PAH, PTX, alveolar collapse, atelectasis Flashcards

1
Q

PH - rare incidence but more common in _____

A

obese

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2
Q

PH mean pressure PAP ______

A

> 25 mmHg

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3
Q

requires ______ to definitively diagnose

A

RHC

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4
Q

5 main categories PH falls into

A
  • pulm arterial HTN
  • left heart disease with low EF
  • lung dz/chronic hypoxia
  • chronic thromboembolic
  • unknown etiologies
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5
Q

PAH is an increase in ____

A

vascular tone

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6
Q

increased proliferation of pulm ______ ______ ______

A

vascular smooth muscle

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7
Q

initially reversible smooth muscle vasoconstriction progresses to ______ ______ _______ _____

A

irreversible smooth muscle hypertrophy

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8
Q

right ventricular overload can lead to ____ ______ with decreased _______ perfusion

A

cor pulmonale
coronary

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9
Q

_______ anesthetic if possible

A

regional

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10
Q

if GA then avoid ______ _______ changes

A

major hemodynamic

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11
Q

avoid _____ since it increases PVR

A

ketamine

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12
Q

avoid any situation that would increase SNS output and increase PVR, such as:

A
  • hypoxemia
  • hypercarbia
  • acidosis
  • pain
  • hypothermia
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13
Q

caution in surgery with potential for _____, _____, ______ embolism

A

air, fat, cement

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14
Q

caution in surgery with ___ __________, ______, ________

[Anesthesia management of PH]

A

Elevated airway pressures, laparoscopic, tredelenburg position

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15
Q

___ Hypotension
[PH management]

A

Avoid

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16
Q

If hypotension fails to correct quickly, then suspect that the ____ may be from ___ and not a drop in ____.
[PH management]

A

Low BP, RV Failure, SVR

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17
Q

Lung parenchyma tear or rupture allows air from inside of lung to escape between___and ___ ___, non-communicating with no atmospheric access, no shifting ___ or ___

[Characteristics, simple pneumo]

A

lung, visceral pleura, mediastinum, hemi-diaphragm

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18
Q

Primary Pneumothorax:

A

absence of diagnosed lung disease, healthy

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19
Q

Causes: (3)
[Primary Pneumothorax]

A

subpleural bleb, smoking, Birt-Hogg Dube’ syndrome speculated drop in atmospheric pressure

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20
Q

Secondary Pneumothorax:

A

complication of lung disease

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21
Q

Causes: (9)
[Secondary Pneumothorax]

A

COPD, emphysema, cystic fibrosis, metastasis, necrotizing bacterial lung infections, pneumocystis, TB, pneumonia, fungal, viral

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22
Q

Traumatic pneumothorax: ___(closed/___) or ___ (open/___) ___ trauma (more common)

A

Blunt, non-communicating, penetrating, communicating, thoracic

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23
Q

Iatrogenic:
[Traumatic Pneumo]

A

medical procedure induced

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24
Q

Non-iatrogneic:
[Traumatic Pneumo]

A

External trauma

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25
____/___ (more common): [Traumatic Pneumo]
Communicating/open
26
___ penetrating injury, air comes from outside, with ___ ___ [Communicating Pneumo part 1]
External, atmospheric access
27
Atmospheric air enters and trapped between ___ ___and___ ___ during inspiration causing a ___ wound and exits chest cavity during ___ [Communicating Pneumo part 2]
parietal pleural, chest wall, sucking, expiration
28
___ moves away from ___ side during ___ and toward the ___ side during ___ (___ ___) [Communicating Pneumo part 3]
Mediastinum, affected, inspiration, affected, expiration, mediastinal flutter
29
___ air enters ___ chest wound during ___ [Tension Pneumo 1/4]
Atmospheric, external, inspiration
30
___ is not able to ___ chest cavity during ___ [Tension Pneumo 2/4]
Air, escape, expiration
31
Air in chest rapidly accumulates ___ lung on ___ side [Tension Pneumo 3/4]
collapses, affected
32
Continued ___ ___ builds [Tension Pneumo 4/4]
intrapleural pressure
33
___, ___, ___ shift to unaffected side [Tension Pneumothorax Physical Findings]
Heart, trachea, esophagus
34
Large vessels collapse and impede___ ___ into chest cavity resulting in ___ ___ ___ [Tension Pneumothorax Physical Findings]
venous return, decreased cardiac output
35
___ ___ ___ ___ (ventilated patient) [Tension Pneumothorax Physical Findings]
Increased peak inspiratory pressure
36
Increased ___ and ___ ___veins [Tension Pneumothorax Physical Findings]
CVP, distended neck
37
Dyspnea, ___, ___, ___ [Tension Pneumothorax Physical Findings]
respiratory distress, cough, tachypnea
38
___or absent ___breath sounds [Tension Pneumothorax Physical Findings]
Decreased, ipsilateral
39
___(most common sign) [Tension Pneumothorax Physical Findings]
Tachycardia
40
___ chest pain [Tension Pneumothorax Physical Findings]
Ipsilateral
41
Hyp__emia [Tension Pneumothorax Physical Findings]
Hypoxemia
42
Hyp___tension [Tension Pneumothorax Physical Findings]
Hypotension
43
Hyp___carbia… but ETCO2 ___due to ___ CO!! [Tension Pneumothorax Physical Findings]
Hypercarbia, decreased, low
44
Tension Pneumothorax Treatment (3)
Observation only Decompression of Pleural Space Supplemental Oxygen
45
___ or ___ then observation only [Tension Pneumothorax Treatment]
Asymptomatic, < 15%
46
Decompression of pleural space ___ angiocath, ___ syringe, 3 ___ ___ Insert at ___intercostal space ___ Or… Insert at ___intercostal space laterally [Tension Pneumothorax Treatment]
14 g. , 50 cc, way stopcock, 2nd, anteriorly, 4th-5th, laterally
47
Supplemental oxygen ___ ___ ___ [Tension Pneumothorax Treatment]
accelerates air reabsorption
48
Inhalation of high concentrations of oxygen may speed the ___ of a pneumothorax by reducing the partial pressure of ___ in the pulmonary capillaries,. This should increase the pressure gradient between the pleural cavity, and pleural capillaries, so increasing the absorption of ___ from the pleural cavity [Tension Pneumothorax Treatment]
resolution, nitrogen, air,
49
Optimizes ___ delivery and ___ ___ [Tension Pneumothorax Treatment]
oxygen, gas exchange
50
Inflammatory condition caused by ___ or ___ Most frequent bacteria: ___ [Pneumonia]
bacteria, virus, pneumococci
51
Alveoli membrane becomes ___ & ___ [Pneumonia]
inflamed, porous
52
Consolidation: Alveoli fills with ___, ___ ___. Entire lobes can become ___ [Pneumonia]
fluid, cell material, consolidated
53
Reduction in ___-___ surface area [Pneumonia]
gas-exchanging
54
V/Q ratios decrease: What does this mean? Increased shunt or deadspace? Hypoxemia, Hypercapnia or both? [Pneumonia]
Shunt, Both
55
Treatment: ___, ___, ___ ___ [Pneumonia]
Antibiotics, Resp Rx, VC breaths
56
A reduction or absence of air in parts of the lung resulting in the collapse of ___, loss of ___ ___, ___-___ shunt and diminished gas exchange. [Atelectasis]
alveoli, lung function, intra-pulmonary
57
___ reduction or absence of air in parts of the lung resulting in the ___ of alveoli, ___ ___lung function, intra-pulmonary ___ ___ gas exchange.
Atelectasis, collapse, loss of, shunt, diminished
58
Oxygen concentration:
the fraction or percentage of inspired oxygen delivered (FiO2).
59
General Anesthesia causes ___
Atelectasis
60
General Anesthesia causes Atelectasis Estimated incidence between ___-___.
50-100%
61
“The prevalence of atelectasis has been estimated to be as high as ___ in patients undergoing ___ ___”
100%, general anesthesia.
62
Average ___, can exceed ___ collapsed lung [General anesthesia causes atelectasis]
3-4%, 20%
63
Difficult to ___postoperatively [General Anesthesia causes Atelectasi]
reverse
64
Reduced inspiratory volumes and chest wall expansion resulting from ___ ___ ___ and a reduced ___tone [General Anesthesia causes Atelectasi]
deeper anesthesia depth, muscle
65
___ ___ due to artificial creation of a significantly higher A-a gradient than ___ [General Anesthesia causes Atelectasi]
Absorption atelectasis, normal
66
Anesthesia= FRC Decreased, Lung Compliance Decreased, Airway Resistance Increased --> Loss of tone, smaller volume, reduced ___ ___ --> ___ ___ atelectasis [General Anesthesia and Lung Volume]
airway dimensions, airway closure
67
Pressure of abdominal contents and resulting FRC Initial upright position ___ Supine position ___ Induction of anesthesia ___
2300 ml, 1400 ml, 950 ml
68
Atelectasis forms regardless of ___ ___
patient position
69
Causes of Atelectasis under General Anesthesia (3)
Mechanical compression Absorption of Alveolar Gas Surfactant dysfunction
70
Mechanical Compression: ___ ___ tone reduced ___ movement cephalad [Causes of Atelectasis under General Anesthesia]
Thoracic muscle, Diaphragmatic
71
Absorption of Alveolar Gas: Under-ventilated airways narrow and close. Air in alveoli rapidly diffuses into capillary. Alveoli ___but ___ continues. Accelerated with ___ ___. [Causes of Atelectasis under General Anesthesia]
collapses, perfusion, higher FiO2
72
Surfactant dysfunction: Positive___ and ____anesthetics [Causes of Atelectasis under General Anesthesia]
pressure, volatile
73
How does a high oxygen concentration cause atelectasis?
Accelerates alveolar absorption
74
Due to oxygen’s rapid diffusing capacity and the pressure difference across the membrane, gas is ___ ___ of the alveolus until it ___…re-opening of the ‘sticky’ atelectasis requires positive pressure of ___ cmH2O
‘sucked out’, collapses, 30–35
75
No ___ splint and a large ___ gradient promotes ___ ___ [Delivery 100% O2, PAO2~600 mmHg, 0% Nitrogen, PaO2(v) 40, PaO2 (a) 500]
nitrogen, A-a, alveoli collapse
76
In less than ___minutes alveoli can ___ or ___collapse. [Delivery 100% O2 PaO2 (v) 40, PaO2 (a) 0)]
5, partially, totally
77
___ ___remains with a reduced A-a gradient causing a ___ in alveoli collapse [Delivery of 40% O2, PAO2 250mmHg, >50% Nitrogen, PaO2 (v) 40, PaO2 (a)200]
Nitrogen splint, delay
78
In PACU: Oxygen sat 92-94%, Combined with shallow respirations, from residual paralysis, residual ___/___. Now sat drops to mid 80s ***___of pts transferred from OR to PACU without oxygen dropped their saturation to ___ [Results of 100% oxygen in OR, Unrecognized atelectasis]
anesthesia/opioids, 30%, <90%.
79
Upper airway obstruction requiring intervention (___ ___, __ ___ or nasal airway) [PACU Respiratory Events]
jaw thrust, oral airway
80
Mild-moderate hypoxemia (SpO2=___ ___) on 3L NC Oxygen that was not improved after active interventions (increasing O2 flows to >3L/min, application of ___-___ ___ ___ verbal requests to ___ ___, ___ ___.) [PACU Respiratory Events]
93%-90%, high-flow face mask, breathe deeply, tactile stimuli
81
Severe hypoxemia (SpO2___) on 3L nasal cannula O2 that was not improved after active interventions (___ ___ ___, application of ___-___ ___ ___ verbal requests to ___ ___, ___ ___.) [PACU Respiratory Events]
<90%, increasing O2 flows to >3L/min, high-flow face mask, breathe deeply, tactile stimuli
82
Signs of respiratory distress or impending ___ ___ (respiratory rate ___, accessory muscle use, ___ ___) [PACU Respiratory Events]
ventilatory failure, >20 bpm, tracheal tug
83
Inability to___ ___ when requested to by the PACU nurse [PACU Respiratory Events]
breathe deeply
84
Patient complaining of symptoms of___ or ___ ____ ____ ___(difficulty breathing, swallowing or speaking) [PACU Respiratory Events]
respiratory, upper airway muscle weakness
85
Patient requiring ___ in the PACU [PACU Respiratory Events]
reintubation
86
Clinical evidence or suspicion of ___ ___ after tracheal ___ (gastric content observed in the ___ and ___) [PACU Respiratory Events]
pulmonary aspiration, extubation, oropharynx, hypoxemia
87
most common cause of early post op hypoxemia is ______ and ______ ______ leading to right to left intrapulmonary shunting
hypoventilation and lobar atelectasis
88
atelectasis can remain for _____
days
89
post op day 1 patient remains on ______ _____ at __/___
nasal cannula 2L/min
90
post op atelectasis can show low grade _____
fever
91
post op atelectasis - coughing up _______ _____ and CXR can show ______ infiltrates
yellow sputum bilateral infiltrates
92
post op atelectasis - start ______ and resp rx
antibiotics
93
post op atelectasis may result in __-__ extra days inpatient stay
2-3
94
these post op atelectasis symptoms are indicative of _____ _____ _____
postoperative pulmonary complication (PPC)
95
is PPC rare?
no
96
PPCs occur in as much as _____ of patients undergoing major non-thoracic sx
30%
97
_______ is a locus for infection
atelectasis
98
atelectasis and _____ account for majority of PPCs
pneumonia
99
incidence of atelectasis following abdominal sx is as high as _____
69%
100
PPCs are a leading cause of ______, ______, and extended ______
mortality, morbidity, and extended hospitalization
101
we can prevent atelectasis at induction with the use of ______
CPAP
102
CPAP has been shown to reduce atelectasis formation even if using _____ _____
high FiO2
103
CPAP may increase _______ risk with gastric insufflation
aspiration
104
semi recumbent vs supine: no ______ in _____
no reduction in atelectasis
105
maintain thoracic and diaphragmatic muscle tone by (3)
1. spontaneous breathing 2. avoid paralytics 3. ketamine use to preserve muscle tone
106
there is evidence that the level of PEEP required to reopen airways may not be high enough to reopen ______ ______
collapsed alveoli (may need recruitment manuever)
107
PEEP of ______ with BMI < 25
6 cmH2O
108
PEEP of ______ with BMI up to 30
8 cmH2O
109
PEEP applied _______ _______ of atelectasis may prevent it
BEFORE formation
110
PEEP of ______ consistently opened collapsed lung tissue
10 cmH2O
111
_____ and ______ maintains open gas exchanging units
PEEP and oxygenation
112
PEEP and oxygenation improves resp mechanics and oxygenation in the _____ _____
morbidly obese
113
PEEP prevents _______ after an alveolar recruitment manuever (ARM)
de-recruitment
114
what is a sigh breath?
double tidal volume breath
115
with sigh breaths, amount of atelectasis is ________
unchanged
116
single sigh breath vs sustained ARM =
new surfactant released
117
ARM - sustained inflation with airway pressure _______
40 cmH2O
118
ARM - 2 goals
1. open airways 2. keep them open
119
ARM - sustained for __-__-__ seconds
7-10-15
120
ARM - MUST be followed by ______ to remain open
PEEP
121
ARM - releases ______ to alveolar wall and terminal bronchiole
surfactant
122
avoid _____ ______
100% oxygen
123
8 RCTs indicated that use of 100% FiO2 during GA resulted in: (4)
1. accelerated atelectasis formation 2. increased atelectatic areas of lung 3. increased intra-pulmonary shunting 4. worsening gas exchange
124
100% FiO2 resulted in atelectasis in less than ___ ______
5 minutes
125
5 RCTs indicated that using lower FiO2 during GA resulted in reduced _______ and ________ of absorption atelectasis
formation and magnitude
126
atelectasis development delayed on average by as much as an hour when less than ____ FiO2 was used
50%
127
_____ FiO2 improves gas exchange during general anesthesia
40%
128
100% FiO2 at the end of GA promotes post op atelectasis regardless of _____
VCM (vital capacity manuever)
129
very little atelectasis developed with ____ FiO2 after induction
30%
130
a vital capacity manuever followed by 40% oxygen ______ _______ post op atelectasis formation
completely prevented
131
high FiO2 is the main mechanism responsible for _______
atelectasis
132
Multiple studies performed to assess optimal FiO2: creating the least amount of absorption atelectasis. Maintain ___ ___. Maintaining acceptable ____.
Nitrogen splint, SaO2
133
current evidence does not indicate that the possible benefits of the use of high ___ ___can overcome the detrimental consequences of postoperative pulmonary complications.”
oxygen concentrations,
134
Ventilation during anesthesia should be done with a moderate fraction of inspired oxygen (e.g., FiO2 of ___ to ___) and should be ___ only if arterial ___ is compromised
0.3 to 0.4, increased, oxygenation
135
Avoiding preoxygenation using 30% FiO2 eliminated atelectasis formation during ___ and subsequent ___
, induction, anesthesia
136
FiO2 100% averaged ___-___ atelectatic lung tissue [Preoxygenation & Atelectasis Formation]
15-20%
137
FiO2 80% averaged __ ___ atelectatic lung tissue [Preoxygenation & Atelectasis Formation]
less than 2%
138
FiO2 60% nearly___ atelectatic lung tissue [Preoxygenation & Atelectasis Formation]
eliminated any
139
FiO2 30% = ___atelectatic lung tissue [Preoxygenation & Atelectasis Formation]
no
140
The final disaster…___ ___ should not be done routinely [Oxygen at Emergence]
post oxygenation
141
Running 100% FiO2 just prior to the end of anesthesia resulted in ___ of lung even following a ___of lung by a vital capacity maneuver [Oxygen at Emergence]
derecruitment, re-expansion
142
Running ___ FiO2 just prior to the end of anesthesia kept the lung open following a ___ ___ ___ [Oxygen at Emergence]
40%, vital capacity maneuver
143
Oxygen consumption equation, VO2
VO2= Fi02-Fe02 x Vm /weight in kg
144
O2 Content of Blood Equation
CaO2=(hgb x oxyhgb x 1.39)+(.003 x PaO2)
145
Oxygen delivery equation
DO2= CaO2 (mls/dL) x CO(mls/min)/kg/100
146
Does using 100% Oxygen Significantly Improve the Amount of Oxygen Delivered to the Tissues?
No Assuming the patient has normal cardiac output & Hgb Using FiO2 21% = delivers ≈ 11.7mlsO2/kg/min Using FiO2 50% delivers ≈ 12.3mlsO2/kg/min Using FiO2 100% delivers ≈ 13.0mlsO2/kg/min
147
The ___ ____ that is the limiting factor in delivery of O2 to the tissues [Why Does Oxygen Delivery Not Change Much?]
cardiovascular system
148
___ is the vehicle and ____is the cargo [Why Does Oxygen Delivery Not Change Much?]
Hemoglobin, oxygen
149
Lower ___promotes higher ___ and O2 delivery [Why Does Oxygen Delivery Not Change Much?]
Vt , CO
150
If sat is near 100% then ___ FiO2 may have___effect on oxygen delivery [Why Does Oxygen Delivery Not Change Much?]
increasing, little
151
O2 consumption ___ [What is the Point about FiO2?]
3.4 mlsO2/kg/min
152
Oxygen Delivery on room air: ___ (mlsO2/kg/min) Nearly ___ more than consumed/need [What is the Point about FiO2?]
11.7 mlsO2/kg/min, 4x
153
No compelling reason to use ___ FIO2 unless indicated [What is the Point about FiO2?]
higher
154
Superphysiologic doses of blood oxygen do not result in a significant ___ in tissue ___ [What is the Point about FiO2?]
increase, oxygen
155
Better to run slightly___sat and keep ___ ____ [What is the Point about FiO2?]
lower, alveoli open
156
2017 WHO recommended ___FiO2 in colon surgery to reduce ___ ____ ____ [Where are We Today Regarding FiO2?]
high , surgical site infections (SSI)
157
___guidelines generated controversy [Where are We Today Regarding FiO2?]
WHO
158
____Guidelines recommend ___ FiO2 for colon surgery [Where are We Today Regarding FiO2?]
ERAS, high
159
…___ Fio2, compared to the ___ ____ Fio2, under the perioperative conditions at this trial site does not meaningfully change clinical outcomes [Where are We Today Regarding FiO2?]
80%, lowest feasible
160
No Proof of ___surgical site infection in patients receiving ____ O2 [Where are We Today Regarding FiO2?]
reduced, 80%
161
CPAP during ____/____ can ____ atelectasis formation
preoxygenation/induction, decrease
162
____ can prevent ____ formation but use it before ____develops
PEEP, atelectasis, atelectasis
163
___ ____ ___ recruits collapsed alveoli followed by ___to prevent reoccurrence
Alveolar recruitment maneuver, PEEP
164
Avoid ___ ETT at emergence
suctioning
165
Follow ___ ____ ERAS-based guidelines
your institution’s
166
___FiO2 worsens atelectasis and ___ while less than 50% prevents atelectasis and reduces ___
100%, PPCs, PPCs
167
Use between____and ___FiO2 during____ ____when not contraindicated
40%, 60%, general anesthesia
168
If you must use ___ oxygen use it only with ___
100%, PEEP
169
Emerge on less than ___ if not contraindicated
100%
170
Pulse Oximetry does not tell the CRNA about the ___ of ___ formation
degree, atelectasis
171
Less than ___ oxygen saturation is acceptable
100%