RESPIRATORY PATHOPHYSIOLOGY modules 1-14 Flashcards

(213 cards)

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
Describe the process of how circulating catecholamines affect airway radius?
B2 receptors present in airway smooth muscle B2 receptors activated by circulating catecholamines NOT sympathetic nerve endings Bronchodilation is effect
26
What activates the B2 receptor in the airway? Function of B2 receptor?
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
27
How is adenylate cyclase activated and what is the subsequent role in airway?
Activation = B2 receptor turning on Gq protein Role second messenger cAMP is activated
28
How is cAMP activated and what is the subsequent role in airway?
Activation = adenylate cyclase, PK Role = reduces Ca++ release from SR, reducing smooth muscle contraction and promotes bronchodilation
29
How is the B2 receptor pathway deactivated?
Phosphodiesterase 3 deactivates cAMP by converting to AMP
30
What is the role of NO is the airway and how?
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
31
Examples of leukotriene modifier drugs
usually end in KAST Montelukast Zafirlukast Zileuton
32
Example of methylxanthine
Theophylline
33
Example of mast cell stabilizer drugs
Cromolyn
34
Examples of corticosteroids for respiratory diseases
Fluticasone Budesonide Beclomethasone Triamcinolone
35
``` What are the classes for each drug Theophylline Zafirlukast Budesonide Cromolyn Triamcinolone Montelukast ```
``` Theophylline = methylxanthine Budesonide/Triamcinolone = corticosteroids Cromolyn = mast cell stabilizer Zafirlukast/Montelukast = leukotriene modifier ```
36
3 classes of pulmonary medications
direct acting bronchodilators anti-inflammatories methylxanthines
37
2 categories of direct acting bronchodilators
Beta 2 agonists | Anticholinergics
38
What are examples of Beta 2 agonists for respiratory diseases. Effect?
albuterol, metaproterenol, salmeterol Bronchodilation
39
Examples of anticholinergics for respiratory disease. Effect?
atropine, glycopyrrolate, ipatropium, tiotropium Bronchodilation
40
3 categories of anti-inflammatory drugs used for bronchodilation
Inhaled corticosteroids Cromolyn Leukotriene modifiers
41
Which 2 anesthetic agents have bronchodilating effects?
Volatile anesthetics | Ketamine
42
2 MOA of bronchodilating beta-2 agonists
B2 stimulation => increased cAMP => decreased Ca++ Stabilizes mast cell membranes => decreases mediator release
43
Side effects of beta-2 agonists for bronchodilation
``` tachycardia dysrhythmias HYPOkalemia HYPERglycemia Tremors ```
44
MOA of anticholinergic bronchodilators
M3 antagonism => decreased IP3 => decreased Ca++
45
Side effects of anticholinergic bronchodilators
``` Dry mouth from decreased secretions Urinary retention Blurred vision Cough Increased IOP ```
46
MOA of corticosteroids for bronchodilation
Stimulates intracellular steroid receptors Regulates inflammatory protein synthesis -decreasing airway inflammation -decreasing airway hyperresponsiveness
47
Side effects of corticosteroids for bronchodilation
Dysphonia Myopathy or laryngeal muscles Oropharyngeal candidiasis Adrenal suppression
48
MOA of cromolyn for bronchodilation
stabilizes mast cells
49
MOA of leukotriene modifiers for bronchodilation
Inhibition of 5-lipoxygenase enzymes which decreases leukotriene synthesis
50
MOA of methylxanthines for bronchodilation
Inhibition of phosphodiesterase => increased cAMP Increased endogenous catecholamine release Inhibition of adenosine receptors
51
Side effects of methylxanthines
Low plasma concentrations: - N/V/D - HA - disrupted sleep High plasma concentrations >30 mcg/mL: - Seizures - Tachydysrhythmias - CHF
52
Which PFT is the most sensitive indicator of small airway disease
Forced expiratory flow 25 - 75%
53
What does forced expiratory flow measure
The average forced expiratory flow during the middle half of the FEV measurement
54
What do static lung volumes measure and examples
Measures how much air the lungs can hold at a single point in time Examples = RV, ERV, Vt, IRV, FRV, IC, VC, TLC
55
What does dynamic lung volume measure and examples
Measures how quickly air can be moved in and out of the lungs over time Examples: FEV1, FVC, FEV1/FVC ratio, MMEF
56
Measure of how much air the lungs can hold
Static lung volume
57
Measure of how quickly air can be moved in an out of the lungs over time
Dynamic lung volume
58
Measure of how well the lungs transfer gas across the alveolar-capillary membrane
Diffusion capacity
59
What is the normal FEV1 value
>80% of predicted value
60
What is the normal FEV1/FVC ratio
>75-80% of predicted value
61
How are lung volumes and capacities measured
Spirometry
62
What does spirometry measure
Lung volumes and capacities
63
Can reserve volume and FRC be measured by spirometry
no
64
What does dynamic lung volume assess?
Airway resistance | Lung recoil
65
What does FVC measure and normal values
Volume of air exhaled after a maximal inhalation ``` Male = 4.8 L Female = 3.7 L ```
66
What does FEV1/FVC ratio measure | Normal values
Compares volume of air expired in 1 second and total volume of air expired Normal = 75-80% predicted value
67
What does an abnormal FEV1/FVC indicate
<70% suggests obstructive disease Normal in restrictive disease Helps differentiate between obstructive vs restrictive disease
68
Measure of volume of air exhaled after a maximal inhalation in 1 second
FEV1
69
Measure of volume of air that can be exhaled after a maximal inhalation
FVC
70
What does FEV1 measure and normal value
Volume of air exhaled after a maximal inhalation in 1 second >80% predicted value
71
What does abnormal FEV1 indicate
Poor pt effort | Declines with age
72
Measures volume of air exhaled after maximal inhalation in 1 second
FEV1
73
What does forced expiratory flow at 45-75% VC measure and normal values
Measures airflow in the middle of FEV (@25-75%) Normal = 100 +/-25% predicted value
74
Measures airflow in the middle of FEV and is most sensitive indicator of small airway disease
Forced expiratory flow at 25-75% VC
75
What does an abnormal forced expiratory flow at 25-75% of VC indicate
REDUCED = obstructive disease NORMAL = restrictive or no disease Most sensitive indicator of small airway disease
76
What does maximum voluntary ventilation measure and normal values
Maximum volumes of air that can be inhaled and exhaled over 1 minute ``` male = 140-180 mL female = 80-120 mL ```
77
Measures maximum volume of air that can be inhaled and exhaled over 1 minute
Maximum voluntary ventilation
78
How is diffusion capacity measured and normal value
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
79
Measure of volume of carbon monoxide that passes thru the alveolocapillary membrane per a given alveolar partial pressure of carbon monoxide
Diffusion capacity
80
What law is diffusion capacity based on
Fick's Law of diffusion
81
What is the importance of lung flow-volume loops
differentiation between obstructive and restrictive disease
82
What patient population is at risk for postop pulmonary complications
``` age>60 yo CHF COPD Cigarette smoker ASA >2 ```
83
What procedure variables increase postop pulmonary complications
Surgical site (Aortic>thoracic>upper abd/neuro/peripheral vascular>emergency) Procedures lasting >2.5 hrs General anesthesia
84
Which diagnostic test can indicate and increased risk for postop pulmonary complications
serum albumin<3.5 g/dl
85
Does a history of asthma increase postop pulmonary complications?
NO
86
What are short-term benefits of smoking cessation
Decreased carboxyhgb, which improves P50 (affinity for O2)
87
From greatest impact to least, list the surgical procedures that can increase postop pulmonary complications
Aortic Thoracic Upper abd, neuro, peripheral vascular emergency
88
6 risk reduction strategies for postop pulmonary complications
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
What is the half-life of carbon monoxide?
4-6 hours
90
Intermediate-term effects of stopping smoking?
``` Return of pulmonary function at least 6 weeks Airway function Mucociliary clearance Sputum production Pulmonary immune function Reduce hepatic enzyme induction ```
91
What peak airway pressure is required for initial reopening of atelectatic regions?
30 cmH2O
92
What benefits could PIP of 40 cm H2O for 8 seconds provide
Reverse anesthesia-induced atelectasis
93
How can anesthesia-induced atelectasis be reversed almost completely?
PIP of 40 mmH2O for 8 seconds
94
What is the relationship between FiO2 and atelectasis
FiO2 significantly contributes to absorption atelectasis Use lowest FiO2 the patient can tolerate
95
Preoperative risk reduction strategies to decrease postop pulmonary complications
Treat expiratory airflow obstruction with bronchodilators and corticosteroids Treat active infxn with antibiotics Educate on pulmonary recruitment maneuvers Treat RV failure
96
Intraoperative risk reduction strategies to decrease postop pulmonary complications
Consider RA vs GA Minimally invasive surgical procedures over open procedures Avoid procedures >3 hours
97
Postoperative risk reduction strategies to decrease postop pulmonary complications
Utilize effective analgesia (NB, Neuraxial opioids, PCA) | Pulmonary recruitment measures (IS, deep breathing, pulm toilet, CPAP)
98
What characteristics (2) define obstructive lung disease
Small airway obstruction Increased expiratory flow Getting air out is the problem
99
What characteristics (2) define restrictive disease
Proportionate reduction in all lung volumes Poor compliance Problem is small lung volumes
100
What lung measures are decreased in restrictive disease
FEV1 and FVC RV, FRC, TLC
101
Which lung measure is normal in restrictive disease
FEV1/FVC | FEF 25-75%
102
Which lung measures are decreased in COPD with gas trapping
FEV1, FVC, FEV1/FVC, FEF 25-75%
103
Which lung measures are increased in COPD with gas trapping
RV, FRC, TLC
104
What is an example of a fixed respiratory lesion. How does the flow-volume loop appear
Ex: tracheal stenosis Inspiratory and expiratory limbs are flat
105
Describe the effect of an extrathoracic obstruction on inhalation and expiration
Inhalation = airway collapse, decreased flow Expiration = pushes obstruction open. Normal flow
106
Describe the effect of an intrathoracic obstruction on inhalation and expiration
Inhalation = obstruction is pulled open, normal flow Expiration = airway collapse, reduced flow
107
Describe the effect of extrathoracic vs intrathoracic obstruction on the flow-volume loop
Extrathoracic = inspiratory limb is flat Intrathoracic = expiratory limb is flat
108
Definition of asthma
Acute, reversible airway obstruction accompanied by airway inflammation and bronchial hyperreactivity
109
Which obstructive lung disease is reversible
Asthma
110
What airway measures are improved in asthma after bronchodilators
FEV1, FEV1/FVC, FEF25-75%
111
What ABG findings may be found in the asthmatic patient
respiratory alkalosis | Hypocarbia
112
What does hypercarbia indicate in the asthmatic patient
Air trapping, respiratory muscle fatigue and impending respiratory failure
113
What anesthetic measures can be taken with the asthmatic patient (6)
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
Which histamine releasing drugs should be avoided in the asthmatic patient
Succinylcholin Atracurium Morphine Meperidine
115
Which anesthetic agents promote bronchodilation in the asthmatic patient
Volatiles (sevo, iso) Ketamine Propofol Lidocaine
116
Which beta blockers should be avoided and which ones used if needed in the asthmatic patient
Avoid = non-selective beta-blockers, beta-2 Ok to use = beta-1 selective
117
Ventilator settings that should be used in the asthmatic patient
Limit inspiratory time Prolong expiratory time Permissive hypercapnia
118
What alternatives should be considered in lieu of airway instrumentation in the asthmatic patient
LMA | Regional techniques
119
Which spirometry measures are altered in the asthmatic patient and how
FEV1, FEV!/FVC, FEF 25-75% All decreased but reversible
120
Why might there be EKG changes during an severe asthmatic attack? What are the changes?
Increased PVR increases the workload of the right heart Changes = RV strain w/ right axis deviation
121
How does bronchospasm cause hypoxemia
due to V/Q mismatch
122
What changes occur with FRC and TLC in the asthmatic patient
FRC may increase d/t air trapping TLC remains normal
123
What are chest xray changes in the asthmatic patient
Hyperinflated lungs | Diaphragm flattening
124
What is the dose of lidocaine for airway reflex suppression in the asthmatic patient
Lidocaine 1-1.5 mg/kg 1-3 minutes p/t extubation
125
How doe NMBD affect bronchospasm
They don't
126
Consideration for toradol in the asthmatic patient
Avoid if the patient has aspirin-intolerant asthma
127
In an OB patient with asthma and poor uterine tone after delivery, which drug is most appropriate and why
Methergine Carboprost can elicit bronchoconstriction in asthmatic patients because of the F2 alpha PG action.
128
How can IV hydration benefit the asthmatic patient
IVF can decrease viscosity of airway secretions
129
What are some anesthetic causes of wheezing
``` Kinked ETT end-bronchial intubation Aspiration Light anesthesia Cuff overinflation Pt biting ETT ```
130
How does intraoperative bronchospasm present (5)
``` Wheezing Decreased breath sounds Increased peak inspiratory pressure Decreased dynamic compliance Increased alpha angle on EtCO2 waveform (expiratory upsloping) ```
131
Treatment for bronchospasm (8)
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
What does a deficiency in alpha-1 antitrypsin lead to?
Increase in alveolar protease activity That enzyme degrades pulmonary connective tissue Leads to development of panlobular emphysema Cigarette smoking doubles rate of destruction
133
What is the treatment for alpha-1 antitrypsin deficiency
Liver transplant
134
Describe expiratory flow in the COPD patient
Reduction in maximal expiratory flow | Slower forced emptying of lungs
135
Definition of chronic bronchitis
Hypertrophied bronchial mucus glands and chronic inflammation
136
Definition of emphysema
Enlargement and destruction of airway distal to terminal bronchioles
137
What volumes and capacities are increased in COPD
RV, FRC
138
Metabolic changes in COPD patient and how does the body compensate
Elevated PaCO2 causing respiratory acidosis Compensation = Kidneys reabsorb HCO3- which provides compensatory metabolic alkalosis
139
How does O2 administration affect CO2 in the COPD patient
Inhibition of hypoxic pulmonary vasoconstriction | Haldane effect
140
SaO2 goal for the COPD patient at risk for O2-induced hypercapnia
88-92%
141
What are components of COPD pathophysiology (4)
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
Why is O2 unloading affected in the COPD patient
If CO2 is returned to normal, the compensatory increase in HCO3- from kidney reabsorption remains. This reduces O2 unloading
143
What is a hematologic compensation for COPD and why
RBC overproduction Compensates for V/Q mismatch (increased dead space) Increases blood viscosity and myocardial work
144
How can supplemental O2 affect patients with severe COPD
It can cause O2-induced hypercapnia
145
How does supplemental O2 lead to O2-induced hypercapnia in the COPD patient (2)
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
When should regional anesthesia be considered in the COPD patient
For procedures involving the extremities and lower abdomen
147
When should neuraxial anesthesia be avoided? Why
When the patient requires sensory blockade >T6 Why = impairment of expiratory muscle function and reduced ERV, hindering cough and clearance of secretions
148
Effects of an interscalene block on COPD patient
IS block causes paralysis of ipsilateral hemidiaphragm d/t phrenic nerve blockade
149
What type of volatile agent is best for COPD patient
An agent with a low blood:gas solubility An anesthetic that bronchodilates i.e. sev/iso>des
150
Considerations for the use of N2O on the COPD patient
N2O is associated with rupture of pulmonary blebs and can lead to PTX
151
Vt, I:E considerations, and PEEP considerations for the COPD patient
``` Vt = 6 - 8 mL/kg IBW I:E = longer expiratory time PEEP = use but be alert for hyperinflation ```
152
Considerations for sedation when using regional anesthesia in the COPD patient
Avoid over-sedation, which depressive ventilation
153
Which volatile anesthetic is least irritating to the airway?
Sevoflurane
154
How does air trapping affect emergence from volatile anesthetic?
Theoretically prolongs emergence d/t agent trapping in alveoli
155
How does slow inspiratory flow improve V/Q matching in COPD patients?
It helps gas redistribute from high compliance areas to areas with longer time constants This maximizes V/Q matching through entire lung
156
How does an increased expiratory time affect COPD ventilation
It minimizes air trapping and auto-PEEP
157
Suggested mechanical ventilation settings for patients with COPD
Vt 6-8 ml/kg IBQ Slow inspiratory flow PEEP Increased expiratory time
158
You should select a volatile agent with a high blood:gas solubility. T/F
FALSE
159
All halogenated anesthetics dilate the lower airways. T/F
TRUE
160
Sevo is more likely than des to irritate the airway. T/F
FALSE
161
Turning on N2O can produce PTX. T/F
TRUE
162
Inhibition of HPV caused by volatile agents can be overcome by increasing FiO2. T/F
TRUE
163
Define dynamic hyperinflation
When a new breath is given before the patient was able to fully exhale the previous breath AKA breath stacking
164
When a new breath begins before complete exhalation is...
dynamic hyperinflation aka auto-PEEP aka breath stacking
165
What are risk factors for dynamic hyperinflation
High minute ventilation Increased airway resistance reduced expiratory flow
166
What are consequences of dynamic hyperinflation (auto-PEEP)
Barotrauma PTX HoTN
167
Interventions for dynamic hyperinflation (auto-PEEP)
Disconnecting patient from circuit to allow for full exhalation to atmospheric pressure Increase I:E ratio
168
How does high minute ventilation contribute to auto-PEEP
Large tidal volumes or fast respiratory rate don't allow enough time for full expiration
169
Factors that contribute to reduced expiratory flow in the COPD patient (3)
Anything that decreases airway diameter: - bronchoconstriction - Airway collapse - Inflammation
170
Factors that contribute to increased airway resistance in the COPD patient
Secretions Obstructed ETT Fighting ventilator
171
What pulmonary consequences may arise d/t auto-PEEP
``` Alveolar overdistension Barotrauma PTX INC PIP INC PP INC work of breathing ```
172
What cardiac consequences may arise d/t auto-PEEP
Impaired venous return HoTN Overestimation of CVP/PAOP
173
List 3 causes of auto-PEEP
High minute ventilation Reduced expiratory flow Increased airway resistance
174
Examples of restrictive lung disease
Sarcoidosis Negative pressure pulmonary edema Flail chest
175
Define restrictive lung disease and what structures may be restricted
# Define = collection of disorders that impair normal lung expansion during inspiration Structures = pulmonary interstitium, pleura, rib cage, abdomen
176
Acute causes of restrictive ventilatory deffects
aspiration | upper airway obstruction (flat inspiratory limb on flow-volume loop)
177
Chronic pulmonary causes of restrictive lung disease
Sarcoidosis | Pulmonary fibrosis d/t amiodarone
178
What defects of the chest wall, mediastinum or pleura can contribute to restrictive lung disease
``` Flail chest Pleural effusion Ankylosing spondylitis PTX Mediastinal mass Pneumomediastinum Neuromuscular disorders i.e. MDs, GBS SC injury ```
179
Other anatomical contributors to restrictive lung deffects
Pregnancy Obesity Ascites
180
Which lung measures are changed and how with restrictive lung disease
FEV1 and FVC are decreased
181
Mechanical ventilator management for patients with restrictive lung disease
Vt 6 mL/kg IBW RR = 14 - 18 bpm PIP < 30 cm H2O I:E = 1:1 All increase inspiration time/volume
182
3 characteristics of restrictive lung disease
1. Decreased lung volumes and capacities 2. Decreased compliance 3. Intact pulmonary flow rates
183
Which lung volumes are affected by restrictive lung disease
All volumes are decreased (VC, TLC, Vt...) | Remember FRC is decreased
184
What is the goal for mechanical ventilation in patients with restrictive lung disease and how is this accomplished
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
When does aspiration most commonly occur
During induction and intubation or within 5 minutes of extubation
186
What are the possible consequences of aspiration (4)
Airway obstruction Bronchospasm Impaired gas exchange Bacterial respiratory infection
187
Risk factors for aspiration
Pregnancy Trauma Emergency surgery GI obstruction
188
What is Mendelson's syndrome
A chemical aspiration pneumonitis d/t gastric pH <2.5 and gastric volume >25 mL
189
List some pharmacologic prophylaxis classes for aspiration
``` Antacids H2 antagonists GI stimulants PPI Antiemetics ```
190
Typical signs and symptoms of aspiration
``` Hypoxemia Dyspnea Tachypnea Cyanosis Tachycardia HTN ```
191
Initial treatment of aspiration includes 4 interventions
head downward or to side Suction upper airway Secure airway if indicated PEEP
192
Criteria for a patient to be discharged home from PACU after aspiration
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
What CXR findings may be present on images s/p aspiration
Pulmonary edema | Infiltrates in perihilar and dependent lung regions
194
How do ETT contribute to VAP
ETT bypass a patients defense mechanisms including cough and mucociliary clearance Micro-aspiration possible between ETT cuff and trachea
195
How does GI prophylaxis affect VAP
PPIs suppress gastric acid leading to bacterial overgrowth in the stomach Any aspirations increase the risk of infection
196
Aspiration pneumonitis causes what 3 potential problems?
1. Airway obstruction 2. Chemical burn to airway and lung parenchyma 3. Bacterial infxn
197
What drug class is not recommended as a prophylaxis for aspiration pneumonitis by decreasing secretions
Anticholinergics
198
What are 3 types of PTX
Closed Communicating Tension
199
What are hallmark characteristics of tension PTX
``` Hypoxemia Increased airway pressures Tachycardia HoTN Increased CVP Absent BS on affected side Tracheal shift to unaffected side ```
200
Which gas should be discontinued immediately if a PTX is suspected
N2O
201
What is emergency treatment of a tension PTX
14 g angiocath to 2nd IC space at mid-clavicular line or at 4-5th IC space at anterior axillary line
202
4 consequences of flail chest
Alveolar collapse Hypoventilation Hypercarbia Hypoxia
203
In a closed PTX, where is the defect located?
Pulmonary tree or lung tissue | Air enters and exits the pleural space through defect
204
Treatment for closed PTX
Observation Cath aspiration CT insertion
205
In an open PTX, where is the defect located?
Defect in the chest wall | Air passes between pleural space and atmosphere
206
What happens to the lung during an open PTX
``` Inspiration = lung collapse Expiration = partial re-expansion ```
207
Treatment for open PTX
Occlusive, unidirectional dressing allowing air out but not in Supplemental O2 CT insertion Possible tracheal intubation
208
Where is the defect when a tension PTX occurs
It can be an open or closed defect
209
Consequence of tension PTX
Increased intrathoracic pressure causes mediastinal shift on contralateral side Compression of heart and vasculature reduces VR and CO
210
Indications for surgical treatment of hemothorax
Initial output >1000 mL Bleeding > 200 mL/hr White lung on CXR Large air leak
211
What can increase the risk of chylothorax
CVC insertion on left side disrupting the thoracic ducts
212
Describe the movement of the flail segment during respiration
Inspiration = the injured ribs move inward and collapse affected region Expiration = Injured ribs move outward and affected region doesn't empty
213
What are the pulmonary consequences of flail chest
Alveolar collapse Hypoventilation Hypercarbia Hypoxia