Last updated: September 11, 2023

Summarytoggle arrow icon

Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation. The numerous causes of shock are classified into hypovolemic shock (e.g., following massive blood/fluid loss), cardiogenic shock (e.g., as a result of acute heart failure), obstructive shock (e.g., due to cardiac tamponade), and distributive shock (due to redistribution of body fluids), which is further classified into septic, anaphylactic, and neurogenic shock. Common clinical findings are hypotension and abnormal heart frequency (most commonly tachycardia; bradycardia in neurogenic shock) accompanied by specific symptoms related to the cause of shock. Diagnosis is mostly clinical but measurement of functional parameters (e.g., PCWP, cardiac output, SVR) can help distinguish between the different types of shock. Management of shock involves circulatory support and treatment of the underlying cause. Shock is associated with a very high mortality rate.

Overviewtoggle arrow icon


  • Shock (circulatory shock): a life-threatening disorder of the circulatory system that results in inadequate organ perfusion and tissue hypoxia, leading to metabolic disturbances and, ultimately, irreversible organ damage [1][2]
  • Shock index = pulse rate/systolic blood pressure
    • Normal range: 0.4–0.7
    • > 1 (positive shock index): consistent with circulatory shock

Types of shock

Overview of the types of shock [3][4][5]
Type Etiology of shock Typical hemodynamic parameters [6] Distinguishing clinical features Treatment options

Hypovolemic shock

(includes hemorrhagic shock)

  • CVP
  • ↓↓ PCWP
  • ↓ CO
  • SVR
  • ↑ HR
  • ↓ SV02
Cardiogenic shock
  • CVP
  • PCWP
  • ↓↓ CO
  • SVR
  • Variable HR
  • ↓ SV02
Obstructive shock
  • CVP
  • ↑ or ↓ PCWP
  • ↓↓ CO
  • SVR
  • ↑ HR
  • ↓ SV02
Distributive shock

Septic shock

(most common)

  • CVP
  • Normal or PCWP
  • ↑ or ↓ CO
  • ↓↓ SVR
  • ↑ HR
  • ↑ SV02

Anaphylactic shock

  • CVP
  • ↓↓ PCWP
  • ↑ or ↓ CO
  • ↓↓ SVR
  • ↑ HR
  • ↑ SV02
Neurogenic shock
  • CVP
  • ↓↓ PCWP
  • ↓ CO
  • ↓↓ SVR
  • ↓ HR
  • Normal or ↑ SV02


CVP: right heart preload

PCWP: pulmonary capillary wedge pressure (a surrogate marker for preload)

CO: cardiac output (CO = HR × stroke volume)

SVR: systemic vascular resistance (a surrogate marker for afterload)

HR: heart rate

SV02: mixed venous content

Hemodynamic parameters in shock

Typical hemodynamic parameters of types of shock [3][4][5][6]
Type Estimated cardiac output (CO) Estimated preload (e.g., PCWP) Estimated afterload (e.g., SVR) Likelihood of fluid responsiveness


  • ↓↓


  • ↓↓
  • ↓ Or ↑


  • Usually ↓
  • ↓↓

Stages of shock

The following stages may not occur in cases of sudden severe cardiovascular collapse , and the progression between stages in septic shock can be indistinct.

Stages of shock
Stage Characteristics
1. Preshock

2. Shock

(progressive phase)

3. End-organ dysfunction

(stage of decompensation)

Clinical features of undifferentiated shocktoggle arrow icon

  • Patients may present at the emergency department with shock or develop shock at any time during hospitalization.
  • Screening for clinical features of shock in patients at risk can allow for early identification and treatment.
  • The clinical picture may vary depending on the stage of shock.
Clinical features of shock [7][8][9]
Feature Classic findings Atypical findings
Vital signs Heart rate
  • Normal or ↓
Blood pressure
  • Normal [7]
Respiratory rate
  • Normal
Pulse pressure
Clinical signs of end-organ hypoperfusion [8] Brain
  • Oliguria: urine output < 0.5 mL/kg/hour

Hypotension may be absent in some patients with shock. [7]

Signs of congestive heart failure alongside shock (e.g., JVP, crackles on lung auscultation) are suggestive of cardiogenic shock.

Managementtoggle arrow icon

Approach [4][7][8]

The following should be performed simultaneously:

Act quickly: Provide immediate hemodynamic support and simultaneously try to identify the type of shock and the underlying cause in order to provide appropriate treatment.

Patients in shock are at risk of cardiopulmonary arrest; if the pulse is lost, start CPR!

Management of patients with severe shock can be recalled with the VIP rule: Ventilation as needed, Infuse IV fluids, and Pump vasopressors as needed. [4]

Respiratory support for patients with severe shock [4]

Pulse oximetry measurements are unreliable in patients with shock due to peripheral hypoperfusion and/or vasoconstriction. Consider initial supplementary O2 for potential hypoxemia in all patients, regardless of pulse oximetry results. [4]

Diagnosticstoggle arrow icon

Routine investigations can help identify the shock subtype but are not required for diagnosis. Consider further investigations if the subtype remains uncertain.

Shock is a clinical diagnosis.

Routine investigations

Findings allow for evaluation of the following:

In all patients with shock, immediately measure ABGs, lactate levels, capillary glucose, perform an ECG, and order a chest x-ray and general laboratory studies.

Compare any available previous studies to the patient's current test results. Previous studies can help determine if alterations to any laboratory or imaging studies are new and likely the cause of shock, or if they are caused by chronic conditions (e.g., CKD, chronic heart failure).

Further investigations

Further studies should be guided by clinical suspicion of the underlying cause.

Further diagnostic studies for patients in shock
Type of shock Studies to consider
Unclear after initial evaluation
Hypovolemic shock Hemorrhagic shock
Nonhemorrhagic shock
Cardiogenic shock
Obstructive shock
Distributive shock Septic shock
Anaphylactic shock
Neurogenic shock
  • Imaging studies can help identify the underlying injury (e.g., CT or MRI spine, CT or MRI brain).

If hemorrhagic shock is suspected, perform blood type and screen and crossmatch as soon as possible. Emergency issue blood products, e.g., Blood type O Rh-negative blood, can be given immediately; however, type-specific and crossmatched blood products are preferred as soon as they become available.

Ultrasoundtoggle arrow icon

Bedside echocardiography

Simplified cardiac ultrasound can help identify pericardial effusion and indirect signs of right heart failure and cardiomyopathy. [14][15]

Rapid assessment by cardiac echo (RACE) [4][7]
Type of shock Possible findings
Hypovolemic shock
  • Small cardiac chambers
  • Contractility: high or preserved
Cardiogenic shock
  • Large cardiac chambers
  • Poor contractility
Obstructive shock
Distributive shock
  • Normal cardiac chambers
  • Contractility is usually preserved.

Other point-of-care ultrasound (POCUS) techniques [16][17][18][19]

Monitoringtoggle arrow icon

Monitoring parameters can be used as treatment targets and should be tailored to the patient.

Monitoring parameters for patients with shock [7][23]
Variable Parameters
Clinical features in shock Vital signs
Laboratory Lactate
  • Aim for a lactate level ≤ 2 mEq/L.
  • Monitor for changes over time (i.e., lactate clearance). [24]
Base deficit (BD)
SvO2 and ScvO2 [6][27][28]
Central venous pressure (CVP) [6][30]
Cardiac function [6]
Bedside echocardiography/POCUS

Signs of an inadequate response to fluid resuscitation include persistently heart rate, ↓ blood pressure, CVP, and ↓ urine output (< 0.5 mL/kg/hour).

Oxygen saturation from peripheral venous blood gases should not be misinterpreted as SvO2 or ScvO2.

Immediate hemodynamic support of undifferentiated shocktoggle arrow icon

IV fluid resuscitation [7][13][32]

Patients with peripheral edema can still be fluid responsive if they have reduced effective arterial blood volume. [4]

Vasopressors [4]

  • Indications: treatment of various shock states in an effort to restore adequate arterial pressure and organ perfusion
  • Available agents
    • Choice is determined based on the underlying shock physiology, the desired pharmacological effects, and potential adverse effects.
    • First-line in undifferentiated shock: norepinephrine
  • Next steps

Additional interventions

Patients with chronic corticosteroid use need steroid stress dosing to prevent adrenal crisis!

Vasopressors and inotropestoggle arrow icon

Vasopressors [3][38]

Blood pressure does not always correlate with blood flow. Agents that increase blood pressure through vasoconstriction can impair tissue perfusion at high doses.

Although certain vasopressors, inotropes, and inodilators can be combined (e.g., to allow for individual agents to be used in moderate doses), this requires careful titration and specialist consultation.


Inoconstrictor drugs [38][39][40][41]


Continuous IV infusion dosages


Clinical applications

Adverse effects

Norepinephrine infusion


  • Initial dosage: 0.01–0.04 mcg/kg/minute
  • Titration increments: 0.02–0.04 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.4 mcg/kg/minute
  • Maximal dosage: 0.5–3.3 mcg/kg/minute [38]
  • α1 > β1
  • ↑↑ SVR , ↑↑ MAP
  • Unchanged/↑ CO, ↑ HR
  • Half-life: ∼ 2 minutes

Epinephrine infusion


  • Initial dosage: 0.01–0.05 mcg/kg/minute
  • Titration increments: 0.02–0.05 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.3 mcg/kg/minute
  • Maximal dosage: 2 mcg/kg/minute
  • β12 > α1
  • ↑↑ CO, ↑↑ HR
  • SVR, ↑↑ MAP
  • Half-life: < 5 minutes
Dopamine infusion [40][41][43][44]
  • Initial dosage: 2–10 mcg/kg/minute
  • Titration increments: 2–5 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 2–20 mcg/kg/minute
  • Maximal dosage: 50 mcg/kg/minute [39][45]
Key: α1 = α1-adrenergic receptor; β1 = β1-adrenergic receptor; β2 = β2-adrenergic receptor; AT1 = angiotensin II receptor type 1; SVR = systemic vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure

Pure vasoconstrictors

  • Mechanism of action: SVR without either significant ↑ cardiac contractility or ↑ HR
Pure vasoconstrictor drugs

Continuous IV infusion dosages




Clinical applications


Adverse effects


Phenylephrine infusion
  • Initial dosage: 0.1–0.3 mcg/kg/minute
  • Titration increments: 0.2–0.4 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 0.1–1.5 mcg/kg/minute
  • Maximal dosage: 6 mcg/kg/minute [46]
Vasopressin infusion
  • Initial dosage: 0.01–0.03 units/minute
  • Titration increments: 0.005 units/minute every 5–15 minutes
  • Usual dosage range: 0.01–0.04 units/minute
  • Maximal dosage: 0.07 units/minute [40]
  • Fixed-dose infusion: 0.03–0.04 units/minute without titration (used as second-line in combination with another vasopressor, e.g., norepinephrine)
Key: α1 = α1-adrenergic receptor; V1 = vasopressin 1a receptor; SVR = systemic vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure


  • Mechanism of action
    • ↑ Cardiac contractility → ↑ CO
    • Peripheral vasodilation SVR afterload (combined with ↑ CO) → improved peripheral blood flow and tissue perfusion

Inodilator drugs


Continuous IV infusion dosages




Clinical applications


Adverse effects


Dobutamine infusion
  • Initial dosage: 2.5–5 mcg/kg/minute
  • Titration increments: 2.5–5 mcg/kg/minute every 5–15 minutes
  • Usual dosage range: 2.5–20 mcg/kg/minute
  • Maximal dosage: 40 mcg/kg/minute [39][40][45]
  • β1 > β2 >> α1
  • ↑↑ CO, ↑ HR
  • Unchanged/↓ SVR, ↑/↓/unchanged MAP, ↓/unchanged PVR
  • Half-life: 2 minutes
Milrinone infusion
  • Initial dosage: 0.1–0.25 mcg/kg/minute
  • Usual dosage range: 0.25–0.75 mcg/kg/minute
  • Maximal dosage: 0.75 mcg/kg/minute
  • PDE-3 inhibitor (β12-like effect)
  • ↑↑ CO, ↑ HR
  • ↓↓ SVR, ↓/unchanged MAP, PVR
  • Half-life: 2–3 hours
Key: α1 = α1-adrenergic receptor; β1 = β1-adrenergic receptor; β2 = β2-adrenergic receptor; PDE-3 = phosphodiesterase 3; SVR = systemic vascular resistance; PVR = pulmonary vascular resistance; MAP = mean arterial pressure; CO = cardiac output; HR = heart rate; BP = blood pressure

Hypovolemic shocktoggle arrow icon



Loss of intravascular fluid volume → preload and SV ↓ CO → compensatory SVR and HR

Management [4][7][8]

The priority of immediate hemodynamic support is aggressive fluid resuscitation to achieve euvolemia. Further treatment depends on the etiologic category of hypovolemia (hemorrhagic vs. nonhemorrhagic).

Hemorrhagic shock

Classification of hemorrhagic shock
Blood loss (% of total blood volume) < 15% 15–30% 30–40% > 40%
Volume loss (in an average adult) ∼ 750 mL ∼ 750–1500 mL ∼ 1500–2000 mL > 2000 mL
Heart rate (bpm) 70–99 100–120 120–140 > 140
Systolic blood pressure Normal Normal
Pulse pressure Normal or ↑
Respiratory rate (rpm) Normal 20–30 30–40 > 35
Urine output > 30 mL/hour 20–30 mL/hour 5–15 mL/hour Absent
Mental status Normal Mildly anxious Anxious, confused Confused, lethargic

Upon suspecting hemorrhagic shock, perform blood grouping and cross-matching and have packed RBCs at hand for transfusion.

Uncrossmatched RBC type O negative units can be transfused if the hemorrhage is severe.

Nonhemorrhagic hypovolemic shock

Cardiogenic shocktoggle arrow icon



Management approach [53]

Management of cardiogenic shock [46][53][54]
Classification Treatment (see “Vasopressors and inotropes” for dosages)
Dry and cold
Wet and cold

IV fluids can worsen cardiogenic pulmonary edema in most cases of cardiogenic shock. Check fluid responsiveness prior to administration of fluid therapy.

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). [57]

Obstructive shocktoggle arrow icon


Pathophysiology [6]

Despite manifesting with high PCWP, many causes of obstructive shock (e.g., severe pulmonary hypertension, cardiac tamponade) are considered preload-dependent states. [6]

Elevation and equalization of pressures in all the cardiac chambers differentiate cardiac tamponade from other causes of obstructive shock.


Distributive shocktoggle arrow icon



Key treatment components

Septic shocktoggle arrow icon


Management of septic shock

See “Management of sepsis” for details on evaluation and definitive treatment of sepsis. The following recommendations relate to septic shock and are consistent with the 2016 and 2018 Surviving Sepsis Campaign guidelines: [12][35]

6–10 L of IV fluids may be necessary during the first 24 hours. [62]

Protocolized resuscitation target strategies [12][35][63]

There is insufficient evidence to support the use of one target over the others in order to inform decisions about escalating hemodynamic support. [12]

Vasopressors for septic shock [12][35][63][64][65]

Anaphylactic shocktoggle arrow icon

Initial management [62][66][67]

Adjunctive treatment (antihistamines and corticosteroids) should only be administered after the initial resuscitation measures (IM epinephrine, fluids and/or vasopressors) have been given.

Refractory anaphylactic shock [62][66][67]

Neurogenic shocktoggle arrow icon


Neurogenic shock is a clinical diagnosis.

In a patient who develops low blood pressure following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive shock have been ruled out.

Management [68][69][70]

Patients with neurogenic shock can have increased vasovagal responses to common procedures (e.g., suctioning, endotracheal intubation), which can trigger rapid changes in heart rate and blood pressure and increase the risk for complications and refractory shock. [74]

Refractory shocktoggle arrow icon

Rescue therapies for shock are for patients who remain in shock despite adequate treatment of the underlying cause. These treatments should be given in consultation with a specialist, and they include: [3]

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Referencestoggle arrow icon

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