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.
- 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 
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 |
|Type||Etiology of shock||Typical hemodynamic parameters ||Distinguishing clinical features||Treatment options|
(includes hemorrhagic shock)
|Distributive shock|| |
HR: heart rate
SV02: mixed venous content
Hemodynamic parameters in shock
|Typical hemodynamic parameters of types of shock |
|Type||Estimated cardiac output (CO)||Estimated preload (e.g., PCWP)||Estimated afterload (e.g., SVR)||Likelihood of fluid responsiveness|
|Hypovolemic|| || || || |
| || || || |
| || || || |
| || || |
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|
|1. Preshock|| |
3. End-organ dysfunction
(stage of decompensation)
Clinical features of undifferentiated shock
- 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 |
|Feature||Classic findings||Atypical findings|
|Vital signs||Heart rate|| || |
|Blood pressure|| || |
|Respiratory rate|| || |
|SpO2|| || |
|Pulse pressure|| || |
|Clinical signs of end-organ hypoperfusion ||Brain|
|Kidney|| || |
Hypotension may be absent in some patients with shock. 
The following should be performed simultaneously:
- Perform ABCDE survey: Identify the need for immediate airway or breathing intervention (e.g., basic airway maneuvers, supplemental O2).
- Establish vascular access immediately: Simultaneously obtain blood samples for testing.
- Begin immediate hemodynamic monitoring.
- Classify the type of shock (see “Overview of types of shock”).
Provide immediate hemodynamic support: can be started for undifferentiated shock
- Begin cardiogenic shock. immediately if there are no or diagnostic evidence of
- Consider a or if is in doubt.
- Determine the need for vasopressors, inotropes, or blood transfusions.
- Determine the need for other critical therapy (e.g., corticosteroids for adrenal crisis, epinephrine for anaphylaxis, needle thoracostomy for tension pneumothorax).
- Call for help early: critical care consult or rapid-response team
- Frequently reassess the patient (e.g., for signs of deterioration or response to therapy): Consider advanced .
Start specific management: according to the identified mechanism and its cause
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.
Respiratory support for patients with severe shock 
- Provide supplementary O2 to avoid complications of hypoxemia.
- Perform as needed.
- Indications for advanced airway maneuvers (e.g., endotracheal intubation
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. 
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.
Findings allow for evaluation of the following:
- Global hypoperfusion
- BMP: ↑ BUN/Cr ratio, hyponatremia, and other
- urinalysis, blood cultures : e.g.,
- ECG: Findings can show evidence of cardiogenic etiology, e.g., arrhythmias , acute coronary syndrome , signs of cardiomyopathy.
- Complications or end-organ dysfunction
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 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|
|Distributive shock||Septic shock|
If hemorrhagic shock is suspected, perform blood and as soon as possible. , e.g., Blood type O Rh-negative blood, can be given immediately; however, type-specific and blood products are preferred as soon as they become available.
|Rapid assessment by cardiac echo (RACE) |
|Type of shock||Possible findings|
|Hypovolemic shock|| |
|Cardiogenic shock|| |
|Distributive shock|| |
Other POCUS) techniques (
- fluid responsiveness, e.g., after a or .  : can be considered alongside other clinical parameters to help predict
- eFAST: can help identify intraperitoneal free fluid and pneumothorax
- Limited abdominal ultrasound: e.g.,
Lung ultrasound findings: Parameters measured include pulmonary A-lines and B-lines and the seashore sign. 
- Pleural effusion: hypoechoic pleural fluid accumulations (> 5–20 mL)
- Pneumothorax: absent lung sliding (e.g., on M-mode) or unilateral loss of B-lines
- Pulmonary fluid overload: bilateral diffuse B-lines (> 3 B-lines visible within an intercostal space are suggestive of interstitial edema)
- Consolidations in pneumonia: hyperechoic and irregular lung tissue 
Monitoring parameters can be used as treatment targets and should be tailored to the patient.
|Monitoring parameters for patients with shock |
|Base deficit (BD)|
|SvO2 and ScvO2 || |
Central venous pressure (CVP) 
|Cardiac function || |
Invasive hemodynamic monitoring: typically reserved for patients with severe shock
- Most patients: urinary catheter to assess urine output
- Patients requiring vasopressors 
- Select patients with refractory shock, RV dysfunction, or high risk of pulmonary edema with uncertain fluid status: pulmonary artery catheterization 
- Protocolized resuscitation targets: e.g., consider or (EGDT) in sepsis.
IV fluid resuscitation 
Clearly apparent hypovolemia: Aggressively replace volume deficit. 
- IV fluid bolus over 10–30 minutes (using glucose-free )
- blood products). : Prioritize as soon as it is available (replace blood losses with
- Uncertain hypovolemia or high-risk patients: includes patients with or 
- Continue with volume titration; further fluid challenges can be performed.
- Proceed with other according to the patient's needs.
- Indications: treatment of various shock states in an effort to restore adequate arterial pressure and organ perfusion
- Available agents
- Adjust infusion according to .
- Titrate down as soon as possible until the patient is weaned.
- Corticosteroids (e.g., hydrocortisone ): not routinely recommended 
- If circulatory collapse is imminent, consider specialist consultation for mechanical circulatory support: e.g., ECMO, IABP, LVAD.
- See also “Management of unstable tachycardia with a pulse” and “Unstable bradycardia.”
- Most vasopressors have inotropic and vasoconstricting effects, i.e., they are inoconstrictor drugs.
- Some are pure vasoconstrictor drugs.
- All have varying degrees of dose-dependent chronotropic effects.
- At higher dosages (e.g., norepinephrine > 0.5 mcg/kg/minute), all can cause harm.
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.
- Mechanism of action
Inoconstrictor drugs 
Continuous IV infusion dosages
|Dopamine || |
|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|
- Mechanism of action: ↑ SVR without either significant ↑ cardiac contractility or ↑ HR
|Pure vasoconstrictor drugs|
Continuous IV infusion dosages
|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
Continuous IV infusion dosages
|Milrinone|| || |
|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|
- Nonhemorrhagic fluid loss
Blood products: Transfuse as soon as possible.
- Ensure adequate vascular access and equipment (e.g., tubing) for blood products.
- Consider emergency transfusion of uncrossmatched blood type O rhesus negative units.
- Switch to crossmatched blood transfusions as soon as available.
- If is expected : Consider transfusing packed RBC, FFP, and platelet concentrate in a 1:1:1 ratio. 
- Consider the use of specialized infusers that allow for rapid administration of warmed blood.
: should be prioritized
- Begin immediate bedside measures: e.g., applying pressure, suturing, or stapling open wounds.
- Consult specialist based on underlying etiology and risk stratification: e.g., surgery, gastroenterology, OB-GYN, interventional radiology.
- Ensure definitive care: See “,” ” ,” “Abnormal uterine bleeding,” “Antepartum hemorrhage,” and “Postpartum hemorrhage.”
- Additional steps to consider
|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|
Uncrossmatched RBC type O negative units can be transfused if the hemorrhage is severe.
Nonhemorrhagic hypovolemic shock
- Treatment of the underlying etiology to stop fluid losses, including:
- Supportive care: e.g., treating any concomitant electrolyte abnormalities (e.g., hyponatremia, hypokalemia)
Next steps (once hemodynamically stable)
- Continue with as needed.
- Attempt .
- Myocardial infarction (MI): most common cause
- Heart failure
- Ventricular septal defect, ventricular rupture
- Valve defects: severe aortic or mitral regurgitation
- Blunt cardiac trauma
- Certain drugs (e.g., beta blockers, calcium channel blockers)
- Underlying event causes dysfunction of the heart → ↓ cardiac contractility and/or SV → ↓ CO
- Systemic circulation: ↓ CO and ↓ BP → ↑ catecholamines → vasoconstriction and ↑ myocardial oxygen demand → ↑ renin-angiotensin-aldosterone system → further ↑ vasoconstriction and retention of sodium and water → shunting of blood to the brain and vital organs → insufficient perfusion of peripheral organs
- Pulmonary circulation: ↓ cardiac contractility and/or ↓ SV → ↑ pulmonary hydrostatic pressure → pulmonary edema
Management approach 
- Determine the type of cardiogenic shock according to the .
- No evidence of congestion (“dry and cold”)
- Evidence of congestion (“wet and cold”)
- Tailor initial treatment according to type.
- Provide supportive care.
- Treat the underlying cause (e.g., revascularization in MI).
- See also “ .”
|Management of cardiogenic shock |
|Classification||Treatment (see “Vasopressors and inotropes” for dosages)|
|Dry and cold|| |
|Wet and cold|
- ↓ Diastolic filling
- ↓ Venous return
- ↑ Ventricular afterload
- Common mechanism: obstruction of the heart or its great vessels → inability of the heart to circulate blood → ↓ CO → compensatory ↑ SVR
- Pulmonary embolism or severe PAH
- Tension pneumothorax
- Cardiac tamponade
- Provide immediate hemodynamic support.
- Treatment based on the underlying cause, including:
- Septic shock
- Anaphylactic shock
- Neurogenic shock
- Acute adrenal insufficiency
- Common mechanism: vasodilation with or without capillary leakage → redistribution of fluid from the intravascular to the extravascular compartment
- Specific mechanisms
- Effect on cardiac output
- Specific mechanism: damage of autonomic pathways → loss of sympathetic vascular tone → unopposed vagal tone → peripheral vasodilation → pooling of peripheral blood
- Effect on cardiac output: can last days to weeks after spinal cord injury 
- Specific mechanism: immunologic anaphylaxis (type I hypersensitivity reaction; IgE-mediated) or nonimmunologic anaphylaxis (not IgE-mediated) → degranulation of mast cells → massive histamine release → systemic vasodilation and increased capillary leakage
- Effect on cardiac output
Key treatment components
- Sepsis and both of the following, despite adequate fluid therapy (i.e., normovolemic patients):
- See also “.”
Management of septic shock
- Begin interventions of the sepsis, including: for
- Consider protocolized resuscitation target strategies in addition to standard .
- The threshold for beginning should be low.
- Consider corticosteroids (e.g., hydrocortisone; ) for shock refractory to the first vasopressor.
6–10 L of IV fluids may be necessary during the first 24 hours. 
Protocolized resuscitation target strategies 
There is insufficient evidence to support the use of one target over the others in order to inform decisions about escalating hemodynamic support. 
Lactate-guided fluid resuscitation strategy 
- If the initial lactate level is elevated (> 2 mmol/L), remeasure every 2–4 hours until normalized.
- Treatment target: 20% decrease in serum lactate every 2–4 hours until normal
- Disadvantages 
- Early goal-directed therapy (EGDT) 
- MAP treatment target: ≥ 65 mm Hg
Vasopressors for septic shock 
- Indications: persistent hypotension during or after fluid resuscitation
- Goal: maintain MAP ≥ 65 mm Hg 
- Stepwise escalation (see “Vasopressors and inotropes” for dosages)
- Additional options
Initial management 
- Assess and secure the airway as needed (see “. ”)
- Remove allergen when possible (e.g., stop medication or IV contrast).
- Administer epinephrine IM 1:1,000 as soon as possible and repeat as needed.
- Provide immediate hemodynamic support with fluid resuscitation.
- See also “ ” for further details.
Refractory anaphylactic shock 
- Refractory to repeated IM epinephrine and fluids: Start continuous IV epinephrine infusion 1:1,000,000 (1 mcg/mL).
- Refractory to IV epinephrine infusion
- Classic presentation: hypotension, bradycardia, vasodilation 
- Exclude other reasons for shock (e.g., other injuries).
- Other neurological deficits may be present.
- Vasopressors: commonly required as shock is often refractory to fluids
- Consider atropine; or cardiac pacing to treat bradycardia (see “Unstable bradycardia” for details). 
- Consult a spine surgeon early to evaluate whether the patient is a candidate for urgent spinal decompression.
- Insert a urinary catheter early. 
- Hemodynamic targets should be individualized in consultation with a specialist.
- Monitor for cardiovascular complications (e.g., ACS, stroke).
Supportive care 
- Prevent hypothermia ; monitor temperature frequently and use warm IV fluids or warming devices as needed.
- Patients may have allodynia; careful patient handling and pain management are required.
- Vasovagal responses can be increased and can lead to refractory shock.
- and vascular dysfunction may be present and can complicate management and recovery. 
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. 
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: 
Corticosteroids (e.g., hydrocortisone): for suspected critical illness-related corticosteroid insufficiency (CIRCI) 
- Diagnosis of CIRCI is based on the presence of critical illness plus one of the following :
- See also “ .”
- Bicarbonate (e.g., ) 
- Mechanical circulatory support
- One-Minute Telegram 37-2021-2/3: Vasopressin plus methylprednisolone for cardiac arrest: Can a cocktail save lives?
- One-Minute Telegram 8-2020-2/3: Should a cocktail of vitamin C, thiamine, and hydrocortisone be given to all patients with septic shock?
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