A man in his sixties with acute dyspnoea, chest pain and syncope

A man in his sixties with inflammatory bowel disease and myopathy treated with prednisolone called for an ambulance during the night due to acute worsening of dyspnoea. He had been short of breath 3–4 weeks beforehand, but experienced a considerable worsening during the night in question. He fainted twice before he called for help. When the ambulance arrived, he reported pain throughout his body, including severe central chest pain.

The patient had central cyanosis, with SpO₂ of 70 % without oxygen, increasing to 93 % with 12 litres of oxygen through a mask with a reservoir. His blood pressure was 115/70 mmHg, and his pulse fluctuated between 130 bpm and 145 bpm.

While transporting the patient to hospital, the ambulance sent an ECG to the cardiology department for prehospital assessment (Figure 1). The ECG revealed sinus tachycardia at a rate of 143 bpm, increased P-wave amplitude in leads II and III consistent with P pulmonale, slight ST elevation in leads V1 and aVR, and ST depression in V4–V6, II, III and aVF.

Ambulance staff sent another ECG 25 minutes later (Figure 2), which revealed atrial fibrillation with a heart rate of 120 bpm, widened QRS complex with right bundle branch block pattern and T-wave inversion in III and V1–V3.

The patient was received by a medical team shortly after the last ECG arrived. He was awake and responded appropriately to questioning. In the initial examination, he had patent airways. His oxygen saturation was 100 % with 12 litres of O₂ and his respiratory rate was 17 breaths per minute. Clear lung sounds were heard on auscultation. His skin was cold and clammy with no peripheral pulses, but with palpable pulses in the groin bilaterally. His blood pressure measured using an arterial line was 50/30 mmHg. The patient monitor showed sinus tachycardia with heart rate of 120 bpm and a QRS configuration associated with right bundle branch block. The patient was afebrile with a temperature of 37.0 °C. Arterial blood gases taken with 12 litres of supplemental oxygen found pH 7.36 (reference range 7.35–7.45), pCO₂ 4.45 kPa (4.7–5.9), pO₂ 13.8 kPa (11.1–14.4) and lactate 4.6 mmol/L (0–2.5).

Screening echocardiography revealed considerable right ventricular dilation; the diameter of the right ventricle (RV) was larger than that of the left ventricle (LV), with an RV/LV ratio of 1.3. A normal ratio is 0.66, and anything over 1.0 is clearly abnormal (1). The right ventricle appeared to have reduced long axis function with TAPSE (tricuspid annular plane excursion) measured at 10 mm (normal > 17). A large flapping mass was observed in the right atrium, which raised suspicion of a thrombus in transit (Figure 3, video). The left ventricle had decreased septal contractility and was compressed by the dilated right heart chambers. Doppler assessments were consistent with underfilling of the left ventricle. The diameter of the ascending aorta was normal, but aortic regurgitation was found, which was hard to grade in the emergency situation.

After a team discussion, 5000 IU heparin was administered intravenously ten minutes after the patient arrived in the emergency department, in accordance with local and international guidelines (2). To increase the patient's blood pressure, 0.01 mg adrenaline was administered intravenously, and a noradrenaline infusion was started at an infusion rate of 0.3 µg/kg/min. An interventional radiologist and radiographer were also called.

The patient was awake and lucid, his respiratory status was stable, but haemodynamic instability persisted following administration of heparin and initiation of a vasopressor. The patient was transported to the radiology department connected to a defibrillator and with alteplase prepared for intravenous administration.

A chest CT scan with pulmonary embolism protocol revealed a saddle embolism, with thrombi in most of the major pulmonary arteries and involvement of all lobes of the lungs at a lobar and segmental level (Figures 4 and 5). The largest impact was in the lower lobes. Aortic dissection was not detected.

A bolus dose of 10 mg intravenous alteplase was administered immediately once the diagnosis of pulmonary embolism had been verified and aortic dissection ruled out, approximately 40 minutes after arrival of the patient in hospital. A maintenance dose of 90 mg alteplase was then started.

In the cardiac intensive care unit, the patient had persistent dyspnoea, severe chest pain and mean arterial pressure (MAP) of approximately 45 mmHg despite the alteplase infusion, titration of noradrenaline up to 0.40 µg/kg/min and initiation of vasopressin at an infusion rate of 0.03 IU/min. Due to haemodynamic instability, repeated doses of dilute adrenaline were administered to prevent further decompensation.

Under local anaesthetic, ultrasound-guided puncture of the common femoral artery was performed, and an angled pigtail catheter was advanced via the inferior vena cava through the right heart chambers to the pulmonary artery (Figure 6). Mean pulmonary artery pressure at the start of the procedure was 37–39 mmHg (<20 mmHg). The thrombectomy device used was the FlowTriever (Inari Medical). Thrombi were aspirated from the vasculature of both lungs using 24 Fr and 16 Fr catheters (Figure 7). In total, ten aspirations were performed.

Blood loss was estimated to be 50–80 ml in total. The patient's systemic pressure rose immediately following aspiration of the thrombi, and the vasopressor treatment could be tapered. Vasopressin was discontinued and the noradrenaline infusion reduced to 0.02 µg/kg/min. There was a rapid objective and subjective improvement in observed dyspnoea. At the end of the procedure, mean pulmonary artery pressure was 19–20 mmHg. Angiography demonstrated acceptable and rapid filling in the major segments of the lungs bilaterally.

Following the procedure, the patient was transferred back to the cardiac intensive care unit. A heparin infusion was started at 1320 IU/hour as further anticoagulant therapy. The infusion rate was guided by the activated partial thromboplastin time (APTT) (reference range 1.5 × baseline value). Clinically, the patient was not in pain at this time, and there was no objective or subjective dyspnoea. SpO₂ was 97 % on 1 litre of oxygen through nasal canula. His skin was dry and warm. His blood pressure rose to 111/62 mmHg as the vasopressor was tapered.

The results of laboratory tests taken on arrival were ready after the intervention, with findings of elevated troponin T at 284 ng/l (0–15) and NT-proBNP at 1571 ng/L (<210).

The following day, the patient had improved, and vasopressor treatment could be discontinued. The patient's anticoagulant therapy was switched to subcutaneous dalteparin (100 U/kg twice daily) since it was considered unlikely that thrombolysis with alteplase would be required again.

Echocardiography follow-up the day after admission found normalised cardiac function and normal dimensions of both ventricles. Pulmonary artery systolic pressure was calculated to be 31 mmHg, which is considered normal. The patient was transferred to the haematology ward and discharged after a total of five days in hospital. He should continue oral anticoagulation with rivaroxaban 20 mg once daily for the first six months, followed by 10 mg once daily indefinitely.