On physical examination, blood pressure between arms and legs differed by up to 40 mmHg, with no perceptible delay on femoral pulses. However, she remained hypertensive, requiring quadruple therapy. Emergent cardiac catheterization excluded coronary disease.ĭuring hospitalization, the patient showed a favourable clinical evolution, allowing extubation in the first 12 hours, and progressive improvement of the pulmonary congestion. Transthoracic echocardiography in the emergency room revealed left chamber dilation, aortic root ectasia, a bicuspid aortic valve, global hypokinesia, and moderate depression of left ventricular systolic function.ĭue to the lack of response to medical therapy, orotracheal intubation and ventilatory support were necessary, and the patient was admitted to the cardiac intensive care unit. Admission laboratory studies showed no significant changes, including myocardial necrosis biomarkers. Arterial blood gas analysis revealed uncompensated metabolic acidaemia (pH 6.9, pCO 2 54.5 mmHg, HCO 3− 16.9 mmol/l) with hyperlacticaemia (11.3 mmol/l). The 12-lead electrocardiogram showed sinus tachycardia and a left bundle branch block. The patient was tachycardic with a heart rate of 132 bpm, and showed peripheral oxygen saturation (in room air) of 78%.Ĭardiac auscultation revealed rhythmic, hypophonetic cardiac sounds, while pulmonary auscultation revealed scattered crackles in both lungs, with no peripheral oedema. Systolic blood pressure was up to 200 mmHg and diastolic up to 100 mmHg in both upper limbs. On physical examination, the patient had shortness of breath, a respiratory rate of over 30 breaths per minute, sudoresis, and jugular venous distention at 45°. A 48-year-old female patient with a history of refractory hypertension since an early age and active smoking was admitted to the emergency room with hypertensive acute pulmonary oedema, referred as sudden dyspnoea and oppressive pre-cordial pain of about 2 hours duration.
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