This case highlights the unusual Doppler finding of a systolic and diastolic antegrade gradient in severe RVOT obstruction and the high risk of fatal hemodynamic collapse when initiating positive pressure ventilation in such patients.
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Intubation may precipitate fatal collapse in severe RVOT obstruction; one case leaves open generalizability of systolic-diastolic gradients.
A 57-year-old male presented with dyspnoea, cough, and weight loss for a month. He was in mild respiratory distress and had BP of 90/60 mmHg and heart rate of 130 bpm. CT scan of the chest showed large mediastinal mass compressing the main pulmonary artery, large pericardial effusion, and no pulmonary embolism (Panel A). His BP dropped to 60/30 mmHg, which responded to fluid challenge. Considering impending clinical cardiac tamponade, 330 cm3 straw colour fluid was drained under transthoracic echocardiogram (TTE) guidance. Right ventricular outflow tract (RVOT) obstruction caused by extrinsic mass was found (Panels B and C and see Supplementary data online,Supplementary Data) with a peak RVOT velocity of 3.3 m/s and gradient of 43 mmHg. There was systolic and diastolic antegrade gradient (peaked at the atrial contraction, red arrow) across the RVOT obstruction, indicating significantly higher pressures in the proximal right ventricular (RV) chamber in systole and diastole avoiding chamber collapse (Panels B and D, see Supplementary data online,Supplementary Data). Following excision biopsy of the lymph node, patient was hypoxic and therefore intubated. Soon after intubation he had asystolic cardiac arrest and could not be resuscitated. Our case highlights the complex physiology of a patient with RVOT obstruction secondary to a mass, which was found to be a lymphoma on the biopsy. TTE did not reveal classic tamponade physiology of chamber collapse, but there were respiratory variations of ≥25% on tricuspid inflows only (Panels E and F). Positive pressure ventilation in the presence of RV obstruction caused reduced venous return and preload as well as an increase in the afterload with eventual cardiogenic shock and cardiac arrest. However, a sudden increase in the vagal tone during the procedure and vasodilatation due to general anaesthesia could also be potential causes of his cardiac arrest. Conflict of interest: none declared. Supplementary data are available at European Heart Journal – Cardiovascular Imaging online.
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Mirrani et al. (2014) studied this question.
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