Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

APEX > Unit 1 - Respiratory Pathophysiology > Flashcards

Unit 1 - Respiratory Pathophysiology Flashcards

1
Q

3 categories of predictors for postoperative pulmonary complications for pts undergoing pulmonary surgery

A
  • lung parenchymal function (gas exchange)
  • respiratory mechanics (airflow)
  • cardiopulmonary reserve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DLCO that predicts postop pulmonary complications in pts undergoing pulmonary surgery

A

< 40% predicted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

FEV1 that predicts postop pulmonary complications in pts undergoing pulmonary surgery

A

< 40% predicted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

normal VO2 max

A

normal male = ~35-40 mL/kg/min

normal female = 27-31 mL/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

VO2 max that predicts postop pulmonary complications in pts undergoing pulmonary surgery

A

< 15 mL/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when is split lung V/Q function testing indicated

A

when preoperative assessment suggests an increased risk of postop pulmonary complications

(DLCO < 40% predicted, FEV1 < 40% predicted, or VO2 max < 15 mL/kg/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what can you ask the patient in the place of VO2 max value

A

ask the patient if she/he can climb 2 flights of stairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when might a right sided DLT be used

A
  • distorted anatomy of left main bronchus (tumor, TAA)
  • left pneumonectomy
  • left lung transplant
  • left sleeve resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

absolute indications for OLV

A
  • isolation of 1 lung to avoid contamination (infection, hemorrhage)
  • control distribution of ventilation (bronchopleural fistula, surgical opening of major airway, large unilateral lung cyst or bulla, life threatening hypoxia d/t lung disease)
  • unilateral bronchopulmonary lavage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

relative indications for OLV

A
  • surgical exposure (high priority): TAA, pneumonectomy, thoracoscopy, upper lobectomy, mediastinal exposure
  • surgical exposure (low priority): middle/lower lobectomy, esophageal resection, thoracic spine surgery
  • pulmonary edema s/p CABG or robotic mitral valve surgery
  • severe hypoxemia r/t lung disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DLT size for females

A

< 160 cm = 35 french

> 160 cm = 37 french

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DLT size for males

A

< 170 cm = 39 french
> 170 cm = 41 french

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DLT depth

A

female ~ 27 cm
male ~ 29 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pediatric DLT sizes

A

8-9 yrs old = 26
10+ = 28 or 32

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DLT alternatives for kids under 8 yrs

A
  • bronchial blocker
  • single lumen ETT advanced into mainstem bronchus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when is DLT contraindicated

A

< 8 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

complication of left sided DLT placed too far on right side with clamped tracheal lumen

A

absent right breath sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

complication of left sided DLT placed too far on left side with clamped tracheal lumen

A

left breath sounds absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

complication of left sided DLT tip in trachea with clamped tracheal lumen

A

left and right breath sounds heard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where on the alveolar compliance curve is alveolar ventilation best

A

steepest part of the curve (where alveolar compliance is best)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how does lateral positioning in awake pt affect V/Q matching

A

alveoli remain on the same part of the alveolar compliance curve as awake upright position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how does lateral positioning affect V/Q matching under GA

A

reduced lung volumes and diaphragmatic excursion is better on the dependent side

results in V/Q mismatching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how is alveolar ventilation affected in the nondependent lung of an anesthetized patient in lateral position

A
  • alveoli move from upper, flatter region of curve to the slope
  • alveolar ventilation better in non-dependent lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how is alveolar ventilation affected in the dependent lung of an anesthetized patient in lateral position

A
  • alveoli move to lower compliance, less ventilation (lower, flatter region of slope)
  • alveolar perfusion better in dependent lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

why is there an increased risk of hypoxemia during OLV

A

V/Q mismatch and increased A-a gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how do NMBs affect V/Q

A
  • worsen mismatch
  • abdominal contents shift towards thorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does positive pressure ventilation affect V/Q

A

worsens mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does the body compensate for V/Q mismatch

A

HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what color is the bronchial cuff of a DLT

A

blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

where should the clamp be placed for a DLT

A
  • to connector piece going to lumen of operative lung
  • place distal to y-piece and proximal to cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

FiO2 to use for OLV

A
  • some say 100%
  • some say 80% or less to minimize absorption atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ideal RR for OLV

A

12-15 breaths/min to maintain PaO2 35-45 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

lab that should be checked serially after OLV is started

A

ABGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

benefit of PEEP in OLV

A
  • increases FRC by pushing the lung up the compliance curve
  • prevents excess shearing stress of repeated alveolar opening and closing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

potential downside of PEEP in OLV

A

may increase shunt flow to non-depdenent lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

vent settings for OLV in COPD patients

A

longer expiratory time (I:E 1:3) and less extrinsic PEEP will improve gas removal from lung (decreased auto-PEEP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how do volatiles affect HPV

A

impaired > 1.5 MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why do procedures that rely on left lung for OLV have a higher incidence of hypoxemia with OLV

A

right lung is larger than the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

steps to take if pt becomes hypoxemic during OLV

A
  1. verify 100% FiO2
  2. check tube position
  3. r/o physiologic causes (dec. CO, bronchospasm, mucus pluc, PTX, etc)
  4. apply CPAP to nondependent lung starting at 2 cm H2O up to 10 cm H2O
  5. PEEP to dependent lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

surgical method to reduce shunt flow to non-dependent lung in pneumonectomy patients

A

early clamping or ligation of pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

can the lumen of a bronchial blocker be used for suctioning?

A

can’t suction blood, pus, or mucus from non-ventilated lung

can suction air from non-ventilated lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

can O2 insufflation be used with a bronchial blocker

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

youngest age a DLT can be used

A

8 years old (size 26 Fr)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how can OLV be accomplished in a pt requiring nasal intubation

A

single lumen tube with bronchial blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how can OLV be accomplished in a pt with a trach

A

bronchial blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

best choice for OLV when lung must be isolated for contamination concerns

A

DLT - not bronchial blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

which lung is ventilated when using a bronchial blocker

A

the lung on the opposite side of the blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

2 most common serious complications of mediastinoscopy

A
  1. hemorrhage
  2. pneumothorax (usually R side)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

most common approach for mediastinoscopy

A
  • small incision at midline of lower neck at suprasternal notch
  • scope placed anterior to trachea and posterior to innominate artery and thoracic aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

risk of mediastinoscopy r/t thoracic aorta

A
  • hemorrhage
  • reflex bradycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

7 vital structures at risk for injury during mediastinoscopy

A
  1. thoracic aorta
  2. innominate artery
  3. vena cava
  4. trachea
  5. thoracic duct
  6. phrenic nerve
  7. RLN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

consequence of innominate artery injury during mediastinoscopy

A

decreased carotid blood flow and cerebral blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

consequence of thoracic duct injury during mediastinoscopy

A

chylothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

consequence of phrenic or right laryngeal nerve injury during mediastinoscopy

A

paresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

only absolute contraindication to mediastinoscopy

A

previous mediastinoscopy d/t scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

relative contraindications of mediastinoscopy

A
  • tracheal deviation
  • thoracic aortic aneurysm
  • SVC obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what should you consider in regards to NMBs in pts having a mediastinoscopy

A
  • procedure used to diagnose & stage lung cancer
  • assoc. between oat cell carcinoma and eaton-lambert syndrome
  • ELS pts sensitive to all NMBs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

vascular anatomy from heart to brain

A

innominate (brachiocephalic) artery → R common carotid → R internal carotid → R cerebral circulation at circle of willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

consequence of innominate artery compression

A
  • compromises circulation to right side of circle of Willis
  • detrimental to pts with cerebrovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

where should pulse ox be placed for mediastinoscopy

A

right upper extremity - of scope compresses innominate artery, waveform will dampen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

where should NIBP placed in mediastinoscopy

A

LUE - if scope compresses innominate a., BP reading on L arm wont be affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

why might it be helpful to have a lower extremity IV in a mediastinoscopy in the event of bleeding

A

fluids and blood given in an upper extrmity will pass through vascular injury and enter mediastinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

indications for tracheal resection

A
  • tracheal stenosis
  • tracheomalacia
  • tumor
  • vascular lesions
  • congenital malformations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

sequence of ETT management in a patient undergoing lower tracheal resection

A
  • place ETT in trachea above lesion
  • after surgeon opens trachea, 2nd ETT place in L mainstem bronchus (used to ventilate L lung)
  • surgeon sutures posterior tracheal anastomosis
  • endobronchial ETT removed and tracheal ETT is advanced past anastomosis and positioned in L bronchus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what artery is at risk for compression during tracheal resection

A

brachiocephalic - follow same rules as mediastinoscopy for NIBP and pulse ox measurement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

complication of neck positioning after tracheal resection surgery

A

tetraplegia - pt must maintain flexed position for several days after surgery to reduce tension on tracheal anastomosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

best choice for reintubation post tracheal resection

A

flexible fiberoptic bronch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

2 core lung protective ventilation strategies

A
  1. low Vt
  2. PEEP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Berlin definition: onset of ARDS

A

within 1 week of initial insult or new/worsening respiratory symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Berlin imaging criteria for ARDS

A

CXT or CT - bilateral opacities not fully explained by effusions, lonar/lung collapse, or nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Berlin definition of ARDS: edema origin

A

resp failure NOT fully explained by cardiac failure or fluid overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Berlin criteria for mild ARDS

A

PaO2/FiO2 ratio 201-300 mmHg with PEEP or CPAP ≥ 5 cm H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Berlin criteria for moderate ARDS

A

PaO2/FiO2 ratio < 101-200 mmHg with PEEP ≥ 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Berlin criteria for severe ARDS

A

PaO2/FiO2 ratio < 100 mmHg with PEEP ≥ 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

pulmonary causes of ARDS

which is the most common?

A
  • pneumonia (most common)
  • COVID 19
  • aspiration
  • smoke inhalation
  • near-drowning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

extrapulmonary causes of ARDS

which is the most common

A
  • sepsis (most common)
  • hematologic (TRALI, TACO, massive transfusion)
  • trauma/shock
  • burns
  • CPB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what causes ARDS

A

neutrophil and platelet mediated inflammation injury that leads to diffuse alveolar destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

4 key pathophysiologic features of ARDS

A
  1. protein-rich pulmonary edema
  2. loss of surfactant
  3. hyaline membrane formation
  4. possible long-term lung injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

stage 1 of ARDS
- onset
- duration

A

exudative
- onset ~6-72 hours after initial insult
- duration ~7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

which phase of ARDS triggers inflammatory cascade and causes diffuse alveolar destruction

A

phase 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what happens to type 1 pneumocytes in stage 1 of ARDS

A

injury disrupts integrity of tight junctions
- leads to capillary leak and protein-rich fluid traverses the alveolar capillary membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

consequences of capillary leak in stage 1 of ARDS

A
  • protein-rich fluids traverse alveolar capillary membrane
  • surfactant damage increases alveolar surface tension
  • alveolar collapse leads to dec. gas exchange
  • inc. WOB d/t decreased alveolar compliance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

role of hyaline membranes in stage 1 of ARDS

A
  • alveoli collapse when there’s not enough surfactant
  • damaged cells accumulate in airways and form hyaline membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

common diagnostic findings in stage 1 of ARDS

A
  • bilateral alveolar infilitrates on CXR
  • hypoxemia despite increased supplemental O2
  • increased A-aDO2 gradient
  • spontaneously breathing pt may have respiratory alkalosis (tachypnea)
  • pHTN in setting of low/normal LV filling pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

hallmark of ARDS

A

hypoxemia despite increased supplemental O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

phase 2 of ARDS

duration?

A

proliferative phase

duration 7-21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

how does the body attempt to repair itself in phase 2 of ARDS

A
  • new pulmonary surfactant
  • new type 1 pneumocytes
  • tight junctions restored
  • alveolar fluid drained by lymphatics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

lasting damage from phase 2 of ARDS

A

fibrotic scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

phase 3 of ARDS

A

extensive fibrotic changes causes irreversible changes to lung archtitecture

fibrosis of pulmonary vasculature leads to irreversible pHTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

typical cause of death in ARDS

A

not from respiratory failure but from underlying complications like sepsis or multiorgan failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

how does ARDS affect alveoli

A

some become very stiff, some maintain normal compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

why is low Vt important in ARDS

A

Vt follows the path of least resistance - the stiff alveoli have poor compliance and fill minimally, normal compliance alveoli fill too much

alveolar overdistention causes volutrauma and barotrauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is biotrauma

A

excessive stretch stimulus in alveoli stimulates release of inflammatory mediators and exacerbates existing ARDS inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

superior ventilator mode in ARDS

A

pressure control - may offer superior pattern of flow distribution vs. volume control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

ideal Vt for ARDS

A

4-6 mL/kg IBW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

target plateau pressure for mechanically ventilating ARDS pts

A

< 30

reduce Vt to as low as 4 mL/kg IBW to achieve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

RR for ARDS ventilation

A

6-35 breaths/min to target pH 7.3-7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

risk of high RR in ventilating ARDS pts

A

dynamic hyperinflation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

how to evaluate RV function in setting of PEEP adjustments

A

point of care echocardiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

PaCO2 goal for ventilating ARDS pts

A

permissive hypercapnia may be required

(the body will retain bicarb to compensate for respiratory acidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

how does prone positioning improve severe ARDS

A
  • may improve V/Q matching and allow higher PaO2 for given FiO2
  • greater number of functional lung units
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

max FiO2 for a regular nasal cannula

A

40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

how does conservative fluid management help in ARDS pts

A

supports oxygenation by reducing hydrostatic pressure in pulmonary capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what are the 3 stages of ARDS

A
  1. exudative
  2. proliferative
  3. fibrotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

2nd messenger in pathway of bronchodilation induced by catecholamines

A

cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

2nd messenger in pathway of bronchoconstriction induced by PNS

A

IP3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what factor has the most significant contribution to airflow resistance

A

radius

108
Q

how does smooth muscle contraction affect airflow

A

decreased airway diameter = increased airway resistance = decreased airflow

109
Q

how does smooth muscle relaxation affect airflow

A

increased airway diameter = decreased airway resistance = improved airflow

110
Q

nerve that supplies parasympathatic innervation to airway smooth muscle

A

vagus

111
Q

releases ACh to M3 receptors in airway smooth muscle

A

cholinergic nerve endings

112
Q

effects of M3 receptor activation in airway smooth muscle

A

= Gq activation = phospholipase C activation = IP3 activation = Ca2+ release from SR = MLK activation = contraction = bronchoconstriction

113
Q

when does the PNS mediated bronchoconstriction pathway turn off

A

when IP3 phosphatase deactivates IP3 to IP2

114
Q

in what part of airway are mast cells highly concentrated

A

smooth airway epithelium

115
Q

proinflammatory mediators involved in bronchoconstriction

A
  • prostaglandins (D2 & F2)
  • leukotrienes (C4, E4, D4)
  • platelet activating factor
  • bradykinin
116
Q

chemicals released by non-cholinergic C fibers that promote bronchoconstriction

A
  • substance P
  • neurokinin A
  • calcitonin gene related protein
117
Q

how are beta 2 receptors in airway smooth muscle activated

A

catecholamines in systemic circulation

118
Q

how does beta 2 activation lead to bronchodilation

A

activation = Gs protein activation = adenylate cyclase activation = cAMP activation = decreased Ca2+ from SR = decreased smooth muscle contraction = bronchodilation

119
Q

how is the pathway of bronchodilation from beta 2 receptor agonism turned off

A

PDE3 deactivates cAMP by converting it to AMP

120
Q

how does vasoactive intestinal peptide affect airway smooth muscle

A

release by noncholinergic PNS nerves = increased NO production = cGMP stimulated = smooth muscle relaxation and bronchodilation

121
Q

MOA of beta-2 agonists

A

beta 2 stim = increased cAMP = decreased Ca2+ = bronchodilation

122
Q

SEs of beta 2 agonists

A
  • tachycardia
  • dysrhythmias
  • hypokalemia
  • hyperglycemia
  • tremors
123
Q

MOA of anticholinergics for bronchodilation

A

M3 antagonism = increased cAMP = decreased Ca2+ = bronchodilation

124
Q

SEs of anticholinergics

A
  • dry mouth
  • urinary retention
  • blurred vision
  • cough
  • increased IOP with narrow angle glaucoma
125
Q

SEs of cortocosteroids

A
  • dysphonia
  • laryngeal muscle myopathy
  • oropharyngeal candidiasis
  • possible adrenal suppression
126
Q

SEs of methylxanthines if plasma conc. > 20 mcg/mL

A
  • N/V/D
  • headache
  • disrupted sleep
127
Q

SEs of methylxanthines if plasma conc. > 30 mcg/mL

A
  • seizures
  • tachydysrhythmias
  • CHF
128
Q

what is FEV1

A

volume of air that can be exhaled in 1 second after maximal inhalation

129
Q

normal FEV1

A

> 80% of predicted value

130
Q

what is FVC?
what’s normal?

A

volume that can be exhaled after maximal inhalation

o Normal male = 4.8 L
o Normal female = 3.7 L

131
Q

what is the FEV1:FVC ratio

when does it suggest obstructive vs. restrictive disease

A

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

  • < 70% suggests obstructive disease
  • Usually normal in restrictive disease
132
Q

normal FEV1:FVC

A

75-80% predicted value

133
Q

what is FEF 25-75%

A

measures airflow in the middle of FEV

134
Q

most sensitive indicator of small airway disease

A

FEF 25-75%

135
Q

FEF 25-75% in obstructive vs. restrictive disease

what is considered normal

A

o Usually ↓ with obstructive disease
o Usually normal with restrictive disease
o Normal: 100 +/- 25% predicted value

136
Q

what is MMV

normal values?

A

Max. Voluntary Ventilation - max volume of air that can be inhaled & exhaled over 1 minute

o Normal male = 140-180 L
o Normal female = 80-120 L

137
Q

PFT that is the best test of endurance

A

MMV

138
Q

PFTs that measure dynamic lung volumes

A
  • FEV1
  • FVC
  • FEV1:FVC
  • FEF 25-75%
  • MMV
139
Q

what is DLCO?
normal values?

A

diffusing capacity: measures alveolocapillary membrane’s ability to exchange gas

• Volume of CO that can transverse alveolocapillary membrane per a given alveolar partial pressure of CO

Normal: 17-25 mL/min/mmHg

140
Q

how can airway resistance be measured

A

dynamic pulmonary function testing

141
Q

which lung volume is represented by the width of the flow volume loop

A

Vital capacity

142
Q

patient related risk factors for postop pulmonary complications

A
  • age > 60
  • ASA > 2
  • CHF
  • COPD
  • smoking
143
Q

procedures at highest risk for postop pulmonary complications

A
  1. aortic
  2. thoracic
  3. upper abd ~ neuro ~ peripheral vascular
144
Q

anesthesia time assoc. with increased postop pulmonary complications

A

2+ hours

145
Q

lab test indicative of risk for postop pulmonary complications

A

albumin < 3.5 g/dL

146
Q

respiratory risks of smoking

A
  • risk for pulm disease
  • decreasd mucociliary clearance
  • airway hyperreactivity
  • decreased pulmonary immune function
147
Q

CV risks of smoking

A
  • CV disease
  • decreased DO2
  • catecholamine release
  • coronary vasoconstriction
  • exercise intolerance
148
Q

short term effects of smoking cessation

A
  • CO t1/2 = 4-6 hours
  • P50 to near normal in 12 hours
  • decreased carboxyhemoglobin within 24 H
  • does not reduce pulmonary complications
149
Q

intermediate-term effects of smoking cessation

A

return of pulmonary function takes at least 6 weeks
- airway function
- mucociliary clearance
- sputum production
- pulmonary immune function

hepatic enzyme induction subsides (6 wks)

150
Q

Best way to reverse anesthesia-induced atelectasis

A

ARM

151
Q

how to perform ARM

A

hold PIP of 40 cm H2O for 8 seconds (best to apply PEEP to keep re-recruited alveoli open)

152
Q

values in obstructive disease:
- FEV1
- FVC
- FEV1:FVC
- FEF 25-75%
- RV
- FRC
- TLC

A
  • FEV1 = decreased
  • FVC = increased to decreased
  • FEV1:FVC= decreased
  • FEF 25-75% = decreased
  • RV = normal (inc if gas trapping)
  • FRC = normal (inc if gas trapping)
  • TLC = normal ( inc if gas trapping)
153
Q

values in restrictive disease:
- FEV1
- FVC
- FEV1:FVC
- FEF 25-75%
- RV
- FRC
- TLC

A
  • FEV1 = decreased
  • FVC = decreased
  • FEV1:FVC = normal
  • FEF 25-75% = normal
  • RV = decreased
  • FRC = decreased
  • TLC = decreased
154
Q

when does airway collapse occur with extrathoracic obstruction

A

inhalation

155
Q

when does airway collapse occur with intrathoracic obstruction

A

exhalation

156
Q

PFTs have not been shown to be predictive of pulmonary postop complications except:

A

lung reduction surgery

157
Q

greatest risk factor for developing asthma

A

atopy

158
Q

most common ABG finding in asthma

A

respiratory alkalosis

159
Q

what does increased PaCo2 indicate in asthmatic pts

A
  • air trapping
  • resp muscle fatigue
  • impending respiratory failure
160
Q

EKG during severe asthma attack

A

may show RV strain with RAD r/t increased PVR/increased R heart workload

161
Q

what causes tachypnea and hyperventilation in asthmatics

A

neural reflexes (not hypoxemia)

162
Q

what does a flow volume loop with a flat inspiratory or expiratory portion suggest in a wheezing patient

A

upper airway obstruction (not asthma)

163
Q

CXR of asthmatics

A
  • hyperinflated lungs
  • diaphragmatic flattening
164
Q

vent settings for asthma

A
  • limit inspiratory time
  • prolong expiratory time
  • tolerate permissve hypercarbia
165
Q

how can hemabate cause adverse effects in asthmatic

A

minimcs action of F2 alpha prostaglandin

166
Q

s/s bronchospasm

A
  • wheezing
  • ↓ breath sounds
  • ↑ airway resistance
  • ↑ PIP with normal plateau pressure
  • ↓ dynamic pulmonary compliance
  • ↑ alpha angle on capnograph (expiratory upsloping)
167
Q

treatment of bronchospasm

A
  • 100% FiO2
  • deepen anesthetic
  • albuterol
  • inhaled ipratropium
  • epi 1 mcg/kg IV
  • hydrocortisone 2-4 mg/kg IV (doesn’t help acutely)
  • aminophylline
  • Heliox
168
Q

factors that contribute to air trapping in COPD

A
  • decreased elastic recoil
  • decreased airway rigidity & collapse during exhalatoin
  • decreased airway pressures & airway collapse
169
Q

common COPD findings

A
  • flattened diaphragm
  • increased AP diameter
  • pulmonary bullae
  • increased WOB
170
Q

why are COPD patients at risk for severe alkalosis if PaCO2 normalized via ventilator settings

A
  • chronically elevated PaCO2 = respiratory acidosis
  • kidneys reabsorb bicarb and cause compensatory metabolic alkalosis
  • changing vent settings doesn’t get rid of excess bicarb
171
Q

most efficacious treatment for improving pHTN and preventing erythrocytosis in chronic bronchitis

A

o2 therapy

172
Q

why do chronic bronchitis patients have erythrocytosis

A

RBCs overproduced to compensate for V/Q mismatch

173
Q

why do chronic bronchitis patients have cor pulmonale

A

chronic hypoxemia & hypercarbia increase PVR and cause right heart strain/RAD

174
Q

why do chronic bronchitis patients have ascites

A

weak right heart creates back pressure on liver/liver congestion

175
Q

assoc. with enlargement and destruction of airways distal to terminal bronchioles

A

emphysema

176
Q

assoc. with hypertrophied bronchial mucus glands & inflammation  limited airflow during exhalation

A

chronic bronchitis

177
Q

what contributes to pHTN in emphysema patients

A

• Destruction of pulmonary capillary bed
• same amount of blood must travel to a smaller network of blood vessels)

178
Q

how do emphysema patients develop right heart failure

A

Late in disease, hypoxemia & hypercarbia further increase PVR

179
Q

PaO2 & PaCO2 in emphysema

A

• Generally normal or slightly reduced PaO2
• Generally normal or decreased PaCO2 (r/t hyperventilation)

180
Q

what causes cirrhosis in alpha 1 antitrypsin deficiency

A

abnormal enzymes can’t be secreted from hepatocyte - accumulation causes cell death and cirrhosis

181
Q

how does alpha 1 antitrypsin deficiency cause emphysema

A

alpha-1 antitrypsin deficiency allows overactivity of alveolar elastase, which breaks down pulmonary connective tissue

causes destruction of pulmonary connective tissue

182
Q

lab values in COPD:
- RV
- FRC
- TLC
- FEV1
- FEV/FVC
- FEF 25-75%

A

• Increased: RV, FRC, TLC
• Decreased: FEV1, FEV/FVC, FEF 25-75%

183
Q

PFTs diagnostic of COPD

A

FEV1/FVC ratio of < 70% after bronchodilator therapy

184
Q

best practice for supplemental O2 in COPD pt

A

Titrate supplemental O2 to maintain arterial O2 sat of 88-92%

185
Q

when should neuraxial anesthesia be avoided in pts with COPD

A

when pt requires sensory blockade > T6

186
Q

why is an interscale block not the best choice for a pt with COPD

A

causes paralysis of ipsilateral hemidiaphragm

187
Q

ideal b:g solubility in a COPD pt

A

low - to minimize postop ventilatory depression

188
Q

how does slower inspiratory time help COPD pts

A

helps gas redistribute from high compliance area to those with longer time constants (matches V/Q throughout lung)

189
Q

expiratory time for COPD pts

A

Increase to minimize air trapping and auto-PEEP

190
Q

how can N2O contribute to PTX in COPD pt

A

can cause rupture of pulmonary blebs

191
Q

flow volume loop that suggests air trapping

A

Flow volume loop that doesn’t return to 0 at end expiration

192
Q

what is auto-PEEP?

A

dynamic hyperinflation or breath stacking
if the patient can’t fully exhale each breath, a portion of that previous breath remains in the lungs

193
Q

flow volume loop that suggest air trapping

A

doesn’t return to 0 at end expiration

194
Q

3 causes of auto PEEP

A
  • increased minute ventilation
  • decreased expiratory flow
  • increased airway resistance
195
Q

methods to treat auto PEEP

A
  • increased expiratory time (inc. I:E - 1:2 to 1:3)
  • decreased RR
  • larger ETT
  • suction secretions
  • d/c from circuit
196
Q

vent settings for pt with restrictive lung disease

A
  • Vt 6-8 mL/kg
  • RR 14-18
  • prolong inspiratory time (I:E 1:1)
197
Q

PFTs in restrictive lung disease

A

decreased FVC and FEV1 (<70%)

ratio unchanged

198
Q

3 characteristics of restrictive lung disease

A
  1. decreased lung volumes and capacities
  2. decreased compliance
  3. intact pulmonary flow rates
199
Q

acute intrinsic causes of restrictive lung disease

A
  • upper airway obstruction
  • aspiration
  • narcan
  • cocaine OD
  • re-expansion of collapsed lung
  • neurogenic
200
Q

chronic intrinsic causes of restrictive lung disease

A

(interstitial lung disease)

  • sarcoidosis
  • amiodarone-induced pulmonary fibrosis
201
Q

structural causes of restrictive lung disease

A
  • kyphoscoliosis
  • ankylosing spondylitis
  • flail chest
  • PTX
  • pleural effusion
  • pneumomediastinum
  • mediastinal mass
  • neuromuscular disorders
202
Q

FRC in restrictive disease

A

decreased

203
Q

3 potential problems with aspiration

A

1) gastric contents in airway = risk obstruction
2) gastric contents cause chemical burn to airway/lung parenchyma = risk bronchospasm
3) infectious material enters airway = bacterial infection

204
Q

when is aspiration most likely to occur

A

most common during induction or within 5 min of extubation

205
Q

what is mendelson’s syndrome & what are the risk factors

A

chemical aspiration pneumonitis

  • gastric pH < 2.5
  • gastric volume > 25 mL (0.4 mL/kg)
206
Q

hallmark symptom of aspiration

A

hypoxemia

207
Q

Most common CXR finding in aspiration pneumonitis

A

pulmonary edema & infiltrates in perihilar and dependent lung regions

208
Q

what should you do first if you suspect your patient has aspirated

A

head down/to the side

209
Q

when should abx be given for aspiration pneumonitis

A

only if pt develops fever or ↑ WBC after 48 hours

210
Q

best method to prevent VAP

A

avoid intubation altogether

211
Q

what should raise suspicion of VAP in intubated pt

A

↑ WBC and/or fever

212
Q

what med should be used for intubated/vented pt with high risk for GI bleed prophylaxis and why

A

sucralfate

PPIs increase bacterial overgrowth

213
Q

drug class not recommended for aspiration pneumonitis prophylaxis

A

anticholinergics

214
Q

treatment of closed PTX

A

obs, catheter aspiration, chest tube

215
Q

treatment of open PTX

A

occlusive dressing (allows air to escape but doesn’t allow air in), supplemental O2, chest tube, +/- intubation

216
Q

closed PTX

A

Defect in pulmonary tree or lung tissue - air enters and exits pleural space through defect

217
Q

open PTX

A

Defect in chest wall - air passes between pleural space and atmosphere

218
Q

which type of PTX is described?

Lung collapses on inspiration & partially re-expands on expiration

A

open

219
Q

what type of PTX is described?

↑ intrathoracic pressure when air enters pleural space through a ball-valve defect in chest wall (air can enter but not exit the pleural space)

A

tension

220
Q

how does mediastinum shift in tension PTX

A

towards contralateral side

221
Q

hallmark characteristics of tension PTX

A

hypoxemia, ↑ airway pressures, ↑ HR, ↓ BP, ↑ CVP

222
Q

POC tension PTX US

A

lack of lung sliding and absence of comet tails (reverberation artifact)

223
Q

emergency tension PTX treatment

A

insertion of 14g angiocath in a) 2nd intercostal space at MCL or b) 4th or 5th intercostal space at AAL

224
Q

definitive treatment of tension PTX

A

chest tube

225
Q

most common cause of hemothorax

A

bleeding intercostal vessel

226
Q

indications for thoracotomy with hemothorax

A

o Initial drainage > 1 L
o Continued bleeding > 200 mL/hr
o White lung on CXR
o Large air leak

227
Q

hemothorax patients who are candidates for VATS management

A
  • bleeding < 150 mL/hr
  • HD stable
228
Q

cause of chylothorax

A

damage to thoracic duct, which empties lymph into L subclavian

229
Q

key characteristics of flail chest

A

paradoxical movement of chest wall at site of rib fractures

230
Q

what happens during inspiration with flail chest

A
  • non-injured ribs move outward
  • injured ribs move inward
  • underlying tissue compressed
  • mediastinum shifts contralateral side
231
Q

what happens during expiration with flail chest

A
  • non-injured ribs move inward
  • injured ribs move outward
  • underlying lung tissue doesn’t empty
  • mediastinum shifts to ipsilateral side
232
Q

consequences of flail chest

A

alveolar collapse, hypoventilation, hypercarbia, hypoxia

233
Q

what causes airlock

A

Gas embolism of significant size can travel to R heart and lodge in pulmonary outflow tract or PA

234
Q

consequences of airlock

A

converts distal alveoli to dead space

235
Q

s/s VAE

A
  • air on TEE
  • “mill wheel” murmur with precordial
  • ↓ ETCO2
  • ↑ EtN2
  • ↑ PAP
  • ↓ BP
  • pulmonary edema
  • hypoxia
  • cyanosis
236
Q

methods to detect VAE from most to least sensitive

A

TEE > doppler > PAP/EtCO2 > CO, CVP > BP, EKG, stethoscope

237
Q

what is durant position

A

L lateral decubitus position (

238
Q

VAE treatment

A
  • 100% O2
  • flood field with NS
  • d/c insufflation
  • L lateral decubitus position (Durant maneuver)
  • aspirate air from CVL
  • HD support (floods, vasopressors, inotropes)
239
Q

how does air trapped in the pulmonary circulation affect the left side of the heart

A
  • decreased LV preload
  • decreased CO
  • asystole/CV collapse
240
Q

diagnosis of pHTN

A

mean PAP > 25 mmHg

241
Q

causes increased PVR

A

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

242
Q

consequences of increased RV afterload in pHTN

A

RV dilation, RVH, ultimately systolic impairment

243
Q

CO in pHTN pt

A

relatively fixed & preload dependent

244
Q

what leads to tricuspid regurg in pHTN pt

A

↓ RV stroke volume = ↑ RV volume at the end of diastole - stretches tricuspid

245
Q

causes of pHTN

A

COPD, hypoxemia, hypercarbia, L heart dysfunction, mitral valve disease. CHD, connective tissue disorders, chronic thromboembolism, portal HTN

246
Q

drugs that increase PVR

A
  • n2o
  • ketamine
  • desflurane
247
Q

causes of increased PVR

A

hypoxemia
hypercarbia
acidosis
SNS stim
pain
hypothermia
↑ intrathoracic pressure
mechanical ventilation
PEEP
atelectasis

248
Q

drugs that decrease PVR

A

iNO, nitro, PDE inhibitors, PGE1, PGE2, CCBs, ACE inhibitors

249
Q

how can increased RA pressure cause a shunt

how is this treated

A

open foramen ovale and lead to R  L intracardiac shunt

Treat: reverse causes of increased pulmonary resistance

250
Q

preferred neuraxial method in pHTN pts

A

epidural - slower sympathectomy vs. spinal

251
Q

drug of choice for increased PVR r/t uterine contractions

A

nitroglycerin

252
Q

Carbon monoxide deprives the tissues of o2 what 2 primary ways

A

1) CO binds to O2 binding site on hgb with affinity 200x that of O2 - displaces O2 from hgb & ↓ CaO2
2) CO causes L shift in carboxyhgb dissociation curve (less O2 at tissue level)

253
Q

how does CO poisoning lead to metabolic acidosis

A

Impairs oxidative phosphorylation - decreased ATP - metabolic acidosis

254
Q

t1/2 of carboxyhemoglobin

A

4-6 hours breathing room air

255
Q

CO poisoning treatment

A

100% supplemental O2 reduces t1/2 to 60-90 min

O2 therapy continued until CoHgb < 5% for 6 hours

256
Q

when is hyperbaric o2 indicated for CO poisoning

A

if CoHgb > 25% or pt symptomatic

257
Q

risk of using dessicated soda lime with des

A

CO formation

258
Q

VC that is a strong indicator for mechanical ventilation

what’s normal?

A

< 15 mL/kg

normal 65-75 mL/kg

259
Q

inspiratory force that is a strong indicator for mechanical ventilation

what’s normal?

A

< 25 cm/H2O

normal 75-100 cm/H2O

260
Q

PaO2 and A-a gradients that are strong indicators for mechanical ventilation

A

@ 21% FiO2:
- PaO2 < 55 mmHg
- A-a gradient > 55 mmHg

@100% FiO2:
- PaO2 < 200 mmHg
- A-a gradient > 450 mmHg

261
Q

single best predictor of postop pulm complications (after pulm surgery)

A

VO2 max

262
Q

how does the PNS affect airway diameter

A

causes bronchoconstriction

263
Q

physiologic systems that contribute to bronchoconstriction

A

mast cells & noncholinergic c fibers
PNS (vagus nerve)

264
Q

physiologic systems that contribute to bronchodilation

A

non-cholinergic PNS (NO)
SNS (circulating catecholamines)

265
Q
A

A = expiration
B = inspiration
C = TLC
D = Residual volume

266
Q

inhalation vs exhalation on flow volume loop

A

inhalation: waveform moves R-L with negative deflection
exhalation: waveform moves L-R with positive deflection

267
Q

PaCO2 that is a strong indicator for mechanical ventilation

A

> 60

APEX (54 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions