Respiratory Failure

• Respiratory failure is defined as inadequate gas exchange due to malfunction of one or more components of the respiratory system.

Respiratory failure means:

• Hypoxaemia – P0₂ <60 mmHg, or y Hypercarbia – PC0₂ >45 mmHg.
• So, respiratory failure may be hypoxaemic, hypercarbic or combined.

• Hypoxemic

  • respiratory failure is defined by arterial O₂ saturation <90% while receiving an inspired O₂ fraction >0.6.
  • Acute hypoxemic respiratory failure can result from pneumonia, pulmonary edema (cardiogenic or noncardiogenic), and alveolar hemorrhage. Hypoxemia results from ventilation-perfusion mismatch and intrapulmonary shunting.

• Hypercarbic

  • respiratory failure is characterized by respiratory acidosis with pH <7.30. Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space.

Respiratory Failure Causes Clinical Features with Management

Respiratory failure may be acute or chronic.

• Acute respiratory failure is sudden and life-threatening.
• Chronic respiratory failure occurs gradually and compensation and adaptations in various organ sys­tems occur ..
• Respiratory insufficiency means that there is a compensated state in a patient with respiratory dis­ease and impaired function.

Four different types of respiratory failure can be present:

• Type I:
  • There is acute hypoxemic respiratory failure. d” There is alveolar congestion.
  • Ex. Pulmonary oedema, pneumonia, lung injury,
• Type II —
  • there is hypercarbia
  • it is seen in bronchial asthma, pneumothorex, drug overdose,
  • brain stem injury,hypothyroidism,
  • sleep disorders, myasthenia gravis,
  • GB syndrome, myopathy etc.
• Type III :
  • This is due to lung collapse.
  • It is also called perioperative respiratory failure.
• Type IV:
  • This occurs in shock due to hypoperfusion of res­piratory muscles.

^aOpen lung ventilation (OLV) involves the use of any of these specific modes with tidal volumes (or applied pressures) to achieve 5—6 mL/kg, and positive end-expiratory pressures achieve maximal alveolar recruitment. ^b FIo₂ is usually set to 1.0 initially, unless there is a specific clinical indication to minimize FIo₂, such as history of chemotherapy with bleomycin. Once adequate oxygenation is documented by blood gas analysis, FIo₂ should be decreased in decrements of 0.1—0.2 as tolerated, until the lowest FIo₂ required for an Sao₂ >90% is achieved. Abbreviations: f, frequency; I/E, inspiration/expiration; FIo₂, inspired O₂; PEEP, positive end-expiratory pressure; for ventilator modes, see text; Vt, tidal ventilation.

Causes of respiratory failure:

• Nervous system

  • The medulla and its neural pathways control res­piration. Dysfunction of this pathway results in central apnoea.

•  Muscles of respiration

   

  • The dia hr m, the intercostal muscles, su­prasternal, sternoCleidomastoid and other small muscles are responsible for the motor part ‘Of respiration. Muscle paralysis results in respira­tory failure.

• Airways

  • If there is obstruction of air passages – ~ airways, bronchi or alveoli, then due to airway system sfunction, there can be respiratory failure.

• Alveolar system

  • In colla se of lung, congestion, injury, there is alveolar system dysfunction. –

• Vasculature

  • The pulmonary vasculature, if diseased, can lead to respiratory failure.

Clinical Features of respiratory failure

• Upper airway should be checked. There may be cen­tral or peripheral ganosis. Respirator .related deth and pattern of respiration ma be altered.
• There may be flarin of nostrils ursed li s use of accessory muscles of respiration.
• Oxygen and CO₂ in arterial blood is estimated by ar­terial blood gas analysis. Pulse oximetry is done.
• To assess which part of the respiratory system is re­sponsible for the respiratory failure, the folloWing table is useful:

 Nervous system

• Respiratory rate is < 12jmin., with hypoxia,hypercarbia and acidemia.

 Muscular dysfunction

• The vital capacity is < 10 ml/kg and inspiratory force is < -20 cm H₂0.
• There is presence of paradoxical respiratory motion.

 Airway dysfunction

• There is wheezing or ronchi and raw airway re­~istance > 10 cm H₂0/ L /sec.

Alveolar disease

• There is consolidation of lungs. PaC0₂ is elevated. Chest x-ray shows infiltrates.

Pulmonary vascular disease

• JVP is raised. ECG shows RVH with strain p~t- tern or RBBB.

Management of Respiratory Failure

• General care of mechanically ventilated pts is reviewed along with weaning from mechanical ventilation. A cuffed endotracheal tube is often used to provide positive pressure ventilation with conditioned gas
• Airway protection, oxygenation, and ventilation is provided.
• Supplemental oxygen is given.
• Noninvasive positive pressure ventilation (NPPV) refers to positive pressure ventilation delivered through a noninvasive interface (nasal mask, facemask, or nasal plugs), rather than an invasive interface (endotracheal tube, tracheostomy).
• Airway is opened with head tilt – chin lift ma­neuver, foreign body removed.
• After an endotracheal tube has been in place for an extended period of time, tracheostomy should be considered, primarily to improve pt comfort and management of respiratory secretions.
• Suction is done for vomit or blood. Tracheostomy may be required.
• Adequate oxygenation – 100% oxygen is given. Artificial ventilation/Mechanical ventilation, if required, is started.
• Endotracheal intubation may be done for me­chanical ventilation.
• PEEP is given in patients with mechanical venti­lation.
• In some circumstances, noninvasive positive pressure ventilation (NPPV) delivered through a tightly fitting nasal or full facemask should be considered for treatment of impending respiratory failure
• Cause of respiratory failure assessed. Treat infections.
• Anti-inflammatory or immuno-suppressive drugs are given.
• Bronchodilators.
• Anticoagulants or thrombolytics. Diuretics.

Triggering —

• Ventilators can be triggered by a change in alveolar pressure (ie, pressure triggered) or flow (ie, flow triggered)
• The trigger sensitivity is usually set at -1 to -2 cmH2O when pressure triggering is used.
• The trigger sensitivity is usually set at 2 L/min when flow triggering is used.

Auto-PEEP —

• Intrinsic positive end-expiratory pressure (ie, intrinsic PEEP or auto-PEEP) can be measured in a relaxed patient by occluding the expiratory port of the ventilator circuit