Shock Syndromes I
| d. | The specific values of PPV and SVV used to predict fluid responsiveness vary by study, specific |
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conditions (e.g., use of vasopressors), and assessment method or device. In a systematic review,
thresholds to predict fluid responsiveness were PPV greater than 12.5% and SVV greater than
11.6%.
IVC variation (also termed IVC collapsibility or IVC distensibility) uses echocardiography to
visualize the diameter of the IVC during positive pressure ventilation. With a positive pressure
breath from mechanical ventilation, venous return is impaired, and the diameter of the IVC
increases (IVC distensibility). The opposite change in IVC diameter occurs in patients breathing
spontaneously (IVC collapsibility). The change in IVC diameter during inspiration is higher in
patients who are fluid responsive than in those who are not fluid responsive.
In one study, the AUC ROC for predicting fluid responsiveness for IVC distensibility was
0.84 (95% confidence interval [CI], 0.63–1.0), and the best cutoff was 16% (sensitivity 67%,
specificity 100%).
ii.
In a larger, multicenter study of mechanically ventilated patients with varied causes of
circulatory shock, IVC distensibility had an AUC ROC for predicting fluid responsiveness
of 0.64 for a threshold of 8% (sensitivity 55%, specificity 70%). In the patient subset with
all assessed dynamic markers of fluid responsiveness available, the AUC ROC for predicting
fluid responsiveness was significantly higher for respiratory variations in superior vena cava
diameter (0.74, threshold of 21% or greater) than PPV (0.66, threshold of 11% or greater,
p=0.01) and IVC distensibility (0.65, threshold of 13% or greater, p=0.02). Of note, superior
vena cava diameter changes must be assessed by transesophageal echocardiography, which is
not commonly performed for this purpose in the United States. IVC variation may be assessed
by transesophageal or transthoracic echocardiography.
The passive leg raise (PLR) test measures the hemodynamic effects of a positional change in the patient’s
legs. Changing the position of the patient’s bed such that the patient’s legs are lifted to a 45-degree angle
with the patient’s head placed horizontally leads to a transfer of blood from the abdominal compartment
and lower extremities to the intrathoracic compartment.
This increase in venous return may subsequently increase SV and CO if the patient is preload
responsive.
An increase in CO by 10%–15% after PLR is considered a positive test.
The benefit of the PLR test is that it can be used in spontaneously breathing or nonintubated patients.
In addition, it does not require the administration of fluid (which may be harmful if the patient is
not fluid responsive) and can easily be reversed by returning patients to their previous position.
| d. | A caveat to use of the PLR test is that a method of evaluating CO is required to determine response |
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(or lack thereof). A change in blood pressure is not an adequate surrogate marker for CO, as noted
earlier. The CO measurement may be obtained from an arterial pulse pressure waveform analysis
monitor (minimally invasive approach) or from a bioimpedance device, bioreactance device, or
echocardiographic LVOT VTI (noninvasive approach).
Several caveats exist for using dynamic markers of fluid responsiveness.
PPV and SVV assume the following: sinus cardiac rhythm, the absence of significant valvular
dysfunction, intubation and mechanical ventilation without spontaneous breaths, and tidal volume
of 8 mL/kg or more of predicted body weight. Values for PPV and SVV above the noted thresholds
do not reliably predict fluid responsiveness in the setting of arrhythmias (e.g., atrial fibrillation). If
these assumptions are not fulfilled, PPV and SVV are not reliable in predicting fluid responsiveness.
IVC distensibility also requires intubation and mechanical ventilation without spontaneous breaths
and is not conducive to continuous monitoring.
The real-time response of CO (or lack thereof) with PLR must be assessed using a CO monitoring
device. In addition, intra-abdominal hypertension reduces the ability of PLR to detect fluid
responsiveness.