For example, a patient with severe heart failure might reach a maximal cardiac output rapidly, even with a low pulmonary capillary wedge pressure (point B). Whether the patient responds to fluid depends on interactions between the preload and cardiac function. wedge pressure, central venous pressure) cannot guide fluid resuscitation because they are static variables which don't measure fluid responsiveness. Technical problems aside, filling pressures (e.g. Thus, the wedge pressure was used as a tool to guide fluid resuscitation. Ideally, the wedge pressure should reflect the preload on the left ventricle (2). Historically, the first variable of interest after a Swan was placed was the pulmonary capillary wedge pressure. Example #1: The Swan doesn't help guide fluid management The following two examples illustrate this problem. The Swan provides only static hemodynamic measurements, which don't actually help us determine how to treat the patient. Although this contains a lot of information, it isn't the information that we need. The swan attempts to give us a snapshot of the patient's hemodynamics. Second reason we fail: The Swan's Curse The swan provides only static variables For example, in the opening case, we were sure that milrinone would increase the patient's cardiac output because this is the average response to milrinone. This gets us into trouble clinically, because it deludes us into believing that we can accurately predict the effect of a drug. The flaw of averages refers to inappropriate assumptions that the average applies to all cases. For example, Kumar 2007 found that patients who survived were more likely to experience an increased stroke volume in response to dobutamine (adjacent figure). Many other studies have also found striking heterogeneity in the responses of septic patients to dobutamine. Without seeing the individual patient data, there is a natural tendency to assume that dobutamine increases the cardiac output in all patients. For example, the average data from this same study by Enrico 2012 shows that dobutamine increases cardiac index (red box below). Unfortunately, most research on hemodynamics focuses on average patient data, ignoring this heterogeneity. In some patients dobutamine increased the cardiac output, but in many patients it had little effect: For example, Enrico 2012 published data from individual patients with septic shock treated with dobutamine (below). Seems simple, right?Ĭloser reading of the hemodynamic literature yields a more complex answer. This is also what every textbook and review article says. Let's consider a simple question: Does dobutamine increase cardiac index in septic shock? There have been about a dozen prospective RCTs investigating this, with a meta-analysis showing that dobutamine increases cardiac index ( Nadeem 2015). First reason we fail: The flaw of averages With a resurgence of the Swan, a resident recently asked me: why don't we use the Swan to guide sepsis resuscitation? Answering this question forced me to recognize that many problems with the Swan continue to haunt us today when using our new darling, bedside echocardiography. This trend may reflect increased utilization of advanced therapies in heart failure (e.g., LVADs). Use of Swan-Ganz catheterization in heart failure is increasing, despite evidence-based recommendations to the contrary ( Pandey 2016). ![]() They caused us to be wrong with confidence, the most dangerous combination in medicine (1). The echo and swan data provided the illusion that we understood his hemodynamics, but failed to predict how he would respond to milrinone. His ventricle was already working at maximal capacity, in the setting of a massive infarction. The patient's cardiac output was not milrinone responsive. With milrinone, his systemic vascular resistance decreased but his cardiac output remained unchanged, causing his blood pressure to fall. A high-dose epinephrine infusion was needed to raise his blood pressure until the milrinone wore off. However, a while after starting the milrinone the patient's blood pressure plummeted to a systolic blood pressure in the 60s. This would shift his physiology closer to normal. The patient's Swan numbers and echocardiogram suggested that he should respond well to milrinone, a drug that ought to increase his ejection fraction while simultaneously reducing his afterload. He had a Swan-Ganz catheter which showed very low cardiac output, high filling pressures, and high systemic vascular resistance. His echocardiogram showed all of the expected features of cardiogenic shock, including a severely reduced ejection fraction and dilated inferior vena cava. Although normotensive, he wasn't perfusing his kidneys. Once upon a time there was a patient with cardiogenic shock due to a myocardial infarction.
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