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Anesthesiology > 8. Respiratory failure > Flashcards

8. Respiratory failure Flashcards

1
Q

Diseases with FRC increase

A
  • Asthma
  • COPD
  • ARDS (?)
  • Airway obstruction
  • DH (dynamic hyperinflation), PEEPi
  • Limited minute ventilation
  • Hypercapnia
  • Elevated WOB
  • Inflammation
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2
Q

COPD

A

Airflow aobstruction due to chronic bronchitis or emphysema

- Progressive and partially reversible

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3
Q

Chronic bronchitis

A

Chronic persistant cough for 3 months in each of 2 consecutive years
- Have excluded other causes

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4
Q

Emphysema

A

Abnormal permanent enlargement of airspaces distal to the terminal bronchioles without obvious fibrosis

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5
Q

Destruction in COPD

A

Lack of uniformity of the pattern of respiratory airspace enlargement - acinus appearance disturbed

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6
Q

AECOPD levels

A

Acute exacerbation
Level I: managed ambulatory
Level II: hospital admission required
Level III: acute respiratory insufficiency

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7
Q

Triggering factors AECOPD

A
  • 50-70 % infection of respiratory tract
  • 10 % environmental dust
  • 30 % unknown
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8
Q

Causes of dynamic hyperinflation (DH)

A
  • Respiratory drive increases
  • COPD exacerbation
  • Tachypnoe
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9
Q

Irreversible causes of airflow limitations

A
  • Fibrosis and narrowing of the airways
  • Loss of elastic recoil due to alveolar destruction
  • Destruction of alveolar support
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10
Q

Reversible causes of airflow limitations

A
  • Accumulations of inflammatory cells, mucus and plasma exudate in bronchi
  • Smooth muscle contraction in central and peripheral airways
  • Dynamic hyperinflation during exercise
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11
Q

COPD EELV (end-expiratory lung volume)

A

Higher than normal

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12
Q

Stages of COPD

A

0: at risk (symptoms, but normal spirometry)
1: Mild (FEV1 > 80 %)
2: Moderate (FEV1 50-80 %)
3: Severe (FEV1 30-50 %)
4: Very severe (FEV1 < 30 % or < 50 % with signs of HF or resp. failure)
* All of stage 1-4 have FEV1/FVC < 70 %

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13
Q

Most common causes of COPD exacerbation

A

Infection and air pollution

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14
Q

Manage COPD exacerbations (medicines)

A
  • Inhaled bronchodilators (b2-antag and/or antocholinergics)
  • Systemic, preferably oral glucocortico-steroids
  • Theophylline can be used
  • If infection: AB
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15
Q

ABG AECOPD

A
  • pH: 7,2-7,35 (decreased)
  • pO2: 25-65 mmHg (decreased)
  • pCO2: 55-90 mmHg (more elevated than stable COPD)
  • Bicarbonate: primarily unchanged from stabel COPD (27-35)
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16
Q

Managed COPD exarcerbations (other)

A
  • Maintain fluid balance
  • Mucus-management
  • NIIPPV - improves blood gases and pH + recovery time
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17
Q

Oxygen therapy COPD

A
  • Hypoxia: give O2 (usually 0,5-2 L/min nasal cannula)
  • Target PaO2: 55-60 mmHg
  • Resolve the hypoxemic vasoconstriction - increased PaCO2 - decreased respiratory drive
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18
Q

Respiratory therpay in obstructive patients

A
  • Oxygenation
  • pH
  • Minimize DH
  • Reduce resistance
  • Reduce WOB
  • Trigger
  • PEEP
  • Early weaning
  • Mucus management
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19
Q

Indication for invasive ventilation

A
  • Oxygen resistant hypoxia
  • Worsening hypercapnia, acidosis, dyspnea with NIV
  • Horowitz < 200
  • Excessive WOB, respiratory muscle fatigue
  • Alteration of consciousness
  • Instable hemodynamics
20
Q

NIV: non-invasive ventilation

A
  • Improves pulmonary ventilation (Va increases, less change in dV/dQ
  • Reduces WOB
21
Q

Mechanical ventilation in COPD - hyperinflation

A

Reduce/keep hyperinflasion

  • Limited MV (minute ventilation?)
  • Limited Ti (?)
22
Q

Dynamic hyperinflation definition

A

Increase in EELV (end-exp. lung volume), thta may occur in patients with airflow limitation when minute ventilation increases (e.g during exercise, hypoxia, anxiety etc)

23
Q

Asthma definition

A

Reversible small-airway narrowing based on the bronchial hyper-responsiveness

24
Q

Status asthmaticus

A

Non-responding to conventional therapy for several hours

25
Q

Extrinsic asthma

A

Exogen - allergic asthma (Type I allergic rect, IgE), onset: child + young adults

26
Q

Intrinsic asthma

A

Endogen - not allergic

  • Unclear pathogenesis
  • Onset: adults
27
Q

Mixed type asthma

A

Mixed signs of intrinsic and extrinsic asthma

28
Q

Causes of airway narrowing in asthma

A
  • Brochoconstriction
  • Mucosa enlargement
  • Dyscrinia (hypersecretion)
29
Q

VD/VT ratio asthma

A

Elevated

30
Q

Mediators asthma

A
  • CD4+ T-cells
  • Eosinophils
  • Completely reversible*
31
Q

Mediators COPD

A
  • CD8+ T-cells
  • Macrophages
  • Neutrophils
  • Completely irreversible*
32
Q

Steroid-resistant asthma

A
  • More towards Th17 (instead of Th2)

- Neutrophils more pronounced than eosinophils

33
Q

Asthma control test

A
  • Controlled (none of the problems)
  • Partly controlled (> 2/wk daytime symptoms, > 2/wk need for rescue treatment, exacerbation once yearly)
  • Uncontrolled (Exacerbations, or 3 or more of problems)
34
Q

Asthma treatment

A

GINA-guidelines - step
1) SABA
2) SABA + low dose ICS (or LT modifier)
3) SABA + low dose ICS + LABA/LT/theophylline
or SABA + medium dose ICS
4) SABA + medium/high dose ICS + LABA/LT/theophylline (?)
5) SABA + Oral glucocorticoids +/- Anti-IgE

35
Q

ICU admission asthma

A
  • Not responding in 30 min
  • High risk pt
  • Mental alteration
  • Severe obstruction
  • Hypoxia
  • Hypercapnia
  • Indications in history (e.g previously intubation due to asthma)
36
Q

2 subtypes of life-treathening asthma

A

1) Gradual airway obstruction + inflammation

2) “Sudden asphyxic asthma” - rapid bronchoconstriction
- Dry airways (not mucus)
- Mainly neutrophils
- Allergen, aspirin or other non-steroids

37
Q

First choice treatment in acute asthma case

A
  • Oxygen
  • Inhalative beta-mimetics (Nebuliser or MDI)
  • Systemic corticosteroid (methylprednisolone)
38
Q

Second choice treatment in acute asthma case

A
  • Inhalative anticholinergic drugs
  • MgSO4
  • Epinephrine
39
Q

Chest imaging ARDS

A

Bilateral opacities

40
Q

ARDS symptoms/signs

A
  • Oxygen-refractory hypoxia! (elevated shunt, deadspace ratio)
  • Elevated WOB, dyspnea
  • Decreased VC, FRC, ineffective cough
  • Spasm or other sounds
  • Uncousciousness, altered mental status, organ failures
  • PAP and PVR elevation
  • PCWP normal/elevated
41
Q

Etiology of ARDS

A

1) Initial injury
- Direct alveolar injury
- Endothel-mediated (sepsis, SIRS etc)

2) Excudative phase
- Inflammatory mediators
- Oxygen radicals, proteases
- Lacking defence system (superoxide dismutase, catalase etc)
- Alveolo-capillary damage

3) Fibroproliferative phase
4) Chronic phase
5) Recovery

42
Q

ARDS pathogenesis

A
  • Microvascular endothel and alveolar epithel damage
  • Neutrophil-dependent lung injury
  • Other proinflammatory mechanisms
  • Cytokines (e.g ventilator-induced lung injury)
  • Fibrotizing alveolitis
43
Q

Treatment of ARDS

A
  • Treat underlying disease
  • Ventilatory support, lung protective care (Inhalative NO and HFO can improve hypoxemia)
  • Supportive care (fluid balance, steroids, ECMO)
44
Q

Most important lung-protective strategies / avoiding VILI

A
  • Late phase: avoiding lung injury
  • Controlling transalveolar pressure (< 35 mmHg)
  • Using low tidal volume (~6 ml/kg)
  • Prone position
45
Q

ECMO types

A
  • A-V (CO2 elimination - spontane circulation)
  • V-V (CO2 removal and O2 supply - pump circulation)
  • V-A (CO2 removal and O2 supply - bypass R. heart+lung)
46
Q

Escape techniques if conventional ventilation fails

A
  • Prone position
  • HFO: High frequency oscillation
  • Superposed Jet ventilation
  • ECMO, ILA

Anesthesiology (13 decks)

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