Question 24

With respect to haemodynamic monitoring in the critically ill patient:

a) Define fluid responsiveness . (10% marks)

b) Outline the physiological basis and the limitations of the following methods of assessment of fluid responsiveness in a patient on mechanical ventilation:

i. Passive leg raise.

ii. Central venous pressure.

iii. Pulse pressure variation. (90% marks)

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College answer

Fluid responsiveness is not synonymous with hypovolaemia and is defined as an increase in stroke volume (or cardiac output/index) by 10 – 15% after fluid administration (volumes vary), depending on technique. The assessment is therefore functional: to induce a change in cardiac preload and observe the effects on cardiac output and arterial pressure.

i. Passive Leg Raise-
Basis- Involves lifting the legs passively from the horizontal position to 45o with the patient supine. This draws venous blood stored in the lower body veins to the inferior vena cava, increasing the right then the left ventricle pre-load. It represents a „reversible volume challenge‟ which can help to predict the haemodynamic response to real volume challenge.

Limitations-
Leg movement may be contraindicated in some patients e.g. pelvic trauma, limbs that are not intact, presence of IABP, femoral ECMO, recent angiography etc.
Unreliable in severely hypovolaemic patients as blood stored in lower body veins may be insufficient to augment stroke volume
May be unreliable in the presence of intra-abdominal hypertension.
Should not be performed in the presence of raised ICP

Central Venous Pressure-
Basis- The CVP is an approximation of right atrial pressure, which is a major determinant of RV filling. It has been assumed that the CVP is a good indicator of RV preload. Furthermore, because RV stroke volume determines LV filling, the CVP is assumed to be an indirect measure of LV preload. A change in the CVP (delta-CVP) with a fluid challenge is thought to be useful in determining fluid management decisions.

Limitations-
CVP is determined by factors other than intravascular volume –i.e. venous tone, intrathoracic pressures, LV and RV compliance, and geometry that occur in critically ill patients, which results in a poor relationship between the CVP and RV end-diastolic volume.
The RV end-diastolic volume may not reflect the patients' position on the Frank-Starling curve and therefore the preload reserve.

Pulse Pressure Variation-
Basis- Pulse pressure variation is derived from the arterial pressure waveform. The reduction in RV preload and increase in RV afterload with positive pressure ventilation both lead to a decrease in RV stroke volume, which is at a minimum at the end of the inspiratory period. The inspiratory reduction in RV ejection leads to a decrease in LV filling after a phase lag of two or three heartbeats because of the long blood pulmonary transit time. Thus, the LV preload reduction may induce a decrease in LV stroke volume, which is at its minimum during the expiratory period when conventional mechanical ventilation is used. The cyclic changes in pulse pressure are greater when the ventricles operate on the steep rather than the flat portion of the Frank-Starling curve.

PPV variation % = (PPmax – PPmin) / PPmean x 100

The magnitude of the respiratory changes in pulse pressure is an indicator of biventricular preload dependence. A PPV of 10-15% is likely to indicate potential for fluid responsiveness. The higher the PPV the more likely the patient is to be fluid responsive.

Limitations-
Unable to interpret in the presence of arrhythmias.
Limited utility in patients ventilated with small tidal volumes (<8 ml/kg) and spontaneously breathing patients
Cannot be used in patients with an open chest.

Candidates were not expected to provide the same level of detail as is in the template.

Additional Examiners' Comments:
For a core topic, the overall understanding of the topic was lacking in a significant number of candidates.

Discussion

There is no agreed-upon definition! Paul Marik suggests that a response to fluids is "an increase of stroke volume of 10-15% after the patient receives 500 ml of crystalloid over 10-15 minutes". Others have used measures like a 10% increase in cardiac output. Stroke volume seems like the most sensible measure, because stroke volume is the main variable which changes in response to changes in preload.

In brief summary, the measures of fluid responsiveness:

Method	Physiology or rationale	Limitations
Static parameters
Clinical signs	Observed resolution of clinical features of shock, in response to a fluid bolus	Only poor capillary refill was found to correlate to fluid responsiveness Significant inter-observer variability In critical care, classical signs may be obscured by an orgy of pathology
CVP	A hypovolemic patient is expected to have a low CVP That patient's CVP should increase in response to fluid challenge If the patient remains relatively hypovolemic, the change in CVPwill be relatively small. A patient who is "well filled" will have a large increase in their CVP.	CVP is unrelated to RA pressure, RV pressure, RV preload, or any of the other validated parameters of fluid responsiveness Apart from RV preload and cardiac function, the CVP is influenced by numerous other physiological variables, including RV compliance, PEEP, tricuspid valve competence, and where in the CVP waveform the measurement is taken
PAWP	A well-placed PAWP measurement should represent LA pressure LA pressure should represent LVEDP LVEDP should be a close surrogate for LV preload Thus, a haemodynamically unstable patient with low PAWP should be challenged with more fluid.	PAWP is confused by many situations in which the PAWP is not equal to LV end-diastolic pressure: It is higher than LVED when there mitral stenosis or regurgitation, left-to-right shunt, COPD, positive pressure ventilation, atrial myxoma, pulmonary venous hypertension or simply poor catheter placement. It is lower than the LVEDP when there is LV failure, high PEEP, a poorly compliant LV (eg. in HOCM) or whenever there is aortic regurgitation
Dynamic parameters
Stroke volume variation and pulse pressure variation	The lower on the Frank-Starling Curve you are, the more stroke volume will vary depending on the phase of ventilation. Decrease in preload due to mechanical inspiration results in a decrease in ventricular wall stretch This results in a decrease in stroke volume Thus, patients who have decreased filling are going to have more difference between their inspiration and expiration stroke volumes.	SVV becomes invalid in the following situations: spontaneously breathing patient cardiac arrhythmia valvular heart disease, especially aortic cardiogenic shock (with poor LV function) intracradiac shunts severe peripheral vascular disease
Passive leg raise autotransfusion	To tip the bed bent at a 45° angle (thus raising the legs above the head) will result in an "autotransfusion" of venous blood into the central veins. This represents a reversible fluid challenge This method of testing fluid responsiveness is well validated	You need a patient with both legs intact You rely on an intact pelvis, so this excludes a lot of messy trauma patients (in whom it would be very useful) It can't be done if you have a balloon pump in situ, or post angiography (because you need to lie flat) - and thus a lot of low-cardiac-output cardiogenic shock patients are excluded, which is a pity It can't be done if you are even slightly concerned about your intracranial pressure.

References

An excellent resource for this topic is a paper by Marik, Paul E. "Hemodynamic parameters to guide fluid therapy." Transfusion Alternatives in Transfusion Medicine 11.3 (2010): 102-112.

Zochios, V., and J. Wilkinson. "Assessment of intravascular fluid status and fluid responsiveness during mechanical ventilation in surgical and intensive care patients." (2011).

Marik, Paul E., et al. "Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature*." Critical care medicine 37.9 (2009): 2642-2647.

Marik, Paul E., and Rodrigo Cavallazzi. "Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense*." Critical care medicine 41.7 (2013): 1774-1781.

Marik, Paul E. "Noninvasive cardiac output monitors: a state-of the-art review."Journal of cardiothoracic and vascular anesthesia 27.1 (2013): 121-134.

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