OACCM Advisor's Blog - May 2011, Dr. McGee on Hemodynamics - William T. McGee, M.D., M.H.A.
I will begin this blog on topics of interest to critical care practitioners. The primary focus will be to put my spin on some of the newer data that appears on the OACCM website along with take-home messages that I derive from reading the medical literature on those topics that I consider important to the practice of critical care medicine at the bedside. Hopefully I will develop a competence for doing this; I would like to include other related issues that are of interest to doctors, especially critical care physicians particularly relevant to the environment of practicing medicine in the United States.
I will begin with a topic that I am familiar with, that is important, and in my experience is being used with widely varying enthusiasm across intensive care units and operating rooms throughout the United States. This is the use of dynamic parameters of volume responsiveness in the care of the critically ill. I will focus on my paper, A Simple Physiologic Algorithm for Managing Hemodynamics Using Stroke Volume and Stroke Volume Variation: Physiologic Optimization Program (Journal of Intensive Care Medicine 2009; Vol 24, No. 6., pp. 352-360.). Dr. Michael Pinsky’s book, “Functional Hemodynamic Monitoring” (Springer-Verlag Berlin Heidelberg NY 2005, ISBN 3-540-22349-5) highlights the inconsistent uptake of these concepts amongst intensive care units. This book published in 2005 representing a broad survey of literature and clinical understanding of dynamic measures of volume responsiveness remains unfamiliar to many, and is not practiced with any degree of consistency throughout the United States. Interestingly, these concepts seem to have been more readily adopted and implemented outside than within the United States.
The way we are training our house staff and fellows to use these data is relatively simple. About two-thirds of the patients in our ICU have an arterial line. Therefore, analysis of the arterial waveform is available from the majority of patients and especially those with hemodynamic instability. We use the FloTrac/Vigileo system; the LIDCO and PICCO systems are also available to analyze the arterial waveform and provide data that facilitates management of hemodynamically unstable patients and additionally those patients with oliguria or volume overload.
A clinical question is required before embarking on interpretation of physiologic data specifically the stroke volume and stroke volume variation to aid patient management. If the patient is clinically well, my opinion is to leave them alone. On the other hand, when clinical questions are asked about hypotension or oliguria obtaining physiologic data that assesses blood flow, cardiac performance and volume responsiveness facilitates management. These data allow precise positioning of the patients on their own Starling Curve. We can thus answer the question; are they volume responsive on the steep part of the Frank Starling Curve or are they residing on the flat volume independent portion of the Frank Starling Curve. Knowing these data along with overall cardiac performance; i.e. stroke volume and cardiac output, quickly allows physiologic based management of patients in shock and those with oliguria. If cardiac performance is judged to be inadequate, and this is a clinical determination considering all our other knowledge of our patients, the common resuscitation paradigm would mandate getting the most benefit from preload augmentation prior to or simultaneous with attempts to improve cardiac performance through pharmacological or other means. Similarly for those patients who we can predict will not respond to volume, additional volume may be harmful and at a minimum would delay appropriate therapy.
To present a clinical example of how we might utilize this for a patient in the intensive care unit who has hypotension would be as follows: we look at the data pair, stroke volume variation and stroke volume, and for purposes of this example stroke volume variation is elevated >13% and the stroke volume is low, we simply assess that this patient will respond to a fluid challenge. We use a bolus of normal saline one liter at a time and assess the change primarily in cardiac performance using stroke volume as the outcome parameter of interest but also are mindful of changes in stroke volume variation. These boluses can be repeated until we are satisfied with the cardiac performance and/or stroke volume variation has come down to < 13%. The relationship between stroke volume variation and volume responsiveness is more appropriately defined as linear so that there may be smaller improvements in cardiac performance starting from a lower threshold value of stroke volume variation let’s say 10%. However, as the variability goes up the improvement in performance is expected to be greater and in the literature most authors consider a change in cardiac output of greater than 12 – 15% to be clinically meaningful. I emphasize this because I do not want 13% to be taken as an absolute, but it will, however, provide good discrimination between those who will respond with a meaningful increase in cardiac output to a volume challenge versus those who will not.
Once an acceptable level of cardiac performance has been achieved or volume responsiveness no longer exists, and as you begin to use these technologies you may need to prove this to yourself several times, i.e. you can always give more volume and then assess the impact on stroke volume and cardiac output independent of what the SVV is but at some point hopefully one would recognize when volume challenge stops producing a meaningful change in cardiac performance, and at that point, if cardiac performance required augmentation, other methodologies (pharmacotherapy) are implemented. I see this as a huge advance over common practice that continues even in my intensive care unit because we either do not avail ourselves of this technology on all of the patients who might benefit from it or we may not be paying attention to it even when in place and simply return to our old habits. Using vital signs and urine output provides a similar opportunity available to the practitioner for at least the past at least 100 years and has repeatedly been shown to have poor predictability for the assessment of a meaningful change in cardiac performance relative to volume challenge.
I think I will stop here with my first attempt at this and may proceed further down the path of how I use these data in the next section to talk about the management of oliguria. Hypotension and oliguria remain clinically relevant questions that we face daily in the ICU.
June , 2011 Blog # 2 - Dr. McGee on Hemodynamics
September , 2011 Blog # 3 - Dr. McGee on Hemodynamics
January, 2012 - Blog # 4 - Dr. McGee on Hemodynamics
September, 2012 - Blog # 5 - Dr. McGee on Hemodynamics
William T. McGee, M.D., MHA, FCCP is Associate Professor of Medicine and Surgery at Tufts University School of Medicine, Boston, Massachusetts. His interests are in ARDS, vascular access (pulmonary artery catheterization), sepsis, nutrition, and nosocomial pneumonia. He has published > 67 papers, chapters and abstracts. He is the principal investigator for clinical trials studying the efficacy and safety of rfPAF-AH for the prevention of ARDS in patients with severe sepsis. He is a three-time recipient of Excellence in Teaching Award from Tufts University School of Medicine, the Society of Critical Care Medicine Internal Medicine Specialty Award for “Influence of Insurance Status on Pulmonary Artery Catheter Use” and The Presidential Citation Award from the Society of Critical Care Medicine for outstanding contribution to the Society. He is a Director for the Fundamentals of Critical Care Support Course for the Society of Critical Care Medicine. Dr. McGee is also a reviewer for several critical care journals.