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Editorial
Myocardial dysfunction in sepsis: no role for NO?
  1. E Belcher,
  2. J Mitchell,
  3. T Evans
  1. Unit of Critical Care, Imperial College School of Medicine, Royal Brompton Hospital, London SW3 6NP, UK
  1. Correspondence to:
    Professor TW Evans, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK;
    t.evans{at}rbh.nthames.nhs.uk

https://doi.org/10.1136/heart.87.6.507

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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

    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).

    MYOCARDIAL DYSFUNCTION IN SEPSIS

    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 features. However, traditional indices of myocardial function, including cardiac and stroke volume index and ejection fraction, may be inaccurate as a significant depression in contractility can be masked by changes in heart rate, preload, and afterload. To quantify intrinsic myocardial depression, an assessment of left ventricular performance using load independent techniques is therefore required. The end systolic pressure–volume relationship (ESPVR) is unaffected by changes in afterload and preload over a wide range. The slope is maximal at end systole (Emax) and has the units of elastance E = ΔP/ΔV. The linear relationship between these parameters is shifted to the left under conditions of increased contractility and to the right with reduced contractility.

    Such techniques have revealed that patients with septic shock have …

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