An 88-year-old man presented with unilateral right-side tongue swelling, progressing over few hours to the dysphagia and dyspnoea. He denied any trauma, allergies, or consumption of new foods. His past medical history included hyperlipidaemia and arterial hypertension treated with 10 mg Ramipril daily for 10 years. He lived independently mobilizing without aid.

Intramuscular and nebulized adrenaline and intravenous dexamethasone were administered in the emergency department (ED), failing to abort progressive swelling of the airways. Nasal endoscopy by ENT confirmed severe oedema of the tongue and the larynx. Mechanical ventilation was initiated following fiberoptic intubation with the patient developing peri-intubation respiratory arrest. Chest X-ray and transthoracic echocardiography (TTE) performed by the cardiology advanced trainee in the ED confirmed negative pressure pulmonary oedema complicated by acute reverse Takotsubo cardiomyopathy. The patient suffered a brief bradycardic episode, followed by asystolic cardiac arrest on ICU arrival, requiring 7 min of CPR, followed by return to spontaneous circulation. Coronary angiography was performed and was deemed unremarkable. Sinus bradycardia and an unstable hemodynamic state demanded concurrent insertion of atrial pacing wire and intra-aortic balloon pump (IABP). The choice of mechanical circulatory support by IABP was dictated by the desire to avoid the use of inotropes in presence of acute left ventricular failure and arterial hypotension. Stable pacing rhythm and excellent augmentation of pressures by IABP provided stabilization of global perfusion. TTE demonstrated persistent left ventricular failure due to catecholamine induced reverse Takotsubo syndrome (good apical left ventricular (LV) contraction with hypokinesis of basal and mid-LV segments). Mitral valve (MV) had normal function. Levosimendan infusion was started. A diagnosis of angiotensin-converting enzyme inhibitor (ACEI)-induced angioedema was confirmed by the immunologist. The first dose of Icatibant was administered.

Patient became haemodynamically unstable again next morning with systolic blood pressure drop to 60 mmHg. Poor TTE windows and ongoing mechanical ventilatory support resulted in suboptimal echocardiographic imaging. Remaining significant upper airways oedema precluded the use of transoesophageal echocardiography. TTE with ultrasound enhancing agent, performed by the intensive care specialist with advanced echocardiographic training, demonstrated hyperdynamic LV with complete recovery of all segments, indicating resolution of reverse Takotsubo. Narrowing of the LVOT was noted on 2D imaging (Fig. 1). Color Doppler revealed a new posteriorly directed mitral regurgitant jet and flow acceleration within the left ventricular outflow tract (LVOT), confirmed by severe aliasing of Pulse Wave Doppler. Continuous Wave Doppler (CWD) had a typical dagger-shaped systolic flow in LVOT (maximum pressure gradient 125 mmHg– Fig. 2 Panel B) and more round-shaped mitral regurgitant flow (maximum pressure gradient 235 mmHg– Fig. 2 Panel A). Changing IABP augmentation ratio from 1:1 to 1:2 (Fig. 2 Panel C) to 1:3 (Fig. 2 Panel D) resulted in reduction of LVOT velocities from 5.5 m/sec to 1.5 m/sec during non-augmented cardiac cycles, remaining high during augmentation. Progressive analysis of LVOT Doppler velocities during amendments of IABP augmentation ratios, confirmed causation of iatrogenic circulatory compromise and the diagnosis of IABP-induced dynamic left ventricular outflow tract obstruction (DLVOTO) was made. Stopping IABP resulted in rapid haemodynamic stabilization. IABP was removed and Levosimendan was discontinued. TTE next day demonstrated normal biventricular systolic function, absence of DLVOTO and completely resolved mitral incompetence.

Systolic frame of the apical 5-chamber TTE view with administered ultrasound enhancing agent and low mechanical index settings of the scanner. Narrowing of the LVOT is noted (red arrows)

Panel A: Continuous Wave Doppler signal sampled from mitral regurgitant jet during IABP support with the ratio 1:1. It demonstrated a maximum LV/LA pressure gradient of 235 mmHg. Note the MR CW signal is late-systolic

Panel B: Continuous Wave Doppler signal sampled from LVOT during IABP support with the ratio 1:1. It demonstrated a maximum LV/aorta pressure gradient of 125 mmHg. Note the typical dagger-shaped Doppler profile compared to the more rounded shape of the MR jet in panel A

Panel C: Continuous Wave Doppler signal sampled from LVOT during IABP support with the ratio 1:2. Red arrows indicate amended by IABP cardiac cycles with elevated maximum pressure gradient across LVOT. Yellow arrows indicate unamended by IABP every second cardiac cycle with normal pressure gradient across LVOT

Panel D: Continuous Wave Doppler signal sampled from LVOT during IABP support with the ratio 1:3. Yellow arrows indicate two unamended by IABP cardiac cycles with normal pressure gradient across LVOT for each one amended by IABP cycles (red arrows)

C3, C4 and C1-estherase inhibitor levels were normal, but persistent angioedema required two more doses of Icatibant. Airways swelling was finally resolved, and the patient was extubated on day 6. He underwent rehabilitation and was discharged home to independent living.

The lessons from our case are centered around prompt multidisciplinary approach to the treatment of life-threatening angioedema and DLVOTO. This case demonstrates how the initial beneficial effects of IABP may rapidly cause near-fatal iatrogenic complications, when causing DLVOTO. Frequent echocardiographic reassessment of unstable patients with mechanical circulatory support in ICU is essential for successful outcome. Echocardiography is best performed by the intensive care or cardiology trained specialist who has sufficient knowledge, training and the authority to temporarily augment IABP settings to allow dynamic echocardiographic assessment.