Journal Pre-proof

How I Do It: Dosing Fluids in Early Septic Shock

Dipayan Chaudhuri, MD, Brent Herritt, MD, Kimberley Lewis, MD, Jose L. Diaz-
Gomez, MD, Alison Fox-Robichaud, MD, Ian Ball, MD, John Granton, MD, Bram
Rochwerg, MD

PII: S0012-3692(20)34890-X
DOI: https://doi.org/10.1016/j.chest.2020.09.269
Reference: CHEST 3688

To appear in: CHEST

Received Date: 27 May 2020

Revised Date: 15 September 2020
Accepted Date: 30 September 2020

Please cite this article as: Chaudhuri D, Herritt B, Lewis K, Diaz-Gomez JL, Fox-Robichaud A, Ball I,
Granton J, Rochwerg B, How I Do It: Dosing Fluids in Early Septic Shock, CHEST (2020), doi: https://
doi.org/10.1016/j.chest.2020.09.269.

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Copyright © 2020 Published by Elsevier Inc under license from the American College of Chest
Physicians.
Abstract word count: 120 words
Full text word count: 2770 words

How I Do It: Dosing Fluids in Early Septic Shock

Dipayan Chaudhuri1,a,3 MD, Brent Herritt2,a MD, Kimberley Lewis1,3 MD, Jose L. Diaz-Gomez4

MD, Alison Fox-Robichaud1,5 MD, Ian Ball6,7 MD, John Granton8 MD, Bram Rochwerg1,3 MD

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a
both authors contributed equally to this work

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Affiliations:
1
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Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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2
Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada
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3
Department of Health Research Methods, Evidence and Impact, McMaster University, Hamilton, Ontario, Canada
4
Division of Cardiovascular Anesthesiology and Critical Care Medicine. Baylor College of Medicine. Houston,
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Texas, USA
5
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Thrombosis and Atherosclerosis Research Institute, McMaster University, Ontario, Canada

6
Department of Medicine, Western University, London, Ontario, Canada
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7
Department of Epidemiology and Biostatistics, Western University, London, Ontario, Canada
8
Division of Respirology, University Health Network and Sinai Health System, Toronto, Ontario, Canada

Corresponding Author and Reprint Requests:

Dr. Bram Rochwerg

Department of Medicine, Division of Critical Care

Juravinski Hospital

711 Concession St, Hamilton ON

L8V 1C1

e-mail: rochwerg@mcmaster.ca
Summary conflict of interest statements: Bram Rochwerg is supported by a Hamilton Health Sciences Early

Career Research Award.

Funding information : There was no funding for this study.

Abbreviation List:

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IV – intravenous

ICU – Intensive care unit

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RCT – randomized control trial

CVP – central venous pressure

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CRT – capillary refill time
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PCWP – pulmonary capillary wedge pressure

LR – likelihood ratio
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CI – cardiac index

AUC – area under the curve

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PPV - pulse pressure variation

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SVV - stroke volume variation

PLR - passive leg raise

TTE – transthoracic echocardiogram

CCE – critical care ultrasound

LVOT – left ventricular outflow tract

Abstract:

Early intravenous fluid administration remains one of the modern pillars of sepsis treatment,

however, questions regarding amount, type, rate, mechanism of action and even the benefits of

fluid remain unanswered. Administering the optimal fluid volume is important as overzealous

fluid resuscitation can precipitate multiorgan failure, prolong mechanical ventilation and worsen

patient outcomes. After the initial resuscitation, further fluid administration should be

determined by individual patient factors and measures of fluid responsiveness. This review

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describes various static and dynamic measures that are used to assess fluid responsiveness and

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summarizes the evidence addressing these metrics. Subsequently, we outline a practical approach
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to the evaluation of fluid responsiveness in early septic shock and explore further areas crucial to
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ongoing research examining this topic.
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Sepsis induces pathogen-mediated molecules which bind to pattern recognition receptors and

initiate a proinflammatory intracellular signalling cascade lead to cytokine release and immune

hyper-responsiveness. This process results in vasoplegia, which in turn can lead to systemic

hypotension or lactic acidosis; a process known as septic shock1. In addition to antimicrobials

and hemodynamic support, intravenous (IV) fluids remain one of the modern pillars of sepsis

treatment2. However, important questions regarding amount, type, rate, mechanism of action and

even the benefits of fluid remain unanswered3–8.

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With the advent of Early Goal Directed Therapy (EGDT)9, large volume fluid resuscitation
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during the first 6 ‘golden hours’ of sepsis management became commonplace. With the
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prioritization of early fluid administration in addition to antibiotics, sepsis became recognized as
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an emergency for clinicians worldwide, a designation that improved the care of millions of
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patients. However, three large subsequent randomized controlled trials (RCTs) enrolling more

than 4200 patients3–5 failed to show a similar benefit with EGDT. Of note, both the intervention
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and control arms in these trials received large amounts of fluid in the initial stages of
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resuscitation, potentially minimizing the difference in treatment between arms. As such, most

clinicians will agree that early fluid administration in sepsis is important; the more pressing

question is how to decide on the optimal amount of fluid to give and how to determine when to

cease resuscitation. Increasingly, data suggest that an overly liberal fluid strategy may be equally

deleterious as one that is too conservative6. In patients with acute respiratory distress syndrome

(ARDS)7 or in early resuscitation of children in a low resource setting8, liberal or bolus fluid

strategies, respectively, tended towards increased harm. A systematic review and meta-analysis
on the topic also supported the conclusion that early, liberal fluid resuscitation may contribute to

worse patient outcomes6.

Thus, the current paradigm for fluid resuscitation in septic shock calls for appropriate fluid

administration. Unfortunately, the term “appropriate” is non-quantifiable. The most recent

Surviving Sepsis guideline strongly recommends that 30 ml/kg of IV crystalloid be given to

patients with septic shock within the first 3 hours of presentation10 . After this, the guideline

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recommends that additional fluid administration should be based on “frequent re-assessment of

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hemodynamic status.” However, these guidelines have been challenged as being too liberal with
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fluid administration especially given that these fluid volumes are not supported by high quality
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data11,12. Furthermore, in the real-world setting, only 50-60% of patients in whom fluid is
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administered actually have objective testing to demonstrate fluid responsiveness13. Moreover,

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important questions remain regarding how to best reassess fluid responsiveness and how to

respond to changes in these assessments. While restricting fluids in non-fluid responsive patients
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is likely beneficial7, is it unclear whether the same is true in patients that are determined to be
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fluid responsive8. Thus, this review aims to summarize the key evidence regarding these

questions and provide a current, evidence-based, practical approach to fluid resuscitation in early

septic shock.

Case

A 58-year-old male presents to the Emergency Department (ED) with a 3-day history of fever,

increasing dyspnea and productive cough. On initial examination his temperature is 38.9 degrees

Celsius, heart rate (HR) 110, blood pressure (BP) 90/40 and oxygen saturation 85% on a
Venturi-mask with a respiratory rate of 25. Cardiac examination reveals a hyperdynamic

precordium with no extra heart sounds. Extremities are cool with brisk palpable pulses. His neck

veins are obscured by a beard. His chest X-ray reveals multi-lobar airspace disease. He is sedated

and intubated. A central venous catheter is inserted in his right internal jugular vein and an

arterial line is placed in his left radial artery. Over the next two hours, he is resuscitated with 40

ml/kg of Ringer’s Lactate and started on broad spectrum antibiotics. He is now requiring a

norepinephrine infusion titrated to 0.1 micrograms/kg/min in order to maintain a mean arterial

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pressure (MAP) of 65 mmHg. His central venous pressure (CVP) is 11mmHg and his digital

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capillary refill time is 5 seconds. Serum lactate is 4.5 g/L and central venous oxygen saturation
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(ScvO2) is 60%. A point of care ultrasound reveals normal right ventricular size and function but
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mildly reduced left ventricular function. One minute after performing a passive leg raise
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maneuver, his cardiac output, measured by his left ventricular outflow tract-velocity time
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integral (LVOT-VTi), increases by 15%. Abdominal ultrasonography reveals an inferior vena

cava (IVC) distensibility index of 10%. The ICU team arrives in the emergency department and
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is unsure about whether or not to administer additional fluid resuscitation.

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Is the patient displaying signs of hypo-perfusion and can this be improved with

fluid administration?

The Surviving Sepsis guidelines recommend that resuscitation be guided by macrocirculation

measures of perfusion, such as heart rate, blood pressure, central venous oxygen saturation,

along with microcirculation measures such as urine output and serum lactate levels10. However,

as mentioned earlier, these guidelines have been challenged for recommending a fluid

resuscitation strategy that is too liberal11,12 without being associated with better outcomes either
earlier or later within the ICU15. Moreover, the ideal macrocirculation (hemodynamic) targets

remain uncertain16 although ongoing trials should help clarify this uncertainty17,18.

Using real-time assessments of the microcirculation to guide ongoing resuscitation remains

difficult. Many of these parameters, such as urine output take too long to respond to treatment,

and therefore are unhelpful in making decisions about further resuscitation. Furthermore, even

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giving fluids to fluid responsive patients, may not actually affect renal resistive index and thus

renal function19.

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A number of studies have been conducted examining lactate as a microcirculatory measure of
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perfusion. A meta-analysis of 5 RCTs enrolling 647 patients compared lactate-guided
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resuscitation in sepsis to other strategies and demonstrated a mortality benefit with lactate-guided
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fluid therapy but no effect on ICU length of stay. However both outcomes were based on low

certainty of evidence10. Furthermore, there is evidence that hyperlactatemia in sepsis may not be
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a specific measure of tissue hypoperfusion, i.e. lactate production has been shown to occur
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within tissues that have normal oxygen tension 20.

The recent Andromeda trial21, enrolled 424 patients with shock and found that capillary refill

time (CRT) guided resuscitation may be as effective as lactate-guided resuscitation at reducing

mortality, while reducing the total amount of fluid administered; however some differences in

co-interventions between study arms may have impacted the conclusions. This trial used a

standardized technique of CRT, which involved applying firm pressure to the ventral surface of
the right index finger with a microscope slide until the skin was blank for 10 seconds. A refill

time greater than 3 seconds was considered abnormal.

Ultimately, there remains no single best way to assess for inadequate tissue perfusion. Clinical

judgement based on the macro and microcirculatory parameters discussed above appears to be a

reasonable approach, however a lot of uncertainty remains.

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Can tissue hypoperfusion be fixed with fluid administration?

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Even with reliable measures of circulatory function, it remains unclear how much fluid is

appropriate. Studies have shown that both too little fluid22 and too much fluid23 can cause harm.
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Physiologically, the administration of fluids primarily influences perfusion by affecting venous
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return to the right side of the heart. Venous return is dependent on the difference between mean
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systemic filling pressure and the right atrial pressure divided by venous resistance24. If mean
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systemic filling pressures remain low after inadequate resuscitation, venous return and hence

cardiac output will remain low24. On the other hand, giving fluid to an already fluid replete
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patient might increase right atrial pressure, and thereby decrease venous return and cardiac

output24.

At our current level of understanding, we would recommend individualizing fluid resuscitation

in sepsis using assessments of fluid responsiveness. In other words, fluids should be

administered only to patients in whom there is expected to be a corresponding response or

improvement in cardiac output. While the risks and benefits of fluid administration in patients

who are fluid responsive remains uncertain 8,25, current evidence suggests giving fluid to patients

who are not fluid responsive appears harmful7. Thus, the next section will discuss the most
frequently used measures of fluid responsiveness, and the benefits and limitations associated

with each.

Is the patient fluid responsive?

Static Measures

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Historically, the most common indicators of inadequate resuscitation used by clinicians were

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derived from the bedside physical exam including dry mucous membranes, low jugular venous

pressure (JVP), tachycardia, and decreased skin turgor 27. More recently, central venous
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pressures (CVP), and pulmonary capillary wedge pressures (PCWP), were commonly employed
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invasive static measures used to guide fluid administration26. However, these static
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measurements, whether assessed independently or in combination with one another, have been
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shown to be a poor predictor of the change in cardiac output following a fluid bolus28–31.
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Dynamic Measures
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Pulse pressure variation (PPV), stroke volume variation (SVV) and the passive leg raise (PLR)

are increasingly being used to guide fluid resuscitation. In principle, positive intrathoracic

pressure delivered by a mechanical ventilator to a passively breathing patient both will increase

LV preload and will decrease LV afterload 26,32. The net effect of a passive positive pressure

breath on cardiac output will depend upon the baseline LV end-diastolic volume and the

slope of the LV cardiac function curve. LV stroke volume variability can be inferred from

changes in pulse pressure.26. Large changes in pulse pressure during passive mechanical

ventilation suggests that baseline LV diastolic filling is low. In practical terms, a PPV greater
than 10% – 12% predicts a 15% increase in cardiac output following a fluid bolus27(Table 1).

Pulse contour analysis, which examines differences in the area under the arterial pressure

waveform during inspiration and expiration, is based on similar principles. Compared to PPV (22

studies, 987 patients), estimates of SVV of greater than 13% based on pulse contour analysis has

a lower sensitivity but similar specificity for fluid responsiveness (9 studies, 343 patients)27

(Table 1).

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Major limitations of PPV and pulse contour analysis are that ventilated patients must not have

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any arrhythmias, cannot be ventilated with low tidal volumes, cannot have low lung compliance
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and cannot be spontaneously breathing27,33. Finally, these methods of assessing fluid
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responsiveness require an arterial line and computer software to optimally capture these
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measures.
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The passive leg raise (PLR) maneuver overcomes some of the limitations of PPV and pulse
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contour analysis (Figure 3). In essence, the concept entails measuring stroke volume before and
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after giving patients an ‘internal bolus’ by augmenting venous return from the legs rather than

exposing them to exogeneous fluid administration. To perform this maneuver, a patient is

positioned in a semi-recumbent position with the head of the bed elevated to 45°. Baseline

hemodynamic assessments are performed and then the bed is repositioned by simultaneously

raising the lower section of the bed 45° and lowering the head. Finally, once repositioned, repeat

hemodynamic assessments are performed. A meta-analysis of 21 studies and 991 adult patients

showed that a 10% +/- 2% increase in cardiac output (as measured by a combination of

echocardiography, pulse contour analysis, bioreactance, esophageal Doppler or PAC) with PLR
predicted fluid responsiveness (AUC 0.95, sensitivity 85%, specificity 91%)27. Unfortunately,

PLR has limitations, such as lack of validation if used with hemodynamic variables other than

cardiac output. It is also challenging to use in patients with obesity, multiple femoral catheters or

abdominal/pelvic injuries. Furthermore, the hemodynamic effects of a passive leg raise reach

their maximum within one minute and rapidly dissipate thereafter27,34.

Critical Care Echocardiography (CCE)

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More recently, point of care ultrasound (POCUS) has gained popularity35 as a method of

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estimating fluid responsiveness in large part due to increased availability, rapidity of assessment
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and lack of need for invasive procedures (Table 2). In principle, echocardiographic evaluation
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can assess cardiac output or stroke volume response to fluid challenge, cardiothoracic interaction
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and PLR. When it comes to echocardiography, the gold standard for stroke volume and thus
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cardiac output assessment in echocardiography is the left ventricular outflow tract volume time

index (LVOT-VTI)36 (Figure 4a and 4b). LVOT-VTI is a doppler-derived measure of the

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distance traveled by midstream blood through the left ventricular outflow tract in a single cardiac
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cycle. The LVOT-VTI is calculated by measuring the maximum diameter of the aortic annulus

multiplied by the velocity time integral of the LVOT.

Other echocardiographic indices are also used to determine whether or not cardiac output

changes in response to fluid trials. One large observational trial of fluid responsiveness studied

540 mechanically ventilated patients. Using echocardiographic assessed LVOT-VTI as the gold

standard, investigators found that respiratory variation in maximal Doppler velocity in left

ventricular outflow tract (∆VmaxAo, Figure 5) was the most sensitive method to determine fluid
responsiveness (sensitivity 79%), whereas respiratory variation of superior vena cava (SVC)

diameter as assessed by transesophageal echocardiogram was the more specific (specificity

84%)35. Generalization of these study results may be limited as all participating centers had

expertise in CCE including TEE and the use of dynamic parameters of fluid responsiveness. In

fact, most of the indices mentioned above are not novice echocardiographic skills and can be

limited by non-ideal acoustic windows. Furthermore, these tests are most reliable under strict

conditions such as passive mechanical ventilatory support with >8 ml/kg of tidal volume, thereby

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limiting their use in many clinical situations (i.e., atrial fibrillation, severe ARDS or right

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ventricular failure).
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Given these limitations, some may argue that measurement of PPV is easier to employ at the
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bedside. However, echocardiography has the additional advantage of being able both to assess
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right ventricular function and to identify pulmonary hypertension, two non-fluid-responsive

conditions that are associated with PPV. Therefore, there may be a complementary role for
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measurement of PPV and CCE in the assessment of fluid responsiveness.

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Emerging technologies

The most important aspect of fluid responsiveness is an improvement in cardiac output following

a fluid bolus. Novel technologies have been developed that permit cardiac output to be measured

non-invasively. Technologies such as thoracic electrical bioimpedance or bioreactance using

surface electrodes, pulse contour analysis using either the vascular unloading technique or radial

artery applanation tonometry, and pulse wave transit time using time differentials between the

EKG “R” wave and the pulse oximetry pulse have each demonstrated promise in their ability to
measure cardiac output accurately and precisely under controlled study conditions37. Notably, a

recent multicenter RCT38 compared the use of bioreactance-guided fluid therapy to usual care in

patients with un-resuscitated sepsis. In patients randomized to the bioreactance group, additional

fluids were withheld if cardiac output failed to increase more by at least 10% from baseline

following a PLR. Those in the bioreactance group had a more negative fluid balance (-1.37L)

and required less renal replacement therapy (RRT) and a shorter duration of mechanical

ventilation compared to those randomized to usual care38. While it is unclear whether the

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difference in outcomes were due to the measures of fluid responsiveness used, the results are

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promising. Unfortunately, some of these novel devices are also not yet widely available.37
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Bottom Line
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An international prospective observational study39 of 2213 critically ill patients showed that the
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number one indication for fluid challenge was hypotension (59%) and that in 43% of the cases in
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which fluid was given, no hemodynamic measures of fluid responsiveness were used. Even in

the cases where a measure of fluid responsiveness was employed, the results of the test were not
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used to inform further fluid administration39. This study nicely illustrates the degree of

uncertainty that currently exists around dosing fluids and measures of fluid responsiveness in

critically ill patients.

As summarized here, the various methods used to asses fluid responsiveness in patients with

septic shock have advantages and disadvantages across diverse patient populations. At present,

dynamic measures are more reliable for guiding fluid resuscitation than static measures however,

higher quality data and expertise, especially in CCE, is required.

While awaiting more definitive evidence, the following approach should be considered: If the

mean arterial pressure remains below 65 mm Hg after the initial 30 cc/kg of crystalloid

resuscitation, we assess for fluid responsiveness. Other than intravenous medications, we

advocate against further fluid administration for patients who are found to be fluid unresponsive.

If a patient is fluid responsive or has uncertain or conflicting assessments, then we would give a

fluid bolus and reassess for clinical improvement. If there are signs of clinical improvement with

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fluid administration and the patient remains fluid responsive based on assessment, then repeated

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bolusing is warranted. Frequent reassessment is require to determine when further fluid
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administration is no longer beneficial. In this situation, if hypotension persists, vasopressors
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should be employed to achieve blood pressure goals.
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Case Follow-up

The patient has a high lactate and elevated capillary refill time, suggesting tissue hypoperfusion,
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but his IVC distensibility index is low. Based on his positive passive leg raise test, his physician
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administered a 500 ml bolus of Ringer’s Lactate.

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Figure Legend

Figure 1: Complications of excessive fluid resuscitation and fluid overload (Malbrain et al,
2014)6

Figure 2: The Frank-Starling curve illustrates how stroke volume is directly dependent on the
end diastolic volume of the heart and how the change in stroke volume is also dependent on the
same

Figure 3: Passive leg raise maneuver40

Figure 4a: Calculating the LVOT-VTI: Measuring the area of the left ventricular outflow tract41

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Figure 4b: Calculating the LVOT-VTI: Calculating the velocity time interval (VTI). This is done
by obtaining an apical five chamber view and then producing a pulse wave doppler wave form of

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the left ventricular outflow tract. The resultant wave form can then produce a VTI.
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Figure 5: Calculating ∆VmaxAo: (Vmax – Vmin)/(Vmax+Vmin/2), where Vmax is the
maximum aortic blood flow during inspiration and Vmin is the minimum aortic blood flow
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during expiration. The pulse wave doppler of the left ventricular outflow tract (LVOT) is used to
calculate velocity of aortic blood flow33
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Table 1: Dynamic Measures of Fluid Responsiveness27

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Spontaneously Breathing Patients

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Maneuver How to perform Finding Accuracy

Stroke Volume The Area Under the Curve Change > 13% meaning Low
Variation (SVV) (AUC) of an arterial line fluid responsive. +LR 1.0-2.3
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tracing represents stroke Change <13% meaning -LR 0.05-0.98

volume. The relative fluid non-responsive.
difference in AUC between
inspiration and expiration
reflects SVV.
Passive Leg 1. Sit patient at 45 Mean threshold of High
Raise (PLR) degrees head up increase in cardiac +LR 7 (3.8-13.1)
change on semi-recumbent output (measured by -LR 0.22 (0.09-0.54)
cardiac output position. echocardiography or
2. Lower patient's transpulmonary
upper body to thermodilution) by 11%.
horizontal and
passively raise legs
45 degrees up.
3. Wait 30-90 seconds.
4. Assess for a 10%
increase in stroke
 volume (cardiac
output monitor) or
using a surrogate
such as pulse
pressure (using an
arterial line).

Mechanically Ventilated Patients

Maneuver How to perform
SVV The Area Under the Curve
(AUC) of an arterial line
tracing represents stroke
volume. The relative
Finding Accuracy
Mean change of >13% Moderate
considered to be FR. +LR 4.9 (2.8-8.5)
-LR 0.30 (0.21-0.44)

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difference in AUC between
inspiration and expiration

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reflects SVV.
Pulse Pressure The pulse pressure, or the In Low Tv patients High
Variation (PPV) distance from top to bottom
of an arterial line tracing is
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(<7cc/kg) >8% PPV is
considered FR.
+LR 7.9 (4.1-16)
-LR 0.3 (0.21-0.44)
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compared between
expiration and inspiration. In High Tv patients High
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(>7cc/kg) >11% PPV is +LR 5.3 (3.5-8.1)

considered FR. -LR 0.3 (0.21-0.44)
Passive Leg 1. Sit patient at 45 Mean threshold of High
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raise degrees head up increase in cardiac +LR 11 (6.3-21)

semi-recumbent output (measured by -LR 0.08 (0.03-0.21)
position. echocardiography or
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2. Lower patient's transpulmonary

upper body to thermodilution) by 11%
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horizontal and
passively raise
legs 45 degrees up.
3. Wait 30-90 seconds.
4. Assess for a 10%
increase in stroke
volume (cardiac
output monitor) or
using a surrogate
such as pulse
pressure (using an
arterial line).
Table 2: Monitoring applications of echocardiography in patients with circulatory
failure requiring assessment of volume status, fluid responsiveness, or volume
intolerance

Echocardiographic Cut-off Diagnostic Pitfalls and Limitations

Monitoring in acute value accuracy
circulatory failure
Central volume status - low
CVP – estimate 0-5 NA Spontaneously breathing patients.
(IVC diameter end exhalation < (3 mmHg) Lack of standardization for the
2.1 cm and collapses >50% negative inspiratory force of a sniff

of
with sniff maneuver)42
LVEDA43 <5,5 cm2/m2 NA Difficult interpretation with lack of

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baseline measure. Most of studies
used TEE. More suggestive of

IVC end exhalation44 <13 mm

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Sensitivity: 29%
severe hypovolemia.
Low sensitivity. Exaggerates IVC
Specificity: 80% collapsibility if out of plane,
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Mistaken interrogation of aorta
Falsely increased: RV failure,
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tamponade, pulmonary embolism,

tricuspid regurgitation.
Falsely decreased: increased intra-
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abdominal pressure (>12 mmHg)

Fluid responsiveness
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LVOT VTI – PLR45 >12% 7 studies; The respiratory variability of

increase Sensitivity: 79% LVOT and aortic velocity Severe
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Specificity: 91% aortic stenosis can be inaccurate in

AUC: 0.88 cases of irregular ventricular
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∆VmaxAo Mech.Ventilation >10% Sensitivity: 79% rhythm, right ventricular failure,
Specificity: 64% low tidal volume ventilation,
AUC: 0.75 decreased pulmonary compliance
∆ LVOT VTI Mech. Ventilation46 >10% Sensitivity: 95% (ARDS), high levels of PEEP.
increase Specificity: 78% PLR: abdominal compartment
after IVF AUC: 0.92 syndrome, open abdomen, unstable
pelvic/low lumbar fracture.
Maximal effect within 1 min.
Severe hypovolemia – lack of
blood in lower limbs
SVC collapsibility index35 >21% Sensitivity: 61% Requires TEE assessment -
Specificity: 84% invasive
AUC: 0.75
IVC distensibility index Mean: 11 studies; Low sensitivity. Exaggerate IVC
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Mech. Ventilation >16% Sensitivity: 67% collapsibility if out of plane,
Specificity: 68% Mistaken interrogation of aorta
 AUC: 0.79 Falsely increased: RV failure,
tamponade, pulmonary embolism,
IVC collapsibility index Mean: 5 studies; tricuspid regurgitation.
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>42% Sensitivity: 52% Falsely decreased: increased intra-
Spontaneous Ventilation
Specificity: 77% abdominal pressure (>12 mmHg
Combined measures: Incorporates TEE – invasive
LVOT VTI + 16 cm Specificity: measurement
E wave velocity mitral inflow + 67 cm/sec 99.3% Atrial fibrillation
SVC collapsibility index48 > 39%
Volume intolerance
IVC end exhalation44 >27mm Sensitivity: 29% Higher cut-off to improve
Specificity: 90% specificity. Same aforementioned

of
pitfalls and limitations
Hepatic vein systolic filling <55% Sensitivity: 86% Requires Doppler imaging of
fraction49

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Specificity: 90% hepatic veins. Tricuspid
regurgitation and atrial fibrillation
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