A 40 year old female presents to the Emergency Department with acute onset breathlessness, palpitations and haemoptysis. She is in acute respiratory distress and an ICU review is requested as she remains hypoxaemic on high-flow oxygen.
Initial observations are:
– Respiratory rate: 34 breaths/minute
– SpO2: 76% on 15L/min O2 through a non-rebreathe mask
– Blood Pressure: 147/105 mmHg
– Heart Rate: 48 beats/minute (sinus)
– Temperature: 36.0˚C
You note a past medical history of anxiety, for which she has taken mirtazapine 15mg OD for several years. There are no known allergies.
On reviewing the notes you notice the patient presented similarly to the Emergency Department 2 weeks previously. On that occasion she experienced acute onset of dyspnoea with accompanying palpitations and a headache. A CXR at that time was undertaken and reported as normal and a CTPA excluded the possibility of a PE. On that occasion the presentation was attributed to worsening anxiety. As a consequence the GP has recently started propranolol 40mg BD to control the somatic symptoms of anxiety.
On examining today’s blood results you notice a mild Acute Kidney Injury (Creatinine 146umol/L, eGFR 67) and a raised venous lactate at 7.0 mmol/L. White cell count is within the normal range and CRP is 1.
A chest X-Ray on this presentation has been taken and reported as “confluent airspace shadowing of both lung fields with predominance in the perihilar regions and lower zones. Given the acute presentation atypical infection or pulmonary oedema should be considered.”
The patient is admitted to the high dependency unit for a trial of CPAP and an arterial line is inserted. Hypoxaemia steadily improves and FiO2 reduces to 40%. However without provocation the invasive blood pressure climbs abruptly to a peak of 220/130mmHg (MAP of 160mmHg).
