EDITORIAL

Myocardial dysfunction in sepsis: no role for NO?

E Belcher, J Mitchell, T Evans

Unit of Critical Care, Imperial College School of Medicine, Royal Brompton Hospital, London SW3 6NP, UK

Correspondence to:
Correspondence to:
Professor TW Evans, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK;
t.evans@rbh.nthames.nhs.uk

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The effects of nitric oxide on myocardial function in clinical sepsis are unclear, with studies in experimental models suggesting both beneficial and deleterious effects

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Keywords: sepsis; myocardial dysfunction; nitric oxide

Abbreviations: EDPVR, end diastolic pressure; volume relationship; ESPVR, end systolic pressure-volume relationship; LVEDV, left ventricular end diastolic volume; MLA, monophosphoryl lipid A; NO, nitric oxide; NOS, nitric oxide synthase; SIRS, systemic inflammatory response syndrome; SVR, systemic vascular resistance

Sepsis and its sequelae¹ represent an important cause of mortality among the critically ill, particularly if cardiovascular dysfunction ensues. In these circumstances, refractory hypotension develops leading to multiple organ failure, and some 50% of such cases fail to survive.² Although sepsis is defined as the systemic response to infection, less than 50% of patients with septic shock have positive blood cultures.³ Indeed, the clinical manifestations of sepsis may be seen in association with a variety of non-infective insults including major trauma, burns, pancreatitis, rhabdomyolysis, and surgery necessitating cardiopulmonary bypass, and are then termed the systemic inflammatory response syndrome (SIRS).

Traditionally, descriptions of septic shock defined an early, hyperdynamic phase, with warm peripheries, low systemic vascular resistance (SVR), and high cardiac output. In non-survivors the "warm" phase was thought to progress to a hypodynamic or "cold" phase in which cool peripheries, increased SVR, and low cardiac output were the dominant clinical . . . [Full text of this article]

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