Shock Syndromes I

General goals of therapy include resolution of altered mental status and adequate urinary output (above

0.5 mL/kg of body weight per hour). However, these goals may be challenging to assess in patients who

are given medications that mask the ability to assess the organ function (e.g., sedatives) or in patients

with chronic organ dysfunction (e.g., end-stage renal disease).

Intravenous fluids are given to increase preload and subsequently increase SV, increase CO, and

increase Do2.

(presumably because of inadequate SV) and if the patient is fluid responsive.

Fluid responsiveness is defined as at least a 10%–15% increase in CO after fluid administration.

This is best assessed by giving a fluid challenge and evaluating the response.

A change in blood pressure is not a reliable indicator of CO response to a fluid challenge; an

assessment of CO (or SV) change should be used instead.

Patients given additional fluid when they are no longer fluid responsive will not experience the

beneficial effects of fluid (increased CO)—only the harmful effects (e.g., pulmonary edema). Although

an argument could be made to determine fluid responsiveness in each patient, it is most critical in

patients for whom harmful fluid effects cannot be tolerated (e.g., those with refractory hypoxemia in

the setting of shock).

Fluid responsiveness may be predicted by static or dynamic markers.

Static markers of fluid responsiveness include the cardiac filling pressures CVP and PCWP.

Dynamic markers of fluid responsiveness include stroke volume variation (SVV), systolic pressure

variation, pulse pressure variation (PPV), and IVC variation.

Although CVP and PCWP may help differentiate shock states and may help to provide an understanding

of static intravascular volume status, they are not reliable predictors of fluid responsiveness.

In one study of patients with sepsis and septic shock, a CVP less than 8 mm Hg and a PCWP less

than 12 mm Hg had fluid responsiveness positive predictive values of 47% and 54%, respectively.

Systematic reviews and meta-analyses suggest that CVP should not be used as a resuscitation

parameter.

Fluid responsiveness is better predicted by dynamic markers of fluid responsiveness than by static

markers of volume status or fluid responsiveness.

The area under the receiver operating characteristic curve (AUC ROC), with the optimal area

of 1, for predicting fluid responsiveness is as follows: PPV 0.94 (95% confidence interval [CI],

0.93–0.95), systolic pressure variation 0.86 (0.82–0.90), and SVV 0.84 (0.78–0.88). In contrast, the

AUC ROC for predicting fluid responsiveness for CVP is 0.55 (0.48–0.62).

Because they can be obtained from monitoring devices (Table 2), PPV and SVV are more commonly

used in practice than is systolic pressure variation.

The dynamic markers, PPV, SVV, and IVC collapsibility, are based on heart-lung interactions in

mechanically ventilated patients.

In mechanically ventilated patients, a controlled positive pressure breath increases pleural pressure.

This increase in intrathoracic pressure leads to a decrease in venous return, decreased RV preload,

and decreased RV SV. LV preload is subsequently decreased, which may lead to a decrease in LV SV.

Patients who are preload (fluid) responsive (on the steep rather than the flat portion of the Frank-

Starling curve) will have relatively large changes in LV SV with positive pressure breaths. This

leads to variation in the LV SV between periods with and without positive pressure breaths.

Some ICU monitors can display automated PPV from an arterial catheter without additional

monitoring equipment or devices.