Pulmonary Disease (CCM Collection) Flashcards
1
Q
PFT
- normal FEV1
A
80-120%
2
Q
PFT
- normal FVC
A
80-120%
3
Q
PFT
- normal absolute FEV1/FVC ratio
A
w/i 5% of predicted ratio
4
Q
PFT
- normal TLC
A
80-120%
5
Q
PFT
- normal FRC
A
75-120%
6
Q
PFT
- normal RV
A
75-120%
7
Q
PFT
- normal DLCO
A
> 60% to < 120%
8
Q
PFT
- obstructive FEV1/FVC
A
reduced, ≤ 70%
9
Q
PFT
- obstructive FEV1
A
reduced, < 80%
10
Q
PFT
- obstructive FVC
A
normal, > 80%
11
Q
PFT
- obstructive TLC
A
normal or increased
12
Q
PFT
- obstructive RV
A
normal or increased
13
Q
diagnosis?
PFT
- FEV1/FVC = reduced,
≤ 70% - FEV1 = reduced, < 80%
- FVC = normal, > 80%
- TLC = normal or increased
- RV = normal or increased
- if DLCO is reduced
A
emphysema
14
Q
diagnosis?
PFT
- FEV1/FVC = reduced,
≤ 70% - FEV1 = reduced, < 80%
- FVC = normal, > 80%
- TLC = normal or increased
- RV = normal or increased
- if DLCO is normal
A
- asthma
- chronic bronchitis
15
Q
diagnosis?
PFT
- FEV1/FVC = normal,
> 70% - FEV1 = variable
- FVC = reduced, < 80%
- TLC = reduced, < 80%
- RV = reduced
- if DLCO is reduced
A
parenchymal
16
Q
diagnosis?
PFT
- FEV1/FVC = normal,
> 70% - FEV1 = variable
- FVC = reduced, < 80%
- TLC = reduced, < 80%
- RV = reduced
- if DLCO is normal
A
- chest wall
- neuromuscular
17
Q
PFT
- restrictive FEV1/FVC
A
normal, > 70%
18
Q
PFT
- restrictive FEV1
A
variable
19
Q
PFT
- restrictive FVC
A
reduced, < 80%
20
Q
PFT
- restrictive TLC
A
reduced, < 80%
21
Q
PFT
- restrictive RV
A
reduced
22
Q
- volume tracing which shows markedly larger inspiratory volume compared to expiratory volume
- partial circuit disconnect
- ruptured ETT cuff
- large bronchopleural fistula
A
circuit leak
23
Q
- phenomenon whereby a patient initiates an inspiratory effort during the delivery of a controlled breath
- usually occurs in heavily sedated patients w/ high control breath rate
A
reverse triggering
24
Q
- MCC of increased breathing frequency in MV patients
- when neural inspiratory time is longer than the mechanical inspiratory time
A
double-triggering
25
empiric treatment for severe CAP
- β-lactam + macrolide
OR
- β-lactam + fluoroquinolone
26
empiric treatment for severe CAP w/ h/o MRSA in sputum
- β-lactam + macrolide
OR
- β-lactam + fluoroquinolone
PLUS
- vancomycin OR linezolid
27
what other clinical scenario is empiric MRSA coverage recommended for severe CAP?
recent hospitalization, < 90 days, w/ receipt of iv abx
28
when empiric MRSA coverage is initiated for CAP what other steps should be taken?
- nasal MRSA PCR swab
- BCs
- sputum cultures
- de-escalation of therapy asap
29
what are the 2 major diagnostic criteria for severe CAP?
- septic shock requiring vasopressors
- respiratory failure requiring MV
30
what are the minor diagnostic criteria for severe CAP? (need 3 or more)
- RR ≥ 30/min
- P:F ratio ≤ 250
- multilobar infiltrates
- AMS
- uremia
- leukopenia
- thrombocytopenia
- hypothermia
- hypotension requiring aggressive fluid resuscitation
31
when can a fluoroquinolone be considered for use as monotherapy in the empiric treatment of CAP?
when it is NOT severe
32
when should empiric treatment of CAP include coverage for Pseudomonas aeruginosa?
- prior respiratory isolation
- recent hospitalization, < 90 days
- recent iv abx
- locally validated risk factors for P aeruginosa
33
ALL patients w/ CAP (BOTH severe and nonsevere) should be empirically covered for what organisms?
- Legionella species
- Mycoplasma pneumoniae
- Chlamydia pneumoniae
- Chlamydia psittaci
34
ALL patients w/ CAP (BOTH severe and nonsevere) should be empirically covered w/ what abx?
either a macrolide or fluoroquinolone
35
what are the mechanical problems that can occur w/i the ECMO circuit?
- recirculation
- chattering
- clotting on the oxygenator
- hemolysis
36
- patient on ECMO
- anemia
- hyperbilirubinemia
- elevated LDH
- low haptoglobin level
hemolysis
37
how can hemolysis occur on ECMO?
- shear stress of blood passing through the ECMO circuit and across the oxygenator
- clotting on the end of the drainage cannula
- hyperinflammatory state induced by the ECMO circuit
- NO dysregulation
38
what are possible solutions for hemolysis on an ECMO circuit?
- decrease pump speed (rpm) to decrease ECMO circuit blood flow
- changing the ECMO circuit
- increasing AC
39
high proportion of oxygenated blood returning to the patient from the ECMO circuit passes directly back into the circuit through the drainage catheter WITHOUT being pumped systemically to the tissues of the body
recirculation
40
what are possible solutions for recirculation on an ECMO circuit?
- decreasing ECMO circuit flow (less negative drainage pressure and lower volume of blood recirculated between return and drainage cannulas)
- repositioning drainage cannula further away from return cannula
- conversion of dual-cannula configuration to SINGLE-cannula configuration
41
highly variable flow rates and rhythmic pulsations of the ECMO tubing
chattering, or chugging
42
what are common causes of ECMO circuit chattering?
- high pump speeds (rpms)
- malpositioned cannulas
- extrinsic kinking or compression of the drainage limb of the ECMO circuit
- increased inspiratory effort
- coughing
- volume depletion
43
what are possible solutions for chattering on an ECMO circuit?
- decrease pump speed (rpm)
- correct cannula positioning or kinking
- increase sweep gas flow to reduce patient inspiratory effort
- volume resuscitation
44
an ECMO circuit oxygenator is a foreign body that creates a thrombophilic environment; clotting is more common under what circumstances?
- lower ECMO circuit blood flows (more time for blood to contact the foreign surface of the oxygenator)
- lower (or no) AC
45
only 2 indications for bilevel NIV
- acute hypercapnic respiratory failure d/t COPD exacerbation leading to respiratory acidosis w/ a pH ≤ 7.35
- acute respiratory failure d/t cardiogenic pulmonary edema
46
should you use NIV for patients w/ acute respiratory failure d/t COPD exacerbation who do NOT have respiratory acidosis?
no
47
causes of INCREASED PIP ONLY
- ETT occlusion (kink, biting)
- ETT cuff herniation
- increased secretions or mucous plugging
- foreign body aspiration
- bronchospasm
48
causes of DECREASED PIP ONLY
- bronchopleural fistula
- disconnection of ventilator tubing
- ETT cuff rupture or leak
- ETT dislodgement
- ventilator dysfunction
49
causes of INCREASED PIP AND PlatP
- ARDS
- pulmonary contusion
- pulmonary edema
- pleural effusion (large)
- PNA
- pneumothorax (tension)
- auto-PEEP
- right mainstem intubation
- circumferential chest wall burn
- chest wall eschar
- abdominal compartment syndrome
- abdominal packing
- abdominal binder
- massive ascites
- Trendelenburg position
50
compliance = 1/elastance =
ΔV / ΔP
- V = volume
- P = pressure
51
LOW compliance means
difficult to inflate
52
HIGH compliance means
easy to inflate
53
airway Pressure =
resistance of airways + alveolar pressure
54
V̇ = flow =
ΔP / R
- P = pressure
- R = resistance
55
P =
- P = pressure
V̇ x R
- V̇ = flow
- R = resistance
56
ØV̇ = ØR
NO flow means NO resistance
57
Plateau P = alveolar P ~
1 / C
- C = compliance
- resistance is not a factor in this equation since there is NO flow meaning there is NO resistance
58
how do you measure the Plateau P on a ventilator?
inspiratory hold
59
C = ΔV / ΔP =
(Vend-insp - Vend-exp) / (Pend-insp - Pend-exp) = TV / PlatP - PEEP = PlatP
60
increase in PIP AND PlatP means what?
DECREASED compliance
61
what is Poiseuille's law?
V̇ = πΔPr^4 / 8nL = ΔP / R
for a kinked ETT, to explain why PIP increases, solve for R
R = 8nL / πr^4
just a small decrease in radius exponentially increases the resistance
62
if hypotensive and increased PIP, next step in management
UNPLUG from the ventilator!!
63
sawtoothing or oscillation of the expiratory flow curve is often seen in this setting
airway obstruction 2/2 mucoid secretions
64
patients who are considered high-risk and have passed SBT should be extubated directly to
NIV
65
which patients are considered high-risk for extubation?
- > 65 yoa
- have underlying cardiac or respiratory disease
66
can you extubate high-risk patients who have passed SBT to HFNC?
it is inferior to NIV
67
in a RCT, MV patients who failed SBT were randomized to early extubation to NIV vs continuing MV until SBT is passed and extubation performed; what were the results of the study?
- median time to liberation from ALL positive pressure ventilation (invasive or NIV) was similar
- NIV was a/w less invasive ventilation and fewer total ventilator days
- no difference in reintubation, tracheostomy rates, or survival
68
for acutely hospitalized patients ventilated more than 24 hours, how should the initial SBT be conducted?
w/ inspiratory pressure augmentation w/ 5-8 cm H2O for at least 30 minutes and not longer than 120 minutes
69
what are the criteria for a successful SBT?
- RR < 35 bpm
- good tolerance to SBTs
- HR < 140, or HR variability of > 20%
- O2 saturation > 90%, or PaO2 > 60 mmHg on FiO2 < 40%
- sbp > 80, and < 180 mmHg, or < 20% change from baseline
- no signs of increased work of breathing or distress
70
what are the signs of increased work of breathing or distress?
- accessory muscle use
- paradoxical or asynchronous rib cage-abdominal movements
- intercostal retractions
- nasal flaring
- profuse diaphoresis
- agitation
71
should a cuff leak test (CLT) be performed on all patients before extubation?
no, since postextubation stridor and reintubation are relatively infrequent and false-positives might subject many patients to unnecessary delay in extubation
72
a failed cuff leak test is defined as a cuff leak volume of?
< 110 ml
73
should you repeat a CLT the day after ppx has been given?
no, not recommended
74
which patients are considered high-risk and are eligible for a CLT?
- traumatic intubation
- female sex
- ETT intubation ≥ 6 days
- trauma to upper airway anatomy
- reintubated after unexpected extubation
- large ETT > 8 mm
75
what are the steps to perform a CLT?
1. suction ETT and oral secretions
2. set the ventilator to assist control moder
3. inflate the cuff
4. record the VTi and VTe to evaluate for differences between the volumes
5. deflate the cuff
6. record the VTe x 6 breathing cycles
7. average the 3 lowest VTe values
8. the cuff leak volume = VTi - averaged VTe
9. a CLT is considered a failure if the cuff leak volume < 110 ml
76
stridor ppx for failed CLT
- methylprednisolone 20 mg iv q4h x 4 doses
- last dose to be administered immediately before extubation
77
treatment for stridor after extubation
- methylprednisolone 40 mg iv x 1
- racemic epinephrine inhalation 2.25% 0.5 ml x 1 hour
- monitor for rebound edema
- cool aerosol
- if stridor persists > 60 minutes, consider reintubation
78
is NIV recommended for stridor treatment after extubation?
no, not recommended; evidence shows increased mortality as it can delay intubation
79
what are the current strategies to improve survival in ARDS?
- treat underlying d/o
- low TV ventilation
- conservative fluid management
- prone ventilation
80
what are contraindications to proning a patient?
- acute bleeding
- multiple or unstable fractures
- spinal instability
- raised ICP
- recent tracheostomy or sternotomy
81
when can steroids be considered as part of the treatment of ARDS?
when the underlying cause is a steroid-responsive process
82
what are the 2 most common and most serious complications during intubation of a critically ill patient?
- hypoxemia
- cardiovascular collapse
83
does BVM between induction and laryngoscopy vs RSI reduce the incidence of severe hypoxemia?
yes, but no difference in incidence of aspiration, MV support required after intubation
84
does a 500 ml crystalloid fluid bolus prior to or during induction reduce the incidence of cardiovascular collapse during or after intubation of a critically ill patient?
no, no difference
85
a single-center RCT found what when routine use of a bougie was applied?
increased first-pass success compare w/ ETT w/ stylet, especially in high-risk patients
86
mechanical ventilation
- what is the trigger phase?
determines when inspiration begins
87
mechanical ventilation
- what is the target phase?
how breath is delivered during inspiration
88
mechanical ventilation
- what is the cycle phase?
what ends inspiration
89
mechanical ventilation
- what is the baseline phase?
airway pressure during expiration
90
what phases occur during inspiration on MV?
trigger, target, and cycle
91
what phase occurs during expiration on MV?
baseline
92
what are the 2 types of triggered breaths?
- ventilator triggered breath = "controlled" breath
- patient triggered breath = "assisted" breath
93
what determines a controlled breath?
time
94
what determines an assisted breath?
pressure or flow (usually flow)
95
how is time determined as the triggered breath?
respiratory rate
96
how is target set?
- pressure target, or
- flow target
97
what is flow?
volume / time
98
what happens when you set the target as pressure target?
- pressure is the independent variable
- always constant
- flow is the dependent variable
99
what happens when you set the target as flow target?
- flow is the independent variable
- flow waveform should be consistent in each breath
- pressure is the dependent variable
99
what are the different waveforms that can be adjusted in flow target mode?
- decelerating ramp
- constant/rectangular
- ascending ramp
- sinusoidal
100
how do you tell a ventilator to stop delivering a breath?
by setting a cycle variable
101
what are the different cycle variables that can be set to tell the ventilator to stop delivering a breath?
- volume-cycle
- time-cycle
- pressure-cycle
- flow-cycle
102
what is a volume-cycle?
inspiration continues until a set VOLUME is delivered
103
what is a time-cycle?
inspiration continues until a set TIME has elapsed
104
what is a pressure-cycle?
inspiration continues until a pressure is reached (doesn't exceed set pressure to avoid barotrauma)
105
what is a flow-cycle?
terminates breath once flow reaches a certain PERCENTAGE of PEAK inspiratory flow
106
what is the baseline phase?
airway pressure during EXPIRATION
107
what does the baseline phase reflect?
PEEP
108
if you're concerned about auto-PEEP what maneuver can be performed on the ventilator?
expiratory hold to check for intrinsic PEEP
109
remember; in pressure assist-control ventilation mode (PACV or PCV) we set the PC AND inspiratory time (Ti), meaning PACV is what type of mode?
pressure-targeted, time-cycled mode
110
remember; in volume assist-control ventilation mode (VACV or VCV) we set the max flow rate (w/ the waveform) AND tidal volume, meaning VACV is what type of mode?
flow-targeted, volume-cycled mode
111
remember; in pressure support ventilation, we set the pressure support and inspiratory cycle off (ICO); there's NO RR, meaning PSV is what type of mode?
pressure-targeted, flow-cycled mode
112
how do you manipulate the inspiratory time on VACV?
by changing the flow rate; the higher the flow rate, the shorter the duration of inspiration needed to achieve the set volume
113
how does pressure-regulated volume control (PRVC) mode work?
- the first breath is a VC breath
- then measures the plateau pressure
- the PlatP becomes the pressure delivered on the second breath
- then measures the volume achieved
- so w/ every breath, a calculated pressure is delivered based on the volume of the previous breath
114
what is a major drawback of using PRVC mode?
if a patient awakens or becomes agitated and spontaneously breaths resulting in larger tidal volumes, the adjusted calculated pressure will continue to decrease, so then the patient will have to work harder for each subsequent breath leading to increased work of breathing, fatigue, and even arrest
115
when does ventilator dyssynchrony occur and what are the types of dyssynchrony?
- occurs at one of the stages of the mechanical breath
- trigger dyssynchrony
- target dyssynchrony
- cycle dyssynchrony
116
what are the 2 types of trigger dyssynchrony?
- ineffective triggering
- extra triggering
117
what is ineffective triggering?
patient tries to initiate a breath, however, ventilator does NOT deliver a breath
118
what is extra triggering?
ventilator delivers an inappropriate breath in the absence of patient effort
119
what are the causes of ineffective triggering?
- flow-trigger set too high?
- pressure-trigger set too high?
- is there diaphragmatic weakness?
- is there significant air-trapping (auto-PEEP)?
120
what are the causes of extra triggering?
- trigger threshold set too low?
- cardiac oscillation
- leak from circuit or chest tube
- condensation sloshing/bubbling in circuit
- peristalsis from large hiatal hernia
(d/t extra-pulmonary causes)
121
if a patient is "flow-starved" in VACV mode, which waveform will you see it reflected on the ventilator?
on the pressure-time scalar, which is the dependent variable
122
what is the only type of target dyssynchrony?
flow-starvation
123
how can you fix flow-starvation aka target dyssynchrony?
- increase flow
- switch from VCV to PCV so flow is now the dependent variable and the patient can have as much flow as they need
124
can you have flow-starvation in pressure-control?
NO! because flow will be your dependent variable, flow can go as high as the patient demands
125
what is cycle dyssynchrony?
dyssynchrony in terminating a breath
126
what are the types of cycle dyssynchrony?
- premature cycling
- delayed cycling
(inspiratory time is either too long or too short)
127
what is premature cycling dyssynchrony?
patient continues to have inspiratory effort AFTER ventilator has cycled-off inspiration (in baseline phase)
128
what is the distinguishing feature of premature cycling dyssynchrony?
2 breaths will be delivered WITHOUT exhalation
129
how do we fix premature cycling dyssynchrony?
INCREASE inspiratory time (how will depend on what ventilator mode)
130
what are the 2 ways to fix premature cycling on VCV?
- increase TV, or
- decrease flow rate
- either solution will increase inspiratory time since time = volume / flow
131
how do we fix premature cycling on PCV?
increase the inspiratory time!
132
what is delayed cycling dyssynchrony?
patient initiates expiratory effort WHILE ventilator still in inspiratory phase
133
what is the distinguishing feature of delayed cycling dyssynchrony?
positive notched deflection in pressure-scalar
134
how do we fix delayed cycling dyssynchrony?
DECREASE inspiratory time
135
what are the 2 ways to fix delayed cycling on VCV?
- decrease TV, or
- increase flow rate
- either solution will decrease inspiratory time since time = volume / flow
136
how do we fix delayed cycling on PCV?
decrease the inspiratory time!
137
how do we fix delayed cycling dyssynchrony in PS mode?
INCREASE ICO (flow-cycle threshold) which will indirectly DECREASE inspiratory time
138
what is the pleural fluid Hct in acute (< 3 days) hemothorax?
typically > 50% of peripheral blood
139
what are the typical lab findings of chronic hemothorax?
- pleural fluid Hct < 50%
- low pH
- elevated WBC count
140
a patient w/ chronic lung collapse w/ hemothorax that has a chest tube placed is at risk of?
reexpansion pulmonary edema
141
can reexpansion pulmonary edema be b/l if a chest tube was placed on only one side?
yes, because there is endothelial injury that can lead to recruitment and activation of inflammatory cells and release of proinflammatory cytokines that can increase permeability in both the affected lung AND contralateral lung
142
what complications can occur during placement of a chest tube that leads to recurrence of a hemothorax?
- thoracic duct injury
- intercostal artery injury
143
ddx for lymphocytopenia
- infection (bacterial, viral, fungal, parasitic)
- congenital immunodeficiency
- acquired immunodeficiency d/t immunosuppressing agents (including chemotherapy and RT)
- systemic disease (AI)
- hematologic disease (eg aplastic anemia, pancytopenia)
144
in a young patient w/ progressing symptoms, what should high on the diagnostic evaluation for lymphopenia?
HIV infection
145
most likely cause in a patient that has a CT chest w/ GGO and lymphopenia
viral PNA
146
can GGO be seen w/ pulmonary edema?
yes; you would also expect to see Kerley B lines and pleural effusions
147
empiric treatment for PJP
tmp-smx
148
empiric treatment for PJP w/ hypoxemia; A-a gradient > 35 mm Hg, or RA SpO2 < 92%
tmp-smx AND corticosteroids
149
what is seen w/ Oil Red O staining in BAL samples that is characteristic of e-cigarette, or vaping, product use-associated acute lung injury (EVALI)?
lipid-laden macrophages
150
foamy macrophages are present in BAL fluid in what pulmonary diseases? (not an inclusive list)
- ILD
- organizing PNA
- bronchiolitis
- amiodarone exposure
151
when are hemosiderin-laden macrophages characteristically found in BAL fluid?
diffuse alveolar hemorrhage (DAH)
152
what are the beneficial effects of positive airway pressure from CPAP on cardiac function?
- reduce LV afterload
- reduce venous return (may be beneficial in patients w/ fluid overload)
- reduces MR
- improvement in gas distribution to dependent lung regions
153
what is the most sensitive and specific sign of narcotic overdose?
bradypnea
154
what are the mechanisms of opioid-induced pulmonary edema?
- stress capillary failure
- negative intrathoracic pressure from inspiring against a closed glottis
- gastric aspiration
155
should you start a naloxone gtt for opioid intoxication if you suspect possible noncardiogenic pulmonary edema 2/2 naloxone?
yes, because the dose needed will likely be lower and it is more likely that the pulmonary edema is from opioid-induced pulmonary edema anyway
156
if VV ECMO circuit blood flow is HIGH relative to the patient's CO, then arterial oxygenation will be
HIGH
157
if VV ECMO circuit blood flow is LOW relative to the patient's CO, such as in a pregnant female whose CO is 10-15 L/min, then ultimate arterial oxygenation will be
LOW, because it's relying heavily on the underlying lung function
158
what intervention in severe ARDS w/ a PO2:FIO2 ratio < 150 mm Hg has shown significant mortality benefit?
early, prolonged prone positioning
159
what intervention in severe ARDS is unclear to have a mortality benefit?
early continuous infusion of cisatracurium
160
what intervention should be considered in very severe ARDS and has been shown to reduce 60-day mortality?
VV-ECMO
161
what medication has not shown a significant difference in hospital mortality rate and should not be routinely used unless otherwise indicated?
methylprednisolone
162
what treatment has been shown to transiently improve hypoxemia w/o a mortality benefit, but may be used as a bridge to VV-ECMO or transfer to a facility for prone positioning?
iNO
163
what adverse effect may occur w/ use of iNO in ARDS patients?
AKI
164
what are the physiologic effects of prone positioning in patients w/ severe ARDS?
- more homogeneous distribution of ventilation
- improved oxygenation
- higher respiratory system compliance
- reduction in ventilator-induced lung injury
- RV unloading
165
in prone positioning, what happens to respiratory compliance?
- reduction in chest wall compliance
- rise in lung compliance
- net result is no change or a modest increase in overall compliance
166
when performing an expiratory hold, an in-line capnograph will show what?
exhaled CO2 that remains at a similar level to the end-tidal CO2 of breaths observed before and after the pause
167
when performing an inspiratory hold, an in-line capnograph will show what?
an absence of CO2 w/ a sudden drop to 0 since the ventilator valve closure occurs at the end of inspiration of fresh gas, which is free of any exhaled CO2
168
what are ominous causes of sudden drop in CO2 on capnography?
- disconnection of ventilator tubing from the ETT
- self-extubation
169
gradual reduction in exhaled CO2 on capnography is indicative of what?
asystole
170
how many phases are there in the capnogram?
4
171
what are the 4 phases of the capnogram?
- phase 1 = absence of exhaled CO2 (represents time from end inspiration to onset of exhalation of dead space gas from the preceding breath)
- phase 2 = rise in exhaled CO2 during the mixing of dead space gas and emptying of alveoli
- phase 3 = alveolar plateau as alveoli empty, reaching a maximum, or end-tidal CO2, immediately prior to the rapid fall in CO2 during inspiration in phase 4
- phase 4 = inspiration
172
information about the lung and circulation is conveyed by the shape of the capnographic waveform, especially in what phases?
phases 2 and 3
173
a dramatic rise in phase 3 on capnography indicates what?
very substantial VQ inhomogeneity, which is seen in severe obstructive disease, such as COPD and status asthmaticus
174
impedance plethysmogram (measures changes in volume) suggest end-expiratory flow and cardiac oscillations, which is typical of?
obstructive lung diseases
175
attempts have been made to use serum biomarkers to define ARDS into what phenotypes?
- hypoinflammatory (uninflamed)
- hyperinflammatory (reactive)
176
empiric treatment for refractory hypoxemic respiratory failure d/t diffuse alveolar hemorrhage (DAH) from pulmonary capillaritis in the setting of untreated vasculitis
high-dose methylprednisolone
177
what should be suspected in patients w/ diffuse b/l radiographic infiltrates, an unexplained drop in hb, and hypoxemia w/ or w/o hemoptysis?
diffuse alveolar hemorrhage (DAH)
178
what test is required to confirm a diagnosis of DAH and rule out infection?
bronchoscopy w/ sequential BAL sampling
179
most cases of DAH are caused by
pulmonary capillaritis and associated systemic AI diseases, such as
- ANCA-associated vasculitis
- anti-GBM disease
- SLE
180
treatment of complicated empyema
- complete drainage w/ thoracostomy tube usually w/ intrapleural fibrinolytics (tPA and DNAse), or
- surgical drainage
181
formula for driving pressure
DP = Pplat - PEEP
but, also
DP = TV / C
where, TV = tidal volume, and C = compliance
and remember, C = ΔV / ΔP
182
what driving pressure might be safe?
< 15-20 cm H2O
183
what is an alternative way to assess compliance during tidal volume delivery?
stress index analysis
184
what are the types of lung injury that can occur as an adverse effect of mechanical ventilation?
- VILI (ventilator-induced lung injury)
- VALI (ventilator-associated lung injury
- SILI (self-induced lung injury)
185
what are the types of ventilator-induced lung injury?
- atelectrauma (cyclic atelectasis)
- biotrauma (inflammation; loss of surfactant leading to decrease in lung compliance)
- rheotrauma (high flow rates)
- volutrauma (high volumes leading to alveolar overdistension)
- barotrauma (high pressures)
186
definition of ventilator-associated lung injury
- if cause is determined then VILI
- if no cause found then VALI; VALI is difficult to discern from ARDS and ALI
187
what parameters must be met when assessing stress index?
- volume controlled breath (no patient effort)
- constant inspiratory flow
188
when assessing stress index, what does an increasing slope suggest?
worsening compliance (tidal overdistension)
189
when assessing stress index, what does a flattened slope suggest?
improving compliance (recruitment during tidal volume)
190
will reduction in RR in the presence of adequate expiratory times have any effect on DP?
no
191
the following findings would be typical of what diagnosis?
- elevated peak airway pressure
- rapid rise of airway pressure very early in the breath
- biphasic expiratory flow w/ abnormally low expiratory flow rates and flow that persists to end-expiration
- presence of autoPEEP demonstrated w/ an end-expiratory pause maneuver
obstructive physiology c/w status asthmaticus or other pulmonary disease
192
the following findings would be typical of what diagnosis?
- elevated peak airway pressure, but pressure rises abnormally only LATER in the breath
- expiratory flow should be normal or fast
- autoPEEP is usually absent unless the diagnosis is d/t severe airflow obstruction
b/l PTX
193
the following findings would be typical of what diagnosis?
- elevated peak airway pressure, but pressure rises abnormally only LATER in the breath
- expiratory flow is usually near normal
- autoPEEP is absent or very minor in degree
ARDS
194
the following findings would be typical of what diagnosis?
- airway pressure is elevated late in inspiration
- expiratory flows are often ELEVATED
- no autoPEEP
idiopathic pulmonary fibrosis
195
one very important observation has emerged from RCT of early vs delayed tracheostomy which is
physicians are not very good at predicting who will need prolonged translaryngeal intubation
196
what are the benefits of early tracheostomy (w/i 3 days) vs delayed tracheostomy (after 10 days) in a patient w/ ALS?
- reduce duration of sedation days
- may be a/w lower mortality (not confirmed)
197
a group of rare d/o's that have various causes, including infectious etiologies, exposures to drugs and toxins, hypersensitivity reactions, neoplasia, and idiopathic causes
pulmonary eosinophilic lung diseases
198
- acute presentation w/ diffuse pulmonary infiltrates and respiratory failure
- 20-40 yoa
- previously healthy
- usually 2-4 weeks duration of illness
- cough, dyspnea, fever
up to 2/3 require intubation
- peripheral eosinophilia is often NOT present initially, but may occur later
idiopathic acute eosinophilic PNA (AEP)
199
diagnostic criteria for idiopathic acute eosinophilic PNA (AEP)
- febrile illness of short duration
- hypoxemic respiratory failure
- diffuse pulmonary opacities on chest radiographs
- BAL demonstrating at least 25% eosinophils
- absence of other causes of pulmonary eosinophilia
200
treatment for idiopathic acute eosinophilic PNA (AEP)
- no controlled treatment trials since rare
- supportive care
- empiric abx
- systemic glucocorticoid therapy a/w rapid clinical course
201
fungal infection that may cause acute pulmonary eosinophilia, endemic to southwestern desert of North America
Coccidioides immitis
202
- should be considered in patients w/ pulmonary eosinophilia
- > 90% patients have asthma
- peripheral eosinophilia
- vasculitic skin lesions
- neurologic findings
- renal disease
eosinophilic granulomatosis w/ polyangiitis
203
what lab test is positive in 30-60% of cases of eosinophilic granulomatosis w/ polyangiitis?
antineutrophil cytoplasmic antibody (ANCA), w/ p-ANCA being most commonly positive
204
condition characterized by a hypersensitivity response to aspergillus
allergic bronchopulmonary aspergillosis (ABPA)
205
diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)
- one predisposing condition must be present
- asthma
- cystic fibrosis
206
diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)
- both obligatory criteria must be present
- aspergillus skin test positivity or detectable IgE levels against Aspergillus fumigatus
- elevated total IgE level, > 1 mg/L (> 1000 IU/L)
207
diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)
- other criteria, at least 2 must be present
- precipitating serum Abs to Aspergillus fumigatus
- radiographic opacities c/w ABPA
- total eosinophil count, > 0.5 x 10^9/L
208
what is the preferred lab test to confirm a diagnosis of severe anaphilaxis?
tryptase
209
when does tryptase peak and for how long does it remain elevated?
- 60-90 minutes
- at least 5 hours
210
what are the prodromal symptoms of anaphylaxis?
- headache
- dyspnea
- flushing
- pruritus
- cough
- abdominal pain
- rhinorrhea
211
what is required to make a diagnosis of anaphylaxis?
- acute-onset illness (minutes to hours)
- involves skin (hives, urticaria, flushing, angioedema), or mucous membranes (lips, tongue, uvula)
- in combination w/ respiratory compromise (bronchospasm), hypotension, or evidence of EOD
- after exposure to a likely trigger
212
what are common triggers of anaphylaxis?
- foods
- drugs
- insect stings
- physical factors (exercise, cold, heat)
- idiopathic
213
ddx for anaphylaxis
- other causes of shock and acute cardiopulmonary complaints
- hereditary angioedema w/ rash
- flushing syndromes (carcinoid, tumors secreting vasoactive intestinal polypeptide (VIP), mastocytosis, mast cell activating syndrome, and medullary thyroid cancer)
- restaurant syndromes (exposure to MSG or scombroidosis)
- nonorganic disease (panic attacks, vocal cord dysfunction syndrome)
214
management recommendations for anaphylaxis
- early administration of epinephrine 0.01 mg/kg IM
- supplemental O2, β-agonists, and close monitoring for patients w/ respiratory distress and airway symptoms
215
for anaphylaxis, what may be considered in patients who fail to respond to multiple injections of epinephrine IM and fluid resuscitation?
epinephrine IV
216
what medications are often administered as adjunctive therapy in more severe cases of anaphylaxis and why?
- histamine receptor (H1 and H2) antagonists and corticosteroids
- to reduce the risk of a late-onset, biphasic reaction that occur 4-8 hours after symptom onset
217
what serologic marker is more sensitive than tryptase in diagnosing anaphylaxis but only remains elevated 30-60 minutes after symptoms onset?
serum histamine
218
self-limited, localized subcutaneous or submucosal swelling that occur in isolation, w/ urticaria, or in a/w anaphylaxis
angioedema
219
initial evaluation of anaphylaxis should include
complement protein C4 level
220
when evaluating anaphylaxis, if the complement protein C4 level is low it should prompt evaluation for what and what should be checked next?
- hereditary or acquired C1 inhibitor deficiency
- C1 inhibitor Ag and functional levels
221
in a patient w/ chronic hypersensitivity pneumonitis, do LFTs obtained during clinical stability correlate w/ an acute event?
no
222
in patients w/ ILD, including hypersensitivity pneumonitis, what is a/w lower survival?
- PEEP > 10 cm H2O
- use of NIV, which may delay intubation
- elevated PlatP
223
although there are no guidelines for ventilator management in patients w/ ILD, what strategies are recommended to follow?
ARDSnet protocol
224
what form of supplemental O2 improves oxygenation by washing out nasopharyngeal dead space?
HFNC
225
what are mechanisms by which HFNC improves oxygenation and gas exchange?
- high-flow rate promotes washout of exhaled gases (CO2) in what is usually upper airway dead space
- reduces entrainment of room air during inhalation
- increases nasopharyngeal airway pressure
- relieves autoPEEP
- decreases work of breathing
226
how much does HFNC increase nasopharyngeal airway pressure when the mouth is closed?
≤ 1 cm H2O for every 15 L/min
- so max is about ≤ 4 cm H2O
227
what is an advantage of using HFNC in patients w/ acute hypoxemic respiratory failure who have secretions?
warmed and humidified air assist in thinning secretions and permits easier sputum expectoration
228
in large, multicenter, RCTs to date, what has not been consistently a/w lower mortality or more ventilator-free days?
cisatracurium gtt
229
definition of massive hemoptysis
- varies
- 100-600 ml of blood w/i 24 hours
230
most common reason for death in a patient w/ massive hemoptysis?
respiratory failure and asphyxia
231
common causes of massive hemoptysis
- DAH from pulmonary vasculitis
- TB
- fungal infections
- bronchiectasis
- heart failure
- cancer
232
initial steps in management of massive hemoptysis
- airway protection
- adequate oxygenation
- localization of the bleeding site
233
in massive hemoptysis, what is the preferred initial imaging modality and why?
- standard cxr
- quick, inexpensive, readily available, can localize bleeding site in at least 1/3 of cases
234
what imaging modality increases sensitivity of bleeding site detection to ~ 80% in massive hemoptysis?
CTA chest
235
in chronic inflammatory d/o's such as TB, what is the source of bleeding in 90% of cases of massive hemoptysis?
neovascularization from collateral bronchial and intercostal arteries
236
what is the treatment of choice for cases of massive hemoptysis (can control ~ 80% of cases)?
bronchial and intercostal arteries angiography w/ embolization
237
bleeding from which site accounts for only 5% of cases of massive hemoptysis?
pulmonary arteries, most of which have a known pulmonary malignancy
238
in patients w/ TB, massive hemoptysis, can rarely occur from what source of bleeding?
Rasmussen's aneurysm, an aneurysm in a pulmonary artery adjacent to a tuberculous cavity
239
in selected cases of massive hemoptysis, if embolization is not an option or is unsuccessful, an experienced operator may use bronchoscopy to place what?
endobronchial blocker (a balloon-tipped catheter that occludes the bleeding segment)
240
is there benefit to transfusing platelets in a patient w/ massive hemoptysis if the platelet count is > 50 x 10^3/mL?
no
241
severe airway obstruction leading to autoPEEP can lead to what type of ventilator dyssynchrony?
trigger dyssynchrony
242
if a lung, or both lungs, have extensive regional consolidation 2/2 PNA, or in a patient w/ severe ARDS, what happens to the volume of lung capable of being ventilated?
functional lung size becomes markedly reduced
243
in a patient w/ PNA or ARDS that has significantly reduced functional lung capacity, what happens if that patient receives "normal" sized TV on MV even if based on ibw?
may produce excessive regional tidal stretch in the reduced functional lung
244
what is one simple approach to avoid overdistention in a patient w/ markedly reduced functional lung size?
scaling TV to compliance (TV / CL) instead of TV to ibw (TV / ibw)
245
in near normal chest wall mechanics, TV / CL is approximated by what?
driving pressure (DP), which is the pressure change across the alveolar structures required to deliver a tidal breath
246
driving pressure (DP) is calculated as
PlatP - PEEP
247
mixing what w/ what to make a cleaning mixture has the potential to explode and produces what gas?
- vinegar and bleach
- chlorine gas
248
hydration of chlorine gas (Cl2) leads to formation of what 2 compounds?
- HCl
- HOCl (hypochlorous acid)
249
inhalation of chlorine gas and penetration into alveolar spaces can lead to
parenchymal lung injury
250
treatment for parenchymal lung injury d/t chlorine gas inhalation
- mostly supportive
- humidified O2
- inhaled β-adrenergic agents
- mechanical ventilation
251
what are other interventions for the treatment of parenchymal lung injury d/t chlorine gas inhalation based on anecdotal evidence?
- inhaled bicarbonate
- systemic or inhaled glucocorticoids
- N-acetylcysteine
252
inflation of alveolar structures and avoidance of expiratory alveolar collapse is driven by what?
transpulmonary pressures (TPP) during breath delivery and during expiration
253
transpulmonary pressures (TPP) is the pressure across alveolar structures which is what?
airway pressure - pleural pressure
Paw - Ppl
254
what key measurements of airway pressures are measured at during the ventilatory cycle?
- end-inspiration w/ no-flow = PlatP
- end-expiration w/ no-flow = PEEP
255
pleural pressures can only be assessed how?
pressure sensors in the pleura or esophagus (Pes)
256
in most MV patients, Ppl is very low, why?
chest wall compliance is normal
257
when chest wall compliance is normal, what is a reasonable surrogate for transpulmonary pressures (TPP)?
airway pressure
258
when are airway pressures not a reliable surrogate for transpulmonary pressures (TPP) and can markedly overestimate TPP and what adverse effect does this have on patients?
- when chest wall compliance (Ccw) is low; eg from obesity
- can lead clinicians to unnecessarily limit inflation and expiratory pressures leading to insufficient TVs, exposing alveoli to repetitive collapse-reopening injury (atelectrauma)
259
would it be beneficial to measure Pes (esophageal pressure) in a patient w/ normal chest wall compliance?
no
260
physiology of prone position and how it helps improve oxygenation; fyi only
- induces a more uniform distribution of TV by reversing the vertical pleural pressure gradient
- decreases the superimposed pressure of both the heart and the abdomen on the dorsocaudal regions of the lungs
- pulmonary perfusion remains preferentially distributed to the dorsal lung regions, thus improving overall alveolar ventilation/perfusion matching
- the larger lung tissue mass suspended from a wider dorsal chest wall effects a more homogeneous distribution of pleural pressures throughout the lung, which in turn reduces abnormal strain and stress development
- this is believed to avoid the development of VILI and may partly explain the reduction in mortality in severe ARDS
261
next best step in a patient that was difficult to intubate, has recurrent cuff leaks, and ETT appears high on cxr
examine the ETT and airway w/ bronchoscopy and advance the ETT w/ direct visualization of the VCs and trachea
262
target SpO2 for all hospitalized patients
≥ 88-92%
263
what happens if hyperoxia, even if it's a modest amount, PO2 120-150 mm Hg?
may still be a/w harm; hyperoxia leads to production of reactive oxygen species (ROS)
264
if hyperoxia is bad, should we allow for "permissive hypoxemia?"
no, there are no data to support doing so
265
what method of supplemental O2 has been shown to be more effective at preventing reintubation in high-risk patients?
NIV
266
what patients are deemed high-risk and should be extubated to NIV?
- ≥ 65 yoa
- h/o underlying cardiac disease
- h/o underlying respiratory disease
267
what patients are deemed low-risk and do not need to be extubated to NIV?
- ≤ 65 yoa
- have a normal PCO2
- no significant respiratory or cardiac comorbidities
- can protect their airway
268
are immunosuppression or PNA as the cause of acute respiratory failure a/w high risk for postextubation respiratory failure and reintubation? and is there benefit in these patient populations for preemptive postextubation NIV?
no and no
269
a patient who has had a CVC removed and shortly afterwards suffers from a stroke should prompt the clinician to think about what?
air embolism, more specifically, paradoxical embolism via patent foramen ovale (PFO)
270
management when arterial embolism is suspected
- immediate oxygenation
- hemodynamic resuscitation
271
severe cases a/w entry of large volumes of air may p/w what?
- LOC
- coma
- cardiac arrest
272
what are additional features of signs of acute ischemia of affected organs from an air embolism?
- chest pain
- wheeze
- crepitus over superficial vessels
- livedo reticularis
- bubbles w/i retinal arteries
273
if a patient on ECMO has a PFO and a large volume of air enters the venous system will the ECMO circuit alarm?
no, they will bypass the ECMO pump since they are not on the outflow of the ECMO circuit
274
severe cases of venous air embolism p/w?
- dyspnea
- substernal chest pain
- light-headedness
- dizziness
275
life-threatening cases of venous air embolism are characterized by
- acute-onset right-sided HF
- acute sense of impending doom
- obstructive shock
- cardiac arrest
276
duration of treatment w/ oseltamivir po or inhaled zanamivir for uncomplicated influenza infection in otherwise healthy, ambulatory patients
5 days
277
management of influenza in patients requiring hospitalization for severe lower respiratory tract manifestations or ARDS
- c/w oseltamivir beyond 5 days
- evaluate for coinfections w/ bacteria or aspergillus
- if persistently positive RT-PCR after 7-10 days check for neuraminidase inhibitors and consider alternate antiviral
278
should severe influenza infection be treated w/ corticosteroids?
no; not unless there is another clinical indication as use has been a/w potential harm including increased mortality
279
should severe influenza infection be treated w/ IVIG?
no
280
should severe influenza infection be treated w/ convalescent plasma from donors who have recovered from confirmed influenza infection or who have been immunized against influenza?
no, it's still under investigation
281
Power (J / min) =
0.098 × RR × (TV^2 × (1/2 × E + RR × (1 + I:E) / (60 × I:E) × Raw) + TV x PEEP
where RR = respiratory rate, TV = tidal volume, E = system elastance, I:E = ratio of inspiratory to expiratory time, and Raw = airway resistance
282
VILI has been linked to
excessive stretch of alveolar tissue
283
the stretch of alveolar tissue that has been linked to VILI is driven by what?
stress (TPP) and resulting tissue strain (volume) both statically (at end inspiration and end expiration), and dynamically (during tidal volume delivery)
284
the use of positive pressure ventilation (BMV) supplied by the operator between the time of induction and translaryngeal intubation of critically ill patients in the ICU is a/w
less severe hypoxemia (defined as pulse oximetry of < 80%)
285
PlatP measurements at end-inspiration are made under what conditions and represent what?
- no-flow conditions
- alveolar distending pressure
286
no-flow conditions to measure PlatP can be created at the end of a breath in any passive mode under what 2 circumstances?
- having a total inspiratory time longer than required for set breath delivery
- manually holding the lung inflated after flow has ceased (inspiratory hold)
287
under what circumstances can you not use the PlatP as a surrogate for end-inspiratory TPP?
when chest wall compliance is LOW
- ACS
- surgical binder
- obesity
288
sudden loss of TV in pressure-targeted ventilation (PCAC and PSV) has a short ddx which is
- sudden decrease in compliance
= flash pulmonary edema
= tension PTX
= lobar collapse
- sudden increase in resistance
= bronchospasm
= tracheal obstruction
= circuit occlusion
= tube occlusion
- sudden loss of patient effort that had been contributing to the tidal breath
= excessive sedation or paralytics
- sudden development of a massive leak
= ruptured ETT cuff
= dislodgement of ETT
= circuit disconnect
- ventilator malfunction
289
3 pathologic states of ARDS
1. acute exudative stage
2. fibroproliferative stage
3. resolution/repair phase OR fibrotic stage
290
explain the pathophysiology of the acute exudative stage of ARDS
- increased alveolar capillary permeability --> alveolar flooding w/ protein-rich fluid
- release of proinflammatory cytokines and neutrophil extravasation
- impaired surfactant synthesis
- alveolar collapse and alveolar hemorrhage
