What it is:Acute, generalized circulatory failure where the cardiovascular system can't deliver enough oxygen to meet tissue demand. Classically defined by SBP <90 mm Hg (or a drop of at least 40 mm Hg from baseline) or MAP <70 mm Hg with tachycardia and signs of organ hypoperfusion, but low blood pressure is not requiredto have shock. Compensatory vasoconstriction can hold the number up while tissue perfusion is already failing.
The core problem:Cells stop getting enough oxygen, flip to anaerobic metabolism, and start dumping lactate. Left uncorrected, this cascades into multi-organ dysfunction.
What you do:Figure out which of the four mechanisms is driving it, because that changes everything downstream. Then restore MAP to at least 65 mm Hg, fluids first, vasopressors (mainly norepinephrine) second, while treating whatever actually caused it.
Think of it as a plumbing problem. Hypovolemic= not enough fluid in the pipes. Cardiogenic= the pump quit. Obstructive= a kink somewhere in the pipes or at the pump. Distributive= the pipes themselves are too wide open and leaky. Every drug you reach for targets one of those four problems specifically, so naming the mechanism before you treat is the whole game.
Four categories, and patients frequently have more than one operating at once (e.g., septic shock with a component of hypovolemia from third-spacing, or cardiogenic shock complicated by a systemic inflammatory response).
Inadequate venous return from internal or external fluid loss (trauma, surgery, hemorrhage). Insufficient preload → decreased stroke volume.
Loss of pump function from decreased contractility (AMI), acute valve failure, or arrhythmia.
Extracardiac obstruction to flow into or out of the heart: tension pneumothorax, cardiac tamponade, pulmonary embolism.
Loss of vascular tone, decreased SVR causing hypoperfusion despite normal or even elevated cardiac output.
Distributive is the umbrella term, vasodilatory is the mechanism, septic is the most common cause.Almost all septic shock is vasodilatory/distributive shock, but not all distributive shock is septic (anaphylaxis, neurogenic shock, and severe pancreatitis can look the same hemodynamically). Exam questions like to swap these words as if they're interchangeable causes rather than a mechanism-and-example pair.
Circulatory shock develops when the CV system can't deliver adequate oxygen to meet tissue demand. That mismatch forces cells into anaerobic metabolism, which produces lactate and, if it persists, drives cellular and organ dysfunction.
| Term | Formula | What it means clinically |
|---|---|---|
| DO2(oxygen delivery) | CO × CaO2 | How much oxygen you're pushing out to tissues, driven by cardiac output and arterial oxygen content (hemoglobin × SaO2) |
| VO2(oxygen consumption) | CO × (CaO2 − CvO2) | How much oxygen tissues are actually extracting and using |
Normally VO2 stays independent of DO2, meaning tissues take what they need and ignore the rest. Below a critical DO2 threshold, VO2 becomes dependenton DO2: further drops in delivery directly cause drops in consumption. That transition point is the pathologic switch from aerobic to anaerobic metabolism, and it's the physiologic reason lactate becomes the number you chase serially in a shock patient.
SvO2 (pulmonary artery) and ScvO2 (central vein) reflect how much oxygen tissues extracted before blood returns to the right heart, and both work as a surrogate for cardiac output when hemoglobin and SaO2 are stable. >70% is normal.<50% is lowand edges toward the critical oxygen extraction ratio where anaerobic metabolism and lactate rise. Counterintuitively, >80% can also be bad: it can mean delivery is fine but the tissue has lost the capacity to extract oxygen at all, a poor prognostic sign rather than a reassuring one.
The body's response to sudden hypoperfusion and its restoration triggers systemic inflammatory response syndrome (SIRS): mediator release that causes further injury on top of the original insult ("ischemia-reperfusion injury"). This produces edematous capillary obstruction, oxygen free-radical membrane damage, activation of white blood cells and platelets, disrupted coagulation and complement pathways, more inflammatory mediator release, and microthrombi formation.
In parallel, the body activates anti-inflammatory and pressure-supporting pathways to fight back: vagally-mediated acetylcholine suppresses proinflammatory cytokines, and the renin-angiotensin-aldosterone and hypothalamic-pituitary-adrenal axes release angiotensin II, vasopressin, and cortisolto hold blood pressure up through vasoconstriction and sodium/water retention. Catecholamine and cortisol release also directly inhibit proinflammatory cytokine production.
Read that hormone list again: angiotensin II, vasopressin, cortisol, catecholamines.Every major drug in this chapter is either a synthetic version of one of the body's own emergency hormones (exogenous norepinephrine, angiotensin II, vasopressin, corticosteroids) or a variant built to hit the same receptors harder (phenylephrine, epinephrine, dopamine, dobutamine). When the endogenous stress response isn't enough to keep MAP up, you're not inventing a new mechanism, you're topping off the same one the body already started.
Symptoms of the underlying cause show up alongside the shock picture itself (cough and fever with pneumonia-driven septic shock, chest pain with an AMI causing cardiogenic shock). Patients commonly report dizziness, lightheadedness, confusion, and low urine output.
| Category | Findings |
|---|---|
| Vitals | Tachycardia (often >120 bpm), tachypnea (often >30/min), hypotension (SBP <90 mm Hg), temperature low-normal (36-37°C) unless infection is present (>38.3°C) |
| Neurologic | Confusion, obtundation |
| Cutaneous | Warm skin (vasodilated states) or cool, clammy skin (vasoconstricted states); impaired capillary refill |
| Renal | Low urine production |
| Labs | Lactate >2 mmol/L, ↑ BUN/SCr with ↓ urine output (<0.5-1 mL/kg/h), ↑ transaminases with hepatic dysfunction, ↓ H&H with hemorrhage, ↑ troponin with AMI |
In septic shock, expect WBC >12,000 cells/mm³and possible thrombocytopenia. In both hemorrhagic and septic shock, PT/INR can rise over time as coagulopathy develops, which is one reason serial coags matter, not just a single baseline draw.
Rapid transthoracic echocardiography can identify the shock type within about 5 minutes when the etiology isn't obvious from the history and exam, and it's the go-to first step whenever the mechanism is unclear.
MAP is the driving pressure for peripheral flow and end-organ perfusion, and it depends on cardiac output and SVR, which is why it tracks with DO2. But compensatory vasoconstriction can preserve MAP while tissue perfusion is already inadequate underneath it. That's the mechanistic reason low BP is common in shock but not required to diagnose it, and it's why you always pair a BP number with a perfusion marker (lactate, urine output, capillary refill, mental status) rather than trusting BP alone.
Gives CVP, pulmonary artery pressure, PAOP (wedge pressure), CO, SVR, and SvO2 in one device. Reserve it for complex or mixed shock states, or when other monitoring is giving you numbers you don't trust. It's more invasive than a central venous catheter, carries a higher complication risk, and is not routinely usedbecause it hasn't been shown to improve outcomes as a default strategy.
The desired outcome is preventing organ damage and reversing what's already occurred. Treatment splits into four overlapping phases: salvage(minimum perfusion and CO to survive, treat the cause), optimization(adequate organ perfusion and DO2), stabilization(prevent further organ injury), and de-escalation(wean vasoactives and fluids as the patient recovers). This chapter, and this doc, is mostly about salvage and optimization.
MAP >65 mm Hgis the usual target to maintain critical organ perfusion, individualized to the patient. Large-bore peripheralIV lines are preferred for initial fluid resuscitation; vasopressors should preferentially run through a centralvenous catheter once one is available.
Stabilization-phase supportive care applies broadly: pain, anxiety/agitation, delirium, immobility, sleep disturbance, nutrition, glycemic control, and thromboembolism prophylaxis all need active management, not just the hemodynamics.
The goal of IV fluid is increasing venous return to raise stroke volume, cardiac output, DO2, and BP. Blood products do the same while also replacing what was actually lost.
Isotonic or near-isotonic crystalloids (lactated Ringer's, 0.9% NaCl) are first-line, given in large volumes except in cardiogenic shock. Balanced salt solutions(LR, Plasma-Lyte A) and normal saline expand plasma volume similarly, but balanced solutions may be safer: excess chloride from normal saline can cause hyperchloremic metabolic acidosis and possibly AKI. If there's tissue hypoperfusion and a fluid-responsive shock state, give an initial challenge of at least 500 mL crystalloid.
Balanced salt solutions should be used with extreme caution in brain-injured patients, they can worsen cerebral edema. Normal saline is the safer default there despite its chloride load elsewhere.
3% hypertonic salinerapidly expands the intravascular space by pulling fluid from the intracellular compartment, but it's not associated with better outcomesas initial resuscitation and carries real risk: hypernatremia, hyperchloremic metabolic acidosis, and peripheral vein damage from its high osmolality (1026 mOsm/L). It's not a shortcut.
Albumin, hydroxyethyl starch, and dextran stay intravascular longer than crystalloids but are expensive and carry real risk.
Hydroxyethyl starch is contraindicated in critically ill patients.It's associated with increased mortality, AKI, and need for renal replacement therapy, which is why the US product labeling was changed. Don't reach for it in shock resuscitation.
PRBCs, FFP, platelets, or cryoprecipitate maintain oxygen-carrying capacity and clotting function. Risks include circulatory overload, transfusion reactions, hypocalcemia from citrate, increased viscosity from supranormal hematocrit, and hypothermia if products aren't warmed before infusion.
The Surviving Sepsis Campaign suggests 30 mL/kg crystalloid within the first 3 hoursof recognition, though the evidence behind that specific number is low-quality. Two broad approaches exist for the first 6 hours: liberal(50-75 mL/kg, reserving vasopressors) versus relatively restrictive(≤30 mL/kg, earlier vasopressor start). More than 30 mL/kg is often needed to hit goal MAP, clear lactate, achieve ScvO2 ≥70%, or restore urine output. Excessive fluid administration is associated with higher mortality, so this is a balance, not a "more is always better" situation, especially with heart failure or impending pulmonary edema.
A single isolated 250-500 mL bolus is unlikely to produce a meaningful BP or acid-base change on its own. Multiple boluses with reassessment after each are usually needed, and IV medication diluents count toward total fluid volume too, they're easy to forget when tallying intake.
This is the exception to "more fluid is safer." Fluid resuscitation beyond minimal levels is harmful in abdominal traumadue to hemodilution and clot destabilization. Instead of immediate plasma expansion, the priority is surgical control of the bleeding source; until that's possible, give fluids in small aliquots to maintain a palpable pulse and keep MAP ≤60 mm Hg and SBP ≤90 mm Hg, not higher. Isotonic crystalloids are preferred over hypertonic saline (equal efficacy, fewer adverse effects); balanced solutions should be avoided with severe traumatic brain injury; hypotonic solutions should be avoided altogether. Once hemostasis is achieved, use a restrictive transfusion threshold of Hgb ≤7 g/dLunless there's active cardiac ischemia, guided further by PT/INR, platelets, or viscoelastic testing. Reversal agents (e.g., prothrombin complex concentrate for warfarin) may be needed for severe bleeding.
Students default to "shock = give fluids aggressively" because that's true in sepsis. In hemorrhagicshock before the bleeding is controlled, aggressive fluids can actively hurt the patient by diluting clotting factors and blowing off the clot that's already forming. Same category (hypovolemic/distributive both need volume), opposite fluid strategy.
Used when volume resuscitation isn't indicated or fails to reach MAP ≥65 mm Hg with ongoing tissue hypoperfusion, or temporarily for life-threatening hypotension during aggressive fluid resuscitation. Inotropes are mainly used to optimize DO2 in septic shock and cardiac function in cardiogenic shock. Note: doses required in practice frequently exceed standard references once you're titrating to a real patient's perfusion markers.
| Agent | Usual dose range | Dominant receptors | Premixed? | Key adverse effects |
|---|---|---|---|---|
| Norepinephrine | 0.02-3 mcg/kg/min | α1 ≈ β1, weak β2 | No, must prepare | Peripheral ischemia, mixed effect on mesenteric perfusion |
| Epinephrine | 0.01-0.05 mcg/kg/min (low); 0.05-3 mcg/kg/min (high) | Low dose β > α; high dose α > β | No | Tachydysrhythmia, ↓PaO2, ↑lactate, hyperglycemia |
| Phenylephrine | 0.5-9 mcg/kg/min | Pure α1 | No | Peripheral ischemia, reflex bradycardia |
| Dopamine | 1-3 (D1) · 3-10 (+β1) · >10-20 mcg/kg/min (+α1) | Dose-dependent D1 → β1 → α1 | Yes | Tachydysrhythmia, ↓PaO2, GI motility inhibition |
| Dobutamine | 2-10 mcg/kg/min (β1β2); >10-20 mcg/kg/min (+α1) | β1 ≫ β2, mild α1 | Yes | Tachycardia, dysrhythmia, hypotension |
| Vasopressin | 0.01-0.1 units/min (adjunct fixed at 0.03-0.04) | V1 ≫ V2, no adrenergic activity | No | Mesenteric hypoperfusion, hyponatremia, thrombocytopenia |
| Angiotensin II | 1.25-80 ng/kg/min | AT1/AT2 only | No | Thrombosis, bronchospasm, infection risk |
Ranked from most to least α1-selective: phenylephrine > norepinephrine > dopamine > vasopressin(vasopressin works through an entirely different receptor, V1, not α1 at all, which is why it's grouped last on a pure α1-activity ranking despite being a potent vasoconstrictor). This exact ranking has shown up as a board-style question.
Only dopamine and dobutaminecome as commercially available premixed, ready-to-use solutions. Norepinephrine, epinephrine, phenylephrine, and vasopressin all require preparation time, which matters when you're the one being paged to get a drip hung emergently.
Both are built along the same biosynthetic line: tyrosine → L-DOPA → dopamine → norepinephrine, with norepinephrine converted to epinephrine by one additional step that happens only in the adrenal medulla, where epinephrine is released as a neurohormone. Both are degraded by monoamine oxidase (MAO) and modified by catechol-O-methyltransferase (COMT), and norepinephrine's action at the synapse is normally ended by reuptake through the norepinephrine transporter (NET), the same transporter targeted by some antidepressants and ADHD medications.
Norepinephrinehas strong α1 agonism with less potent β1 activity and weak β2 vasodilatory effect. It's the vasopressor of choice in most shock statesfor a cluster of reasons: it may reduce mortality in septic shock, reverses inappropriate vasodilation and low global oxygen extraction, attenuates myocardial depression without dropping CO, improves renal perfusion and filtration, enhances splanchnic perfusion, and is less arrhythmogenic than most alternatives. Heart rate often dropsinitially from reflex bradycardia as SVR rises, which trips up students expecting a pure adrenergic agonist to always speed the heart up.
Older course material frames norepinephrine (Levophed) as the drug for an "acute hypotensive crisis," raising BP withoutmeaningfully raising heart rate, which is exactly the profile the current shock algorithm relies on: pressure support without piling on tachyarrhythmia risk.
Epinephrinemixes α and β effects, with β dominant at low doses (↑ stroke volume and CO) and α dominant at higher doses (↑ SVR and MAP). It's as effective as norepinephrine for MAP response in distributive shock and is an acceptable option, but it's typically considered adjunctivebecause of its tachydysrhythmia risk, lactate elevation, and unpredictable pH effects. Younger patients tend to respond better, likely from greater β-adrenergic reactivity.
Phenylephrineis a pure α1 agonist, raising BP through vasoconstriction and improving stroke index via enhanced venous return. Because it does almost nothing at β1, tachydysrhythmias are uncommon, making it the go-to swap when norepinephrine or epinephrine triggers one. The tradeoff: in patients with impaired myocardial performance, phenylephrine can actually worsencardiac output by raising afterload against a weak pump, so it's not a safe first choice when cardiogenic physiology is in play.
Vasopressinworks through an entirely separate receptor system. V1 stimulation constricts efferent arterioles and dilates afferent arterioles, which paradoxically increasesglomerular perfusion and can enhance urine output even while raising SVR systemically; V2 stimulation promotes water retention in the collecting duct. Its vasoconstrictive effect is preserved during hypoxemia and severe acidemia, unlike catecholamines, which lose potency in that setting. Doses up to 0.04 units/minlet you reduce catecholamine requirements; doses above that risk worsening cardiac output and mesenteric perfusion. It causes reflex bradycardia after starting, similar logic to norepinephrine's SVR-driven HR drop.
Vasopressin is used adjunctively, fixed-dose, to spare catecholamines, not titrated up and down as a primary pressor. It is not commercially available premixed.
Dopamineis the natural precursor to norepinephrine and epinephrine, and its receptor activity shifts with dose, though this dose-response relationship isn't as clean in critically ill patients as it is in the textbook diagram: 1-3 mcg/kg/minis mostly D1 agonism (renal vasodilation, natriuresis), 3-10 mcg/kg/minadds β1 stimulation (↑ contractility and rate), and >10-20 mcg/kg/minadds meaningful α1 activity (vasoconstriction). In practice, significant hemodynamic overlap occurs even at doses as low as 3 mcg/kg/min, and low-dose "renal-protective" dopamine does notimprove renal function or survival, a myth worth actively unlearning. It's largely fallen out of first-line use because the doses needed to hit goal MAP are frequently limited by tachycardia and tachydysrhythmias.
Dobutamineis marketed as a β1-selective inotrope, but it's actually a racemic mix: the (+) isomer is a β agonist and weak α1 antagonist, while the (−) isomer is an α1 agonist. The two roughly cancel each other's effect on peripheral resistance (the β2-mediated vasodilation and weak α1 antagonism from the (+) isomer offset the (−) isomer's vasoconstriction), leaving the net clinical effect as increased cardiac output with little change in SVR, an "inodilator." It's the go-to inotrope for low CO with high filling pressures(e.g., LV dysfunction on echo) or ongoing hypoperfusion despite adequate volume, typically raising CO by 25-50%. Because it increases myocardial oxygen demand, use it cautiously in cardiogenic shock specifically. Receptor desensitization limits its practical window to roughly the first several days of use.
Angiotensin IIraises SVR through AT1/AT2 receptors and can be considered for distributive shock refractory to catecholamines and vasopressin. Start at 10-20 ng/kg/minwith rapid titration, as often as every 5 minutes, to goal MAP; in the first 3 hours the dose may climb to 80 ng/kg/min, and after that it should not exceed 40 ng/kg/min. It's only been studied in patients without depressed cardiac output, so use it cautiously with impaired LV systolic function. It raises thromboembolism risk (give VTE prophylaxis), infection risk, and has been linked to bronchospasm, so avoid it with asthma or active bronchospasm.
Corticosteroidsin septic shock improve hemodynamics and let you use lower catecholamine doses, with a relatively clean short-term safety profile. Consider them when fluids and vasopressors aren't restoring stability, when weaning vasopressors keeps failing, or when adrenal insufficiency is suspected (e.g., a patient on long-term steroids before shock onset), though routine adrenal function testing to guide the decision isn't recommended. Courses are typically short, around 7 days, and while GI bleeding and superinfection risk don't appear meaningfully increased at that duration, watch for hypernatremia, hyperglycemia, and possible neuromuscular weakness.
The most common distributive shock, and the scenario the current sequencing algorithm is built around.
Within 1 hour of recognition:measure blood lactate (remeasure if >2 mmol/L), begin rapid 30 mL/kg crystalloid for hypotension, start vasopressors if hypotensive during or after fluids to reach MAP ≥65, and give antibiotics. All four happen in the same hour, not sequentially over a shift.
Medications are a distant secondto fluid resuscitation and hemorrhage control here, the opposite emphasis from septic shock. Peripheral resistance is already elevated from the body's own compensatory mechanisms trying to preserve perfusion; adding a vasopressor early or overzealously can push that resistance high enough to stop flow altogetherrather than help it.
Vasopressors are reserved as a temporizing measure or a last resortonce every other option to maintain perfusion has been tried. When one is needed, norepinephrineis the first-line choice, same as most other shock states, just used far more sparingly and later in the sequence.
| Parameter | When | Watching for |
|---|---|---|
| Vital signs, mental status | Continuously / every assessment | Trend toward or away from perfusion goals |
| Blood lactate | Baseline, remeasure if >2 mmol/L, then serially | Clearance = improving global perfusion; rising = worsening anaerobic metabolism |
| Urine output | Hourly via catheter | Goal ≥0.5 mL/kg/h; regional (renal) perfusion marker |
| MAP / SBP | Continuous arterial line during titration | Goal MAP ≥65 mm Hg (or SBP 80-90 in trauma) |
| Capillary refill | Every assessment | Goal <3 seconds; quick bedside perfusion check |
| ScvO2 / SvO2 | Via central or PA catheter, serially | Goal ≥70%; <50% signals critical extraction |
| Echocardiography | Initial workup, repeat if not responding | Re-classify shock type, guide added therapy |
| Electrolytes, BUN/SCr, CBC | Regularly through resuscitation | Renal function, oxygen-carrying capacity, infection (WBC), ongoing bleeding |
| Hepatic transaminases | If sustained hypotension | "Shock liver" from reduced hepatic blood flow, should trend down with recovery |
| PT/INR, platelets | Serially in bleeding patients | Coagulopathy; consider viscoelastic testing (TEG) |
Once a patient is responding, the goal is discontinuing vasopressors and inotropes as soon as it's safe, but taper slowlyand reassess fluid responsiveness frequently rather than stopping abruptly. Doses are typically titrated downward roughly every 10 minutesto check tolerance. Vasopressor/inotrope-dependent shock usually resolves over several days to about a week; if it isn't trending that way, that's a signal to re-image and reassess the mechanism.
Most shock patients can't hold a normal counseling conversation while they're actively decompensating, sedated, or intubated. On an ICU rotation, the "counseling" moment is usually with the bedside nurse, the family, or the patient once they've stabilized enough to talk, so frame it that way.