Volume status

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Contents

Static indices

Central venous pressure (CVP), left ventricular end-diastolic area, E/Ea and wedge pressure are indicators of ventricular filling, but do not reliably predict volume responsiveness. In a study in septic patients, CVP< 8 mmHg had less than 47% positive predictive value for predicting responsiveness to volume challenge (1).


This can be explained with the Frank-Starling curves:
Schema Frank Starling curves.jpg
For the same baseline pre-load (A, assessed by CVP) and same increase in pre-load (amount of fluid given: A -> B), the hemodynamic response assessed by the variation in stroke volume is not significant in patients on the flat portion of the Frank Starling curve (poor LV systolic function) : a = b. In these patients, pre-load increase won't have beneficial effects and may worsen the patient's condition. In patients who are on the steep portion of the curve, the same increase of pre-load (A -> B) will lead to significant increase in stroke volume: b' > a'.


Ideally, the volume status is a “functional assessment”: to induce a change in cardiac preload and observe the effects on cardiac output and arterial pressure.

How to assess the hemodynamic response to volume challenge?

The objective is to distinguish responders (=patients who will benefit from volume expansion) from non-responders (=patients for whom volume expansion may be deleterious).

Clinical parameters can be used: blood pressure, heart rate, urine output... but are not sensitive nor specific.

Stroke volume, thus cardiac output and cardiac index give a real-time, direct assessment of hemodynamics in a patient. They can be accurately calculated by trans-thoracic or trans-esophageal echocardiography (2). Please go to cardiac output calculation chapter for detailed method on how to measure cardiac output.

In most studies, > 15% increase in cardiac output is considered as a positive response to volume challenge.


To monitor a patient, serial measurements of cardiac output are necessary: before and after leg raising or volume challenge. LVOT area does not change in a given patient, thus the initial LVOT area measurement should be kept in all calculations in the same patient.  


How to predict the hemodynamic response to volume challenge?


Passive legs raising 

Schema passive leg raising.jpg
Passive legs raising draws the venous blood stored in the lower body veins to the inferior vena cava, increasing the right then the left ventricle pre-load. Thus passive legs raising represents a reversible volume challenge which can help to predic the hemodynamic response to real volume challenge.

Left ventricle stroke volume variations reflect the hemodynamic response to volume challenge or passive legs raising. It has been demonstrated that the hemodynamic response to passive legs raising predicts the hemodynamic response to volume challenge, defined as variation > 15% cardiac output .



Patients with mechanical ventilation and no spontaneous breathing activity

Schema respiratory variations positive pressure ventilation.jpg
In patients with mechanical ventilation and no spontaneous breathing activity, the cyclic variations of intra-thoracic pressure induced by the ventilation create cyclic variations in right ventricle pre-load, mimicking reversible and limited volume expansion:

-during insufflation, the intra-thoracic pressure is positive. The positive pressure is transmitted to the pericardium and to the right atrium, creating a decrease in the pressure gradient of the venous return, defined as the difference between the mean systemic pressure and the right atrial pressure. This pressure gradient leads to reduced right atrium filling.

-during expiration, intra-thoracic pressure is much lower. The pressure gradient of the venous return is increased, leading to increase of right atrium filling from the IVC.

These consequences of mechanical ventilation on variations of venous return are not altered by positive pressure ventilation.

 

The cyclic variations of venous return induced by mechanical ventilation will have interesting consequences:

1. If the ventricles are still pre-load dependant (steep portion of Frank-Starling curve), increase in right ventricle filling will lead to increased right ventricle output, which will increase the left ventricle filling and output. Thus the cardiac output will follow the variations in venous return, leading to respiratory variations of stroke volume.

It has been validated (5) that respiratory variations > 20% of stroke volume predict positive hemodynamic response to volume expansion. VTI or maximum velocity of LVOT flow can be used as surrogates of stroke volume.


2. Respiratory variations of IVC diameter will be observed only in patients in whom the right atrial pressure is not high, indicating right ventricle pre-load dependance. IVC diameter respiratory variations can therefore predict the hemodynamic response to volume challenge (6-7):

  • respiratory variations of IVC diameter are greater in patients who will respond to fluid expansion
  • after fluid infusion, respiratory variations of IVC diameter decreased significantly in these patients
  • small IVC (<1.2 cm) had a 100% specificity for a RA pressure of less than 10 mm Hg with a low sensitivity (8)

Assessment of respiratory variations of IVC diameter is an easy and useful tool to help predict the response to volume challenge, even with minimal experience.


Severe hypovolemia

Collapsed cardiac chambers

The measurement of cardiac chambers size is generally not a reliable indice to assess the patients' volume status. It depends on the quality of the images recorded, on the heart rate and on the ventricular systolic function. The only exception is in severe hypovolemia.

In severely hypovolemic patients, the pre-load is insufficient to ensure adequate cardiac filling. The left and right ventricles are small and hyperkinetic. In the most severe cases, the left ventricle collapses in systole.


Collapsed IVC

The IVC diameter is easy to measure and reflects the right chambers pre-load. A small IVC (<1.2 cm) has a 100% specificity for a RA pressure of less than 10 mm Hg with a low sensitivity (8).


Hemodynamic LVOT obstruction

References

1 - Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge.Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL. Crit Care Med 2007, 35:64-68.

2 - Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window. Lewis JF, Kuo LC, Nelson JG, Limacher MC, Quinones MA. Circulation. 1984 Sep;70(3):425-31

3- Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneously breathing activity. Lamia B, Ochagavia A, Monnet X, Chemla D, Richard C, Teboul JL. Intensive Care Med. 2007 Jul;33(7):1125-32.

4- Non-invasive stroke volume measurement and passive leg raising predict volume responsiveness in medical ICU patients: an observational cohort study.Thiel SW, Kollef MH, Isakow W. Crit Care. 2009 Jul 8;13(4):R111.

5- Echocardiographic measurement of fluid responsiveness. Charron C, Caille V, Jardin F, Vieillard-Baron A. Curr Opin Crit Care. 2006 Jun;12(3):249-54
6- The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Feissel M, Michard F, Faller JP, Teboul JL. Intensive Care Med. 2004 Sep;30(9):1834-7. Epub 2004 Mar 25

7- Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Barbier C, Loubieres Y, Schmit C, Hayon J, Ricome JL, Jardin F, Vieillard-Baron A.  Intensive Care Medicine 2004; 30 (9): 1740-6
8- Does inferior vena cava size predict right atrial pressures in patients receiving mechanical ventilation? Jue J., Chung W., Schiller N.B.,  J Am Soc Echocardiogr (1992) 5 : pp 613-619


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