assessment of volume status and fluid responsiveness in … · 2018-03-20 · 1 ana-catarina...

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Ana-Catarina Pinho-Gomes [ST2 Cardiothoracic Surgery] Manchester Royal Infirmary – 06 December 2016

Assessment of volume status and fluid responsiveness in intensive care

Before completing this tutorial please answer the following MCQs:

1 Regarding the Frank-Starling mechanism, which statement is true?

• An increase in preload will shift the curve up and to the left.

• The cardiac output continuously increases as the preload increases.

• An increase in afterload shifts the curve down and to the right.

• If the inotropy increases, the stroke volume will decrease for the same preload.

2 Each 1 litre of positive fluid balance during the first 72 h of ICU stay was associated

with an increase mortality of:

• 5%

• 10%

• 30%

• 50%

3 Regarding static measurements of volume status, which statement is true:

• CVP depends solely on venous return to the right heart.

• A low CVP is a reliable marker of hypovolaemia.

• In ideal circumstances, PCWP is proportional to the LV preload.

• Echocardiographic parameters have been validated to predict fluid response in critical patients.

4 Regarding dynamic measurements of fluid status, which statement is false:

• Dynamic measurements are affected by the changes in intrathoracic pressure during respiration.

• The respiratory variation of SV is more pronounced in the flat portion of the Frank-Starling curve.

• Pulse pressure variation is more reliable than stroke volume variation at predicting fluid responsiveness.

• Dynamic parameters can only be obtained with transoesophageal echocardiography.

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5 Regarding passive leg raise, which statement is false:

• It is a quick and reversible way of increasing preload.

• It should be performed by elevating both lower limbs to 90°.

• It is not possible to perform in mechanically-ventilated patients.

• It is influenced by intra-abdominal pressure.

Key points:

• Accurate assessment of volume status as well as whether cardiac output will

respond positively to a fluid challenge is a common albeit challenging task in the

care of critically ill patients.

• The ability of clinical acumen to adequately assess fluid status is limited and should

be combined with ancillary tests.

• Static pressure measurements, such as the CVP and PCWP, have little utility and

should not be routinely used to assess volume status or fluid responsiveness.

• Newer dynamic measurements, like PPV and echocardiographic parameters, hold

great promise for determining fluid status but often require sedation and invasive

monitoring.

• Passive leg raise can provide useful information to complement clinical assessment

in spontaneously breathing patients.

• Clinical judgement is required to interpret the results of volume measurements in the

context of the individual patient.

Introduction

It is a typical morning intensive care round. There is a septic, mechanically ventilated

patient, who remains hypotensive despite aggressive fluid therapy overnight. The

patient is dependent on vasopressors to meet with the targets of ‘early goal directed

therapy’. A lively debate ensues with someone advocating a fluid bolus, whilst someone

else feels the patient is already overloaded. How can the conflict be resolved? How can

volume status be accurately assessed?

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The underlying principle: the Frank-Starling law

The Frank-Starling law describes the relationship between preload, mainly influenced by

venous return, and contractility (Figure 1). It resulted from the joint work of two scientists:

Otto Frank observed, using isolated frog hearts, that the strength of ventricular

contraction was increased when the ventricle was stretched prior to contraction; later

Ernest Starling and colleagues in the early 20th century found that increasing venous

return to the heart, which increased the filling pressure (left ventricular end-diastolic

pressure; LVEDP) of the ventricle, led to increased stroke volume (SV). Conversely,

decreasing venous return decreased filling pressure and SV. This ventricular response to

changes in venous return is intrinsic to the heart but it can be modified by extrinsic

neurohumoral mechanisms. Therefore, the ventricle can operate on several Frank-

Starling curves depending on the afterload and inotropic state, which is influenced by

neurohumoral systems (e.g. noradrenaline, angiotensin-aldosterone, dopamine).

As shown in Figure 2, increasing afterload (the resistance against ventricular

contraction) or decreasing inotropy (the contractility of the myocardium) shifts the curve

down and to the right, which means that at a given preload (LVEDP) the ventricular

response (SV) will be lower. On the contrary, decreasing afterload and increasing

inotropy shifts the curve up and to the left, which means that at a given preload (LVEDP)

the force generated by the ventricle and so the SV will be higher.

Figure 1 [left]: Frank-Starling curve (basal) Figure 2 [right]: Multiple Frank-Starling curves in response to changes in afterload and inotropy

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Figure 3: Pressure-Volume Loop: basal conditions and response to increase in preload

The underlying mechanisms for the increase in ventricular contraction with increased

preload (LVEDP) are related to the degree of stretching of cardiac myocytes. There is

an optimal sarcomere length in which force generation and thus ventricular contraction

are maximal, which is at least partly explained by increased activation of contractile

proteins.

Based on the Frank-Starling mechanism, pressure-volume loops can be created to

depict how changes in venous return affect end-diastolic and end-systolic volumes

(Figure 3). When venous return increases, there is increased filling of the ventricle along

its passive pressure curve leading to an increase in LVEDV. If the ventricle now contracts

at this increased preload, provided that afterload and inotropy remain constant, the

ventricle empties to the same LVESV, which then results in an increase in SV (width of

the pressure-volume loop). This demonstrates how a normal ventricle can match stroke

volume to physiological increases in venous return; the loss of this response explains the

inability of failing ventricles to cope with increases in preload.

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Why is it important to assess intravascular volume?

Although aggressive fluid resuscitation targeted to central venous pressure (CVP) and

physiological variables has been the mainstay of early goal directed therapy to reduce

organ failure and improve survival in patients with severe sepsis and septic shock [1],

more recent studies in critically ill patients have demonstrated that excessive fluid

resuscitation and markedly positive net fluid balance is associated with higher rates of

complications and increased mortality [2]. In a European multicentre observational

study of patients admitted to the ICU, each 1 litre of positive fluid balance during the

first 72 h of ICU stay was associated with a 10% increase in mortality after adjustments

for other risk factors [3]. A more conservative fluid management strategy seems

particularly beneficial for patients with acute lung injury in the ICU due to the

detrimental effects of fluid overload on gas exchange [4]. Although both insufficient and

excessive resuscitation are associated with worse clinical outcomes, most decisions

regarding fluid therapy are still made empirically.

The two crucial questions in fluid resuscitation are: (1) what is the current state of the

patient’s intravascular volume? and (2) if the patient receives continued fluid

resuscitation or a fluid bolus, will physiological variables such as blood pressure, tissue

perfusion, and urine output improve (i.e. is the patient fluid-responsive)?

History and examination

History and examination provide the earliest evidence of volume status (Table 1). The

most reliable symptoms of volume overload are paroxysmal nocturnal dyspnoea,

orthopnoea and peripheral oedema [5]. For blood-loss hypovolaemia, postural

hypotension was the most useful physical finding but only for large blood losses (>1

litre). However, the accuracy of physical findings is more limited for non-blood loss

related hypovolaemia, for which laboratory tests are required (Table 2)[6].

Chest radiograph and echocardiography

The daily chest X-ray (CXR) in the ICU is an established diagnostic tool to complement

history and physical examination findings, and is commonly used to assess volume

status. However, common CXR findings (e.g. venous redistribution, interstitial oedema)

are highly variable and insensitive and more complex measurements like cardiac index

and vascular pedicle width although more reliable are technically difficult [7, 8].

Therefore, the utility of physical findings and CXR to assess volume status is limited and

so more sensitive and specific techniques are needed.

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Static measurements:

Central venous pressure

Central venous pressure (CVP), obtained using a pressure transducer attached to a

central venous catheter, is probably the most popular parameter used to guide fluid

therapy in ICU, because it is simple, static and easy to interpret. In addition,

randomized controlled trials (RCT) have used CVP to set targets for fluid therapy for

instance in sepsis [1] and ARDS [4]. However, CVP does not predict whether the

patient’s cardiac output (which depends on SV and HR) will increase in response to a

fluid bolus [9, 10]. CVP is dependent on venous return (VR) to the heart, right ventricular

compliance, peripheral venous tone, and posture, and the CVP is particularly unreliable

in pulmonary vascular disease, right ventricular disease, patients with tense ascites,

isolated left ventricular failure, and valvular heart disease. In patients with an intact

sympathetic response to hypovolemia, the CVP may fall in response to fluid, as

compensatory venoconstriction is reduced [11]. Therefore, it is possible to have a low

CVP and not be volume responsive, as well as have a high CVP and be volume

responsive [12].

Pulmonary capillary wedge pressure (PCWP)

Pulmonary artery occlusion pressure or PCWP has been widely used to assess volume

status and fluid responsiveness in the ICU and operating room because in ideal

circumstances it is proportional to LVEDV/preload. However, most studies demonstrated

a poor correlation with volume responsiveness, which might be due to changes in

vascular and cardiac compliance, distribution of fluids in the various compartments of

the cardiovascular system, and the compromised cardiac response to an increase in

preload in critically ill patients [11, 13].

Echocardiography

There are several two-dimensional and Doppler flow measurements that can be

obtained from transthoracic or transoesophageal echocardiography (TTE or TOE) that

provide cardiac chamber volume assessment [14]. However, in the absence of baseline

echocardiographic data, isolated measurements are hard to interpret due to individual

variability, which compromises their usefulness in the assessment of preload and

volume responsiveness.

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Dynamic measurements

Dynamic measurements have been developed to overcome the limitations of static

parameters to better discriminate between those patients who increase SV with fluid

therapy (‘fluid responders’) and those who do not (‘nonresponders’). The degree of

variation of those dynamic parameters depends on the changes in intrathoracic

pressure induced by spontaneous and mechanical ventilation [15]. Furthermore, the

changes in RV and LV SV with respiration/ventilation are more pronounced on the steep

(‘volume responsive’) compared with the flat portion of the Frank–Starling curve (that is,

significant hypovolaemia results in more pronounced changes in arterial pressure

during the respiratory cycle) [16].

Systolic pressure variation, SVV and PPV

For a given arterial compliance, the amplitude of the pulse pressure is directly related

to SV. This makes SVV and PPV potentially more useful parameters over SPV as they are

less affected by changes in diastolic pressure that affect the systolic pressure and could

confound interpretation [17]. PPV is calculated by one of several techniques that

calculate the difference between maximum and minimum pulse pressures during

mechanical breaths, and SVV is computed through pulse contour analysis and

computation of the area under the systolic portion of the arterial pressure curve.

There are several systems available to calculate SPS, SVV and PPV. Edwards

Lifesciences (Irvine, CA) manufactures a system that calculates SVV (the Vigileo monitor

and FloTrac sensor) by means of an arterial catheter and analysis of the arterial

pressure waveform and it has been shown to optimise fluid management strategies [18,

19]. Another system for determining beat-to-beat measurement of CO along with the

ability to ascertain SVV, PPV, and SPV is the LiDCO Plus System (LiDCO, Cambridge, UK).

This calibrated system combines the LiDCO system for the measurement of CO using a

lithium-based indicator dilution method along with the PulseCO system, which calculates

continuous beat-to-beat analysis of CO [20]. Data derived from this system can be used

to derive SVV, PPV, and SPV. However, evidence hitherto available is insufficient to

either support or discard its routine use [21].

A less invasive alternative to these techniques is pulse pressure analysis during

mechanical ventilation using dynamic changes in both the peak and amplitude of the

pulse oximeter plethysmographic wave form. These volume changes in arterial vessels

correlate with PPV and provide a good estimate of fluid responsiveness [22, 23].

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Several studies have demonstrated the superior performance of PPV in comparison to

SVV, perhaps because PPV is directly measured on an arterial-line tracing whilst SVV is

calculated from pulse contour analysis [24, 25].

However, those parameters have only been validated in mechanically ventilated

patients who were paralysed, which undermines the accuracy of extrapolations to

spontaneously breathing patients [26, 27].

Passive leg raise (PLR)

PLR [28, 29] is a simple manoeuvre that can be performed in spontaneously breathing

patients. This quick and reversible way of increasing preload offers a good estimation

of cardiac response to volume with no risk of causing unnecessary harm, as is increases

venous return to the heart without the need for an actual increase in total volume.

Moreover, it does not require any sophisticated equipment or training. However, for

reasons yet to be understood, it has never become standard of practice for assessment

of volume status. From a more technical point of view, PLR ideally should be obtained

by simultaneously elevating the lower limbs to 45° and lowering the patient into the

supine position from a 45° degree semi-recumbent position. Several devices are

available to translate the assess the response of SV and CO to the increase preload

induced by PLR. For instance, the FloTracVigleo (Edwards Lifesciences, Irvine, CA)

system shows how SVV responds to PLR [30], whilst transpulmonary thermodilution

(PiCCO system, Pulsion Medical Systems, Munich, Germany) shows the effects of PLR on

cardiac output with pulse pressure analysis [31]. A noninvasive alternative to those

systems is the noninvasive CO monitor (NICOM, Cheetah Medical, Portland, OR), which

allows continuous haemodynamic monitoring based on bioreactance [32] and can

predict cardiac response to PLR or an IV fluid challenge [33, 34].

Oesophageal Doppler

Oesophageal Doppler monitoring, by means of a probe placed in the oesophagus

through the nose or mouth, allows measuring aortic blood flow in the descending

thoracic aorta and hence provides good estimates of SV and cardiac output [35].

However, the probe is poorly tolerated in awake patients and it needs to be refocused

prior to each measurement, making it more suitable for repeated measurements than

for continuous monitoring.

In the UK, NICE has approved the use of the CardioQ-ODM oesophageal doppler

monitor in people who are having major surgery or people having surgery who would

otherwise be monitored with a more invasive method [36]. The approval was granted

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on the grounds that it reduces the use of central venous catheters, complications after

surgery and the length of stay in hospital without increasing the need for readmission to

hospital or repeat surgery. However, further evidence is required to fully clarify the

actual benefit of oesophageal Doppler for predicting fluid responsiveness [37].

Echocardiography

Bedside transthoracic echocardiography has met with increased interest for the last

years and it is now commonly used for volume assessment [38, 39]. Nevertheless, there

is ongoing controversy on which measurements are better at predicting response to a

fluid bolus. Inferior vena cava (IVC) diameter or the extent of respiratory cycle variation

[16, 40, 41] together superior vena cava (SVC) collapsibility index [42] are the most

often employed to assess fluid responsiveness. Respiratory SVC variation seems to have

the best specificity and overall accuracy, whereas maximal Doppler velocity in the left

ventricular outflow track has the best sensitivity for predicting fluid response [43].

However, those measurements cannot be obtained on a continuous basis and may be

technically difficult due to body habitus. In addition, IVC diameter is influenced by intra-

abdominal pressure and thus has limited use in patients post laparotomy or with

suspected high intra-abdominal pressures. On the other hand, SVC measurements

require TOE, which is logistically difficult to obtain in unstable, critically ill patients.

Bioimpedance vector analysis

Bioimpedance vector analysis is a new technique that is currently under investigation

and appears promising as noninvasive, real-time measurement of static volume status

[44]. It relies on the relative conduction of electrical current by different body tissues,

including water. Although it might be useful in managing patients with volume overload

[45-47], it is not able to differentiate between compartmentalised oedema and

increased total body water. It is thus unable to assess intravascular volume and

response to fluid therapy.

Conclusion

Early recognition and treatment of acute circulatory failure and tissue hypoperfusion are

crucial in the management of critically ill patients but accurate assessment of

intravascular volume remains one of the most challenging tasks for clinicians. Accurate

identification of patients who would benefit from fluid resuscitation is paramount to

optimise haemodynamic parameters and avoid the deleterious consequences of fluid

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overload, particularly pulmonary oedema, in patients for whom inotropic and/or

vasopressor support would be preferable.

Although clinical experience and acumen remain the cornerstone of assessment of

volume status, additional diagnostic tests are useful to support or refute clinical

assessments (Table 3). Static pressure measurements have been progressively replaced

by newer dynamic measurements. Although the latter are more accurate at predicting

response to fluid therapy, the common requirement for sophisticated equipment and

training as well as invasiveness preclude more routine use [48]. None of the methods

hitherto available has demonstrated enough accuracy and reliability to override clinical

judgement, considering the context of each individual patient.

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Answers to MCQs:

1 FFTF

2 FTFF

3 FFTF

4 FTFF

5 FTFF

References

1 Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of

severe sepsis and septic shock. N Engl J Med 2001; 345: 1368-77.

2 Investigators RRTS, Bellomo R, Cass A, et al. An observational study fluid balance

and patient outcomes in the Randomized Evaluation of Normal vs. Augmented Level

of Replacement Therapy trial. Crit Care Med 2012; 40: 1753-60.

3 Vincent JL, Sakr Y, Sprung CL, et al. Sepsis in European intensive care units: results of

the SOAP study. Crit Care Med 2006; 34: 344-53.

4 National Heart L, Blood Institute Acute Respiratory Distress Syndrome Clinical Trials

N, Wiedemann HP, et al. Comparison of two fluid-management strategies in acute

lung injury. N Engl J Med 2006; 354: 2564-75.

5 Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT Does this dyspneic patient in

the emergency department have congestive heart failure? JAMA 2005; 294: 1944-56.

6 McGee S, Abernethy WB, 3rd, Simel DL The rational clinical examination. Is this

patient hypovolemic? JAMA 1999; 281: 1022-9.

7 Saugel B, Ringmaier S, Holzapfel K, et al. Physical examination, central venous

pressure, and chest radiography for the prediction of transpulmonary thermodilution-

derived hemodynamic parameters in critically ill patients: a prospective trial. J Crit

Care 2011; 26: 402-10.

8 Ely EW, Smith AC, Chiles C, et al. Radiologic determination of intravascular volume

status using portable, digital chest radiography: a prospective investigation in 100

patients. Crit Care Med 2001; 29: 1502-12.

9 Durairaj L, Schmidt GA Fluid therapy in resuscitated sepsis: less is more. Chest 2008;

133: 252-63.

10 Marik PE, Cavallazzi R Does the central venous pressure predict fluid

responsiveness?An updated meta-analysis and a plea for some common sense. Crit

Care Med 2013; 41: 1774-81.

11 Michard F, Teboul JL Predicting fluid responsiveness in ICU patients: a critical

analysis of the evidence. Chest 2002; 121: 2000-8.

14


12 Marik PE, Baram M Noninvasive hemodynamic monitoring in the intensive care unit.

Crit Care Clin 2007; 23: 383-400.

13 Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to

predict hemodynamic response to volume challenge. Crit Care Med 2007; 35: 64-8.

14 Josephs SA The use of current hemodynamic monitors and echocardiography in

resuscitation of the critically ill or injured patient. Int Anesthesiol Clin 2007; 45: 31-59.

15 Michard F, Teboul JL Using heart-lung interactions to assess fluid responsiveness

during mechanical ventilation. Crit Care 2000; 4: 282-9.

16 Feissel M, Michard F, Faller JP, Teboul JL The respiratory variation in inferior vena

cava diameter as a guide to fluid therapy. Intensive Care Med 2004; 30: 1834-7.

17 Tavernier B, Makhotine O, Lebuffe G, Dupont J, Scherpereel P Systolic pressure

variation as a guide to fluid therapy in patients with sepsis-induced hypotension.

Anesthesiology 1998; 89: 1313-21.

18 McLean AS, Huang SJ, Kot M, Rajamani A, Hoyling L Comparison of cardiac output

measurements in critically ill patients: FloTrac/Vigileo vs transthoracic Doppler

echocardiography. Anaesth Intensive Care 2011; 39: 590-8.

19 Benes J, Chytra I, Altmann P, et al. Intraoperative fluid optimization using stroke

volume variation in high risk surgical patients: results of prospective randomized

study. Crit Care 2010; 14: R118.

20 Sundar S, Panzica P LiDCO systems. Int Anesthesiol Clin 2010; 48: 87-100.

21 Moppett IK, Rowlands M, Mannings A, Moran CG, Wiles MD, Investigators N LiDCO-

based fluid management in patients undergoing hip fracture surgery under spinal

anaesthesia: a randomized trial and systematic review. Br J Anaesth 2015; 114: 444-

59.

22 Feissel M, Teboul JL, Merlani P, Badie J, Faller JP, Bendjelid K Plethysmographic

dynamic indices predict fluid responsiveness in septic ventilated patients. Intensive

Care Med 2007; 33: 993-9.

23 Cannesson M, Besnard C, Durand PG, Bohe J, Jacques D Relation between

respiratory variations in pulse oximetry plethysmographic waveform amplitude and

arterial pulse pressure in ventilated patients. Crit Care 2005; 9: R562-8.

24 Monnet X, Bleibtreu A, Ferre A, et al. Passive leg-raising and end-expiratory

occlusion tests perform better than pulse pressure variation in patients with low

respiratory system compliance. Crit Care Med 2012; 40: 152-7.

25 Marx G, Cope T, McCrossan L, et al. Assessing fluid responsiveness by stroke volume

variation in mechanically ventilated patients with severe sepsis. Eur J Anaesthesiol

2004; 21: 132-8.

15


26 Freitas FG, Bafi AT, Nascente AP, et al. Predictive value of pulse pressure variation

for fluid responsiveness in septic patients using lung-protective ventilation strategies.

Br J Anaesth 2013; 110: 402-8.

27 Marik PE, Cavallazzi R, Vasu T, Hirani A Dynamic changes in arterial waveform

derived variables and fluid responsiveness in mechanically ventilated patients: a

systematic review of the literature. Crit Care Med 2009; 37: 2642-7.

28 Preau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL Passive leg raising is

predictive of fluid responsiveness in spontaneously breathing patients with severe

sepsis or acute pancreatitis. Crit Care Med 2010; 38: 819-25.

29 Teboul JL, Monnet X Prediction of volume responsiveness in critically ill patients with

spontaneous breathing activity. Curr Opin Crit Care 2008; 14: 334-9.

30 Biais M, Vidil L, Sarrabay P, Cottenceau V, Revel P, Sztark F Changes in stroke

volume induced by passive leg raising in spontaneously breathing patients:

comparison between echocardiography and Vigileo/FloTrac device. Crit Care 2009;

13: R195.

31 Squara P, Denjean D, Estagnasie P, Brusset A, Dib JC, Dubois C Noninvasive cardiac

output monitoring (NICOM): a clinical validation. Intensive Care Med 2007; 33: 1191-

4.

32 Marik PE Noninvasive cardiac output monitors: a state-of the-art review. J

Cardiothorac Vasc Anesth 2013; 27: 121-34.

33 Kossari N, Hufnagel G, Squara P Bioreactance: a new tool for cardiac output and

thoracic fluid content monitoring during hemodialysis. Hemodial Int 2009; 13: 512-7.

34 Lamia B, Ochagavia A, Monnet X, Chemla D, Richard C, Teboul JL

Echocardiographic prediction of volume responsiveness in critically ill patients with

spontaneously breathing activity. Intensive Care Med 2007; 33: 1125-32.

35 Dark PM, Singer M The validity of trans-esophageal Doppler ultrasonography as a

measure of cardiac output in critically ill adults. Intensive Care Med 2004; 30: 2060-6.

36 CardioQ-ODM oesophageal doppler monitor. UK: National Institute for Clinical

Excellence, 2011.

37 Mowatt G, Houston G, Hernandez R, et al. Systematic review of the clinical

effectiveness and cost-effectiveness of oesophageal Doppler monitoring in critically

ill and high-risk surgical patients. Health Technol Assess 2009; 13: iii-iv, ix-xii, 1-95.

38 Boyd JH, Sirounis D, Maizel J, Slama M Echocardiography as a guide for fluid

management. Crit Care 2016; 20: 274.

39 Charbonneau H, Riu B, Faron M, et al. Predicting preload responsiveness using

simultaneous recordings of inferior and superior vena cavae diameters. Crit Care

2014; 18: 473.

16


40 Yanagawa Y, Nishi K, Sakamoto T, Okada Y Early diagnosis of hypovolemic shock by

sonographic measurement of inferior vena cava in trauma patients. J Trauma 2005;

58: 825-9.

41 Weekes AJ, Tassone HM, Babcock A, et al. Comparison of serial qualitative and

quantitative assessments of caval index and left ventricular systolic function during

early fluid resuscitation of hypotensive emergency department patients. Acad Emerg

Med 2011; 18: 912-21.

42 Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a

gauge of volume status in ventilated septic patients. Intensive Care Med 2004; 30:

1734-9.

43 Vignon P, Repesse X, Begot E, et al. Comparison of Echocardiographic Indices Used

to Predict Fluid Responsiveness in Ventilated Patients. Am J Respir Crit Care Med

2016.

44 Peacock WFt Use of bioimpedance vector analysis in critically ill and cardiorenal

patients. Contrib Nephrol 2010; 165: 226-35.

45 Peyton PJ, Chong SW Minimally invasive measurement of cardiac output during

surgery and critical care: a meta-analysis of accuracy and precision. Anesthesiology

2010; 113: 1220-35.

46 Alves FD, Souza GC, Clausell N, Biolo A Prognostic role of phase angle in

hospitalized patients with acute decompensated heart failure. Clin Nutr 2016.

47 Pillon L, Piccoli A, Lowrie EG, Lazarus JM, Chertow GM Vector length as a proxy for

the adequacy of ultrafiltration in hemodialysis. Kidney Int 2004; 66: 1266-71.

48 Mohsenin V Assessment of preload and fluid responsiveness in intensive care unit.

How good are we? J Crit Care 2015; 30: 567-73.

49 Kalantari K, Chang JN, Ronco C, Rosner MH Assessment of intravascular volume

status and volume responsiveness in critically ill patients. Kidney Int 2013; 83: 1017-

28.

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