 Hypervolemic shock results from fluid loss. Now there are two main causes for hypervolemic shock, hemorrhage and plasma depletion. Now the latter occurs because of extravascular fluid sequestration or gastrointestinal or urinary fluid losses. Extravascular fluid sequestration may be difficult to recognize and it follows infection and inflammation from diseases such as pancreatitis from trauma or surgery. This leads to increased capillary permeability and loss of intravascular fluid to the interstitium. Physiological changes take place to compensate for hypervolemia irrespective of the type of hypervolemia. This is done in order to protect cerebral and coronary blood flow. These changes are driven by sympathetic activity, the release of stress hormones, the resorption of interstitial fluid, mobilization of intracellular fluid and renal fluid conservation. Hemorrhage as an example of hypervolemic shock is easier to quantify than plasma losses. So we talk about class 1 hemorrhage which occurs when 10 to 15 percent of the total blood volume is lost in a 70 kilogram human being. This equates to about 500 to 750 milliliters. This is usually well tolerated especially in the supine position and mild tachycardia may be the only finding. In class 2 hemorrhage we have a 15 to 30 percent loss that equates to about 750 to one and a half liters that's 750 milliliters to one and a half liters. These patients present with anxiety, tachycardia and a drop in their pulse pressure. Now the central perfusion is maintained through peripheral vasoconstriction which leaves the peripheries cold and pale with diminished capillary refill. A mild oliguria develops from elevated levels of vasopressin, aldosterone and adrenergic mediated renal arteriola constriction. Now class 1 and class 2 shock are termed compensated forms of shock. It is important to recognize and manage these classes before decompensation sets in. Now class 3 hemorrhage represents a 30 to 40 percent loss that's about 1500 to 2000 mills one and a half to two liters. These patients have a pronounced tachycardia they have tachypnea at a pressed mental state and they become hypotensive. Class 4 hemorrhage represents a total loss in excess of 40 percent that's more than two liters. Severe hypertension is noted and the mental state deteriorates through restlessness, agitation and obtundation. Finally a loss of consciousness sets in as the cerebral perfusion becomes totally inadequate. If the hypervelemic state is not recognized and managed, decompensation leads to cellular damage with the release of inflammatory mediators that may set up a self-propagating cascade leading to multi-organ dysfunction. Now while external hemorrhage is easy to recognize, internal bleeding and plasma losses may remain hidden. There's a few points I want you to note. Never rely solely on supine vital signs. Patients with early stages that's compensated hemorrhage develop dizziness when sitting upright and their heart rates might increase. Remember also that capillary refill time has a very low sensitivity. Don't rely on it. Hematocrit and hemoglobin levels are maintained early on hemorrhage and only start to drop when fluid shifts into the vascular space by means of compensation or when crystalloids are administered. Lastly plasma losses difficult to diagnose may lead to hemoconcentration.