The paradox of reduced myocardial shortening in the
presence of preserved EF is explained mathematically
through geometric factors, where EF can be constant
for a large variation in shortening if other geometric
factors are altered to compensate. Increased wall
thickness and/or reduced ED volume augment EF,
and therefore can maintain a normal EF despite
reduced shortening. EF is quadratically dependent
on circumferential shortening and only linearly
dependent on longitudinal shortening; hence, EF is
less sensitive to a reduction in longitudinal shortening.
Our findings suggest that strain measurements reflect
systolic function better than EF in patients with
preserved EF.
Comparison Between Ejection Fraction and Strain
Editorial Comment V. Fuster MP4
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Wednesday, August 16, 2017
Oliguria is a poor marker for perfusion
Oliguria is an overused parameter to guide resuscitation and must always be interpreted within the clinical context
The 2016 version of the “Surviving Sepsis Campaign” no longer mentions a UO of ≥0.5 mL/
kg/h as a goal of resuscitation. Isolated oliguria with-out signs of vasoplegia, hypovolemia, or low cardiac output is unlikely to be explained by a systemic hemo-dynamic cause and must not evoke the administration of additional fluids or vasopressors.
Oliguria should also not trigger further hemodynamic interventions in the clinical setting of established AKI.
Oliguria resulting from vasodilatory hypotension should preferably be treated with a vasopressor. However, a MAP of 80–85 mmHg as target does not seem to be a beneficial strategy, except in patients with chronic hypertension.
Reference articles:
Does this critically ill patient with oliguria need more fuids, a vasopressor, or neither?
The Ten Principles behind Arterial Pressure
The 2016 version of the “Surviving Sepsis Campaign” no longer mentions a UO of ≥0.5 mL/
kg/h as a goal of resuscitation. Isolated oliguria with-out signs of vasoplegia, hypovolemia, or low cardiac output is unlikely to be explained by a systemic hemo-dynamic cause and must not evoke the administration of additional fluids or vasopressors.
Oliguria should also not trigger further hemodynamic interventions in the clinical setting of established AKI.
Oliguria resulting from vasodilatory hypotension should preferably be treated with a vasopressor. However, a MAP of 80–85 mmHg as target does not seem to be a beneficial strategy, except in patients with chronic hypertension.
Reference articles:
Does this critically ill patient with oliguria need more fuids, a vasopressor, or neither?
The Ten Principles behind Arterial Pressure
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