Intraoperative hypotension (IOH) is a major concern to the anesthesiologist. Its appropriate identification and management require an understanding of the physiology of blood pressure regulation, prudent blood pressure monitoring, and treatment. Even short durations of low mean arterial pressure have been associated with adverse postoperative clinical outcomes. The challenge is for the clinician to respond proactively, address the specific etiology of IOH, and keep in mind any changes to the patient's physiology. Predictive technology, such as the Hypotension Prediction Index, offers the clinician new insight into IOH. It has been shown to predict hypotension up to 15 minutes before occurrence. It also calculates stroke volume variation, dynamic arterial elastance, and left ventricular contractility, which can inform the anesthesiologist of the etiology of IOH to direct management. This new technology has the potential to reduce duration or even prevent IOH. In the authors' opinion, it is an example of how human-machine interaction will contribute to future advances in medicine. Additional studies should evaluate the effects of its use on postoperative outcomes.

SUPERIOR VENA cava (SVC) syndrome is characterized by a mechanical obstruction to the SVC, decreasing preload to the heart and causing the constellation of neck vein distention, facial, and upper extremity edema, and sometimes cerebral edema.1,2 Malignancy has been the historic cause of SVC syndrome, although there has been a shift toward nonmalignant etiologies accounting for up to half of cases.3,4 Malignancies arising in the anterior mediastinum are well-known to cause SVC syndrome by direct tumor invasion or SVC compression.

MORE THAN 300 million people undergo surgery annually,1 and intraoperative hypotension (IOH) is a common event, with an incidence ranging from 5% to 99%.2 There is no standardized definition of IOH, but the commonly agreed-on definition is an absolute systolic pressure <100 mmHg and/or a relative decrease of 30% from baseline.3 IOH increases the potential for adverse effects on cardiac, renal, and nervous systems, as well as increases both hospital length of stay and mortality.4

To the Editor: A 63-year-old woman presented with double vision and intermittent headaches. A cerebral angiogram showed a 27-mm globular wide-based basilar apex aneurysm. Preoperative cardiac catheterization revealed severe stenosis involving the left anterior descending (LAD) (80%) and the right coronary artery (90%). The LAD lesion required surgical repair rather than stenting. The plan was to proceed with the combined surgical approach under deep hypothermic cardiac arrest. The patient was monitored with arterial, central venous, and pulmonary arterial catheters, as well as electroencephalogram, brainstem auditory evoked potentials, bladder/nasal temperature, intracranial pressure via a lumbar drain, and transesophageal echocardiography. Anesthesia was induced with fentanyl, sodium thiopental, and vecuronium. Anesthesia was maintained with isoflurane and IV infusions of fentanyl and midazolam. We administered mannitol and hyperventilated to a Paco2 of 30 mm Hg, allowed the temperature to decrease to 34°C, and drained spinal fluid to maintain a cerebral perfusion pressure >60 mm Hg. Craniotomy and exposure of the aneurysm preceded median sternotomy. Aprotinin was administrated for antifibrinolysis. The patient was placed on cardiopulmonary bypass, with arterial blood pressure maintained at approximately 60 mm Hg. Dexamethasone and sodium thiopental were used for additional cerebral protection. Distal coronary anastamoses were performed while cooling to a nasopharyngeal temperature of 18°C. Once the patient was deeply hypothermic, bypass was stopped and the neurosurgery team dissected and clipped the aneurysm within 39 min. Cardiopulmonary bypass resumed, and the proximal coronary anastomosis were completed during rewarming. The patient was easily weaned off bypass with one defibrillation. Protamine was administered. The total bypass time was 107 min. Craniotomy closure followed chest closure. An intraoperative cerebral angiogram showed no residual aneurysm. The patient did well until the fourth postoperative day, when an undiagnosed pneumothorax from a central line placed postoperatively led to a prolonged hypoxic event, with a poor neurological outcome unrelated to the surgery. This is a unique case that required the cooperation among many teams including cardiac and neuroanesthesia, nursing, cardiac surgery, neurosurgery, and critical care. The anesthetic technique was unique in order to involve the two procedures. Except for the postoperative hypoxic event that eventually took the life of the patient, our example would be good for future for similar cases. Bachar Hachwa, MD Department of Anesthesia The Ohio State University [email protected] Michele Walker, MD Anesthesiologist Grant Hospital Columbus, Ohio Ryan Dalton, MD Mark Gerhardt, PhD, MD Sergio D. Bergese, MD Department of Anesthesia The Ohio State University Columbus, Ohio