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| | Myocardial dysfunction in sepsis: no role for NO? -- Belcher et al. 87 (6): 507 -- Heart |
 | | Left ventricular end diastolic pressure (LVEDP) then increases in a curvilinear manner during addition of further volume. |
 | | 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 |
 | | While NO may be responsible for the reduction in systolic contractility, the septic patient is able to maintain end systolic volume because of a reduction in systemic vascular resistance; therefore the overriding haemodynamic effect of NO in sepsis may be facilitation of ventricular dilatation, which acts to further stroke volume and maintain cardiac output. |
| heart.bmjjournals.com /cgi/content/full/87/6/507 |
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