Hypovolemic Shock

Catch it before the pressure falls - Narrowing pulse pressure with a rising diastolic, tachycardia, tachypnea, and cool mottled extremities with delayed capillary refill all precede the systolic drop. By the time systolic pressure falls, 25% to 30% of the blood volume is already gone.

Separate it from the other shock states first - Hypovolemic shock runs a low CVP with a high systemic vascular resistance; cardiogenic and obstructive shock (tamponade, tension pneumothorax) run a high CVP. In trauma, use FAST — specificity is above 99% for free fluid, though a negative scan does not rule out intra-abdominal injury.

Pick a fluid-responsiveness test that actually works - CVP and pulse pressure variation are only valid without spontaneous breaths or arrhythmias, and both degrade with right heart failure, poor lung or chest wall compliance, and high respiratory rates. Passive leg raise with echo assessment of contractility is the most accurate bedside measure.

Access before induction - Two large-bore peripheral IVs or a central line, in place before you take away the sympathetic tone holding the pressure up.

Induction removes the compensation - Everything keeping this patient normotensive is sympathetic outflow and peripheral vasoconstriction, and that is precisely what induction agents blunt. Expect the pressure the compensation was hiding.

Non-hemorrhagic resuscitation - Warm isotonic crystalloid 30 mL/kg infused rapidly, repeated as needed. Crystalloid over colloid — albumin has not improved outcomes and hyperoncotic starch increases mortality and renal failure. Large volumes of normal saline give a hyperchloremic metabolic acidosis; balanced crystalloids appear to cause less renal injury in big resuscitations.

Hemorrhagic resuscitation - Blood products beat crystalloid. Balanced ratios of 1:1:1 or 1:1:2 plasma to platelets to packed cells gave no mortality difference at 24 hours or 30 days, but 1:1:1 patients were less likely to exsanguinate in the first 24 hours and more likely to achieve hemostasis. Shorter time to first plasma reduces mortality.

Tranexamic acid early - CRASH-2 showed antifibrinolytic given within 3 hours of traumatic injury decreases death from major bleeding, with the greatest benefit inside 3 hours.

Permissive hypotension, with caveats - In hemorrhagic shock without head trauma, damage control resuscitation targets a systolic around 90 mmHg until bleeding is controlled, accepting brief suboptimal end-organ perfusion rather than blowing fresh clot off vessels. Studies conflict, and the call depends on blunt versus penetrating mechanism, likelihood of intracranial injury, injury severity, and how far away definitive hemorrhage control is.

Fight the lethal triad - Acidosis, hypothermia, and coagulopathy feed each other. Acidosis degrades coagulation factor activity, fibrinogen, and platelet number; hypothermia below 34 °C impairs coagulation and is an independent risk factor for death. Warm the fluids, warm the room, warm the patient — trauma-induced coagulopathy is already present in 25% to 56% of patients before resuscitation even starts.

Vasopressors are a bridge, not the treatment - They worsen tissue perfusion in a volume-depleted patient. Use them only to catch up during the initial phase while volume is going in, and treat their need as a prompt to find the bleeding.

Track the resuscitation with endpoints you can see - Heart rate, blood pressure, urine output, mental status, and peripheral edema. Lactate reflects the anaerobic debt; acid-base can mislead, since heavy GI losses can leave the patient alkalotic.

Don't trust vitals in the elderly or beta-blocked - Beta blockade blocks the compensatory tachycardia, physiologic reserve is lower with age, and a chronically hypertensive patient is functionally hypotensive at a systolic of 110. Heart rate and blood pressure cannot be the sole basis for the diagnosis.

Complications come from the treatment too - Circulatory overload, abdominal compartment syndrome, and transfusion reactions, on top of whatever the surgical or interventional radiology source control costs.

Venous oxygen saturation, and the number that should worry you - Mixed venous saturation normally runs 65% to 75%, meaning tissues pull 25% to 35% of the oxygen you deliver. As delivery falls from blood loss, anemia, or hypoxemia, extraction climbs and the saturation drops, which tracks with the bleeding. The trap is a high number: a saturation above 90% means oxygen is being delivered and not used - septic shock, arteriovenous shunting, or cyanide - not a resuscitated patient.

What lactate tells you and what it does not - Normal is under 2 mmol/L, 2 to 4 mmol/L is hyperlactatemia, and 4 mmol/L or higher is severe. Every shock state produces type A lactic acidosis, the kind that comes from hypoperfusion and hypoxia. Type B has nothing to do with either, and hyperlactatemia occurs in the presence of perfectly adequate perfusion and oxygenation, so a high lactate is a prompt rather than a diagnosis. The number carrying the prognosis is clearance: the longer it takes to normalize, the greater the risk of death. Lactate is cleared by the liver and kidney, so hepatic or renal failure slows the fall for reasons that have nothing to do with your resuscitation. Shock with a pH under 7.2 carries roughly 50% mortality, and no survival has been reported for shock with a pH below 7.0.

Put a number on the perfusion exam - Capillary refill under one second, with warm skin and bounding pulses, is the compensated vasodilated picture; refill beyond three seconds with cool extremities and thready pulses is the decompensated clamped-down one. Score mental status with the Glasgow Coma Scale rather than writing altered, so the next person can tell whether it moved.

Volume loss inside a vasodilated circulation - Third-spacing from pancreatitis, burns, or any massive inflammatory insult produces genuine hypovolemia at the same moment the inflammatory response drops systemic vascular resistance. The high-resistance, cold-periphery fingerprint you were going to use to call this hypovolemic shock is gone - the patient is warm with flash capillary refill and still profoundly volume down. Give the volume anyway, and stop waiting for the exam to look like textbook hypovolemia before you believe it.

In trauma, expect more than one - Hemorrhage is the usual answer, but tension pneumothorax and tamponade produce obstructive shock in the same patient, and head or neck trauma adds neurogenic shock. An inappropriately low heart rate in a hypotensive trauma patient points at neurogenic shock, but that is a diagnosis of exclusion; hemorrhage is the more common cause of hypotension in trauma and gets ruled out first.

Induction agents in the volume-depleted patient - Etomidate 0.2 to 0.3 mg/kg injected over 30 to 60 seconds gives the most forgiving induction hemodynamics: cardiac output and heart rate essentially unchanged, mean arterial pressure maintained or only modestly lower. Two catches belong to this patient specifically. Etomidate is about 77% protein bound, so in a low-albumin critically ill patient the same milligram dose puts more free drug in the brain. And a single induction dose inhibits 11-beta-hydroxylase, with cortisol suppressed for 24 to 48 hours. Ketamine's sympathetic stimulation makes it a good choice in hypovolemia at an induction dose of 1 to 2.5 mg/kg, but its direct negative inotropy is only masked by intact catecholamine reserve - in someone who has been compensating for hours, expect the mask to come off and cut the dose.

Hypovolemic shock is circulatory failure from loss of effective intravascular volume — hemorrhagic (trauma, GI bleeding, obstetric, vascular, surgical) or non-hemorrhagic (vomiting and diarrhea, bowel obstruction, fistula and stoma output, osmotic diuresis and diuretics, burns and skin losses, third-space sequestration in pancreatitis or any large inflammatory insult). Falling preload drops cardiac output, oxygen delivery stops meeting demand, cells switch to anaerobic metabolism, and lactic acidosis builds.

Compensation hides it early. Sympathetic tone raises heart rate and contractility and clamps the periphery, so at roughly 10% volume loss the diastolic pressure rises, pulse pressure narrows, and the cuff still reads normal. Only at 25% to 30% loss does systolic pressure fall, with tachycardia and oliguria. That same vasoconstriction starves non-vital beds, deepening the acidosis toward refractory hypotension, multiorgan failure, and death.

Shock sorts into four categories - distributive, hypovolemic, cardiogenic, and obstructive - and three of the four end the same way, with a low cardiac output and reduced oxygen transport. Distributive shock is the outlier: peripheral vascular resistance falls and oxygen extraction itself becomes abnormal. That matters here because distributive shock is the most common form in adults, so it is the one hypovolemic shock is most often confused with, and the two overlap constantly. In children the order flips, and hypovolemic shock is the most common type, driven by diarrheal illness.

Beyond the pressure and the pulse, the findings that pin the problem to lost volume are flattened jugular venous pulsations, dry mucous membranes, decreased skin turgor, thirst, muscle cramps, and orthostatic hypotension. The kidney gives it away too, with a fractional excretion of sodium under 1%, a low urine sodium, and a high urine osmolality as it conserves salt and water. Both have limits: urine sodium is also low in the euvolemic patient with heart failure, cirrhosis, or nephrotic syndrome, and urine osmolality rises simply from impaired concentrating ability. Hematocrit is the least trustworthy of all - critically low with brisk bleeding, but falsely raised by hemoconcentration as plasma volume drops.