Association of arterial blood pressure and vasopressor load with septic shock mortality: a post hoc analysis of a multicenter trial

Dünser, Martin W.; Ruokonen, Esko; Pettilä, Ville; Ulmer, Hanno; Torgersen, Christian; Schmittinger, Christian A.; Jakob, Stephan M.; Takala, Jukka

doi:10.1186/cc8167

Cited by 200 publications

(155 citation statements)

References 31 publications

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“…While catecholamines are effective in counteracting haemodynamic instability [116], excessive use might be harmful. In a retrospective analysis, mean arterial pressures maintained >70 mmHg were not associated with improved survival though mortality was progressively higher in those given increasing doses of vasopressor to achieve this [117].…”

Section: Inotropes For Contractilitymentioning

confidence: 92%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

CVP

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Septic shock is characterized by circulatory compromise, microcirculatory alterations and mitochondrial damage, which all reduce cellular energy production. In order to reduce the risk of major cell death and a diminished likelihood of recovery, adaptive changes appear to be activated. As a result, cells and organs may survive in a non-functioning hibernation-like condition. Sepsis-induced cardiac dysfunction may represent an example of such functional shutdown. Sepsis-induced myocardial dysfunction is common, corresponds to the severity of sepsis, and is reversible in survivors. Its mechanisms include the attenuation of the adrenergic response at the cardiomyocyte level, alterations of intracellular calcium trafficking and blunted calcium sensitivity of contractile proteins. All these changes are mediated by cytokines. Treatment includes preload optimization with sufficient fluids. However, excessive volume loading is harmful. The first line vasopressor recommended at present is norepinephrine, while vasopressin can be started as a salvage therapy for those not responding to catecholamines. During early sepsis, cardiac output can be increased by dobutamine. While early administration of catecholamines might be necessary to restore adequate organ perfusion, prolonged administration might be harmful. Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine reduces myocardial oxygen expenditure and ameliorates diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. All these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice. While early administration of catecholamines might be necessary to restore adequate organ perfusion and pressure, prolonged administration might be harmful.Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine will reduce myocardial oxygen expenditure and ameliorate diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. However, all these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice.-3 -Alain Rudiger & Mervyn Singer: The heart in sepsis

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Section: Inotropes For Contractilitymentioning

confidence: 92%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

CVP

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“…Algunos estudios han documentado buenos resultado clínicos en pacientes con shock séptico en quienes se ha empleado como meta hemodinámica una PAM ≥ 65 mmHg [29][30][31][32] . No obstante, algunos pacientes con hipertensión arterial crónica pueden requerir mayores niveles de PAM para asegurar una adecuada presión de perfusión a los diferentes órganos, lo que debe ser determinado en forma individualizada y evaluado a través del comportamiento de los diferentes marcadores de oxigenación tisular.…”

Section: En Presencia De Hipotensión Y/ounclassified

Actualización del bundle de reanimación inicial y monitorización integral de la perfusión tisular en la sepsis severa

P¹,

P²

2013

Rev. méd. Chile

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“…In contrast to the clinical trials mentioned above [9,10], retrospective observational studies suggest that MAP levels between 60 and 65 mmHg can best predict survival from septic shock [13,14]. Elevating MAP above 70 mmHg by intensifying vasopressor therapy was even associated with an increased risk of adverse events [11]. To allow for more definite conclusions, better compliance with the protocol and more data regarding concomitant interventions and actual hemodynamic values are needed in future trials (Table 1).…”

mentioning

confidence: 99%

“…On the basis of previous study results, many intensive care nurses and physicians seem to consider a MAP between 70 and 85 mmHg as the 'comfort zone' . However, vasopressors may have serious adverse effects in critically ill patients with shock [10][11][12], and, therefore, titration of these agents to the lowest necessary dose may be beneficial. In contrast to the clinical trials mentioned above [9,10], retrospective observational studies suggest that MAP levels between 60 and 65 mmHg can best predict survival from septic shock [13,14].…”

mentioning

confidence: 99%

“…The objective to identify a population at specific risk for adverse vasopressor effects is though clinically relevant. Observational studies have suggested that age per se is not an independent risk factor for the occurrence of adverse events during vasopressor therapy [11,12], which emphasizes the need for large-scale RCTs with predefined subgroups and stratification by subgroup before any conclusions can be made. Instead, the intensity of vasopressor therapy and the disease severity may be the most relevant independent risk factors to predict complications.…”

mentioning

confidence: 99%

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