JOURNAL READING AND INTERPRETATION

Fluid Responsiveness : An evolution in our

understanding
BY NURSHAWINA KAMALUDIN
112014180
Faculty of medicine
Krida Wacana Christian university (Ukrida)
Co-assistant
Department of Anesthesiology
(10 August 2015 29 August 2015)
TARAKAN General Districts Hospital

WHAT IS FLUID
RESPONSIVENESS?
Fluid responsiveness is an increase of stroke
volume of 10-15% after the patient receives
500 ml of crystalloid over 10-15 minutes
Fluid responsive patients have preload
reserve and will have an increase in stroke
volume (and usually cardiac output) when
fluid is administered

WHY IS IT REALLY
IMPORTANT?! WHAT WE
UNDERSTAND ABOUT FLUID
RESPONSIVENESS?
The PRESUMPTION is that increased cardiac
output will lead to increased oxygen delivery
(DO2) and increased tissue oxygenation
Fluid therapy acts by increasing the stressed
venous volume, thereby increasing venous return
to the heart.
Venous system has a much greater capacity for
blood compared with the arterial system, it is a
normal physiologic condition to be a fluid
responder.
Other haemodynamic parameters are sometimes
used as surrogates for stroke volume.

WHAT WE MISUNDERSTOOD ABOUT

FLUID RESPONSIVENESS?
Clinicians would agree that both hypovolaemia and volume
overload increase the morbidity and mortality of patients
Being a fluid responder is not equal to being hypovolaemic.
This suggests that not all patients who are fluid responders
necessarily require volume expansion.
Fundamentally, the only reason to give any patient a fluid
challenge is to increase their SV; if this does not happen,
the fluid administration serves no useful purpose and is
likely to be harmful.
Furthermore, the increase in SV (and thus cardiac output)
must be judged to be beneficial.

WHAT WE SHOULD KNOW ABOUT

FLUID RESPONSIVENESS?
When a fluid challenge is given on
clinical grounds, only 50% of
haemodynamically unstable patients (in
the OT, ICU, or ED) are volume
responders.
Fluid loading per se is not always the
correct therapy for hypotension or a
reduced urine production.
Our homeostatic mechanisms have
evolved (over thousands of years) to deal
with hypovolaemia (tachycardia,
vasoconstriction, and blood flow
redistribution), whereas volume overload

WHAT HAPPENED IF PATIENT

BECOME FLUID UNRESPONSIVE ?
As patients become less fluid responsive,
EVLW(and tissue oedema) increases markedly
because of the increased cardiac filling pressures
and transmitted hydrostatic pressures.
This process is accentuated in patients with
endothelial damage (sepsis, ARDS, pancreatitis,
burns). Increased cardiac filling pressures trigger
the release of natriuretic peptides, presumably to
assist in fluid removal.
Therefore, excessive volume expansion increases
the release of natriuretic peptides, which in turn
damages the endothelial glycocalyx, and this is
followed by a rapid shift of intravascular fluid into
the interstitial space leading to a marked increase
in EVLW and tissue oedema.

TECHNIQUES FOR ASSESSING FLUID

RESPONSIVENESS

PREDICTING FLUID
RESPONSIVENESS
Static tests (less sensitive, less specific and less
useful than dynamic tests)
Clinical static endpoints (e.g. heart rate, blood
pressure, collapsed veins, capillary refill time,
previous urine output)
~not sensitive
~poor inter-observer reliability
CVP/PCWP (also delta CVP post fluid challenge)
~poor predictors
CXR (chest x-ray)
~look for pulmonary edema
~unreliable
PiCCO
~ EVLW and Intra Thoracic Blood Vol

Dynamic tests
Passive leg raising
~ transiently increases venous return in patients who
are preload responsive, as such it is a diagnostic test
not a treatment
~ it is a predictor of fluid responsiveness (i.e helps
identify patient who are on the ascending portion of
their Starling curve, and will have an increase in stroke
volume in response to fluid administration
~ can use with pulse pressure change, PPV, VTI (echo),
NICCOM, carotid Doppler flow, or ETCO2 (if ventilation
and metabolic status constant)

TECHNIQUE
sit patient at 45 degrees head up semirecumbent position ( induces a larger increase
in cardiac preload beacuse it induces the shift
of venous blood not only from both legs but
also from abdominal compartment)
lower patients upper body to horizontal and
passively raise legs at 45 degrees up
maximal effect occurs at 30-90 seconds
assess for a 10% increase in stroke volume
(cardiac output monitor) or using a surrogate
such aspulse pressure (using an arterial line)

PERFORMANCE CHARACTERISTICS
o 9% increase in stroke volume has 86%sensitivity and
90%specificity
o 10% increase in pulse pressure has 79%sensitivity and
85%specificity
ADVANTAGES
Reversible ( its effect are reversed once the legs are tilt
down)
non-invasive
Easy to perform in patients breathing spontaneously and
with arrhythmias (but must use measures other than stroke
volume variation and pulse pressure variation)
can be repeated many times to reassess preload
responsiveness without any risk of inducing pulmonary
edema or cor pulmonale in potential nonresponders

DISADVANTAGES
unreliable in severely hypovolemic patients
the blood volume mobilized by leg-raising (which is
dependent on total blood volume) could be small
and can show minimal to no increase in CO and
blood pressure, even in fluid responsive patients
need to stop any other interventions during the
test
positional changes may be contra-indicated in
some patients
not useful in patients with raised intra-abdominal
pressure (impair venous return & reduces the
ability of PLR to detect fluid responsiveness)

 End-expiratory occlusion test

~ Occluding the circuit at end-expiration prevents
the cyclic effect of inspiration to reduce left
cardiac preload and acts like a fluid challenge
~ A 15 second expiratory occlusion is performed
and an increase in pulse pressure or cardiac index
predicts fluid responsiveness with a high degree
of accuracy
~ The patient must be able to tolerate the 15
second interruption to ventilation without
initiating a spontaneous breath

During mechanical ventilation, each insufflation

increases increases intrathoracic pressure, thus

reduces the systemic venous return
~ Interrupting mechanical insufflation during an
end-

expiratory occlusion can increase cardiac

preload sufficiently for such a test being used to

predict fluid response.
~ Patient who will increase their CO> 15% in
response to sebsequent 500 ml fluid challenge the
EEO test increased both arterial pulse and pulse
contour cardiac output
~An increase in CO > 5% predicted fluid
responsiveness with a good accuracy

CONT.
Ultrasound (can be used dynamically)
Echocardiography
~ subaortic velocity time index (VTI) allows
measurement of stroke volume
~ End diastolic volume (EDV) approximates
preload
Lung ultrasound
~ can be used to detect pulmonary edema, i.e.
lack of fluid tolerance

CONT.
Respiratory variation tests (can be used dynamically)
Inferior Vena Cava (IVC) ultrasound
~ assess size and degree of inspiratory collapse
~ correlates with CVP, but CVP is a poor indicator of
fluid responsiveness
systolic pressure, pulse pressure (PPV) and stroke
volume (SVV)
~ generally limited to mechanically ventilated
patients in sinus rhythm
aortic blood velocity

THINGS THAT WE SHOULD KNOW IN

FLUID THERAPY
Fluid responsiveness does not mean that a patient
should be given fluids!
However, if a patient has low cardiac output that
requires correction, fluid responsiveness means that
stroke volume (and usually cardiac output, unless heart
rate falls) will improve if fluids are given
It means patients are on the ascending portion of their
Starling curve, in other words, they have preload
reserve
We should probably use different cutoff values for fluid
responsiveness depending on the clinical context. For
example, patients with severe respiratory failure need
higher specificity and lower sensitivity tests of fluid
responsiveness, whereas the opposite may be

CONCLUSION
As our understanding of this complex topic evolves,
it is likely that new and improved methods of
assessing fluid responsiveness and more
physiological targets of fluid therapy will emerge.
The methods for assessing fluid responsiveness have
evolved from static pressure and volume
parameters, which are unable to predict fluid
responsiveness, to dynamic indices based on heart
lung interactions during mechanical ventilation,
which have a modest degree of accuracy, to those
techniques based on either a virtual or a real fluid
challenge, which have a high degree of accuracy in

Thank you
For Your Time