Causes of respiratory failure

Respiratory failure

 

• Results from a failure of the respiratory apparatus to meet to gas exchange requirements of the body
• Type I respiratory failure – hypoxia with a PaO₂ of less than 8kPa but normal CO₂
  • It is also called oxygenation failure
• Type II respiratory failure – PCO₂ raised above 6kPa
  • Also known as ventilatory failure

 

Causes of respiratory failure;

• Type I
  • Acute asthma
  • Left heart failure
  • ARDS
  • Pneumonia
  • Pulmonary fibrosis
  • Emphysema
  • Cystic fibrosis
  • Pulmonary vascular disease
• Type II
  • CNS;
    • Trauma
    • Cerebral tumour
    • Increased ICP
    • Drugs
  • Neuromuscular
    • Cervical cord lesion
    • Bilateral phrenic nerve trauma
    • Guillan-Barre
    • MND
    • Polio
    • MS
    • Muscular dystrophy
    • Myasthenia gravis
  • Thoracic cage and pleura
    • Crushed chest
    • Kyphosis
    • Thoracoplasty
    • AS
    • Obesity
  • Lungs and airways
    • Severe asthma or pneumonia
    • Upper airway obstruction e.g. obstructive sleep apnoea
    • Severe COPD
    • Bronchietasis

 

Mechanism of Type I respiratory failure

• V-Q perfusion mismatch with areas of low ventilation compared with perfusion contributing to hypoxaemia
• Intrapulmonary or intrathoracic shunts – where by venous, deoxygenated blood bypasses ventilated alveoli

 

Mechanisms of Type II respiratory failure

• Alveolar ventilation insufficient to excrete CO₂. Usually from reduced ventilatory effort, increased resistance to ventilation, failure to compensate for increased deadspace (e.g. COPD, chest wall deformities, aspirin overdose).
• Acute: pH is low, bicarbonate is normal.
• Chronic: pH has normalised by a raised bicarbonate (but can get acute on chronic from an exacerbation – watch for a lowering pH with high bicarbonate).

 

 

Pulmonary Oedema

 

• Can be caused by haemodynamic causes e.g. heart failure or direct increases in capillary permeability owing to microvascular injury

 

Causes of pulmonary oedema

• Haemodynamic
  • Increased hydrostatic pressure;
    • Left sided heart failure
    • Volume overload
    • Pulmonary vein obstruction
  • Decreased oncotic pressure;
    • Hypoalbubinaemia
    • Nephrotic syndrome
    • Liver disease
    • Protein losing enteropathies
  • Lymphatic obstruction (rare)
• Oedema sue to microvascular injury
  • Infections – pneumonia, septicaemia
  • Inhaled gases – oxygen, smoke
  • Liquid aspiration – gastric contents, near drowning
  • Drugs and chemicals – chemotherapeutic agents (bleomycin), Amphotericin B, heroin, kerosene
  • Shock, trauma
  • Radiation
  • Transfusion related
  • Oedema of unknown origin
  • High altitude
  • Neurogenic (CNS trauma)

 

Haemodynamic pulmonary oedema

• Most commonly due to increased hydrostatic pressure as occurs with left sided heart failure
• Characterised by heavy wet lungs
• Fluid accumulates at the bases of the lungs because hydrostatic pressure is greater here
• Histologically the alveolar capillaries are engorged and an intra alveolar granular pink precipitate is seen
• Alveolar micro-haemorrhages may be seen along with haemosiderin-laden macrophages (called heart failure cells)

 

Oedema caused by microvascular injury

• Due to injury of the capillaries of the alveolar septa
• Oedema results from damage to the vascular endothelium of damage to alveolar epithelial cells
• This results in leakage of fluids first into the interstitial space and then into the alveoli
• When diffuse it contributes to acute respiratory distress syndrome

 

Acute Respiratory Distress syndrome

 

• A clinical syndrome caused by diffuse alveolar capillary damage
• Characterised clinically by the rapid onset of severe respiratory insufficiency, cyanosis, hypoxia that is refractory to oxygen therapy which may progress to multi-organ failure
• CXR show diffuse alveolar infiltration
• Diffuse alveolar damage is the histological manifestation
• Mortality is around 60%

 

Causes of ARDS

• Infection;
  • Sepsis
  • Diffuse pulmonary infections; viral, mycoplasma, PCP, military TB
  • Gastric aspiration
• Physical injury;
  • Mechanical trauma including head injuries
  • Pulmonary contusions
  • Near drowning
  • Fractures with fat embolism
  • Burns
  • Ionising radiation
• Inhaled irritants
  • Oxygen toxicity
  • Smoke
  • Irritant gases and chemicals
• Chemical injury;
  • Heroin or methadone injury
  • Acetylsalicylic acid
  • Barbiturate overdose
  • Paraquat
• Haematologic conditions
  • Multiple transfusions
  • DIC
• Pacreatitis
• Uraemia
• Cardiopulmonary bypass
• Hypersensitivity reactions

 

Morphology

• Acute stage;
  • Lungs are firm, red, boggy and
  • There is congestion, interstitial and intra-alveolar oedema, acute inflammation and fibrin deposition
  • The alveolar membranes become lined with hyaline membranes
• Organizing sate
  • Interstitial fibrosis and proliferation of Type II pneumocytes
  • Fatal cases often have superimposed bronchopneumonia

 

Pathogenesis

• Central to the causation is diffuse damage to alveolar capillary wall, initially involving the endothelium but also the epithelium eventually
• Early ARDS is characterized by increased capillary permeability, oedema, fibrin exudation, formation of hyaline membranes and septal inflammation
• Activated neutrophils damage the endothelium by secreting proteases and releasing oxygen derived free radicals as well as arachidonic acid metabolites which facilitate further inflammation
• Activated macrophages release oxidants, proteases and inflammatory cytokines
• There is loss of surfactant contributing to atelectasis
• The exudates and tissue destruction of ARDS can be easily resolved and results in organization resulting in scaring and chronic disease

 

Neonatal respiratory distress syndrome

 

• Many causes of respiratory distress of the newborn including, aspiration of blood or amniotic fluid during delivery, brain injury affecting respiratory centers, umbilical cord around the baby’s neck or excessive maternal sedation
• The most common cause however is HYALINE MEMBRANE DISEASE

 

Aetiology and pathogenesis

• RDS primarily occurs in the immature lung due to a deficiency in surfactant produced by Type II pneumocytes
• Type II pneumocytes are most abundant after 35 weeks gestation
• Decreased surfactant results in;
  • Increased alveolar surface tension
  • Progressive alveolar ateclectasis
  • Increasing inspiratory pressures required to expand the alveoli
• Hypoxaemia results in;
  • Acidosis
  • Pulmonary vasoconstriction
  • Pulmonary hypoperfusion
  • Capillary endothelial and alveolar epithelial damage
  • Plasma leakage into the alveoli
  • Plasma proteins combine with fibrin and necrotic alveolar pneumocytes to form hyaline membranes
• Corticosteroids help prevent RDS by inducing formation of surfactant lipids and apoprotein in the fetal lung

 

Morphology

• Grossly the lungs are solid, airless and reddish purple
• Microscopically the alveoli are poorly developed and often collapsed
• Proteinaceous “membranes” line respiratory bronchioles, alveolar ducts and random alveoli

 

Clinical

• Strong association with male infants, diabetic mothers (surfactant synthesis suppressed by high insulin levels) and caesarian section
• Typical infant is preterm but appropriate for the gestational age
• Early on the CXR may reveal a ground glass appearance due to minute reticulogranular densities
• Treatment is most based on prevention, delaying labour until the fetal lung reaches maturity or iducing maturation of the fetal lung with corticosteroids
• In uncomplicated cases treated with surfactant recovery begins in 3 to 4 days but they are at risk of developing retinopathy of prematurity and bronchopulmonary dysplasia (BPD) both due to high concentration oxygen therapy

The major histopathological abnormalitiy in BPD is decreased alve