I read with great interest the Letter to the Editor "Labetalol May Decrease Cerebral Perfusion in Beach Chair Position," and wish to thank Dr. Lofsky for pointing out important issues related to the clinical pharmacology of labetalol. I would like to mention some additional supporting and relatively under-appreciated aspects of this drug and would like to stress the need for us to understand each patient's hemodynamic situation and how our actions affect it.
At our institution we frequently monitor cardiac output and its components with the esophageal Doppler. Monitoring esophageal Doppler hemodynamics confirms and underscores the fact that labetalol's stronger beta-1 blocking decreases heart rate and contractility preferentially. We have seen profound effects on contractility with this drug, including frequent decreases in aortic peak velocities by 50% and greater. Cerebral, as well as overall perfusion, is not well supported with low perfusion pressure, low cardiac output, and low flow velocities.
Anesthesiologists need to be very certain that any method used for decreasing, or increasing, blood pressure is the desired mechanism for the given clinical situation. The mechanism of labetalol-reduced blood pressure is just one example of how little we know about each individual's hemodynamics when we lack objective information regarding left ventricular filling and emptying characteristics, when we lack real-time data as to how our treatments affect these, and blindly give convenient drugs to change the blood pressure one way or another. We need to assure that our therapeutic actions are providing conditions for safe and favorable outcomes, and to do so we need to understand the hemodynamic situation in real time.