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Peter Bentzer, MD, PhD, discusses the clinical examination for fluid responsiveness in hemodynamically unstable patients.
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Peter Bentzer, MD, PhD, discusses the clinical examination for fluid responsiveness in hemodynamically unstable patients.
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Segment:0 .
[ Music ] >> Hello and welcome to JAMAevidence, our monthly podcast focused on core issues in evidence-based medicine. I'm David Simel, the Editor of the Rational Clinical Examination series, and Professor of Medicine at the Durham Veterans Affairs Medical Center in Duke University. Today, we're discussing the clinical evaluation for fluid responsiveness in hemodynamically unstable patients.
Joining me to talk about this topic is Dr. Peter Bentzer who is a consultant in anesthesia and intensive care at Helsingborg Hospital, Helsingborg, Sweden, and Associate Professor at the Department of Anesthesia and Intensive Care, Lund University in Sweden. Welcome, Peter, and thanks for joining us. To start off, can you tell us about the risk of administering excessive intravenous fluid therapy to a patient who has been resuscitated but is still hypotensive?
>> Like any potent medication, fluid can have side effects. In the case of fluids, the most important side effects would be edema formation and compartment syndromes, which can then result in poor organ function and ultimately influence outcome. So the concept that a positive fluid balance adversely affect outcomes is supported by observational studies showing a correlation between a positive fluid balance and mortality.
The caveat being, of course, that the sicker the patients are, the more fluid they are likely to get. Causality, however, is not established as firmly as one could expect. To my knowledge, only one study so far has investigated the impact of reducing or restricting fluid therapy and that was one of the studies published by the ARDS Network group in 2006 in New England Journal of Medicine showing that if you applied a restrictive fluid administration therapy to a patient suffering from ARDS their lung function and duration of mechanical ventilation was decreased.
[inaudible] potential adverse effects of fluids, it's very important to carefully consider if more fluids will actually improve the patient's hemodynamics. And by predicting fluid responsiveness, it's possible that we can actually avoid adverse effects and eventually improve outcome. >> Well, after you resuscitate a patient, while everyone is giving themselves high fives, it's not unusual to see that your patient remains hypotensive. So when you think about those patients, what's the probability that a patient like that is going to respond to continued fluid administration after the initial resuscitation?
>> Based on the studies that we included in our analysis, about 50% of the patients that remains hemodynamically unstable after the initial resuscitation will respond to further fluids. And by responds, I mean an increase in cardiac output by 10 to 15% after a fluid bolus. However, I think it's important to realize that the majority of studies that we included in our analysis included patients that were suffering from sepsis.
Having said that, I'm not certain that we can say that the 50% figure applies to all pathophysiological conditions. It might very well be different, for example, in trauma or other conditions. >> Well, after your resuscitation, what signs and symptoms are going to help the clinician assess whether the hemodynamic instability is actually due to hypovolemia? >> That is a tricky question.
So basically, what we want to find out is if the patient in front of us is likely to improve in hemodynamic status if we increase pre-load by administering fluid. So in essence, what we want to do at the bedside is try to establish whether our patient is on the steep or flat part of the so-called Frank-Starling curve. That is the curve that describes the relation between pre-load and cardiac output.
So the clinical examination findings that are traditionally associated with hypovolemia include, for example, prolonged capillary refill time, tachycardia, decreased tissue turgor, and decreased jugulovenous pressure. And in our search, we could only find two studies that investigated the accuracy of these clinical examination findings to predict fluid responsiveness. As it turned out, these signs and symptoms were very poor predictors of fluid responsiveness with likelihood ratios crossing one in both of these studies.
And perhaps it's not extremely surprising as these findings align very well with the 50% prevalence of fluid responsiveness in the other studies that I mentioned before. In fact, in those studies, inclusion criteria usually included symptoms like tachycardia and increased capillary refill time. So to conclude, clinical signs and symptoms at the bedside are very poor predictors of response to fluids.
>> Well, after the resuscitation, a lot of these patients are going to be mechanically ventilated. Does that make it easier or harder to assess their volume status? >> Well, I guess it depends. For the most part, it would make a prediction of fluid responsiveness easier provided, at least, that the patients are ventilated in a controlled manner and that they don't make any spontaneous breathing efforts. The reason for that is that positive pressure ventilation induced cyclic changes in the preload of the heart.
And if the patient is on the steep part of the Frank-Starling curve, those changes in preload will cause cyclic changes in stroke volume, and those changes, in turn, can be quantified by calculating either pulse pressure variation, or for example, stroke volume variation by using data obtained in an arterial line. Also, positive pressure ventilation will lead to cyclic changes in central venous pressures. And if compliance of large venous vessels is high, these changes can induce changes in dimension, so for example, the inferior vena cava, that can be measured bedtime by using ultrasound.
So what happens is that in inspiration the vena cava gets wider and in expiration, vena cava gets smaller. And these changes can be quantified by calculating what's called the distensibility index. And a high variation in dimension of the vena cava with respiration suggests a low intervascular volume and that the patient may be fluid responsive.
In fact, we found four studies evaluating this method to predict fluid response ability and it turned out that it was pretty good in predicting fluid responsiveness with positive likelihood ratios of about five and negative likelihood ratios of about 0.3. >> Well, our hospital medicine physicians are looking for all kinds of uses for bedside ultrasound. So what you've described is that a large filling and then collapse of the inferior vena cava suggests volume depletion.
Does this same technique work for evaluating hypovolemia in a spontaneously breathing patient as opposed to one who is being ventilated? >> The simple answer is we don't know yet. But it's unlikely to be as good in spontaneously ventilated patients as in positive pressure ventilated patients because in spontaneously breathing patients, inspiratory effort will influence the variability in vena cava.
We only found two studies in our search that evaluated variability in vena cava dimensions in spontaneously breathing patients and those could not demonstrate the good accuracy that we found in patients that were receiving positive pressure ventilation. >> I'm disappointed. Okay, so what special challenges do clinicians face when deciding if a patient is going to be responsive to the additional fluids that they give?
>> Well, I would say that the most challenging situation is the spontaneously breathing patient. In this situation, only one method show reasonable accuracy and that is a method called passive leg raising. Passive leg raising is based on the principle that the preload of the heart is increased by transferring blood from the lower extremities to the central compartment.
And in order to maximize the change in preload induced by the leg raising, the patient is commonly semi-recumbent at baseline, and then by tilting the bed the legs are raised to a degree of about 40 degrees and with the torso being in a flat position. And following this passive leg raise, the response in terms of cardiac output is measured by either invasive measurements or actually by a bedside ultrasound.
And an increasing cardiac output by more than 10% within the first 60 seconds of the leg raise indicates that the patient is a responder to fluids. This is actually the most versatile test and can be used both in spontaneous breathing patients and in ventilated patients. >> To actually do the test, do I lower the head of the bed or can I have someone hold both feet and raise the legs up? >> That is a good question.
In most studies that we found, what the authors actually did was that they tilted the bed. But I guess that if you raise the legs and lower the torso, that would be equally good but that is actually not studied in those studies. >> Is there anything else you'd like to tell our listeners about fluid responsiveness in unstable patients? >> I think the most important take-home message that we perhaps didn't get across in the article is that fluid responsiveness is a very dynamic feature, which is most likely going to change with changing doses of vasopressors or inotropes.
So I think it's important to realize that it has to be reassessed frequently. And also I think it's very important to realize that the decision to give fluids or not should not be based solely on whether the patient is deemed to be a responder or a potential responder or not but should be based on the clinical context. Etiology of hemodynamic instability in critically ill patients is often complex and involves other components than hypovolemia.
And fluid is perhaps not always the optimal way to improve the circulation in an unstable patient even if he or she is likely to respond favorably to fluids. For example, spontaneously breathing patients with bilateral crackles and hypotension may be better off if we start him or her on vasopressors or an inotrope than giving more fluids, which could eventually lead to respiratory failure and an intubation with all the consequences on outcome that that has.
Another take-home message is that cutoff values for each of the different predictors that we evaluated in the study differs between different studies. So one should perhaps not regard the cutoff values as absolute limits but rather an indication of whether the patients are likely to be responsive or not to fluids. Last but perhaps not least important is that if you want to use any of the methods that we described in the manuscript, you have to realize that there are caveats with each of the methods and that you have to take into account that when evaluating the accuracy of the different methods.
>> Well, Dr. Bentzer, thanks for joining me today in this discussion. More information about this topic is available in the Rational Clinical Examination and on our website, JAMAevidence, that is all one word, JAMAevidence.com, where you can listen to our entire roster of podcasts. I'm David Simel and I'll be back with you soon for another edition of JAMAevidence. [ Music ]
Segment:0 .
[ Music ] >> Hello and welcome to JAMAevidence, our monthly podcast focused on core issues in evidence-based medicine. I'm David Simel, the Editor of the Rational Clinical Examination series, and Professor of Medicine at the Durham Veterans Affairs Medical Center in Duke University. Today, we're discussing the clinical evaluation for fluid responsiveness in hemodynamically unstable patients.
Joining me to talk about this topic is Dr. Peter Bentzer who is a consultant in anesthesia and intensive care at Helsingborg Hospital, Helsingborg, Sweden, and Associate Professor at the Department of Anesthesia and Intensive Care, Lund University in Sweden. Welcome, Peter, and thanks for joining us. To start off, can you tell us about the risk of administering excessive intravenous fluid therapy to a patient who has been resuscitated but is still hypotensive?
>> Like any potent medication, fluid can have side effects. In the case of fluids, the most important side effects would be edema formation and compartment syndromes, which can then result in poor organ function and ultimately influence outcome. So the concept that a positive fluid balance adversely affect outcomes is supported by observational studies showing a correlation between a positive fluid balance and mortality.
The caveat being, of course, that the sicker the patients are, the more fluid they are likely to get. Causality, however, is not established as firmly as one could expect. To my knowledge, only one study so far has investigated the impact of reducing or restricting fluid therapy and that was one of the studies published by the ARDS Network group in 2006 in New England Journal of Medicine showing that if you applied a restrictive fluid administration therapy to a patient suffering from ARDS their lung function and duration of mechanical ventilation was decreased.
[inaudible] potential adverse effects of fluids, it's very important to carefully consider if more fluids will actually improve the patient's hemodynamics. And by predicting fluid responsiveness, it's possible that we can actually avoid adverse effects and eventually improve outcome. >> Well, after you resuscitate a patient, while everyone is giving themselves high fives, it's not unusual to see that your patient remains hypotensive. So when you think about those patients, what's the probability that a patient like that is going to respond to continued fluid administration after the initial resuscitation?
>> Based on the studies that we included in our analysis, about 50% of the patients that remains hemodynamically unstable after the initial resuscitation will respond to further fluids. And by responds, I mean an increase in cardiac output by 10 to 15% after a fluid bolus. However, I think it's important to realize that the majority of studies that we included in our analysis included patients that were suffering from sepsis.
Having said that, I'm not certain that we can say that the 50% figure applies to all pathophysiological conditions. It might very well be different, for example, in trauma or other conditions. >> Well, after your resuscitation, what signs and symptoms are going to help the clinician assess whether the hemodynamic instability is actually due to hypovolemia? >> That is a tricky question.
So basically, what we want to find out is if the patient in front of us is likely to improve in hemodynamic status if we increase pre-load by administering fluid. So in essence, what we want to do at the bedside is try to establish whether our patient is on the steep or flat part of the so-called Frank-Starling curve. That is the curve that describes the relation between pre-load and cardiac output.
So the clinical examination findings that are traditionally associated with hypovolemia include, for example, prolonged capillary refill time, tachycardia, decreased tissue turgor, and decreased jugulovenous pressure. And in our search, we could only find two studies that investigated the accuracy of these clinical examination findings to predict fluid responsiveness. As it turned out, these signs and symptoms were very poor predictors of fluid responsiveness with likelihood ratios crossing one in both of these studies.
And perhaps it's not extremely surprising as these findings align very well with the 50% prevalence of fluid responsiveness in the other studies that I mentioned before. In fact, in those studies, inclusion criteria usually included symptoms like tachycardia and increased capillary refill time. So to conclude, clinical signs and symptoms at the bedside are very poor predictors of response to fluids.
>> Well, after the resuscitation, a lot of these patients are going to be mechanically ventilated. Does that make it easier or harder to assess their volume status? >> Well, I guess it depends. For the most part, it would make a prediction of fluid responsiveness easier provided, at least, that the patients are ventilated in a controlled manner and that they don't make any spontaneous breathing efforts. The reason for that is that positive pressure ventilation induced cyclic changes in the preload of the heart.
And if the patient is on the steep part of the Frank-Starling curve, those changes in preload will cause cyclic changes in stroke volume, and those changes, in turn, can be quantified by calculating either pulse pressure variation, or for example, stroke volume variation by using data obtained in an arterial line. Also, positive pressure ventilation will lead to cyclic changes in central venous pressures. And if compliance of large venous vessels is high, these changes can induce changes in dimension, so for example, the inferior vena cava, that can be measured bedtime by using ultrasound.
So what happens is that in inspiration the vena cava gets wider and in expiration, vena cava gets smaller. And these changes can be quantified by calculating what's called the distensibility index. And a high variation in dimension of the vena cava with respiration suggests a low intervascular volume and that the patient may be fluid responsive.
In fact, we found four studies evaluating this method to predict fluid response ability and it turned out that it was pretty good in predicting fluid responsiveness with positive likelihood ratios of about five and negative likelihood ratios of about 0.3. >> Well, our hospital medicine physicians are looking for all kinds of uses for bedside ultrasound. So what you've described is that a large filling and then collapse of the inferior vena cava suggests volume depletion.
Does this same technique work for evaluating hypovolemia in a spontaneously breathing patient as opposed to one who is being ventilated? >> The simple answer is we don't know yet. But it's unlikely to be as good in spontaneously ventilated patients as in positive pressure ventilated patients because in spontaneously breathing patients, inspiratory effort will influence the variability in vena cava.
We only found two studies in our search that evaluated variability in vena cava dimensions in spontaneously breathing patients and those could not demonstrate the good accuracy that we found in patients that were receiving positive pressure ventilation. >> I'm disappointed. Okay, so what special challenges do clinicians face when deciding if a patient is going to be responsive to the additional fluids that they give?
>> Well, I would say that the most challenging situation is the spontaneously breathing patient. In this situation, only one method show reasonable accuracy and that is a method called passive leg raising. Passive leg raising is based on the principle that the preload of the heart is increased by transferring blood from the lower extremities to the central compartment.
And in order to maximize the change in preload induced by the leg raising, the patient is commonly semi-recumbent at baseline, and then by tilting the bed the legs are raised to a degree of about 40 degrees and with the torso being in a flat position. And following this passive leg raise, the response in terms of cardiac output is measured by either invasive measurements or actually by a bedside ultrasound.
And an increasing cardiac output by more than 10% within the first 60 seconds of the leg raise indicates that the patient is a responder to fluids. This is actually the most versatile test and can be used both in spontaneous breathing patients and in ventilated patients. >> To actually do the test, do I lower the head of the bed or can I have someone hold both feet and raise the legs up? >> That is a good question.
In most studies that we found, what the authors actually did was that they tilted the bed. But I guess that if you raise the legs and lower the torso, that would be equally good but that is actually not studied in those studies. >> Is there anything else you'd like to tell our listeners about fluid responsiveness in unstable patients? >> I think the most important take-home message that we perhaps didn't get across in the article is that fluid responsiveness is a very dynamic feature, which is most likely going to change with changing doses of vasopressors or inotropes.
So I think it's important to realize that it has to be reassessed frequently. And also I think it's very important to realize that the decision to give fluids or not should not be based solely on whether the patient is deemed to be a responder or a potential responder or not but should be based on the clinical context. Etiology of hemodynamic instability in critically ill patients is often complex and involves other components than hypovolemia.
And fluid is perhaps not always the optimal way to improve the circulation in an unstable patient even if he or she is likely to respond favorably to fluids. For example, spontaneously breathing patients with bilateral crackles and hypotension may be better off if we start him or her on vasopressors or an inotrope than giving more fluids, which could eventually lead to respiratory failure and an intubation with all the consequences on outcome that that has.
Another take-home message is that cutoff values for each of the different predictors that we evaluated in the study differs between different studies. So one should perhaps not regard the cutoff values as absolute limits but rather an indication of whether the patients are likely to be responsive or not to fluids. Last but perhaps not least important is that if you want to use any of the methods that we described in the manuscript, you have to realize that there are caveats with each of the methods and that you have to take into account that when evaluating the accuracy of the different methods.
>> Well, Dr. Bentzer, thanks for joining me today in this discussion. More information about this topic is available in the Rational Clinical Examination and on our website, JAMAevidence, that is all one word, JAMAevidence.com, where you can listen to our entire roster of podcasts. I'm David Simel and I'll be back with you soon for another edition of JAMAevidence. [ Music ]
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