Re-thinking resuscitation goals: an alternative point of view!

Abstract

We respectfully disagree with several key assertions made by Dunser and colleagues [1] in this issue of Critical Care and consider their approach to resuscitation to be potentially harmful. Septic shock is not primarily a volume-depleted state, and attempts to treat vasoplegic shock with fl uids alone will compound the macro- and micro-circulatory abnormalities of sepsis. A vasopressor with both α1 and β1 adrenergic activity (norepinephrine) will increase arterial tone, preload, and cardiac contractility [2]. Early administration of norepinephrine is associated with improved hemodynamics and reduced mortality in patients with sepsis [2,3]. Permissive hypotension is an untested and potentially dangerous concept. When the mean arterial pressure (MAP) falls below an organ’s autoregulatory threshold, organ blood fl ow decreases in an almost linear fashion [4]. Because the autoregulatory ranges of the heart, brain, and kidney are above 45 mm Hg [4], such a blood pressure will, as one would expect, predictably decrease organ blood fl ow. Lehman and colleagues [5] have convincingly demonstrated that the risk of kidney injury and death increases sharply with an MAP of below 60 mm Hg. Th e notion that sepsis is associated with tissue hypoxia is unproven and, as Hotchkiss and Karl [6] argued over 20 years ago, is likely to be incorrect. Attempts to titrate therapy to a nonexistent oxygen debt on the basis of an elevated lactate concentration are doomed to fail. Similarly, the use of central venous oxygen saturation to guide the resus ci tation of patients with sepsis is problematic. Although urine output may be a valuable marker of renal perfusion in hypovolemic states, this clinical sign becomes un reliable in sepsis-associated acute kidney injury, in which experimental models show that oliguria occurs in the presence of marked global renal hyperemia [7]. In summary, we consider that the fi rst step in the resus citation of patients with septic shock is to achieve an MAP of at least 60 to 65 mm Hg with the use of vasoactive agents (norepinephrine) and small volumes of balanced fl uid. A simultaneous goal would be to ensure adequate fl ow (cardiac output) as determined by echocardiography and minimally invasive cardiac output monitoring and supported by an integrated assessment that includes monitoring the patient’s clinical response to therapy.