Assessing Fluid Intolerance with Doppler Ultrasonography: A Physiological Framework

Abstract

Ultrasonography is becoming the favored hemodynamic monitoring utensil of emergentologists, anesthesiologists and intensivists. While the roles of ultrasound grow and evolve, many clinical applications of ultrasound stem from qualitative, image-based protocols, especially for diagnosing and managing circulatory failure. Often, these algorithms imply or suggest treatment. For example, intravenous fluids are opted for or against based upon ultrasonographic signs of preload and estimation of the left ventricular ejection fraction. Though appealing, image-based algorithms skirt some foundational tenets of cardiac physiology; namely, (1) the relationship between cardiac filling and stroke volume varies considerably in the critically ill, (2) the correlation between cardiac filling and total vascular volume is poor and (3) the ejection fraction is not purely an appraisal of cardiac function but rather a measure of coupling between the ventricle and the arterial load. Therefore, management decisions could be enhanced by quantitative approaches, enabled by Doppler ultrasonography. Both fluid ‘responsiveness’ and ‘tolerance’ are evaluated by Doppler ultrasound, but the physiological relationship between these constructs is nebulous. Accordingly, it is argued that the link between them is founded upon the Frank–Starling–Sarnoff relationship and that this framework helps direct future ultrasound protocols, explains seemingly discordant findings and steers new routes of enquiry.

Wearable ultrasound and provocative hemodynamics: a view of the future

“…A recently published framework speculates how simultaneously acquired venous and arterial Doppler ultrasound could inform patient therapy and posits that Doppler ultrasound accompany all advanced critical care echocardiography to better delineate unique hemodynamic phenotypes [ 6 ]. For instance, dynamic fluid intolerance describes a hypo-perfused patient subtype with suggestive signs of low filling pressure (e.g., flat jugular vein, collapsing inferior vena cava, low central venous pressure) who is, nevertheless, found to be fluid unresponsive during a dynamic maneuver such as a PLR [ 6 ]. We envision how this phenotype could be detected using the ultrasound system described by Wang and colleagues.…”

“…Though not explicitly described by Wang and colleagues, we believe what is most exciting about these data is simultaneous, noninvasive venous and arterial ultrasound surrogates for cardiac input and output, respectively. This novel paradigm has substantial inpatient and outpatient diagnostic and therapeutic implicationsfor example, real-time inferences of the Frank-Starling mechanism [2,[4][5][6]. This is of particular interest in the ICU.…”

“…*Correspondence: jon-emile@heart-lung.org phenotypes [6]. For instance, dynamic fluid intolerance describes a hypo-perfused patient subtype with suggestive signs of low filling pressure (e.g., flat jugular vein, collapsing inferior vena cava, low central venous pressure) who is, nevertheless, found to be fluid unresponsive during a dynamic maneuver such as a PLR [6]. We envision how this phenotype could be detected using the ultrasound system described by Wang and colleagues.…”

A Wireless, Wearable Carotid Doppler Ultrasound Aids Diagnosis and Monitoring of Pericardial Tamponade: A Case Report

“…In these cases, a wearable Doppler device could guide sufficient, but not excessive, pericardial drainage. Additionally, the Doppler patch could be used to assess the hemodynamic response of intravenous fluids (9)(10)(11) and vasopressors for patients before drainage or in situations where the risk and benefits of drainage are less clear.…”

The time cost of physiologically ineffective intravenous fluids in the emergency department: an observational pilot study employing wearable Doppler ultrasound

“…At its core is the notion that intravenous (IV) fluid has an intended effect, that is, to increase stroke volume (SV) [ 4 , 5 ]. This cause-and-effect relationship between cardiac input (i.e., preload, IV fluids) and SV is described by the ‘Starling’, or ‘cardiac function’, curve [ 6 , 7 ]. Critically, during acute illness many patients flatten their cardiac function curve such that augmenting preload with IV fluid does not have the intended effect of improving SV [ 8 , 9 ].…”