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Although guidelines provide excellent expert guidance for managing patients with septic shock, they leave room for personalization according to patients’ condition. Hemodynamic monitoring depends on the evolution phase: salvage, optimization, stabilization, and de-escalation. Initially during the salvage phase, monitoring to identify shock etiology and severity should include arterial pressure and lactate measurements together with clinical examination, particularly skin mottling and capillary refill time. Low diastolic blood pressure may trigger vasopressor initiation. At this stage, echocardiography may be useful to identify significant cardiac dysfunction. During the optimization phase, echocardiographic monitoring should be pursued and completed by the assessment of tissue perfusion through central or mixed-venous oxygen saturation, lactate, and carbon dioxide veno-arterial gradient. Transpulmonary thermodilution and the pulmonary artery catheter should be considered in the most severe patients. Fluid therapy also depends on shock phases. While administered liberally during the resuscitation phase, fluid responsiveness should be assessed during the optimization phase. During stabilization, fluid infusion should be minimized. In the de-escalation phase, safe fluid withdrawal could be achieved by ensuring tissue perfusion is preserved. Norepinephrine is recommended as first-line vasopressor therapy, while vasopressin may be preferred in some patients. Essential questions remain regarding optimal vasopressor selection, combination therapy, and the most effective and safest escalation. Serum renin and the angiotensin I/II ratio may identify patients who benefit most from angiotensin II. The optimal therapeutic strategy for shock requiring high-dose vasopressors is scant. In all cases, vasopressor therapy should be individualized, based on clinical evaluation and blood flow measurements to avoid excessive vasoconstriction. Inotropes should be considered in patients with decreased cardiac contractility associated with impaired tissue perfusion. Based on pharmacologic properties, we suggest as the first test a limited dose of dobutamine, to add enoximone or milrinone in the second line and substitute or add levosimendan if inefficient. Regarding adjunctive therapies, while hydrocortisone is nowadays advised in patients receiving high doses of vasopressors, patients responding to corticosteroids may be identified in the future by the analysis of selected cytokines or specific transcriptomic endotypes. To conclude, although some general rules apply for shock management, a personalized approach should be considered for hemodynamic monitoring and support.

To evaluate hemoadsorptive therapy in treating refractory septic shock in a non-concurrent cohort of patients by analyzing clinical and laboratory parameters. A non-concurrent review of patients admitted to the intensive care unit (ICU) with refractory septic shock who received hemoadsorptive therapy over five years was conducted. Clinical variables, including age, gender, APACHE II and SOFA scores, vasopressor requirements, and laboratory parameters, as well as in-hospital mortality and mortality at 30 and 90 days, were analyzed. Descriptive statistics were calculated, and pre- and post-therapy variables were compared using the Mann-Whitney test. The median age of the cohort was 65.5 years, with a male-to-female ratio of 0.43. Hemoadsorptive therapy was associated with a reduction in vasopressor requirements, with a median initial noradrenaline requirement of 0.7 μg/kg/min (IQR 0.45–0.8875) decreasing to 0.12 μg/kg/min (IQR 0–0.225) post-therapy. The total normalized vasopressor requirement at the beginning of the therapy was 0.8125 (IQR 0.56–1.08), and post-therapy, it was 0.175 (IQR 0.01–0.29). Adrenaline was used in 0.64 of patients, vasopressin in 0.43, and 0.28 received inotropic therapy. Median APACHE II scores pre- and post-therapy were 30.5 and 20.5, respectively, while SOFA scores were 13.5 and 11.5. Both scores decreased without statistical significance according to the Wilcoxon test. Median lactate levels decreased by 62%, from 7,86 mmol/l pre-therapy to 2,97 mmol/l post-therapy. Inflammatory parameters, such as C-reactive protein (CRP), decreased from 206 mg/dL to 180 mg/dL, and procalcitonin (PCT) decreased from 58 to 8.91. In-hospital mortality was 0.57, increasing to an index of 0.64 at 90 days of follow-up. Eight out of 14 patients died during hospitalization, with an additional patient succumbing to the illness within the 90-day follow-up period. Hemoadsorptive therapy demonstrated encouraging efficacy in the management of refractory septic shock in our non-concurrent cohort of 14 patients. A significant decrease in vasopressor requirements, lactate levels, and inflammatory parameters was observed, although changes in APACHE II and SOFA scores were not statistically significant. These promising results warrant further investigation through larger cohort studies to evaluate the impact of hemoadsorptive therapy on long-term mortality and to explore its potential role as a standard treatment option for refractory septic shock.

Catecholamines are used to increase cardiac output and blood pressure, aiming ultimately at restoring/improving tissue perfusion. While intuitive in its concept, this approach nevertheless implies to be effective that regional organ perfusion would increase in parallel to cardiac output or perfusion pressure and that the catecholamine does not have negative effects on the microcirculation. Inotropic agents may be considered in some conditions, but it requires prior optimization of cardiac preload. Alternative approaches would be either to minimize exposure to vasopressors, tolerating hypotension and trying to prioritize perfusion but this may be valid as long as perfusion of the organ is preserved, or to combine moderate doses of vasopressors to vasodilatory agents, especially if these are predominantly acting on the microcirculation. In this review, we will discuss the pros and cons of the use of catecholamines and alternative agents for improving tissue perfusion in septic shock.

The aim of this study was to collect and describe all published reports of local tissue injury or extravasation from vasopressor administration via either peripheral intravenous (IV) or central venous catheter. A systematic search of Medline, Embase, and Cochrane databases was performed from inception through January 2014 for reports of adults who received vasopressor intravenously via peripheral IV or central venous catheter for a therapeutic purpose. We included primary studies or case reports of vasopressor administration that resulted in local tissue injury or extravasation of vasopressor solution. Eighty-five articles with 270 patients met all inclusion criteria. A total of 325 separate local tissue injury and extravasation events were identified, with 318 events resulting from peripheral vasopressor administration and 7 events resulting from central administration. There were 204 local tissue injury events from peripheral administration of vasopressors, with an average duration of infusion of 55.9 hours (±68.1), median time of 24 hours, and range of 0.08 to 528 hours. In most of these events (174/204, 85.3%), the infusion site was located distal to the antecubital or popliteal fossae. Published data on tissue injury or extravasation from vasopressor administration via peripheral IVs are derived mainly from case reports. Further study is warranted to clarify the safety of vasopressor administration via peripheral IVs.

The optimum spinal cord perfusion pressure (SCPP) after traumatic spinal cord injury (TSCI) is unknown. Here, we describe techniques to compute and display the optimum SCPP in real time. We recruited adults within 72 h of severe TSCI (American Spinal Injuries Association [ASIA] grades A-C). A pressure probe and a microdialysis catheter were placed on the injured cord. SCPP was computed as mean arterial pressure (MAP) minus intraspinal pressure (ISP), spinal pressure reactivity index (sPRx) as the running ISP/MAP correlation coefficient, and continuous optimum SCPP (cSCPPopt) as the SCPP that minimizes sPRx in a moving 4-h window. In 45 patients, we monitored ISP and blood pressure. In 14 patients, we also monitored injury site metabolism. cSCPPopt could be computed 45% of the time. Mean cSCPPopt varied by up to 60 mm Hg between patients. Each patient's cSCPPopt varied with time (standard deviation 10-20 mm Hg). Color-coded maps showing the sPRx/SCPP curve evolution enhanced visualization of cSCPPopt. Periods when SCPP ≈ cSCPPopt were associated with low injury site glucose, high pyruvate, and high lactate. Mean SCPP deviation from cSCPPopt correlated with worse neurological outcome at 9–12 months: ASIA grade improved in 30% of patients with <5 mm Hg deviation, 10% of patients with 5–15 mm Hg deviation, and no one with >15 mm Hg deviation. We conclude that real-time computation and visualization of cSCPPopt after TSCI are feasible. cSCPPopt appears to enhance glucose utilization at the injury site and varies widely between and within patients. Our data suggest that targeting cSCPPopt after TSCI might improve neurological outcome.

Fever control may improve vascular tone and decrease oxygen consumption, but fever may contribute to combat infection. To determine whether fever control by external cooling diminishes vasopressor requirements in septic shock. In a multicenter randomized controlled trial, febrile patients with septic shock requiring vasopressors, mechanical ventilation, and sedation were allocated to external cooling (n = 101) to achieve normothermia (36.5-37°C) for 48 hours or no external cooling (n = 99). Vasopressors were tapered to maintain the same blood pressure target in the two groups. The primary endpoint was the number of patients with a 50% decrease in baseline vasopressor dose after 48 hours. Body temperature was significantly lower in the cooling group after 2 hours of treatment (36.8 ± 0.7 vs. 38.4 ± 1.1°C; P < 0.01). A 50% vasopressor dose decrease was significantly more common with external cooling from 12 hours of treatment (54 vs. 20%; absolute difference, 34%; 95% confidence interval [95% CI], -46 to -21; P < 0.001) but not at 48 hours (72 vs. 61%; absolute difference, 11%; 95% CI, -23 to 2). Shock reversal during the intensive care unit stay was significantly more common with cooling (86 vs. 73%; absolute difference, 13%; 95% CI, 2 to 25; P = 0.021). Day-14 mortality was significantly lower in the cooling group (19 vs. 34%; absolute difference, -16%; 95% CI, -28 to -4; P = 0.013). In this study, fever control using external cooling was safe and decreased vasopressor requirements and early mortality in septic shock.

Intensive care unit (ICU) nurses frequently manually titrate norepinephrine to maintain a predefined mean arterial pressure (MAP) target after high-risk surgery. However, achieving this task is often suboptimal. We have developed a closed-loop vasopressor (CLV) controller to better maintain MAP within a narrow range. After ethical committee approval, fifty-three patients admitted to the ICU following high-risk abdominal surgery were randomized to CLV or manual norepinephrine titration. In both groups, the aim was to maintain MAP in the predefined target of 80–90 mmHg. Fluid administration was standardized in the two groups using an advanced hemodynamic monitoring device. The primary outcome of our study was the percentage of time patients were in the MAP target. Over the 2-hour study period, the percentage of time with MAP in target was greater in the CLV group than in the control group (median: IQR25–75: 80 [68–88]% vs. 42 [22–65]%), difference 37.2, 95% CI (23.0–49.2); p < 0.001). Percentage time with MAP under 80 mmHg (1 [0–5]% vs. 26 [16–75]%, p < 0.001) and MAP under 65 mmHg (0 [0–0]% vs. 0 [0–4]%, p = 0.017) were both lower in the CLV group than in the control group. The percentage of time with a MAP > 90 mmHg was not statistically different between groups. In patients admitted to the ICU after high-risk abdominal surgery, closed-loop control of norepinephrine infusion better maintained a MAP target of 80 to 90 mmHg and significantly decreased postoperative hypotensive when compared to manual norepinephrine titration.

Conventional vital signs alone have limitations in determining the physiological status. Age-adjusted shock-index (SIPA), a comprehensive physiological variable, defined as the ratio of heart rate (HR) and systolic blood pressure (SBP) may be better at predicting hemodynamic stability and outcome than vital signs. To compare discriminatory power of SIPA against vital signs in assessing higher level of care (vasopressor use and mechanical ventilation) and early mortality in severe sepsis/septic shock. Prospective cohort study of 116children <14 years with severe sepsis/septic shock admitted at emergency department of a tertiary care hospital. Association between abnormal signs (raised heart-rate; HR, lower systolic blood-pressure; SBP, high SIPA) and higher level of care and early mortality at 0 and completed 6 hours (t0, t6) were assessed using univariate/multivariate analysis. Area-under-receiver-operating-characteristic curves (AUROC) of SIPA and conventional vital signs for outcome variables and their correlation with arterial lactate using Pearson's-coefficient were noted. High SIPA was independently associated with higher level of care i.e. vasopressor use, mechanical ventilation (AUROC t0: 0.698, 0.730; AUROC t6; 0.733, 0.735) as well as early mortality (AUROC t0: 0.638; AUROC t6:0.721) at t0 and t6. At t0, only high SIPA (r2 = 0.313) fairly correlated with arterial lactate (4.5 mmol/L). At t6, HR and SBP showed weak and SIPA (r2 = 0.434) demonstrated moderate correlation with arterial lactate. SIPA performs better than conventional vital-signs in recognising higher-level-of-care and early mortality.

This case addressed patient and free flap survival after cardiac arrest with the contentious use of vasopressors amid concerns about potential vasoconstrictive effects on flap vitality. A 59-year-old male with mucoepidermoid carcinoma underwent post-total maxillectomy and double free flap reconstruction (free fibular flap and anterolateral thigh free flap). Intraoperatively, he experienced cardiac arrest after anastomosis due to hypovolemia or hypoxia, requiring external cardiac massage and vasopressor administration. Despite the initial restoration of circulation, subsequent cardiac arrest ensued, necessitating further resuscitation. Postoperatively, vasopressors were also administered due to hemodynamic instability. Contrary to concerns, both flaps demonstrated sustained vitality, challenging prevailing apprehensions about vasopressor-induced vasoconstriction compromising flap viability. This observation suggests that vasopressors may not significantly threaten flap viability, prompting reconsideration of hesitations and encouraging further investigation. The study advocates for a judicious evaluation of vasopressor administration in free flap procedures, enriching clinical considerations for optimal patient care.

Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that vasopressor-induced pulmonary hypertension is caused by increased pulmonary blood volume and tested this hypothesis in dogs under general anesthesia. In normal hearts (model 1), phenylephrine (2.5 μg/kg/min) transiently increased right but decreased left cardiac output, associated with increased pulmonary blood volume (63% ± 11.8, P  = 0.007) and pressures in the left atrium, pulmonary capillary, and pulmonary artery. However, the trans-pulmonary gradient and pulmonary vascular resistance remained stable. These changes were absent after decreasing blood volume or during right cardiac dysfunction to reduce pulmonary blood volume (model 2). During double-ventricle bypass (model 3), phenylephrine (1, 2.5 and 10 μg/kg/min) only slightly induced pulmonary vasoconstriction. Vasopressin (1U and 2U) dose-dependently increased pulmonary artery pressure (52 ± 8.4 and 71 ± 10.3%), but did not cause pulmonary vasoconstriction in normally beating hearts (model 1). Pulmonary artery and left atrial pressures increased during left ventricle dysfunction (model 4), and further increased after phenylephrine injection by 31 ± 5.6 and 43 ± 7.5%, respectively. In conclusion, vasopressors increased blood volume in the lung with minimal pulmonary vasoconstriction. Thus, this pulmonary hypertension is similar to the hemodynamic pattern observed in left heart diseases and is passive, due to redistribution of blood from systemic to pulmonary circulation. Understanding the underlying mechanisms may improve clinical management of patients who are taking vasopressors, especially those with coexisting heart disease.