Acute Respiratory Failure

Overview

 Acute Respiratory failure causes hypoxia and/or impaired ventilation with hypercapnia, leading to severe hypoxemia and rapid deterioration. Two main types of respiratory failure:

• Type I respiratory failure (non-hypercapniec respiratory failure)
  • Primarily from failure of oxygenation (PaO2 <60mmHg)
  • Normal or low CO2
  • pH 7.5
  • Usually responds to Oxygen therapy
• Type II respiratory failure (hypercapniec respiratory failure)
  • Increased CO2 (PaCO2 >50mmHg)
  • Normal or low O2
  • pH <7.3
  • Failure of ventilation as well as oxygenation
  • Requires ventilator support as well as supplemtntal oxygen

Aetiology and Risk Factors

Clinical Manifestation

Clinical Presentation

Increased work of breathing

• Increased RR
• Use of accessory muscles
• Tracheal tug
• Abdominal recession
• Increased HR
• Sweating or clammy skin
• Anxiety or agitation
• Exhaution and confusion
• *Other signs and symptoms depending on cause

Signs of Hypoxia

• Cyanosis
• Low O2
• Arrthymia (from hypoxia)
• Anxiety, agitation
• Acidosis (tissue hypoxia)

Hypoventilation

• Vasodilation
• Headache, fatigue
• Asterixis
• Acidosis

Obstruction

• Inability to speak
• Accumulation of secretion

Treatment

Acute Management

• Oxygenation in all hypoxic patients
  • Nasal prongs
  • Simple Mask
  • Venturi mask
• Monitor and regular ABG
• Treat underlying cause
  • Bronchodilators – if bronchoconstriction
  • Antibiotics – if infection
  • Diuretics – if fluid overload

Ongoing Management If CO2 still increasing or O2 saturation is not improving (>88%) in order:

• Non-invasive mechanical ventilation
  • Bag-valve-mask
  • CPAP/PEEP
  • BiPAP – if CO2 continuous to increase (Type II Respiratory Failure)
• Invasive mechanical ventilation
  • Endotracheal Tube
  • Tracheostomy

Respiratory Failure Type I

Overview 

Hypoxaemia (PaO2<60mmHg) without hypercapnia. Caused by conditions affecting oxygenation: right-to-left shunts or V/Q mismatch.

Pathophysiology

• V/Q mismatch
  • Pneumonia
  • ARDS
  • Interstitial Lung disease
  • PE
  • Pneumothorax
• Right-to-left shunt
  • Physiological: Pneumonia, acute pulmonary oedema, atelectasis
  • Anatomical: intra-cardiac shunts (VSD, ASD), pulmonary AVM
• Low inspired O2 partial pressure (FiO2)
  • High altitude
• Diffusion impairment
  • Interstitial lung disease – Restrictive
  • Acute pulmonary oedema
  • ARDS
• Hypoventilation
  • Obesity

Management

• Oxygenation (non-invasive)
  • Nasal prongs
  • Simple Mask
  • Venturi mask
• Treat underlying cause
  • Ventalin – if asthma or COPD to reduce bronchoconstriction
  • Antibiotics – if infection
  • Diuretics – if fluid overload
• Monitor clinically and with ABG
• Non-invasive mechanical ventilation
  • CPAP/PEEP
    • Maintain recruitment of collapsed lung
    • Increased functional residual capacity
    • Minimise intrapulmonary shunt
  • BiPAP
• Invasive mechanical ventilation – if not improving
  • Endotracheal Intubation
  • Tracheostomy Tube

Respiratory Failure Type II

Overview 

Hypoxaemia with hypercapnia (PaCO2>50mmHg).

Clinical Presentation

• Increased work of breathing
  • ↑RR
  • Use of accessory muscles
  • Tracheal tug
  • Abdominal recession
  • Increased HR
  • Sweating or clammy skin
  • Anxiety or agitation
  • Exhaution and confusion
  • *Other signs and symptoms depending on cause
• Hypoxaemia
  • Altered mental state
  • Dyspnoea
  • Confusion
  • Cyanosis
• Hypercapnia:
  • Mild & moderate: dyspnoea, daytime sluggishness, hypersomnolence, delirium, paranoia, confusion, coma
  • Severe: asterixis, myoclonus, seizures, papilloedema

Pathophysiology – Hypercapnia when alveolar ventilation insufficient to excrete volume of CO2 produced by tissue metabolism due to:

• Decreased minute ventilation
  • COPD
  • Asthma
  • Heart failure
  • Neurological causes
  • Kyphoscoliosis
  • Obesity
• Increase in dead space ventilation
• Increased CO2 production
  • Fever, sepsis, seizure, acidosis, carbohydrate load

• Oxygenation (non-invasive)
  • Nasal prongs
  • Simple Mask
  • Venturi mask
• Treat underlying cause
  • Ventalin – if asthma or COPD to reduce bronchospasm
  • Antibiotics – if infection
  • Diuretics – if fluid overload
• Monitor clinically and with ABG
• Non-invasive mechanical ventilation
  • BiPAP
• Invasive mechanical ventilation – if not improving
  • Intubation

Acute Respiratory Distress Syndrome

Overview 

ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue. Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage.

More Information on Acute Respiratory Distress Syndrome 

Lung Transplantation

Overview

Contraindications

Relative

• Diabetes
• Osteoporosis
• Alcohol excess
• Still smoking
• Likely compliance problems
• Atypical mycobacterial colonization of lungs
• Weight (over and under)

Absolute

• HIV
• Hepatitis B
• Hepatitis C
• Liver disease
• Malignancy
• Other organ failure

Ventilator setting

Intermittant Mandatory Ventilation: Patient Paralysed/Sedation [No spontaneous effort]

Volume Control Ventilation

• Fraction inspired oxygen (FiO2) – initially 100% then wean to maintain SaO2 90 – 94% and/or PaO2 60mmHg – 90mmHg
• Respiratory Rate – 12-14 (higher rate for patient with increased metabolic demand/severe metabolic acidosis (require higher minute ventilation therefore higher RR)
• Tidal Volume – 5-8mls/kg
• PEEP – 5cm H2O
• Airway Pressure [Limit alarm]– 35mmHg

Pressure Control Ventilation

• Airway Pressure Alarm – 30mmHg
• PEEP – 5cmH20
• Inspiratory Pressure – adjust to achieve desired tidal volume, normally between 5-15mmHg
• FiO2 – 100% initially then wean as above
• Respiratory rate