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APEX-CV & Respiratory > RESPIRATORY PATHOPHYSIOLOGY modules 1-14 > Flashcards

RESPIRATORY PATHOPHYSIOLOGY modules 1-14 Flashcards

1
Q

What mediates bronchoconstriction (2)

A

PNS (muscarinic-3 receptors)

immune response

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2
Q

What mediates bronchodilation

A 
Catecholamines
VIP receptors (NO pathway)
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3
Q

What is the most significant contribution to airflow resistance in the airways

A

Radius of airway

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4
Q

What physiologic systems determine airway diameter (4)

How: bronchoconstriction/dilation

A

PNS (Vagus) = bronchoconstriction
Mast cells and non-cholinergic PNS = bronchoconstriction
Non-cholinergic PNS (NO) = bronchodilation
SNS (catecholamines) = bronchodilation

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5
Q

Which nerve supplies PNS innervation to airway smooth muscles and what is the result?

A

Vagus n (CN 10) = M3 receptors

Result = bronchoconstriction

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6
Q

What effect do mast cells and non-cholinergic C-fibers produce in the airway

A

Bronchoconstriction

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7
Q

How do sympathetic nerve endings affect airway smooth muscle

A

They DON’T

Sympathetic nerve endings do not exist in airway smooth muscle

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8
Q

How does sympathetic response occur in airway smooth muscle? What is the response

A

B2 receptors in the airway are activated by circulating catecholamines

response = bronchoconstriction

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9
Q

What product does non-cholinergic PNS stimulation produce in the airway? What is the response

A

Nitric Oxide

Result = bronchodilation

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10
Q

What is the physiologic result of decreased airway radius and how

A

smooth muscle contraction => decreased airway diameter => increased airway resistance => reduced airflow

How = PNS vagus n., mast cells, and non-cholinergic C-fibers

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11
Q

What is the result of increased airway radius and how

A

smooth muscle relaxation => increased airway diameter => decreased airway resistance => improved airflow

how = Non-cholinergic PNS NO, SNS circulating catecholamines at B2 receptors

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12
Q

Which nerve provides PNS innervation to airway smooth muscles

A

Vagus N

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13
Q

How doe cholinergic nerve endings function in the airway

A

Release ACh on to M3 receptors

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14
Q

Describe the M3 receptor response to ACh

A

M3 is coupled to Gq protein.

M3 activation turns ON the Gq protein which activates phospholipase C (PLC)

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15
Q

What activates phospholipase C in the airway and what is PLC response

A

Activation = Gq protein is turned on by the M3 receptor activating PLC

Response = inositol triphosphate (IP3) is activated as a second messanger

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16
Q

What is IP3 role in the airway and what activates it?

A

Activation = PLC via Gq protein and M3 receptor

Role = stimulation of Ca++ release from sarcoplasmic reticulum

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17
Q

What is the role of Ca++ and how is it released

A

Release = IP3 stimulation of sarcoplasmic reticulum

Role = activates myosin light chain kinase. This enzyme enables the contractile mechanism leading to bronchoconstriction

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18
Q

How is the bronchoconstriction pathway deactivated?

A

When IP3 phosphatase deactivates IP3 to IP2

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19
Q

How do mast cells mediate airway radius

A

High concentrations of mast cells in smooth airway epithelium = Bronchoconstriction

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20
Q

What are the mast cell and pro-inflammatory mediators that alter airway radius and how? Result

A

mediators = IgE, cytokines, complement, histamine, PG, leukotrienes, bradykinin, plt activating factor

How = cough, allergy, or infection activate mediators and amplify the inflammatory process

Bronchoconstriction

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21
Q

How do non-cholinergic C-fibers affect airway radius?

A

Release chemicals that promote bronchoconstriction

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22
Q

What receptors respond to mast cells and other pro-inflammatory cells in the airway? result

A 
Histamine-1
Thromboxane-specific prostanoid receptor
CysLT1
PAF
Bradykinin-2

Bronchoconstriction

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23
Q

What C-fiber mediators are released in the airway? Result

A

Substance P
Neurokinin A
Calcitonin gene related peptide

Bronchoconstriction

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24
Q

Which receptors respond to C-fiber mediator release? Result

A

Neurokinin-2
CGRP

Bronchoconstriction

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25
Q

Describe the process of how circulating catecholamines affect airway radius?

A

B2 receptors present in airway smooth muscle
B2 receptors activated by circulating catecholamines NOT sympathetic nerve endings

Bronchodilation is effect

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26
Q

What activates the B2 receptor in the airway? Function of B2 receptor?

A

ACtivation = circulating catecholamines

Function = B2 receptor coupled to Gq protein which is turned on thus activating adenylate cyclase.
Second messanger cAMP is activated by adenylate cyclase and, with PK, decreases Ca++ release from SR.
Smooth muscle contraction is reduced = bronchodilation

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27
Q

How is adenylate cyclase activated and what is the subsequent role in airway?

A

Activation = B2 receptor turning on Gq protein

Role second messenger cAMP is activated

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28
Q

How is cAMP activated and what is the subsequent role in airway?

A

Activation = adenylate cyclase, PK

Role = reduces Ca++ release from SR, reducing smooth muscle contraction and promotes bronchodilation

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29
Q

How is the B2 receptor pathway deactivated?

A

Phosphodiesterase 3 deactivates cAMP by converting to AMP

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30
Q

What is the role of NO is the airway and how?

A

Role = bronchodilation

How = non-cholinergic PNS nerves release vasoactive intestinal peptide onto airway smooth muscles
This increases NO production
NO stimulates cGMP which leads to smooth muscle relaxation

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31
Q

Examples of leukotriene modifier drugs

A

usually end in KAST
Montelukast
Zafirlukast
Zileuton

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32
Q

Example of methylxanthine

A

Theophylline

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33
Q

Example of mast cell stabilizer drugs

A

Cromolyn

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34
Q

Examples of corticosteroids for respiratory diseases

A

Fluticasone
Budesonide
Beclomethasone
Triamcinolone

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35
Q 
What are the classes for each drug
Theophylline
Zafirlukast
Budesonide
Cromolyn
Triamcinolone
Montelukast
A 
Theophylline = methylxanthine
Budesonide/Triamcinolone = corticosteroids
Cromolyn = mast cell stabilizer
Zafirlukast/Montelukast = leukotriene modifier
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36
Q

3 classes of pulmonary medications

A

direct acting bronchodilators
anti-inflammatories
methylxanthines

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37
Q

2 categories of direct acting bronchodilators

A

Beta 2 agonists

Anticholinergics

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38
Q

What are examples of Beta 2 agonists for respiratory diseases. Effect?

A

albuterol, metaproterenol, salmeterol

Bronchodilation

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39
Q

Examples of anticholinergics for respiratory disease. Effect?

A

atropine, glycopyrrolate, ipatropium, tiotropium

Bronchodilation

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40
Q

3 categories of anti-inflammatory drugs used for bronchodilation

A

Inhaled corticosteroids
Cromolyn
Leukotriene modifiers

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41
Q

Which 2 anesthetic agents have bronchodilating effects?

A

Volatile anesthetics

Ketamine

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42
Q

2 MOA of bronchodilating beta-2 agonists

A

B2 stimulation => increased cAMP => decreased Ca++

Stabilizes mast cell membranes => decreases mediator release

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43
Q

Side effects of beta-2 agonists for bronchodilation

A 
tachycardia
dysrhythmias
HYPOkalemia
HYPERglycemia
Tremors
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44
Q

MOA of anticholinergic bronchodilators

A

M3 antagonism => decreased IP3 => decreased Ca++

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45
Q

Side effects of anticholinergic bronchodilators

A 
Dry mouth from decreased secretions
Urinary retention
Blurred vision
Cough
Increased IOP
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46
Q

MOA of corticosteroids for bronchodilation

A

Stimulates intracellular steroid receptors
Regulates inflammatory protein synthesis
-decreasing airway inflammation
-decreasing airway hyperresponsiveness

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47
Q

Side effects of corticosteroids for bronchodilation

A

Dysphonia
Myopathy or laryngeal muscles
Oropharyngeal candidiasis
Adrenal suppression

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48
Q

MOA of cromolyn for bronchodilation

A

stabilizes mast cells

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49
Q

MOA of leukotriene modifiers for bronchodilation

A

Inhibition of 5-lipoxygenase enzymes which decreases leukotriene synthesis

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50
Q

MOA of methylxanthines for bronchodilation

A

Inhibition of phosphodiesterase => increased cAMP
Increased endogenous catecholamine release
Inhibition of adenosine receptors

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51
Q

Side effects of methylxanthines

A

Low plasma concentrations:

  • N/V/D
  • HA
  • disrupted sleep

High plasma concentrations >30 mcg/mL:

  • Seizures
  • Tachydysrhythmias
  • CHF
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52
Q

Which PFT is the most sensitive indicator of small airway disease

A

Forced expiratory flow 25 - 75%

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53
Q

What does forced expiratory flow measure

A

The average forced expiratory flow during the middle half of the FEV measurement

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54
Q

What do static lung volumes measure and examples

A

Measures how much air the lungs can hold at a single point in time

Examples = RV, ERV, Vt, IRV, FRV, IC, VC, TLC

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55
Q

What does dynamic lung volume measure and examples

A

Measures how quickly air can be moved in and out of the lungs over time

Examples: FEV1, FVC, FEV1/FVC ratio, MMEF

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56
Q

Measure of how much air the lungs can hold

A

Static lung volume

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57
Q

Measure of how quickly air can be moved in an out of the lungs over time

A

Dynamic lung volume

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58
Q

Measure of how well the lungs transfer gas across the alveolar-capillary membrane

A

Diffusion capacity

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59
Q

What is the normal FEV1 value

A

> 80% of predicted value

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60
Q

What is the normal FEV1/FVC ratio

A

> 75-80% of predicted value

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61
Q

How are lung volumes and capacities measured

A

Spirometry

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62
Q

What does spirometry measure

A

Lung volumes and capacities

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63
Q

Can reserve volume and FRC be measured by spirometry

A

no

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64
Q

What does dynamic lung volume assess?

A

Airway resistance

Lung recoil

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65
Q

What does FVC measure and normal values

A

Volume of air exhaled after a maximal inhalation

Male = 4.8 L
Female = 3.7 L
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66
Q

What does FEV1/FVC ratio measure

Normal values

A

Compares volume of air expired in 1 second and total volume of air expired

Normal = 75-80% predicted value

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67
Q

What does an abnormal FEV1/FVC indicate

A

<70% suggests obstructive disease
Normal in restrictive disease
Helps differentiate between obstructive vs restrictive disease

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68
Q

Measure of volume of air exhaled after a maximal inhalation in 1 second

A

FEV1

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69
Q

Measure of volume of air that can be exhaled after a maximal inhalation

A

FVC

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70
Q

What does FEV1 measure and normal value

A

Volume of air exhaled after a maximal inhalation in 1 second

> 80% predicted value

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71
Q

What does abnormal FEV1 indicate

A

Poor pt effort

Declines with age

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72
Q

Measures volume of air exhaled after maximal inhalation in 1 second

A

FEV1

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73
Q

What does forced expiratory flow at 45-75% VC measure and normal values

A

Measures airflow in the middle of FEV (@25-75%)

Normal = 100 +/-25% predicted value

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74
Q

Measures airflow in the middle of FEV and is most sensitive indicator of small airway disease

A

Forced expiratory flow at 25-75% VC

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75
Q

What does an abnormal forced expiratory flow at 25-75% of VC indicate

A

REDUCED = obstructive disease
NORMAL = restrictive or no disease
Most sensitive indicator of small airway disease

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76
Q

What does maximum voluntary ventilation measure and normal values

A

Maximum volumes of air that can be inhaled and exhaled over 1 minute

male = 140-180 mL
female = 80-120 mL
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77
Q

Measures maximum volume of air that can be inhaled and exhaled over 1 minute

A

Maximum voluntary ventilation

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78
Q

How is diffusion capacity measured and normal value

A

Measured by volume of carbon monoxide that can traverse the aveolocapillary membrane per a given alveolar partial pressure of carbon monoxide

normal = 17-25 mL/min/mmHg

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79
Q

Measure of volume of carbon monoxide that passes thru the alveolocapillary membrane per a given alveolar partial pressure of carbon monoxide

A

Diffusion capacity

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80
Q

What law is diffusion capacity based on

A

Fick’s Law of diffusion

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81
Q

What is the importance of lung flow-volume loops

A

differentiation between obstructive and restrictive disease

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82
Q

What patient population is at risk for postop pulmonary complications

A 
age>60 yo
CHF
COPD
Cigarette smoker
ASA >2
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83
Q

What procedure variables increase postop pulmonary complications

A

Surgical site (Aortic>thoracic>upper abd/neuro/peripheral vascular>emergency)
Procedures lasting >2.5 hrs
General anesthesia

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84
Q

Which diagnostic test can indicate and increased risk for postop pulmonary complications

A

serum albumin<3.5 g/dl

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85
Q

Does a history of asthma increase postop pulmonary complications?

A

NO

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86
Q

What are short-term benefits of smoking cessation

A

Decreased carboxyhgb, which improves P50 (affinity for O2)

87
Q

From greatest impact to least, list the surgical procedures that can increase postop pulmonary complications

A

Aortic
Thoracic
Upper abd, neuro, peripheral vascular
emergency

88
Q

6 risk reduction strategies for postop pulmonary complications

A
  1. Smoking cessation (at least 6 weeks)
  2. Alveolar recruitment + PEEP
  3. Bronchodilators and corticosteroids for expiratory airflow obstruction
  4. Treat active infections
  5. Consider options other than GA
  6. Teach patient pulmonary recruitment maneuvers
89
Q

What is the half-life of carbon monoxide?

A

4-6 hours

90
Q

Intermediate-term effects of stopping smoking?

A 
Return of pulmonary function at least 6 weeks
Airway function
Mucociliary clearance
Sputum production
Pulmonary immune function
Reduce hepatic enzyme induction
91
Q

What peak airway pressure is required for initial reopening of atelectatic regions?

A

30 cmH2O

92
Q

What benefits could PIP of 40 cm H2O for 8 seconds provide

A

Reverse anesthesia-induced atelectasis

93
Q

How can anesthesia-induced atelectasis be reversed almost completely?

A

PIP of 40 mmH2O for 8 seconds

94
Q

What is the relationship between FiO2 and atelectasis

A

FiO2 significantly contributes to absorption atelectasis

Use lowest FiO2 the patient can tolerate

95
Q

Preoperative risk reduction strategies to decrease postop pulmonary complications

A

Treat expiratory airflow obstruction with bronchodilators and corticosteroids
Treat active infxn with antibiotics
Educate on pulmonary recruitment maneuvers
Treat RV failure

96
Q

Intraoperative risk reduction strategies to decrease postop pulmonary complications

A

Consider RA vs GA
Minimally invasive surgical procedures over open procedures
Avoid procedures >3 hours

97
Q

Postoperative risk reduction strategies to decrease postop pulmonary complications

A

Utilize effective analgesia (NB, Neuraxial opioids, PCA)

Pulmonary recruitment measures (IS, deep breathing, pulm toilet, CPAP)

98
Q

What characteristics (2) define obstructive lung disease

A

Small airway obstruction
Increased expiratory flow

Getting air out is the problem

99
Q

What characteristics (2) define restrictive disease

A

Proportionate reduction in all lung volumes
Poor compliance

Problem is small lung volumes

100
Q

What lung measures are decreased in restrictive disease

A

FEV1 and FVC

RV, FRC, TLC

101
Q

Which lung measure is normal in restrictive disease

A

FEV1/FVC

FEF 25-75%

102
Q

Which lung measures are decreased in COPD with gas trapping

A

FEV1, FVC, FEV1/FVC, FEF 25-75%

103
Q

Which lung measures are increased in COPD with gas trapping

A

RV, FRC, TLC

104
Q

What is an example of a fixed respiratory lesion. How does the flow-volume loop appear

A

Ex: tracheal stenosis

Inspiratory and expiratory limbs are flat

105
Q

Describe the effect of an extrathoracic obstruction on inhalation and expiration

A

Inhalation = airway collapse, decreased flow

Expiration = pushes obstruction open. Normal flow

106
Q

Describe the effect of an intrathoracic obstruction on inhalation and expiration

A

Inhalation = obstruction is pulled open, normal flow

Expiration = airway collapse, reduced flow

107
Q

Describe the effect of extrathoracic vs intrathoracic obstruction on the flow-volume loop

A

Extrathoracic = inspiratory limb is flat

Intrathoracic = expiratory limb is flat

108
Q

Definition of asthma

A

Acute, reversible airway obstruction accompanied by airway inflammation and bronchial hyperreactivity

109
Q

Which obstructive lung disease is reversible

A

Asthma

110
Q

What airway measures are improved in asthma after bronchodilators

A

FEV1, FEV1/FVC, FEF25-75%

111
Q

What ABG findings may be found in the asthmatic patient

A

respiratory alkalosis

Hypocarbia

112
Q

What does hypercarbia indicate in the asthmatic patient

A

Air trapping, respiratory muscle fatigue and impending respiratory failure

113
Q

What anesthetic measures can be taken with the asthmatic patient (6)

A
  1. Suppress airway reflexes during instrumentation
  2. Limit inspiratory time, prolong expiratory time, permissive hypercapnia
  3. Avoid non-selective beta-blockers (beta-1 are best)
  4. Deep extubate if possible
  5. Chose anesthetics that promote bronchodilation
  6. Avoid histamine releasing drugs
114
Q

Which histamine releasing drugs should be avoided in the asthmatic patient

A

Succinylcholin
Atracurium
Morphine
Meperidine

115
Q

Which anesthetic agents promote bronchodilation in the asthmatic patient

A

Volatiles (sevo, iso)
Ketamine
Propofol
Lidocaine

116
Q

Which beta blockers should be avoided and which ones used if needed in the asthmatic patient

A

Avoid = non-selective beta-blockers, beta-2

Ok to use = beta-1 selective

117
Q

Ventilator settings that should be used in the asthmatic patient

A

Limit inspiratory time
Prolong expiratory time
Permissive hypercapnia

118
Q

What alternatives should be considered in lieu of airway instrumentation in the asthmatic patient

A

LMA

Regional techniques

119
Q

Which spirometry measures are altered in the asthmatic patient and how

A

FEV1, FEV!/FVC, FEF 25-75%

All decreased but reversible

120
Q

Why might there be EKG changes during an severe asthmatic attack? What are the changes?

A

Increased PVR increases the workload of the right heart

Changes = RV strain w/ right axis deviation

121
Q

How does bronchospasm cause hypoxemia

A

due to V/Q mismatch

122
Q

What changes occur with FRC and TLC in the asthmatic patient

A

FRC may increase d/t air trapping

TLC remains normal

123
Q

What are chest xray changes in the asthmatic patient

A

Hyperinflated lungs

Diaphragm flattening

124
Q

What is the dose of lidocaine for airway reflex suppression in the asthmatic patient

A

Lidocaine 1-1.5 mg/kg 1-3 minutes p/t extubation

125
Q

How doe NMBD affect bronchospasm

A

They don’t

126
Q

Consideration for toradol in the asthmatic patient

A

Avoid if the patient has aspirin-intolerant asthma

127
Q

In an OB patient with asthma and poor uterine tone after delivery, which drug is most appropriate and why

A

Methergine

Carboprost can elicit bronchoconstriction in asthmatic patients because of the F2 alpha PG action.

128
Q

How can IV hydration benefit the asthmatic patient

A

IVF can decrease viscosity of airway secretions

129
Q

What are some anesthetic causes of wheezing

A 
Kinked ETT
end-bronchial intubation
Aspiration
Light anesthesia
Cuff overinflation
Pt biting ETT
130
Q

How does intraoperative bronchospasm present (5)

A 
Wheezing
Decreased breath sounds
Increased peak inspiratory pressure
Decreased dynamic compliance
Increased alpha angle on EtCO2 waveform (expiratory upsloping)
131
Q

Treatment for bronchospasm (8)

A
  1. 100% FiO2
  2. Deepen anesthetic
  3. Short-acting inhaled beta-2 agonist
  4. Inhaled ipratropium
  5. Epi 1 mcg/kg IV
  6. Hydrocortisone 2-4 mg/kg IV
  7. Aminophylline
  8. Helium-O2 mixture
132
Q

What does a deficiency in alpha-1 antitrypsin lead to?

A

Increase in alveolar protease activity
That enzyme degrades pulmonary connective tissue
Leads to development of panlobular emphysema
Cigarette smoking doubles rate of destruction

133
Q

What is the treatment for alpha-1 antitrypsin deficiency

A

Liver transplant

134
Q

Describe expiratory flow in the COPD patient

A

Reduction in maximal expiratory flow

Slower forced emptying of lungs

135
Q

Definition of chronic bronchitis

A

Hypertrophied bronchial mucus glands and chronic inflammation

136
Q

Definition of emphysema

A

Enlargement and destruction of airway distal to terminal bronchioles

137
Q

What volumes and capacities are increased in COPD

A

RV, FRC

138
Q

Metabolic changes in COPD patient and how does the body compensate

A

Elevated PaCO2 causing respiratory acidosis

Compensation = Kidneys reabsorb HCO3- which provides compensatory metabolic alkalosis

139
Q

How does O2 administration affect CO2 in the COPD patient

A

Inhibition of hypoxic pulmonary vasoconstriction

Haldane effect

140
Q

SaO2 goal for the COPD patient at risk for O2-induced hypercapnia

A

88-92%

141
Q

What are components of COPD pathophysiology (4)

A
  1. Progressive deterioration of elastic components in lungs
  2. Reduced airway rigidity causing exhalation collapse
  3. Increased gas velocity decreasing airway pressures
  4. Secretions obstructing airflow
142
Q

Why is O2 unloading affected in the COPD patient

A

If CO2 is returned to normal, the compensatory increase in HCO3- from kidney reabsorption remains. This reduces O2 unloading

143
Q

What is a hematologic compensation for COPD and why

A

RBC overproduction
Compensates for V/Q mismatch (increased dead space)
Increases blood viscosity and myocardial work

144
Q

How can supplemental O2 affect patients with severe COPD

A

It can cause O2-induced hypercapnia

145
Q

How does supplemental O2 lead to O2-induced hypercapnia in the COPD patient (2)

A
  1. Inhibition of HPV increases shunt and dead space. Increased DS decreases CO2 excretion
  2. Haldane effect describes how O2 in the blood determines the blood’s ability to buffer O2. Well oxygenated blood has lower capacity to buffer CO2 which causes hypercapnia
146
Q

When should regional anesthesia be considered in the COPD patient

A

For procedures involving the extremities and lower abdomen

147
Q

When should neuraxial anesthesia be avoided? Why

A

When the patient requires sensory blockade >T6

Why = impairment of expiratory muscle function and reduced ERV, hindering cough and clearance of secretions

148
Q

Effects of an interscalene block on COPD patient

A

IS block causes paralysis of ipsilateral hemidiaphragm d/t phrenic nerve blockade

149
Q

What type of volatile agent is best for COPD patient

A

An agent with a low blood:gas solubility

An anesthetic that bronchodilates i.e. sev/iso>des

150
Q

Considerations for the use of N2O on the COPD patient

A

N2O is associated with rupture of pulmonary blebs and can lead to PTX

151
Q

Vt, I:E considerations, and PEEP considerations for the COPD patient

A 
Vt = 6 - 8 mL/kg IBW
I:E = longer expiratory time
PEEP = use but be alert for hyperinflation
152
Q

Considerations for sedation when using regional anesthesia in the COPD patient

A

Avoid over-sedation, which depressive ventilation

153
Q

Which volatile anesthetic is least irritating to the airway?

A

Sevoflurane

154
Q

How does air trapping affect emergence from volatile anesthetic?

A

Theoretically prolongs emergence d/t agent trapping in alveoli

155
Q

How does slow inspiratory flow improve V/Q matching in COPD patients?

A

It helps gas redistribute from high compliance areas to areas with longer time constants
This maximizes V/Q matching through entire lung

156
Q

How does an increased expiratory time affect COPD ventilation

A

It minimizes air trapping and auto-PEEP

157
Q

Suggested mechanical ventilation settings for patients with COPD

A

Vt 6-8 ml/kg IBQ
Slow inspiratory flow
PEEP
Increased expiratory time

158
Q

You should select a volatile agent with a high blood:gas solubility. T/F

A

FALSE

159
Q

All halogenated anesthetics dilate the lower airways. T/F

A

TRUE

160
Q

Sevo is more likely than des to irritate the airway. T/F

A

FALSE

161
Q

Turning on N2O can produce PTX. T/F

A

TRUE

162
Q

Inhibition of HPV caused by volatile agents can be overcome by increasing FiO2. T/F

A

TRUE

163
Q

Define dynamic hyperinflation

A

When a new breath is given before the patient was able to fully exhale the previous breath
AKA breath stacking

164
Q

When a new breath begins before complete exhalation is…

A

dynamic hyperinflation aka auto-PEEP aka breath stacking

165
Q

What are risk factors for dynamic hyperinflation

A

High minute ventilation
Increased airway resistance
reduced expiratory flow

166
Q

What are consequences of dynamic hyperinflation (auto-PEEP)

A

Barotrauma
PTX
HoTN

167
Q

Interventions for dynamic hyperinflation (auto-PEEP)

A

Disconnecting patient from circuit to allow for full exhalation to atmospheric pressure

Increase I:E ratio

168
Q

How does high minute ventilation contribute to auto-PEEP

A

Large tidal volumes or fast respiratory rate don’t allow enough time for full expiration

169
Q

Factors that contribute to reduced expiratory flow in the COPD patient (3)

A

Anything that decreases airway diameter:

  • bronchoconstriction
  • Airway collapse
  • Inflammation
170
Q

Factors that contribute to increased airway resistance in the COPD patient

A

Secretions
Obstructed ETT
Fighting ventilator

171
Q

What pulmonary consequences may arise d/t auto-PEEP

A 
Alveolar overdistension
Barotrauma
PTX
INC PIP
INC PP
INC work of breathing
172
Q

What cardiac consequences may arise d/t auto-PEEP

A

Impaired venous return
HoTN
Overestimation of CVP/PAOP

173
Q

List 3 causes of auto-PEEP

A

High minute ventilation
Reduced expiratory flow
Increased airway resistance

174
Q

Examples of restrictive lung disease

A

Sarcoidosis
Negative pressure pulmonary edema
Flail chest

175
Q

Define restrictive lung disease and what structures may be restricted

A

Define = collection of disorders that impair normal lung expansion during inspiration

Structures = pulmonary interstitium, pleura, rib cage, abdomen

176
Q

Acute causes of restrictive ventilatory deffects

A

aspiration

upper airway obstruction (flat inspiratory limb on flow-volume loop)

177
Q

Chronic pulmonary causes of restrictive lung disease

A

Sarcoidosis

Pulmonary fibrosis d/t amiodarone

178
Q

What defects of the chest wall, mediastinum or pleura can contribute to restrictive lung disease

A 
Flail chest
Pleural effusion
Ankylosing spondylitis
PTX
Mediastinal mass
Pneumomediastinum
Neuromuscular disorders i.e. MDs, GBS SC injury
179
Q

Other anatomical contributors to restrictive lung deffects

A

Pregnancy
Obesity
Ascites

180
Q

Which lung measures are changed and how with restrictive lung disease

A

FEV1 and FVC are decreased

181
Q

Mechanical ventilator management for patients with restrictive lung disease

A

Vt 6 mL/kg IBW
RR = 14 - 18 bpm
PIP < 30 cm H2O
I:E = 1:1

All increase inspiration time/volume

182
Q

3 characteristics of restrictive lung disease

A
  1. Decreased lung volumes and capacities
  2. Decreased compliance
  3. Intact pulmonary flow rates
183
Q

Which lung volumes are affected by restrictive lung disease

A

All volumes are decreased (VC, TLC, Vt…)

Remember FRC is decreased

184
Q

What is the goal for mechanical ventilation in patients with restrictive lung disease and how is this accomplished

A

GOAL = minimize risk of barotrauma

Accomplished = Small Vt (6 mL/kg) and faster RR (14-18 bpm). Keep PIP <30 cmH2O by prolonging inspiratory time

185
Q

When does aspiration most commonly occur

A

During induction and intubation or within 5 minutes of extubation

186
Q

What are the possible consequences of aspiration (4)

A

Airway obstruction
Bronchospasm
Impaired gas exchange
Bacterial respiratory infection

187
Q

Risk factors for aspiration

A

Pregnancy
Trauma
Emergency surgery
GI obstruction

188
Q

What is Mendelson’s syndrome

A

A chemical aspiration pneumonitis d/t gastric pH <2.5 and gastric volume >25 mL

189
Q

List some pharmacologic prophylaxis classes for aspiration

A 
Antacids
H2 antagonists
GI stimulants
PPI
Antiemetics
190
Q

Typical signs and symptoms of aspiration

A 
Hypoxemia
Dyspnea
Tachypnea
Cyanosis
Tachycardia
HTN
191
Q

Initial treatment of aspiration includes 4 interventions

A

head downward or to side
Suction upper airway
Secure airway if indicated
PEEP

192
Q

Criteria for a patient to be discharged home from PACU after aspiration

A
  1. No new cough or wheeze
  2. No CXR evidence of pulmonary injury
  3. No decrease in SpO2 >10% of preop value on RA
  4. A-a gradient <300 mmHg
193
Q

What CXR findings may be present on images s/p aspiration

A

Pulmonary edema

Infiltrates in perihilar and dependent lung regions

194
Q

How do ETT contribute to VAP

A

ETT bypass a patients defense mechanisms including cough and mucociliary clearance

Micro-aspiration possible between ETT cuff and trachea

195
Q

How does GI prophylaxis affect VAP

A

PPIs suppress gastric acid leading to bacterial overgrowth in the stomach
Any aspirations increase the risk of infection

196
Q

Aspiration pneumonitis causes what 3 potential problems?

A
  1. Airway obstruction
  2. Chemical burn to airway and lung parenchyma
  3. Bacterial infxn
197
Q

What drug class is not recommended as a prophylaxis for aspiration pneumonitis by decreasing secretions

A

Anticholinergics

198
Q

What are 3 types of PTX

A

Closed
Communicating
Tension

199
Q

What are hallmark characteristics of tension PTX

A 
Hypoxemia
Increased airway pressures
Tachycardia
HoTN
Increased CVP
Absent BS on affected side
Tracheal shift to unaffected side
200
Q

Which gas should be discontinued immediately if a PTX is suspected

A

N2O

201
Q

What is emergency treatment of a tension PTX

A

14 g angiocath to 2nd IC space at mid-clavicular line or at 4-5th IC space at anterior axillary line

202
Q

4 consequences of flail chest

A

Alveolar collapse
Hypoventilation
Hypercarbia
Hypoxia

203
Q

In a closed PTX, where is the defect located?

A

Pulmonary tree or lung tissue

Air enters and exits the pleural space through defect

204
Q

Treatment for closed PTX

A

Observation
Cath aspiration
CT insertion

205
Q

In an open PTX, where is the defect located?

A

Defect in the chest wall

Air passes between pleural space and atmosphere

206
Q

What happens to the lung during an open PTX

A 
Inspiration = lung collapse
Expiration = partial re-expansion
207
Q

Treatment for open PTX

A

Occlusive, unidirectional dressing allowing air out but not in
Supplemental O2
CT insertion
Possible tracheal intubation

208
Q

Where is the defect when a tension PTX occurs

A

It can be an open or closed defect

209
Q

Consequence of tension PTX

A

Increased intrathoracic pressure causes mediastinal shift on contralateral side
Compression of heart and vasculature reduces VR and CO

210
Q

Indications for surgical treatment of hemothorax

A

Initial output >1000 mL
Bleeding > 200 mL/hr
White lung on CXR
Large air leak

211
Q

What can increase the risk of chylothorax

A

CVC insertion on left side disrupting the thoracic ducts

212
Q

Describe the movement of the flail segment during respiration

A

Inspiration = the injured ribs move inward and collapse affected region

Expiration = Injured ribs move outward and affected region doesn’t empty

213
Q

What are the pulmonary consequences of flail chest

A

Alveolar collapse
Hypoventilation
Hypercarbia
Hypoxia

APEX-CV & Respiratory (8 decks)

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