
  2. what angle for right and for left?
  3. how far down mainstem is RUL bronchi?
A
  1. bronchi are generation 1
  2. right is 25 degrees; left is 40-60 degrees
  3. RUL is 2.5 cm past the carina
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9
Q

section 1: anatomy of respiration

  1. what airways are generation 2?
  2. how many do you have?
A
  1. lobar bronchi are generation 2

2. you have 3 right and 2 left (one for each lobe)

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10
Q

section 1: anatomy of respiration

  1. generation 3 are?
  2. how many are there?
A
  1. segmental bronchi

2. 18

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11
Q

section 1: anatomy of respiration

  1. generations 4-9
  2. what happens to the size and cartilage?
  3. how much airway resistance below the glottis normally occurs here?
  4. what begins to emerge here?
A
  1. subsegmental bronchi #4-9
  2. size from 4 mm to 1 mm with decreasing amounts of cartilage
  3. 80% of RAW (airway resistance) below the glottis occurs here
  4. emergence of goblet cells and mucosal glands
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12
Q

section 1: anatomy of respiration

  1. broncioles are generation #?
  2. tube diameter is how big? (what is that the same size as?)
  3. what happens to the walls? How is patency maintained?
  4. how much of the RAW is found in these airways (2 mm or less)?
  5. how is this possible?
A
  1. broncioles are generation #s 10-15
  2. tube diameter is 1mm (same diameter as a period “.”).
  3. no cartilage in walls. patency is maintained by elasticy of surrounding parynchyma
  4. less than 20% (in airways
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13
Q

section 1: anatomy of respiration

  1. what is the last portion of the airways to only conduct (and not exchange gasses)? what generation are they?
  2. what is their diameter?
  3. what cells start here? what do they produce?
A
  1. terminal bronchioles (generation 16)
  2. diameter is 0.5 mm
  3. contains surfactant producing Clara cells
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14
Q

section 1: anatomy of respiration

  1. what is the name of the respiratory pathways of generations 17-19?
  2. what is this the beginning of?
  3. what factors influence airway patency here?
A
  1. respiratory bronchioles
  2. beginning of lung parenchyma (gas exchange units of the lung)
  3. airway patency factors are same that influence alveolar patency
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15
Q

section 1: anatomy of respiration

  1. alveolar ducts…what generation?
  2. how many of these?
  3. alvolar ducts arise from?
A
  1. generation 20-24
  2. 9 million of these
  3. ducts arise from walls of respiratory bronchioles
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16
Q

section 1: anatomy of respiration

  1. what is generation 25?
  2. what percentage of alveoli arise from what 2 origins?
A
  1. alveolar sacs

2. 65% arise from sacs; 35% arise from ducts

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17
Q

section 1: anatomy of respiration

  1. generation 26…?
  2. what is the surface area?
  3. how are alveoli connected?
  4. why have so many (how many)?
A
  1. alveoli
  2. 9m x 9m (80 m squared or 29 ft x 29 ft)
  3. connected by “pores of Kohn”
  4. by having 300,000,000 single alveoli, surface area for gas exchange is increased
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18
Q

section 1: anatomy of respiration

  1. how much of lung volume is alveolated?
  2. how much of total lung volume is dead space?
A
  1. 3L

2. 150 ml

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19
Q

section 1: anatomy of respiration

  1. what is TLC (total lung capacity) in Liters?
  2. what is FRC (functional residual capacity) in liters?
  3. what is
A
  1. TLC=6L
  2. FRC=2.5L
    3.
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20
Q

section 1: anatomy of respiration

where is blood distributed in the body at any one momemt?

A

a) veins= 65%
b) arteries= 15%
c) pulmonary vessels= 9%
d) heart= 7%
e) capillaries= 5%

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21
Q

section 1: anatomy of respiration

how much distending pressure does it require to take a 500 mL breath

A

3 cmH2O

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22
Q

section 1: anatomy of respiration

  1. Where does most of the RAW is below the glottis occur?
  2. where does the rest occur?
A
  1. 80% of the RAW below the glottis occurs at the subsegmental bronchi (generations 4-9)
  2. the other 20% occurs at the bronchioles (generations 10-15)
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23
Q

section 2: regulation of respiration:

  1. inspiration is always ____?
  2. exhalation is always ____ except for ____?
A

regulation of respiration:

  1. inspiration is always -active?
  2. exhalation is always -passive except for -with active expiration?
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24
Q

section 2: regulation of respiration:

what muscle groups are used in inspiration?

A
  1. diaphragm
  2. external intercostals
  3. accessory muscle group
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25
Q

section 2: regulation of respiration:

how do the external intercostals work?

A
  • elevate anterior end of each rib

- increases AP and transverse diameter by bucket handle

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26
Q

section 2: regulation of respiration:

  1. what innervates the diaphragm
    2a. how much excursion does the diaphragm cause with normal excursion ?
    2b. with effort?
A
  1. controlled by phrenic nerve c3,4,5
    2a. 1.5 cm
    2b. 7-8 cm
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27
Q

section 2: regulation of respiration:

What are the layers of alveolar epithelium (that we need to know)?

A
  1. type I, type II, type III
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28
Q

section 2: regulation of respiration:

what is type I alveolar epithelium?

A

specialized for gas exchange, form the thin alveolar walls

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29
Q

section 2: regulation of respiration:

what are type II epithelium (what do they do)?

A
  • cover 10% of the alveolar surface
  • produce surfactant
  • regenerate type I cells
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30
Q

section 2: regulation of respiration:

what are type III cells (what do they do)?

A

phagocytic macrophages which aid in cleaning debris

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31
Q

section 2: regulation of respiration:

  1. what are the major accessory muscles used in inspiration?
  2. what type of respiration are accessory muscles active in?
A
  1. sternocleidomastoid, scalenes (anterior, middle, posterior), pec major & pec minor
  2. not used during resting ventilation (used during exercise, strenuous breathing)
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32
Q 
section 2: regulation of respiration:
central chemoreceptors:
1. how do they work?
2. where are they located?
3. what are the effects of stimulating central chemoreceptors?
A
  1. sense changes in pH of CSF (monitor arterial CO2 concentration)
  2. located in medulla of brain
  3. increase ventilatory drive by stimulating inspiratory and vasomotor centers in the medulla (causing increased VT followed by increased RR, increased CO and increased SVR).
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33
Q 
section 2: regulation of respiration:
peripheral chemoreceptors:
1. what do they respond to?
2. where are they located?
3. what does their stimulation result in?
A
  1. respond to decreased O2 levels (decreased paO2, SaO2, Hb, pH as well as vastly increased paCO2 and methemoglobinemia)
  2. located in carotid bodies
  3. stimulation results in increased VE and CO (by increasing VT, RR, HR, BP, PVR also increased bronchial smooth muscle tone, adrenal cortical and cerebral cortex activity).
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34
Q

section 3. gas transport:

  1. what is pO2 AT the nose?
  2. what is pO2 at the larynx? why?
  3. what is pO2 at the alvoeli? why? what is co2?
  4. what is pO2 at the left ventricle? why?
  5. what is pO2 at right ventricle/ PA? why? what is CO2?
A
  1. at nose=160 mmhg
  2. at larynx=150 mmhg; d/t mixing with H20 (.21 x (760-47))
  3. at alveoli=102 mmhg; d/t mixing with CO2 (which is 40mmhg)
  4. at LV=94 mmhg; d/t mixing with “blue” shunt blood from thebesian, bronchial and pleural vessels
  5. at RV/PA=40 mmhg; 46 mmhg d/t drop off of O2 to tissues and pick up of co2
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35
Q

section 3. gas transport:

what happens to barometric pressure (pB) with an increase in altitude?

A

pB drops as altitude increases

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36
Q

section 3. gas transport:

  1. what percentage of air is oxygen?
  2. nitrogen?
  3. Co2?
A
  1. 21%
  2. 78%
  3. 0%
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37
Q

section 3. gas transport:

what is the alveolar pressure at end expiration?

A

equal to atmospheric pressure

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38
Q

section 3. gas transport:

what does an increase in pACO2 (alveolar CO2) do to pAO2 (alveolar O2)?

A

increased pACO2 decreases pAO2 (since nitrogen level doesnt change and vapor pressure is dependent on temp; if one tension increases (co2) the other (o2) must decrease).

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39
Q

section 3. gas transport:

  1. what does the respiratory quotent (R) state?
  2. what does this mean for pAO2 when pACO2 increases?
A
  1. that for every 250 ml of oxygen that enters the body, 200 ml CO2 must leave (quotent=0.8)
  2. for every increase in CO2 by 1 mmHg, PAO2 will decrease by 1.2 mmHg
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40
Q

section 3. gas transport:

1. Is alveolar O2 (pAO2) equal to arterial O2 (paO2)?

A
  1. shunted blood causes arterial O2 to ALWAYS be lower than pulmonary end capillary (or alveolar) pO2
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41
Q

section 3. gas transport:

what is the formula for (alveolar) pAO2?

A

pAlvO2=(Fio2 x [pB-47]) - (1.2 x paCO2)

ex. —.21 x (760-47) - 1.2 x 40 =
- –149.73-48

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42
Q

section 3. gas transport:

what does an elevated alveolar-arterial gradient reflect?

A

lung disease

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43
Q

section 3. gas transport:

how much oxygen does nasal canula give you?

A

1 to 6 L=24 to 44% (4% per Liter)

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44
Q

section 3. gas transport:

how much oxygen does a face mask give?

A

8 to 10 liters (at least more than 5 Liters) equals 40-60%

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45
Q

section 3. gas transport:

How much oxygen does a face mask with reservior (NRB)give?

A

a flow of 6 to 10 L; yields 60-100%

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46
Q

section 3. gas transport:

venturi mask delivers how much oxygen?

A

4-8L yields 24-48%

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47
Q

section 3. gas transport:

what is denitrogenation absorptive atalectasis?

A
  • when there is a stenosis of an alveolar duct and a patient is given 100% o2 (for denitrogenation), the oxygen leaves the alveoli faster than more oxygen can get in (past the narrowing)
  • the alveoli then collapses
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48
Q

section 3. gas transport:

a. what are potential hazards of O2 therapy in adults?
b. in neonates?

A

a. in adults:
1. denitrogen absorbtion atalectasis
2. inhibition of HPV??
3. pulmonary toxicity
4. reduction of hypoxic ventilatory drive
5. issues due to mode of administration of O2:
- drying of mucous membranes
- nasal stuffiness
- sores from plastic tubing
- artificial airway hazards
b. in neonates:
1. bronchopleural dysplasia and
2. retrolental fibroplasia (eyes)

49
Q

section 4. blood gasses/ acid base:

  1. what is a normal PO2?
  2. what happens as you get older?
A
  1. normally 95 mmhg;

2. falls to 85 at age 60 d/t increased VA/Q inequality

50
Q

section 4. blood gasses/ acid base:
“anchors” of the Hb/O2 dissociation curve:
1. what is your sat when your pO2 is 40 mmhg?
2. what is your sat when your pO2 is 60 mmHg?
3. what is your sat when your pO2 is 100 mmHg?

A
  1. po2 of 40= o2 sat of 75% (mixed venous)
  2. po2 of 60= o2 sat of 90% (at the “knee” of the curve)
  3. po2 of 100=o2 sat of 97% (arterial blood)
51
Q

section 4. blood gasses/ acid base:

what are 5 causes of arterial hypoxemia?

A
  1. hypoventilation
  2. diffusion impairment
  3. shunt
  4. VA/Q inequality (#1 by far!!!!!)
  5. reduction of FI02
52
Q

section 4. blood gasses/ acid base:

  1. what is hypoventilation (really)?
  2. what causes it?
A
  1. decreased alveolar ventilation

2. usually caused by diseases outside the lungs

53
Q

section 4. blood gasses/ acid base:

what 10 situations can cause hypoventilation?

A
  1. resp center depression
  2. medullary disease
  3. spinal conduction abnormalities (cervical dislocation etc.)
  4. anterior horn cell diseases (polio-myelitis)
  5. disease of peripheral nerves (gullian-barre)
  6. diseases of NMJ (MG, serin gas (anticholinesterase poisoning)
  7. muscular dystrophy
  8. crushed chest cage
  9. upper airway obstruction
  10. pickwickian syndrome (obesity, decreased resp fxn, polycythemia, sleep apnea)
54
Q

section 4. blood gasses/ acid base:

what are 2 cardinal features of hypoventilation?

A
  1. increased paCO2 (always); if VA is halved, paCO2 will double
  2. hypoxia is easily abolished by increasing Fi02
55
Q

section 4. blood gasses/ acid base:

what is the danger of supplemental oxygen in a sedated patient with inadequate respiration (high CO2 and low pH)?

A

this will give them a normal spO2 which can lull you into thinking respiration is adequate

56
Q

section 4. blood gasses/ acid base:

what is the oxygen content forumla?

A

(Hgb x 1.34 x Sao2) + (0.0031 x Pao2)

ex: (15 hgb x 1.34 x .97) + (.0031 x 100)
15 x 1.34=20.1
20.1 x .97= 19.47
19.47+ .31= 19.78 (note that only 1/3 of 1% (.31) of oxygen is free floating as PaO2)

57
Q

section 4. blood gasses/ acid base:

  1. why do some patients develop CO2 retention?
  2. which patient will usually have CO2 retention; an asthmatic, an emphysematous or a chronic bronchitis patient?
A
  1. usually from high WOB (work of breathing) d/t increased RAW (airway resistance)
  2. bronchitis patients usually retain CO2, asthma or emphysma usually do not.
58
Q

section 4. blood gasses/ acid base:

what is the henderson-hasselbach equation:

A
  • pH=pK + log [(HCO3-) / 0.03 (pCO2)]

- where pK=6.1

59
Q

section 4. blood gasses/ acid base:

what does an increase in CO2 of 10 mmhg do to the ph?

A

increase of 10 mmHg causes a decrease in pH of 0.1

ex: increase of co2 from 40 to 80 mmhg causes a pH drop from 7.4 to 7.0

60
Q

section 4. blood gasses/ acid base:

  1. what is the biggest consequence of hypoventilation?
  2. why not hypercapnia?
A
  1. hypoxemia/ hypoxia

2. brain tells body to breathe faster, but decreased oxygenation is hard to make up

61
Q

section 4. blood gasses/ acid base:

what is the difference in pH between an acute and chronic co2 retention?

A

chronic co2 retention will have a smaller ph drop d/t increase in bicarb retention (compensated resp. acidosis)

62
Q

section 4. blood gasses/ acid base:

what causes resp alkalosis?

A

acutely increased VE d/t pain, fear, anxiety, sepsis, asa o.d., liver failure, hypoxemia, interstitia lung disease, acute lung/airway disease or chronic in high altitudes
also seen in chronically ill resp patients which are ventiated too vigorously

63
Q

section 4. blood gasses/ acid base:

what causes resp acidosis:

A

severe impairment of chest bellows, CNS depression, severe lung airway disease

64
Q
  1. what is the difference between a:
    a) true shunt (aka physiological shunt)
    b) capillary shunt?
    c) shunt effect?
  2. what is the significant about shunts and hypoxemia?
A

1a. a TRUE SHUNT (aka physiological/ ANATOMIC shunt) is when “blue blood” mixes from an unventilated lung region or an ASD or AV fistula “blue blood” from thebesian, bronchial and pleural veins which never sees oxygen (3-5% of c.o. is from here). (BLUE Q WITHOUT V)
1b. a CAPILLARY SHUNT is when the lung is NOT ventilated but IS perfused (can be caused by fluid or gunk between the alveoli (ARDS, pneumonia etc.) (Q WITHOUT V)
1c. SHUNT EFFECT: blood is going one way and ventilation is going another way (in general) (Q WITH MINIMAL V)
2. shunt is the only cause of hypoxemia which does not respond to O2 therapy because you can only go to 100%fio2 (therefore you cannot compensate for deoxygenated blood in the mix).

65
Q

does shunting cause an increase in paCO2?

A

no, because ventilation will increase d/t chemoreceptors and blow off excess

66
Q
  1. what does QS/QT mean?

2. what does it explain

A
  1. QS=shunt flow (total right heart C.O. that doesnt pick up oxygen)
    QT= total flow (total right heart C.O. (includes QS)
  2. describes the type of shunt
67
Q

what is VD?

  1. what is VD physiol?
  2. what is VD mech?
  3. what is VD anat?
  4. what is VD alv?
A

VD stands for Dead Space Volume

  1. zone 1 (an area of ventilation with little to no perfusion)-VQ mismatch …
  2. mechanical dead space (from intubation or mask)
  3. anatomic dead space (150 ml from nose to terminal bronchioles)
  4. alveolar dead space (oxygenated alveoli which have no perfusion-can be zone 1 as well)
68
Q

what does intubation do to deadspace?

A

increases dead space

69
Q

what is DOT-1-2-3?

A

for every pound of weight you:
have 1 cc of dead space (x150 lbs=150 cc dead space)
need 2 cc of oxygen (x 150=300 cc of oxygen)
need 3 cc of tidal volume (x 150 equals 450 tidal volume)

70
Q

what affects zone 1?

A

cardiac output (what is needed to push blood up to the apices)

71
Q

what type of shunting is responsible for most of the hypoxemia of COPD and pulmonary embolism?

A

shunt effect (Va/Q inequality)

72
Q

arterial pCO2:
1. normal values-
2 a,b. causes of co2 retention-
3. what does paCO2(arterial) measurement reflect?

A
  1. normal pCO2=37-43 (or ~35-45)
    2a. hypoventilation
    2b. Va/Q inequality (however it may be compensated)
  2. direct measure of adequacy of alveolar ventilation (inversely proportonal)=increased alveolar ventilation= decreased co2
73
Q

what respiratory disease patients develop hypercapnea and what ones may not?

A
  • bronchitis patients retain co2

- asthma and emphysema may not

74
Q

when arterial pco2 retention is mentioned, what 2 things should pop into your mind?

A
  • respiratory acidosis

- ventilatory failure

75
Q

why do some patients develop co2 retention?

A

high work of breathng (WOB) d/t increased airway resistance(RAW)

76
Q
  1. anion gap is calculated how?

2. what is a normal anion gap?

A
  1. cations (metals) minus anions (non-metals)
    i. e. ([K+] + [Na+]) - ( [Cl-] + [HCO3])
    ex: (4 + 140) - (109 + 24)»> 144-133=11
  2. normal is 8-12 mEq/L
77
Q

what is a normal value of:

  1. HCO3:
  2. chloride:
  3. paO2:
  4. pCO2:
A
  1. HCO3= 22-26
  2. Chloride=95-110
  3. paO2=90-110
  4. pCO2= 35-45
78
Q

what is the formula for compliance?

A

change in volume/ change in pressure

79
Q

what causes increased anion gap acidosis:

A

poisons, toxins, methanol, ethylene glycol, (think mudpiles)

80
Q

what causes non anion gap acidosis (NAGMA)?

A

internal issues;

  1. loss of bicarb renal: renal tube acidosis, interstitial nephritis, early renal failure
  2. loss of bicarb GI: diarrhea, ureteral diversion procedures
  3. other: carbonic anhydrase inhibitors, acids containing Cl-, hyperalimentation
81
Q

what MNEMONIC for non anion gap acidosis (NAGMA)?

A

HARDUP

  • H-hyper al
  • A-acetazolamide use
  • R-renal tube acidosis/ renal issues/failure
  • D-diarrhea
  • U-uretosigmoid fistula
  • P-pancreatic fistula
82
Q

what is the MNEMONIC for increased anion gap acidosis?

A

MUDDPALES:

  • M-methanol
  • U-uremia
  • D-diabetic keto acidosis
  • P-parahaldehyde
  • I-iron infusion /INH
  • L-lactic acidosis
  • E-ethanol
  • S-salicylates (ASA)
83
Q
  1. what is HPV?

2. what do volatile agents do th HPV?

A
  1. hypoxic pulmonary vasoconstriction (hypoxia causes vasoconstiction to non oxygenated areas of the lungs, shunting blood to oxygenated areas; so that blood goes where it is most useful)…a good thing
  2. volatile agents decrease HPV (vasodilate pulmonary vasculature)
84
Q
  1. elastic forces in the chest wall tend to do what to the chest volume?
  2. elastic forces in the lungs tend to do what to the chest volume?
  3. what is the average intrapleural pressure
  4. what is the maximum inspiratory effort pressure?
  5. what is the maximum expiratory effort pressure?
A
  1. elastic forces in chest wall help to expand intrathoracic volumes;
  2. elastic forces in lung contract the intrathoracic volme
  3. negative 4-5 cmH20
  4. max inspiratory (against closed glottis)= negative 50 cmH20
  5. max expiratory (forced exhalation)= positive 70 cmH20
85
Q

what makes up transairway pressure?

A

Pmouth + Palveoli

86
Q

what makes up transpulmonary pressure?

A

Pmouth + Pintrapleural

87
Q

what does a laryngospasm during emergence cause?

A

negative pressure pulmonary edema

88
Q

what causes gas flow in the tracheobrachial tree?

A

changes in pressure gradients between mouth and alveoli (transairway and transpulmonary)

89
Q

what happens when the diaphragm descends? what gas law is it?

A
  • intrapleural pressure becomes more negative and volume increases
  • boyle’s law (when temp is constant, a decrease in pressure causes an increase in volume).
90
Q

static compliance vs. dynamic compliance:

what is the difference?

A
  • static compliance is the point at which gas flow has ceased (equilibrium of gas)
  • dynamic compliance is when there are changes in gas flow occuring (airway resistance)
91
Q
  1. what does the law of la place have to do with alveolar collapse in smaller alveoli?
  2. what prevents this?
A
  1. law of la place states that the smaller the diameter, the easier the collapse (especially when there is surface tension)
  2. surfactant breaks surface
92
Q

what is alveolar critical volume?

A

the point at which the surface tension and elastic forces causing collapse of alveoli is higher than the volume keeping the alveoli open

93
Q
  1. what is the law of laplace (for a sphere)?
A
  1. P=2T/R
  2. P= distending pressure necessary to maintain alveolar volume
    T= surface tension
    R= radius
  3. in other words, the P(distending pressure) is balanced with the T (surface tension of air-liquid interface) and the R (radius of the alveoli).
    If the surface tension remains the same but the alveolar radius decreases, the amount of distending pressure would have to increase to maintain alveolar volume (keep the alveoli open).
94
Q

what is significant about shunt affect vs. capillary and anatomical shunt

A

shunt effect is responsive to oxygenation (O2 therapy)—

perfusion > ventilation

95
Q

how does a capillary shunt differ from shunt effect?

A
  • capillary shunt is when a whole region of the lung is bypassed (d/t not being oxygenated
    i. e. regional/ lobar pneumonia
  • shunt effect is a shunt when there is perfusion with some ventilation to some of the alveoli (not a whole region)
    i. e. atalectasis
96
Q

what is another name for non anion gap acidosis

A

hyperchloremic acidosis

97
Q

What normal functions cause CO2 to

  1. rise?
  2. fall?
A
  1. co2 rises slightly during sleep

2. falls slightly during exercise

98
Q

what is the paco2 level in many patients with altered VA/Q ratios?

A

normal, but it can be high

99
Q

what happens when the lung pressure change doesnt yield an equivalent volume change

A

the lung is not very compliant (the lung doesnt respond correctly to the pressure)

100
Q
  1. what is lung compliance?
  2. what is lung elasticity?
  3. when a lung is on a gas machine and is less compliant, what is needed to give the tidal volume?
  4. what type of loop will be seen and on what graph?
A
  1. lungs ability to give (stretch)
  2. the lungs ability to recoil
  3. increased pressure
  4. the loop will be more horizontal than normal on the pressure volume loop
101
Q
  1. what does the flow volume loop depict?

2. what is the “R” in that statement?

A
  1. RAW (airway resistance)

2. “R” stands for “change in pressure/ flow (Q)

102
Q
  1. what is laminar flow characterized by?

2. what is the shape of the flow?

A
  1. less friction in the middle but the most friction (drag) along the sides of the tube;
  2. causes a cone shaped flow
103
Q

how does Q change with change in radius?

A

Q will vary directly with the fourth power of the radii of the airway

104
Q

what are common causes of increased RAW below the glottis?

A

brohchospasm and inflammation

105
Q

what determines the respitory pattern in patients with lung disease?

A

the pattern that allows for the least work (path of least resistance) NOT by effeciency.
ex: asthmatic should breathe slwo and deep because deep and slow breathing is opposed by elastic forces (recoil) and asthmatics have more issue with RAW (resistance)

106
Q
  1. what type of breathing is opposed by RAW?

2. what type of breathing is opposed by elastic forces?

A
  1. rapid and shallow breathing is opposed by RAW

2. deep and slow breathing is opposed by elastic forces

107
Q
  1. what is normal O2 consumption?
  2. how much is spent on work of breathing?
  3. how much of that is lost as heat energy?
  4. how much of that actually moves gas in and out?
A
  1. 250 ml/min
  2. 5% is used for work of breathing
  3. ninety percent (of that 5%) is lost as heat
  4. 10% (of that 5%) is used to move air
108
Q
  1. what is the equal pressure point?

2. for whom does the equal pressure point increase, thus obstructiong airflow and causing mortality?

A
  1. the point at which lung volumes close; it is usually only reached during forced exhalation when lung volume is below FRC (at the end of FEV the bronchioles will start to close (you will hear wheezing)
  2. this can occur during tidal volume in someone with asthma, bronchitis and emphysema
109
Q

what are the attributes of each zone (pA-Pa-Pv):

  1. zone 1
  2. zone 2
  3. zone 3
A
  1. zone 1= PAvenous)
  2. zone 2=Pavenous)
  3. zone 3=PaAlveolar)
110
Q

what determines perfusion to lungs?

A

cardiac output and gravity (perfusion of lung is directly proportional to C.O.)

111
Q

distribution of ventilation:

what is the difference in pressure on the alveoli at the apices vs the bases?

A

there is a 7 cm of water difference (intrapleural at apex is -10, at base is -2).
transpulmonary at apex is +10, at base is +2
3. the higher negative pressure at the apices tends to hold the alveoli open all the time; the alveoli at the bases are therefore smaller

112
Q

what is VA?
what is VE?
what is Vd?

A

VA=alveolar ventilation
VE=minute ventilation (or “exhaled sample)
VD=dead space ventilation

113
Q

what is VE?

A

minute ventilation= VT x RR

114
Q

what is the formula for VA?

A

VA=(VT-VD) x RR

(alveolar ventilation = (tidal volume minus dead space ventilation) x resp rate

115
Q

what is the formula for VE?

A

minute ventilation is VA + VD

116
Q

what is the hallmark of ventilatory failure?

A
  1. increased paCO2

2. inadequate VA as compared to VCO2

117
Q

what three situations would cause inadequate VA compared to VCO2?

A
  1. decreased VA caused by decreased VE
  2. decreased VA caused by increased VD
  3. decreased VA from diminished VE and increased VD
118
Q

most common cause of arterial hypoxemia?

A

VQ mismatch

119
Q
  1. what makes up VD?
  2. what makes up VD physiol?
  3. what makes up QS physiologic (or total)?
A
  1. VD is made up of VD physiol + VD mech
  2. VD physiol is made up of VD anatomic + VD alveolar
  3. QS physiologic is made up of QS anat + QS capillary + QS shunt effect
120
Q

what is the difference between:

  1. VD physiological
  2. VE anatomical?
A
  1. VD physiological: has to do with the physiology of the lungs (up or down) the up lung or portion of the lung is zone 1 (standing up or lying laterally; physiologically up is zone 1)
  2. VD anatomical: has to do with anatomical and does not change because anatomy does not change. It is the air in the communicating airways that does not exchange oxygen.

adv princip II exam 2 (6/13) (5 decks)

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