Hypovolemia

Recognize it before induction. Symptoms are non-specific - weakness, fatigue, dizziness, muscle cramps, thirst. On exam look for dry mucous membranes, decreased skin turgor, orthostatic tachycardia, and hypotension. Send BUN and creatinine, serum and urine sodium, hematocrit, and a blood gas; these point at the etiology, and the etiology is what actually determines the treatment. Blood pressure is the fastest surrogate for extracellular volume and the least specific one.

Static filling pressures lie - use dynamic measures. CVP and volumetric preload parameters only approximate preload. Systolic pressure variation, pulse pressure variation, and stroke volume variation are more precise, but they are valid only in a mechanically ventilated patient - spontaneous breathing generates the stroke volume swings by a different mechanism and the numbers come out wrong. Passive leg raise works in the spontaneously breathing patient but is cumbersome to perform.

Put the probe on. POCUS of the IVC gives a volume estimate in seconds. A normal IVC collapsibility index is 20% to 50% during spontaneous respiration; above 50% indicates high collapsibility and suggests hypovolemia or fluid responsiveness, while a low index suggests overload and argues for restriction or diuresis. IVC respiratory variation has not been validated in patients without spontaneous breaths or with arrhythmias, so do not make it the only measure. LVOT diameter with velocity time integral for stroke volume variation is more accurate in the ventilated patient; SVC distensibility works as well but requires TEE.

Neuraxial anesthesia converts a deficit into hypotension. Spinal blocks sympathetic outflow and vasodilates, producing relative hypovolemia, and most patients presenting for neuraxial anesthesia are already in a preoperative fluid deficit. Common practice is 10 to 20 mL/kg of IV fluid 15 minutes before the block, but crystalloid preload redistributes to the extravascular compartment quickly, so many providers co-load instead - the volume then arrives as the vasodilation does. Post-spinal hypotension is not benign: it is associated with myocardial infarction, acute renal disease, and mortality. Higher-risk patients are the elderly and those with preoperative hypotension, emergency surgery, autonomic dysfunction, or pregnancy.

Treat the tachycardia by treating the volume. Before reaching for a beta blocker in a tachycardic patient, confirm they are euvolemic - the tachycardia often resolves with fluid alone. Blunting the compensatory rate in a patient who is volume-down, already hypotensive, or actively bleeding removes the only thing holding cardiac output up.

Fluid choice, and knowing when to stop. Crystalloid remains the standard of care for resuscitation; several meta-analyses suggest colloids may increase mortality, and CRISTAL found similar mortality between colloids and crystalloids in hypovolemic shock. Once the resuscitation target is met, stop - further fluid accumulates beyond the intravascular space and buys you pulmonary and cardiac consequences.

Children compensate, then crash. In pediatrics hypotension is a late and ominous finding; a child may hold a normal blood pressure until 35% of blood volume is lost. Tachycardia is sensitive but not specific, and its resolution helps guide therapy. Capillary refill over 2 seconds is more specific, especially alongside tachycardia. Weak pulses, mottling, cyanosis, cold skin, decreased urine output, and impaired consciousness all precede hypotension.

When it stops being a deficit. If fluid does not restore perfusion and the patient shows peripheral vasoconstriction, cyanosis, oliguria, and altered mental status, you are managing hypovolemic shock rather than a volume deficit - see the Hypovolemic Shock entry for resuscitation targets and vasopressor management.

Hypovolemia is a low extracellular fluid volume, generally from combined sodium and water loss. Total body water is roughly 50% to 60% of body weight; the extracellular compartment holds about 25% to 45% of that, divided between intravascular and interstitial space, and it is the intravascular fraction the anesthetic acts on. Causes split into renal - diuretics, osmotic diuresis, salt wasting - and extrarenal - hemorrhage, vomiting, diarrhea, third-spacing, burns, and preoperative fluid deficit.

Absolute hypovolemia is actual loss of blood or plasma from the circulation. Relative hypovolemia is loss of effective circulating volume to vasodilation and redistribution, which is precisely what a neuraxial block or an induction dose produces. Compensation holds the blood pressure until it does not, at which point the patient crosses into hypovolemic shock.