Shock is the clinical manifestation of inadequate tissue perfusion secondary to
circulatory collapse. Shock can be grouped into four groups, based on etiology:
hypovolemic, cardiogenic, obstructive, and distributive. The first three groups are
characterized by low cardiac output. Distributive shock, which encompasses sepsis and
anaphylaxis, is usually a problem of the periphery, with high cardiac output and very
low systemic vascular resistance. Treatment of shock is dependent on the underlying
pathology, but end organ perfusion remains the goal of therapy. Current guidelines
recommend a combination of MAP, CVP, urine output, lactate, and central oxygen
saturation to determine effectiveness of resuscitation. We will discuss the current
guidelines, review the pathophysiological basis for each endpoint, as well as touch on
ongoing controversies within this field of study.
The primary goal of resuscitation in shock should be restore adequate tissue
perfusion, and therefore, cellular metabolism (1). Although the mechanisms behind
shock are varied, initially resuscitation is problem based. Therefore, a patient with
severe pneumonia and one with tamponade both face issues with tissue hypoperfusion,
but with very different etiologies. Identification of tissue hypoperfusion is very
important, as is monitoring effectiveness of therapies. The landmark study by E. Rivers
in 2001 introduced us to early goal directed therapy, and the resuscitation end points
utilized. His team included mean arterial pressure (MAP), central venous pressure
(CVP), central venous saturation (ScvO2), urine output, and oxygen saturation as the
endpoints of resuscitation (2). These endpoints were chosen due to evidence
supporting their role in monitoring global and molecular oxygenation, although there
are benefits and caveats for each one.
The use of these endpoints has been widely accepted by critical care (3), and has
been studied as a prognostic marker as well as an endpoint (4). Although there has been
improvement in outcomes in patients with severe sepsis, circulatory shock continues to
have a high mortality. Septic shock is characterized by a derangement of
microcirculation, something not necessarily seen in other forms of shock. Ongoing
research is centered on evaluation of these endpoints, and the relationship of oxygen
consumption, delivery, and tissue perfusion. For example, lactate has long been used as
a marker for tissue perfusion, but concerns regarding clearance in the face of renal and
hepatic dysfunction, as well as epinephrine induced elevations, have led many to
question its utility as an endpoint (4, 5). Furthermore, there is ongoing debate whether
we are targeting the correct thing; whether pressure is equivalent to flow, or if lactate is
truly a measure of metabolism, or if lactic acidemia is merely an epi-phenomenon (5, 6).
1. Vincent, Jean-Louis, DeBacker, Daniel. Circulatory Shock. NEJM 2013; 369
(28): 1726-1734.
2. Rivers E et al. Early goal directed therapy in the treatment of severe sepsis and
septic shock. NEJM 2001; 345 (19): 1368-1377.
3. Dellinger, R et al. Surviving Sepsis Campaign: International Guidelines for
Management of Severe Sepsis and Septic Shock: 2012. Crit Care Med 2013; 41
(2): 580-637.
4. Jansen, Tim C et al. Early lactate-guided therapy in intensive care unit patients.
Am J Resp Crit Care Med 2010; 182: 752-761.
5. Bakker, Jan et al. Clinical use of lactate monitoring in critically ill patients.
Annals of Intensive Care 2013; 3:12.
6. Dunser, Martin W et al. Re-thinking resuscitation: leaving blood pressure
cosmetics behind and moving forward to permissive hypotension and a tissue
perfusion-based approach. Crit Care 2013; 17:326.