Does desflurane alter left ventricular function when used to control surgical stimulation during aortic surgery?

BACKGROUND: Although desflurane is commonly used to control surgically induced hypertension, its effects on left ventricular (LV) function have not been investigated in this clinical situation. The purpose of the present study was to evaluate the LV function response to desflurane, when used to control intraoperative hypertension. METHODS: In 50 patients, scheduled for vascular surgery, anesthesia was induced with sufentanil 0.5 microg/kg, midazolam 0.3 mg/kg and atracurium 0.5 mg/kg. After tracheal intubation, anesthesia was maintained with increments of drugs with controlled ventilation (N2O/O2=60/40%) until the start of surgery. A 5 Mhz transesophageal echocardiography (TEE) probe was inserted after intubation. Pulmonary artery catheter and TEE measurements were obtained after induction (to)(control value), at surgical incision (t1) if it was associated with an increase in systolic arterial pressure (SAP) greater than 140 mmHg (hypertension) and after control of hemodynamic parameters by administration of desflurane (return of systolic arterial pressure to within 20% of the control value) (t2) in a fresh gas flow of 31/ min. RESULTS: Sixteen patients developed hypertension at surgical incision. SAP was controlled by desflurane in all 16 patients. Afterload assessed by systemic vascular resistance index (SVRI), end-systolic wall-stress (ESWS) and left-ventricular stroke work index (LVSWI) increased with incision until the hypertension returned to post-induction values with mean end-tidal concentration of 5.1+/-0.7% desflurane. No change in heart rate, cardiac index, mean pulmonary arterial pressure, stroke volume, end-diastolic and end-systolic cross-sectional areas, fractional area change and left ventricular circumferential fiber shortening was noted when desflurane was added to restore blood pressure. CONCLUSION: This study demonstrates that in patients at risk for cardiac morbidity undergoing vascular surgery, desflurane is effective to control intraoperative hypertension without fear of major cardiac depressant effect.

Treating anesthesia-induced hypotension by angiotensin II in patients chronically treated with angiotensin-converting enzyme inhibitors.

UNLABELLED: Although angiotensin II bolus administration may be used to increase blood pressure in patients chronically treated with angiotensin-converting enzyme inhibitors (ACEI) who have severe hypotension on anesthetic induction, no data are available describing its time course and its effects on the left ventricular function. Fourteen patients chronically treated with ACEI for hypertension and scheduled for vascular surgery were prospectively studied. Patients with cardiac insufficiency were excluded. A transesophageal echocardiography probe was inserted to assess systolic left ventricular function. When hypotension was observed (systolic arterial pressure [SAP] <85 mm Hg), an I.V. bolus of 2.5 microg of angiotensin II (AII) was given, and hemodynamic variables were recorded each 30 s over 5.5 min. Results are expressed as mean +/- SEM. Sixty seconds after the AII bolus injection, the SAP increased from 78 +/- 3 to 152 +/- 6 mm Hg. SAP remained higher than control until the 5th min. This was associated with significant increases in end-diastolic area (from 15.1 +/- 0.6 to 19.3 +/- 1.0 cm2, P < or = 0.001), end-systolic area (from 6.6 +/- 0.4 to 10.7 +/- 0.7 cm2, P < or = 0.001), end-systolic wall stress (from 32 +/- 0.05 to 82 +/- 7 kdynes/cm2, P < or = 0.001). In addition, a decrease in fiber-shortening velocity (from 1.1 +/- 0.05 to 0.76 +/- 0.04 circ/s, P < or = 0.05) and in fractional area change (from 0.57 +/- 0.02 to 0.44 +/- 0.02, P < or = 0.05) was observed. Heart rate did not significantly change during the study. Increases in preload and afterload were observed. However, the administration of AII causes a transient impairment in left ventricular function. We conclude that AII, given as an I.V. bolus of 2.5 microg, is effective in restoring arterial blood pressure within 60 s in patients chronically treated with ACEI. IMPLICATIONS: Severe hypotension on anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors for hypertension could be treated with an I.V. bolus of 2.5 microg of angiotensin II.