A 26-year-old woman was seen in the emergency department (ED) for chest pain and hypertension.

She was found to have a urinary tract infection and was sent home with an antibiotic and thiazide diuretic.

Two days later, she returned with epigastric pain, nausea, emesis and myalgias.

The patient had no significant medical history and denied cardio-respiratory symptoms; however, she complained of a low exercise tolerance for the last year.

There was no family history of cardiac or pulmonary disease or of sudden cardiac death.

She was born in the USA and had neither travelled recently nor had any sick contacts.

On examination, she was hypertensive (170/105 mm Hg), tachycardic (125 bpm), had dry mucous membranes and appeared ill looking.

She was found to have an elevated serum creatinine of 160 μmol/l (normal 60–110 μmol/l).

After receiving 1.5 l of intravenous fluids for presumed volume depletion and prerenal azotaemia she became short of breath.

Crackles were noted on auscultation of her chest and a portable chest film demonstrated hazy infiltrates that likely represented pulmonary oedema.

She then developed hypotension with systolic pressures in the 90s.

Non-invasive positive pressure ventilation was initiated.

An ECG demonstrated sinus tachycardia with a rate of 130 bpm and minimal ST depression on the precordial leads.

In consultation with a cardiologist, the patient received 40 mg of intravenous furosemide.

An echocardiogram demonstrated global hypokinesis with a left-ventricular ejection fraction <10% (see figure 1).

The patient was transferred to the intensive care unit where she became more anxious and tachycardic to 170 bpm.

She was intubated and sedated.

Despite the placement of a Foley catheter and administration of intravenous loop diuretics, she remained anuric for the first 12 h of hospitalisation.

She developed signs of acute kidney injury with a creatinine that increased to 350 μmol/l within the first 24 h of hospitalisation.

She received norepinephrine and milrinone to improve cardiac output.

On the second day of hospitalisation, she was evaluated by a cardiologist and cardiothoracic surgeon for emergent circulatory support as she had developed signs of poor tissue perfusion with a lactic acidosis (8.4 mmol/l; normal <2.2 mmol/l) and transaminitis with aspartate aminotransferase/alanine transaminase  >150 IU/l (normal <40 U/l).

She was taken to the cardiac catheterisation laboratory for emergent right heart catheterisation and biopsy to exclude acute myocarditis.

Over the next few days, she was gently fluid resuscitated (guided by bioreactance non-invasive cardiac output), the pressors were gradually weaned off and she became non-oliguric.

She slowly regained renal function and organ perfusion improved with resolution of the lactic acidosis and a decrease in liver transaminases.

On hospital day 5 she was transferred to the medical ward and was eventually discharged home on non-selective β blockade, an ACE inhibitor and nitrate with planned follow-up at the heart-failure clinic.

The patient returned to the ED 4 days later with an elevated blood pressure, nausea and abdominal pain.

A contrast scan of her abdomen revealed pancreatitis and an adrenal mass.

During her treatment for pancreatitis she began to have paroxysms of headaches, nausea, emesis and abdominal pain with corresponding hypertension to the 220s systolic and tachycardia to 120s with a baseline systolic pressure of 90–110 mm Hg (see figure 2).

Her urinary and plasma catecholamines were elevated and confirmed on repeat testing.

She was given aggressive fluid rehydration and α and β blockade for a planned adrenalectomy.

Prior to surgery her left-ventricular ejection fraction had improved to 55% on medical management (see figure 1).

Pathology of her adrenal gland was consistent with a non-malignant pheochromocytoma (see figure 3).