Is β-adrenergic receptor stimulation crucial for splanchnic O₂availability in septic shock?

Background

Septic shock is characterized by arterial hypotension despite adequate fluid resuscitation, and treatment with vasopressors is current practice [1]. Vasopressors, however, may impair capillary exchange capacity in the splanchnic region [2]. Therefore we tested the effect of replacing noradrenaline (NOR) by phenylephrine (PHE) on splanchnic hemodynamics and O₂ kinetics in septic shock.

Methods

In up to now four patients with hyperdynamic septic shock (CI ≥ 41/min/m²) all requiring NOR (0.25 ± 0.22 μg/kg min) to maintain mean arterial pressure NOR was replaced by PHE (4.2 ± 3.9 μg/kg min) adjusted to achieve similar systemic hemodynamics. In addition to global oxygen delivery (DO₂sys) and uptake (VO₂sys) (indirect calorimetry) we measured gastric intramucosal pH (pHi) as well as splanchnic blood flow (Qspl), O₂ delivery (DO₂spl) and uptake (VO₂spl) using the indocyanine-green steady state-infusion technique corrected for hepatic dye extraction. Data were obtained after at least 2 h of stable hemodynamic conditions.

Results

See table.

Conclusions

Replacing NOR by PHE selectively reduced Qspl and DO₂spl without influencing pHi. Since VO₂sys remained constant, this fall in Qspl, however, was unlikely to be to due to reduced regional O₂ demands resulting from decreased β-adrenergic receptor-mediated thermogenesis [3]. Suppression of β-receptor stimulation, hence, may cause supply-dependency of VO₂spl in septic shock.

Table