Apex- Respiratory Pathophys Flashcards

1
Q

Chemicals that contribute to increased airway resistance (select 3):

  • nitric oxide
  • inositol tirphosphate
  • vasoactive intestinal peptide
  • phospholiapase C
  • leukotrienes
  • cyclic AMP
A
  • inositol triphosphate
  • phospholiapse C
  • leukotrienes
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2
Q

Bronchoconstriction is mediated by what 2 things?

What about bronchodilation?

A

Bronchoconstriction:

1. PNS:

  • CNX >ACH > muscarinic-3 receptor (GQ > phospholipase C > IP3 >CA+ release from SR> Myosin light-chain kinase activation> contraction)

2. The immune response:

  • Histamine, leukotrienes, mast cells, ect

Bronchodilation:
1. Circulating catecholamines

  • Epi, NE > B2 receptor (GS) > activates adenylate cyclase > cAMP (2nd mes) > DECREASED release of CA+ from SR > bronchodilation

2. VIP receptor (nitric oxide pathway)

  • Nitric oxide - potent smooth muscle relaxant
  • non-cholinergic PNS nerves release VIP (Vasoactive intestinal peptide) onto airway smooth muscle > increase NO > activates cGMP > smooth muscle relaxation and bronchodilation.
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3
Q

What turns off the adenylate cyclase > cAMP > decreased CA+ release from SR > bronchodilation pathway?

How?

A

PDE III

*deactivates cAMP by converting it to AMP

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4
Q

What cranial nerve supplies parasympathetic innervation to the airway smooth muscle?

A
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5
Q

With all other things being equal, what part of the airway has the most significant contribution to airflow resistance?

A

Radius

(R^4)

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6
Q

T/F: there are NO sympathetic nerve endings in the airway smooth muscle

A

True

Instead, B2 receptors embedded in the airway smooth muscle are activated by catecholamines in the systemic circulation (ok?)

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7
Q

Match the drug with it’s corresponding drug glass

  • Theophylline:
  • Zafirlukast:
  • Cromolyn:
  • Triamcinolone:

Corticosteroid, Leukotriene modifier, Methylxanthine, Mast cell stabilizer

A
  • Theophylline: Methylxanthine
  • Zafirlukast: Leukotriene modifier
  • Cromolyn: Mast Cell stabilizer
  • Triamcinolone: Corticosteroid
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8
Q

2 anesthetic agents with bronchodilating properties

A

volatile anesthetics and ketamine

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9
Q

Pulmonary medications can be broken down into what 3 classes?

A
  1. Direct acting Bronchodilators
  • Beta 2 agonists = albuterol, metaproterenol, salmeterol
    • B2 stimulation → increased cAMP → decreased CA+
  • Anticholinergics = atropine, glycopyrrolate, ipratropium
    • M3 antagonism = decreased IP3 → decreased CA+
  1. Anti-inflammatories
  • Inhaled corticosteroids: beclomethasone, fluticasone, triamcinolone
    • Stimulates intracellular steroid receptors
      • Regulates inflammatory protein synthesis
  • Cromolyn
    • Mast cell stabilizer → decreased release of mediators
  • Leukotriene modifiers: zileuton, montelukast
    • Inhibits 5-Lipoxygenase enzyme → decreased leukotriene synthesis
  1. Methylxanthines
  • Theophylline
    • Inhibits phosphodiesterase (PDE) (usually turns off cAMP pathway) → increased cAMP → increased release of endogenous catecholamines to stimulate B2
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10
Q

What PFT is the MOST sensitive indicator of small airway disease?

  • Forced expiratory volume in 1 second
  • Forced expiratory flow 25-75%
  • Forced vital capacity
  • diffusion capacity of carbon monixide (DLCO)
A

-Forced expiratory flow 25-75%

The average forced expiratory flow during the middle half of the FEV measurement.

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11
Q
A
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12
Q

Normal FEV 1

A

>80% of predicted value

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13
Q

Normal FEV1/FVC ratio value

A

>75-80% of the predicted value

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14
Q

What does FEV1 measure

A

the volume of air that can be exhaled after a maximal inhalation over 1 second

(>80% predicted volume)

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15
Q

What does Forced Vital Capacity (FVC) measure?

Normal volumes for males/females

A

The volume of air that can be exhaled after a maximal inhalation

Male= 4.8 L

Female = 3.7L

(can we just say 3.8 to make it easier?)

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16
Q

What does the FEV1 to FVC ratio compare?

What is it useful for

A

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

useful in diagnosing obstructive vs restrictive disease

Normal = 75-80% of predicted value

< 70% suggests obstructive disease (have a problem getting air out)

normal in restrictive disease (no problem getting air out, but problem getting it in, but the small amount they take in is the same amount they can exhale)

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17
Q

FEV1/FVC of < 70%

A

obstructive disease

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18
Q

What does Forced Expiratory Flow at 25-75% vital capacity measure?

(FEF25-75%)

how does it measure in obstructive vs restrictive disease?

Normal Value

AKA

A

Measures airflow in the middle of FEV

  • reduced with obstructive disease (prob getting air out)
  • normal with restrictive disease (no prob getting air out)

normal = 100 +/- 25% predicted value (whatever the hell that means)

AKA- Mid-Maximal Expiratory Flow Rate (MMEF)

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19
Q

What does the Maximum Voluntary Ventilation (MMV) Measure?

A

The maximum volume of air that can be inhaled and exhaled over the course of 1 minute

  • Male = 140-180
  • Female = 80-120
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20
Q

What is the best test of endurance?

A

Maximum Voluntary Ventilation (MMV)

max volume of air that can be inhaled and exhaled over the course of 1 minute

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21
Q

What does DLCO (diffusing capacity) measure?

How is it measured?

What law?

Normal Value?

A

the ability of the alveolocapillary membrane to exchange gas

  • CO ususally used to measure this
  • Ficks law
  • normal value 17-25ml/min/mmHg
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22
Q

How does restrictive disease affect the FEV1/FVCC ratio?

A

It’s usually normal

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23
Q

What do flow-volume loops allow us to differentiate between?

A

obstructive and restrictive respiratory diseases

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24
Q

What’s ABC&D

A

A- Exhalation

B- Inhalation

C- Total Lung capacity

D- Residual volume

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25
All of the following are independent ris kfactors for postop pulmonay complications **EXCEPT:** - Age \>65yo - COPD - CHF - Asthma
Asthma
26
What 3 things _alone_ are **not** shown to be indepedent predictors of postop pulm complications?
1. Asthma 2. PFTs/ABGs 3. Obestiy
27
What are the 4 C's and 4 S's of risk of postop pulmonary complications?
Class 3 ASA Cigg smoking CHF COPD Sixty or older Serum albumin \<3.5 (malnutrition) Surgery duration \> 2.5 hours Surgical site: uppder abd/thorax/peripheral vascular
28
Serum albumin less than what puts patient at risk for postop pulmnary complications?
\< 3.5g/dL
29
How long should patients stop smoking before surgery?
6 weeks
30
What is the t 1/2 life of carbon monoxide?
4-6 hours
31
After you stop smoking, how long until P50 returns to normal?
12 hours (reduction in carboxyhemoglobin \> improved P50 [but does not reduce risk of postop pulm complications])
32
2 ways to reverse anesthesia-induced atelectasis
**_1. ARMs_** \*PIP to 40cm H20 for 8 seconds **_2. Use the lowest FiO2 the patient will tolerate_** (high FiO2 contributes to absorption atelectasis)
33
What blood test indicates a higher risk of postop pulmonary complications?
Serum Albumin \< 3.5
34
A patient with severe kyphoscoliosis is expected to have a reduced: select 2: - FEV1/FVC ratio - FRC - FEF 25%-75% - FEV1
**-FRC & FEV1** - restrictive lung disease - all volumes are decreased - since TLC is smaller , there is less volume to exhale , so the FEV1/FVC ratio is usually unchanged (they can get out what they bring in) but the FEV1 will be decreased bc they are taking in decreased volumes - the FEF 25-75% is sensitive to increased air flow resistance in the small airways; not a problem for those with restrictive lung disease
35
How does obstructive disease affect the following: FEV1, FEV, FEV1/FVC ratio
FEV1 & FEV - normal or decreased **FEV1/FVC ratio always decreased** (they cant get out what they brought in)
36
How are the following affected with restrictive disease: FEV1, FVC, FEV1/FVC ratio
FEV1 and FVC are decreased (taking in and expiring small volumes bc they cant get air in) **FEV1/FVC ratio is NORMAL** (they can exhale everything they take in)
37
T/F- Obstructive disease is characterised by small airway obstruction
True Small airway obstruction & increased resistance to expiratory flow Problem = getting air out
38
How is compliance in someone with restricitive disease?
decreased
39
Identify each
Blue = obstructive (icream cone, left shift) * Someone took a bite of my icecream cone (COPD) Red = fixed (rock) * Someone smashed my icecream cone; it needs to be **fixed** Green = Normal Purple = Restrictive (narrow, shift right) * On a **restrictive** diet, you'll have to eat a smaller ice cream cone
40
What kind of obstructions do these loops represent
**_1. Extrathoracic_** * pt inhales, airway colllapses, reduces flow being inhaled * pt exhales and pushes the obstruction open; flow out is normal * Inspiratory limb is flat in an Extrathoracic obstruction **_2. Intrathoracic_** * pt inhales, pulls open the obstruction; flow going in = normal * pt exhales, airway collapses; flow going out = reduced * Expiratory limb is flat in the Intrathoracic obstruction
41
A patient with astham expereinces bronchospasm immediately following tracheal intubation. This is **most** likely the result of: - mast cell degranulation - decreased sympathetic tone - histamine release - vagal stimulation
**_Vagal Stimulation_** - Bronchospasm can be due to direct PNS stimulation OR consequence of an immune response (mast cell degranulation) - intubation does not cause an immune response; however, it can activate vagal afferents leading to bronchospasm
42
What is defined by an acute, resversible airway obstruction that is accompanied by chronic airway inflammation and bronchial hyperreactivity?
Asthma
43
What is the greatest risk factor for developing asthma?
Atopy -the condition of being "hyper-allergic"
44
What's to be noted about FEV1, FEV1/FVC ratio, and FEF25-75% in the astmatic?
They are all reduced but will improve following bronchodilator therapy (asthma = reversible)
45
What is the most common ABG finding in the asthmatic and why? What would suggest impending respiratory failure?
**_Resp. Alkalosis with hypocarbia_** Hypercarbia would suggest impending respiratory failure due to air trapping and respiratory muscle fatigue
46
5 Histamine releasing agents that should be avoided in the asthmatic patient (mneumonic)
**_MMAST_** Morphine Meperidine Atracurium Sux Thiopental (mast cells implicated in immune response)
47
What might an EKG show during a severe asthma attack?
Right ventricular strain with right axis devation due to the increased pulm vasc resistance increasing the workload of the right heart
48
T/F: during an asthma attack, tachypnea and hyperventilation are the result of hypoxemia
FALSE -result of neural reflexes (whatever the hell that means)
49
PFTs are not predictive of postop pulm complications. What is the exception to this?
lung reduction surgery
50
T/F - a flow volume loop where the inspiratory or expiratory portion of the loop is flat suggests that wheezing is cuased by asthma.
FALSE -suggesting wheezing is a reslt of uppper airway obstruction (tracheal stenosis or foregin body)
51
What will an asthma CXR show
hyperinflated lungs with diaphragmatic flattening
52
How should you adjust vent settings for an asthamatic
-limit inspiratory time, prolong expiratory time & tolerate moderate permissive hypercapnia
53
What does stimulation of presynaptic H2 receptors result in?
decreased histamine release (H2 blockers [famotidine and ranitidine] can allow for unopposed H1 stimulation which can produce bronchospasm) - risk is very low though but hey, why not know it
54
What's the problem with giving a beta-2 agonist to an asthmatic pregnant patient?
beta-2 agonists relax the uterus which can slow the progression of labor and lead to post-delivery bleeding .
55
What drug used to stop uterine bleeding in the OR can cause bronchoconstriction in asthmatics? By what mechanism?
**_Carboprost (Hemabate)_** -it mimics the action of F2 alpha prostaglandin .... great
56
Would you want to keep asthmatics on the drier side or hydrated side in terms of giving IV fluids
hydrated side to reduce the viscosity of airway secretions
57
What 4 things would indicate intraop bronchospasm
1. Wheezing 2. Decreased breath sounds 3. Increased PIPs (increased plats) 4. increased alpha angle on ETCO2
58
Treatment for acute bronchospasm: 6 key steps + 2 more
**1. 100% FIO2** **2. Deepen anesthetic (crank up gas and give propofol)** **3. Albuterol** **4. Ipratropium** **5. Epi 1mcg/kg IV** **6. Hydrocortisone 2-4mg/kg IV** 7. Aminophylline 8. Helium-oxygen gas mixture
59
_Alpha-1 antitrypsin deficiency: (select 2):_ - increases risk of bronchospasm - caues panlobular emphysema - can be treated with IgG - is the most common metabolic disease affecting the liver
- increases risk of bronchospasm **-caues panlobular emphysema** -can be treated with IgG **-is the most common metabolic disease affecting the liver**
60
Treatment for Alpha-1 antitrypsin deficiency
liver transplant
61
What is alpha-1 antitrypsin deficency casue an increase in?
alveolar protease activity \> an enzyme that degrades pulmonary connective tissue and leads to the development of panlobular emphysema.
62
How can you minimize the risk of oxygen-induced hypercapnia in the patient with severe COPD?
Titrate the FiO2 to maintain SaO2 between 88-92%
63
-Why would you see hypercarbia in a COPD patient receiving O2 therapy? and don't say because o2 decreases their hypoxic drive to breathe (How many times have you given o2 to a COPD patient and they stop breathing? never. )
1. What does happen is O2 is a very potent pulmonary vasodilator, so if you give them oxygen your going to **inhibit their HPV** and worsen VQ matching - your going to have blood going to non-ventilated alveoli which will **increase CO2** bc it cant be dropped off at these non-ventilated alveoli to be exhaled **2. Haldane effect**- hemoglobin that's not bound to oxygen will bind hydrogen ions ; so when you give supplemental o2, the hgb kicks off the hydrogen ions and picks up the o2; the excess H+ ions will bind bicarbonate and produce more CO2
64
How is chronic bronchitis defined?
Cough + sputum production for more than 3 months for 2 consecutive years
65
What spirometry test is diagnositic of COPD
An FEV1/FVC ratio of \< **70%** after bronchodilator therapy
66
If oxygen therapy can cause hypercapneia in the COPD patient, what is the best practice in treating hypoxia?
O2 titrated to maintain a sat of 88-92%
67
Identify the MOST appropriate stategy for mechanical ventilation in the patient with COPD - I:E ratio of 1:1 - Fio2 \< 50% - RR 7bpm - TV 10-12ml/kg
RR 7bpm
68
Vent setting benificial to COPD: I:E ratio: Inspiratory flow: FiO2: RR: TV: PEEP? - why or why not
I:E ratio: increased (1:2.5-3 to allow more air to be exhaled) Inspiratory flow: slow (improve VQ matching) FiO2: adjusted to maintain SpO2 88-92% (avoid oxygen induced hypercapnia) RR: slow- allows for increased expiratory times between breaths TV: small (6-8ml/kg) to minimize risk of hyperinflation and PEEP to keep the small airways open instead of collapsing
69
neuraxial anesthesia should not be considered for COPD patients if a sensory blockade \> ____ is required
T6
70
What block should be avoided in the COPD patient and why
interscalene block bc it causes paralysis of the ipsilateral hemidiaphagm
71
T/F: all halogenated agents are bronchodilators
True (sevo and iso are better than des)
72
The COPD patient should receive a volatile agent with a (high/low) blood:gas solubility. Why?
low to minimize postop resp depression- fast on fast off.
73
74
A patient with COPD is mechanically ventilated. Which interventions will improve this condition? What is this condition? - increase I-time - Decrease RR - Disconnect the circuit - Increase inspiratory flow
- Decrease RR - Disconnect the circuit \*Breath stacking (AKA dynamic hyperinflation)
75
Increasing inspiratory time is another way of saying
reducing expiratory time
76
What does inspiratory flow determine
How fast the tidal volume is delivered to the patient
77
All of the following are examples of restrictive lung disease EXCEPT: - sarcoidosis - cystic fibrosis - negative pressure pulmonary edema - flail chest
**_Cystic Fibrosis_** It's an autosomal recessive genetic disorder than affects *chloride* channels. -Excessive pulmonary secretions plug the airways and create an obstructive ventilatory defectl
78
What is diagnostic of restrictive lung disease?
FEV1 and FVC \<70% with a normal FEV1/FVC ratio
79
Ventilatory strategies for the restrictive lung disease patient: TV: RR: PIP: I:E ratio:
TV: 6ml/kg IBW RR: faster, 14-18BPM PIP: \< 30cm H20 (significant risk of barotrauma) I:E ratio: 1:1 (increase inspiratory time by decreasing expiratory time; less time expiring = more time to inhale)
80
Your patient has restrictive lung disease, what is one of your main concerns-re:induction
that they have decreased FRC and will desat fast on you on induction
81
All of the following reduce the incidence of ventilator-associated pneumona EXCEPT: - oropharyngeal decontamination - minimizing duration of mechanical ventilation - limited sedation - proton pump inhibitors
- PPIs - they increased gastric pH which provides an enviornment for bacteria to flourish; microaspiration can introduce these bacteria into the lungs
82
When does aspiration most commonly occur?
During induction and intubation or within 5 minutes of extubation.
83
Risk fators for mendelson's syndrome and what is it?
Gastic pH \< 2.5 gastric volume \> 25mls (0.4ml/kg) -it's a chemical aspiration pneumonitis
84
Do patients who aspirate have to be admitted overnight?
No, but they must be observed for 2 hours after aspiration event and can be discharged home only if there is no: - new cough/wheeze - cxr evidence of injury - SpO2 decrease \> 10% of preop values on RA - A-a gradient \> 300mHg
85
Hallmark sign of aspriation pneumonitis
Hypoxemia
86
When are antibiotics indicated after an aspiration event?
only if the patient develops a fever or increased WBC count \> 48 hours
87
2 most common culprits of VAP
Pseudomonas aeruginosa and S. aureus
88
What is the first-line treatment for this patient? A. Chest tube insertion B. 14g angiocath insertion at 2nd intercostal space, midclavicular line C. pericardiocentesis D. Cardiopulmonary resusitation
**B. 14g angiocath insertion at 2nd intercostal space, midclavicular line** (emergency treatement for tension PTX) -chest tube insertion is definitive treatment as all the angiocath does is release the tension and improve hemodynamic instability - does not relieve the underlying ptx
89
A chest ultrasound that reveals lack of lung sliding and the absence of comet tails indicates what
tension PTX
90
other place you can shove a 14g angiocath other than 2nd intercostal space mid-clavicular line
4th-5th intercostal space at the anterior axillary line
91
Treatment of flail chest
pain reducing measures (epidural or intercostal nerve blocks) -some patients may require mechanical ventilation and surgical fixation
92
With an open pneumothorax, does the lung collapse on inspiration or expiration
inspiration tx = occlusive dressing that does not let air in but allows air to escape, o2, chest tube , possibly intubation
93
Which 3 blocks are associated with a risk for PTX?
Supraclavicular, interscalene, intercostal
94
Blood:gas partition coefficient of nitrous oxide vs nitrogen. Importance?
Nitrous oxide = 0.47 nitrogen = 0.014. \*Nitrous oxide is 34x more soluble in blood than nitrogen
95
75% Nitrous oxide can double the size of a PTX in \_\_\_\_minutes.
10
96
The thoracic duct empties lymph into where?
The left subclavian vien
97
Key characteristic of flail chest
paradoxical movement of the chest wall at the site of rib fractures
98
What happens with the non-injured vs injured ribs during inspiration and exhalation for flail chest
okay so inspiration = negative intrathoracic pressure, injured ribs get sucked in and normal ribs expand out as per usual (mediastinum shifts to contralateral side) expiration = postive intrathoracic pressure; injured ribs move outward due to the postive pressure; normal ribs move inward as per usual (mediastinum shifts to ipsilateral side) [think mediastimum follows injured ribs]
99
Order the monitors of VAE accordign to their relative sensitivities (1 = most sensitive, 4 = least sensitive): transesophageal echocardiography, precordial doppler, ETCO2, CVP
**#1 = TEE** 2- precordial doppler 3 - EtCO2 4 - CVP
100
What does the presence of a mill wheel murmer on precordial doppler indicate?
VAE
101
What would you see hemodynamically for VAE? (4)
1. End tidal would drop off (air embolus blocking blood from getting to alveoli for CO2 to be exhaled) 2. Hypotension (blood cant get through the lungs \> LV \> systemic = decreased CO) 3. tachycardia to try and get more volume through 4. hypoxia- no blood can get through to pick up o2
102
Treatment for VAE: (4)
1. 100% FIO2 2. Flood surgical field 3. D/C insufllation if applicable 4. Durant maneuver (left lateral decub position)
103
What is the durant maneuver and when should it be utlized?
left lateral decub position ; VAE
104
A patient with pulmonary HTN develops TR, which treatments MOST likely will improve the patient's condition? (Select 3) - Hypothermia - Nitric Oxide - Nitroglycerine - Nitrous Oxide - PEEP - Hyperventilation
Hyperventilation (Blow off CO2) Nitric Oxide Nitroglycerine
105
What 3 things is PVR reduced by?
1. hyperventilation 2. Nitric oxide 3. Nitroglycerine
106
What 5 things is PVR increased by?
Hypoxia Hypercarbia/Acidosis Hypothermia Nitrous oxide PEEP
107
Pulmonary artery hypertension is defined as a mean PAP \> \_\_\_\_\_mmHg
mean PAP \> 25mmHg
108
Formula for PVR + normal values
(mean PAP - PAOP) / \*80 CO **150-250 dynes/sec/cm^5**
109
Why should you treat hypotension aggressively in the patient with pulmonary hypertension
Because CO is relatively fixed and dependent on preload increase PVR = less amount of blood able to get to left heart to be expelled
110
Why is epidural favored over spinal for someone with pulm htn
bc they are preload dependent and a slow sympathectomy is best
111
Drug of choice to reduce preload in the pregnant mother with pulmonary htn having contractions (contractions \> increased preload \> may worsen PAH and RV function)
Nitroglycerine
112
**_Increase or decrease PVR:_** CCBs
decrease (less calcium in vascular smooth muscle = dilation)
113
**_Increase or decrease PVR:_** hypothermia
increases PVR =cold = clamp down
114
**_Increase or decrease PVR:_** PEEP
Increases PVR (don't shove easter PEEPs in the pulmonary vasculature)
115
**_Carbon Monoxide:_** A. Shifts the oxyhemoglobin dissociation curve to the right B. Production is highest with isoflurane C. Binds to the oxygen binding site on hemoglobin with an affinity 200x that of oxygen D. Poisioning is reversed with methylene blue
C. Binds to the oxygen binding site on hemoglobin with an affinity 200x that of oxygen
116
what 3 populations are at risk for carboxyhemoglobinemia
1. burn victims 2. smokers 3. those exposed to desiccated soda lime
117
What is required for the diagnosis of carboxyhemolobinemia?
A co-oximeter ...whatever the fuck that is
118
T/F: oxygen administration is the treatment for carboxyhemoglobinemia
True hyperbaric o2 therapy may also be required
119
When soda lime is desiccated, the risk of carbon monoxide formation is greatest with which volatile anesthetic?
Des \> Iso \>\>\> Sevo
120
Oxygen therapy should be continued until CoHgb is \< \_\_\_% for \_\_\_\_hrs.
\<5% for 6 hours
121
Hyperbaric oxygen is indicated if CoHgb exceeds \_\_\_\_% or if the patient is symptomamtic
\>25%
122
Sodalime is hydrated to ____ - _____ %
13-15%
123
_What are the strongest indications for intubation and mechanical ventilation?/ (Select 2)_ - PaCO2 \> 60mmHg - Vital capacity 25ml/kg - Inspiratory force \<25cm H20 - RR 35BMP
- PaCO2 \> 60 - Inspiratory force \<25cm H20 \*vital capacity **\<15ml/kg** \*RR **\>40bpm** \*keep in mind that no single variable indicates the need for intubation and mechanical ventilation
124
Drugs that can be given via ETT (+mneumoic)
**_NAVEL_** Narcan Atropine Vasopressin Epi Lidocaine
125
3 absolute indications for one-lung ventilation
- Bronchopleural fistula - Pulmonary infection - massive hemorrhage
126
What are the 3 best predictors of postop pulmonary complications for patietns undergoing pulmonary surgery?
127
Instances a right-sided tube would be used
left main bronchus is distorted (tumor/TAA)
128
Ideal DLT sizing for males vs females
female = 35-37F male = 39-41F
129
double lumen tube should not be used for children under what age? So what would you do?
kids under 8 -bronchial blocker or single lumen tube into the main bronchus
130
If VO2 max is not available preop for lung surgery, what can you do?
Ask the patient if they can climb 2 flights of steps without stopping if no, pt is at risk
131
Insertion depth for a DLT; males vs females
females = 27cm males = 29cm (think females 37tube @ 27cm; males 39tube @ 29cm)
132
You placed a left-sided DLT and clamped the tracheal lumen. Match the complication of tube position with the region where breath sounds will be heard - DLT in too far: - DLT tip in trachea: - DLT too far in on right side: with -Right breath sounds absent, left and right breath sounds heart, left breath sounds absent
**_-DLT in too far on left side:_** Right breath sounds absent **_-DLT tip in trachea:_** Left and Right breath sounds heard **_-DLT too far in on right side:_** Left breath sounds absent
133
In the anesthetized lateral decub position, where is alveolar ventilation vs perfusion better? **How does this compare to the awake lateral decub position patient?**
aleveolar ventilation better in nondependent lung persuion better in dependent lung **In the awake lateral decub patient; VQ matching is preserved** * Not preserved with GA on board bc GA reduces lung volumes and diaphragmatic excursion is better on the dependent side
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1 lung ventilation, Ideal: Vent mode: TV: RR: FiO2: \*What are you going to do before starting OLV?
**_Vent mode:_** PC with ideal PIP \< 20cm H20 above PEEP **_TV:_** 6mL/kg of IBW **_RR:_** 12-15 to maintain PaCO2 35-45 (permissive hypercanpia ok as long as pt isnt sensitive to a rise in PVR) **\*Do an ARM before starting OLV**
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Why would it be important to do serial ABGs after starting OLV?
Bc once the SpO2 reaches 100%, then the PaO2 could be either 100 or 500mmHg and you wont know without an ABG
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What poses a higher risk of hypoxemia during OLV, ventilating the right or left lung only and why?
ventilating the left lung only bc the right lung is bigger
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What is the most common complication of the DLT?
poor positioning
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5 steps in treating hypoxia during OLV what if these fail?
**_1. verify 100% O2_** **_2. check position of tube_** **_3. rule out physiologic causes_** such as: * decreased CO (reduced amount of blood able to go pick up oxygen) * bronchospasm (O2 unable to get to alveoli \> blood), * mucus plug (same), * PTX of dependent lung **_4. Apply CPAP to the non-dependent lung_** * start at 2cm H2o (up to 10) * Reduces shunt flow to the non-depedent lung * Can either use the CPAP device to provicde itnermittent PPV (talk to surgeon first) OR, insufflate oxygen to the non-dependent lung by passing a suction catheter through the DLT lumen on the non-depedent side (won't cause lung inflation) **_5. Apply PEEP to the depedent lung:_** * 5-10cm H20 * This may improve FRC or worsen shunt by directing more blood flow to the non-dependent lung so pay attention * consider doing ARM before applying PEEP to ventilated lung *If none of these work:* * *intermittently reinflate with non-depedent lung (communicate with surgeon)* * *surgeon can clamp the pulmonary artery if doing a pneumonectomy to reduce shunt flow to the non-dependent lung* * *think about drugs that inhibit HPV (can you decrease your inhalational agent or convert to tiva?)*
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With OLV, how does applying CPAP to the nondepedent lung improve oxygenation?
By reducing shunt flow (blood no air); your providing air, will improve VQ matching.
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**_Unlike a DLT, the bronchial blocker CANNOT: (select 3):_** - insufflate oxygen itno the isolated lung - ventilate the isolated lung - provide lung separation in the patient requiring naasotracheal intubation - prevent contamination from contralateral lung infection - provide lung separation in children - suction secretions from the isolated lung
- prevent contamination from contralateral lung infection - ventilate the isolated lung - suction secretions from the isolated lung
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T/F: a bronchial blocker cannot provde lung seperation for hte patient requiring nasotracheal intubation
FALSE- it can (DLT's cannot- think you cant shove that big ass tube up someones nose)
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T/F: both the DLT and the bronchial blocker allow you to insufflate oxygen into the isolated lung
True \*but remember the bronchial blocker cannot provide ventilation nor suction secretions from the isolated lung
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Advantage of a bronchial blocker
Since it is plased through a single lumen ETT, the patient wont need to be reintubated with a single lumen ETT if they require postop ventilation
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When you put a bronchial blocker in, which lung is ventilated and which side is not (lung same side vs opposite side of blocker)
same side of blocker = not ventilated opposite side of blocker = ventilated just think the blocker BLOCKS ventilation (goes through the Single lumen ETT- placement can be guided by fiberoptic
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T/F - the lumen of the bronchial blocker can be used to suction blood, pus, or secretions from the non-ventilated lung
False- it is very narrow, so it can only suction (and/or insufflate) air
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What is the smallest sizes DLT and who would you use that for?
26F kids 8-10yo (no DLT \< 8yo, just no DLT small enough)
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How would you provide one-lung ventilation to someone with a trach?
throw a bronchial blocker down there
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Main issue with bronchial blockers
it's a high pressure balloon so it can easily slip into the trachea which can lead to contamination from the other lung or even block ventilation of both lungs
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**_What is the MOST common serious complications of mediastinoscopy (select 2):_** - Chylothorax - Pneumothorax - Left RLN injury - Hemorrhage
PTX (usually right side- bigger) & Hemorrhage
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What is mediastinoscopy used for?
to diagnose and stage lung CA
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Absolute contraindication to mediastinoscopy
Previosu mediastinoscopy (due to scarring)
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Why do you have to be strategic with placing monitors for a mediastinoscopy?
Bc it can compress the innominate artery and impair cerebral perfusion (right side of the circle of willis) - pulseox (or a-line) should go in the RUE; if the scope compresses the innominate artery (which feeds the right subclavian \> ax and right ICA), the waveform will dampen or dissapear - BP cuff on LUE to measure BP (Pro tip- POX on RUE , A-line on left so you dont lose your BP measurement if that happens)
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What 2 things should you have availalbe due to severe hemorrhage being a risk of mediastinoscopy?
1. large bore IV access (lower extremity) * If bleeding occurs, fluid and blood given in the upper extremity will past through the vascular injury and enter the mediastinum. * Large bore IV in a lower extremity avoids this problem (doen't it eventually need to go through the heart though lol - maybe im just missing something) 2. PRBCs available
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What syndrome is oat-cell carcinoma associated with?
Eaton- Lambert Syndrome \*Sensitive to BOTH sux and non-depolarizers -think nany eaton is so extra, shes sensitive to EVERYTHING (both NMBs)
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Mediastinoscopy: **_Incision:_** **_Scope anterior to:_** **_Scope posterior to:_**
**_Incision:_** suprasternal notch **_Scope anterior to:_** trachea **_Scope posterior to:_** innominate and thoracic aorta
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What things would you want to look at preop before mediastinoscopy? (2)
airway imaging on CT evidence of cerbrovascular disease or hx stroke
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Best choice if a patient needs to be reintubated after trachea resection
flexible fiberoptic bc the neck must be maintained in a flexed position for several days after surgery to reduce tension on the tracheal anastomosis while it heals
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**_What are the MOST important strategies for managing mechanical ventilation in the patient with acute redspiratory distress sysndrome (Select 2):_** - low tidal volume - reducing plateu pressure - high-frequency oscillatory ventilation - permissive hypocapnia
**_- low tidal volume (4-6ml/kg IBW)_** * ARDS doesn't affect alveoli in the same way (some become very stiff while others maintain normal compliance) * If you give a poositive pressure breath; the TV will follows the path of least resistance: * stiff alveoli (poor compliance)- will only minimally fill if at all * normal alveoli- will fill way too much as they will get the extra TV unable to go to the stiff alveoli * Can cause volutrauma and barotrauma, which stimulates release of inflammatory mediators, worsening inflammation in the lungs **_-reducing plateu pressure_** * \<30cm H20 * If this isn't being achieved, reduce TV to 4ml/kg IBW
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What is the most common pulmonary etiology of ARDS vs most comon extra-pulmonary etilogy
pulmonary etilogoy = PNA extra-pulmonary = Sepsis
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4 key pathophysiolologic features of ARDS
1. protein-rich pulmonary edema 2. loss of surfactant 3. Hyaline membrane formation 4. potential for long-term lung injury
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Time of onset of ARDS
within 1 week of initial insult or new/worsening resp symptoms
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how will ARDS present on CXR or CT?
Bilateral opacities -not fully explained by effusions, lobar/lung collapse, or nodules
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ARDS is caused by inflammation injury (mediated by neutrophils and platelets) that leads to what
diffuse alveolar destruction
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Hallmark of ARDS
hypoxemia despite increased supplemental O2
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What vent mode would be best for somone with ARDS?
Pressure control will goals of keeping lower tidal volumes
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Goal RR for ARDs patient
6-35 -titrate to a target pH of 7.3-7.45 (dynamic hyperinflation is a risk when using a high RR) [i think thats autopeep/breath stacking]
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oxygen goal for ARDS patients
Target a PaO2 of 55-80 or SpO2 88-95%
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Why should FiO2 be reduced to 50% whenever possible?
because a high concentration of inspired oxygen (likely over 50%) causes oxidatative stress to the lung
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Max Fio2 delivered for a regular nasal cannula
40%
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PEEP strategies for ARDs patients
Increase PEEP to allow for lowest FiO2
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What is the most approrpiate sized DLT for a woman who is 5'2"?
35F (62" x 2.54 = 157.5cm) \<160 = 35, \>160 = 37
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How to convert someones height to cm
inches x 2.54
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**_What is the definitive treatment for hypoxemia during OLV in the lateral decub position?_** - Resume 2 lung ventilation - Pulm artery ligation - Apply CPAP to the non-dependent lung - Apply PEEP to the dependent lung
Resume 2-lung ventilation
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**_Anesthetic considerations for hte patient with pulmonary HTN secondary to lung disease (select 2):_** - permissive hypercapnia - volume loading before anesthetic induction - continuing the patient's sildenafil preoperatively - treating right heart failure with inhaled nitric oxide
**-continuing the patient's sildenafil preoperatively** **-treating right heart failure with inhaled nitric oxide** (fluid therapy should be careful, CO is relatively fixed and pts can be sensitive to inadequate preload but you cant overload them either)
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**_Which variable is reduced by dynamic hyperinflation?_** A. Inspiratory capacity B. Expiratory reserve volume C. Tidal Volume D. FRC
A. Inspiratory capacity - Dynamic hyperinflation = breath stacking = autopeep - pt's fully cant exhale delivered tidal volume, FRC rises, IC decreases
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**_What are the primary mechanisms by which carboxyhemoglobinemia produces metabolic acidosis (Select 2):_** - Impaired krebs cycle - decreased CaO2 - left shifted oxyhgb dissociation curve - accelerated o2 consumption
**_-decreased CaO2:_** * CO2 binds to o2 binding site on the hgb with 200x afinity than o2 * This displaced o2 from hgb and reduces CaO2 **_-left shifted oxyhgb dissociation curve_** * Less O2 is released at the tissue level \*The net result is an impairment of *oxidative phyosphorlation*, reducing ATP production \> metabolic acidosis