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Physiology > Obstructive Lung Diseases > Flashcards

Obstructive Lung Diseases Flashcards

1
Q

What is obstructive lung disease?

A

pulmonary conditions characterized by airflow limitation

  • inside lumen
  • bronchial wall
  • peribronchial region (reversible vs non-reversible)
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2
Q

OSA define

A

mechanical obstruction of breathing that occurs during sleep when pharyngeal muscles relax

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3
Q

What does OSA lead to?

A

increased morbidity
chronic hypoxemia & hypercarbia
other pathologies: artherosclerosis, HTN, stroke, insulin resistance, DM

LOW FRC

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4
Q

Cardiac effects of OSA

A

chronically hypoxic –> changes in vasculature –> RHF
systemic & pulmonary HTN
IHD
CHF

these pt are very unstable

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5
Q

Diagnosis of OSA

A

polysomnography
> 5 sleep-related symptoms
> 15 dx for moderate OSA
> 30 severe OSA

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6
Q

Obstructive diseases & peak flow rates

A

Peak flow rates are decreased b/c small airways close on expiration, thus decreasing flow

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7
Q

FEV1

A

forced expiratory volume in 1 second
normal: 80-120%
COPD: 20%

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8
Q

FVC

A

forced vital capacity
the volume of air forcefully exhaled after a deep inhalation

normal: 3.7L (Female), 4.8L (male)

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9
Q

FEV1 to FVC ratio

A

normal: 75 - 80%

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10
Q

FEV25-75

A

measurement of air flow at midpoint of a forced exhalation

most effort independent and most sensitive indicator of small airway disease

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11
Q

Maximum voluntary ventilation

A

usually do it for 15m and extrapoalte it

-maximum amount of air that can be inhaled and exhaled in 1 minute

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12
Q

MVV male

A

140 - 180L

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13
Q

MVV female

A

80 - 120 L

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14
Q

Diffusing capacity

A

Volume of carbon monoxide transferred across the alveoli into the blood per minute per unit of alveolar partial pressure

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15
Q

DLCO normal value

A

17 - 25 mL/m/mmHg

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16
Q

What are some things that could affect DLCO?

A

Fick’s Law of Diffusion

  • emphysema (increased SA)
  • fibrosis (increased thickness)
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17
Q

How long do you wait after an acute upper respiratory infection?

A

6 weeks (only if ACTIVELY febrile)

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18
Q

Acute Upper Respiratory Infection case tips

A

avoid OPA, run them deep to avoid bronchospasm, extubate deep (turn on side)

  • hydrate
  • reduce secretions
  • limit airway manipulation (best thing you can do)
  • LMA
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19
Q

adverse respiratory events

A

bronchospasm
laryngospasm
airway obstruction
postoperative croup

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20
Q

Asthma (3)

A

REVERSIBLE airway obstruction characterized by

  1. bronchial hyperactivity
  2. bronchoconstriction
  3. chronic inflammation of lower airways
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21
Q

Pathophys of asthma

A

activation of the inflammatory pathway leads to infiltration of airway mucosa w/ eosinophils, neutrophils, mast cells, T cells & B cells

inflammatory mediators include: histamine, prostaglandin D, leukotrienes

airway edema results = thickened basement membrane

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22
Q

S/S Asthma (4)

A

EPISODIC (may lasts minutes to hours but pt completely recovers)

  1. wheezing
  2. productive and non-productive cough
  3. dyspnea & chest discomfort –> air hunger
  4. eosinophilia (sputum)
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23
Q

Severe bronchospasm VS

A

RR > 30, HR > 120

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24
Q

Dx asthma

A
  • wheezing, chest tightness, SOB
  • airflow obstruction that is partially reversible w/bronchodilators
  • PFTS (FEV1 < 35%)
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25
Q

Expiratory limb of loop w/asthma

A

scoooooping

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26
Q

What happens w/FRC and TLC in asthma?

A 
FRC increases (usually RV)
TLC normal
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27
Q

DLCO in asthma?

A

samesies

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28
Q

ABGs in asthma

A
  • normal in mild dx
  • hypocarbia & respiratory alkalosis common (reflecting neural reflex changes in lungs; not hypoxemia)
  • severe obstruction associated w/PAO2 < 60
  • rises in PaCO2 noted when FEV1 < 25%
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29
Q

CXR in asthma

A

normal

severe - hyperinflation, hilar congestion d/t mucus plugging and pulmonary HTN

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30
Q

EKG in asthma

A

only in severe attacks

  • RV strain (d/t increased pulmonary pressures)
  • T wave inversion (V1-V4, II, III, avF)
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31
Q

Treatment of asthma

A

treat inflammation & bronchospasm

  1. corticosteroids
  2. long-acting bronchodilators
  3. leukotriene modifiers
  4. anti-igE monoclonal antibody (omalizumab)
  5. methylxanthines (theophylline)
  6. mast cell stabilizer (cromolyn)
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32
Q

corticosteroid example

A

beclomethasone

give 1-2h preop (ideally 5 days)
alters gene transcription, inhibits mast cells, apoptosis of inflammatory cells, increase B2 agonist effectiveness

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33
Q

long-acting bronchodilator example

A

salmetrol (50 mcg) DOA 12 - 24 h

combination (symbicort & advair) = LABA + steroid

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34
Q

leukotriene modifier

A

singulair

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35
Q

PFT’s & ASTHMA

A

if FEV1 > 50% of normal, symptom free

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36
Q

Status asthmaticus

A

life threatening emergency in which bronchospasm does not respond to treatment

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37
Q

Status asthmaticus s/s

A 
low oxygen
blunted CO2 waveform
wheezing
mucus hypersecretion
PIPs increased
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38
Q

Status asthmaticus tx

A 
B2 agonist (albuterol - 4 puffs (400 mcg total))
IV steroids
O2
Mg (1-2 g over 20 m)
Oral leukotriene inhibitor

Resistant? think airway edema & secretions

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39
Q

Terbutaline

A

0.25 mg SQ q15m (beta agonist)

40
Q

Bronchospasm tx

A
  1. deepen (propofol)
  2. 100% O2
  3. SABA
  4. Epi 10 mcg/kg
  5. Hydrocort 2-4 mg/kg
  6. ipraprotium 0.25 - 5 mg
41
Q

What increases risk for perioperative event for asthma (think PFTS)

A

FVC < 70%

FEV1/FVC < 65%

42
Q

When do you stress dose steroids?

A

only IF systemic therapy in the last six months

43
Q

Anesthesia considerations for asthma

A
  1. deep induction
  2. IV or transtracheal lidocaine
  3. VA (sevo)
  4. avoid histamine releasing drugs (no morphine, no succinylcholine)
  5. Adequately hydrated
  6. avoid acei?
  7. use PEEP
44
Q

COPD define

A

non-reversible loss of alveolar tissue and progressive airway obstruction

45
Q

COPD RF:

A 
cigarette smoking
occupational exposures
pollution
recurrent respiratory infections
low birth weight
a1 antitrypsin deficiency
46
Q

type B COPD

A

bronchitis

blue bloater

47
Q

type A COPD

A

emphysema

pink puffer

48
Q

emphysema pathophys

A

destruction of parenchyma
loss of SA, elastic recoil & structural support
inability to maintain airway patency

49
Q

bronchitis pathophys

A

narrowing of small airways by inflammation & mucuous production

50
Q

emphysema definition

A

enlargement of air spaces distal to the terminal bronchiole with destruction of walls

  • loss of alveoli & damage to capillaries
  • small airways are thin, tortuous, atrophied

shunting & deadspace

51
Q

what is an acinus

A

tissue distal to terminal bronchioles

52
Q

centriacinar (centrilobular) emphysema

A

more common in apex

proximal

53
Q

panacinar (panlobular) emphysema location & cause

A

more common distally d/t a1 antitrypsin deficiency

54
Q

paraseptal emphysema

A

regional

55
Q

bullae emphysema

A

one big sac

56
Q

what does elastase do?

A

degrades pulmonary connective tissue

it is released by smoking

57
Q

what does alpha 1 antitriptase do

A

blocks elastase

58
Q

chronic bronchitis definition

A

dx characterized by excessive sputum production (expectoration of sputum most days for at least 3 mo for 2 successive years)

59
Q

hallmark findings of chronic bronchitis (5)

A
  1. hypertrophy of mucus glands of large bronchi
  2. inflammatory changes in small airways
  3. granulation of tissue, smooth muscle increases
  4. peribronchial fibrosis
  5. chronically hypoxic (paO2 < 60)
60
Q

COPD diagnosis

A

SPIROMETRY

severity determined by GOLD

61
Q

FEV1/FVC for COPD

A

decrease < 70% of predictive

not reversible w/bronchodilators

62
Q

FEV25-75 for COPD

A

decreased

63
Q

FRC and TLC for COPD

A

increased RV

64
Q

COPD treatment

A

smoking cessation
long term O2 admin (2LPM)
hct > 55%, paO2 < 55, usually have corpulmonale

65
Q

Drug treatment of COPD

A 
O2 
long acting B2agonist
steroids
long acting anticholinergic (ipaprotrium)
vaccines
diuretics
theophylline
66
Q

Sx treatment COPD

A

lung volume reduction surgery for severe COPD cases

-increases pel, decreases hyperinflation, improves diaphragmatic/chest wall movement, decreases V/Q mismatch

67
Q

COPD anesthetic considerations for lung volume reduction

A

double lumen tube
avoid nitrous
avoid excessive positive pressure (low Vt, high RR)

68
Q

what is most predictive of COPD pulmonary compliactions

A

clinical symptoms (wheezing, cough)

69
Q

preop pulmonary functon testing

A 
hypoxemia
home O2
NaHCO3 > 33 mEq/L
PaCO2 > 50 mm Hg
hx resp failure
severe SOB
planned pneumonectomy
difficulty assessing pulmonary status through clinical means
differential dx needed
determine response to bronchodilators
pulmonary htn
70
Q

smoking cessation

A

at least six weeks

or morning of only

71
Q

COPD malnutrition leads to —>

A

increases risk of pleural leaks after surgery

72
Q

interscalene block risks

A

ipsilateral phrenic nerve palsy

73
Q

why do you avoid NO for COPD pt

A

attenuates HPV, increases V/Q MISMATCH

74
Q

PIP

A

< 30 CM H2O

75
Q

Why does air trapping occur?

A

positive pressure ventilation applied w/o sufficient expiration –> increasing intrathoracic pressure –> decreasing VR –> increases PAP

76
Q

Capnography for air trapping

A

sloped carbon dioxide concentration; expiratory flow does not reach baseline

77
Q

bronchospasm COPD pt

A

light? deepen anesthetic

pathologic? bronchodilator, magnesium, epi, IV steroids, suction secretions

78
Q

Name 5 other expiratory outflow obstructions

A 
bronchiectasis
cystic fibrosis
primary ciliary dyskinesia
bronchiolitis obliterans
tracheal stenosis
79
Q

bronchiectasis

A

irreversible airway dilation and collapse d/t inflammation d/t chronic infections

80
Q

bronchiectasis s/s

A

significant hemoptysis (200 mL over a 24 hour period)
dyspnea/wheezing
pleuritic chest pain
FINGER CLUBBING

81
Q

bronchiectasis dx

A 
hx chronic cough w/purulent sputum
CT confirms (usually lower lobes)
82
Q

anesthetic considerations for bronchiectasis

A

GETTA w/frequent suctioning
double lumen tube to avoid infecting both sides
avoid nasal intubations

83
Q

cystic fibrosis definition

A

autosomal recessive d/o affect a single gene on chromosome 7 - this prevents chloride transport and movement of salt and water

84
Q

cystic fibrosis damage

A 
lungs (COPD, bronchiestasis)
pancreas (DM)
GI (ileus)
sinusitis
liver (cirrhosis)
reproductive organs
85
Q

cf dx

A

sweat chloride > 70 mEq/L
chronic purulent sputum, malabsorption
bronchoalveolar lavage high in neutrophils
older adults –> COPD
normal sinuses is strong evidence CF is NOT present

86
Q

CF tx

A

alleviation of symptoms

  1. clear airway secretions
  2. correct organ dysfunction
  3. nutrition (VIT K)
  4. prevent GI obstruction
87
Q

CF anesthesia considerations (6)

A
  1. optimize pt (elective procedures)
  2. vit k to help absorb fat soluble vitamins
  3. general anesthesia w/VA (increased oxygen concentrations, relax smooth airways)
  4. avoid anticholinergic
  5. awake extubation
  6. pain control
88
Q

primary ciliary dyskinesia

A

congenital impairment of ciliary activity in respiratory tract epithelial cells and sperm cells

89
Q

what is kartagener’s syndrome?

A

PCD

  • chronic sinusitis
  • bronchiectasis
  • sinus inversus (ORGANS REVERSED)
  • decreased fertility
90
Q

primary ciliary dyskinesia anesthesia

A 
regional anesthesia
reverse position of EKG leads
left IJ vein cannulation
right uterine displacement
avoid nasal pharyngeal airways
91
Q

bronchiolitis obliterans

A

disease of small airways and alveoli in children from RSV

92
Q

adult bronchiolitis obliterans

A

d/t viral pneumonia

  • collagen vascular dx (RA)
  • silo filler’s disease (nitrogen dioxide inhalation)
  • graft vs host dx
93
Q

Bronchiolitis obliterans organizing pneumonia (BOOP)

A

shares features of interstitial lung dx and bronchiolitis obliterans

treatment innefective

94
Q

tracheal stenosis

A

occurs following prolonged intubation or over-inflation of ETT (may not appear for several weeks)

95
Q

when does tracheal stenosis become symptomatic

A

tracheal diameter decreases < 5 mm
dyspnea prominent at rest
accessory muscles used in all phases of breathing

96
Q

tracheal stenosis tx

A
  1. tracheal dilation (temporary) - balloon or surgical dilators, lasering of scarred tissue
  2. Tracheobronchial stent can be short term or long term
  3. Tracheal resection w/anastomosis is the best treatment (intubate below resection)
97
Q

tracheal stenosis anesthetic considerations

A

translaryngeal intubation
VA to ensure maximum inspired oxygen concentration
helium

Physiology (5 decks)

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