Effect of Increasing Blood Pressure With Noradrenaline on the Microcirculation of Patients With Septic Shock and Previous Arterial Hypertension.

OBJECTIVES: To assess whether an increase in mean arterial pressure in patients with septic shock and previous systemic arterial hypertension changes microcirculatory and systemic hemodynamic variables compared with patients without arterial hypertension (control). DESIGN: Prospective, nonblinded, interventional study. SETTING: Three ICUs in two teaching hospitals. PATIENTS: After informed consent, we included patients older than 18 years with septic shock for at least 6 hours, sedated, and under mechanical ventilation. We paired patients with and without arterial hypertension by age. INTERVENTIONS: After obtaining systemic and microcirculation baseline hemodynamic variables (time 0), we increased noradrenaline dose to elevate mean arterial pressure up to 85-90 mm Hg before collecting a new set of measurements (time 1). MEASUREMENTS AND MAIN RESULTS: We included 40 patients (20 in each group). There was no significant difference in age between the groups. After the rise in mean arterial pressure, there was a significant increase in cardiac index and a slight but significant reduction in lactate in both groups. We observed a significant improvement in the proportion of perfused vessels (control: 57.2 ± 14% to 66 ± 14.8%; arterial hypertension: 61.4 ± 12.3% to 70.8 ± 7.1%; groups: p = 0.29; T0 and T1: p < 0.001; group and time interaction: p = 0.85); perfused vessels density (control: 15.6 ± 4 mm/mm to 18.6 ± 4.5 mm/mm; arterial hypertension: 16.4 ± 3.5 mm/mm to 19.1 ± 3 mm/mm; groups: p = 0.51; T0 and T1: p < 0.001; group and time interaction: p = 0.70), and microcirculatory flow index (control: 2.1 ± 0.6 to 2.4 ± 0.6; arterial hypertension: 2.1 ± 0.5 to 2.6 ± 0.2; groups: p = 0.71; T0 and T1: p = 0.002; group and time interaction: p = 0.45) in both groups. CONCLUSIONS: Increasing mean arterial pressure with noradrenaline in septic shock patients improves density and flow in small vessels of sublingual microcirculation. However, this improvement occurs both in patients with previous arterial hypertension and in those without arterial hypertension.

Short-term effects of passive mobilization on the sublingual microcirculation and on the systemic circulation in patients with septic shock.

BACKGROUND: Active mobilization is not possible in patients under deep sedation and unable to follow commands. In this scenario, passive therapy is an interesting alternative. However, in patients with septic shock, passive mobilization may have risks related to increased oxygen consumption. Our objective was to evaluate the impact of passive mobilization on sublingual microcirculation and systemic hemodynamics in patients with septic shock. METHODS: We included patients who were older than 18 years, who presented with septic shock, and who were under sedation and mechanical ventilation. Passive exercise was applied for 20 min with 30 repetitions per minute. Systemic hemodynamic and microcirculatory variables were compared before (T0) and up to 10 min after (T1) passive exercise. p values <0.05 were considered significant. RESULTS: We included 35 patients (median age [IQR 25-75%]: 68 [49.0-78.0] years; mean (±SD) Simplified Acute Physiologic Score (SAPS) 3 score: 66.7 ± 12.1; median [IQR 25-75%] Sequential Organ Failure Assessment (SOFA) score: 9 [7.0-12.0]). After passive mobilization, there was a slight but significant increase in proportion of perfused vessels (PPV) (T0 [IQR 25-75%]: 78.2 [70.9-81.9%]; T1 [IQR 25-75%]: 80.0 [75.2-85.1] %; p = 0.029), without any change in other microcirculatory variables. There was a reduction in heart rate (HR) (T0 (mean ± SD): 95.6 ± 22.0 bpm; T1 (mean ± SD): 93.8 ± 22.0 bpm; p < 0.040) and body temperature (T0 (mean ± SD): 36.9 ± 1.1 °C; T1 (mean ± SD): 36.7 ± 1.2 °C; p < 0.002) with no change in other systemic hemodynamic variables. There was no significant correlation between PPV variation and HR (r = -0.010, p = 0.955), cardiac index (r = 0.218, p = 0.215) or mean arterial pressure (r = 0.276, p = 0.109) variation. CONCLUSIONS: In patients with septic shock after the initial phase of hemodynamic resuscitation, passive exercise is not associated with relevant changes in sublingual microcirculation or systemic hemodynamics.

Efeito do treinamento físico aeróbio sobre a reativação vagal cardíaca em jovens sedentárias / Effect of aerobic physical training on cardiac vagal reactivation in young sedentary

O objetivo foi comparar o comportamento parassimpático cardíaco durante a fase de recuperação de um exercício incremental (EI), realizado antes e após programa de treinamento aeróbio (TA). Para isso, 15 jovens sedentárias saudáveis, com idades entre 18 e 25 anos, se submeteram a um EI em esteira, com velocidade inicial de 4,0Km/h e acréscimos de 1,0Km/h/min, até atingirem a exaustão. Após, seus batimentos cardíacos foram registrados durante 10min e enviados a um computador para processamento da análise da variabilidade da frequência cardíaca (VFC), pelos índices pNN50, RMSSD e AF (u.n.) dos tempos 0-5min e 5-10min pós-esforço. Depois, submeteram-se a um TA de 12 sessões de 40min com intensidade equivalente a 65% da FC pico. Após, o EI foi repetido até que atingissem a mesma velocidade do EI da fase pré TA. Os dados pré e pós TA foram comparados por meio do teste de Kruskal-Wallis. As análises da VFC 0-5min e VFC 5-10min, não mostraram diferença entre os dados, com: a) 0-5min: pNN50 (0,3±0,7 % pré TA e 0,4±1,1 % pós TA), RMSSD (8,4±5,5ms pré TA e 9,6±7,5ms pós TA), AF(u.n.) 27,6±17,0% pré TA e 28,2± 13,8% pós TA); e b) 5-10min: pNN50 (0,1±0,4 % pré TA e 0,4±0,8 % pós TA), RMSSD (8,0±4,6ms pré TA e 10,6±7,9ms pós TA), AF(u.n.) 27,6±18,3% pré TA e 29,8± 17,5% pós TA). A aplicação do programa de TA de curta duração não se mostrou efetiva na ampliação da interferência do sistema nervoso parassimpático sobre o coração durante a fase de recuperação após EI.

The objective was to compare the cardiac parasympathetic behavior during the recovery phase of an incremental exercise (IE), before and after an aerobic training (AT) program. For this, fifteen healthy sedentary young people, aged between 18 and 25 years, underwent the IE in treadmill with initial velocity of 4.0 km/h and increments of 1.0 km/h/min until exhaustion. After the MIE the heart beats were recorded during 10min. The register was sent to a computer to be processed the heart rate variability (HRV) analysis using the index pNN50, RMSSD and HF (u.n.) of the times 0-5min and 5-10min post-effort. After, underwent an AT with 12 sessions of 40min at intensity equivalent to 65% of HR peak. Subsequently, the IE was repeated until they reached the same speed of IE of the first phase before AT. The data were compared using Kruskal-Wallis test with significant level of p<0.05. The HRV analysis 0-5min and 5-10min showed no differences between the data, with: a) 0-5min: pNN50 (0.3±0.7 % pre AT and 0.4±1.1 % post AT), RMSSD (8.4±5.5ms pre AT and 9.6±7.5ms post AT), HF(u.n.) 27.6±17.0% pre AT and 28.2± 13.8% post AT); and b) 5-10min: pNN50 (0.1±0.4% pre AT and 0.4±0.8% post AT), RMSSD (8.0±4.6ms pre AT and 10.6±7.9ms post AT), HF(u.n.) 27.6±18.3% pre AT and 29.8± 17.5% post AT). The application of a short duration AT was not effective to increase the parasympathetic nervous system interference on the heart during the recovery phase after IE.