PATIENTS who are in shock associated with infection continue to present difficult therapeutic problems. In addition to the multiple effects of bacterial toxins, patients in septic shock have invariably had associated problems which affect the hemodynamic and metabolic responses to shock, including hypovolemia from dehydration or hemorrhage, and diseases of the heart, lungs, kidneys, liver, or other organ systems.1
Clinical sepsis is often associated with extensive inflammation, which may impose hemodynamic burdens which the circulation is unable to support.2 Patients in septic shock are commonly found to have hypotension associated with a normal or high cardiac output, ie, "low-resistance," or "hyperdynamic" septic shock.3-6
Inadequate perfusion of tissues in these patients may result in part, at least, from arteriovenous shunting of blood in areas of inflammation,2,3,5,7 either through greatly dilated capillary beds or through arteriovenous communications, thereby creating a form of "high output cardiac failure."
The controversy