A woman in her forties with chest pain and life-threatening bradycardia

The patient was a woman in her forties with known Crohn's disease, chronic pain and short bowel syndrome following repeated surgery for stenoses. Her remaining small bowel length was 170 cm, and she had also undergone resection of the sigmoid colon following spontaneous perforation. Her Crohn's disease had been highly refractory to treatment and had not responded to treatment with anti-tumour necrosis factor (TNF) agents or interleukin inhibitors. She was now being treated with budesonide tablets 9 mg once daily, subcutaneous methotrexate 25 mg once weekly and intravenous vedolizumab 300 mg once every 8 weeks. She was also taking pain relief in the form of oxycodone tablets 30 mg in the early morning, 25 mg mid-morning and 30 mg in the evening, paracetamol tablets 1 g four times daily and amitriptyline tablets 25 mg once daily in the evening. She had several previous admissions for severe hypokalaemia secondary to short bowel syndrome and required high-dose potassium supplementation. At the time in question, she was taking potassium chloride tablets 4.5 g four times daily. She was also taking loperamide tablets 2 mg as required for loose stools and desogestrel 75 µg once daily for contraception.

The patient had been feeling increasingly unwell and nauseous for 2–3 days, but on the day of admission she had developed chest pain radiating to the left arm and dyspnoea. She then telephoned the local emergency medical communication centre. When the ambulance came, she had oxygen saturation of 88 %, pulse 34 bpm, blood pressure 98/51 mmHg and respiratory rate 24 breaths per minute. Her skin was pale and clammy, and her radial pulse was not palpable, but she was awake and talking in full sentences.

A pre-hospital ECG was taken, which was sent to the local hospital for interpretation (Figure 1). The ambulance team was informed that the patient had a probable ST-elevation myocardial infarction and that the plan should be to transport her to the university hospital if she was clinically stable. In the meantime, the patient's condition had declined. She developed bradycardia with a pulse of 17 bpm recorded on the ECG monitor, and her level of consciousness was decreasing. The ambulance team assessed that she was not stable enough to be transported to a centre for percutaneous coronary intervention (PCI), and therefore she was taken directly to the local hospital.

The patient arrived in the Emergency Department and was received by the medical team. She was cyanotic, had a respiratory rate of 8 breaths per minute and oxygen saturation of 75 % despite 12 litres of oxygen through a non-rebreather mask. It was noted that she was emptying the whole reservoir with every breath. Initially, her blood pressure was not measurable, with the best pulse being a weak pulse in the groin. She was no longer responsive and scored 6–7 on the Glasgow Coma Scale (GCS). ECG revealed severe bradycardia, a heart rate of 23 bpm, absent P waves and extreme widening of the QRS complex (Figure 2).

Focused echocardiography did not reveal decreased regional cardiac muscle motion (hypokinesia), reduced global function or any other signs of acute myocardial infarction. However, it did find clear flattening of the dividing wall between the right and left ventricles (septal flattening), which raised suspicion of increased right ventricular pressure, referred to as right heart strain.

Following repeated attempts, it was not possible to insert peripheral venous catheters or take blood gases from the radial artery. Therefore, blood gases were taken from the femoral artery. Analysis found pH 7.22 (reference range 7.35–7.45), pCO₂ 3.5 kPa (4.7–5.9), pO₂ 8.6 kPa (11.0–14.4), base excess (BE) −15.9 mmol/L (−3 to 3), HCO₃^- 10.3 mmol/L (22–26), sodium 134 mmol/L (137–145), potassium 10.6 mmol/L (3.6–4.7), chloride 123 mmol/L (98–110), glucose 25 mmol/L (4.2–6.3), lactate 6.8 mmol/L (0.0–2.0). The patient's potassium levels were confirmed in a follow-up blood gas analysis.

The patient received high-dose nebulised terbutaline 5 mg. At the same time, a triple lumen central venous catheter was inserted, as well as an arterial cannula in the groin. Once these lines had been established, 20 ml calcium gluconate (4.5 mmol calcium) was immediately administered intravenously. Within the space of a few minutes, the patient's pulse increased to 40 bpm and QRS width decreased.

The patient was administered repeated doses of calcium gluconate 10 ml (2.25 mmol calcium), totalling 80 ml. She was also administered fluid resuscitation with 6 litres of fluids in total, with the aim of achieving systolic blood pressure > 100 mmHg. Sodium chloride 0.9 % was administered initially, switching rapidly to 1000 mL glucose 5 % mixed with 20 IU insulin aspart. Her respiratory rate increased to 21 breaths per minute, and her O₂ saturation rose to 89 % on 12 litres of O₂. Follow-up blood gases after 30 minutes found pO₂ increased to 9.8 kPa, potassium decreased to 8.8 mmol/L, but also glucose increased to 33 mmol/L, lactate increased to 8.2 mmol/L and pH decreased to 7.06. Therefore, the patient was administered an infusion of 1000 mL sodium bicarbonate 167 mmol/L over 30 minutes.

One hour after the patient's arrival in the Emergency Department, her pulse was increasing, pH had increased to 7.21 and lactate levels had fallen to 3.3 mmol/L. Two hours after arrival, she was transferred to the intensive care unit. She was stable, awake and breathing for herself at that time. She had sinus rhythm of 90–100 bpm, adequate blood pressure, potassium of 5.9 mmol/l and pH had almost normalised (7.29).

Twelve hours after arrival, her glucose levels had returned to normal (5.4 mmol/L) and remained within the normal range for the entire hospital admission with no need for insulin administration. Venous blood tests found leukocytes 28.3 × 10⁹/L (3.5–11), CRP 3 mg/L (< 5), creatinine 80 µmol/L (45–90), with estimated glomerular filtration rate (GFR) of 79 mL/min/1.73 m² (> 70). Phosphate levels were 0.60 mmol/L (0.85–1.50), urea 2.8 mmol/L (2.6–6.4) and HbA_1c 38 mmol/mol (27–42).

Repeat echocardiography revealed regression of right heart strain. A chest CT was performed, which confirmed that there was no pulmonary embolism. A dialysis catheter was placed in the patient's right internal jugular vein and continuous haemodialysis took place overnight.

The woman was transferred to a general ward after 24 hours. At that time, she had normal potassium levels of 4.5 mmol/L. She had no neurological sequelae and no symptoms other than fatigue. Potassium supplementation was resumed at a lower dose, potassium chloride tablets 750 mg four times daily for the first 24 hours, followed by 1.5 g four times daily afterwards. The patient was discharged three days later with stable potassium levels.

The patient was able to report that she had struggled with loose stools for a long time and had therefore started to take loperamide 2 mg capsules on her own initiative. Previously, she had only taken these occasionally and not regularly. These were effective in firming stools. Since loperamide works by prolonging intestinal transit time, the absorption of potassium was improved at the same time. When she eventually noticed muscular weakness, malaise and nausea, she suspected this was caused by hypokalaemia, a condition she had experienced several times before. She later admitted that her symptoms did differ slightly from previous episodes of hypokalaemia, but they were similar enough that she misinterpreted the symptoms. She had never had symptomatic hyperkalaemia before. Therefore, on her own initiative, she had started to increase her potassium intake. As her symptoms increased, she continued to increase the doses. This led to a vicious cycle of rapidly increasing potassium levels.

Following discharge, the patient was followed up by her general practitioner with measurement of potassium levels three times a week. There is an agreement with the hospital laboratory that any abnormal potassium levels will be reported by telephone to the general practitioner or the internal medicine specialist on duty if the general practitioner is not available. Furthermore, she is free to return to the Emergency Department for potassium measurement if she notices symptoms of potassium imbalance.