Effects of phenylephrine on cardiac output and venous return depend on the position of the heart on the Frank-Starling relationship

Introduction: phenylephrine is used daily during anesthesia for treating hypotension. However, the effects of phenylephrine on cardiac output (CO) are not clear. We hypothesized that the impact of phenylephrine on cardiac output is related to preload dependency. Methods: eight pigs were studied at a preload independent stage (after CO augmentation) and at a preload dependent stage (after a 21 ml/kg hemorrhage). At each stage, phenylephrine boluses (0.5, 1.0, 2.0, and 4.0 μg/kg) were given randomly while mean arterial pressure (MAP), CO, inferior vena cava flow (IVCf) (both measured using ultrasonic flow probes), and pulse pressure variation were measured. Results: at the preload independent stage, phenylephrine boluses induced significant increases in MAP (from 72 ± 6 to 100 ± 6 mmHg; P < 0.05) and decreases in CO and IVCf (from 7.0 ± 0.8 to 6.0 ± 1.1 l/min and from 4.6 ± 0.5 to 3.8 ± 0.6 l/min, respectively). At the preload-dependent stage, phenylephrine boluses induced significant increases in MAP (from 40 ± 7 to 65 ± 9 mmHg), CO (from 4.1 ± 0.6 to 4.9 ± 0.7 l/min), and IVCf (from 3.0 ± 0.4 to 3.5 ± 0.6 l/min; all data presented are for 4 μg/kg). Incremental doses of phenylephrine induced incremental changes in cardiac output. A pulse pressure variation >16.4% before phenylephrine predicted an increase in stroke volume with a 93% sensitivity and a 100% specificity. Conclusion: impact of phenylephrine on cardiac output is related to preload dependency. When the heart is preload independent, phenylephrine boluses induce on average a decrease in cardiac output. When the heart is preload dependent, phenylephrine boluses induce on average an increase in cardiac output.

Effect of inspiration on inferior vena caval blood flow in dogs

Inferior vena cava flow of anesthetized open-chest dogs was drained to a reservoir from a cannula above the diaphragm and returned to the atrium at constant rate. At selected base-line caval pressures, the caval flow and pressures in the abdomen (Pab), iliac vein (Piv), and downstream cavae (Pvc) were recorded during spontaneous breathing, cyclic phrenic nerve stimulation, and cyclic lowering of caval drain pressure. Each augmented flow unless Pab exceeded Pvc by at least ca. 5 cmH2O. In other dogs a cannulating flow probe was placed in the thoracic inferior cava and the chest was reclosed. Flow was augmented throughout most or all of spontaneous inspiration and was never depressed even though Pab exceeded right atrial pressure and Piv. I conclude that the collapse of hepatic veins and proximate cava does not occur at most normal pressures and a Starling resistor analog of abdominal veins based solely on abdominal and venous pressures is inappropriate. Both falling atrial pressure and rising Pab probably augment inspiratory abdominal venous return.