Predicting volume responsiveness

One of the current Holy Grails of ED critical care is to find a reliable measure of fluid responsiveness in those patients with impaired organ perfusion, such as those with severe sepsis. This would enable us to identify those patients whose cardiac output would be improved by fluid therapy, and avoid subjecting ‘non-responders’ to the risks associated with fluid overload. Thanks to the uptake of early goal-directed therapy in sepsis, under-resuscitation is now much less common in the ED. However a growing evidence base reveals the dangers of over-resuscitation. We have a responsibility to optimise fluid therapy as best we can with the equipment we have, according to the latest evidence.

Inferior Vena Cava Ultrasound
Some tests of fluid responsiveness rely on the effect of respiration-induced changes in pleural pressure on the circulation. Inferior vena cava (IVC) size and degree of inspiratory collapse correlate with central venous pressure (CVP), but CVP is not a reliable predictor of volume status or responsiveness. Skinny, collapsing IVCs detected on ultrasound suggest volume responsiveness, but the lack of this finding does not exclude fluid responsiveness. IVC size and measurement can be affected by patient position, probe position, and a variety of health states from athleticism to increased abdominal pressure.

Pulse Pressure Variation
Respiratory pulse pressure variation derived from an arterial line trace in mechanically ventilated patients who are adequately sedated and receiving large tidal volumes can predict fluid responsiveness too. Variability in tidal volume, the presence of spontaneous breathing activity in a ventilated patient, and cardiac dysrhythmia can all confound the usefulness of this method.

End expiratory occlusion
Another test in mechanically ventilated patients is the end expiratory occlusion test. A positive pressure inspiratory breath cyclically decreases the left cardiac preload. Occluding the circuit at end-expiration prevents this cyclic impediment in left cardiac preload and acts like a fluid challenge. A 15 second expiratory occlusion is performed and an increase in pulse pressure or (if you can measure it) 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.

Passive Leg Raise
Passive leg raising (PLR) involves measuring cardiac output (or its surrogate, velocity-time integral, or VTI) before and after tilting the semirecumbent patient supine and raising the legs to 45 degrees. This ‘autotransfuses’ blood from the lower limbs to the core and acts as a reversible fluid challenge. An increase in VTI identifies fluid responders. It would be nice if a PLR-induced increase in blood pressure revealed the answer, but BP does not reliably inform us of changes in cardiac output.

All these tests have limitations. Pulse pressure variation fails in patients with low respiratory system compliance, such as is found in ARDS(1). End-expiratory occlusion and PLR work in low respiratory system compliance, but the former still requires mechanical ventilation, and the latter requires a means of estimating cardiac output or a surrogate – oesophageal Doppler, the velocity-time integral measured by transthoracic echocardiography, and femoral artery flow (measured by arterial Doppler) have all been used. Non-invasive cardiac output monitors that are not operator dependent exist, such as the NICOM(TM) bioreactance device. Bioreactance cardiac output measurement is based on an analysis of relative phase shifts of an oscillating current that occurs when this current traverses the thoracic cavity. Its advantages are that it is noninvasive, it does not require endotracheal intubation or an arterial line, and it provides a good estimate of stroke volume in patients with atrial fibrillation.

A recent study evaluating the combination of PLR with NICOM(TM) bioreactance monitoring revealed that another tool could indicate volume responsiveness: an increase in carotid blood flow after PLR, as measured by carotid Doppler flow imaging(2). A threshold increase in carotid Doppler flow imaging of 20% for predicting volume responsiveness had a sensitivity and specificity of 94% and 86%, respectively. This was studied in a heterogenous group of hemodynamically unstable patients, suggesting applicability to the kind of patients who present to the ED, although numbers were small so more validation is required.

End-tidal carbon dioxide
End-tidal carbon dioxide (ETCO2) levels depend on cardiac output. Increasing cardiac output with a fluid challenge or PLR increases ETCO2,as long as ventilatory and metabolic conditions remain stable. In a recent small study, a PLR-induced increase in ETCO2 ≥ 5 % predicted a fluid-induced increase in cardiac index ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %(3). The maximal effects of PLR on CI and ETCO2 were observed within 1 min.

So what can I use?
In summary, differentiating fluid responders from non-responders in the ED remains a challenge. The method used depends on available equipment and expertise, and whether the patient is spontaneously breathing or mechanically ventilated. The NICOM(TM) shows great promise but until your department can afford one, ultrasound is the way to go; small collapsing IVCs suggest fluid responders. Learning to measure a VTI on transthoracic echo or carotid Doppler flow will help you assess the response to a PLR in spontaneously ventilating patients. If they’re mechanically ventilated, then looking for an ETCO2 rise after PLR could be a simpler alternative.

 
I look forward to more studies on these modalities, and to trying some of them in the resus room at every available opportunity.

1. 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 Jan;40(1):152-7
Abstract

2. The use of bioreactance and carotid doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients
Chest. 2013 Feb 1;143(2):364-70
Abstract

3. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test
Intensive Care Med. 2013 Jan;39(1):93-100
Abstract

Identifying the febrile kid who’s too tachypnoeic

Body temperature raises heart rate and respiratory rate in kids, potentially affecting our interpretation of these clinical signs.

Dutch investigators developed centile charts of respiratory rates for specific body temperatures (derivation study), so that abnormally high rates could be identified as a means of predicting lower respiratory infection (validation set).

Respiratory rate increased overall by 2.2 breaths/min per 1°C rise (standard error 0.2) after accounting for age and temperature in the model, which is similar to a previous UK study that suggested a rise in respiratory rate of around 0.5-2 breaths per minute and an increase in heart rate of about 10 beats per minute for every 1 degree celcius above normal.

Cut-off values at the 97th centile were more useful in detecting the presence of LRTI than existing (Advanced Paediatric Life Support) respiratory rate thresholds.

The respiratory rate charts are available here.

Derivation and validation of age and temperature specific reference values and centile charts to predict lower respiratory tract infection in children with fever: prospective observational study
BMJ. 2012 Jul 3;345:e4224

Free Full Text Link

Targeted ICP reduction in TBI

A South American randomised controlled trial has demonstrated no improvement in mortality when traumatic brain injured patients had therapy targeted at keeping intracranial pressure below or equal to 20 mmHg as measured by an intraparenchymal monitor. The control group’s management was guided by neurologic examination and serial CT imaging(1).

Editorialist Dr Ropper summarises what we should do with this information well(2):

“[The authors]…do not advocate abandoning the treatment of elevated intracranial pressure any more than the authors of studies on wedge pressure reject the administration of fluid boluses in the treatment of shock”

BACKGROUND

Intracranial-pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently, but the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed.

METHODS
We conducted a multicenter, controlled trial in which 324 patients 13 years of age or older who had severe traumatic brain injury and were being treated in intensive care units (ICUs) in Bolivia or Ecuador were randomly assigned to one of two specific protocols: guidelines-based management in which a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring group) or a protocol in which treatment was based on imaging and clinical examination (imaging–clinical examination group). The primary outcome was a composite of survival time, impaired consciousness, and functional status at 3 months and 6 months and neuropsychological status at 6 months; neuropsychological status was assessed by an examiner who was unaware of protocol assignment. This composite measure was based on performance across 21 measures of functional and cognitive status and calculated as a percentile (with 0 indicating the worst performance, and 100 the best performance).

RESULTS
There was no significant between-group difference in the primary outcome, a composite measure based on percentile performance across 21 measures of functional and cognitive status (score, 56 in the pressure-monitoring group vs. 53 in the imaging–clinical examination group; P=0.49). Six-month mortality was 39% in the pressure-monitoring group and 41% in the imaging–clinical examination group (P=0.60). The median length of stay in the ICU was similar in the two groups (12 days in the pressure-monitoring group and 9 days in the imaging–clinical examination group; P=0.25), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging–clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P=0.002). The distribution of serious adverse events was similar in the two groups.

CONCLUSIONS
For patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination

1. A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury
N Eng J Med 367;26:2471-2381 Full Text

2. Brain in a Box
N Eng J Med DOI: 10.1056/NEJMe1212289 Full Text

Aeromedical retrieval: invasive vs noninvasive blood pressure

The chaps from the Emergency Medical Retrieval Service in the UK compared invasive (IABP) and non-invasive blood pressure (NIBP) measurements on the ground and in the air. They concluded that NIBP was unreliable, although it was no worse in the aeromedical environment than in the hospital. Not surprisingly there was a better correlation between the mean IABP and NIBP than systolic or diastolic pressures (oscillometric NIBP devices measure the mean BP and derive systolic and diastolic using an algorithm specific to the device).

In their summary, they recommend:

• IABP monitoring should be used in any unwell patient in whom accurate blood pressure measurement is desirable.
• The aeromedical transport environment does not lead to less precise NIBP results than the non-transport environment.
• Where NIBP measurement is the only option, the mean blood pressure should be used in preference to systolic measurements

Blood pressure measurement is an essential physiological measurement for all critically ill patients. Previous work has shown that non-invasive blood pressure is not an accurate reflection of invasive blood pressure measurement. In a transport environment, the effects of motion and vibration may make non-invasive blood pressure less accurate.

Consecutive critically ill patients transported by a dedicated aeromedical retrieval and critical care transfer service with simultaneous invasive and non-invasive blood pressure measurements were analysed. Two sets of measurements were recorded, first in a hospital environment before departure (pre-flight) and a second during aeromedical transport (in-flight).

A total of 56 complete sets of data were analysed. Bland-Altman plots showed limits of agreement (precision) for pre-flight systolic blood pressure were -37.3 mmHg to 30.0 mmHg, and for pre-flight mean arterial pressure -20.5 mmHg to 25.0 mmHg. The limits of agreement for in-flight systolic blood pressure were -40.6 mmHg to 33.1 mmHg, while those for in-flight mean blood pressure in-flight were -23.6 mmHg to 24.6 mmHg. The bias for the four conditions ranged from 0.5 to -3.8 mmHg. There were no significant differences in values between pre-flight and in-flight blood pressure measurements for all categories of blood pressure measurement.

Thus, our data show that non-invasive blood pressure is not a precise reflection of invasive intra-arterial blood pressure. Mean blood pressure measured non-invasively may be a better marker of invasive blood pressure than systolic blood pressure. Our data show no evidence of non-invasive blood pressures being less accurate in an aeromedical transport environment.

Comparison of non-invasive and invasive blood pressure in aeromedical care
Anaesthesia. 2012 Dec;67(12):1343-7

What is ‘hypotension’ in penetrating trauma?

I previously noted an article demonstrating that a ‘lowish’ – as opposed to a low – systolic blood pressure is a reason to be vigilant in blunt trauma patients, as a significant increase in mortality has been demonstrated with a systolic blood pressure (SBP) < 110 mmHg.

The same researchers have found similar results in patients with penetrating trauma.
Compared with the reference group with SBP 110-129mmHg, mortality was doubled at SBP 90-109mmHg, was four-fold higher at 70-89mmHg and 10-fold higher at <70mmHg. SBP values ≥150mmHg were associated with decreased mortality.

Systolic blood pressure below 110 mmHg is associated with increased mortality in penetrating major trauma patients: Multicentre cohort study
Resuscitation. 2012 Apr;83(4):476-81
Click for abstract

Don’t ignore the diastolic

Most of us are pretty good at spotting hypotension and activating help or initiating therapy.

But ‘hypotension’ in many practitioners’ minds refers to a low systolic blood pressure. Who pays serious attention to the diastolic blood pressure? A low diastolic in a sick patient to me is a warning sign that their mean arterial pressure (MAP) is – or will be – low. After all, we spend about twice as long in diastole as in systole, so the diastolic pressure contributes more to the MAP than does the systolic.

A recent study showed that a low diastolic BP was one of several factors predictive of cardiac arrest on hospital wards: the most accurate predictors were maximum respiratory rate, heart rate, pulse pressure index, and minimum diastolic BP. These factors were more predictive than some of the variables included in the commonly used Early Warning Scores that trigger an emergency review.

The ‘pulse pressure index’ examined in the study is the pulse pressure divided by the systolic blood pressure (ie. [SBP-DBP]/SBP) which of course will be higher with lower diastolic blood pressures.

Importantly, the authors point out:

“In addition, our findings suggest that for many patients there is ample time prior to cardiac arrest to provide potentially life-saving interventions.”

…suggesting that there is still room for improvement in the identification and management of patients at risk for cardiac arrest, as the NCEPOD report ‘Cardiac Arrest Procedures: Time to Intervene?’ also showed.

They also recommend:

“…although systolic BP is commonly used in rapid response team activation criteria, incorporation of pulse pressure, pulse pressure index, or diastolic BP in place of systolic BP into the predictive model may be superior.”

Perhaps this may remind all of us to keep an eye on the diastolic as well as systolic BP when patients first present to us, and to include the importance of recognising diastolic hypotension in the teaching we provide our medical, paramedical and nursing students.

Predicting Cardiac Arrest on the Wards: A Nested Case-Control Study
Chest. 2012 May;141(5):1170-6 Free Full Text here
Click to read abstract

Confidential stuff – in hospital cardiac arrests

A new report describes room for improvement in the care of cardiac arrest patients in hospital¹.

The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) aimed to describe variability and identify remediable factors in the process of care of adult patients who receive resuscitation in hospital, including factors which may affect the decision to initiate the resuscitation attempt, the outcome and the quality of care following the resuscitation attempt, and antecedents in the preceding 48 hours that may have offered opportunities for intervention to prevent cardiac arrest.

Data were captured over a 14 day study period in late 2010 from UK hospitals, and were reviewed by an expert panel.

The summary is available here. I have picked out some findings of interest:

• An adequate history was not recorded in 70/489 cases (14%) and clinical examination was incomplete at first contact in 117/479 cases (24%).
• Appreciation of the severity of the situation was lacking in 74/416 (18%).
• Timely escalation to more senior doctors was lacking in 61/347 (18%).
• Decisions about CPR status were documented in the admission notes in 44/435 cases (10%). This is despite the high incidence of chronic disease and almost one in four cases being expected to be rapidly fatal on admission.
• Where time to first consultant review could be identified it was more than 12 hours in 95/198 cases (48%).
• Appreciation of urgency, supervision of junior doctors and the seeking of advice from senior doctors were rated ‘poor’ by Advisors.
• Physiological instability was noted in 322/444 (73%) of patients who subsequently had a cardiac arrest.
• Advisors considered that warning signs for cardiac arrest were present in 344/462 (75%) of cases. These warning signs were recognised poorly, acted on infrequently, and escalated to more senior doctors infrequently.
• There was no evidence of escalation to more senior staff in patients who had multiple reviews.
• Advisors considered that the cardiac arrest was predictable in 289/454 (64%) and potentially avoidable in 156/413 (38%) of cases.
• The Advisors reported problems during the resuscitation attempt in 91/526 cases (17%). Of these, 36/91 were associated with airway management.
• Survival to discharge after in-hospital cardiac arrest was 14.6% (85/581).
• Only 9/165 (5.5%) patients who had an arrest in asystole survived to hospital discharge.
• Survival to discharge after a cardiac arrest at night was much lower than after a cardiac arrest during the day time (13/176; 7.4% v 44/218; 20.1%).

In the opinion of the treating clinicians, earlier treatment of the problem and better monitoring may have improved outcome:

Compare these findings with a smaller scale confidential enquiry into the care of patients who ended up in intensive care units, published exactly 14 years ago by McQuillan et al²:

“The main causes of suboptimal care were failure of organisation, lack of knowledge, failure to appreciate clinical urgency, lack of supervision, and failure to seek advice.”

One of the co-authors of the McQuillan study, Professor Gary Smith , has spent years improving training in and awareness of the importance of recognition of critical illness, and pioneered the “ALERT” Course ^TM: Acute Life-threatening Emergencies, Recognition, and Treatment. Professor Smith provides commentary on the NCEPOD report and the slides are available here, including a reminder of the ‘Chain of Prevention’³.

It’s a shame these issues remain a problem but it is heartening to see NCEPOD tackle this important topic and provide recommendations that UK hospitals will have to act upon. It is further credit to the vision of Pete McQuillan, Gary Smith and their colleague Bruce Taylor (another co-author of the 1998 confidential inquiry). These guys opened my eyes to the world of critical care and trained me for 18 months on their ICU, which remains a beacon site for critical care expertise and training. Without their inspiration, I may not have ended up in emergency medicine-critical care and I doubt very much that Resus.ME would exist.

1. Cardiac Arrest Procedures: Time to Intervene? (2012)
National Confidential Enquiry into Patient Outcome and Death (NCEPOD)

2. Confidential inquiry into quality of care before admission to intensive care
BMJ 1998 Jun 20;316(7148):1853-8 Free Full Text
Click to read abstract

3. In-hospital cardiac arrest: is it time for an in-hospital ‘chain of prevention’?
Resuscitation. 2010 Sep;81(9):1209-11
Click to read abstract

Is diastolic worse than systolic dysfunction in sepsis?

Septic myocardial dysfunction is a well recognised contributor to shock in sepsis but for many of us we assume this to be gross systolic impairment. Interestingly a recent study highlights that patients with severe sepsis and septic shock frequently have diastolic dysfunction¹. They found that diastolic dysfunction was the strongest independent predictor of early mortality, even after adjusting for the APACHE-II score and other predictors of mortality.

In this study, 9.1% of severe sepsis/septic shock patients had isolated systolic dysfunction, 14.1% had combined systolic and diastolic dysfunction, and 38% had isolated diastolic dysfunction.

Importantly, the authors point out that although diastolic dysfunction is associated with age, hypertension, diabetes mellitus, and ischaemic heart disease, diastolic dysfunction is a stronger independent predictor of mortality than age and the other co-morbidities. However, a limitation of the study acknowledged by the authors is that it did not include follow-up echocardiography examinations, so we do not know whether sepsis was responsible for a transient diastolic dysfunction or whether the observed diastolic dysfunction was a pre-existing condition.

Both troponin and NT-ProBNP elevations also predicted mortality.

Want to know how to measure diastolic dysfunction? These authors measured mitral annular early-diastolic peak velocity, or the e’-wave (called ‘e prime’). It is a way of seeing how fast myocardial tissue relaxes in diastole, and if its peak velocity is slow (in this case < 8cm/s) there is diastolic dysfunction. We measure speed using Doppler, and in this case we’re looking at the speed of heart tissue (as opposed to the blood cells within the heart chambers) so we do ‘Tissue Doppler Imaging’, or TDI. You need an echo machine with pulsed-wave Doppler, and you need to be able to get an apical view. This is explained really nicely here² but if you don’t have the time or the echopassion to read a whole article on TDI watch this one minute video (BY emergency physicians FOR emergency physicians!) on diastology, where TDI measurement of e’ is shown from 45 seconds into the video.

For reference, there is some more detail on diastolic function measurements at the Echobasics site.

If you think you can cope with any more of this level of awesomeness and want these geniuses to talk to you from your smartphone in the ED then get the free One Minute Ultrasound app for Android or Apple devices.

AIMS: Systolic dysfunction in septic shock is well recognized and, paradoxically, predicts better outcome. In contrast, diastolic dysfunction is often ignored and its role in determining early mortality from sepsis has not been adequately investigated.

METHODS AND RESULTS: A cohort of 262 intensive care unit patients with severe sepsis or septic shock underwent two echocardiography examinations early in the course of their disease. All clinical, laboratory, and survival data were prospectively collected. Ninety-five (36%) patients died in the hospital. Reduced mitral annular e’-wave was the strongest predictor of mortality, even after adjusting for the APACHE-II score, low urine output, low left ventricular stroke volume index, and lowest oxygen saturation, the other independent predictors of mortality (Cox’s proportional hazards: Wald = 21.5, 16.3, 9.91, 7.0 and 6.6, P< 0.0001, <0.0001, 0.002, 0.008, and 0.010, respectively). Patients with systolic dysfunction only (left ventricular ejection fraction ≤50%), diastolic dysfunction only (e’-wave <8 cm/s), or combined systolic and diastolic dysfunction (9.1, 40.4, and 14.1% of the patients, respectively) had higher mortality than those with no diastolic or systolic dysfunction (hazard ratio = 2.9, 6.0, 6.2, P= 0.035, <0.0001, <0.0001, respectively) and had significantly higher serum levels of high-sensitivity troponin-T and N-terminal pro-B-type natriuretic peptide (NT-proBNP). High-sensitivity troponin-T was only minimally elevated, whereas serum levels of NT-proBNP were markedly elevated [median (inter-quartile range): 0.07 (0.02-0.17) ng/mL and 5762 (1001-15 962) pg/mL, respectively], though both predicted mortality even after adjusting for highest creatinine levels (Wald = 5.8, 21.4 and 2.3, P= 0.015, <0.001 and 0.13).

CONCLUSION: Diastolic dysfunction is common and is a major predictor of mortality in severe sepsis and septic shock.

1. Diastolic dysfunction and mortality in severe sepsis and septic shock
Eur Heart J. 2012 Apr;33(7):895-903

2. A clinician’s guide to tissue Doppler imaging
Circulation. 2006 Mar 14;113(10):e396-8 Free Full Text

End-Tidal CO2 as a Predictor of Cardiac Arrest Survival

In one of largest studies to date of prehospital capnography in cardiac arrest, an initial EtCO2 >10 mmHg (1.3 kPa) was associated with an almost five-fold higher rate of return of spontaneous circulation (ROSC). In addition, a decrease in the EtCO2 during resuscitative events of >25% was associated with a significant increase in mortality, independent of other variables known to affect outcome.

The authors conclude: “EtCO2 values should be included as important variables in protocols to terminate or continue resuscitation in the prehospital setting“.

OBJECTIVE: The objective of this study was to evaluate initial end-tidal CO2 (EtCO2) as a predictor of survival in out-of-hospital cardiac arrest.

METHODS: This was a retrospective study of all adult, non-traumatic, out-of-hospital, cardiac arrests during 2006 and 2007 in Los Angeles, California. The primary outcome variable was attaining return of spontaneous circulation (ROSC) in the field. All demographic information was reviewed and logistic regression analysis was performed to determine which variables of the cardiac arrest were significantly associated with ROSC.

RESULTS: There were 3,121 cardiac arrests included in the study, of which 1,689 (54.4%) were witnessed, and 516 (16.9%) were primary ventricular fibrillation (VF). The mean initial EtCO2 was 18.7 (95%CI = 18.2-19.3) for all patients. Return of spontaneous circulation was achieved in 695 patients (22.4%) for which the mean initial EtCO2 was 27.6 (95%CI = 26.3-29.0). For patients who failed to achieve ROSC, the mean EtCO2 was 16.0 (95%CI = 15.5-16.5). The following variables were significantly associated with achieving ROSC: witnessed arrest (OR = 1.51; 95%CI = 1.07-2.12); initial EtCO2 >10 (OR = 4.79; 95%CI = 3.10-4.42); and EtCO2 dropping <25% during the resuscitation (OR = 2.82; 95%CI = 2.01-3.97).The combination of male gender, lack of bystander cardiopulmonary resuscitation, unwitnessed collapse, non-vfib arrest, initial EtCO2 ≤10 and EtCO2 falling > 25% was 97% predictive of failure to achieve ROSC.

CONCLUSIONS: An initial EtCO2 >10 and the absence of a falling EtCO2 >25% from baseline were significantly associated with achieving ROSC in out-of-hospital cardiac arrest. These additional variables should be incorporated in termination of resuscitation algorithms in the prehospital setting.

End-Tidal CO2 as a Predictor of Survival in Out-of-Hospital Cardiac Arres
Prehosp Disaster Med. 2011 Jun;26(3):148-50

Passive leg raise predicted fluid responsiveness in kids

Passive leg raising (PLR) is a great ‘free reversible fluid challenge’ to see if a shocked or hypotensive patient is likely to respond to volume therapy. A new study assesses its applicability in children.

PLR predicted fluid responders with 85% specificity but a lack of response did not rule out fluid responsiveness. Also, the effect of the PLR on cardiac index measured by echocardiography was the only way of predicting response – there was no relation to the more easily monitored effects of PLR on systolic blood pressure or heart rate.

Want to learn how to measure cardiac output using ultrasound? Mike Mallin from the Emergency Ultrasound Podcast shows you how here

OBJECTIVE: Fluid challenge is often used to predict fluid responsiveness in critically ill patients. Inappropriate fluid expansion can lead to some unwanted side effects; therefore, we need a noninvasive predictive parameter to assess fluid responsiveness. We want to assess the hemodynamic parameter changes after passive leg raising, which can mimic fluid expansion, to predict fluid responsiveness in pediatric intensive care unit patients and to get a cutoff value of cardiac index in predicting fluid responsiveness in pediatric patients.

DESIGN: Nonrandomized experimental study.

SETTING: Tertiary academic pediatric intensive care.

PATIENTS: Children admitted to pediatric intensive care.

INTERVENTION: Hemodynamic parameters were assessed at baseline, after passive leg raising, at second baseline, and after volume expansion (10 mL/kg normal saline infusion over 15 mins).

MEASUREMENTS AND MAIN RESULTS: We measured the heart rate, systolic blood pressure, and stroke volume and cardiac index using Doppler echocardiography. The hemodynamic parameter changes induced by passive leg raising were monitored. Among 40 patients included in the study, 20 patients had a cardiac index increase of ≥10% after volume expansion (responders). Changes in heart rate, systolic blood pressure, and stroke volume after passive leg raising did not significantly relate to the response to volume expansion. There was significant relation between changes in cardiac index to predict fluid responsiveness (p = .012, r = .22, 95% confidence interval 1.529 to 31.37). A cardiac index increase by ≥10% induced by passive leg raising predicted preload-dependent status with sensitivity of 55% and specificity of 85% (area under the curve 0.71 ± 0.084, 95% confidence interval 0.546-0.874).

CONCLUSION: The concomitant measurements in cardiac index changes after the passive leg raising maneuver can be helpful in predicting who might have an increase in cardiac index with subsequent fluid resuscitation.

The role of passive leg raising to predict fluid responsiveness in pediatric intensive care unit patients.
Pediatric Critical Care Medicine. 13(3):e155-e160, May 2012

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