- 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)

- 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

8. Respiratory failure Flashcards by JR SV

Diseases with FRC increase

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

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COPD

Airflow aobstruction due to chronic bronchitis or emphysema

- Progressive and partially reversible

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Chronic bronchitis

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

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Emphysema

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

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Destruction in COPD

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

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AECOPD levels

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

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Triggering factors AECOPD

50-70 % infection of respiratory tract
10 % environmental dust
30 % unknown

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Causes of dynamic hyperinflation (DH)

Respiratory drive increases
COPD exacerbation
Tachypnoe

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Irreversible causes of airflow limitations

Fibrosis and narrowing of the airways
Loss of elastic recoil due to alveolar destruction
Destruction of alveolar support

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Reversible causes of airflow limitations

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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COPD EELV (end-expiratory lung volume)

Higher than normal

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Stages of COPD

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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Most common causes of COPD exacerbation

Infection and air pollution

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Manage COPD exacerbations (medicines)

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

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ABG AECOPD

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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Managed COPD exarcerbations (other)

Maintain fluid balance
Mucus-management
NIIPPV - improves blood gases and pH + recovery time

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Oxygen therapy COPD

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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Respiratory therpay in obstructive patients

Oxygenation
pH
Minimize DH
Reduce resistance
Reduce WOB
Trigger
PEEP
Early weaning
Mucus management

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Indication for invasive ventilation

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

NIV: non-invasive ventilation

Improves pulmonary ventilation (Va increases, less change in dV/dQ
Reduces WOB

Mechanical ventilation in COPD - hyperinflation

Reduce/keep hyperinflasion

Limited MV (minute ventilation?)
Limited Ti (?)

Dynamic hyperinflation definition

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)

Asthma definition

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

Status asthmaticus

Non-responding to conventional therapy for several hours

Extrinsic asthma

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

Intrinsic asthma

Endogen - not allergic - Unclear pathogenesis - Onset: adults

Mixed type asthma

Mixed signs of intrinsic and extrinsic asthma

Causes of airway narrowing in asthma

- Brochoconstriction - Mucosa enlargement - Dyscrinia (hypersecretion)

VD/VT ratio asthma

Elevated

Mediators asthma

- CD4+ T-cells - Eosinophils * Completely reversible*

Mediators COPD

- CD8+ T-cells - Macrophages - Neutrophils * Completely irreversible*

Steroid-resistant asthma

- More towards Th17 (instead of Th2) | - Neutrophils more pronounced than eosinophils

Asthma control test

- 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)

Asthma treatment

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

ICU admission asthma

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

2 subtypes of life-treathening asthma

1) Gradual airway obstruction + inflammation 2) "Sudden asphyxic asthma" - rapid bronchoconstriction - Dry airways (not mucus) - Mainly neutrophils - Allergen, aspirin or other non-steroids

First choice treatment in acute asthma case

- Oxygen - Inhalative beta-mimetics (Nebuliser or MDI) - Systemic corticosteroid (methylprednisolone)

Second choice treatment in acute asthma case

- Inhalative anticholinergic drugs - MgSO4 - Epinephrine

Chest imaging ARDS

Bilateral opacities

ARDS symptoms/signs

- 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

Etiology of ARDS

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

ARDS pathogenesis

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

Treatment of ARDS

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

Most important lung-protective strategies / avoiding VILI

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

ECMO types

- 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)

Escape techniques if conventional ventilation fails

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