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increased base deficit or blood lactate level, may also signal diminished organ
perfusion early in shock.
As shock continues, early compensatory mechanisms fail to maintain cardiac
output and SVR and blood pressure falls. Shock with hypotension is referred to as
uncompensated shock. In addition to hypotension, clinical signs include
worsening tachycardia (or bradycardia in infants) and tachypnea, mottled skin,
cold extremities, and markedly delayed capillary refill (>4 seconds). Tachypnea
and respiratory distress may herald underlying pulmonary disease, but may also
reflect an increase in minute ventilation (to decrease PaCO2 ) to compensate for
an increasing metabolic acidosis. Signs of organ dysfunction are typically
evident, including further alterations in mental status (agitation, confusion,
lethargy,
stupor),
gastrointestinal
ileus,
azotemia,
coagulopathy,
thrombocytopenia, and hyperbilirubinemia.
All types of shock encompass some degree of absolute or functional
hypovolemia. Absolute hypovolemia exists in cases of dehydration from fluid
losses (e.g., diarrhea, severe emesis, hyperthermia), hemorrhage, and “third
spacing” of fluid due to increased vascular permeability, as in sepsis or burn
injuries. Functional hypovolemia exists when vascular capacity increases, as in
septic shock, spinal cord injury, anaphylaxis, or certain medication effects. In
addition to volume loss, microcirculatory dysfunction is characterized by a
maldistribution of capillary blood flow and is common to all types of shock. Even
with reestablishment of global circulation, the activation of inflammatory
cytokines in response to pathogen-associated molecular patterns (PAMPs) from
invading microorganisms in sepsis and danger-associated molecular patterns
(DAMPs) from cell injury in trauma, as well as endothelial cell activation and
microthrombi formation, leads to regional changes in blood flow within and

across organ systems. This contributes to local tissue ischemia that fuels a vicious
cycle of tissue injury and inflammation that can result in the multiorgan
dysfunction syndrome (MODS). Furthermore, a second wave of reperfusion
injury may occur due to an increase in oxidant and nitrogenous stress even after
the primary insult of decreased tissue perfusion in shock is corrected.