Exam 3 Flashcards

1
Q

What is ventilation?

A

ventilation is the process of exchanging gas (O2 and Co2) between the atmosphere and the lungs

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2
Q

Ventilation 2 critical functions:

A
  1. O2 delivered to Hgb too support aerobic metabolism
  2. CO2 (primary end product of aerobic metabolism) eliminated from the blood.
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3
Q

_____& _______contract during inspiration (tidal breathing)

A

diaphragm and external intercostals

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4
Q

Is exhalation passive or active?

A

passiveW

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5
Q

What is exhalation driven by?

A

recoil of the chest wall

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6
Q

Accessory muscles for inspiration?

A

sternocleidomastoid and scalene muscles

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7
Q

Accessory muscles for active expiration

A

internal intercostals (secondary)

TIRE
Transverse abdominis
Internal Oblique
Rectus abdominis
External oblique

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8
Q

When does exhalation become an active process?

A

when minute ventilation increases or in patients with lung disease, such as COPD

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9
Q

What vital capacity is required for an effective cough?

A

15ml/kg
A forced exhalation is required to cough and clear the airway of secretions

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10
Q

Function of the conducting zone

A

bulk gas movement
-does not participate in gas exchange
it is anatomic dead space

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11
Q

Where is the conducting zone?

A

begins at the nares and mouth and ends with terminal bronchioles

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12
Q

What are the last structures perfused by the bronchial circulation?

A

terminal bronchioles

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13
Q

What does the transitional zone contain?

A

respiratory bronchioles

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14
Q

function of the transitional zone?

A

bulk gas movement

-respiratory bronchioles serve dual function of air conduit and gas exchange

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15
Q

function of the respiratory zone?

A

gas exchange

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16
Q

Where does the respiratory zone begin?

A

at the alveolar ducts and extends to the alveolar sacs

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17
Q

gas exchange occurs across flat epithelium (type 1 pneumocytes) by _________.

A

diffusion

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18
Q

What is transpulmonary pressure?

A

the difference between the pressure inside the airway and pressure outside the airway

TPP=alveolar pressure-intrapleural pressure

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19
Q

What determines the rate of removal of carbon dioxide from the body?

A

alveolar ventilation

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20
Q

When is TPP negative?

A

during forced expiration.

If it is negative the airway collapses.

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21
Q

What is the amount of gas that is inhaled and exhaled during a breath?

A

tidal volume Vt

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22
Q

normal TV

A

6-8ml/kg

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23
Q

normal dead space

A

2ml/kg or 150ml

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24
Q

When you exhale, which zone’s gas is removed first?

A

conducting zone gas removed first.

Any condition that increases the volume of the conducting zone (Vd) makes itmore difficult to eliminate expiratory gases from the lungs

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25
Q

Minute ventilation (Ve)

A

amount of air in a single breath multiplied by number of breaths per minute

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26
Q

What only measures the fraction of VE that is available for gas exchange and removes dead space from MV equation?

A

alveolar ventilation

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27
Q

Definition of anatomic dead space

A

air confined to conduction airways
ex. nose and mouth–>terminal bronchioles

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28
Q

definition alveolar dead space

A

alveoli that are ventilated but not perfused

ex. decreased pulmonary blood flow

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29
Q

physiologic dead space

A

anatomic Vd + alveolar Vd

variable

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30
Q

increased Vd–>airway

A

-facemask
-heat and moisture exchanger
-positive pressure ventilation

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31
Q

Which drugs increase Vd

A

-atropine because its bronchodilator action increases the volume of the conduction airway
anticholinergics

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32
Q

does old age increase or decrease Vd?

A

increase dead space

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33
Q

Which neck position increases dead space?

A

neck extension because it opens the hypopharynx and increases its volume

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34
Q

What neck position decreases dead space?

A

flexion

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35
Q

what pathophysiology increases dead space?

A

-decreased cardiac output
-COPD
-PE (thrombus, air, amniotic fluid)

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36
Q

Which position increases Vd?

A

sitting

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37
Q

Which position decreases Vd?

A

supine and trendelenberg (head down)

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38
Q

What can physiologic dead space be calculated with?

A

bohr equation

Vd/Vt= (paCO2-PeCO2)/PaCO2

compares partial pressure of CO2 in blood vs the partial pressure of CO2 in exhaled gas. The greater the difference between these values the greater amount of dead space

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39
Q

in the circle system, where does dead space begin?

A

at the y-piece
anything proximal to the y-piece does not influence dead space nor does increasing the length of the circuit.
Only exception to the rule is an incompetent valve in the circle system. In this situation the entire limb with the faulty valve becomes apparatus dead space.

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40
Q

What is the most common cause of increased Vd/Vt under general anesthesia?

A

reduction in cardiac output. If ETCO2 acutely decreases you should first rule out hypotension before considering other causes of increased dead space

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41
Q

Ventilation is ___L/min and perfusion is _____L/min

A

ventilation=4L/min
Perfusion=5L/min

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42
Q

What is the V/Q ratio assuming patient is standing

A

0.8

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43
Q

What is alveolar compliance?

A

change in alveolar volume for a given change in pressure

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44
Q

Where is ventilation poorest?

A

in the alveoli in the apex due to poorest compliance.

The slope of the curve is less steep in this region so there’s a smaller volumetric change throughout the respiratory cycleW

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45
Q

Where is the ventilation the greatest?

A

the alveoli in the base due greatest compliance.

The slope of the curve is steeper in this region so there’s a greater volumetric change throughout the respiratory cycle

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46
Q

What is the most common cause of hypoxemia in the PACU?

A

V/Q mismatch specifically atelectasis

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47
Q

The tendency of the alveolus to collapse is directly proportional to:

A

surface tension (more tension==more likely to collapse)

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48
Q

The tendency of the alveolus to collapse is inversely proportional to

A

-alveolar radius (smaller radius=more likely to collapse)

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49
Q

What does surfactant do?

A

equalizes the effet of surface tension by type 2 pneumocytes. This prevents alveolar collapse

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50
Q

When do type 2 pneumocytes begin producing surfactant?

A

22-26 weeks

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51
Q

When is peak production occur for surfactant?

A

35-36 weeks

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52
Q

zone 1

A

dead space
PA>Pa>Pv

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53
Q

zone 2

A

waterfall

Pa>PA>Pv

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54
Q

zone 3

A

shunt
Pa>Pv>PA

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55
Q

zone 4

A

pulmonary edema
Pa>Pis>Pv>PA

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56
Q

Normal A-a gradient

A

<15mmHg

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57
Q

Normal IRV

A

3,000 mL

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58
Q

IRV

A

volume of gas that can be forcibly inhaled after tidal inhalation

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59
Q

ERV normal

A

1,100 mL

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60
Q

ERV

A

Volume of gas that can be forcibly exhaled after tidal exhalation

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61
Q

Normal RV

A

1,200 ml

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62
Q

RV

A

volume of gas that remains in the lungs after complete exhalation
-the volume cannot be exhaled from the lungs
-this provides a “windbag” of alveolar gas that provides an oxygen reservoir during apnea

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63
Q

Total Lung capacity

A

IRV+TV + ERV +RV

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64
Q

Normal TLC

A

5,800mL

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65
Q

normal VC

A

4,500 ml

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66
Q

normal IC

A

3,500 ml

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67
Q

normal FRC

A

2,300ml

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68
Q

normal CC

A

variable

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69
Q

VC

A

IRV + TV + ERV

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70
Q

IC

A

IRV + TV

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71
Q

FRC

A

RV + ERV

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72
Q

What is Functional residual capacity?

A

The volume of air in the lungs at end-expiration
-the reservoir of oxygen that prevents hypoxemia during apnea

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73
Q

What is static equilibrium?

A

At FRC, the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall

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74
Q

What effects do GA have on FRC?

A

decrease FRC
-diaphragm shifts cephalad 4cm due to decreased inspiratory muscle tone and increased expiratory muscle tone

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75
Q

What effects does obesity have on FRC?

A

decrease FRC
-decreased chest wall compliance
increased airway collapsibility

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76
Q

What effects does pregnancy have on FRC?

A

decreased FRC
-diaphragm shifts cephalad as a result of gravid uterus
-decreased chest wall complaince

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77
Q

What effects does a neonate have on FRC?

A

decreased FRC
less aveoli
decreased lung compliance
cartilaginous ribcage that is prone to collapse during inspiration

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78
Q

What effects does advanced age have on FRC?

A

increased FRC
decreased lung elasticity–> increased air trapping–> increased residual volume–>increased FRC

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79
Q

Which positions decrease FRC?

A

supine
lithotomy
t-burg

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80
Q

which positions increase FRC?

A

prone
sitting
lateral none or increased

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81
Q

What effects do NMB have on FRC?

A

decreased FRC
diaphragm shifts cephalad–>decreased lung volumes

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82
Q

What effects does light anesthesia have on FRC?

A

decreased FRC
straining–>forcefu expiration–>decreased lung volumes

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83
Q

What effects does excessive IVF have on FRC?

A

decreased FRC
fluid accumilation in dependent lung regions favor zone 3 development

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84
Q

What effects does high FiO2 have on FRC?

A

decreased FRC
-absorption atelectasis –>conversion of low v/q unit–?shunt unit
-newer evidence suggests FiO2< 80% at emergence PEEP or CPAP reduces atelectasis

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85
Q

What effects does COPD have on FRC?

A

increase FRC
airtrapping–>increased RV–>increased FRC

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86
Q

What effects does PEEP have on FRC?

A

increase FRC
recruits collapsed alveoli
partially overcomes effects of GA

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87
Q

What effects do sigh breaths have on FRC?

A

increased FRC
recruits collapsed alveoli

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88
Q

Factors that increased closing volume

A

CLOSE-P
COPD
LV failure
Obesity
Surgery
Extremes of Age
Pregnancy

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89
Q

At age 30, CC~FRC when

A

under general anesthesia

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90
Q

by age 44, CC ~FRC when

A

supine

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91
Q

by age 66, CC ~ FRC when

A

standing

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92
Q

a right shifted curve means what?

A

Hgb has a decreased affinity for oxygen. During normal physiology, this occurs at the metabolically active tissue

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93
Q

a left shifted curve means what?

A

hgb has increased affinity for oxygen. During normal physiology, this occurs in the lungs

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94
Q

What is the Bohr effect?

A

CO2 & hydrogen ions cause a conformational change in the hgb molecule; this facilitates the release of oxygen
-An increase in the partial pressure of CO2 and a decrease in pH cause Hgb to release oxygen

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95
Q

What is 2,3 DPG

A

produced during RBC glycolysis (Rapoport-Leubering Pathway)
-it maintains the curve in a slightly right shifted position at all times

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96
Q

What effect does hypoxia have on 2,3 DPG?

A

increased 2,3 DPG production. This facilitates O2 offloading
-2,3 DPG is an important compensation mechanism during chronic anemia
-

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97
Q

what happens to 2,3 DPG in banked blood

A

concentration fo 2,3 DPG falls. This shifts the curve to the left and reduces the amount of O2 available to the tissue load

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98
Q

Does Hgb F respond to 2,3 DPG?

A

no, which explains why Hgb F has a left shift (P50 =19 mmHg)

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99
Q

What is the primary substrate used for ATP synthesis?

A

Glucose

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100
Q

Glycolysis =net gain of how many ATP?

A

2

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101
Q

Kreb’s cycle =net gain of how many ATP?

A

2

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102
Q

Oxidative phosphorylation =net gain of how many ATP?

A

34

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103
Q

In the absence of oxygen, pyruvic acid is converted to what?

A

ATP

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104
Q

What is the primary bi-product of aerobic metabolism?

A

carbon dioxide

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105
Q

3 primary ways CO2 is transported (buffered) in the blood?

A
  1. as bicarbonate (70%)
  2. bound to hemoglobin as carbamino compounds
  3. Dissolved in plasma (7%)
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106
Q

What enzyme facilitates the formation of carbonic acid from H20 and CO2?

A

carbonic anyhydrase

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107
Q

Haldane effect

A

describes CO2 carriage.
It says that oxygen causes the erythrocyte to release CO2.

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108
Q

Hypercapnia is defined as

A

PaCO2 greater than 45mmHg

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109
Q

causes of Hypercapnia-increased CO2 production

A

-sepsis
-overfeeding
-MH
-intense shivering
-prolonged seizure activity
-thyroid storm
-burns

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110
Q

cause of hypercapnia-decreased CO2 elimination

A

-airway obstruction
-increased dead space
-increased Vd/Vt
-ARDS
-COPD
-repiratory center depression
-drug overdose
-inadequate NMB reversal

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111
Q

causes of hypercapnia-rebreathing

A

-exhausted soda lime
-incompetent unidirectional valve in the circle system
-inadequate fresh gas flow with mapleson circuit

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112
Q

pathophysiology of hypoxemia

A

increased alveolar CO2 displaces alveolar O2–>arterial hypoxemia

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113
Q

pathophysiology increased P50

A

oxyglobin curve shifts to the right releases more O@ to the to the tissues
-partially compensates for hypoxemia

114
Q

increased PVR-patho of CO2

A

CO2 is a smooth muscle dilator except in the pulmonary vasculator
-CO2 increased PVR-increases workload in the right heart

115
Q

How does hypercarbia affect blood pH

A

during respiratory acidosis, the kidneys excrete hydrogen and conserve bicarb to return pH to normal. This process begins within hours but may require several days for full compensation to occur

116
Q

The carbon dioxide ventilatory response curve describes the relationship between pa CO2 and minute ventilation

117
Q

What is the primary monitor of PaCO2?

A

central chemoreceptor in the medulla

118
Q

What play a secondary role in monitoring PaCO2?

A

peripheral chemoreceptors in the carotid bodies and transverse and aortic arch

119
Q

What is the apneic threshold?

A

highest PaCO2 at which a person will not breathe. Once the PaCO2 exceeds the apneic threshold the patient will begin to breathe.

120
Q

Left shift in CO2 curve implies that apneic threshold has_______.

121
Q

right shift in CO2 curve implies that apneic threshold has_______.

122
Q

causes of a left shift of the CO2 curve

A

-hypoxemia
-metabolic acidosis
-surgical stimulation
-CNS etiologies: increased ICP, fear, anxiety

Drugs:
-salicylates
-aminophylline
-doxapram
-norepinephrine

123
Q

causes of right shift of CO2 curve

A

-metabolic Alkalosis
-carotid endarterectomy
-natural sleep
-drugs:
-volatile anesthetics
-opioids
-NMBs

124
Q

Where is the respiratory center located in?

A

The reticular activating system in the medulla and pons

125
Q

What is the primary job of the respiratory center?

A

Determine how fast and deep you breathe

126
Q

What modifies the responses of the respiratory center?

A

cerebral cortex

127
Q

location of the DRG?

A

medulla
nucleus tractus solitarus

128
Q

function of the DRG

A

pacemaker for inspiration
primarily active during inspiration

129
Q

location of the VRG?

A

medulla
-nucleus ambiguous
-nucleus retroambigus

130
Q

function of the VRG

A

inspiration and expiration functions (primarily active during expiration

131
Q

what contains the pre-Botzinger complex?

132
Q

What group inhibits the DRG?

A

pneumotaxic center

133
Q

function of the pneumotaxic center (upper pons)

A

triggers end inspiration by inhibiting DRG
-strong stimulus–>rapid shallow breathing
weak stimulus–>slow and deep breathing

134
Q

pontine respiratory centers

A

pneumotaxuic and apneustic center

135
Q

apneustic center -lower pons funciton

A

antagonized the pneumotaxic center which causes inspiration
-action is inhibited by pulmonary stretch receptors (J receptors)

136
Q

Classic teaching says the DRG is considered the primary respiratory pacemaker. Newer evidence says that this function is performed by the :

A

-central pattern generator which includes the DRG, pre-Botzinger complex ( in the VRG) and other medullary structures

137
Q

What do central chemoreceptors respond indirectly to

A

PaCO2 and this region sends stimulatory impulses to the dorsal respiratory center

138
Q

What ions doesnt pass through the BBB

139
Q

Chief responsibility of the carotid monitor

A

for hypoxemia (PaO2< 60mmHg) they do not respond to SaO2 or CaO2

140
Q

Why do we not do bilateral CEA simultaneously?

A

carotid endarterectomy severs the afferent limb of the hypoxic ventilatory response.
takes time for the body to recalibrate

141
Q

sub-anesthetic doses of inhalation and intravenous anesthetics ____MAC depress the hypoxic ventilatory drive.

142
Q

Hering breuer deflation reflex

A

when lung volume is too small, this reflex helps prevent atelectasis by stimulating the patient to take a deep breath

143
Q

paradoxical reflex of the head

A

causes a newborn baby to take her first breath

144
Q

What does J receptor stimulation cause?

A

tachypnea
The J receptors are activated by things that JAM traffic in the pulmonary vasculatture such as pulmonary embolism or CHF

145
Q

Pulmonary C fiber receptors also called

A

J receptoras

146
Q

What is a local reaction that occurs in response to a reduction in alveolar oxygen tension (not arterial PO2)

A

hypoxic pulmonary vasoconstriction

147
Q

What does HPV minimize?

A

shunt flow during atelectasis or one0lung ventilation

148
Q

What is the only region in the body that responds to hypoxia with vasoconstriction?

A

pumonary vascular bed

149
Q

What factors inhibit HPV?

A

-volatile anesthetics >1.5 MAC reduce effectiveness of HPV
-vasodilators, PDEI, dobutamine, some CCB increase shunt flow by inhibiting HPV

150
Q

What has the most significant contribution to airflow resistance?

A

radius of the airway

151
Q

Which physiologic systems determine airway diameter?

A

PNS (vagus nerve)–>bronchoconstriction
mast cells and non-cholinergic PNS–>bronchoconstriction
non-cholinergic PNS (nitric oxide)–>bronchodilation
SNS (circulating catecholamines)–>bronchodilation

152
Q

Are there SNS nerve endings in the airway smooth muscle?

A

no. Instead B2 receptors embedded in airway smooth muscle are activated by catecholamines in the systemic circulation

153
Q

Beta 2 agonists MOA

A

B2 stimulation–>increased cAMP–>decreases iCa+2
-stabilizes mast cell membranes –>decreased mediator release

154
Q

Side effects of B2 agonists

A

-tachycardia
-dysrhthmias
-hypokalemia
-hyperglycemia
-tremors

155
Q

Beta-2 agonist drugs

A

-albuterol
-metaproterenol
-salmeterol

156
Q

Anticholinergics MOA

A

M3 antagonist–>decreased IP3–>decreased iCa2+

157
Q

anticholinergics used for bronchodilation

A

-atropine
-glycopyrrolate
-ipatropium

158
Q

side effects of anticholinergics

A

-inhibits secretions
-dry mouth
-urinary retention
-blurred vision
-cough
-increased intraocular pressure with narrow angle glaucoma

159
Q

corticosteroids moa

A

-stimulates intracellular steroid receptors
-regulates inflammatory protein synthesis
-decrease airway inflammation
-decreases airway hyperresponsiveness

160
Q

side effects of corticosteroids

A

-dysphonia
-mypathy of larygneal muscles
-oropharyngeal candidiasis
-possible adrenal suppression

161
Q

corticosteroid drugs

A

-beclomethasone
-budesonide
-flunisolide
-fluticasone
-tramcinolone

162
Q

cromolyn moa

A

stabilizes mast cell membranes

163
Q

leukotriene modifiers moa

A

inhibits 5-lipooxygenase enzyme
decreases leukotriene synthesis

164
Q

leukotriene modifier drugs

A

-zileuton
-monteleukast
-pranlukast
-zafirlukast

165
Q

theophylline moa

A

inhibits phosphodiesterase–>increases cAMP
increases endogenous catecholamine release
inhibits adenosine receptors

166
Q

theophylline se plasma concentration >20mcg/ml

A

-N/V/D
-headache
-disrupted sleep

167
Q

theophylline se plasma concentration >30mcg/ml

A

-seizures
-dysrythmias
-CHF

168
Q

normal FEV1

A

> 80% predicted value

169
Q

FVC male normal

170
Q

FVC female normal

171
Q

FEV1/FVC normal

A

75-80% predicted value

172
Q

MMEF normal

A

100+/- predicted value

173
Q

MMV normal male

174
Q

MMV normal value female

175
Q

DLCO normal

A

17-25ml/min/mmHg

176
Q

What is the volume of air that can be exhaled after maximal inhalation in 1 second?

A

FEV1
-depends on patient’s effect
-declines with age, so predicted value takes age into account

177
Q

Volume of air that can be exhales after a maximal inhalation

178
Q

<___% of FEV1/FVC suggests obstructive disease

179
Q

is FEV1/FVC normal or abnormal with restrictive disease?

180
Q

What value is useful in dx of obstructive vs. restrictive disease?

181
Q

What is the most sensitive indicator of small airway disease?

A

MMEF (mid maximal expiratory flow rate)

182
Q

What is the best test of endurance?

A

MMV (maximal voluntary ventilation

183
Q

What measures airflow in the middle of FEV ?

A

mmef
mid maximal expiratory flow

184
Q

MMEF obstructive disease

185
Q

MMEF in restrictive disease

186
Q

Maximum value of air that can be inhaled and exhaled over the course of 1 minute

A

MMV
-maximum voluntary ventilation

187
Q

What is DLCO (diffusing capacity)

A

-volume of carbon monoxide that can transver the alveolocapillary membrane per a given alveolar partial pressure of carbon monoxide
-based on Fick’s law of diffusion

188
Q

In a flow-volume loop flow is zero at _______

A

the line that transverses the loop

189
Q

In a flow-volume loop , flow occurs during_____

A

inspiration (it moves away from zero)

190
Q

In a flow-volume loop , flow becomes zero at ____.

A

end inspiration

191
Q

In a flow-volume loop , what is the width of the loop?

A

Vital capacity

192
Q

Patient examples of independent risk factors for pulmonary complications

A

-age >60 years
-ASA >2
-CHF
-COPD
-cigarette smoking

193
Q

procedure examples of independent risk factors for pulmonary complications

A

aortic> thoracic
upper abdominal ~neuro~peripheral vascular>emergency
general anesthesia
duration of anesthesia >/=2 hours

194
Q

diagnostic testing examples of independent risk factors for pulmonary complications

A

albumin <3.5g/dL

195
Q

What are the short term benefits of smoking cessation?

A

-carbon monoxide t1/2 =4-6 hours
-P50 returns to near normal in 12 hours
-short term cessation does not reduce pulmonary complications

196
Q

what are the intermediate term benefits of smoking cessation?

A

-return of pulmonary function takes atelast 6 weeks
this includes:
-airway functin
-mucociliary clearance
-sputum production
-pulmonary immune function
-hepatic enzyme induction also subsides after 6 weeks

197
Q

How can you reduce PPC (postop pulmonary complications) in preop?

A

-tx expiratory outflow obstruction with bronchodilators and corticosteroids
-tx active infection with abx (no indication for prophylaxis from pulmonary infection)
-instruct patient on pulmonary recruitment maneuvers
-tx RV failure

198
Q

How can you reduce PPC (postop pulmonary complications) intraop?

A

-consider regional instead of general
-minimally invasive surgical approaches instead of open
-avoid procedures lasting >3 hours

199
Q

How can you reduce PPC (postop pulmonary complications) postop?

A

utilize effective analgesia
-use pulmonary recruitment manuevers (incentive spirometer, deep breathing, pulmonary toilet, CPAP)

200
Q

obstructive disease is characterized by

A

-small airway obstruction and increased resistance to expiratory flow
-the problem is getting air out

201
Q

restrictive disease is characterized by

A

a proportionate reduction in all lung volumes along with poor compliance
-the problem is small lung volumes

202
Q

asthma is defined by an

A

acute, reversible airway obstruction that is accompanied by chronic airway inflammation and bronchial hyperreactivity

203
Q

What is the greatest risk factor for developing asthma?

A

atopy
The condition of being “hyper-allergic”

204
Q

s/s of asthma

A

wheezing
-dspnea
-chest discomfort or tightness
-production or non-productive cough
-prolonged expiratory phase
-eonsinophilia

205
Q

most common ABG finding in asthma

A

respiratory alkalosis with hypocarbia

206
Q

an elevated PACO2 on abg in asthma suggests:

A

-air trapping
-respiratory muscle fatigue and impending respiratory failure

207
Q

in asthma, ekg may show

A

right ventricular strain and right axis deviation during a severe attack
-pulmonary vascular resistance increases the workload of the right heart

208
Q

Are PFTs predictive of postop respiratory complications?

A

no, the exception is for lung reduction surgery

209
Q

severe bronchospasm can cause

A

hypoxemia due to V/Q mismatch

210
Q

what does CXR show with asthma

A

hyperinflated lungs with diaphragmatic flattening

211
Q

Ventilator goals for asthmatic patients

A

-limit inspiratory time
-prolong expiratory time and tolerate moderate permissive hypercapnia

212
Q

True/false: avoidance of tracheal intubation is a good idea if patient can safely receive regional or LMA

213
Q

Which volatile anesthetics reduce airway resistance?

A

all VA dilate the airway and reduce airway resistance
sevo reduces risk of coughing and may reduce risk of bronchospasm

214
Q

Which IV induction agent causes bronchodilation?

A

ketamine-only IV indiction drug that causes bronchodilation

215
Q

What dose of lidocaine reduces airway reflexes at extubation?

A

1-1.5mg/kg before extubation suppresses airway reflexes

216
Q

are anticholinesterases safe in a patient with asthma?

A

although they can precipitate bronchospasm coadministration of anticholinergics negates risk

217
Q

How does intraop bronchospasm present?

A

-wheezing
-decreased breath sounds
-increased airway resistance
-increased PIP with normal plateau pressure
-increased alpha angle on capnogram (expiratory upsloping)

218
Q

How is intraoperative bronchospasm treated?

A

-100% FiO2
-deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
-short-acting inhaled B2 agonist (albuterol)
-inhaled ipatropium
-epi 1mcg/kg IV
-hydrocortisone 2-4 mg/kg IV (does not tx acute symptoms but prevents problems later)
-aminophylline(theophylline doesn’t work well for acute bronchospasm)
-helium-oxygen (heliox) reduces airway resistance

219
Q

is montelukast used in the tx of acute bronchospasm?

220
Q

COPD is characterized by

A

a reduction in maximal expiratory flow and a slower forced emptying of the lungs. Unlike asthma, the airflow obstruction is not fully reversible

221
Q

Etiologies of COPD

A

-cigarette smoking
-respiratory infection
-exposure to dust with higher risk in the coal mining, gold mining, and textile industries
-alpha 1 antitrypsin deficiency

222
Q

In COPD, chronically elevated PACO2 causes what?

A

respiratory acidosis. The kidneys reabsorb bicarbonate which provides a metabolic alkalosis

223
Q

What happens to a patient with COPD who is administered supplemental O2?

A

it can ause oxygen induced hypercapnia
-it does not inhibit the hypoxic drive

224
Q

Goal SPo2 Sat in COPD patients to minimize risk of oxygen-induced hypercapnia in a patient with severe cOPD

225
Q

Do not consider neuraxial anesthesia if the patient requires sensory blockade higher than__________.

A

T6
This impairs expiratory muscle function and reduces ERV. This hinders the patient’s ability to cough and clear secretions

226
Q

Which block causes paralysis of the ipsilateral hemidiaphragm so isn’t the best block for a patient with severe COPD.

A

interscalene

227
Q

For COPD patients which type of volatile agent is best?

A

low blood: gas solubility to minimize post op respiratory depression.
All halogenated anesthetics are bronchodilators (sevo and iso> des)

228
Q

Volatile agents impair hypoxic pulmonary vasoconstriction >____MAC and increase shunt.

229
Q

nitrous oxide is associated with

A

rupture of pulmonary blebs–>pneumothorax

230
Q

How should you set the ventilator in a patient with COPD?

A

-use TV 6-8ml/kg IBW
-slow inspiratory flow helps has redistribute from high compliance areas to those with longer time constants. This maximizes matching of ventilation and perfusion throughout the entire lung.
-peep maintains airway patency in the alveoli at the flat portion of alveolar compliance curve.
increased expiratory time to minimize air trapping and auto peep

231
Q

What can cause dynamic hyperinflation? (AUTO peep)

A

-if patient is unable to fully exhale with each breathe the portion of the previous breath remains in the lungs. If this occurs with subsequent breaths the effect is additive and airway pressure continues to rise.
-this is most evident by watching the waveforms baseline increase with each breath

232
Q

Tx for dynamic hyperinflation

A

-risk can be reduced by emplying manuevers that prolong expiratory time (this allows patient to get the air out)
-options include decreasing the I:E ratio (such as 1:2 to 1:3)) reducing respiratory rate and reducing flow resistance
-for immediate tx you can disconnect the circuit you will hear whooshing sound as volume of air exits the lungs

233
Q

Acute intrinsic restrictive lung disease examples

A

pulmonary edema
-upper airway obstruction
-aspiration
-reversal of opioid overdose
-cocaine overdose
-reexpansion of collapsed lung
-neurogenic

234
Q

Chronic intrinsic restrictive lung disease examples.

A

-sarcoidosis
-drug induced pulmonary fibrosis
-amiodarone

235
Q

How should you set the ventilator in restrictive lung disease?

A

-best ventilator strategy is to minimized risk of barotrauma
-best accomplished with smaller TV (6ml/kg IBW) and faster RR (14-18 breaths/min)
-keep peak inspiratory pressure below 30cmH20
-prolonged inspiratory time I:E 1:1

236
Q

When does aspiration most commonly occur?

A

during anesthetic induction and intubation or within 5 minutes of extubation

237
Q

What complications arise from aspiration?

A
  1. gastric contents enter the airway–>risk of airway obstruction
  2. gastric contents cause chemical burn to the airway and lung parenchyma–>risk of bronchospasm and impaired gas exchange
  3. Infectious material enters the airway (bacterial infection)
238
Q

Risk factors for aspiration

A

-trauma
-emergency sx
-pregnancy
-GI obstruction
-GERD
-peptic ulcer dz
-hiatal hernia
-ascites
-difficult airway management
-cricoid pressure
-impaired airway reflexes
-head injury
-seizures
-residual nBNM

239
Q

s/s of aspiration

A

-most asymptomatic
-hypoxemia=hallmark
additional findings
-dyspnea
-tachypnea
-cyanosis
-tachycardia
-HTN

240
Q

Initial tx for aspiration

A

1st head tilt down or to side
-upper airway suction to remove particulate matter
-lower airway suction is only useful for removing particulate matter. does not help chemical burn from gastric acid
-secure airway to support oxygenation
-peep to reduce shunt
-bronchodilators to reduce wheezing
-IV lidocaine to help reduce neutrophil response
-steroid probably wont help
-abx only indicated if patients develop a fever or increased WBC count >48 hours

241
Q

How can you determine readiness for discharge if patient has aspirated

A

if they have not experienced any of the following within 2 hours of aspiration event:
-new cough or wheeze
-radiographic evidence of pulmonary injury
-SPO2 decrease >10% of preeop values on room air
-A-a gradient > 300mmHg

242
Q

The best method to prevent ventilator associated pneumonia is _______

A

to avoid intubation altogether
if intubation unavoidable, the next best preventative measure is to minimize duration of mechanical ventilation

243
Q

in pneumothorax POCUS will reveal

A

lack of lung sliding or absence of comet tails

244
Q

emergency tx of tension pneumothorax includes____

A

insertion of a 14g angiocath into:
-2nd intercostal space at the mid-clavicular line or
-4th or 5th intercostal space at the axillary line

245
Q

risk factors for pneumo

A

-central line insertion
-supraclavicular, interscalene and intercostal nerve blocks
-surgical procedures including radical neck dissection, shoulder arthroscopy, mastectomy, axillary lymph node dissection, mediastinoscopy, laparoscopy, nephrectomy
-chest trauma increased peak inspiratory pressure following chest trauma should raise suspicion
-barotrauma, higher or high inspiratory pressures
-lung cysts or bullae can explain and rupture when nitrous used

246
Q

tx of flail chest

A

reducing pain with epidural catheter or intercostal nerve block

247
Q

patient position risk of VAE highest to lowest

A

sitting>supine>prone>lateral

248
Q

consequences of air trapped in pulmonary circulation from vneous air embolism include:

A
  1. increased pulmonary artery pressure
  2. increased RV stroke work index
  3. RV failure
  4. decreased pulmonary venous return
  5. decreased LV preload
  6. decreased CO
  7. aasystole/CV collapse
249
Q

S/s of VAE

A

-air observed on TEE
-mill wheel murmur on precordial doppler
-decreased ETCO2
-increased ETN2
-increased pumonary artery pressures
-hypotension
-dysrhthmias
-pulmonary edema
-hypoxia
-cyanosis

250
Q

how to treat VAE

A

administer 100% FiO2
-flood surgical field with NS

-if surgical insufflation used, d/c gas insufflation and release pneumoperitoneum
-place patient left lateral decubitus position (durant’s maneuver)
-Aspirate air from CVC

251
Q

pulmonary ertery HTN is defined as mean PAP>

252
Q

pulmonary vascular resistance increases as a function of:

A

-increased vascular smooth muscle tone
-vascular cell proliferation
and/or pulmonary thrombi

253
Q

normal PVR

A

150-250 dynesxsec x cm-5

254
Q

things that increase PVR

A

-hypoxemia
-hypercarbia
-acidosis
-SNS stimulation
-pain
-hypothermia
-increased intrathoracic pressure
-mechanical ventilation
-PEEP
atelectasis

Drugs:
-nitrous oxide
-ketamine
-desflurane

255
Q

things that decrease PVR

A

-increased PaO2
-hypocarbia
-alkalosis
-decreased intrathoracic pressure
-spontaneous ventilation
-preventing coughing/straining

drugs:
inhaled nitric oxide
-nitroglycerin
-phosphodiesterase inhibitors (sildenafil)
-prostaglandins PGE1 and PGI2
-calcium channel blockers
-ACE inhibitors

256
Q

Carbon monoxide binds to the oxygen binding site on hgb with an affinity ___x that of oxygen. This displaces O2 from Hgb which reduces ____

257
Q

Does CO shift the curve?

258
Q

T1/2 of carboxyhemoglobin

A

4-6 hours breathing room air

259
Q

Does pulse ox measure COhgb?

A

no and may give falsely elevated result.

260
Q

What is required to diagnose carboxyhemoglobinemia?

A

co-oximeter

261
Q

What is the treatment for carboxyhemoglobinemia?

A

100% supplemental O2. Hyperbaric Oxygen therapy may be required

262
Q

Hyperbaric o2 is indicated if COHgb exceeds _____.

A

25% or if patient is symptomatic

263
Q

What drugs can you give down the ETT?

A

NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine

264
Q

Strong indications for mechanical ventilation-Vital Capacity

265
Q

Strong indications for mechanical ventilation-inspiratory force

266
Q

Strong indications for mechanical ventilation-PaO2 at 21% FiO2

267
Q

Strong indications for mechanical ventilation-PaO2 at 100% FiO2

268
Q

Strong indications for mechanical ventilation-A-a gradient at 21% FIO2

269
Q

Strong indications for mechanical ventilation-A-a gradient at 100% FiO2>

270
Q

Strong indications for mechanical ventilation-PaCO2

271
Q

Strong indications for mechanical ventilation-respiratory rate

A

> 40 or <6

272
Q

What testing is indicated when preop assessment suggested an increased risk of postop pulmonary complications?

A

split lung V/Q function testing

273
Q

normal VO2 max male

A

35-40 ml/kg/min

274
Q

normal VO2 max female

A

27-31 ml/kg/min

275
Q

best predictors of postoperative pulmonary complications for patients undergoing pulmonary surgery:

A

FEV1: <40% predicted
DLCO: <40% predicted
VO2 max < 15ml/kg/min

276
Q

FRC can be measured indirectly by:

A
  1. nitrogen washout
  2. helium wash-in
  3. body plethysmography
277
Q

Vo2

A

3.5ml/kg/min
250ml/min (assuming 70 kg male)

278
Q

Respiratory rate and pattern are determined by:

A
  1. neural control in the respiratory center-medulla
  2. chemical control in the central chemoreceptors-medulla
  3. chemical control in the peripheral chemoreceptors carotid body and aortic arch
  4. baroreceptors-lungs
279
Q

Which surface of the medulla is the central chemoreceptor located?

280
Q

What are the type 1 Glomus cells

A

sensors that transduce PaO2 into an action potential and mediate the hypoxic ventilatory drive