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A Guide to Use of Crystalloids
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Jeetinder Kaur Makkar, Mandeep Tundak
A patient will be fluid responsive if fluid bolus increases the stressed blood volume with a resultant increase in mean circulating filling pressure, thereby increasing the gradient of venous return if ventricles are functioning on an ascending limb of the Frank–Starling curve. Fluid responsiveness can be defined by various parameters:Passive leg raise (PLR) test – Passively raising the lower limbs mobilizes almost 300 ml of fluid from the lower limb to intravascular space. A more than 10% increase in pulse pressure or stroke volume indicates patient is fluid responsive.An increase in SV by at least 10% after 500 ml of crystalloid infusion indicates fluid responsiveness.Pulse pressure variation or SV variation more than 12% upon arterial pressure contour analysis indicates fluid responsiveness.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
A non-invasive practical method of clinically assessing ventricular preload is the passive leg raise manoeuvre. This relies on the principle that raising the legs above the level of the heart increases venous return to the heart by about 300–500mL. The increase in ventricular preload will transiently increase the cardiac output in those patients who are fluid-deficient. This approach had the benefits of predicting those patients who will increase their stroke volume when given additional fluid, without the deleterious consequences of fluid overload, as the legs can be returned to the supine position if no improvement is seen. Patients who respond to the passive leg raise manoeuvre can safely be given a fluid bolus/challenge as required (Picket et al. 2017).
Hemodynamic changes during aortic valve surgery among patients with aortic stenosis
Published in Scandinavian Cardiovascular Journal, 2022
Rasmus Carter-Storch, Søren Mose Hansen, Jordi S. Dahl, Kasper Enevold, Nils Sofus Borg Mogensen, Henrik Berg, Marie-Annick Clavel, Jacob E. Møller
Conversely, after fluid challenge, we observed a marked increase in both SVi and CO, likely caused by increased preload and the Frank-Starling mechanism. This is in contrast to a study by Sonny et al., studying the CO response to passive leg raise in sedated patients with severe AS [24]. They found that passive leg raise did not improve CO, and concluded that patients with severe AS were already in the upper end of the Starling curve and consequently did not benefit from increased preload. In our study, the majority of patients had normal ejection fraction and only mildly elevated LV filling pressure, and it is likely that the increase in Svi would be lower in patients with heart failure and ischemic heart disease. Although patients almost uniformly increased SVi after fluid bolus, this increase was negatively associated with baseline heart rate. The combination of decreased LV compliance associated with AS and shortened LV filling time caused by relative tachycardia may have caused a reduced SVi response. Further, similarly to the findings regarding dobutamine infusion, the patients with a larger decrease in SVi after general anesthesia also had the largest increase in SVi after fluid bolus, which would support that the decrease in SVi after general anesthesia is in part caused by a reduction in preload [25], which can be restored when preload is increased.