The resuscitation of a patient in shock is a highly complex endeavor that should go beyond normalizing mean arterial pressure and protocolized fluid loading. We propose a holistic, four-interface conceptual model of shock that we believe can benefit both clinicians at the bedside and researchers. The four circulatory interfaces whose uncoupling results in shock are as follows: the left ventricle to arterial, the arterial to capillary, the capillary to venular, and finally the right ventricle to pulmonary artery. We review the pathophysiology and clinical consequences behind the uncoupling of these interfaces, as well as how to assess them, and propose a strategy for approaching a patient in shock. Bedside assessment of shock may include these critical interfaces in order to avoid hemodynamic incoherence and to focus on microcirculatory restoration rather than simply mean arterial pressure. The purpose of this model is to serve as a mental model for learners as well as a framework for further resuscitation research that incorporates these concepts.

The use of lactate as a marker of the severity of circulatory shock was popularized by Dr. Weil in the 1970’s. Dr. Weil promoted the idea that blood lactate concentration increased in circulatory shock due to anaerobic metabolism following decreased oxygen delivery. This concept becomes entrenched with 1992 ACCP/SCCM consensus conference definition of sepsis. Since then, the central role of lactate in the definition and management of septic shock has only been expanded and become more ingrained. This review will discuss the wisdom of such an approach, an updated model describing the origins of hyperlactatemia in sepsis, and how such improvements in our knowledge of the underlying physiology should change our approach to resuscitation in patients presenting with septic shock.

The resuscitation of the patient in shock is a highly complex endeavor which should go beyond normalizing mean arterial pressure and protocolized fluid loading. We propose a holistic, four interface conceptual model of shock which we feel can benefit both clinicians at the bedside and researchers. The four circulatory interfaces whose uncoupling result in shock are the left ventricle to arterial, the arterial to capillary, the capillary to venular and finally the right ventricle to pulmonary artery. We review the pathophysiology and clinical consequences behind the uncoupling of these interfaces as well as how to assess them and propose a strategy on how to approach the patient in shock. Bedside assessment of shock may include these critical interfaces in order to avoid hemodynamic incoherence and focus on microcirculatory restoration rather than simply mean arterial pressure. Further research may incorporate these concepts.