Key result
The Trendelenburg position produces only small, transient increases in cardiac output (mean 8%) and blood pressure (mean 9 mm Hg), and may cause harmful cardiopulmonary and neurological effects.
Why the study?
Does use of the Trendelenburg position (head-down or passive leg raising) cause clinically significant increases in blood pressure and CO/CI in hypotensive patients?
Does use of the Trendelenburg position (head-down or passive leg raising) cause clinically significant increases in blood pressure and CO/CI in hypotensive patients?
The Trendelenburg position does not produce sustained, clinically significant improvements in blood pressure or cardiac output in hypotensive patients and may cause harmful cardiopulmonary and neurological effects.
Does not support routine Trendelenburg use for hypotension; leaves open targeted trials on alternatives or subgroups.
In the mid-19th century, Friedrich Trendelenburg—pioneering German surgeon (1844–1924)—popularized the technique known in the Middle Ages as the “head-down position.” In his surgical text of 1873, Trendelenburg recognized that raising a patient’s hips caused the bulk of abdominal viscera to slide toward the diaphragm, providing a less cluttered operative field for lower abdominal and pelvic procedures. Later in the early-20th century, American physiologist Walter Cannon promoted the Trendelenburg position to displace blood from the lower extremities to enhance venous return in the treatment of hemorrhagic shock. This action was thought to cause an “autotransfusion” to the central circulation, increasing right and left ventricular preloads, stroke volume, and cardiac output (CO)/cardiac index (CI).1–3Despite surgeons questioning the position’s effectiveness in the 1950s because of adverse consequences,4 use of the Trendelenburg position continued as a mainstay of resuscitation.3 Although current Advanced Cardiac Life Support and first aid guidelines from the American Red Cross (ARC)/American Heart Association (AHA) state that patients with evidence of shock should be positioned supine,5,6 use of the Trendelenburg position may remain a ritualistic practice in response to hypotension. Thus, the following question was prompted: Does use of the Trendelenburg position (head-down or passive leg raising) cause clinically significant increases in blood pressure and CO/CI in hypotensive patients?The strategy included searching MEDLINE, CINAHL, and the Cochrane database. Key words included Trendelenburg, head-down, passive leg raising, hypotension, cardiac output, and hemodynamics. The search was not limited by date in order to present scientific evidence about this practice over time.The hemodynamic effects of the Trendelenburg position were tested in more than 20 studies. Although the effects on blood pressure and CO/CI are the main focus of this review, changes in other variables were evaluated: heart rate, blood pressure, systemic vascular resistance, filling pressures, ventricular index, blood volume, blood flow dynamics, and oxygenation/gas exchange. Most studies used observational methods, enrolling small heterogeneous samples ranging from animals or healthy volunteers to postoperative and other acute/critical care patients. The Trendelenburg position (10º–30º) and the modified Trendelenburg position with passive leg raising (45º–60º) were studied, with duration of position change ranging from 1 to 30 minutes.Table 1 outlines the predominant effect of Trendelenburg positioning on hemodynamic and physiological variables across studies, as well as less common changes that were also statistically significant.7–31 First, CO/CI increased significantly in healthy populations,12,15,23 although the effects were transient, lasting 1 to 3 minutes. Of the 13 studies of acutely ill patients, almost half showed significant increases in CO/CI with a mean change of 8%, but these effects were largely transient, lasting 3 to 5 minutes.14,17,18,25,30,31 In 1 study,17 significant increases remained at 30 minutes but CO/CI changes were only 6% to 9%. Although CO/CI increased, the predominant effect of use of the Trendelenburg position on blood pressure was no change. In the few studies17,18,20,30,31 in which increased blood pressure was observed, the mean change was only 9 mm Hg.Normal physiology provides evidence that changes in body position cause shifts in blood volume that affect preload. However, Bivins et al13 reported that only a small amount of total blood volume (1.8%) is displaced centrally with Trendelenburg positioning. In the face of hypovolemia, preload changes are limited because venous capacitance vessels are rapidly depleted and have little blood volume to add to the central circulation. Thus, the autotransfusion effect associated with use of the Trendelenburg position is small and unlikely to have clinical significance. Additionally, when blood pressure is low and patients are tilted, abdominal contents shift35 and compress the vena cava, putting pressure on and fooling baroreceptors that blood pressure is back to normal. As a result, the normal baroreceptor response to low blood pressure—heightened sympathetic and reduced parasympathetic activity to increase systemic vascular resistance and blood pressure—is halted and instead, vasodilatation ensues, further aggravating the hypotensive problem.Additional studies reveal potential harmful effects associated with use of the Trendelenburg position (Table 1), such as reduced blood flow and oxygenation. Although most of this evidence is from 1 observational study or studies with small samples, it needs to be considered clinically. In a review of physiological changes, Martin3 outlined the sequence of symptoms that typically occur after a patient is tilted into the Trendelenburg position (see Figure). The Trendelenburg position is poorly tolerated by conscious patients, whereas hypotensive and mentally obtunded patients may first become transiently more alert and then subsequently lose the will to struggle. Disease conditions set patients up for more deleterious effects. Patients with coronary artery disease are at risk for increased myocardial oxygen consumption that provokes dysrhythmias, whereas patients with lower limb ischemia may experience more reduction in perfusion as segmental blood flow gradually decreases the longer the position is maintained.15 Respiratory expansion and vital capacity also decrease, especially in obese patients, promoting hypoventilation or atelectasis and altered ventilation-perfusion ratios as blood gravitates to poorly ventilated apices. Patients with neurological impairment face other unfavorable effects, including increased intraocular/intracranial pressure and cerebral edema from increased venous congestion inside and outside the cranium.32 It is conceivable that the steeper the tilt—as well as the longer it is maintained—the more pronounced the physiological impact will be.Most of the evidence for this intervention is grade B evidence (Table 2), indicating that use of the Trendelenburg position does not lead to beneficial changes in blood pressure or CO/CI. As a result, this position is probably not useful in rescue efforts. The associated hemodynamic effects are small and unsustained and thus are unlikely to have a clinically significant impact on hypotensive patients. Furthermore, because use of the Trendelenburg position may be associated with harmful cardiopulmonary, neurological, and vascular effects, especially in the presence of disease, the position should be used with caution even when immediate/transient benefits are desired. Instead, clinicians should position patients flat and seek or initiate available orders for additional interventions such as fluid boluses, pharmacological therapies, or other devices targeted to the cause of the hypotension.Although the results are dated, Ostrow34 conducted a survey of nearly 500 critical care nurses about use of the Trendelenburg position. Most of the responding nurses reported that use of the Trendelenburg position was an immediate and independent intervention routinely used to treat hypotension/shock almost half of the time. Despite the limited hemodynamic effects and adverse consequences associated with use of the Trendelenburg position, anecdotal evidence suggests that clinicians still use this position today. Thus, use of the Trendelenburg position is an example of an intervention that is based on tradition rather than scientific evidence.32,35,36 Perhaps tilting the patient gives clinicians satisfaction that they have initiated some intervention until they can start other therapies such as administration of fluid boluses or inotropic agents. Or the explanation could be that because these interventions are often initiated almost simultaneously, clinicians attribute a blood pressure response to the effects of using the Trendelenburg position and not to the other therapies. Furthermore, current ARC/AHA first aid guidelines6 state that because the evidence is mixed, passive raising of the legs 6 to 12 inches (30º–45º) may be helpful for patients with no signs of trauma or injury as long as the position does not cause pain or discomfort. The presence of such guidelines in the prehospital setting may add to the confusion among clinicians in the acute care setting about continued use of the Trendelenburg position.Challenge practice in your unit with a small test of change: Repeat Ostrow’s survey with your colleagues to determine if implementation science has been effective in changing their initial response to hypotensive episodes. If reliance on the intervention remains, use the evidence to teach your colleagues about the limited therapeutic and potentially harmful effects of using the Trendelenburg position. Only with continued commitment and discipline to access and integrate the best available evidence at the bedside can we move our practice beyond the confines of our initial nursing education, professional experience, and unit rituals or traditions to evidence-based practice.
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Margo A. Halm (2012) conducted a review in Hypotension. Trendelenburg position was evaluated on Blood pressure and cardiac output/cardiac index (CO/CI). The Trendelenburg position produces only small, transient increases in cardiac output (mean 8%) and blood pressure (mean 9 mm Hg), and may cause harmful cardiopulmonary and neurological effects.
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