Cardiovascular management of septic shock

Clinical and Experimental Emergency Medicine

Journal of Pediatric Critical Care

Mean Arterial Pressure (MAP)-Central venous pressure (CVP) (MM of Hg) Term Newborn 120 to 180 55 Up To 1 year 120 to 180 60 Up To 2 years 120 t0 160 65 Up To 7 years 100 t0 140 65 Up To 15 years 90 to 140 65 ABSTRACT Severe sepsis and septic shock are complications of infection leading to high morbidity and mortality. Hemodynamic outcomes are considered surrogate markers for survival-an ultimate goal of treatment strategies. The goal of vasoactive agents is to improve arterial blood pressure (age related norms) without associated adverse effects. Early initiation of a vasoactive agent in fl uid-refractory septic shock has a signifi cant role in the outcome; initiation within an hour of presentation is recommended and is associated with favorable outcomes. The choice of the correct vasoactive agent in a given scenario has a pivotal role on the desired outcome as well as the duration to achieve it. Cardiac dysfunction is a well recognized complication of septic shock, occurring in about 60% of the patients. So ionotropes may play a role in septic shock patients with associated myocardial dysfunction and signs of organ hypoperfusion despite achieving adequate preload and mean arterial pressure. In children presentation of septic shock is more complex, predominantly vasoconstricted with low cardiac output. Sometimes they can have deranged myocardial contractility and SVR problems requiring combination of inotropes and vasopressors. Hence the choice of inotrope remains empirical. Vasoactive therapy should be guided by clinical end points.

Critical Care, 2022

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.

Annals of Intensive Care, 2018

CHEST Journal, 2004

Study objectives: To determine possible differences in morbidity and mortality between early and late onset of septic shock in ICU patients. Design: Systematic data collection. Setting: Thirty-one-bed, mixed, medicosurgical ICU in a university hospital. Patients: All 65 patients who acquired septic shock after admission to the ICU between February 1999 and April 2000. Interventions: None. Measurements and results: Forty-one of the 65 patients presented with septic shock within 24 h of admission to the ICU (early septic shock [ESS]); the other 21 patients acquired septic shock > 24 h after ICU admission (late septic shock [LSS]). Eleven patients had a second episode (7 patients in the ESS group, and 4 patients in the LSS group), and 1 patient in the LSS group had a third episode of septic shock. Patients with ESS had higher APACHE (acute physiology and chronic health evaluation) II (mean ؎ SD, 26 ؎ 6 vs 20 ؎ 6; p ‫؍‬ 0.002) and sequential organ failure assessment (SOFA) scores (11 ؎ 3 vs 7 ؎ 3, p < 0.001) on ICU admission, and a higher blood lactate concentration at the onset of shock (median 3.70 mEq/L; interquartile range, 2.6 to 6.6 mEq/L; vs median, 2.50 mEq/L [interquartile range, 1.8 to 4.0 mEq/L], p ‫؍‬ 0.03) than patients with LSS. However, the duration of septic shock (median, 42 h [interquartile range, 21 to 97 h] vs median, 93 h [interquartile range, 32 to 241 h], p ‫؍‬ 0.058) and the length of ICU stay after the onset of septic shock (median, 75 h; [interquartile range, 38 to 203 h] vs median, 321 h [interquartile range, 96 to 438 h], p ‫؍‬ 0.018), was shorter in patients with ESS than patients with LSS. The ICU mortality rate was 63% (26 patients) in the ESS group, and 88% (21 patients) in the LSS group (p ‫؍‬ 0.071). At the onset of the first episode of shock, patients with ESS had higher SOFA scores (11 ؎ 3 vs 9 ؎ 3, p ‫؍‬ 0.045), lower pH (7.24 ؎ 0.15 vs 7.33 ؎ 0.12, p ‫؍‬ 0.01), and were treated with higher doses of dopamine (median, 20 g/kg/min [interquartile range, 14 to 20 g/kg/min] vs median, 12 g/kg/min [interquartile range, 8 to 20 g/kg/min], p ‫؍‬ 0.028) than patients with LSS. Conclusions: Septic shock is more severe when of early onset, as reflected by more severe organ dysfunction, greater lactic acidosis, and higher vasopressor requirements, yet the outcome is better, as reflected by a shorter duration of the shock episode, shorter ICU stay, and slightly lower mortality rates. These differences may influence clinical trials of therapeutic agents for sepsis, and should be taken into account when analyzing the results.

Canadian Journal of Anaesthesia, 1997

Many patients with sepsis require surgery for their management, often on an urgent or emergency basis. Anaesthetists are commonly required to manage patients with sepsis and septic shock in the operating room, post anaesthesia recovery area, and the intensive care unit. Since little has been written in the Anaesthesia literature on sepsis and septic shock, a review of this topic was considered appropriate. Source: References were obtained from computerized searches of the National Library of Medicine (English language), recent review artides and personal files. Principle ]Finding;s: Septic shock is a common cause of morbidity and mortality. Its presentation may be subtle or catastrophic. Successful management depends on an understanding of the pathophysiology of the syndrome, allowing rapid, appropriate resuscitation. This often requires aggressive correction of volume deficit. maintenance of adequate perfusion pressure with inotropic and vasopressor therapy, mechanical ventilation and correction of coagulopathy. Appropriate cultures must be taken and antibiotic therapy started, often empirically. Anaesthetic management should indude careful haemodynamic monitoring. Anaesthesia induction and maintenance must be tailored to the haemodynamically unstable patient. C.,ondusiorts: The management of the septic patient in the perioperative period presents a challenge for the anaesthetist. Haemodynamic and respiratory instability should be anticipated. Management requires multisystem intervention and careful anaesthetic management.

IMPORTANCE Definitions of sepsis and septic shock were last revised in 2001. Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination. OBJECTIVE To evaluate and, as needed, update definitions for sepsis and septic shock. PROCESS A task force (n = 19) with expertise in sepsis pathobiology, clinical trials, and epidemiology was convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine. Definitions and clinical criteria were generated through meetings, Delphi processes, analysis of electronic health record databases, and voting, followed by circulation to international professional societies, requesting peer review and endorsement (by 31 societies listed in the Acknowledgment). KEY FINDINGS FROM EVIDENCE SYNTHESIS Limitations of previous definitions included an excessive focus on inflammation, the misleading model that sepsis follows a continuum through severe sepsis to shock, and inadequate specificity and sensitivity of the systemic inflammatory response syndrome (SIRS) criteria. Multiple definitions and terminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepancies in reported incidence and observed mortality. The task force concluded the term severe sepsis was redundant. RECOMMENDATIONS Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%. In out-of-hospital, emergency department, or general hospital ward settings, adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following clinical criteria that together constitute a new bedside clinical score termed quickSOFA (qSOFA): respiratory rate of 22/min or greater, altered mentation, or systolic blood pressure of 100 mm Hg or less. CONCLUSIONS AND RELEVANCE These updated definitions and clinical criteria should replace previous definitions, offer greater consistency for epidemiologic studies and clinical trials, and facilitate earlier recognition and more timely management of patients with sepsis or at risk of developing sepsis.

Journal of Critical Care, 2020

Critical Care, 2018

Background: Vasopressin (AVP) is commonly added to norepinephrine (NE) to reverse shock in patients with sepsis. However, there are no data to support the appropriate strategy of vasopressor tapering in patients on concomitant NE and AVP who are recovering from septic shock. Therefore, the objective of this study was to evaluate the incidence of hypotension while tapering vasopressors in patients on concomitant NE and AVP recovering from septic shock. Methods: Patients with septic shock receiving concomitant NE and AVP were randomly assigned to taper NE first (NE group) or AVP first (AVP group). The primary end point was the incidence of hypotension within one hour of tapering of the first vasopressor. We also evaluated the association between serum copeptin levels and the occurrence of hypotension. Results: The study was stopped early due to a significant difference in the incidence of hypotension after 38 and 40 patients were enrolled in the NE group and the AVP group, respectively. There were 26 patients (68.4%) in the NE group versus 9 patients (22.5%) in the AVP group who developed hypotension after tapering the first vasopressor (p < 0.001). There was a similar finding during the subsequent tapering of the second vasopressor (64.5% in the NE vs 25.0% in the AVP group, p = 0.020). Finally, NE tapering was significantly associated with hypotension during the study period (hazard ratio, 2.221; 95% confidence interval, 1.106-4.460; p = 0.025). The serum copeptin level was lower in patients in whom hypotension developed during tapering of AVP than it was in those without hypotension. Conclusions: Tapering NE rather than AVP may be associated with a higher incidence of hypotension in patients recovering from septic shock who are on concomitant NE and AVP. However, further studies with larger sample sizes are required to better determine the appropriate strategy for vasopressor tapering.

Emergency Care Journal

Much research, both pathophysiological and clinical, has been produced about septic shock during the last 20 years. Nevertheless, many aspects of treatment are still controversial, among these the approach to the administration of fluids and vasopressors. After the first clinical trial on Early goal-directed therapy (EGDT) was published, a liberal approach to the use of fluids and conservative use of vasopressors prevailed, but in recent years a more restrictive use of fluids and an earlier introduction of vasopressors seem to be preferred. Although both treatments are based on sound pathophysiological knowledge, clinical evidence is still inadequate and somehow controversial. In this non-systematic review, recent research on the hemodynamics of septic shock and its treatment with fluids and inotropes is discussed. As a conclusion, general indications are proposed for a practical approach to patients in septic shock.