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Variations of Cutaneous Capnometry and Perfusion Index During a Heating Challenge is Early Impaired in Septic Shock and Related to Prognostic in Non-Septic Shock

Vallée, Fabrice∗,†,‡; Nougué, Hélène∗,§; Mari, Arnaud||; Vodovar, Nicolas§; Dubreuil, Guillaume; Damoisel, Charles; Dépret, François; Mateo, Joaquim

Author Information
doi: 10.1097/SHK.0000000000001216



Alterations in microcirculatory perfusion are present in all cases of shock, i.e., septic, hemorrhagic, or cardiogenic shocks (1–4). In addition, several studies have demonstrated an association between the severity of microvascular hypoperfusion and the development of organ dysfunction and prognosis (5–7). However, the underlying mechanisms involved are different. In cardiogenic or hemorrhagic shock, tissue hypoperfusion is typically secondary to macrocirculatory failure (4, 8, 9). In septic shock, microcirculatory alterations are presumed to play a primary role in triggering and maintaining hypoxia via a combination of compromised vascular auto-regulation, increased blood viscosity, neutrophil activation, and reduced red cell deformability (1). These findings have brought the concept of “hemodynamic coherence,” i.e., macro/microcirculation coupling, whereby resuscitation based on systemic hemodynamic variables is likely to be effective if regional and microcirculatory perfusion is corrected (10, 11). For these reasons, monitoring microcirculation seems mandatory for the evaluation of hemodynamic coherence in circulatory failure. However, microcirculatory assessment remains challenging in daily clinical practice (5, 7, 12, 13), and the impact of microcirculation monitoring on the outcome of patients with shock has not been demonstrated to date.

Tissue CO2 or tissue-to-arterial carbon dioxide pressure (Pc-aCO2) appears to be a well-evidenced candidate tool to assess local perfusion (14) or microcirculatory alterations (15, 16). Therefore, capnometric devices could offer the opportunity to monitor hemodynamic coherence and persistent microcirculatory impairment despite macrohemodynamic stabilization (10). In addition, this method could be used with cutaneous sensors which have the advantage of being noninvasive, continuous, and compatible with daily clinical practice (17–19). In a previous study, we showed that cutaneous PCO2 (PcCO2) and cutaneous-to-end tidal carbon dioxide pressure measured at 37°C at the earlobe provided a rapid and continuous depiction of the peripheral microcirculatory perfusion in septic shock (20).

In the aforementioned study, PcCO2 values were obtained at 37°C instead of the commonly used 42° to 44°C to limit tissue vasodilatation and increase local blood flow and “arterialization.” However, we hypothesized that this heat-induced vasodilatation and arterialization could be used intermittently to evaluate the microcirculatory status by serially measuring PcCO2 at 37°C and increasing the temperature sensor to 45°C as a heating challenge (HC). We also included the perfusion index (PI) in this analysis, which is derived from the plethysmographic signal already captured by the sensor. PI could then be measured concomitantly with PcCO2 in the HC as a functional index of peripheral vasomotor tone and peripheral perfusion (21–23). We hypothesized that adding a dynamic vascular reactivity test as the HC to the continuous PcCO2 monitoring could provide additional arguments for classifying the severity of microperfusion alterations in shock. Thus, the aims of this proof-of-concept study were as follows: to describe the variations in PcCO2 and PI induced by HC in various types of shock and to assess the potential prognosis of HC parameters in the evolution of shock patients during the first days after ICU admission.



After approval by the ethics committees (N IRB0006477) and informed consent signatures were obtained, shock patients (with septic, hemorrhagic, and cardiogenic shocks), and the ICU-controls and healthy volunteers were enrolled in the study. This study was performed in the ICU at Lariboisière Hospital from January 2012 to February 2013.

The inclusion criteria for the shock group were as follows: septic shock as defined according to international guidelines, suspected or documented infection and acute increase in the Sequential Organ Failure Assessment (SOFA) score (≥2) and vasopressor therapy needed to elevate mean arterial pressure ≥65 mm Hg and lactate > 2 mmol/l despite adequate resuscitation (24, 25); or cardiogenic shock defined by a systolic blood pressure < 90 mm Hg in the absence of hypovolemia, or the requirement of vasopressors/inotropes to achieve a systolic blood pressure ≥90 mm Hg with a reduction of cardiac index and elevated left ventricular filling pressures (26); or hemorrhagic shock defined by a blood loss leading to acute circulatory deficiency with systolic blood pressure ≤ 90 mm Hg and the requirement of vasopressor associated ≥ four packed red blood cells within 6 h of hospital care (27). The exclusion criteria were cutaneous ear lobe injury, age < 18, and refusal to enroll to the study. Shock patients were included within 24 h after the onset of shock, and if one investigator (FV, HN, GD, or JM) was present. Shock patients who died within 48 h after admission were excluded from the final analysis on prognosis.

The ICU-controls were chosen from stable ICU patients who were admitted after scheduled major neurosurgery without any hemodynamics or respiratory instability. The patients were monitored with an arterial catheter for the surgery and the HC was performed in the 4 h following ICU admission. The healthy volunteers were maintained in an air-conditioned room set at 22°C and were at rest for at least 15 min before the test and 10 min after the test.

Study protocol

All included shock patients were mechanically ventilated with an end-tidal capnography monitoring system (Siemens; Berlin, Germany). Patients were set up with a radial or femoral arterial catheter and a central venous catheter and were continuously monitored for cardiac output with a pulmonary arterial catheter (Vigilance CCO catheter; Edwards Lifesciences Corporation; Irvine, Calif) or transesophageal Doppler (Deltex Medical Group plc; Chichester, England). All shock patients were treated according to the standard practice of our ICU, regardless of the HC results. Patients were maintained in an air-conditioned room set at 22°C. The following parameters were collected at baseline (H0), 6 h (H6), 12 h (H12), 24 h (H24), 36 h (H36), and 48 h (H48) after admission in ICU: temperature; systemic hemodynamic parameters; arterial, venous, end-tidal and cutaneous PCO2; arterial and central venous blood gas; arterial lactate concentration; and treatment. The Simplified Acute Physiology Score (28) and SOFA score (29) were calculated at baseline, day 1 and day 2. The outcome was assessed according to outcome at 28 days (D28) after admission in ICU (dead or alive).

PcCO2 and PI measurements

PcCO2 was measured by clipping the sensor to the earlobe after application of conductive gel with a TOSCA 500 monitor (TOSCA; Radiometer Basel Ag; Basel, Switzerland) at 37°C as previously described (20). The temperature of the sensor is permanently maintained at 37°C. The sensor was calibrated before use and every 12 h (based on manufacturer's recommendations (18, 30)). The TOSCA 500 monitor also enables us to measure SpO2, hence the PI (31).

Heating challenge: HC

The HC was designed to evaluate dynamic changes in microvascular vasoreactivity induced by an increase in temperature and was performed in a timeframe during which circulatory parameters, administration of vasoactive agents, and ventilatory settings remained unchanged. All subjects were placed in the supine position during the HC and for at least 15 min for the healthy volunteers.

The HC consisted of first equilibrating the sensor at 37°C, then increasing the sensor temperature to 45°C for 5 min while continuously recording PcCO2 and PI. A typical response to the HC in a healthy volunteer is illustrated in Figure 1. The increase in temperature provoked a decrease in PcCO2, and a transient increase in PI. From these measurement, we extracted two parameters for subsequent analysis: the variation in PcCO2 expressed in % (ΔPcCO2 = (PcCO2end – PcCO2start)/PcCO2start × 100), and the ratio between the maximal PI at 45°C and the PI at 37°C (PImax/min = PImax/PImin). The initial values considered are taken after setting the sensor at 45°C since the TOSCA 500 monitor applies different correction factors for of PcCO2 and PI measurements between 37°C and 45°C (30).

Fig. 1:
Flowchart of the subjects included in this study.

Statistical analysis

All statistical analyses were performed using R-statistical software ( Data are expressed as median [interquartile range]. Variables were tested using the Wilcoxon rank-sum test or χ2 test as appropriate. P values for multiple comparisons were adjusted using the Holm method. Paired data were analyzed using the paired Wilcoxon rank-sum test. Repeated measured were analyzed using two-way ANOVA. The predictive value on mortality at D28 was calculated using a receiver operator characteristic (ROC) curve, and the AUC was computed. A two-sided P value < 0.05 was considered statistically significant.



Eighty-one subjects were included as follows: Shock patients (n = 59), including 37 septic shock, and 22 non-septic shock (14 cardiogenic and eight hemorrhagic); and 10 ICU-controls and 12 healthy volunteers (Fig. 2). The characteristics of the population are described in Table 1.

Fig. 2:
Stereotypical examples of the HC performed in healthy volunteer (light gray), non-septic shock (hemorrhagic in this example, medium gray), septic shock patient (black).
Table 1:
Characteristics of the patients at baseline

Heating challenge at baseline

As expected, shock patients (septic, cardiogenic, and hemorrhagic) had a baseline PcCO2 at 37°C that was significantly higher than healthy volunteers and ICU-controls (57.9 ± 14.8 vs. 47.3 ± 3.0 and 48.2 ± 2.0 mm Hg, P < 0.05 respectively, Fig. 3A). The PI was higher in healthy volunteers compared with ICU-controls and all shock patients (1.1 ± 0.6 vs. 0.6 ± 0.3 and 0.5 ± 0.4, P = 0.02 and P < 0.05 respectively; Fig. 3B).

Fig. 3:
Results of heating challenge at baseline in the different groups.

A representative curve for ΔPcCO2 and PImax/min during the HC for healthy volunteers, non-septic and septic shocks is represented in Figure 1. In the healthy volunteers and ICU-controls, the response to HC led to a ∼10% decrease in PcCO2 (ΔPcCO2: −9.0 ± 4.6% and −11.1 ± 4.7, respectively, Fig. 3A) and ∼5-fold increase in PI (PImax/min: +5.5 ± 1.9 and +5.2 ± 2.8, Fig. 3B). Interestingly, non-septic shock patients were similar to the healthy volunteers and ICU-controls with respect to both ΔPcCO2 and PImax/min (ΔPcCO2: −11.6 ± 10.6% and PImax/min: 4.2 ± 2.7, Fig. 3, A and B). In marked contrast, the ΔPcCO2 and PImax/min were significantly lower in septic shock patients when compared with healthy volunteers (−1.9 ± 7.9 vs. −9.0 ± 4.6% and +2.9 ± 2.2 vs. +5.5 ± 1.9, P < 0.05 for ΔPcCO2 and PImax/min respectively). Of note, this difference was significant with ICU-controls and non-septic shock at baseline (Fig. 3).

Evolution and predictive value of HC in the shock group

Next, we evaluated the predictive value of the HC with respect to mortality at D28 after 48 h following admission. In shock patients, mortality at D28 was 38% (23 patients). The characteristics at baseline of survivors and non-survivors are shown in Table 2. We excluded four patients (three with septic shock and one with hemorrhagic shock) from the prognosis analysis because they died within the first 48 h after inclusion. In shock patients, the evolution of macrohemodynamic parameters, such as the mean arterial pressure, central venous oxygen saturation, central venous pressure, and cardiac output was similar between survivors and non-survivors during the first 48 h (Supplementary appendix 1, In contrast, the trends in the arterial lactate concentration, SOFA score, Pc-aCO2, and ΔPcCO2 were significantly different in survivors compared to non-survivors (P < 0.05, Supplementary appendix 1,, and Fig. 4A). Finally, we observed a trend in the evolution of PI and PImax/min in survivors compared with non-survivors; however, the results were not statistically significant (Supplementary appendix 1,, and Fig. 4B).

Table 2:
Characteristics of survivors and non-survivors patients at baseline
Fig. 4:
Evolution of the HC during the first 48 h after inclusion in non-septic (left) and septic (right) shock patients according to prognosis (black: non-survivor and gray: survivors).

At H36, lactate and Pc-aCO2 were significantly higher and ΔPcCO2 lower in non-survivors compared with survivors. At H36, the areas under the ROC curve for lactate, Pc-aCO2, and ΔPcCO2 were 0.89, 0.86, and 0.80, respectively (Fig. 5A–C). Interestingly, when combining the Pc-aCO2 and ΔPcCO2 analysis with the respective thresholds of 17 mm Hg and 0%, the AUC increased at 0.95 with a specificity of 82% and a sensitivity of 93% (Fig. 5D).

Fig. 5:
Receiver operating characteristic (ROC) curve for the plasma lactate level, Pc-aCO2, ΔPcCO2 and Pc-a CO2 + ΔPcCO2 at H36 for predicting death at D28 in all shocked patients, with an optimal cut-off value of 1.9 mmol/L (sensitivity 87%, specificity 79%) for lactate (A), 17 mm Hg (sensitivity 80%, specificity 76%) for Pc-aCO2 (B), 0 mm Hg (sensitivity 87%, specificity 74%) for ΔPcCO2 (C) and (D) combined Pc-a CO2 + ΔPcCO2 (sensibility 93%, specificity 82%).

HC parameters in non-septic shock versus septic shock patients

Since non-septic shock patients (cardiogenic and hemorrhagic) were similar at baseline and different from septic shock patients, we further analyzed the evolution over the first 2 days of these two subpopulations separately.

In non-septic shock and in septic shock, the mortality at D28 was 19% (4/21) and 38% (12/34), respectively. In non-septic patients, during the first 12 h, the ΔPcCO2 trend was similar between survivors and non-survivors. However, from 12 h onward, ΔPcCO2 deviated in survivors, while in non-survivors the trend appeared to remain the same with a gradual worsening of vascular reactivity (Fig. 4C). Of note, PImax/min decreased in non-survives while remaining stable in survivors (Fig. 4D). In contrast, in septic shock patients, neither the ΔPcCO2 nor the PImax/min trend was different between survivors and non-survivors during the first 48 h (Fig. 4, E and F). In fact, after 12 h, the HC parameters of the non-septic patients with a poor prognosis begin to resemble those of septic shock patients.


In this preliminary study, the results of the cutaneous heating challenge were as follows: HC causes a 10% decrease in PcCO2 and a 5-fold increase in PI in the healthy volunteers and ICU-controls; at admission, HC parameters were only impaired in septic shock compared with non-septic shock patients; and the combination of Pc-aCO2 and ΔPCO2 after the first day of resuscitation is strongly related to prognosis.

The HC consists of simultaneously monitoring PI and PcCO2 at the earlobe before and after heating to 45°C. The variation in PcCO2 at 37°C was previously shown to be correlated to skin blood flow assessed to laser Doppler flowmetry (20), strongly suggesting that PcCO2 is a marker of microcirculatory flow (32, 33). The PI is related to tissue perfusion and capillary recruitment by studying the evolution of PcCO2 and PI between 37°C and 45°C, we took advantage of local temperature-induced vasodilation, arterialization, and increase in blood flow as an integrative tool to monitor the status of microcirculatory reactivity. The ability of microvessels to respond to heating has been studied by laser Doppler and validates the relationship between local heating and vascular reactivity and is maintained with aging (34). Interestingly in a recent article (35), this hypothesis was also tested in ICU patients; the results showed the microcirculatory reactivity is decreased in circulatory shock patients and has prognostic value. To train the system with PcCO2 and PI, we studied healthy volunteers in which the microcirculation was normal. As expected in this population, the increase in temperature was associated with an increase in PI and a decrease in PcCO2 (5.2 ± 3.8 and −11.1 ± 4.7%). Interestingly, in non-septic shock patients, even if the baseline values of PcCO2 and PI were significantly different, the vascular reactivity induced by HC could be viewed as identical in this population compared with the healthy volunteers and the ICU-controls (Fig. 3). By contrast, in septic shock patients, HC parameters at baseline were markedly impaired without any decrease in PcCO2 during the heating period. This result confirmed that the microcirculation of early-stage septic shock patients is highly compromised (7, 10). Additionally, when studying the relationship of cutaneous PcCO2 together with HC and prognosis in all shock patients, we found that, after the first day of evolution, the combination of a Pc-aCO2 >17 mm Hg with a ΔPcCO2 ≥ 0 could predict mortality with a specificity of 87% and a sensitivity of 93%. This result has to be confirmed in a larger cohort but is at least as effective as the arterial lactate value. Therefore, PcCO2 monitoring with HC could constitute a noninvasive and continuous tool to test vasoreactivity in patients with shock without specific training or blood sample analysis.

From a clinical standpoint, we observed that from 12 h postinclusion onward, the HC could differentiate survivors from non-survivors in patients admitted with cardiogenic or hemorrhagic shock. Indeed, from 12 h onward, ΔPcCO2 deviated in survivors while the value in non-survivors appeared to remain the same with a gradual worsening of vascular reactivity (Fig. 4A). In contrast, in septic shock patients, HC parameters were not different between survivors and non-survivors during the first 48 h (Fig. 4, C and D). In fact, after 12 h, the HC parameters of the non-septic patients with poor prognosis could reflect persistent tissue hypoxia provoked by shock which, in turn, leads to a “sepsis-like state” associated with a local inflammatory response, oxidative stress, and vascular permeability among other factors (3).

Study limitations

This study has several limitations. First, the study is monocentric with a limited number of patients included in each group. However, this study was designed to establish a proof-of-principle that HC can be used to monitor the microcirculation. Furthermore, the number of events during follow-up was limited in the non-septic shock group. Thus, further larger-scale studies will be needed to fully validate this approach. Second, due to technical limitations, we could not compare the HC with other tissue perfusion monitoring, such as laser Doppler or orthogonal polarization spectral imaging, which could add to the understanding of HC as a test for microcirculation and vascular reactivity (20, 36, 37).

Finally, all patients were monitored after the very early initial stabilization, i.e., not at the onset of shock.

In conclusion, this preliminary study suggests that the noninvasive continuous monitoring of cutaneous CO2 and PI coupled with intermittent dynamic heating challenge could assess cutaneous vasoreactivity, and is early comprised in septic shock. The association between Pc-aCO2 and ΔPcCO2 during HC was strongly related to prognosis in all shock patients.


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Heating challenge; microcirculation; PcCO2; perfusion index; shock; CVP; central venous pressure; HC; heating challenge; ICU; intensive care unit; IGS; Index Gravity Score; IQ; interquartile; MAP; mean arterial pressure; Pc-aCO2; difference of the gradient between PcCO2 and PaCO2; PcCO2; cutaneous carbon dioxide partial pressure; Pc-etCO2; difference of the gradient between end-tidal PCO2 and PcCO2; PcvCO2; central venous PCO2; PI; perfusion index; Pv-aCO2; difference of the gradient between central venous PCO2 and PaCO2; SaO2; arterial oxygen saturation; ScvO2; central venous saturation; SOFA; Sequential Organ Failure Assessment

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