Related Subjects: Asthma
|Acute Severe Asthma
|Exacerbation of COPD
|Pulmonary Embolism
|Cardiogenic Pulmonary Oedema
|Pneumothorax
|Tension Pneumothorax
|Fat embolism
|Hyperventilation Syndrome
|Acute Respiratory Distress Syndrome (ARDS)
|Respiratory Failure
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It is quite possible for a patient with COPD to also have a PE. Patients may go from Type 1 to become Type 2 when they tire and hypoventilate or receive sedation. Intubation and ventilation treat both types.
About
- Respiratory failure (PaO₂ < 8 kPa) is a common medical emergency,
- Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination.
- It may be classified as either hypoxaemic with or without hypercapnia.
- Oximeters estimate arterial oxygen saturation are useful in assessment or monitoring.
- Oximeters tell us nothing about Carbon dioxide levels. For that we need an ABG.
Classification:
Types | Oxygen | Carbon Dioxide |
1 | PaO₂ < 8 Kpa | PaCO₂ levels < 6 Kpa. |
2 | PaO₂ < 8 Kpa | PaCO₂ levels > 6 Kpa.
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How much Oxygen should I give
- Normally Patients should have enough oxygen to achieve Sats 94-98%
- In COPD/T2 RF Patients should have enough oxygen to achieve Sats 88-92% and PO₂ > 7 Kpa
- Generally If O₂ sats > 98% then wean back on oxygen
- Generally If O₂ sats < 94% then consider increasing oxygen
- There are always exceptions to this e.g. In COVID we initially changed target to > 90% to conserve oxygen stocks. take advice if unsure.
Causes
- Type 1:Is the commonest form and usually due to alveolar fluid and similar pathologies. Often due to mismatch of ventilation and perfusion in the pulmonary alveolar bed.
- Pulmonary oedema,
- Pulmonary embolism
- ARDS
- Asthma
- Pneumonia
- High altitude
- Upper airways obstruction
- Type 2: It is usually due to ventilatory weakness, sedation or diseases that impair ventilation Hypercapnia causes acidosis for which there is over days a corresponding rise in renal retention of bicarbonate.
- Causes of Type 1 when tired, sedation, hypoventilation
- CNS disease e.g. stroke, tumour
- Exacerbation of COPD
- Pneumonia
- Neuromuscular weakness (Polio, GBS, MND, Spinal muscular atrophy)
- Muscle weakness (Muscular dystrophy, Myotonic dystrophy, Pompe disease)
- Flail chest, Rib#, Kyphoscoliosis
- Obesity, sedation, hypercarbia, alcohol
- Sputum and mucus plugs
Investigations
- Oxygen saturation probe: does not detect CO₂ levels.
- ABG: can tell pH, PO₂, PCO₂, HCO3 and base excess
- ECG: STEMI, AF, S1Q3T3 PE, RV Changes of COPD
- CXR: may show COPD changes, pneumonia, pneumothorax but will not show PE
- CTPA: if T1RF and Wells score suggest possible PE
Management of Type 1 RF
- ABC, High flow oxygen unless suspected COPD - see below
- Make a diagnosis and manage cause
- Diuretics if fluid, Chest drain if PTX, Antibiotics if infection
- Bronchodilators/Steroids if Asthma/COPD
- Thrombolysis/Anticoagulation if PE
- May need CPAP or NIV depending on cause
- May need intubation or ventilation or ECMO
Management of Type 2 RF
- ABC, Controlled Oxygen therapy start with 24% venturi mask aim for PaO₂ > 7 kPa. The goal of treatment in acute on chronic type II respiratory failure is to achieve a PaO₂ (> 7.0 kPa or 52 mmHg) without increasing PaCO₂ and acidosis, while identifying and treating the precipitating condition.
- CO₂ retention is seen with warm dilated peripheries and the patient is sleep and has bounding pulses and may have a flapping tremor
- Often with COPD the patients have prolonged expiration phase and wheeze as well as inflated lungs and intercostal indrawing. lips are pursed to help keep collapsed small airways open
- if there is significant right heart failure then there will be signs of peripheral oedema, raised jugular venous pressure, hepatomegaly, ascites.
- Make a diagnosis and manage cause
- Frequent physiotherapy ± pharyngeal suction if mucus plugs or sputum to expectorate
- COPD+/- Pneumonia: Treat exacerbation if present.
- See other causes of Type 1 which may need addressed
- Noninvasive ventilation and if this fails to work then escalate to ITU
- CPAP nasal or mask: Start at 5 cm H₂O
- BiPAP Nasal or mask: Start at 10 cm H₂O inspiration/5 cm H₂O expiration
- May need intubation or ventilation: Initial ventilator settings:
- FiO₂ 1.0
- Tidal Volume- 6–10 ml/kg
- RR 10 -12
- PEEP- 5 cmH₂O
- Pressure Support - 5 cmH₂O
- ECMO may be considered
- Drug-induced Hypoventilation: consider naloxone for opiates and flumazenil for benzodiazepines if drugs recently taken. May need Naloxone infusion.
Important scenarios to recognise
- Impending Respiratory arrest: HR> 120/min. RR >30. Low BP, Pale and sweaty, agitation, confusion. Rising PaCO₂ or fall in PaO₂. Needing higher FiO₂, rapid desaturation on disconnection from O₂
- Masks may be poorly tolerated leading to Hypoxia in confused patients. It might be best to see if Oxygen via nasal prongs at 1 or 2 L/min is more effective and continuous with less interruptions if it gives a satisfactory PaO₂.
- If a patient has normal PaO₂ on high flow oxygen this is abnormal as you would expect the patient to have a PaO₂ well above the normal range. These needs investigating as high FiO₂ can hide worsening pathology. Patients should have only enough oxygen to achieve Sats 94-98%.
- If a hypoxic asthmatic patient has an ABG with a normal paCO₂ (it should be low) this is a sign that they are tiring or worsening for some other reason and they need urgent ITU review
- A very low PaO₂ in a patient who looks completely well, is not short of breath and has normal O₂ saturations is likely a venous sample
References