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Anesthesia MM/TL > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

What is the alveolar gas equation?

A

PA= FiO2 (Patm-PH2O) - PaCO2/0.8

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2
Q

What is the equation for mean alveolar pressure?

A

PIP - PEEP (IT/TT) + PEEP

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3
Q

What are the 3 ways to improve oxygenation by adjusting the vent?

A

Increase FiO2
Increase Peep (thereby increase Paw)
Increase inspiratory time

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4
Q

What is dead space?

A

Ventilation without perfusion

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5
Q

What is functional residual capacity?

A

Volume of air left in the lungs at the end of breathing

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6
Q

What is closing capacity?

A

The volume of air in the lungs at which airways begin to close

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7
Q

What is expiratory reserve volume?

A

The amount of air that can be actively exhaled at the end of a tidal breath

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8
Q

What is residual volume?

A

The amount of air left in the lungs at the expiratory reserve volume.

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9
Q

What is vital capacity?

A

The amount of air that is moved with a maximal inhalation and forced exhalation

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10
Q

What does FRC equal?

A

30 ml/kg
Residual volume + expiratory reserve volume
Total lung capacity - inspiratory capacity

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11
Q

What enzymes are activated in the lungs?

A 
Angiotensin I (converted to ANG II by ACE) 
Arachidonic acid
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12
Q

What enzymes are inactivated in the lungs?

A 
Adenosine
ATP/ADP/AMP
ANP
Bradykinin
Endothelin
Leukotrienes 
Norepinephrine
Prostaglandin 
Serotonin
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13
Q

What enzymes are not changed or removed in the lungs?

A 
Epinephrine 
Dopamine
Histamine
Oxytocin
Vasopressin
Prostaglandin I
Ang IIl
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14
Q

How do the lungs metabolize norepinephrine and serotonin?

A

Takes up and degrades them intracellularly with MAO and COMT

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15
Q

What are the chemoreceptors in the body sensitive to.

A

Hypoxia
Hypercapnea
Acidosis

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16
Q

Why is the ventilatory response to respiratory acidosis more pronounced than in metabolic acidosis?

A

Because CO2 is more permeable to the bbb

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17
Q

Where are the chemoreceptors in the body?

A

Carotid and aortic body

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18
Q

What do the chemoreceptors in the carotid body do?

A

Change minute ventilation

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19
Q

What causes the most significant change to minute ventilation?

A

PaO2

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20
Q

What two values do not stimulate the chemoreceptors

A

SaO2

CaO2

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21
Q

At what levels of PaCO2 is the change in ventilation linear?

A

PaCO2 of 20-80

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22
Q

At what value of PaO2 does the firing increase in the chemoreceptors

A

Below 100

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23
Q

At what value of PaO2 does minute ventilation change?

A

60-65

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24
Q

What is the onset of ipratropium?

A

30-60 minutes

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25
Q

What is this duration of action of ipratropium

A

6-8 hours

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26
Q

What is ipratropium used in?

A

COPD

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27
Q

What is the mechanism of theophylline?

A

Increased cGMP causing bronchodilation

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28
Q

How does ipratropium cause bronchodilation?

A

Through muscarinic receptors which are coupled with Gq and therefore have PLC-IP3-Calcium second messengers

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29
Q

What drug improves lung function over a period of years and reduces exacerbations and mortality in COPD patients?

A

Tiotropium

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30
Q

What does atelectasis cause?

A

A shunt

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31
Q

What is functional residual capacity?

A

Residual volume + expiratory reserve volume

The amount of gas remaining in the lungs at the end of passive exhalation

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32
Q

What is vital capacity?

A

Tidal volume
Expiratory reserve volume
InspIratory reserve volume

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33
Q

How is FRC decreased in obese patients?

A

Increase adipose tissue and pulmonary blood decrease lung compliance
Decreased excursion decreases ERV

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34
Q

Why do obese patients have more V/Q mismatch?

A

Their FRC is lower but their closing capacity is unchanged so you get closure of the smaller airways thus more atelectasis

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35
Q

Why do obese patients have an increased A-a gradient?

A

More V/Q mismatch

Higher oxygen consumption due to metabolically active adipose tissue

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36
Q

What is the gradient between PaCO2 and ETCO2 in spontaneously breathing patient?

A

2-5 mm Hg (PaCo2 higher)

5-10 in an anesthetized patient

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37
Q

What is PaCO2 a function of?

A 
CO2 production
CO2 elimination (alveolar ventilation)
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38
Q

What causes an increase in the PaCO2/ETCO2 gradient? (low ETCO2)

A 
Decreased Lung perfusion (decreased CO)
Cardiogenic shock
Hypotension
PE
High PEEP
Right to left intra cardiac shunt 
Esophageal intubation
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39
Q

What is the most effective first line treatment of hypoxemia in one lung ventilation?

A

Applying CPAP to the non-dependent (nonventilated) lung because it allows some oxygenation to blood that is otherwise going through a nonventilated lung

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40
Q

What the physiology behind hypoxemia in one lung ventilation?

A

Intra pulmonary shunt from the non-dependent (non ventilated) lung still receiving perfusion (mixing of deoxygenated blood into the circulation)

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41
Q

What is the second line treatment for hypoxemia during one lung ventilation?

A

Add PEEP to the dependent lung

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42
Q

What is the treatment for persistent hypoxemia in a situation where lung re-expansion would be unacceptable?

A

Ligate the pulmonary artery to the non dependent lung

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43
Q

Why does trendelburg cause hypoxemia?

A

It increases intrapulmonary shunting

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44
Q

What strategy is used to decrease postpneumonectomy pulmonary edema?

A

Careful fluid administration

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45
Q

Which side pneumonectomy is associated with a higher mortality rate?

A

Right sided (10% vs 2%)

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46
Q

When does postpneumonectomy pulmonary edema occur?

A

POD 3

or Bimodal POD3-10

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47
Q

What are the risk factors for postpneumonectomy pulmonary edema

A

Excessive fluid administration
Hyperinflation during one-lung ventilation
Impaired lymphatic drainage of hilar lymph nodes from lymphadenopathy
Pulmonary hypertension

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48
Q

What is postpneumonectomy pulmonary edema look like?

A

Protein rich fluid - ARDS

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49
Q

How does postpneumonectomy pulmonary edema present?

A

Hypoxemic respiratory failure with diffuse infiltrates on CXR

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50
Q

What are the other complications of pneumonectomy

A

Bronchi pleural fistula
PE
Postpneumonectomy syndrome

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51
Q

What is postpneumonectomy syndrome?

A

Occurs 6 months after surgery

Due to shifting of trachea and mediastinum to side of pneumonectomy

52
Q

What are the signs/symptoms of bronchi pleural fistula?

A 
Fever
Productive cough
Hemolysis
Subcutaneous emphysema 
1-2 weeks postop
53
Q

What is the treatment of bronchopleural fistula?

A

Antibiotics
Drainage of the pleural space
Muscle flap for leakage repair

54
Q

What is the benefit of smoking cessation in the first 24-48 hours?

A

Decreased carboxyhemoglobin which causes a right shift in the oxygen dissociation curve

55
Q

How long does it take for improved ciliary function, closing capacity and FEF 25-75% after smoking cessation?

A

2-3 months

56
Q

Which agents cause a right shift in the oxygen dissociation curve?

A

Sulfonamides
Metoclopramide
Sumatriptan
Dapsone

Because the sulfur atom binds irreversibly to the porphyrin ring of the heme moiety

57
Q

What color is sulfhemoglobin blood?

A

Dark greenish black

Vulcan/Romulus

58
Q

What color is methemoglobinemia

A

Chocolate

59
Q

After how many weeks of smoking cessation does the risk of postoperative pulmonary complications drastically decline and begin to approach the rate of observed no Smokers?

A

8 weeks

60
Q

What is closing capacity equal to?

A

Residual volume and closing volume

61
Q

When is closing capacity reached while supine?

A

During forced exhalation with the apices emptying first

62
Q

What happens as closing volume reached zero?

A

The differential between FRC and closing capacity is increased reducing atelectasis

63
Q

What is absorption atelectasis

A

Profound reduction in the partial pressure of nitrogen in the lung which served to inflate the lung space.

64
Q

Who responds the most to bronchodilator therapy on PFTs?

A

Moderate COPD

65
Q

What is split lung function testing?

A

The next step is the patient’s PFTs suggest it will not tolerate pneumonectomy

Determines which lung is less involved in ventilation and oxygenation

66
Q

What is used to test ventilation in the split lung test?

A

Xenon

67
Q

What is used to test oxygenation in the split lung test?

A

Technetium

68
Q

What is a normal SID?

A

~40

69
Q

What will increase SID?

A

Alkalosis
Dehydration
Vomiting
Hypoalbuminemia

70
Q

What happens to PaO2 at advanced age and why?

A

It decreases due to an increase in closing capacity

Closing capacity may be higher than FRC causing air to be trapped behind closed airways. These airways reopen at the end of inspiration when lung volume is greater than closing capacity

71
Q

What is intermittent air trapping?

A

When closing capacity is higher than FRC, air is trapped behind closed airways preventing full exhalation

This is a cause of venous admixture, decreasing PaO2

72
Q

How does high FiO2 promote atelectasis?

A

Because oxygen is quickly absorbed from alveoli causing alveolar collapse.

With lower FiO2, there is more nitrogen left in the alveoli which is very slowly absorbed

73
Q

What is the normal P50 of the oxygen dissociation curve

A

27 mm Hg

74
Q

What is the half life of CO?

A

4-6 hour

1 hour with exercise

75
Q

What adverse effects does smoking cessation have in the first 24-48 hours?

A

More secretions

More reactive airway

76
Q

What is the risk of VAP in the first week of intubation?

A

3%

77
Q

Is transpulmonary pressure higher or lower in the apices?

A

Higher due to higher volumes and more negative pressure compared to dependent regions.

78
Q

What percent maximum voluntary ventilation of the predicted value is associated with good postoperative prognosis after pneumonectomy?

A

Greater than 50%

79
Q

What is MVV?

A

Effort dependent

The patient is asked to inhale deeply and quickly for 10 seconds assessing cardiopulmonary status

80
Q

What is the first phase of preop PFTs?

A

ABG + spirometer

81
Q

What are the ABG criteria that predict increased perioperative morbidity and mortality?

A

PaO2 < 50

PaCO > 45

82
Q

What are the spirometers criteria that predict increased perioperative morbidity and mortality?

A 
FVC < 50%
FEV1 < 2L
Fev1/FVC < 50%
MVV < 50%
DLCO < 50%
83
Q

What is the indication for chronic bronchodilator therapy?

A

> 15% FEV1 improvement

84
Q

What is contraindicated during bronchopulmonary lavage in pulmonary alveolar proteinosis?

A

CPAP to nonventilated lung because one lung ventilation is being done specifically for lung isolation to protect the ventilated lung from contamination

Also, could drown the dependent lung with the lavage solution

85
Q

What are the three main causes of auto-PEEP?

A
  1. Dynamic hyperinflation with intrinsic expiratory flow limitation (COPD)
  2. Dynamic hyperinflation: volume delivered is too high
    Exaggerated expiratory activity
86
Q

How do you remedy auto-PEEP.

A

Decrease tidal volumes
Increased expiratory time
Decrease respiratory rate
Reduce anxiety, pain, fever
Use larger ETT, suction, give bronchodilators
Give PEEP for people with obstructive lung disease

87
Q

What is the mechanism for increased shunt fraction in a patient breathing 100% FiO2

A

Blunting of hypoxic pulmonary vasoconstriction

88
Q

What are the diagnostic criteria for postpneumonectomy pulmonary edema

A

PaO2/FiO2 < 200
PCWP < 18
Bilateral infiltrates

89
Q

What are the risk factors for postpneumonectomy pulmonary edema?

A

Pre-op alcohol use
Right side pneumonectomy
Periop fluid overload (> 3-4L in first 24 hours)
High intraoperative airway pressures (>40)
High urine output in post op period

90
Q

Bilateral injury to what nerve causes acute respiratory distress after total thyroidectomy?

A

Recurrent laryngeal due to unopposed tension of the cricothyroid leaving the vocal cords adducted

91
Q

What nerve innervated the cricothyroid muscle?

A

Superior laryngeal nerve (external branch)

92
Q

What happens with unilateral superior laryngeal nerve injury?

A

Difficulty with phonation

93
Q

What happens with bilateral superior laryngeal nerve injury?

A

Hoarseness and tiring of the voice

94
Q

When does normalization of pulmonary immune system happen after smoking cessation?

A

4-6 weeks

95
Q

What is the resting tone of airway smooth muscle mediated by?

A

Parasympathetic neurons

96
Q

Where are the neuronal fibers controlling the bronchial tree?

A

Medulla : nucleus solitarius, ambiguous

97
Q

What parasympathetic mediators can cause bronchodilation?

A

VIP
NO
Pacap

98
Q

What pulmonary conditions are associated with RA?

A

Fibrosis
Effusions
Nodules

99
Q

What is the first sign of bleomycin pulmonary toxicity?

A

A decrease in DLCO

100
Q

What increases toxicity of bleomycin?

A

High FiO2

101
Q

How does nitric oxide improve ARDS?

A

By improving VQ mismatch by improving blood flow in only the ventilated areas as opposed to nitroprusside or nitroglycerin which vasodilation everywhere

102
Q

What happens to residual volume with aging?

A

It increases due to increased closing capacity

103
Q

What happens to vital capacity and total lung capacity with aging?

A

They both decrease due to increased closing capacity

104
Q

Why do the elderly have an increased closing capacity

A

Because with aging, there is a loss of elasticity in the lungs so the smaller airways have less radial traction on them and are stiffer.

105
Q

At what age, does closing capacity surpass FRC?

A

Mid-60s

106
Q

What is the equation for pulmonary vascular resistance?

A

PVR = 80(Mean pulmonary artery pressure - PCWP)/CO

107
Q

What is the Hering-Breuer reflex?

A

Prevents inspiration so a patient can exhale to prevent over inflation of the lungs

108
Q

How do the lungs inactivate bradykinin?

A

ACE

109
Q

How do the lungs metabolize serotonin and norepinephrine?

A

Intracellular degradation via MAO

110
Q

What other enzyme degraded norepinephrine?

A

catecholamines methyltransferase

111
Q

What hormones are not metabolized by the lungs?

A

Epi
Dopamine
Histamine

112
Q

What is dominant determinant of bronchoconstriction?

A

The parasympathetic nervous system

113
Q

What is the action of Vip in the lungs?

A

Vasodilation and bronchodilation

114
Q

What is a frequent complication of subplot tic jet ventilation?

A

Hypercarbia due to small tidal volume delivery (more dead space ventilation, less alveolar ventilation) and obstructed upper airway as is usually the case when using this airway management technique

115
Q

What is the normal gradient between PaCO2 and ETCO2 in a spontaneously breathing patient?

A

2-5 mm Hg

116
Q

What is the normal gradient between PaCO2 and ETCO2 in an anesthetized patient?

A

5-10 mm Hg

117
Q

What is the most common reason for an acute increase in the PaCO2-ETCO2 gradient?

A

Decreased CO causing decreased lung perfusion.

118
Q

How much positive pressure is needed to completely reverse anesthesia induced atelectasis?

A

40 cm H2O for 7-8 seconds

119
Q

What is the mechanism behind an obese patient desaturation on induction?

A

Increased V/Q mismatch with development of shunt

120
Q

What factors increase closing capacity?

A 
Age
COPD
Smoking
Surgery
Heart failure

Cause changes in transpulmonary pressures that make it easier for and airways to collapse at higher lung volumes

121
Q

When should Heliox be used?

A

When there is turbulent flow in the medium to large sized always (subglottic stenosis)

122
Q

What is the mechanism of pulmonary edema?

A

Increased preload and pulmonary blood volume –> increases pulmonary transudative pressures
Increased PVR causes bulging of intra ventricular septum –> decreases diastolic dysfunction causing further increases in pulmonary hydrostatic pressure
Increased afterload which decreases cardiac output

123
Q

What is the treatment of negative pressure pulmonary edema?

A

Supportive - positive pressure with ventilation or CPAP

124
Q

What is the FiO2 of a face mask at 5-10 L of oxygen?

A

35-50%

125
Q

How much FiO2 do nasal cannulas provide?

A

25-40%

126
Q

How much FiO2 is provided with a partial rebreathing mask?

A

40-70%

127
Q

How much FiO2 will a nonrebreather give?

A

60-80% at flows of 10L or more

Anesthesia MM/TL (36 decks)

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