false
Catalog
Multiprofessional Critical Care Review: Adult (202 ...
11: Case Studies: Cardiovascular Monitoring (David ...
11: Case Studies: Cardiovascular Monitoring (David A. Kaufman, MD)
Back to course
[Please upgrade your browser to play this video content]
Video Transcription
Hello, welcome to the multi-professional critical care review course for adults. This is the program on case studies for cardiovascular monitoring in critical care. My name is David Kaufman. I'm a critical care physician, and I just need you to know that I have some conflicts of interest regarding this topic. I have received grant funding and travel reimbursement from the company Cheetah Medical, which is now part of the Baxter Corporation, and I've also participated on a number of levels with the company Pulsion Medical Systems. I'm a member of the Medical Advisory Board. I have received travel reimbursement, and I have received speaking honoraria. For this program, the objectives are to understand indications for IV fluid administration and shock resuscitation, to get an idea of which patients are likely to benefit from IV fluid administration, and to understand the role of cardiovascular monitoring and making treatment decisions around IV fluid resuscitation specifically. For the first case, we're going to discuss a 38-year-old man who presents to the emergency department with dizziness and lightheadedness. An hour before coming to the emergency department, he finished running a half marathon. That's 21.1 kilometers in hot and humid weather. On presentation, he's noted to have a heart rate of 144 beats per minute, a blood pressure of 78 over 47 millimeters of mercury, and the physical exam reveals hot, dry skin. His laboratory values show a serum sodium of 131 and a serum creatinine of 1.6. Would you give IV fluids to this patient? Yes, no, or not sure, I need more information. I think the correct answer here is yes, you would give IV fluid to this patient because there is a strong history that suggests that this patient has hypovolemia. If you were to give IV fluids to this patient, would you give Ringer's Lactate, 0.9% sodium chloride solution, otherwise known as normal saline, 0.45% sodium chloride solution, otherwise known as half normal saline, albumin solution, or not sure? I think the answer here would be reasonable to give either as a Ringer's Lactate or 0.9% sodium chloride. We would want to give this patient isotonic crystalloid solution. This patient already has hyponatremia, so we would not want to give a hypotonic solution such as half normal saline, and there's no strong indication to give a colloid-containing solution at this time. Do you think this patient needs additional monitoring, and if so, would you check the central venous pressure, check the pulmonary artery occlusion pressure, otherwise known as the wedge pressure, check the inferior vena cava diameter with bedside ultrasound, perform echocardiography, or none of the above? For additional monitoring, would you check the central venous pressure, check the pulmonary artery occlusion pressure or wedge pressure, check the diameter of the inferior vena cava with bedside ultrasound, perform echocardiography, or none of the above? The correct answer here is probably none of the above. This person probably is a healthy adult who does not have a high probability of having an underlying cardiac problem, and the history strongly suggests hypovolemia due to high body temperature and exposure, as well as probably a decreased intake of enough oral fluids. So you don't really need more monitoring here to guide your therapy. This is case two, and it regards a 68-year-old man with a known history of arterial hypertension, type 2 diabetes mellanus, and coronary artery disease. He had undergone percutaneous coronary intervention with a stent to the right coronary artery about three years prior to admission. And he comes in with stuttering chest pain for the last three days. He has known systolic left ventricular dysfunction with a depressed ejection fraction that you can see there. And on presentation, he has a low blood pressure, tachycardia, tachypnea, and a low oxygen saturation. You can see in these clinically pertinent images that he has an electrocardiogram that shows some ischemic ST segment depressions, principally in the lateral leads. You can see them circled there. And he also has a chest radiograph that shows pulmonary vascular congestion with increased interstitial markings and possibly some fluffy alveolar infiltrates in the central portion of the x-ray. So would you give intravenous fluid to this tachycardic hypotensive patient? Yes, no, not sure. I need more information. I think rightly, most people would choose not to give intravenous fluid to this individual. He appears to be having an acute MI with acute worsening of already compromised left ventricular systolic function and an x-ray that suggests cardiogenic pulmonary edema. And so increasing the left ventricular preload might be expected to increase the pulmonary vascular congestion and worsen his hypoxemia. If you were to give IV fluids, would you give Ringer's Lactate, 0.9% saline, 0.45% saline, an albumin-containing solution, or not sure, none of the above? Well, following the likely correct answer to the last question, most of us would give none of the above. It may be worth mentioning at this juncture, and many of you know this information, that when we choose to give isotonic crystalloids such as Ringer's Lactate or 0.9% saline, emerging evidence suggests that balanced crystalloids such as Ringer's Lactate or others such as Hartman's or Plasmolyte may be associated with better outcomes than giving 0.9% saline. For additional monitoring, would you check the central venous pressure, check the wedge pressure, check the IVC diameter with bedside ultrasound, perform echocardiography, or none of the above? I think here most people would perform an echocardiogram. It would give a lot of additional information that would help diagnostic and potentially therapeutic thinking. I don't know that there's a lot of utility to checking the central venous pressure or the inferior vena cava diameter, but some people would advocate putting in a pulmonary artery catheter and checking the wedge pressure as well as measuring cardiac output and other relevant pulmonary vascular pressures to help understand how better to care for this patient. This slide is basically a reminder, goes back to the other presentation that I have placed up here, in which we discuss shock as a failure to deliver or utilize adequate amounts of oxygen and typically in basic arithmetic we say that the oxygen consumption, VO2, is greater than the oxygen delivery, DO2, and if we remember the DO2 is equal to the product of the cardiac output times the oxygen carrying capacity of arterial blood where the oxygen carrying capacity of the arterial blood is essentially the product of the hemoglobin saturation times the hemoglobin concentration plus a very small contribution of the oxygen dissolved in plasma. Even though that's a relatively technical definition, we often clinically use low blood pressure to define shock although it has a relatively low sensitivity for diagnosing it. When we consider the various kinds of shock, we can consider that there are three ways that the heart, the pump, can be working insufficiently. One, the pump could be empty as in hypovolemia. In one, the pump could be blocked as in a pulmonary embolism or a pericardial effusion causing tamponade. The pump can be broken like with a myocardial infarction or cardiomyopathy. And finally, the pipes could be broken. That is, you could have excessive vasodilation such as occurs with sepsis, anaphylaxis, adrenal failure, and so forth. And while the pump being empty is relatively straightforward to remedy with volume resuscitation, the other kinds of shock reversal require usually a specific kind of therapy to resolve the problem. And very frequently, while we're waiting, we provide some kind of supportive care with intravenous fluids, vasopressors, inotropes, or other instruments that help the myocardium perform better. Clinically, we recognize that intravenous fluids are often the first choice of supportive therapy because they're readily available, they're inexpensive, and many practitioners see them as benign. And the main questions here are, which fluid should we choose? Will this fluid help? And when should we stop fluid? That is, how much do we give? And how do we know when we've given just enough? And we all also recognize that the administration of intravenous fluid is codified in expert guidelines such as the Surviving Sepsis Campaign Guidelines, which recommend giving 30 mls per kilogram of body weight of intravenous fluid to patients with sepsis and evidence of poor perfusion. Intravenous fluid eventually comes in two varieties. There's crystalloids, in which small molecules such as sodium chloride or other small molecules provide osmolarity and tonicity. You could give a dextrose solution, you could give a saline-based solution, which could be hypo or hypertonic, or you could give what we call balanced solutions such as Ringer's Lactate, Plasmolyte A, or Hartman solution. We also can give colloids in which larger molecules, macromolecules, provide the osmolarity and tonicity. Sometimes that large molecule is a protein, as in albumin or gelatin-containing solutions, and sometimes it's a starch such as hydroxyethyl starch or dextran. Theoretically, isotonic crystalloids, or all crystalloids, will distribute into all the extracellular fluid with only about a third of the administered volume effectively expanding the plasma volume. When the crystalloid is dextrose, because of the metabolism of dextrose and the ability of dextrose to cross the cell membrane, dextrose in water will distribute into all of the total body water, including the intracellular volume, leaving only about seven to eight percent of the volume administered available for plasma volume expansion. In contrast, at least in theory, isotonic crystalloids expand the plasma in an almost one-to-one ratio with the volume that's administered, and that effect should last at least until the macromolecule is metabolized. Because of these properties, colloids in theory enjoy an advantage over crystalloids if you believe in Starling's law, which says that the flow of water in and out of the vascular compartment is governed by the balance between plasma oncotic pressure and interstitial hydrostatic pressure. However, more recent research has begun to suggest that endothelial barrier properties, especially the intact nature of the glycocalyx layer on top of endothelial cells, is very, very important in maintaining a patent barrier between the plasma compartment and the interstitial compartment. Despite multiple studies, no advantage, no patient-centered advantage for colloids has been identified. We do know after much study that hydroxyethyl starch is very likely to be harmful, and that many of the studies associated with hydroxyethyl starch may have contained fraudulent data. We'll move along to our next case, which is somewhat more complicated than the previous cases that we've reviewed. In this case, a 51-year-old man with history of multiple myeloma presents, and he also has known amyloid infiltration of the myocardium with a resulting dilated and restrictive cardiomyopathy, and a transthoracic echocardiogram performed only one week prior to this admission showed that he had a left ventricular ejection fraction of 35%. He comes into the emergency department with dyspnea, leg swelling, but also is noted to have a pretty substantial fever. In the emergency department, he's noted to have basically a normal heart rate, but a low blood pressure, as well as some mild tachypnea, but well-preserved oxygen saturation, at least initially. He is Lurtin-oriented, but has jugular venous distension notable on the physical exam. He has an unremarkable precordial exam and also chest auscultation. He has a soft abdomen, but he's noted to have pitting edema all the way up to the thighs. When a urinary catheter is inserted, a very low volume of urine is left in the bag, and despite intravenous fluid loading, his hypotension persists. He has leukocytosis with a left shift. He has some anemia and he has a normal platelet count. He has some hyponatremia and mild hyperkalemia but no obvious metabolic acidosis. He has some renal insufficiency especially when you look at the serum creatinine which is now 3.4 compared to 0.8 just a few weeks ago. The urine is concentrated and has a small leukocyte esterase and a lot of protein as well as some ketones and bilirubin in it. He has some evidence of liver dysfunction and an elevated B-type natriuretic peptide. His condition deteriorates some and an arterial blood gas shows hypoxemia despite an increased amount of supplemental oxygen. He has a plain chest radiograph which shows a somewhat enlarged cardiac silhouette with a loss of concavity in the left atrial border and he has some plump pulmonary vessels that could represent pulmonary vascular congestion. No obvious increase in alveolar infiltrates or really increased interstitial markings and he has clear costophrenic angles. Would you give intravenous fluid to this patient? Yes. No. Not sure. I need more information. Okay. This case presents a lot of therapeutic dilemmas. He remains hypotensive with evidence of poor organ function despite initial intravenous volume loading but he also has some clinical signs that his gas exchange is deteriorating and some of that could be attributable to pulmonary edema potentially related to the initial administration of intravenous fluid and giving more intravenous fluid could make this situation worse. If you were to give intravenous fluid, would you give Ringer's Lactate, normal saline, half normal saline, albumin, or you're not sure? Well, here again, if you're going to give intravenous fluid, you're probably going to want to give isotonic crystalloid as opposed to hypotonic crystalloid for volume resuscitation. As we mentioned before, balanced solutions probably enjoy benefit compared with a high chloride containing solutions. Intriguingly, some small studies have shown that the infusion of hyper-oncotic albumin, so 20% or 25% albumin, may be associated with improvements in the blood volume as well as lowering the amount of pulmonary edema, but those findings are very, very preliminary and probably are not strong enough to drive clinical decision making. If you were to add a monitoring device to this patient who seems like he's bound for the intensive care unit, would you check the central venous pressure? Would you check the wedge pressure? Would you check the IVC diameter with bedside ultrasound? Would you perform echocardiogram? Or would you do none of the above? Like I said, this patient presents pretty important clinical dilemmas, and I think our choice of monitoring system might here be none of the above, and we'll go into that in just a moment. I included this slide in my other presentation on hemodynamic monitoring in critical illness, and it comes from a consensus of people who have been in clinical care for a number of years, a consensus statement, an expert consensus statement published a few years ago in intensive care medicine that looked at the use of less intensive hemodynamic monitoring systems in critically ill patients. And as you can see, when patients present with shock, like the patient who is under consideration, we want to do things like put in a central venous catheter, potentially measuring the central venous pressure, obviously do a clinical assessment, check the blood lactate levels, insert an arterial catheter to be sure that we're getting good blood pressure, and perform echocardiography to assess the state of the mitochorium and look for any rapidly reversible dysfunction. But then we see that either if the patient has severe ARDS or looks like he might be headed in the direction of severe ARDS, or if the patient has an insufficient response to initial therapy, that these experts recommend the use of transpulmonary thermodilution systems or a pulmonary artery catheter to assist with the care of the patient. We have been using intravenous fluids to resuscitate people with shock or cardiovascular insufficiency for almost 200 years at this point. And in the first reports of the use of intravenous fluid during a cholera epidemic in Britain, the object of giving these fluids is to place the patient in nearly his ordinary state as to the quantity of blood circulating in the vessels. Often we translate this clinical question at the bedside is, is my patient wet or dry? But I would submit to you that the question is not really is my patient wet or dry, or really is the quantity of the blood circulating in the vessels sufficient or ordinary, but rather it's actually a different question. If we recall that shock essentially is synonymous with low blood pressure, and that blood pressure is the product of the cardiac output and the systemic vascular resistance, and we recall that the goal of shock resuscitation is to improve oxygen delivery, it pays to keep in mind that what we are trying to do is improve cardiac output and therefore blood pressure or oxygen delivery with intravenous fluids by increasing the cardiac output. Because it's not increasing the systemic vascular resistance, it's not increasing the hemoglobin concentration, and it's not increasing the oxygen content of the blood. As I said, I think that the question for us at the bedside is not so much is my patient wet or dry, but rather if I give intravenous fluid, will I increase left ventricular stroke volume? And if I increase left ventricular stroke volume, do I effectively increase cardiac output? And if I increase cardiac output, do I increase oxygen delivery? And if I increase oxygen delivery, does organ function eventually improve? We can answer the first three questions here with monitoring. We do not presently have we do not presently have any means of answering the second two questions effectively. Related questions that we ask at the bedside could include, is giving fluid harmful? If I'm going to give fluid, which kind of fluid should I give? Isotonic crystalloids, colloids, blood components, and when do I stop? And it pays to keep in mind that there are possible adverse effects of fluids such as pulmonary edema, increasing inflammation, causing interstitial edema of the kidneys or intestines, elevating the intra-abdominal pressure, or disrupting the endothelial glycocalyx. Some of these questions can be answered with monitors today. Many of the monitors that we use today, and the ones that some of the ones that we discussed in our earlier presentation on hemodynamic monitoring, help us understand the Frank-Starling curve. And we see that if patients are operating on the steep part of the Frank-Starling curve, the part in green, potentially increasing ventricular preload by increasing, by giving intravenous fluid voluses, will increase the left ventricular stroke volume. However, if patients are in the flatter part of the Frank-Starling curve, up there in the tan or red portion of this figure, increasing the left ventricular preload by giving intravenous fluids is very unlikely to increase stroke volume much. Again, the questions we ask at the bedside are, will my patient improve with IV fluids? We can try to answer that question by looking at changes in cardiac preload that are induced either by positive pressure ventilation, by giving a rapid fluid bolus, or by performing a passive leg raise maneuver. Knowing whether any of these maneuvers identify patients who might improve with IV fluids requires monitoring of the stroke volume and cardiac output. Furthermore, trying to answer the question, will intravenous fluids cause harm, can possibly be answered by some of the monitors that we use. For the last 20 plus years, lots of technology has been available to perform continuous pulse contour analysis of the arterial waveform. When paired with patients who are on positive pressure mechanical ventilation, we recognize that ventilator breaths cause cyclic changes in the intrathoracic pressure, which results in cyclic changes to the preload, that is a fall or a rise in right atrial volume and pressure. These changes lead to cyclic changes in the stroke volume, which can be detected by analyzing the time pulse wave on the arterial catheter. And we can read a number of different indices. One is the stroke volume variation, and another is the pulse pressure variation. There's a lot of enthusiasm about looking at the inferior vena cava diameter to try to understand which patients might or might not be fluid responsive. The advantages of using this technique include the wide availability of the equipment in almost every emergency department, hospital, ward, or intensive care unit, and the fact that it's non-invasive. The disadvantages of this technique are that it requires some expertise. There's a lot of variability of the location of the inferior vena cava measurement and where the probe is placed accurately to assess the diameter. And that the parameters that need to be met or the criteria that need to be met for this technique to be accurate are the same and are quite limiting. And they're the same as the criteria that you need to meet for pulse pressure variation or stroke volume variation to be accurate. And we discussed those in my previous talk. Because of the complicated nature of patients like the last one we mentioned, who appears to have some combination of sepsis and cardiomyopathy driving his circulatory insufficiency, advanced monitoring with devices such as transpulmonary thermodilution can potentially be helpful in resolving therapeutic dilemmas and making good decisions at the bedside. So for example, understanding whether or not this patient is fluid responsive could help guide decision making about whether or not to administer any further intravenous fluids. Also, understanding the extravascular lung water would help understand how much edema potentially is forming, at least in the lung compartment and potentially in other compartments. And that could provide a guide for the prescription of further intravenous fluids. So giving patients who are complicated advanced monitoring with a pulmonary artery catheter that measures cardiac output and wedge pressure or transpulmonary thermodilution systems potentially give providers a lot of information that helps navigate these very, very difficult waters. Some of the important take-home points are that intravenous fluids are ubiquitous, but we must learn to treat them with the same kind of risk-benefit or harm-benefit analysis to which we ought to be subjecting all of our clinical decisions. We use IV fluid resuscitation with the sole objective of increasing cardiac stroke volume by increasing the venous return and the cardiac preload. Newer and current monitoring tools and techniques permit bedside clinicians to identify which patients are likely to show an increase in stroke volume when they receive more intravenous fluids, but also help identify patients who are not likely to show such an increase. Some of these monitors tell us when interstitial edema is accumulating, especially in the lung. Unfortunately, as we talked about in the other presentation that I made, knowing that a person is fluid responsive does not tell us whether giving IV fluid will actually benefit the patient. They do, however, give some information about when giving IV fluids may harm the patient, specifically when the extravascular lung water is rising. There are several good review articles that can help provide a good knowledge framework to understand fluid status, food responsiveness, the potential harms of intravenous fluid, and how we can think about clinical decision-making with regard to giving intravenous fluids, especially in complex conditions like sepsis. Thank you very much for your attention.
Video Summary
The video discusses case studies for cardiovascular monitoring in critical care. The first case study involves a 38-year-old man who presented to the emergency department with dizziness and lightheadedness after running a half marathon. The presenter suggests giving IV fluids to this patient due to the strong history suggesting hypovolemia. Ringer's Lactate or 0.9% sodium chloride solution would be reasonable choices for fluid administration. There is no indication for additional monitoring in this case.<br /><br />The second case study involves a 68-year-old man with a history of hypertension and coronary artery disease. He presents with chest pain and signs of cardiogenic shock. The presenter advises against giving IV fluids to this patient as it may worsen pulmonary edema. If fluids were to be given, isotonic crystalloids like Ringer's Lactate or 0.9% saline would be appropriate choices. Additional monitoring with echocardiography may be helpful in this case.<br /><br />The video also discusses the goals of IV fluid administration, different types of fluids, potential harm from fluids, and the use of monitoring devices to guide fluid therapy. The importance of considering the underlying condition and the patient's response to fluids is emphasized.
Keywords
cardiovascular monitoring
IV fluids
hypovolemia
Ringer's Lactate
0.9% sodium chloride solution
echocardiography
Society of Critical Care Medicine
500 Midway Drive
Mount Prospect,
IL 60056 USA
Phone: +1 847 827-6888
Fax: +1 847 439-7226
Email:
support@sccm.org
Contact Us
About SCCM
Newsroom
Advertising & Sponsorship
DONATE
MySCCM
LearnICU
Patients & Families
Surviving Sepsis Campaign
Critical Care Societies Collaborative
GET OUR NEWSLETTER
© Society of Critical Care Medicine. All rights reserved. |
Privacy Statement
|
Terms & Conditions
The Society of Critical Care Medicine, SCCM, and Critical Care Congress are registered trademarks of the Society of Critical Care Medicine.
×
Please select your language
1
English