Introduction: In shock, the increase in cutaneous-to-arterial carbon dioxide partial pressure (Pc-aCO2) and the decrease in the perfusion index (PI) are related to macrovascular or microvascular alterations. We hypothesized that inducing cutaneous vasodilation and local perfusion with heat could provide a noninvasive tool to monitor microvascular reactivity.
Objectives: This study aimed to develop a noninvasive approach, the heating challenge (HC), to monitor the microvascular reactivity of patients with shock and to evaluate the potential relationship with outcome.
Methods: After ethics committee agreement was obtained, 59 shock patients, including 37 septic shock, 22 non-septic shock (14 cardiogenic and eight hemorrhagic), 10 intensive care unit (ICU)-controls and 12 healthy volunteers, were included in this study. The HC consisted of heating the ear lobe PcCO2 sensor from 37° to 45° over 5 min and recording PcCO2 and PI variations (ΔPcCO2 and PImax/min). HC was performed on admission and during the first 48 h of hospitalization.
Results: Pc-aCO2 was significantly higher in shock patients than ICU-controls at baseline (P < 0.05). HC led to a decrease in PcCO2 and an increase in PI in the healthy volunteers (ΔPcCO2 = -9.0 ± 4.6% and PImax/min = 5.5 ± 1.9). On admission, non-septic shock patients (cardiogenic and hemorrhagic shocks) had an HC response profile identical to that of healthy volunteers and ICU-controls. In contrast, septic shock patients had a lower ΔPcCO 2 and PImax/min compared to healthy volunteers and all other groups (P < 0.05). After the first day, the combination of a Pc-aCO2 >17 mm Hg with a positive ΔPcCO2 could predict mortality with a specificity of 82% and a sensitivity of 93%.
Conclusions: HC appears to be a dynamic test to classify vascular reactivity alterations in shock. At baseline, HC results were impaired in septic patients and conserved in non-septic patients. After the first day, the association between Pc-aCO2 and ΔPcCO2 was strongly related to prognosis in shock patients.
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