Robert Glatter, MD; David A. Farcy, MD

Disclosures

April 18, 2014

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Robert Glatter, MD: Hi. I am Dr. Robert Glatter, editorial board member of Medscape Emergency Medicine, and I want to welcome everyone to the 2014 American Academy of Emergency Medicine Scientific Assembly.

With me is Dr. David Farcy, Chairman of Emergency Medicine at Mount Sinai Medical Center in Miami Beach, Florida, and Director of the Surgical Intensive Care Unit at Mount Sinai. Today we will be discussing whether CVP (central venous pressure) is useless and whether other markers of dynamic resuscitation would be more useful. Welcome.

David Farcy, MD: Thank you very much for having me. It is a pleasure to spend some time with you.

Dr. Glatter: Thank you very much.

Dr. Farcy: CVP as a marker for resuscitation has been used for about the past 20 years. CVP really has come to light with Manny Rivers' paper[1] on early goal-directed therapy that used a CVP level from 8 to 12 mm Hg as a marker to guide resuscitation in septic patients. Recently, CVP has come under a lot of scrutiny, especially from Dr. Paul Marik's group, which has completed 2 meta-analyses, the latest in 2013,[2] and found that CVP is useless. It does not gauge the fluid responsiveness, especially when the CVP is low, high, or medium. They show that CVP has been a static form of resuscitation.

Dr. Glatter: CVP is something we have been using for a long time and have considered to be tried-and-true. Are you saying that this article's finding is something that should change our practice, possibly?

Dr. Farcy: Yes. I would definitely change my practice. I would not put in a central line just to measure CVP. If my patient is hypotensive, in need of a vasopressor, then yes -- I will use a central line and maybe I will use one of the CVP ports to get a measurement, but I will also want a dynamic method of finding my patient's fluid responsiveness.

Dr. Glatter: What is the best way to do that?

Dr. Farcy: There are several dynamic methods. Dr. Paul Marik talks a lot about the passive leg raise, which requires a special monitor, the Edwards Lifesciences monitor; it is essentially an arterial line with a CVP line that takes the pulse pressure under the arterial line and calculates cardiac output and the cardiac index. Then you elevate the patient's legs and remeasure the cardiac output and cardiac index, and this basically tells you whether the person is fluid depleted or not.

That is one method. It uses an expensive monitor that not every emergency department has. I believe the easier way is to use ultrasound and calculate the IVC (inferior vena cava) diameters, and calculate the collapse and the difference in the IVC diameter during inspiration and expiration.

Dr. Glatter: How sensitive is that?

Dr. Farcy: Great question. Unfortunately, we have very little data on this. Two papers have addressed this. The paper in favor of this method was in the Journal of Trauma-Injury Infection & Critical Care,[3] I believe, which found it to be significantly sensitive -- 96% to 98%. Unfortunately, this included a very small patient population. Newer articles are saying that this is not as sensitive as one thought because of the position of the IVC and the angle at which we are using the IVC.

Personally, when I am in the emergency department or the ICU and see that my patient's IVC is collapsing, then I know that the patient requires fluid. If my IVC is not completely collapsing or it is staying at 100%, then the patient is probably fluid overloaded and does not need fluid. We know that fluid therapy recently has come under a lot of scrutiny, especially under the ARDSNet trial,[4] which looked at fluid in patients with acute respiratory distress syndrome (ARDS), and we know that lower fluid is better for patients with ARDS.

Dr. Glatter: Would you say that, in 2014, using ultrasound is the best way to estimate someone's right atrial pressure, or CVP, for that matter?

Dr. Farcy: Yes. As of right now, I would say yes, until a new trial comes out with something else. Critical care is a very fast-changing field, and until a new trial shows us new data, ultrasound is what I am using right now. I am in the ICU, and for my patient who is on vasopressors, I am using the CVP and correlating these CVP measurements with ultrasound. I am noticing that my CVP may be all over the place. I had a patient with a CVP of 18% on low positive end-expiratory pressure levels and my IVC was completely collapsed. I was guiding my therapy based on these measurements, only to find out that the transducer was in the wrong place. Once we recalibrated the CVP we had a better number, but now I am using ultrasound to guide my fluid therapy.

Dr. Glatter: Could you address the controversy around using mixed venous oxygen saturation (SvO2) along with arterial or venous lactate? Is one method better than another? Do you have any preference when you are resuscitating patients?

Dr. Farcy: I have an unpopular approach. I use both. SvO2 is a great marker in early goal-directed therapy, as Dr. Manny Rivers showed us; he was able to reduce mortality in patients with severe sepsis and septic shock by 21% in 28 days. That study came under a lot of scrutiny; everyone was criticizing it. As of right now, I do not use the monitor. I send an SvO2 from the distal port of the triple lumen. I send a venous blood gas every hour, to look at the O2 saturation.

The question that the Jones group[5] brought to us was, can we use lactate instead of SvO2? I have an issue with this because, as you know, 20% to 25% (I'll be generous) of septic patients do not have elevated lactate levels.

Dr. Glatter: What is the reason behind that?

Dr. Farcy: They may not be producing lactates. Is it a liver insufficiency? Is it poor flow state? I do not think we have the answer to that, but significant data show that 20% to 25% of patients with severe sepsis and septic shock do not have elevated lactate levels. Lactate by itself has a lot of issues. A patient with liver function abnormalities, poor perfusion, who does not metabolize the lactate will have elevated levels, for example.

I do a lot of jujitsu. After 45 minutes of jujitsu competition my lactate level is 4.0. What does that mean? The Jones group utilized a lactate clearance by 10%. I prefer the term "lactate normalization" rather than "clearance." If your lactate is 8.0 and you clear it by 10%, we are talking 0.8 less; so 7.2, for me, is still a very alarming number. I favor normalizing the numbers all the way down to less than 4.0.

I use this in conjunction with other numbers: my patient's SvO2, blood pressure, and general status.

Dr. Glatter: What is your timeframe for normalization of lactate? Is that typically 2 hours or is it 1 hour, 4 hours?

Dr. Farcy: According to the Surviving Sepsis campaign,[6] we should try to achieve normalization within the first 6 hours. Again, I mentioned that giving fluid is not safe -- that is, it is safe in a small quantity, when you do not want to "re-sink the Titanic." Chasing a number because a patient's lactate level is 6.0 and you are giving 6 liters of fluid is alarming. You must begin to wonder, "Am I on the right path or am I going down the wrong path?"

Dr. Glatter: Would you say that the venous lactate level correlates well with arterial lactate level?

Dr. Farcy: Absolutely. All of the studies have shown that there is no difference between venous lactate and arterial lactate. Actually, at my center in Miami Beach, we place IOs (intraosseous catheters) for all patients in cardiac arrest because we find that it takes a significantly short time to place an IO. We even send blood for lactate levels from the IO, and the numbers remain the same between venous and arterial; there is really no significant difference.

Dr. Glatter: Thank you very much for taking the time out from the meeting.

Dr. Farcy: Thank you very much. It has been an honor.

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