Shock

Etiology and Risk Factors

Shock is classified by the primary hemodynamic failure (Mitrovic, 2019; Norris, 2020; Wood, 2026):

• Hypovolemic: Loss of circulating volume from hemorrhage, gastrointestinal losses, burns, excess urinary losses, or third spacing
• Cardiogenic: Pump failure from myocardial infarction, sustained arrhythmias, acute valve damage, severe heart failure, or cardiomyopathy
• Obstructive: Mechanical obstruction to filling or outflow from massive pulmonary embolism, tension pneumothorax, cardiac tamponade, or aortic dissection
• Distributive: Loss of vascular tone that enlarges the vascular space beyond the circulating volume, including septic, anaphylactic, and neurogenic shock

Epidemiology and Clinical Context

In a large trial of patients in shock, septic shock accounted for more than 60% of cases, with cardiogenic and hypovolemic shock at about 16% each and obstructive shock at about 2%. Hemorrhage from trauma is a major cause of death worldwide, and mortality in cardiogenic shock approaches 50% (Wood, 2026). Septic shock is the most common cause of death in U.S. intensive care units (Mitrovic, 2019). See Sepsis and Septic Shock for sepsis definitions and management.

Pathophysiology

Oxygen delivery depends on cardiac output and arterial oxygen content, and blood pressure depends on cardiac output and systemic vascular resistance. Each type of shock disrupts a different part of this system (Mitrovic, 2019; Wood, 2026):

• Hypovolemic shock: Loss of preload lowers stroke volume and cardiac output. Systemic vascular resistance rises in compensation, and central venous pressure is low.
• Cardiogenic shock: Loss of contractility lowers stroke volume while blood backs up, raising filling pressures and causing pulmonary congestion.
• Obstructive shock: Mechanical obstruction prevents filling or outflow, lowering cardiac output while right-sided pressures rise.
• Distributive shock: Vasodilation lowers systemic vascular resistance and enlarges the vascular space so a normal blood volume no longer fills it.

Compensated Shock

Falling pressure reduces baroreceptor firing and triggers sympathetic discharge within seconds. Heart rate and contractility increase, arterioles constrict in the skin, muscle, kidneys, and gut, and venoconstriction mobilizes stored blood, while flow to the brain and heart is preserved. Angiotensin II, aldosterone, and antidiuretic hormone conserve sodium and water, and falling capillary pressure draws interstitial fluid into the vessels (Mitrovic, 2019; Norris, 2020).

These responses can maintain blood pressure through a substantial loss. Symptoms of hypovolemic shock begin in adults after a loss of about 1500 to 2000 mL, roughly 30% to 40% of blood volume, and cardiac output and tissue perfusion fall before hypotension appears (Norris, 2020; Wood, 2026).

Progressive Shock

As compensation fails and tissue perfusion falls, shock enters a progressive stage. Cells shift to anaerobic glycolysis, producing little adenosine triphosphate (ATP) and large amounts of lactate. Failure of the sodium-potassium pump causes cellular swelling, lysosomal enzymes are released, and cell death releases inflammatory mediators and oxygen free radicals that extend the injury (Norris, 2020). Lactic acidosis depresses the myocardium and reduces vascular responsiveness to catecholamines (Mitrovic, 2019). Sustained vasoconstriction that initially preserved pressure deepens tissue ischemia (Norris, 2020).

Refractory Shock

With prolonged shock, precapillary sphincters relax while postcapillary venules remain constricted, so blood pools in capillaries. Cerebral ischemia depresses vasomotor output, and reduced coronary flow weakens the heart, creating feedback loops in which low pressure worsens perfusion and poor perfusion lowers pressure further (Mitrovic, 2019).

Distributive Mechanisms

• Septic shock: Cytokines such as tumor necrosis factor and interleukin-1, nitric oxide-mediated vasodilation, endothelial injury with capillary leak, and activation of coagulation with depletion of natural anticoagulants. Myocardial depression can add a cardiogenic component (Mitrovic, 2019; Norris, 2020).
• Anaphylactic shock: Histamine and other mediators cause vasodilation and increased capillary permeability (Norris, 2020).
• Neurogenic shock: Loss of sympathetic vasomotor tone from brain or spinal cord injury, anesthesia, or drugs causes vasodilation and venous pooling (Mitrovic, 2019; Norris, 2020).

Clinical Manifestations

Common manifestations include (Norris, 2020; Wood, 2026):

• Tachycardia
• Tachypnea
• Thirst
• Restlessness, anxiety, or agitation progressing to confusion and coma
• Narrow pulse pressure
• Cool, pale, clammy, or mottled skin
• Oliguria, with urine output of 20 mL/h or less signaling inadequate renal perfusion
• Hypotension, often late
• Metabolic acidosis and rising lactate

Type-specific findings include:

• Hemorrhagic shock: Pallor and signs of the bleeding source. Bleeding into an injured thigh can hide about a liter of blood (Mitrovic, 2019).
• Cardiogenic shock: Pulmonary congestion and edema, elevated filling pressures, and sometimes cyanosis (Mitrovic, 2019; Norris, 2020).
• Obstructive shock: Elevated central venous pressure and jugular venous distention. Cardiac tamponade can produce pulsus paradoxus, an inspiratory fall in systolic pressure of 10 mm Hg or more (Mitrovic, 2019; Norris, 2020).
• Septic shock: Fever, often warm and flushed skin early, low systemic vascular resistance, and abrupt changes in cognition or behavior (Norris, 2020).
• Anaphylactic shock: Urticaria, angioedema, laryngeal edema, bronchospasm, and abdominal cramping (Norris, 2020).
• Neurogenic shock: Hypotension with bradycardia and warm, dry skin (Norris, 2020).

Diagnostic Evaluation

Immediate Stability Assessment

Assess airway, breathing, circulation, mental status, skin perfusion, and urine output at the same time resuscitation begins. The diagnosis is clinical and is supported by arterial hypotension, signs of tissue hypoperfusion, and hyperlactatemia (Wood, 2026).

Laboratory Testing

Initial testing includes (Wood, 2026):

• Complete blood count
• Electrolytes and renal function
• Liver function tests
• Prothrombin time, international normalized ratio, and activated partial thromboplastin time
• Serum lactate
• Arterial blood gas
• Troponin when acute coronary syndrome is suspected
• Blood cultures from at least two sites before antibiotics when sepsis is possible (Norris, 2020)

Identifying the Type

History and examination findings, including skin temperature, neck veins, heart sounds, and lung examination, help identify the type of shock. Continuous electrocardiographic monitoring, echocardiography, and invasive measurement of filling pressures and cardiac output may be needed (Norris, 2020; Wood, 2026).

Expected Findings

Findings that support each type include (Mitrovic, 2019; Norris, 2020; Wood, 2026):

• Hypovolemic: Low central venous pressure, high systemic vascular resistance, cool skin, and, in hemorrhage, falling hemoglobin after fluid shifts
• Cardiogenic: High filling pressures, low cardiac output, high systemic vascular resistance, and pulmonary congestion
• Obstructive: High right-sided pressures, jugular venous distention, and low cardiac output
• Distributive: Low systemic vascular resistance, often warm skin early, and bradycardia in neurogenic shock
• All types: Rising lactate, metabolic acidosis, oliguria, and evidence of organ dysfunction

Differential Diagnosis

Among the Types of Shock

The four types can coexist. Septic shock can include hypovolemia from capillary leak and myocardial depression, and any prolonged shock can become cardiogenic as coronary perfusion falls (Mitrovic, 2019; Norris, 2020).

Vasovagal and Postural Syncope

Transient loss of consciousness from reflex bradycardia and vasodilation or from orthostatic pooling usually resolves promptly when the patient lies flat. It must still be distinguished from cardiac syncope and other serious causes (Mitrovic, 2019).

Medication-Related Hypotension

Drugs that block sympathetic activity or dilate vessels can cause hypotension, particularly on standing, without the progressive hypoperfusion of shock (Mitrovic, 2019; Norris, 2020).

Findings That Reduce Diagnostic Probability

Few findings exclude shock by themselves. The following findings should lower its position in the differential or prompt evaluation for an alternative:

• Normal mentation, warm well-perfused skin, adequate urine output, and a normal lactate make significant shock less likely, even with a low blood pressure reading (Norris, 2020; Wood, 2026).
• Prompt recovery of consciousness and blood pressure after lying flat favors postural or vasovagal syncope (Mitrovic, 2019).
• Warm skin with bradycardia after spinal cord injury favors neurogenic shock over hypovolemic shock (Norris, 2020).

Treatment and Management

All forms of shock share early priorities: secure the airway and oxygenation, restore perfusion, and correct the cause. Common resuscitation goals include a mean arterial pressure above 60 to 65 mm Hg, heart rate below 100, urine output above 0.5 mL/kg/h, and normalization of lactate and mental status (Wood, 2026).

Hypovolemic Shock

Management includes (Wood, 2026):

• Control the source of loss.
• Isotonic crystalloids are first-line for all hypovolemic shock.
• Blood products are reserved for hemorrhage, severe anemia, or coagulopathy.
• In traumatic hemorrhage, damage control resuscitation limits crystalloid, gives red cells, plasma, and platelets in roughly equal ratios, and accepts permissive hypotension until bleeding is controlled.
• Vasopressors are added only when fluids alone have not restored mean arterial pressure and perfusion.

Cardiogenic Shock

Management includes (Norris, 2020; Wood, 2026):

• Restore coronary flow with percutaneous coronary intervention, fibrinolysis, or bypass surgery when myocardial infarction is the cause.
• Dobutamine is the standard inotrope.
• Norepinephrine may be added for hypotension, recognizing that increased afterload can lower cardiac output.
• Titrate fluids carefully to filling pressures.
• Mechanical support such as an intra-aortic balloon pump can augment coronary perfusion and reduce afterload.

Obstructive Shock

Remove the obstruction: pericardiocentesis for cardiac tamponade, chest tube insertion for tension pneumothorax, and thrombolysis or embolectomy for massive pulmonary embolism (Huynh et al., 2026; Norris, 2020). See Pulmonary Embolism.

Septic Shock

Begin resuscitation immediately with at least 30 mL/kg of crystalloid within the first 3 hours, obtain cultures, and start empiric broad-spectrum antibiotics without delay. Norepinephrine is the first-line vasopressor to maintain a mean arterial pressure of 65 mm Hg, vasopressin can be added for refractory shock, and dopamine is not used routinely (Branan & Smith, 2026). See Sepsis and Septic Shock.

Anaphylactic Shock

Give epinephrine, which constricts blood vessels and relaxes bronchial smooth muscle. Remove the trigger, keep the patient supine, and add oxygen, antihistamines, and corticosteroids (Norris, 2020).

After Resuscitation

Many patients accumulate excess fluid during resuscitation, which can impair organ function. Deresuscitation, through reducing or stopping fluid administration, diuresis, or renal replacement therapy, is increasingly recognized as part of recovery (Wood, 2026).

Complications and Red Flags

Urgent escalation is required for:

• Persistent hypotension, rising lactate, or worsening metabolic acidosis despite resuscitation
• Declining mental status or urine output below 0.5 mL/kg/h
• New arrhythmia, chest pain, hypoxemia, or increasing oxygen requirement
• Bleeding, falling platelet count, or prolonged clotting times
• Jugular venous distention with hypotension

Complications include acute respiratory distress syndrome, acute kidney injury, gastrointestinal ulceration, disseminated intravascular coagulation, and multiple organ dysfunction syndrome (Norris, 2020).

Clinical Reasoning Priorities

Mentation, skin perfusion, urine output, and lactate should guide both recognition and reassessment, because compensation can hold blood pressure near normal until late in the course (Norris, 2020; Wood, 2026). The type of shock should be identified early because fluids, inotropes, vasopressors, and procedures help different forms of shock, and an intervention suited to one type can worsen another; vasopressors in uncorrected hypovolemia and liberal fluids in cardiogenic shock are examples (Norris, 2020; Wood, 2026).

---

---

References

Branan, T. N., & Smith, S. E. (2026). Sepsis and septic shock. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed.). McGraw Hill.

Huynh, N. S., Cantrell, M., & Lee, J. C. (2026). Venous thromboembolism. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed.). McGraw Hill.

Mitrovic, I. (2019). Cardiovascular disorders: Vascular disease. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed.). McGraw-Hill Education.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Wood, G. C. (2026). Circulatory shock syndromes. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed.). McGraw Hill.