8. Respiratory failure Flashcards
Diseases with FRC increase
- Asthma
- COPD
- ARDS (?)
- Airway obstruction
- DH (dynamic hyperinflation), PEEPi
- Limited minute ventilation
- Hypercapnia
- Elevated WOB
- Inflammation
COPD
Airflow aobstruction due to chronic bronchitis or emphysema
- Progressive and partially reversible
Chronic bronchitis
Chronic persistant cough for 3 months in each of 2 consecutive years
- Have excluded other causes
Emphysema
Abnormal permanent enlargement of airspaces distal to the terminal bronchioles without obvious fibrosis
Destruction in COPD
Lack of uniformity of the pattern of respiratory airspace enlargement - acinus appearance disturbed
AECOPD levels
Acute exacerbation
Level I: managed ambulatory
Level II: hospital admission required
Level III: acute respiratory insufficiency
Triggering factors AECOPD
- 50-70 % infection of respiratory tract
- 10 % environmental dust
- 30 % unknown
Causes of dynamic hyperinflation (DH)
- Respiratory drive increases
- COPD exacerbation
- Tachypnoe
Irreversible causes of airflow limitations
- Fibrosis and narrowing of the airways
- Loss of elastic recoil due to alveolar destruction
- Destruction of alveolar support
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
COPD EELV (end-expiratory lung volume)
Higher than normal
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 %
Most common causes of COPD exacerbation
Infection and air pollution
Manage COPD exacerbations (medicines)
- Inhaled bronchodilators (b2-antag and/or antocholinergics)
- Systemic, preferably oral glucocortico-steroids
- Theophylline can be used
- If infection: AB
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)
Managed COPD exarcerbations (other)
- Maintain fluid balance
- Mucus-management
- NIIPPV - improves blood gases and pH + recovery time
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
Respiratory therpay in obstructive patients
- Oxygenation
- pH
- Minimize DH
- Reduce resistance
- Reduce WOB
- Trigger
- PEEP
- Early weaning
- Mucus management
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
