Vasopressor and inotropic support in septic shock: An evidence-based review

Beale, Richard; Hollenberg, Steven M.; Vincent, Jean‐Louis; Parrillo, Joseph E.

doi:10.1097/01.ccm.0000142909.86238.b1

Cited by 223 publications

(148 citation statements)

References 106 publications

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“…In a direct comparison with dopamine, noradrenaline caused less arrhythmia [45] and less skin ischaemia [114,115]. 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: 99%

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: 99%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

CVP

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“…[42][43][44][45] The 2012 Surviving Sepsis Guidelines suggest using norepinephrine as the first line agent for these patients. 46 Norepinephrine vs Dopamine.…”

Section: Question 5: Which Vasopressors and Inotropes Should Be Used mentioning

confidence: 99%

Vasopressor and Inotrope Use in Canadian Emergency Departments: Evidence Based Consensus Guidelines

Djogovic

MacDonald

Wensel

et al. 2015

CJEM

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“…No choque séptico, ocorre uma complexa interação entre vasodilatação patológica, hipovolemia relativa e/ou absoluta, disfunção miocárdica e alteração da distribuição do fluxo sanguíneo secundário a resposta inflamatória à infecção e, mesmo após o restabelecimento da normovolemia, anormalidades microcirculatórias podem persistir (BEALE et al, 2004;DRIES, 2007).…”

Section: Classificação Do Choque Circulatóriounclassified

“…A diminuição do nível de consciência e da diurese são sinais precoces de choque (MARSON et al, 1998). Como a hipovolemia é um achado primário dos vários tipos de choque e o restabelecimento da pressão sanguínea um dos objetivos terapêuticos, a mensuração acurada e contínua de pressão sanguínea é essencial nos casos de choque (BEALE et al, 2004).…”

Section: Diagnósticounclassified

Choque circulatório em equinos

et al. 2010

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ResumoChoque circulatório pode ser definido como uma falha circulatória aguda com liberação inadequada de oxigênio e nutrientes aos tecidos, resultando em hipóxia celular. O choque pode ser classificado como cardiogênico, obstrutivo, hipovolêmico ou distributivo. As consequências fisiopatológicas da perfusão tecidual inadequada estão diretamente relacionadas à isquemia celular, liberação inadequada de O 2 e produção de potentes mediadores inflamatórios. Caso as anormalidades de perfusão tecidual se perpetuem, a função de vários órgãos se torna inadequada. A consequente reperfusão poderá exacerbar a disfunção orgânica e, nos casos graves, culminar na síndrome da disfunção orgânica múltipla. O reconhecimento precoce de equinos em choque circulatório e o fornecimento imediato de suporte circulatório efetivo são essenciais. Em todos os casos o objetivo é restaurar a perfusão e a liberação de oxigênio aos tecidos, enquanto se corrige a causa primária. A demora em fazer o diagnóstico e iniciar o tratamento, bem como a ressuscitação sub-ótima, contribuem para o desenvolvimento de falha vascular periférica e alterações irreversíveis na utilização de oxigênio, culminando na disfunção orgânica. Palavras-chave: Equino, fluidoterapia, hipovolemia, perfusão tecidual, mediadores inflamatórios AbstractCirculatory shock can be defined as an acute circulatory failure with an inadequate tissue delivery of oxygen and nutritive substrates to the tissues, resulting in generalised cellular hypoxia. Shock can be classified as cardiogenic, obstructive, hypovolaemic, or distributive. The pathophysiologic consequences of inadequate tissue perfusion are directly related to cell ischemia, inadequate O 2 delivery, and the production of proinflammatory mediators. If abnormalities of tissue perfusion are allowed to persist, the function of vital organs will be impaired. The subsequent reperfusion will exacerbate organ dysfunction and, in severe cases, may culminate in multiple organ dysfunction syndrome. Early recognition of equine that are shocked and immediate provision of effective circulatory support is therefore essential. In all cases the objective is to restore oxygen delivery to the tissues while correcting the underlying cause. Delays in making the diagnosis and initiating treatment, as well as suboptimal resuscitation, contribute to the development of peripheral vascular failure and irreversible defects in oxygen use which can culminate in vital organ dysfunction.

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Vasopressor and inotropic support in septic shock: An evidence-based review

Cited by 223 publications

References 106 publications

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Vasopressor and Inotrope Use in Canadian Emergency Departments: Evidence Based Consensus Guidelines

Choque circulatório em equinos

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