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ACE Review - Pulm Flashcards

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1
Q

Cause of neurogenic pulm edema

A

Sympathetic discharge

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2
Q

When does neurogenic pulm edema occur

A

Within 12 hrs. As as soon as 4 hrs

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3
Q

Common cause of neurogenic pulm edema

A

Head trauma

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4
Q

in a tension pneumo, where should a large bore needle be placed

A

mid clavicular 2nd intercostal

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5
Q

in a tension pneumo, where should a chest tube be placed

A

mid clavicular 6th intercostal

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6
Q

If an abg had an air bubble in it,how would the pao2 and paco2 be affected

A

Increased pao2 and decreased paco2

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7
Q

How does the pao2 increase bc of an air bubble?

A

Air fio2 is 0.21, thus partial pressure is 160mmhg(.21x760). O2 will diffuse into blood that only has an o2 partial pressure of 60-100 if pt is on room air

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8
Q

How does the paco2 decrease with an air bubble.

A

Same idea. Air partial co2 pressure is 0.04%

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9
Q

how many steps are there in lung injury when aspiration occurs

A

two steps

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10
Q

what is the first step of aspiration lung injury

A

loss of type 1 alveolar cells leads to pulmonary edema

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11
Q

what is the second part of aspiration lung injury

A

lung acute reactive airway disease

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12
Q

what is the first goal of aspiration

A

provide oxygenation and

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13
Q

what is the recommended tx for liquid aspiration

A

suction with a large bore catheter

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14
Q

should you do bronch lavage with liquid aspiration

A

no, it will push the contents down further

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15
Q

should you give antibiotics

A

no, because you are now making the patient more prone to vent assoc pna with resistant bacteria

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16
Q

should you give steriods

A

no, because it has been shown to increase risk of mortality in criticlly ill patients

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17
Q

what patient would benefit cpap

A

patients suffering soley from hypoxemia, like osa

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18
Q

what patient would benefit from bipap

A

pts suffering from hypercarbia or mixed hypercarb/hypoxemia

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19
Q

4 most common reasons for bipap

A

postop thoracic / ab surgery, pulm edema 2ndry heart failure, acute copd exacerbation, immunosupression

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20
Q

6 contraindications to bipap

A

ams, decreased resp drive, aspiration risk, untreated pneumothorax, hemodynamic instable, refusal

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21
Q

What is the leading cause of

A

TRALI

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22
Q

What are the other 2 major causes for transfusion associated mortalities

A

TAS - Transfusion Associated Sepsis, ABO Hemolytic transfusion reactions

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23
Q

what component makes transfusion more likely to have TRALI

A

plasma components

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24
Q

what is an example of plasma rich component

A

plateletes…it is 1000x more likely than prbc

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25
Q

what is the percent of death by trali

A

5-10%

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26
Q

what is the mechanism of action of trali

A

neutrophils are sequestered in the lungs…they are then triggered by high concentration of leukocyte antibodies

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27
Q

what kind of donors have higher likely hoold of giving blood components with high chance of trali

A

female multiparous pts bc they have developed more HLA antibodies

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28
Q

what kind of compenents have multiparous female donors have shown to increase risk of trali

A

ffp and plateletes, cryo and prbc not shown much difference

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29
Q

where does angioedema occur

A

mucocutaneous tissues primarily in lungs and bowel

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30
Q

who are prone to angioedema

A

hereditary…those who lack c1 easterase inhibitor enzyme

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31
Q

what drugs are associated with angioedema

A

pcn and sulfa drugs

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32
Q

what drugs causes pseudo-angioedema

A

NSAIDS…bc they inhibit prostaglandin synth

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33
Q

what is the most common cause for angioedema admission to ER

A

ACE inhibitors 17-38%

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34
Q

what is the moa for ace-I causing angioedema

A

it accumulates bradykinin that causes increase in vascular permeability

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35
Q

what 3 drugs are used to treat angioedema

A

epi, benadryl, steriods

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36
Q

how long should a pt with angioedema be followed

A

at least 24 hours bc relapse can occur

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37
Q

do patients with hereditary cause of angioedema have any preventative meds for acute angio tx

A

epsilon-aminocaproic acid and danazol(steriod)

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38
Q

does lasix cause angioedema

A

no

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39
Q

what is the calculation for static compliance of the lungs

A

tidal volume/ Plateau pressure minus peep

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40
Q

what is the purpose of static lung compliance

A

it is to test the elasticity of the respiratory system

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41
Q

when is static lung compliance measured

A

at the end of inspiration when lung volume is kept constant

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42
Q

xxxxxxxxxxxxxxxxxxxxxxxxxx

A

xxxxxxxxxxxxxxxxxxxxxxxxxx

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43
Q

what can increase pulmonary hypertension

A

hypercarbia, acidosis, hypoxia

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44
Q

what is ards

A

oxygenation problem 2ndry non cardiogenic protienacious pulmonary edema

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45
Q

what has been assoc with decrease mortality in pt w ards

A

prevention of ventilator associated lung injury

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46
Q

what are the ventilator goals for decreasing ards assoc vent mortality

A

less than 6cc/kg of predicted body wt tidal volume and peak pressures less than 30mmHg

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47
Q

should we target to get a Pao2/Fi02 over 300 for ards pt

A

no

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48
Q

what may be used to help oxygenation in ards pt

A

peep

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49
Q

should high peep pressure be used in ards pt

A

no, may cause barotrauma…hi peep not recommended

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50
Q

should increasing fi02 to maintain o2% greater than 94% be targeted in ards pt

A

no…may lead to oxygen toxicity in pt

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51
Q

what is the cause of hereditary angioedema

A

it is autosomal dominant lesion that leads to a C1 esterase Inhibitor deficiency

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52
Q

what is the prob with hereditary angio edema

A

it causes swelling of mucos membranes including those of airway and gi tract

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53
Q

what are 2 prophylactic meds for hereditary angioedema

A

attenuated androgens, antifibrinolytics

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54
Q

what are examples of attenuated analbolic androgens

A

danazol and stanozolol

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55
Q

whare is an example of antifibrinolytic

A

epsilon amino caproic acid

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56
Q

which is prefered for prophylactic use for hereditary angio edema

A

androgen steriods bc antifibrinolytics have been assoc with thrombosis

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57
Q

what are drugs used for acute attacks of hereditary angio edema

A

FFP and synthetic C1 easterase inhibitors

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58
Q

what are 2 examples of C1 esterase inhibitor synthetics

A

CinRyze and Berinert P

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59
Q

which is c1 esterase inhibitor can be used for acute attack

A

only Berinert P can be used for acute attacks

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60
Q

is FFP better than synthetic C1esterase inhibitor

A

no because it is assoc with TRALI

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61
Q

if patient is to get a short proceedure, and they have Hereditary angioedema…what is the recommeneded treatment

A

avoide airway manipulation with the following: androgens 2 days before surgery, c1esterase inhibitors 24 hrs before surgery,or ffp 6-12 hours before surgery

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62
Q

what if airway manipulation is required?

A

ideal to achieve normal c1easterase inhibitor levels, but 40-50% is ok

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63
Q

how to achieve normal c1 esterase levels

A

5-7 days of androgen steriods, FFP on day of surgery, Berinert P on day of surgery

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64
Q

What prostacyclin is used to treat pulm hypertension.

A

Epoprostenol flolan

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65
Q

How does epoprostenol work

A

It vasodilates and inhibits platelet aggregation.

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66
Q

How is epoprostenol administered.

A

It is given as an infusion.

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67
Q

What phosphodiesterase inhibitor is used for pulm htn

A

Sildenafil

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68
Q

What drug in obstetric patients is contraindicated in pulm hypertension

A

15-methylprostaglandin- it vasconstricts. This is also known as hemabate

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69
Q

What is the p50 in adults

A

26.7

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70
Q

Which way does the oxyhemoglobin curve shift with carbon monoxide.

A

Left

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71
Q

Which way does the oxyhemoglobin curve shift with methemoglobin

A

Left

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72
Q

Which way does the oxyhemoglobin curve shift with fetal hg

A

Left

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73
Q

Which way does the oxyhemoglobin curve shift with preggos

A

Right

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74
Q

What settings can be set for high oscillatory freq ventilatoin

A

Fio2, inspiratory time, bias gas flow rate, frequency, amplitude,

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75
Q

What are alcoholics at risk for postoperatively

A

Postoperative pneumonia

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76
Q

which way does carbon monoxide shift oxyhemoglobin curve

A

left because it makes the o2 that is bound higher affinity to heme group…and not get kicked out

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77
Q

how does carbon monoxide work

A

besides competing for heme, it also inhibits cytochrome oxideases

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78
Q

what is similar to carbon monoxide in moa

A

cyanide…which also inhibits cytochrome oxidases

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79
Q

what is the most common presentation of carbon monoxide

A

altered mental status

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80
Q

how is carbon monoxide tested for

A

co-oximetry

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81
Q

how to treat carbon monoxide posioning

A

high flow non rebreather o2 mask, then ett with o2, then hyperbaric oxygen

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82
Q

what drug inhibit hypoxic pulm vasoconstriction

A

inhaled anesthtic

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83
Q

What problem can pectus excavatum cause

A

The sternum can cause Compression of the right heart And cause right ventricle outflow tract compression

84
Q

What kind of PFT Is seeing with pectus excavatum

A

restrictive pattern

85
Q

What common cardiac lesion is associated with pectus excavatum

A

50% of patients have mitral insufficiency

86
Q

If Marfan’s is associated with pectus excavatum , What must you look out for him

A

Aortic insufficiency aortic dissection aortic aneurysm

87
Q

What is adult P 50

A

26.5 mmHg

88
Q

What is Fetal P 50

A

20 mmhg

89
Q

What a sickle cell P 50

A

30 mmhg

90
Q

What is the effect called when increased CO2 causes decreased O2 affinity in hemoglobin

A

bohr effect

91
Q

What do inhaled anesthetic gases do to the Oxyhemoglobin curve

A

right shift

92
Q

obesity…what happens to work of breathing

A

increse work of breathing

93
Q

obesity…what happens to frc

A

decrease

94
Q

obesity…what happens to vital capacity

A

decrease

95
Q

obesity…what happens to dead space

A

no change

96
Q

obesity…what happens to closing capacity

A

increase

97
Q

obesity…what happens to hemoglobin

A

increase - polycythemia

98
Q

obesity…what happens to fev1

A

decrease

99
Q

obesity…what happens to fvc

A

decrease

100
Q

obesity…why is there less time for 100% saturation on induction

A

supine postion decreases frc, increases shunt fraction, and worsen vq mismatch

101
Q

Myasthenia gravis…what is the oral med used in MG

A

Pyridostigmine

102
Q

Myasthenia gravis…what test is done before surgery to check if the patient needs optimization for surgery

A

Pulmonary function test.

103
Q

Myasthenia gravis…what to look for in pulmonary function test

A

Vital capacity…they should have a vital capacity greater than 2 liters…or else that means that they will most likely end up intubated post thymectomy

104
Q

Myasthenia gravis…ok, you got a low vital capacity…what should you do

A

Plasmapheresis

105
Q

Myasthenia gravis…how should the patient be induced

A

Rapid sequence because they are at high risk for aspiration.

106
Q

myasthenia gravis…how do these patients respond to succinylcholine

A

They are more resistant

107
Q

Myasthenia gravis…why are they resistant to succinylcholine

A

Because the antibodies occupy most ach receptors…thus only a few ach receptors left for succ to work on….

108
Q

Myasthenia gravis…how do they respond to nondepolarizing mm relaxants

A

They are more sensitive…only the few ach receptors left over need to be blocked

109
Q

Myasthenia gravis…are neuraxial anesthesia contraindicated?

A

No…actually they help. They decrease the use of narcotics…and thus less chance of respiratory depression by narcotics

110
Q

Myasthenia gravis…what are the 4 indicators of postoperative ventilator dependance

A
  1. Pyridostigmine dose greater than 750 daily. 2. Vital capacity less than 2.9liters, 3. MG for greater than 6 years 4. Coexisting copd
111
Q

Myasthenia gravis…what other treatment can be used before surgery to decrease chance of postoperative intubation

A

Immunoglobulin administration

112
Q

Beach chair…what happens to alveolar dead space in this position

A

There is increase alveolar dead space

113
Q

Beach chair…what is the mechanism for increased alveolar dead space

A

It causes more dead space at the apex of the lungs…and also positive pressure ventilation causes decrease preload

114
Q

Trali…what are 4 criteria

A

Onset within 6hrs of transfusion, hypoxia, chest X-ray bilateral infiltrate, pulm artery occlusion pressure below 18mmhg

115
Q

Trali…how do u know there is hypoxia

A

Pao2/fio2 ratio less than 300, or spo2. Less than 90 on room air at sea level

116
Q

Trali…what is the treatment

A

Supportive with oxygen supplementation

117
Q

Axillary roll. What is the purpose

A

To prevent the head of the humerus from compressing the brachial plexus…to prevent brachial artery occlusion.

118
Q

Axillary roll. Where should it be placed…

A

Caudal to the axillary pulse.

119
Q

Axillary roll. What danger can be caused if it is placed to cephalad

A

Brachial nerve injury, arm ischemia, compartment syndrome

120
Q

Axillary roll. What is a common complaint in people using axillary roll

A

Nondependant shoulder pain.

121
Q

Axillary roll. What is a treatment for Nondependant shoulder pain

A

Interscalene block. ..but ketorlac is the first line treatment.

122
Q

Sepsis. What are the 4 goals of early goal directed therapy for sepsis patients

A

Cvp 8-12, map 65-90, central venous oxygenation greater than 70.

123
Q

Sepsis. What if you cannot get central venous oxygenation above 70?

A

Transfuse to get the hematocrit above 30

124
Q

Sepsis. What kind of shock is septic shock

A

Distributive shock

125
Q

ards. what is the treatment

A

low tidal volumes to prevent vent associated trauma

126
Q

ards. what treatment may improve hypoxemia

A

prone positioning

127
Q

Preoxygenation. Where does the extra oxygen go to

A

Frc

128
Q

Preoxygenation. Does that affect the hypoxic pulmonary vasoconstriction

A

No. It does not alter it.

129
Q

Preoxygenation. Does it affect the second gas effect.

A

No it does not alter it.

130
Q

Preoxygenation. Does it alter diffusion hypoxia

A

No it does not alter it.

131
Q

Preoxygenation. What is the second gas effect.

A

It is the high concentration effect of one gas that causes the increase in concentration of another gas.

132
Q

Preoxygenation. What is diffusion hypoxia.

A

During extubation. When a patient begins to breaths room air, and nitrous oxide is discontinued, hypoxemia then develops.

133
Q

Lung mechanics. What is elastance.

A

Inward recoil of the lung.

134
Q

Lung mechanics. How is elastance and compliance related

A

Inverse of eachother

135
Q

Lung mechanics. What are the components of total lung compliance.

A

Lung paranchyma and chest wall compliance

136
Q

Lung mechanics. What conditions decrease compliance.

A

Fibrosis. Pulm edema. Consolidations

137
Q

Lung mechanics. What condition is increase compliance.

A

Emphysema.

138
Q

Lung mechanics. What does general anesthesia do to compliance.

A

Decrease compliance

139
Q

pneumonectomy. what is a complication that can mimick ards

A

postpneumonectomy pulm edema

140
Q

pneumonectomy. what side of operation is at risk for pppe

A

right side

141
Q

pneumonectomy. what kind of fluid management is associated with pppe

A

excessive fluid resuscitation

142
Q

pneumonectomy. what peak pressures are associated with pppe

A

peak pressures greater than 25mmhg

143
Q

pneumonectomy. what pt factor can cause increase in pppe

A

alcohol abuse

144
Q

pneumonectomy. what is the rate of pppe in a lobectomy

A

1-7%

145
Q

pneumonectomy. what is the rate of pppe in a total pneumonectomy

A

4-7%

146
Q

pneumonectomy. what is the mortality of pppe

A

30-100% regardless of lobectomy or pneumonectomy

147
Q

carbon monoxide. which is the order of anesthetic gases that make carbon monoxide over dessicated soda lyme

A

desflurane>enflurane>isoflurane,sevoflurane>halothane

148
Q

carbon monoxide. which co2 absorbant has higher carbon monoxide production if dessicated

A

baralyme more than sodalyme

149
Q

Plateau pressure. When is this measured

A

At the middle of an inspiratory hold.

150
Q

Plateau pressure. What does it represent

A

Pressure in the small airways and alveoli

151
Q

Plateau pressures. How do you measure pressures of the large airways and trachea.

A

It is not plateau pressure but it is the peak pressure.

152
Q

Plateau pressure. What can it be used to measure.

A

The static compliance of the respiratory system.

153
Q

Compliance. How do you calculate static compliance.

A

Tidal volume/(plateau pressure - PEEP)

154
Q

Compliance. How do calculate dynamic compliance.

A

Tidal volume /(peak pressure - PEEP)

155
Q

Mediastinal mass. What 3 symptoms can u see with this

A

Orthopnea, chest pain. Superior vena cava syndrome.

156
Q

Mediastinal mass. What dangers can occur after muscle relaxant.

A

Compression Of tracheal bronchial tree after relaxation.

157
Q

Mediastinal mass. Would tracheostomy be useful in this case.

A

No. Because the obstruction may be distal to the tracheostomy.

158
Q

Mediastinal mass. How would a pt be optimized for surgery.

A

Radiation or chemo to reduced the size of the lesion.

159
Q

Mediastinal mass. How should anesthesia be given to the pt.

A

Pt should be kept spontaneous.

160
Q

Mediastinal mass. What should you have ready when induction of these pt

A

Rigid brochoscope. To visualize and ventilate through.

161
Q

Mediastinal mass. What should be done for these pt with your use of muscle relaxants.

A

It should be avoided.

162
Q

Mediastinal mass. How is the pt positioned for awake fiber optic.

A

Semifowler position.

163
Q

Mediastinal mass. What should you have ready if there is tracheal tree bronchial obstruction.

A

Be able to intubate with reinforced tube, have a ventilating rigid bronch, have cardiopulmonary bypass available.

164
Q

Mediastinal mass. What should you have ready if there is pulmonary artery obstruction

A

Avoid negative ionotrops and have cardiopulmonary bypass available.

165
Q

Mediastinal mass. What should you do to IV line if there is superior vena cava syndrome.

A

Place IV lines in the lower limbs.

166
Q

pulmonary hypertension. what factors can increase pulmonary hypertension

A

hypoxia, hypercapnea, acidosis, peep, hypOthermia

167
Q

pulmonary hypertension. what agents can be used to decrease pvr

A

phosphodiesterase inhibitor, nitric oxide, prostaglandins, btype naturetic peptide

168
Q

pulmonary hypertension. how does milrinone work

A

inhibits phosphodiesterase III in the heart, increasing cAMP, influx of calcium, improve ionotropy, pulm and systemic vasodilation

169
Q

pulmon hypertension. how does nitric oxide work

A

it acts to increase guanylate cyclase activity…thus increase cGMP on smooth cells…thus pulm vasc relax

170
Q

pulmonary hypertension. how does b-naturetic peptide work to decrease pvr

A

it increase cGMP like nitric oxide

171
Q

pulmon hypertension. how long does b-naturetic peptide work

A

around 18 minutes

172
Q

pulmonary hypertension. what kind of prostaglandins work for pulm htn

A

pge1 and pgi2

173
Q

Aspiration. What should be done when there is gastric content seen in the oral pharynx

A

Head down position. Suction of gastric. Content. Intubation. Suction of ett.

174
Q

flow volume loops. what is the positive y axis

A

expiration

175
Q

flow volume loops. what is the negative y axis

A

inspiration

176
Q

flow volume loops. what is the x axis.

A

measurement of the lung volume

177
Q

flow volume loops. what is the capacity as demonstrated by the width of the loop

A

vital capacity

178
Q

flow volume loops. what are 2 characteristics to look at when describing lesions

A

intra vs extrathoracic. fixed or variable

179
Q

flow volume loops. what do you see with a fixed airway obstruction

A

both values of extra and intrathoracic flows are decreased (the y values are decreased)

180
Q

flow volume loops. what do you see wiht a variable extrathroacic obstruction

A

you see a decrease in the inspiration flow value (less negative y value)

181
Q

flow volume loops. why do u see dampened inspiration flow with a variable extrathoracic obstruction

A

because during inspiration, a variable extrathroacic obstruction causes obstruction. but during expiration, the positive intrathoracic pressure releaves and resolved the variable obstruction…thus almost normal expiration flow loop

182
Q

flow volume loops. what do you see with a variable intrathoracic obstruction.

A

you see decrease amplitude on the positive y axis…aka the expiratory flow is decreased in amplitude.

183
Q

flow volume loops. why do you see a dampened expiratory flow loop with variable intrathoracic obstruction

A

because when you expire, the positive intrathoracic pressure will cause that mass or obstruction to clamp down on airways and decrease expiratory flow. however, during inspiration, the negative intrapleural pressure will pull up on the obstruction and help have a normal inspiratory flow

184
Q

flow volume loops. what is unilateral paralyzed vocal cord considered as for an obstruction

A

variable extrathoracic obstruction

185
Q

flow volume loops. what is special about the V25-75% of the flow volume loops

A

this portion is not effort dependant..but is independant of the patients effort

186
Q

flow volume loops. what disease has alterations of the v25-75% area of the expiratory limb

A

copd…this is a dease of the small airway disease that is obstructed intrathoracic….these small airways is not dependant on pt effort to get obstruction

187
Q

flow volume loops. what does a restrictive lung look like

A

a very narrow skinny loop

188
Q

flow volume loops. why is it skinny loop vor restrictive lung disease

A

because there is a decrease in lung capacity…but the inspiratory and expiratory flows are normal

189
Q

flow volume loops. what is a restrictive lung disease loop an inverse of?

A

it is an inverse of a fixed obstructive leison

190
Q

mediastinal mass. what must be available

A

rigid bronchoscope to intervene when intubation cannot ventilate

191
Q

mediastinal mass. what if the pt does not have svc compression…should u still place a central line above the diaphram?

A

no…bc the svc may be clamped in these cases…so u need ivc access.

192
Q

mediastinal mass. what population of pt are at highest risk for airway compromise

A

pediatric pts

193
Q

Tongue. Motor.

A

Hypoglossal. Cn12

194
Q

Tongue. Taste. Posterior 1/3

A

Glossylpharyngeal. Cn9

195
Q

Tongue. Taste. Anterior 2/3.

A

Cn7. Chordatymapni branch.

196
Q

Tongue. Taste. Epiglottis and Root.

A

Cn10.

197
Q

Tongue. Sensation. Anterior 2/3

A

Cn5. Mandibular v3 portion

198
Q

Tongue. Sensation. Posterior 1/3.

A

Cn9. Glossylpharyngeal.

199
Q

atelectasis. what IV agent does not cause atelectasis

A

ketamin

200
Q

obstructive lung disease. what is decreased

A

max breathing capacity, max midexpiratory flow rate, fev1/fvc ratio

201
Q

obstructive lung disease. what is increased

A

residual volume, total lung capacity

202
Q

obstructive lung disease. what happens to vital capacity

A

normal

203
Q

obstructive lung disease. what happens to total lung capacity

A

increased but can be normal

204
Q

restrictive lung disease. what is decreased

A

vital capacity, total lung capacity, residual volume

205
Q

restrictive lung disease. what is increased

A

fev1/fvc ratio…it can be normal as well

206
Q

restrictive lung disease. what happens to max breathing capacity

A

normal

207
Q

restrictive lung disease. what happens to max mid expiratory flow rate

A

normal

ACE (18 decks)

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