A 64-year-old hypertensive patient treated with atenolol maintained blood pressure levels of 140/85 mm Hg.
The echocardiogram showed good systolic function and left ventricular hypertrophy.
Right hepatic lobectomy was performed, with no intraoperative major incidents.
Approximately 12 h after surgery, the patient presented a decrease in blood pressure to 80/50 mm Hg and heart rate of 135, with no response to the administration of 500 ml of Voluven®.
Dobutamine infusion was started and increased up to 7 ug/kg/min cardiac index, greater deterioration of hemodynamic conditions, so a pulmonary artery catheter showing a pulmonary capillary pressure of 18 mmHg, 1.2 mmHg (P2).
A TEE showed a hypertrophic left ventricle with a small cavity, with good overall function and no changes in segmental motility, and normal aortic valve appearance and mobility.
During systole, the anterior mitral valve leaflet dislodged or displaced 70% of the LVOT, producing moderate mitral regurgitation (MR).
A diagnosis of MAS was made, 1000 ml of Voluven® were administered, noradrenaline infusion was initiated up to 2 ug/kg/min, dobutamine was suspended, and 3 mg of metoprol was administered.
Within the following 20 minutes, there was a decrease in the obstruction of the LVOT and MI, blood pressure was reduced by 100/60 mm Hg, and heart rate by 100.
Twelve hours later, a new episode of hemodynamic compromise of similar characteristics occurred.
Due to the possibility of the existence of a hemoperitoneum that could perpetuate the condition of hypovolemia resulting from the development of an MAS, an exploratory laparotomy was performed, finding 300 ml of blood.
Volume was provided, norepinephrine was increased from 0.05 to 1.5 ug/kg/min, reestablishing BP 100/70 mm Hg, PCWP 22 mm Hg/m, and CI 3.2 l.
No other hemodynamic problems were observed postoperatively.
The patient was discharged on day 30 due to intra-abdominal abscess requiring percutaneous drainage.
