Static measures of fluid responsiveness such as central venous pressure, pulmonary artery occlusion pressure, right ventricular end-diastolic volume, and global end-diastolic volume have limitations in accurately predicting a patient's fluid responsiveness. While some studies found statistically significant differences in these measures between fluid responders and non-responders, the overlap between individual values means no threshold can reliably discriminate the two groups. Due to their poor accuracy, static measures are best used alongside dynamic tests of fluid responsiveness to guide fluid management in critically ill patients.

1. Static indices of fluid responsiveness

2. Hemodynamic optimization is the key to provide the supply of oxygen and
metabolic substrates to tissues according to their metabolic needs

3. fluid resuscitation
FLUID
RESPONDER
BENEFITS &
RISK
increase of stroke
volume of 10–15%
after administration
of 500 mL of
crystalloids in 10–
15 minutes
3

4. Fluid overload
tissue edema
delays in weaning
from mechanical
ventilation
increased length in
ICU and hospital
stays
predictor of
increased mortality in
septic shock, acute
distress respiratory
syndrome (ARDS),
worsening in gas
exchange,
hemodilution
intra-abdominal
hypertension and
acute kidney injury

5. ◎ Static measures have been used for the last decades and are used to estimate preload
(venous return).
◎ Preload in steady-state conditions is equal to cardiac output.
◎ Preload is determined by the relationship of venous resistance with systemic filling pressure
and right atrial pressure.
◎ Venous capacitance is important because influences venous return and central venous
pressure (CVP)

6. 6

7. ◎ Static indicators - supposed to reflect preload, but are not accurate
◎ Stroke volume and cardiac output also depends upon cardiac
contractility apart from preload.
◎ So static indices can be used to confirm that the fluid boluses have
filled the cardiac chambers
Used as safety
parameter to
stop further
infusion

8. Why preload alone may not predict stroke volume?

9. Michard F, Teboul JL. Predicting Fluid Responsiveness in ICU Patients. Chest 2002;121:2000-8.

10. Michard F, Teboul JL. Predicting Fluid Responsiveness in ICU Patients. Chest 2002;121:2000-8.

11. Central venous pressure
The origins of CVP monitoring can be traced back to Hughes and Magovern , who in 1959 described
a complicated technique for right atrial pressure monitoring.
The technique of CVP monitoring was further popularized by Wilson and Grow
and soon became routine in patients undergoing thoracic surgery.
CVP is considered equivalent to right atrial pressure (RAP) when the vena cava
is continuous with the right atrium .
Central venous catheterization is the gold standard measurement of CVP and
RAP

12. Central venous pressure
Weak relationship between CVP and blood volume.
The evaluation of CVP has not a standard pattern although frequently is determined immediately
after the atrial contraction (A wave) and the valve closure (C wave)
Although it varies from one patient to someone else, and in the same patient, between different
times
The CVP correspond to right atrial pressure (RAP)
A low RAP indicate the ascending limb of the Frank- Starling curve; a high RAP suggest that the
patient is on the plateau
Few link between CVP and RVEDV. Because of variations in venous tone, intrathoracic pressures,
ventricular functions.
CVP has a low accuracy for predicting fluid responsiveness

13. it is widely used with other static
markers to test preload
responsiveness in 1/3 of cases, as
shown by the FENICE study an
observational study operated in
intensive care units all over the
Earth

14. In a study about hemodynamic monitoring in patients under high-risk surgery, 73% of American and
84% of European anesthesiologists reported the use of CVP to govern fluid management

15. A systematic review including 803
patients analyzed CVP with measured
circulating blood volume and the
relationship between CVP/ΔCVP
following a fluid challenge.
The difference in CVP at baseline in
responders (8.7±2.32 mmHg) versus
non-responders (9.7±2.2 mmHg)
resulted not statistically significant
(P=0.3)
There are no data to
support the widespread
practice
of using central venous
pressure to guide fluid
therapy. This
approach to fluid
resuscitation should be
abandoned.

16. Right atrial pressure
Examination of the jugular venous pulse (JVP) to estimate right atrial (RA) pressure (RAP) is a
commonly performed bedside technique.
However, the JVP is often difficult to accurately ascertain because of patient body habitus or poor
examiner technique.
Even when it is visualized, there is a poor correlation between JVP estimation of RAP and invasive
measurements.
The most commonly used technique involves measurement of the inferior vena caval (IVC) size
along with its respirophasic variation
RAP measurement is highly influenced by the transmitted pressure (i.e., the pleural or pericardial
pressure), and its measurement is altered by numerous technical factors.

17. Right atrial pressure
◎ Before volume expansion, RAP
was not significantly lower in
responders than in non
responders in three of five
studies
◎ The marked overlap of
individual RAP values did not
allow the identification of a RAP
threshold value discriminating
responders and nonresponders
before fluid was administered.
Michard F, Teboul JL. Predicting Fluid Responsiveness in ICU Patients. Chest 2002;121:2000-8.

18. Pulmonary artery occlusion pressure
Pulmonary artery catheters (PACs) measure the PAOP which corresponds to the end-diastolic
pressure of the left-ventricle (LVEDP)
PAOP could be subject to several valuables: compliance of myocardial tissue alternated (as in
septic state or ischemia), pericarditis, increase of pulmonary vascular resistance, right ventricular
overload, mitral stenosis and increased intra thoracic pressure due to mechanical ventilation
Insert a PAC is an invasive operation with risk of arrhythmias, pulmonary infarction, catheter
knotting, and rupture of the vessels

19. In a study with 96 patients, Osman et al.
evaluated the relationship between the
evaluation of PAOP and patients “fluid
responders”:
responders had smaller values of PAOP before
the infusion than non-responders (10±4 vs. 11±4
mmHg, P=0.05),
But they noted a big overlapping of values in
different persons.

20. ◎ A study by Michard et al. measured PAOP
before and after a fluid increase in the two
categories of patients: responders and non-
responders; they showed a not-significant
evidence of measurement of PAOP in seven of
nine studies
◎ However, in none of these studies, a PAOP
cutoff value was proposed to predict the
hemodynamic response to volume expansion
before fluid was administered.

21. ◎ The PAOP is highly dependent on left ventricular compliance, which is frequently
decreased in ICU patients (sepsis, ischemic, or hypertrophic cardiomyopathy).
◎ RAP and PAOP have been shown to over estimate transmural pressures in
patients with external or intrinsic PEEP.

22. ◎ Wagner and Leatherman, suggested that the lower RAP or PAOP before volume expansion, the
greater the increase in stroke volume in response to fluid infusion.
◎ However, although statistically significant, these relationships were weak because a given value of
RAP or of PAOP could not be used to discriminate responders and non responders before fluid was
administered.
◎ It has been suggested that a beneficial hemodynamic effect of volume expansion cannot be
expected in critically ill patients with a RAP > 12 mm Hg and/or a PAOP >12 mm Hg or > 15 mm Hg.
◎ Wagner JG, Leatherman JW. Right ventricular end-diastolic volumeas a predictor of the hemodynamic response to a fluid
challenge. Chest 1998; 113:1048–1054

23. Right ventricular end diastolic volume (GVEDV)
◎ The increase in stroke volume as a result of end-diastolic volume increase, depends on
ventricular function
◎ Therefore, only 40 to 72% of critically ill patients have been shown to respond to volume
expansion by a significant increase in stroke volume or cardiac output in studies designed to
examine fluid responsiveness.

24. ◎ Before volume expansion, RVEDV index was not significantly lower in responders than in non
responders in four of six studies.

25. ◎ In the two remaining studies of Diebel et al, RVEDV index was significantly lower at baseline in
responders than in nonresponders
◎ RVEDV index < 90 mL/m2 was associated with a high rate of response (100% and 64%,
respectively), and RVEDV index > 138 mL/m2 was associated with the lack of response to
volume expansion.
◎ However, when the RVEDV index ranged from 90 to 138 mL/m2, no threshold value was
proposed to discriminate responder and non responder patients before volume expansion

26. Beneficial hemodynamic effect of volume
expansion was likely when the RVEDV index was
below 90 mL/m2
Very unlikely when the RVEDV index was >138
mL/m2.
No significant difference was observed between re-
sponders and nonresponders with regard to the
baseline value of RVEDV index
The evaluation of RVEDV by thermodilution has been shown influenced by tricuspid regurgitation, which
is frequently encountered in patients with pulmonary hypertension (ARDS, mechanical ventilation with
PEEP).

27. Global end-diastolic volume (GEDV)
GEDV and the derived global end-diastolic volume index (GEDI) estimate the blood volume of all
the four cardiac chambers with the technique of transpulmonary thermodilution (TPTD)
PiCCO® (Pulse Contour Cardiac Output) monitor or EV1000 monitor (Vigileo®) are employed to
obtain these measurements.
The monotoring system PiCCO utilizes TPTD method through a central venous catheter (CVC) and
a thermodilution-tipped arterial catheter
GEDV/GEDI is an evaluation of preload and of stroke volume because estimates the volume in the
four hearth-chambers, although the relationship between GEDV-measurement and patients fluid
responders is lacking.
Venous capacitance and heart chambers compliance are important to identify a change in preload,
influenced by different GEDV values

28. ◎ Michard et al. reported a significant
association with stroke volume index (SVI)
(r=0.72, P=0.001) in 36 patients comparing
GEDI with SVI before and after a fluid
challenge;
◎ pre-infusion GEDI was smaller in patients
fluid responders than in non-responders
(637±134 vs. 781±161 mL/m2, P=0.001)

29. ◎ Endo et al. found GEDV to be unpredictable in
prediction of fluid responsiveness on 93
mechanically ventilated patients
Due to the poor data and the heterogeneity
of the results about GEDV/GEDI to predict
fluid responsiveness, further research is
needed
During the early phase of patients with severe sepsis on mechanical ventilation, there was no constant
relationship between GEDI and fluid reserve responsiveness, irrespective of the presence of SIMD,
defined as LVEF ≤50%.
GEDI should be used as a cardiac preload parameter with awareness of its limitations.

30. Inferior vena cava diameter

31. ◎ The inferior vena cava (IVC) is a compliant vessel whose size and
shape vary with changes in CVP and intravascular volume.
◎ Therefore, sonographic measurement of the IVC represents an
effective and noninvasive method of estimating CVP

32. Factors affecting IVC measurements
- Luminal factors
Factor Comments
RV compliance LV diastolic dysfunction is usually associated with
RV diastolic dysfunction
ICU patients may have transient ventricular
dysfunction
Tricuspid valve
disease
TR and TS falsely results in raised RAP
independent of fluid status
Obstructed right
atrium
Pulmonary artery
hypertension
Increased RAP
Portosystemic
shunting
Blood flows through veins other than IVC

33. Extra Luminal factors affecting IVC
Factor Comments
Tension
pneumothorax
Raised intrathoracic pressure distends the IVC
Spontaneous
ventilation
Increased respiratory efforts result in compression
of IVC during diaphragmatic excursion
Standardization therefore cannot be done for
spontaneously breathing patients
Mechanical ventilation PEEP, tidal volume mode of ventilation, paralysis
all affect IVC diameter
Pericardial
tamponade
Increased intra pericardial pressure
Intra abdominal
pressure
Edema, ascites may all increase intra abdominal
pressure and may falsely decrease IVC diameter
in an already volume overloaded patient

34. Other factors affecting IVC
FACTOR COMMENTS
Position Smallest in left lateral, intermediate in supine,
largest in right lateral position
Age and ethnicity Decreases with age
Technical difficulty May not be visualized in up to 18%
Inter observer
variability
Intra abdominal
pressure
Edema, ascites may all increase intra abdominal pressure
and may falsely decrease IVC diameter in an already
volume overloaded patient

35. Theoretically changes in relation to preload and its increase should correspond to an increment
Its accuracy is operator-dependent and needs image acquiring and analysis. preload and right
atrial filling pressure.
Many components like obesity, lung hyperinflation pneumothorax, abdominal distention or
elevated intra-abdominal pressure (>12 mmHg) may cause unsatisfying sonographic windows.
The diameter of the IVC is correlated with RAP

36. The diameter of the IVC is correlated with RAP

37. The correlation between the IVC diameter and RAP
has been shown to be weak and inconsistent in
mechanically ventilated patients .
Ciozda W, Kedan I, Kehl D, Zimmer R, Khandwalla R, Kimchi A
(2016) The efficacy of sonographic measurement of inferior vena
cava diameter as an estimate of central venous pressure.
Cardiovasc Ultrasound 14:33
A large overlap between the measured and
estimated RAP based on IVC diameter
measurement has also been reported in
spontaneously breathing patients
Seo Y, Iida N, Yamamoto M, Machino-Ohtsuka T, Ishizu T,
Aonuma K (2017) Estimation of central venous pressure
using the ratio of short to long diameter from cross-
sectional images of the inferior vena cava. J Am Soc
Echocardiogr 30:461–467

38. Positive pressure ventilation leads to increased intrathoracic pressure, decreased systemic venous
return, and increased volume of venous blood in the IVC.
The dimension and distensibility of the IVC is consequently affected.
Therefore, the use of IVC measurements to estimate RAP in mechanically ventilated patients is
usually unreliable.

39. IVC-EE
In contrast, the end-expiratory IVC diameter ( IVCEE) better reflect the transmural RAP and hence
cardiac preload.
IVCEE was measured approximately 2 cm from the junction with the right atrium in the IVC long
axis, usually caudal to the hepatic vein inlet for the best accuracy

40. In a multicenter study, in 22% of patients was not
possible to obtain the IVCd; in only 29% of the ICU-
ventilated patients was possible to predict fluid
responsiveness with a specificity of 80%.
Even so, a value of end-expiratory IVCd less than 8
mm or more than 28 mm could predict patients
fluid responders with a specificity of 95%
Conclusions: Measurement of IVCEE in ventilated patients is moderately feasible and poorly predicts FR, with
IAP acting as a confounding factor.
IVCEE might add some value to guide fluid therapy but should not be used alone for fluid prediction
purposes.

41. Left ventricular end-diastolic area (LVEDA)
LVEDA is estimate with transthoracic echocardiogram (apical 4-chamber view) or transesophageal
echocardiography (TEE)
It should increase with fluid expansion in responding subjects.

42. Swenson et al reported a significant relationship between baseline LVEDA and changes in cardiac
output induced by IV fluid therapy, suggesting that LVEDA could be an indicator of fluid
responsiveness.
Michard et al. analyzed twelve studies and showed that static indicators of cardiac preload (RAP,
PAOP, RVEDV, LVEDA) in patients in ICU, before fluid infusion, were not significantly decreased in
responders than in non-responders
Swenson JD, Harkin C, Pace NL, et al. Transesophageal echocardiography:an objective tool in defining maximumventricular response to IV fluid therapy. Anesth Analg 1996;
83:1149–1153

43. In two studies, the LVEDA before volume expansion was significantly lower in responders than in
non responders.
◎

44. ◎ In the study of Tousignant et al, a marked overlap of baseline individual LVEDA values was
observed
◎ So that a given value of LVEDA could not be used to predict the hemodynamic response to
fluid infusion.

45. ◎ In another study, responder and non responder patients were not different with regard to the
baseline value of LVEDA index.
◎ No significant relationship (r2 0.11, p 0.17) was observed between the baseline value of
LVEDA index and the percentage of increase in cardiac index in response to volume
expansion.

46. The estimation of the LVEDA by echocardiography does not always accurately reflect left
ventricular end diastolic volume and hence LV preload.
In case of right ventricular dysfunction, a beneficial hemodynamic effect of volume expansion
cannot be expected, even in the case of low left ventricular preload.
Hypovolemia can be associated with a normal or high LVEDA value in patients with dilated
cardiopathy.

47. Decrease in ventricular contractility decreases the relationship between end-diastolic volume and
stroke volume.
So, the rise in stroke volume as a result of end diastolic volume increase depends on ventricular
function.
The increase in end diastolic volume as a result of fluid therapy depends on the partitioning of the
fluid into the different cardiovascular compliances organized in series.
Therefore, a patient can be nonresponder to a fluid challenge because of high venous compliance,
low ventricular compliance and/or ventricular dysfunction.
Therefore bedside indicators of cardiac chambers dimensions are not accurate predictors of fluid
responsiveness in ICU patients in whom venous capacitance, ventricular compliance,and
contractility are frequently altered.

48. E/e’
LV diastolic dysfunction can be defined as an increase in myocardial stiffness or a reduction in the
rate of relaxation of the heart muscle
This condition can be assessed echocardiographically, with the tissue Doppler, through indices like
e’ and E/e’;
e’ wave provides information on the maximum speed of movement of the mitral annulus during
the rapid ventricular filling phase;
Values of e’ less than 7 cm·s−1 for septal and less than 10 cm·s−1 for lateral tissue velocity, are
considered abnormal.
E wave represents the maximum velocity of the rapid ventricular filling;
E/e’ is the ratio between these two values

49. The values of the ratio E/e’ correlate with the LAP (left atrial pressure) and with the capillary Wedge
pressure,
Values below 8 indicate a non-elevated LAP, values above 14 indicate an increase in the filling
pressures of the left heart chambers
During circulatory failure, fluid administration is often used to increase stroke volume;
If we assume that this volume is able to correct the LVDD, the variables of e’ and E/e’ seems useful
and reliable for testing fluid responsiveness.

50. Mahjoub et al. shown that the administration of liquids (500 mL of NS) causes an increase in the
values of e’ higher in the patients considered responders (SV increased more than 15%)
On the other hand the value of E/e’ had increased more markedly in the group of non-responders
E/e’ ratio proved to be a good predictive value of LV filling pressures in the patient with septic
shock.
Sanfilippo et al found a significant correlation between mortality in critically ill patients and low
levels of e’ and high values of E/e’ patients.

51. The assessment of LVDD in critically ill patients remains difficult and the evaluation of E and E / e is
probably the most used tool because it is easy to perform at patients’ bedside .