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Health Assessment > Obstructive Disease > Flashcards

Obstructive Disease Flashcards

1
Q

What is obstructive sleep apnea?

A
  • Recurrent upper airway collapse during sleep
  • causes ↓ or complete cessation of airflow
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2
Q

What 3 things will polysomnography recordings show?

A
  • Apnea
  • Hypopnea
  • Respiratory effort-related arousals
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3
Q

What is the definition of apnea?

A
  • 90% ↓ in amplitude of airflow signal
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4
Q

What are 3 classifications of apnea? How long do the episodes have to last?

A
  • Obstructive
  • Central
  • Mixed
  • Duration of 10 seconds or more
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5
Q

What is the definition of hypopnea?

A
  • ↓ of 30% or 50% or more in amplitude of nasal presure that last for 90% or more of the breath
  • Also has a 4% or greater ↓ in SpO2
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6
Q

What is the Apnea-hypopnea index (AHI)

A
  • Number of apnea and hypopnea events per hour of sleep
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7
Q

What is respiratory effort-related arousals?

A
  • A limitation in the airflow followed by an arousal on the EEG channel. (Flattening of the airflow in a way that does not meet the criteria for apnea or hypopnea)
  • Duration of 10 seconds or more
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8
Q

How is sleep apnea or hypopnea diagnosed?

A
  • If AHI ≥ 15
  • If AHI ≥ 5 plus S/Sx or associated medical or psychiatric disorder such as HTN CAD CHF insomnia snoring etc
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9
Q

How is Obstructive sleep apnea syndrome (OSAS) diagnosed?

A
  • AHI ≥ 5
  • Daytime somnolence ≥ 2 days/week
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10
Q

What are the 3 severity levels of OSA?

A
  • Mild → AHI 5-15
  • Moderate → AHI 15-30
  • Severe → AHI ≥ 30
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11
Q

What are the 3 direct physiologic mechanisms for Apnea/obstruction?

A
  • Anatomic and functional upper airway obstruction
  • ↓ respiratory-related EEG arousal response
  • Unstable ventilatory response to chemical stimuli
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12
Q

How are apnea episodes resolved by the body?

A
  • ↑ muscular activity at upper airway and thoracoabdominal respiratory muscles
  • EEG arousal
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13
Q

What are some of the neurocognitive consequence of OSA?

A
  • Slower EEG
  • Sleep deprivation
  • Sleepy in daytime
  • ↓ cognition performance
  • ↓ quality of life
  • ↑ car accidents
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14
Q

What are some of the metabolic consequences of OSA?

A
  • Hypoxic injury
  • inflammation
  • ↑ SNS activity
  • Hormonal changes
  • Insulin resistance / DM2
  • central obesity
  • Metabolic syndrome
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15
Q

What are the most common sites of upper airway obstruction?

A
  • Retropalatal and retroglossal regions of the oropharynx
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16
Q

What are some signs that a patient may have an issue with airway obstruction?

A
  • Bony craniofacial abnormalities
  • Excess soft tissue
  • Acromegaly thyroid enlargement and hypothyroidism
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17
Q

When will the airway collapse?

A
  • When the forces that can collapse airway > than forces the dilate the airway
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18
Q

What are the collapsing forces of the airway?

A
  • intraluminal negative inspiratory pressure
  • extraluminal positive pressure
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19
Q

What are dilating forces on the airway?

A
  • Pharyngeal dilating muscle tone
  • longitudinal traction on upper airway d/t ↑ lung volume
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20
Q

When the patient is ________ airway obstruction is enhanced?

A
  • Supine → supine enhances airway obstruction
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21
Q

Which patient position ↑ the effect of extraluminal positive pressure against the pharynx?

A
  • Supine position
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22
Q

Altered neuromuscular control of the airway is related to what 2 things?

A
  • Inflammatory infiltrates
  • Denervation chagnes
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23
Q

Respiratory related arousal response is related to what 4 things?

A
  • Hypercapnia
  • Hypoxia
  • Upper airway obstruction
  • Work of breathing
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24
Q

What are som clinical symptoms of OSA/apnea?

A
  • Day → dry mouth headache sleepy cognitive impairment
  • Night → wake up often snoring choking sensation breathing pauses
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25
Q

What are some comorbidities associated with OSA?

A
  • HTN
  • CAD
  • MI
  • HF
  • ESRD
  • Graves disease
  • DM2
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26
Q

What are some risk factors for OS?

A
  • elderly
  • Obesity
  • non-caucasian
  • male
  • pregnant
  • craniofacial abnormalities
  • smoking
  • narrow airway
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27
Q

What are some treatments for OSA?

A
  • CPAP
  • oral appliances
  • Eletrical stim → stiimulates hypoglossal nerve (CN12) with every breath
  • Weight reduction
  • Surg
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28
Q

What are 4 surgeries that might help OSA?

A
  • tonsillectomy
  • maxillomandibular advancement
  • ubulopalatopharyngoplasty
  • adenotonsillectomy
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29
Q

For every 1 point ↑ in Mallampati score how much do the odds ratio for OSA increase?

A
  • ↑ by 2.5 for every 1 point ↑ in Mallampati
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30
Q

During induction what are 4 things we can do to help reduce issues with OSA?

A
  • elvate HOB
  • Pre oxygenate
  • Know they might be difficult to mask ventilate or intubate
  • Minimize or don’t use opioids
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31
Q

What anesthetic type might be preferred for OSA patients?

A
  • Regional more than GA
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32
Q

What are two mnemonics to help assess OSA?

A
  • STOP
  • BANG
33
Q

What is the most common cause for acute URI?

A
  • viral or bacterial nasopharyngitis (95% of cases)
34
Q

What are 2 possible noninfectious nasopharyngitis?

A
  • allergic
  • vasomotor
35
Q

What are some S/Sx of URI?

A
  • nonproductive cough
  • sneezing
  • rhinorrhea
36
Q

IF the patient has had a URI that is not getting better how does that affect their surgery? What if it’s stable or getting better?

A
  • Unstable → delay 6 weeks
  • Stable → proceed with surg
37
Q

If the patient has had a recent URI what airway device might be preferred?

A
  • LMA > ETT
38
Q

What are some adverse respiratory events for a patient that had URI?

A
  • bronchospasm
  • airway obstruction
  • postintubation croup
  • desat
  • atelectasis
39
Q

What can we do to help ↓ risk r/t recent URIs when anesthetizing a patient?

A
  • Hydrate
  • ↓ secretions
  • limit airway manipulation → URI causes hyperreactive airway
  • Nebulized or topical anesthetic to the vocal cords → URI causes hyperreactive airway
  • LMA > ETT
40
Q

What is asthma?

A
  • reversible airway obstruction
  • bronchial hyperreactivity
  • bronchoconstriction
  • chronic airway inflammation
41
Q

What are some things that ↑ risk for asthma?

A
  • Heriditary
  • Family Hx
  • mom smoked while pregnant
  • childhood exposure to infectious environments
42
Q

What is status asthmaticus?

A
  • life threatening bronchospasm that persists despite treatment
43
Q

What are some things that can provoke an asthma attack?

A
  • allergens
  • aspirin / β antagonists / NSAIDS
  • respiratory viruses
  • excercise → typ following exertion than during it
  • emotional stress
44
Q

What is the pathogenesis of asthma?

A
  • chronic inflammation in lower airways activates inflammatory cascade
  • Leads to bronchi and airway edema and thickened airways
  • Simultaneous areas of inlammation and repair in airways
45
Q

In a patient with asthma which inflammatory infiltrate the airway mucosa?

A
  • Eosiniphils / neutrophils
  • mast cells
  • T-cells / B-cells
  • LTs
46
Q

What are some S/Sx of asthma?

A
  • wheezing
  • cough
  • dyspnea
  • chest tightness
47
Q

How long can an asthma attack last?

A
  • minutes to hrs
48
Q

How can we determine if someone has severe asthma?

A
  • prior intubation / ICU admission
  • ≥ 2 hospitalizations in a year
  • presence of coexisting disease
49
Q

How is asthma diagnosed?

A
  • report wheezing chest tightness SOB
  • Airflow obstruction on PFT that is partially reversible with bronchodilators
50
Q

How is severity of Asthma diagnosed?

A
  • clinical symptoms
  • PFTs
  • Med useage
51
Q

What are some PFT changes we would see in an asthmatic?

A
  • FEV1 < 35% of normal
  • FRC → may ↑
52
Q

What are some ABG changes we might see with an asthmatic?

A
  • hypocarbia
  • respiratory alkalosis
53
Q

For mild asthma how will PaO2 and PaCO2 be affected on ABG?

A
  • will be normal
54
Q

For sever asthma how will PaO2 and PaCO2 be affected on ABG?

A
  • PaO2 < 60 mmHg on RA
  • PaCO2 ↑ when the FEV1 < 25%
55
Q

What changes on CXR will we see with an asthma patient?

A
  • Mild/moderate → normal
  • Severe → hyperinflation and vascular congestion of hilum d/t mucous plugging and PHTN
56
Q

What changes on ECG will we for an asthmatic?

A
  • RV strain / irritability
57
Q

What are 2 goals of treating asthma?

A
  • Prevent / control bronchial inflammation
  • Treat bronchospasm
58
Q

What are 2 SABA meds we talked about?

A
  • Albuterol (Proventil)
  • levalbuterol (xopenex)
59
Q

What are the 7 long term treatments for asthma we discussed in class?

A
  • Inhaled corticosteroids → budesonide fluticasone
  • LABA → arformeterol (brovana)
  • Combo steriods + LABA → symbicort or advair
  • LT modifier → montelukast (singulair)
  • Anti- IgE MAB → omalizumab
  • Methylxanthines → theophyline aminophylline
  • Mast cell stabilzer → Cromolyn
60
Q

What are some ways to treat status asthmaticus?

A
  • O2
  • β2 agonist
  • Steroids → hydrocortisone or methylprednisolone
  • IV fluid and IV mag sulfate
  • broad spectrum ABX
  • Ipratropium
  • Intubate when PaCO2 > 50 mmHg
61
Q

When preopping an asthma patient what are some things to consider?

A
  • onset age
  • triggers
  • accessory muscle use wheezing
  • stress dose steroids ABX bronchodilators
62
Q

For an asthmatic what type of anesthesia is preferred?

A
  • regional > GA
63
Q

What meds can be used to suppress hyperreactive airway?

A
  • fentanyl
  • remifentanil
  • lidocaine
  • prop
  • ketamine
64
Q

What NMBDs should we avoid in an asthma patient?

A
  • histamine releasing nmbds
65
Q

What is COPD?

A
  • progressive loss of alveolar tissue that is not reversible
66
Q

What deficiency do COPD patients have?

A
  • α1 - Antitrypsin
67
Q

What is emphysema?

A
  • destruction of lung parenchyma
68
Q

What is chronic bronhitis?

A
  • cough and sputum production
69
Q

What are some risk factors for COPD (this is not exhaustive list)?

A
  • smoking
  • occupational exposure to bad things
  • recurrent resp infections
  • low birth weight
  • asthma
  • age
  • female
70
Q

What are some S/Sx of COPD?

A
  • Dyspnea on exertion or at rest
  • chronic cough and sputum production
71
Q

What is a COPD exacerbation?

A
  • acute worsening of airflow obstruction
72
Q

How is COPD diagnosed?

A
  • FEV1/FVC < 70% normal
  • ↑ RV FRC and TLC
  • CXR → hyperinflation hyperlucency
73
Q

What is Bullae associated with?

A
  • emphysema
74
Q

How do we treat COPD medically?

A
  • Stop smoking
  • O2→ if PaO2 < 55mmHg Hct > 55% or if cor pulmonale
  • LABA corticosteroids anticholinergics
  • Flu / pneumonia vaccines
  • Diuretics
75
Q

What is the goal of O2 therapy for COPD?

A
  • PaO2 > 60 mmHg
76
Q

How can we treat COPD surgically? How does it help?

A
  • Lung volume reduction surgery
  • Help ↑ elastic recoil ↓ hyperinflation ↓ V/Q mismatch
77
Q

What are some things to consider for COPD patient preop eval?

A
  • smoking Hx
  • current meds
  • comorbidities
  • do they have RV failure
  • prior hospitalizations
  • optimize before surg
  • PFTs/ABGs
  • Ventilation
78
Q

What are some preop risk reductions we can do for COPD patients?

A
  • stop smoking for 6 weeks
  • treat respiratory infections
  • treat expiratory airflow obstructions
  • lung volume expansion maneuvers

Health Assessment (7 decks)

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