Abstract
BackgroundWe hypothesized that the cardiovascular responses to Surviving Sepsis Guidelines (SSG)-defined resuscitation are predictable based on the cardiovascular state.MethodsFifty-five septic patients treated by SSG were studied before and after volume expansion (VE), and if needed norepinephrine (NE) and dobutamine. We measured mean arterial pressure (MAP), cardiac index (CI), and right atrial pressure (Pra) and calculated pulse pressure and stroke volume variation (PPV and SVV), dynamic arterial elastance (Eadyn), arterial elastance (Ea) and left ventricular (LV) end-systolic elastance (Ees), Ees/Ea (VAC), LV ejection efficiency (LVeff), mean systemic pressure analogue (Pmsa), venous return pressure gradient (Pvr), and cardiac performance (Eh), using standard formulae.ResultsAll patients were hypotensive (MAP 56.8 ± 3.1 mmHg) and tachycardic (113.1 ± 7.5 beat min−1), with increased lactate levels (lactate = 5.0 ± 4.2 mmol L−1) with a worsened VAC. CI was variable but > 2 L min−1 M−2 in 74%. Twenty-eight-day mortality was 48% and associated with admission lactate, blood urea nitrogen (BUN), and creatinine levels but not cardiovascular state. In all patients, both MAP and CI improved following VE, as well as cardiac contractility (Ees). Fluid administration improved Pra, Pmsa, and Pvr in all patients, whereas both HR and Ea decreased after VE, thus normalizing VAC. CI increases were proportional to baseline PPV and SVV. CI increases proportionally decreased PPV and SVV. VE increased MAP > 65 mmHg in 35/55 patients. MAP responders had higher PPV, SVV, and Eadyn than non-responders. NE was given to 20/55 patients in septic shock, but increased MAP > 65 mmHg in only 12. NE increased Ea, Eadyn, Pra, Pmsa, and VAC while decreasing HR, PPV, SVV, and LVeff. MAP responders had higher pre-NE Ees and lower VAC. Dobutamine was given to 6/8 patients who remained hypotensive following NE. It increased Ees, MAP, CI, and LVeff, while decreasing HR, Pra, and VAC. At all times and all steps of the protocol, CI changes were proportional to Pvr changes independent of treatment.ConclusionsThe cardiovascular response to SSG-based resuscitation is highly heterogeneous but predictable from pre-treatment measures of cardiovascular state.
Highlights
Human sepsis is the result of a complex pathological process characterized by an infection-induced generalized intravascular inflammatory state causing marked dysregulation of cardiovascular adaptive responses [1, 2]
Thirty-day mortality was associated with higher admission lactate, blood urea nitrogen (BUN), and creatinine levels, but not with any other measured or derived hemodynamic variables
35 patients resolved their hypotension with volume expansion (VE) alone but retained a 44% 30-day mortality rate, whereas those in septic shock had a 52% 30-day mortality rate of which was not significantly different
Summary
Human sepsis is the result of a complex pathological process characterized by an infection-induced generalized intravascular inflammatory state causing marked dysregulation of cardiovascular adaptive responses [1, 2]. As defined by the Surviving Sepsis Guidelines (SSG), focuses on source control, early broad-spectrum antibiotics, and cardiovascular stabilization [3]. Intravascular fluid infusion to restore an adequate pressure gradient for venous return, vasop ressor-induced increased vasomotor tone to maintain organ perfusion pressure, and inotropes to improve cardiac contractility represent the three primary cardiovascular therapies used to restore cardiovascular stability in septic shock patients [3]. We hypothesized that the cardiovascular responses to Surviving Sepsis Guidelines (SSG)-defined resuscitation are predictable based on the cardiovascular state
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