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C HAPTER 2 1 / Hemodynamic Monitoring 485
with hemorrhage (PPV% baseline 12% 9%, posthemorrhage shock, a PLR-induced increase of 10% in aortic bloodflow (as
28% 11%, p .001; SPV% baseline 12.5% 6.5%, posthem- measuredby TEE) predicted a fluidbolus-induced increase of
orrhage 21% 8, p .05). The increase in values reflects increased 15% in aortic bloodflow (sensitivity 97%, specificity
fluid responsiveness, but may also reflect the effect of decreased SBP 94%). 278 On the basis of the random and systematic variability in
and pulse pressure on the absolute values. In the same animals, the CO measurements, De Backer 291 recommends that at a mini-
subsequent addition of norepinephrine caused a decrease in PPV mum a 15% PLR-induced change in CO or SV be the threshold
(14.5% 6.2%) and SPV (15.5% 4.5%). In this case, the de- to predict fluid responsiveness. In contrast to earlier research that
crease in SPV and PPV does not reflect resolution of the intravas- demonstrated a strong correlation (r 0.89, p .001) between
cular volume deficit, but rather an increase in vascular tone. In PLR-induced change in pulse pressure and the response to a
contrast, nitroprusside will increase variation. 282 Treatment would 300-mL fluidbolus, 288 a PLR-induced increase of 12% in pulse
be a decrease in the vasodilator, not a fluid bolus. As described be- pressure was not as useful a marker offluid responsiveness (sensi-
low, the integration of standard and functional indices may aid in tivity 60%, specificity 85%). 278
tailoring therapy for a patient. Interpretation of the PLR-induced change is based on the as-
The mode of ventilation may affect the absolute values of the sumption that there is adequate volume translocation from the
functional indices. In an animal model, under conditions of nor- legs to the central circulation and a change in ventricular preload,
movolemia and moderate hypovolemia the mode of ventilation which can be assessed with a change in CVP or an echocardio-
(pressure versus volume controlled) does not affect the absolute graphic preload indicator (e.g., FTc) or end-diastolic volume. 293
values of the functional indices. With severe hypovolemia (hem- Of note, the change in preload is greater with a position trans-
orrhage 30% estimated blood volume), functional indices are fer from the semirecumbent to the flat, supine position withlegs
higher with volume-controlled versus pressure-controlled ventila- raised versus the flat, supine position with the legs raised and
tion, which reflects the variable effects of the ventilator modes on provides a more sensitive and specific indicator offluid respon-
intrathoracic pressure. 283 In addition, ventilation with variable siveness. 295 In contrast to other functional indices, evaluation of
VT (e.g., pressure support ventilation) also affects the accuracy of fluid responsiveness with PLR can be performed in patients who
these measurements. 250 are spontaneously breathing or have arrhythmias. 278,292,296,297
Intra-abdominal hypertension (intra-abdominal pressure PLR can cause RV compromise and should be performed cau-
[IAP] 12 mm Hg), may occur in up to 50% of ICU pa- tiously in patients withdecreased RVEF ( 40%) 298 and care
tients. 284 Absolute functional hemodynamic indicator values are should be taken to avoid any noxious stimuli during the ma-
affected by intra-abdominal hypertension. In an animal model, neuver as this may cause changes in vascular tone and affect the
independent of intravascular volume, as the IAP increased the response.
SPV, PPV, and SVV also increased. 285 Caution should be exer-
cised when interpreting functional indices if the IAP is greater
than RAP. 285,286 In patients with intra-abdominal hypertension CO MEASUREMENT
or perhaps during laparoscopic surgery where a pneumoperi-
toneum is created, the use of PPV or SVV are recommended over Measurement of CO by the thermodilution method (thermodilu-
the SPV or static indices (CVP or PAOP), as the PPV and SVV tion CO [TDCO]) is based on the injection of a known volume
are less affected by the initial ventilator-induced increase in ve- of cold or room temperature sterile D5W through the proximal
nous return that occurs with moderate increases in IAP. 286,287 If port of the PA catheter into the RA. The blood is temporarily
the IAP and pleural pressure are not changing, then changes in cooledby the injectate, and thechange in temperature is sensed
the functional indices may reflect fluid responsiveness, but ab- by a thermistor on the distal end of the PA catheter. A computer
solute thresholds indicative of fluid responsiveness remain to be connected to the PA catheter calculates the CO on the basis of
defined. the area under the curve (AUC) using the Stewart–Hamilton equa-
A
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tion. The temperature of the blood is assumed to be stable; thus,
Passive Leg Raising theoretically any change in blood temperature is causedby the in-
jectate. This assumption may be incorrect, particularly if a patient
Evaluation of the reversible change in flow-related indices (e.g., is on mechanical ventilation, which causes a ventilator-induced
aortic blood flow or SV by transthoracic echocardiography or variability in blood temperature or during rapid core temperature
TEE, transpulmonary thermodilution (TPTD) CO, arterial pulse changes (induced hypothermia or rewarming). Most CO com-
pressure, or PVI) in response to PLR is another method to assess puters display the CO time–temperature curve, which allows for
fluid responsiveness. 274,278,288–293 The PLR maneuver, which is confirmation of a correct waveform.
performed by either elevating the legs to 30 to 45 degrees with the
thorax horizontal or moving the patient from a head of bed ele- Factors Influencing Thermodilution
vated position to a horizontal position and concurrently elevating CO Measurement
the legs to 30 to 45 degrees, causes a reversible translocation (au-
totransfusion) of approximately 300 mL of blood from the legs to Technicalfactors that affect the accuracy of thermodilution CO
the central circulation and increases RV preload. 294 If the patient is measures include the catheter position, site of injection, use of the
fluid responsive, the increased RV preload causes an increase in left correct calibration constant, injection technique, and volume and
ventricular preload and if the LV is also fluid responsive, the SV and temperature of the injectate (Display 21-7). Pathophysiological
CO increase. The increase in SV and CO occurs immediately and conditions, such as tricuspid insufficiency and ventricular septal
reaches a maximum approximately 1 minute after starting the PLR defect, inhibit adequate mixing of the thermal indicator and
maneuver, 278 with evaluation of SV or pulse pressure 30 to 90 sec- bloodbefore it is sensedby the thermistor, and may cause under-
onds after the PLR maneuver. For example, in patients with septic estimation of the TDCO. 191

