• This is type 1 respiratory failure. The PO2 is low with a low CO2.
• The accompanying alkalosis is a response, due to the patient blowing off CO2 due to her likely high respiratory rate.

• The differential diagnosis in this case is:
  • Pulmonary embolus (PE)
  • Pneumonia
  • Asthma
  • Pulmonary oedema
  • Pneumothorax
  • Severe atelectasis

• Look at the patient!
  • Acutely unwell: ABCDE and call for help
• Check the observations
  • All of these conditions can may you tachypnoeic and tachycardic. Wheeze will predominate in asthma. Pyrexia points more towards pneumonia (but PE can give a mild pyrexia). Pulmonary embolus will be the only condition that will likely be normal on auscultation.
• Take a full history and examination
  • Sudden onset: more likely PE
  • Purulent cough: more likely pneumonia
  • Raised JVP, ankle swelling, fine basal creps: more likely oedema
• Investigations
  • CXR
  • Bloods
  • Cultures if pyrexial
• Management (depends on cause)
  • PE: Heparinisation or thrombolysis if unstable. Remember this patient is post-op so it is a complex decision.
  • Pneumonia: Antibiotics for hospital acquired pneumonia
  • Asthma: Salbutamol, ipatropium and steroid in the first instance
  • Pulmonary oedema: Sit patient up, furosemide, consider catheter

See relevant pages in the respiratory section for further information.

•  This is a compensated respiratory acidosis.
  • This does not represent acute pathology.
  • Rather it reflects a compensation for a chronic respiratory acidosis secondary to chronic pulmonary disease.
  • Note this is an acidosis, not an acidaemia (pH normal, but only due to compensatory mechanisms: the high bicarbonate).

• Nothing acutely as this man does not meet the criteria for long-term oxygen therapy (LTOT).
  • Lifestyle advice and smoking cessation of necessary.
• LTOT criteria are:
  • PaO₂ less than 7.3 kPa when stable.
  • OR…
  • PaO2 greater than 7.3 and less than 8.0 kPa when stable AND with any of:
    • Secondary polycythaemia
    • Peripheral oedema
    • Nocturnal hypoxaemia
    • Pulmonary hypertension

• This is Type 2 respiratory failure. See ABG interpretation for more details.
  • Note that the HCO3 is raised in this patient despite the abnormal pH.
  • With the above history this is likely to represent an acute on chronic respiratory acidosis.
  • This would indicate that the patient normally retains CO2 and has a chronically raised HCO3.
  • The drop in pH represents the normal mechanisms of compensation being over whelmed.
  • This is one of the cases where having an old ABG from a previous admission can be useful.

• Oxygen administration in this group is a complicated issue. 100% oxygen makes subsets of COPD patients retain CO2, decreasing respiratory drive and worsening hypoxia and hypercapnia.
• More information can be found on this page: Prescribing oxygen in COPD patients
• The British Thoracic Society have produced guidelines which give a helpful overview and can be found here.

• This is a respiratory alkalaemia
• Differential diagnosis:
  • Pulmonary disease
  • Hypermetabolic states (e.g. infection or fever)
  • Pain
  • Anxiety hyperventilation

• Based on the history, anxiety hyperventilation is the most likely cause here. However, it is very important to have considered the other options, in particular and to have ruled out a primary respiratory pathology or infection.
• In the anxious patient who is short of breath and persistently tachycardic have you thought of PE?

• The anion gap is the difference between primary measured cations (sodium and potassium) and the primary measured anions(chloride and bicarbonate). It is calculated by subtracting the concentrations of chloride and bicarbonate (anions) from the concentrations of sodium and potassium (cations):
  • Anion gap = ([Na⁺] + [K⁺]) − ([Cl⁻] + [HCO₃⁻])
  • Reference range usually 7–16 mEq/L (but varies between hospitals, some using 3-11)

• Potassium is commonly left out of the equation as potassium concentrations, being very low, usually have little effect on the gap. This leaves the following equation:
  • Anion gap = [Na⁺] − ([Cl^–] + [HCO₃⁻])

 

• Anion gap = ([Na⁺] + [K⁺]) − ([Cl⁻] + [HCO₃⁻]) = 28.5
  • Normal range is 7 – 16.
    • N.B. Some analysers won’t include potassium in their calculations therefore for them >15 constitutes a raised anion gap.
• Either way, this is a raised anion gap metabolic acidosis.

The traditional mnemonic for the causes of a metabolic acidosis with raised anion gap is ‘MUDPILES’:

• Methanol
• Uraemia
• Diabetic ketoacidosis (and alcoholic/starvation ketoacidosis)
• Propylene glycol
• Isoniazid
• Lactate
• Ethylene glycol
• Salicylates

However, another way is to think about the mechanism of acidosis:

• Excess production of acids
  • DKA, lactic acidosis (produced by poorly perfused tissues)
• Ingestion of acids
  • Methanol, ethanol, ethylene glycol
• Inability to clear acids
  • Renal failure

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• Loss of bicarbonate:
  • From the GI tract (diarrhoea or high-output stoma)
  • From the kidneys (renal tubular acidosis)

• This is metabolic alkalaemia

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Differential diagnosis of a metabolic alkalosis or alkalaemia:

• Persistent vomiting
  • E.g. gastric outlet obstruction (the classic example is pyloric stenosis in a baby)
• Hyperaldosteronaemia
• Diuretic use
• Milk alkali syndrome
• Massive transfusion

• This is the classic picture of aspirin overdose.
• There is an initial respiratory alkalosis due to central respiratory centre stimulation causing  increased respiratory drive.
• In the later stages a metabolic acidosis develops along side the respiratory alkalosis as a result of direct effect of the metabolite salicylic acid and more complex disruption of normal cellular metabolism.

How do you manage an aspirin overdose?

Presentation of aspirin overdose

• Hyperventilation
• Sweating
• Nausea & vomiting
• Epigastric pain
• Tinnitus
• Deafness
• ARDS (rare)
• Hypoglycaemia (children in particular)

Investigations in aspirin overdose

• Plasma salicylate concentration (initial and repeats)
• Paracetamol levels (always check in any case of poisoning by anything)
• ABG
• Urea and electrolytes
  • Renal failure (rare) sometimes other electrolyte imbalances
• Chest x-ray
  • If dropping sats or any suspicion of ARDS (non-cardiogenic pulmonary oedema)

Management of aspirin overdose

• ABCDE and supportive care
• Gastric lavage within 1h of ingestion (although no evidence for mortality reduction)
• Activated charcoal
• Correct electrolyte abnormalities
• In mild/moderate cases (plasma concentration 500-700mg/l)
  • Alkalinise urine
    • Give 225ml of 8.4% bicarbonate solution over 1hr
    • Ensure urine pH over 7.5 (use indicator paper)
      • Bicarbonate will increase any pre-existing hypokalaemia – so don’t let it happen
      • Additional boluses of bicarbonate to maintain alkalinisation
        • N.B. Acidosis increases salicylate transfer across the blood brain barrier
  • Monitor U+Es regularly
• In severe cases (plasma concentrations >700mg/l)
  • Haemodialysis

Prognosis in aspirin overdose

• Generally good with treatment.

• This is diabetic ketoacidosis (DKA).

• Priorities for management include fluid resuscitation, insulin administration and careful management of potassium levels. Click here for a page detailing this, and click here for DKA questions 

• This patient has asthma, ongoing difficulty in breathing and a rising CO2 (the fact that it is in the normal range is irrelevant) .
• This is an extremely worrying sign as it shows that the patient is tiring.
• This patient should be managed in a high dependency area and closely monitored for further deterioration.

The management of acute asthma will be found on the respiratory sections of this website.

• Note that despite the low pH the pCO2 is also high.
• This is a picture of a mixed respiratory and metabolic acidosis.
• Given the history of diabetes and ankle swelling, renal failure is a unifying diagnosis with pulmonary oedema contributing to a respiratory acidosis whilst the failure to clear acids causes a metabolic acidosis.