Abstract

The patient was a twenty-five-year-old male individual, who suddenly started feeling faint and malaise at fainted on February 18th, 2009. He was taken to the medical emergency service of the local hospital by family members approximately one hour after symptom onset. The patient was previously healthy and asymptomatic. There was no history of hypertension, diabetes, dyslipidemia, heart disease or use of illegal drugs. At physical examination the patient had lowered level of consciousness, 60/50 mmHg blood pressure, heart rate (HR) of 150 beats per minute (bpm), no palpable pulses in the upper limbs and symmetrical pulses in the lower limbs. Several tests were performed on the day of hospital admission. The electrocardiogram (ECG) showed sinus tachycardia, with a HR of 150 bpm, PR interval of 120 ms, QRS duration of 80 ms (Figure 1). Chest radiography showed cardiomegaly, mediastinal enlargement and clear pulmonary fields (Figure 2). The transthoracic echocardiography showed dissection of the ascending aorta with cardiac tamponade (compression of the right atrium). Figure 1 Resting electrocardiogram showing sinus tachycardia. Figure 2 Chest radiography showing cardiomegaly, mediastinal enlargement and clear pulmonary fields. Laboratory assessment showed hemoglobin of 14.2 g/dL, hematocrit 42.9%, leukocytes 12,400/mm3 (78% neutrophils, 2% eosinophils, 14% lymphocytes and 6% monocytes), platelets 202.000/mm3, urea 30.5 mg/dL, creatinine 1.2 mg/dL, potassium 3.8 mEq / L, sodium 146 mEq/L, glucose 132 mg/dL, alkaline phosphatase 46 IU/L, gamma-glutamyl transpeptidase 37 IU/L, aspartate aminotransferase 21 IU/L and alanine aminotransferase 34 IU/L. Due to the patient's clinical instability, tracheal intubation for ventilatory support was required, as well as volemic expansion with 0.9% saline solution and a vasoactive drug (norepinephrine) to elevate blood pressure. After volume expansion and noradrenaline administration, blood pressure increased to 126/40 mmHg, with a heart rate of 135 bpm, and due to the severity of the clinical picture, his transfer to the Emergency Department of Instituto do Coracao (InCor) was requested in the same evening. Upon admission to InCor on February 19, 2009, the patient was sedated, assisted by mechanical ventilation and with pallor (++/6). The cardiorespiratory examination, showed a heart rate of 110 bpm, blood pressure 110/70 mmHg, normal pulmonary auscultation; however, cardiac auscultation showed muffled heart sounds (no accessory heart sounds, murmurs or pericardial friction rubs were identified). Abdominal examination was normal and there were no arterial pulses in the upper limbs, with bilateral cyanosis in the fingers. The arterial pulses were palpable and symmetrical in the lower limbs. The laboratory assessment performed on February 19, 2009 showed: hemoglobin of 17.1 g / dL, hematocrit 54%, 26,900/mm 3 leukocytes (1% rods, 84% segmented neutrophils, 7% lymphocytes and 8% monocytes), 107.000/mm 3 platelets, urea 39 mg/dL, creatinine 2.6 mg/dL (glomerular filtration, 32 mL/min/1.73m2), sodium 134 mEq/L, potassium 4.9 mEq/L, lactate 33 mg/dL, prothrombin time (International Normalized Index, INR) of 3.8 and activated partial thromboplastin time ratio of 1.53. Arterial blood gas analysis showed a pH of 7.22, partial pressure of Carbon Dioxide (pCO2) of 32.9 mmHg, partial pressure of oxygen (pO2) of 206 mm Hg, O2 saturation of 99.9%, bicarbonate 13 mEq/L and excess of base (-) of 13.7 mEq/L. The ECG was suggestive of electrical alternans (Figure 3). Figure 3 Resting electrocardiogram showing electrical alternans. Transesophageal echocardiography showed left ventricular hypertrophy with normal systolic function and a 62-mm aneurysmal dilation in the ascending aorta with the dissection lamina starting 1.7 cm from the valve. The dissection extended up after the aortic arch and affected the innominate artery, the left common carotid artery and the left subclavian artery. Severe aortic valve regurgitation and large pericardial effusion were also observed, with signs of right ventricular restriction to diastolic inflow. Surgical treatment of the aortic dissection was indicated; however, the patient had bradycardia in the perioperative period, followed by asystole unresponsive to resuscitation maneuvers and died.

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