Shock

Topic Overview

Summary

Shock is a life-threatening syndrome of acute circulatory failure resulting in inadequate cellular oxygen delivery and tissue hypoperfusion. It represents a final common pathway of critical illness characterized by the inability of the cardiovascular system to maintain adequate tissue perfusion to meet metabolic demands.[1] The condition progresses through compensated and decompensated phases, ultimately leading to irreversible cellular injury and multi-organ failure if untreated.[2]

Shock is classified into four primary mechanisms: hypovolaemic (inadequate circulating volume), cardiogenic (primary pump failure), distributive (pathological vasodilation), and obstructive (mechanical impediment to circulation).[3] Each type has distinct haemodynamic profiles, but all share the common endpoint of tissue hypoxia and metabolic acidosis.

Early recognition through clinical assessment (hypotension, tachycardia, altered consciousness, oliguria) combined with biomarker measurement (lactate elevation) is critical for survival.[4] Management requires simultaneous resuscitation and identification of the underlying cause. The cornerstone of treatment includes fluid resuscitation (except in cardiogenic shock), vasopressor support when required, and definitive treatment of the precipitating condition.[5]

Mortality remains high despite advances in critical care, ranging from 20% in hypovolaemic shock to 40-60% in cardiogenic and septic shock, emphasizing the importance of early goal-directed therapy.[6]

Key Facts

• Definition: Acute circulatory failure causing inadequate cellular oxygen delivery and tissue hypoperfusion
• Classification: Four main types—hypovolaemic, cardiogenic, distributive (including septic), and obstructive
• Pathophysiology: Tissue hypoxia → anaerobic metabolism → lactic acidosis → cellular dysfunction → organ failure
• Key diagnostic markers: Hypotension (SBP less than 90 mmHg or MAP less than 65 mmHg), elevated lactate (> 2 mmol/L), oliguria, altered consciousness
• Haemodynamic monitoring: Trends in blood pressure, heart rate, urine output, and lactate clearance guide resuscitation
• Treatment priorities: Airway, breathing, circulation (ABCDE), fluid resuscitation (most types), vasopressors (if fluid-refractory), treat underlying cause
• Septic shock specificity: Most common form in hospitalized patients; requires early antibiotics (within 1 hour) and source control[7]
• Cardiogenic exception: Fluid restriction often required; excessive fluids worsen pulmonary oedema
• Lactate clearance: Serial lactate measurements predict outcomes; failure to clear lactate indicates inadequate resuscitation[8]
• Mortality: Type-dependent: hypovolaemic 10-30%, cardiogenic 40-60%, septic 30-50%, with MODS conferring worst prognosis[6]

Clinical Pearls

Lactate trends matter more than absolute values: Rising or persistently elevated lactate despite resuscitation indicates ongoing tissue hypoxia and poor prognosis. Target ≥10% reduction per hour during early resuscitation.[8]

Skin examination differentiates shock types: Cold, clammy, vasoconstricted peripheries suggest hypovolaemic or cardiogenic shock (high SVR response); warm, flushed, bounding pulses suggest early distributive shock (low SVR). Late shock of any type presents with cold, mottled skin.[3]

Septic shock is the most common shock in hospitalized patients: Represents 60-70% of ICU shock cases. Any unexplained hypotension with suspected infection should trigger sepsis protocol and early antibiotics.[7]

MAP targets individualized: Standard MAP ≥65 mmHg is initial goal, but patients with chronic hypertension may require higher targets (70-80 mmHg) for adequate organ perfusion, while lower targets may be acceptable in younger patients without comorbidities.[9]

Cardiogenic shock paradox: Despite low cardiac output, aggressive fluid resuscitation worsens outcomes by increasing pulmonary oedema and afterload. Small fluid challenges (250 mL) with close monitoring of respiratory status and JVP are safer.[10]

Obstructive shock mimics cardiogenic: Elevated JVP with hypotension suggests obstructive (tamponade, massive PE, tension pneumothorax) or cardiogenic shock. Bedside echocardiography differentiates—look for RV strain (PE), pericardial effusion (tamponade), or LV dysfunction (cardiogenic).[11]

Early vasopressors may be lifesaving: In profound shock (MAP less than 50 mmHg), initiate vasopressors early (even peripherally if necessary) while establishing central access, rather than delaying for fluid resuscitation alone. Severe hypotension causes critical hypoperfusion of brain and coronary arteries.[12]

Hypotension is a late sign: Compensatory mechanisms (tachycardia, vasoconstriction) maintain blood pressure until 30-40% blood volume loss in hypovolaemic shock. Normal blood pressure does not exclude shock—look for tachycardia, narrow pulse pressure, reduced capillary refill, and oliguria.[13]

Why This Matters Clinically

Shock is a time-critical emergency where minutes determine survival and neurological outcome. The brain tolerates only 4-6 minutes of profound hypoperfusion before irreversible injury occurs. Delayed recognition or inadequate resuscitation leads to a cascade of organ failure (kidneys within hours, liver and lungs within days) with exponentially increasing mortality.[2]

The "golden hour" concept in trauma applies equally to all shock: early, aggressive resuscitation within the first hour significantly improves survival.[4] Septic shock mortality increases by 7.6% for every hour delay in antibiotic administration.[14] Cardiogenic shock mortality drops from > 80% to 40-50% with early revascularization for acute MI.[10]

Understanding shock classification allows targeted therapy: fluids for hypovolaemia, vasopressors for distributive, inotropes for cardiogenic, and procedural intervention for obstructive. Misclassification leads to harmful treatment—fluid overload in cardiogenic shock worsens pulmonary oedema; inadequate fluids in hypovolaemic shock prolongs hypoperfusion.[3]

Shock is also a marker of disease severity across all specialties: the patient in septic shock requires ICU-level care regardless of the source; the post-MI patient in cardiogenic shock needs urgent catheterization; the trauma patient in haemorrhagic shock needs damage control surgery. Recognition triggers appropriate escalation and resource mobilization.[15]

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Visual Summary

Visual assets to be added:

• Four types of shock comparison table with haemodynamic profiles
• Shock recognition and classification algorithm
• ABCDE approach to shock management flowchart
• Lactate clearance targets and prognostic implications
• Vasopressor and inotrope selection guide
• Fluid responsiveness assessment diagram
• Surviving Sepsis Campaign Hour-1 Bundle visual
• Cardiogenic shock mechanical support options

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Epidemiology

Incidence and Prevalence

Shock is encountered across all healthcare settings but is most prevalent in critical care environments. Approximately 30% of ICU admissions involve shock as the primary or contributing diagnosis.[1] In emergency departments, shock accounts for 1-3% of all presentations but contributes disproportionately to morbidity and mortality.[15]

The incidence varies by type and clinical setting:

Septic Shock: Most common form in hospitalized patients, accounting for 60-70% of ICU shock cases.[7] Incidence is rising globally, estimated at 270 cases per 100,000 person-years in developed countries, with increasing prevalence due to aging populations, immunosuppression, and antimicrobial resistance.[16]

Cardiogenic Shock: Complicates 5-10% of acute myocardial infarctions, though incidence has decreased with modern reperfusion strategies.[10] Represents 15-20% of ICU shock cases. Non-ischaemic causes (acute decompensated heart failure, myocarditis, arrhythmias) account for 20-30% of cardiogenic shock.[17]

Hypovolaemic Shock: Accounts for 10-15% of ICU shock cases.[3] Trauma-related haemorrhagic shock is most common in younger populations and varies by geographic region and injury patterns. Non-haemorrhagic hypovolaemia (dehydration, gastrointestinal losses) is more common in elderly and pediatric populations.

Obstructive Shock: Least common (2-5% of ICU shock cases) but often immediately life-threatening.[3] Massive pulmonary embolism causes shock in 5-10% of PE cases; cardiac tamponade is rare outside of trauma, cardiothoracic surgery, and malignancy; tension pneumothorax is primarily trauma-related but occurs iatrogenically in mechanically ventilated patients.

Demographics and Risk Factors

Age: All ages are affected, but elderly patients (> 65 years) have higher incidence across all shock types and significantly elevated mortality (2-3 times higher than younger patients).[6] Neonates and infants are particularly vulnerable to hypovolaemic shock due to limited physiological reserve.

Sex: Septic shock has slight male predominance (55-60% male), likely reflecting higher rates of pneumonia and intra-abdominal infections in men.[16] Cardiogenic shock mirrors the male predominance of acute MI in younger age groups but equalizes after menopause.

Comorbidities: Chronic conditions dramatically increase shock risk and mortality:

• Diabetes mellitus: 2-fold increase in septic shock risk; impaired immune function and microvascular disease worsen outcomes
• Chronic kidney disease: Reduced reserve for hypoperfusion; shock-induced AKI more likely to require dialysis
• Immunosuppression: Chemotherapy, HIV, chronic steroids increase septic shock risk 3-5 fold
• Heart failure: Baseline low cardiac output predisposes to cardiogenic shock with any additional stressor
• Cirrhosis: Baseline vasodilatory state predisposes to distributive shock; hepatorenal syndrome complicates shock resuscitation

Healthcare-associated factors: Invasive devices (central lines, urinary catheters, mechanical ventilation) increase nosocomial infection and septic shock risk. Recent surgery predisposes to bleeding (hypovolaemic), infection (septic), and PE (obstructive shock).

Geographic and Temporal Variation

Septic shock incidence is higher in developed countries due to aging populations and aggressive medical interventions, but mortality is lower (30-40%) compared to resource-limited settings (50-70%) where access to ICU care, antibiotics, and vasopressors is restricted.[16]

Trauma-related haemorrhagic shock varies by region: higher in areas with armed conflict, limited traffic safety measures, or inadequate trauma systems. Seasonal variation occurs in some shock types: septic shock from community-acquired pneumonia peaks in winter; heat-related hypovolaemia increases in summer months.

Outcomes and Burden

Despite advances in critical care, shock mortality remains high:

• Septic shock: 30-50% mortality, higher with multi-drug resistant organisms or delayed treatment[7]
• Cardiogenic shock: 40-60% mortality, improved from > 80% pre-mechanical circulatory support era[10]
• Hypovolaemic shock: 10-30% mortality, heavily dependent on etiology and time to control (trauma less than 10% with rapid surgery; massive GI bleeding 20-40%)[13]
• Obstructive shock: Variable—tension pneumothorax less than 5% if recognized early; massive PE 30-50%; tamponade 10-20% with pericardiocentesis

Multi-organ dysfunction syndrome (MODS) develops in 30-50% of shock patients and confers 60-80% mortality when three or more organ systems fail.[2]

Survivors face significant morbidity: chronic critical illness (prolonged ventilation, delirium), post-intensive care syndrome (PICS) with physical disability, cognitive impairment, and psychiatric disorders (PTSD, depression), and chronic organ dysfunction (CKD, restrictive lung disease).

Economic burden is substantial: ICU care for shock averages £2,000-4,000 per day (NHS) or $5,000-10,000 per day (US), with mean ICU length of stay 7-14 days for survivors. Long-term disability reduces quality-adjusted life-years (QALYs) and workforce participation.[15]

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Pathophysiology

Fundamental Concepts

Shock represents the final common pathway of acute circulatory failure where oxygen delivery (DO₂) is insufficient to meet cellular metabolic oxygen consumption (VO₂). Under normal conditions, DO₂ exceeds VO₂ by 3-4 fold, providing substantial physiological reserve. Shock occurs when this balance is disrupted.[1]

Oxygen delivery is determined by three factors:

DO₂ = Cardiac Output × Arterial Oxygen Content
DO₂ = (HR × SV) × (Hb × 1.34 × SaO₂ + 0.003 × PaO₂)

Where:

• HR = heart rate
• SV = stroke volume (preload × contractility / afterload)
• Hb = haemoglobin concentration
• SaO₂ = arterial oxygen saturation

Therefore, shock can result from:

1. Reduced cardiac output (cardiogenic, hypovolaemic, obstructive)
2. Impaired oxygen-carrying capacity (anaemia, carbon monoxide poisoning—distributive)
3. Maldistribution of blood flow (distributive shock—blood bypasses capillary beds)
4. Rarely, increased metabolic demands exceeding supply (thyroid storm, malignant hyperthermia)

The Shock Cascade: From Hypoperfusion to Cell Death

Stage 1: Initial Insult and Compensatory Response

The precipitating event (haemorrhage, myocardial infarction, sepsis, etc.) reduces effective circulating volume, cardiac output, or vascular tone. Baroreceptors in the carotid sinus and aortic arch detect reduced pressure and trigger immediate compensatory mechanisms:[2]

Neuroendocrine activation:

• Sympathetic nervous system: Catecholamine release (adrenaline, noradrenaline) increases heart rate, contractility, and vasoconstriction
• Renin-angiotensin-aldosterone system (RAAS): Angiotensin II causes vasoconstriction and aldosterone-mediated sodium retention
• Vasopressin (ADH): Potent vasoconstriction and water retention
• Cortisol: Stress response, permissive for catecholamine action

Cardiovascular compensation:

• Tachycardia: Maintains cardiac output despite reduced stroke volume
• Increased contractility: Augments stroke volume
• Peripheral vasoconstriction: Redistributes blood from skin, splanchnic, and renal beds to preserve brain and heart perfusion
• Venoconstriction: Increases venous return and preload

Respiratory compensation:

• Tachypnoea: Compensates for metabolic acidosis (respiratory alkalosis)
• Increased minute ventilation: Enhances oxygen uptake

This compensated shock phase can maintain blood pressure and vital organ perfusion despite 25-30% reduction in circulating volume (hypovolaemic) or significant cardiac impairment. However, this comes at the cost of hypoperfusion to "non-essential" organs (kidneys, gut, skeletal muscle), setting the stage for subsequent organ dysfunction.[13]

Stage 2: Decompensation and Cellular Hypoxia

As shock progresses, compensatory mechanisms are overwhelmed. Blood pressure drops, and perfusion pressure to vital organs becomes critically reduced. Cellular hypoxia ensues when oxygen delivery falls below the critical threshold.[2]

Cellular metabolic crisis:

• Aerobic metabolism failure: Mitochondria cannot sustain ATP production via oxidative phosphorylation
• Anaerobic glycolysis: Cells switch to inefficient anaerobic pathways, producing only 2 ATP per glucose (vs. 36 ATP aerobic)
• Lactate accumulation: Pyruvate is converted to lactate in the absence of oxygen, causing metabolic acidosis
• ATP depletion: Cellular energy stores deplete, impairing all ATP-dependent functions

Cellular dysfunction cascade:

• Na⁺/K⁺-ATPase failure: Loss of membrane potential, cellular swelling, and necrosis
• Ca²⁺ dysregulation: Intracellular calcium overload activates proteases, lipases, and endonucleases
• Mitochondrial injury: Opening of mitochondrial permeability transition pore (MPTP) triggers apoptosis
• Oxidative stress: Reactive oxygen species (ROS) production damages membranes, proteins, and DNA
• Inflammatory activation: Damaged cells release damage-associated molecular patterns (DAMPs) triggering systemic inflammation

Stage 3: Systemic Inflammatory Response and Organ Failure

Tissue hypoxia and cellular injury trigger a profound systemic inflammatory response syndrome (SIRS), mediated by cytokines (TNF-α, IL-1, IL-6), complement activation, and leukocyte-endothelial interactions.[2]

Microcirculatory dysfunction:

• Endothelial injury increases capillary permeability (third-spacing of fluids)
• Microthrombosis from disseminated intravascular coagulation (DIC)
• Loss of autoregulation in cerebral, renal, and splanchnic beds
• No-reflow phenomenon: Capillary obstruction by swollen endothelium and activated leukocytes

Organ-specific failure mechanisms:

Multi-organ dysfunction syndrome (MODS) develops when two or more organ systems fail, creating a vicious cycle where each failing organ worsens others (e.g., renal failure causes volume overload worsening pulmonary oedema; hepatic failure impairs lactate clearance worsening acidosis).[2]

Stage 4: Irreversible Shock

Beyond a critical threshold, shock becomes irreversible despite correction of the precipitating cause and aggressive resuscitation. Cellular injury is too extensive, inflammatory cascades are self-perpetuating, and microvascular thrombosis prevents perfusion restoration. Mitochondrial dysfunction becomes permanent, and cellular apoptosis progresses unchecked. Death is inevitable from refractory cardiovascular collapse or MODS.[1]

Type-Specific Pathophysiology

Hypovolaemic Shock

Mechanism: Reduced circulating volume decreases venous return (preload), leading to reduced stroke volume and cardiac output.[13]

Etiologies:

• Haemorrhagic: Trauma, GI bleeding, ruptured AAA, ruptured ectopic pregnancy, postpartum haemorrhage
• Non-haemorrhagic: Vomiting/diarrhoea, burns (plasma loss), third-spacing (pancreatitis, bowel obstruction), osmotic diuresis (DKA, HHS)

Haemodynamic profile:

• Cardiac output: ↓↓
• Systemic vascular resistance (SVR): ↑↑ (compensatory vasoconstriction)
• Central venous pressure (CVP): ↓ (empty right atrium)
• Pulmonary capillary wedge pressure (PCWP): ↓ (empty left atrium)

Compensatory classification (haemorrhagic shock):

Note: Compensatory mechanisms maintain blood pressure until Class III (30% loss), emphasizing that "normal BP" does not exclude significant hypovolaemia.[13]

Cardiogenic Shock

Mechanism: Primary myocardial dysfunction reduces cardiac output despite adequate preload.[10]

Etiologies:

• Ischaemic: Acute MI (large territory, mechanical complications—VSD, acute MR, free wall rupture), post-cardiac arrest
• Non-ischaemic: Acute decompensated heart failure, myocarditis, dilated cardiomyopathy, stress cardiomyopathy (Takotsubo)
• Arrhythmic: Sustained VT/VF, profound bradycardia, atrial fibrillation with rapid ventricular response
• Valvular: Acute severe MR/AR, prosthetic valve thrombosis
• Other: Myocardial contusion (trauma), cardiomyopathy (peripartum, chemotherapy-induced)

Haemodynamic profile:

• Cardiac output: ↓↓
• SVR: ↑↑ (compensatory)
• CVP: ↑ (RV failure or biventricular failure)
• PCWP: ↑↑ (LV failure, pulmonary oedema)
• Cardiac index: less than 2.2 L/min/m²
• PCWP: > 18 mmHg

Vicious cycle: Low cardiac output → hypotension → reduced coronary perfusion pressure → worsening myocardial ischaemia → further reduction in contractility → worsening shock.[17]

Pulmonary oedema: Elevated LV end-diastolic pressure (LVEDP) transmits backward to pulmonary capillaries. When capillary hydrostatic pressure exceeds oncotic pressure (> 25 mmHg), fluid extravasates into alveoli, impairing gas exchange.

Distributive Shock

Mechanism: Pathological vasodilation reduces systemic vascular resistance (SVR), causing relative hypovolaemia despite normal or increased cardiac output.[3] Microvascular dysfunction causes maldistribution—blood bypasses capillary beds, reducing oxygen extraction despite adequate macrocirculatory flow.

Septic Shock (Most Common Distributive Shock)

Pathogen-host interaction:[7]

1. Infection: Bacteria, fungi, viruses release pathogen-associated molecular patterns (PAMPs—endotoxin, lipopolysaccharide)
2. Immune activation: Toll-like receptors (TLRs) on macrophages and endothelium trigger massive cytokine release (TNF-α, IL-1β, IL-6)
3. Endothelial dysfunction: Nitric oxide (NO) overproduction causes profound vasodilation; capillary leak from endothelial glycocalyx degradation
4. Microvascular thrombosis: Procoagulant state with platelet activation and microthrombi formation
5. Mitochondrial dysfunction: Direct pathogen toxins and inflammatory mediators impair cellular oxygen utilization (cytopathic hypoxia—oxygen present but not used)

Haemodynamic profile (early/warm shock):

• Cardiac output: ↑ or normal (hyperdynamic)
• SVR: ↓↓ (vasodilation)
• CVP: ↓ or normal
• Mixed venous oxygen saturation (SvO₂): ↑ (oxygen delivery exceeds extraction due to shunting)

Late/cold septic shock: Myocardial depression from inflammatory mediators, acidosis, and hypoperfusion reduces cardiac output. Haemodynamics resemble cardiogenic shock despite preserved ejection fraction ("septic cardiomyopathy").[16]

Anaphylactic Shock

Mechanism: Type I hypersensitivity reaction. IgE-mediated mast cell and basophil degranulation releases histamine, leukotrienes, and tryptase, causing:

• Massive vasodilation (histamine on H1/H2 receptors)
• Increased capillary permeability (third-spacing)
• Bronchospasm
• Cardiac depression (direct histamine effect on myocardium)

Triggers: Foods (peanuts, shellfish), medications (penicillin, NSAIDs), insect stings, latex.

Neurogenic Shock

Mechanism: Loss of sympathetic tone (spinal cord injury above T6, high spinal anaesthesia) causes:

• Vasodilation (loss of vascular smooth muscle tone)
• Bradycardia (unopposed vagal tone)
• Inability to compensate (fixed heart rate despite hypotension)

Distinguishing feature: Bradycardia with hypotension (all other shock types cause tachycardia).

Obstructive Shock

Mechanism: Mechanical impediment to ventricular filling or ejection reduces cardiac output despite normal myocardial function.[11]

Massive Pulmonary Embolism

• Mechanism: Thrombus obstructs > 50% of pulmonary vasculature → acute RV pressure overload → RV dilation and failure → septal bowing into LV → reduced LV filling → reduced cardiac output
• Haemodynamics: Low CO, high CVP, high RV pressures, normal PCWP (pre-LV obstruction)
• Characteristic: RV strain on echo (D-shaped LV, McConnell's sign), ECG (S1Q3T3, RBBB)

Cardiac Tamponade

• Mechanism: Pericardial fluid accumulation → external compression of all cardiac chambers → impaired ventricular filling → equalization of diastolic pressures → reduced stroke volume
• Haemodynamics: Low CO, elevated and equalized diastolic pressures (CVP ≈ PCWP ≈ PAD), pulsus paradoxus
• Causes: Trauma, malignancy, post-MI free wall rupture, aortic dissection, uraemia, post-cardiac surgery

Tension Pneumothorax

• Mechanism: One-way valve allows air entry into pleural space but not exit → increasing intrapleural pressure → ipsilateral lung collapse → mediastinal shift → compression of contralateral lung and great veins → reduced venous return → reduced cardiac output
• Clinical: Tracheal deviation away, hyperresonant percussion, absent breath sounds ipsilaterally, JVP elevation, hypotension
• Management: Clinical diagnosis—do not wait for CXR. Immediate needle decompression (2nd intercostal space, midclavicular line) followed by chest tube.

Haemodynamic Profiles Summary Table

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Clinical Presentation

General Features Common to All Shock Types

Regardless of etiology, shock manifests with signs of inadequate tissue perfusion:[3]

Haemodynamic instability:

• Hypotension: SBP less than 90 mmHg, or MAP less than 65 mmHg, or SBP drop > 40 mmHg from baseline
• Tachycardia: HR > 100-110 bpm (except neurogenic shock, which may show bradycardia)
• Narrow pulse pressure: Difference between systolic and diastolic less than 25 mmHg (hypovolaemic, cardiogenic)
• Thready, weak pulse

End-organ hypoperfusion markers:

• CNS: Altered mental status (confusion, agitation, obtundation), anxiety, restlessness, eventual loss of consciousness
• Renal: Oliguria (less than 0.5 mL/kg/hr, typically less than 30 mL/hr in 70 kg adult), anuria in severe shock
• Skin: Pallor, cool peripheries, mottled skin (livedo reticularis), delayed capillary refill (> 3 seconds)
• Metabolic: Lactic acidosis (lactate > 2 mmol/L, often > 4 mmol/L in severe shock)

Respiratory distress:

• Tachypnoea (> 20-22 breaths/min): Compensatory response to metabolic acidosis
• Dyspnoea, increased work of breathing
• In late shock: Respiratory failure from ARDS or respiratory muscle fatigue

Type-Specific Clinical Features

Hypovolaemic Shock

History:

• Bleeding: Trauma, GI bleeding (haematemesis, melaena, haematochezia), vaginal bleeding (ectopic pregnancy, PPH)
• Fluid loss: Vomiting, diarrhoea, polyuria (DKA), burns
• Third-spacing: Pancreatitis (retroperitoneal fluid sequestration), bowel obstruction

Examination:

• Dry mucous membranes, reduced skin turgor, sunken eyes (dehydration)
• Collapsed neck veins (flat JVP, even when supine)
• Cold, clammy, pale skin (peripheral vasoconstriction)
• Postural hypotension (in early/compensated shock)

Haemorrhagic shock-specific:

• Obvious external bleeding or signs of concealed haemorrhage (distended abdomen—haemoperitoneum; femoral/flank bruising—retroperitoneal bleed)
• Pale conjunctivae, nail beds

Cardiogenic Shock

History:

• Cardiac chest pain (acute MI)
• Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea (heart failure)
• Palpitations (arrhythmia)
• Cardiac history: Previous MI, known heart failure, recent cardiac surgery

Examination:

• Elevated jugular venous pressure (JVP) despite hypotension (key distinguishing feature from hypovolaemic)
• Pulmonary oedema: Bibasal crackles, pink frothy sputum in severe cases
• S3 gallop rhythm (ventricular dysfunction)
• Displaced apex beat, cardiomegaly
• Cool, clammy peripheries (low cardiac output state)
• Peripheral oedema (chronic heart failure)

Mechanical complications (acute MI):

• New murmur: Acute mitral regurgitation (papillary muscle rupture—high-pitched, apical systolic); VSD (pansystolic, parasternal)
• Pericardial rub (free wall rupture with contained haematoma)

Distributive Shock: Septic Shock

History:

• Infection source: Pneumonia (cough, dyspnoea), UTI (dysuria, frequency), intra-abdominal (abdominal pain), skin/soft tissue (cellulitis, abscess), CNS (meningitis—headache, photophobia)
• Risk factors: Recent surgery, invasive devices (lines, catheters), immunosuppression

Examination:

Early/hyperdynamic ("warm") septic shock:

• Fever (> 38°C) or hypothermia (less than 36°C in severe sepsis)
• Warm, flushed, vasodilated peripheries
• Bounding pulses
• Wide pulse pressure
• Tachycardia, tachypnoea

Late/hypodynamic ("cold") septic shock:

• Cold, mottled peripheries (myocardial depression, peripheral vasoconstriction in late stage)
• Altered consciousness, confusion, agitation
• Oliguria, anuria

Source identification:

• Respiratory: Bronchial breathing, crackles
• Abdominal: Peritonism, guarding, rigidity
• Skin: Cellulitis, purpura (meningococcal), necrotizing fasciitis (crepitus, rapidly spreading erythema, skin necrosis)
• Lines/devices: Erythema, purulence at insertion sites

Distributive Shock: Anaphylactic Shock

History:

• Acute onset (minutes to less than 2 hours) after allergen exposure
• Known allergies or previous reactions
• Common triggers: Foods (peanuts, tree nuts, shellfish, milk, eggs), drugs (penicillin, NSAIDs, contrast media), insect stings (bee, wasp)

Examination:

• Skin: Urticaria (hives), angioedema (lip, tongue, face swelling), flushing, pruritus
• Respiratory: Wheeze, stridor (laryngeal oedema), respiratory distress, cyanosis
• GI: Nausea, vomiting, abdominal cramping, diarrhoea
• Cardiovascular: Tachycardia, hypotension, dizziness, syncope
• Warm peripheries initially, then cold if severe

Severity markers: Stridor, cyanosis, SpO₂ less than 92%, confusion indicate life-threatening anaphylaxis requiring immediate IM adrenaline.

Distributive Shock: Neurogenic Shock

History:

• Spinal cord injury (trauma, spinal surgery)
• High spinal or epidural anaesthesia

Examination:

• Bradycardia with hypotension (pathognomonic—distinguishes from all other shock types)
• Warm, dry skin (loss of sympathetic tone → no vasoconstriction or sweating)
• Flaccid paralysis, loss of reflexes below level of injury (spinal shock)
• Priapism (may occur in acute spinal injury)

Obstructive Shock: Massive Pulmonary Embolism

History:

• Risk factors: Recent surgery, prolonged immobility, malignancy, pregnancy/postpartum, oral contraceptives, DVT history
• Acute dyspnoea, pleuritic chest pain, haemoptysis (may be absent in massive PE)
• Syncope (suggests massive PE with haemodynamic compromise)

Examination:

• Tachycardia, tachypnoea, hypotension
• Elevated JVP (RV strain)
• Loud P2 (pulmonary hypertension)
• RV heave (acute RV dilation)
• Hypoxia (SpO₂ less than 90%), cyanosis
• DVT signs: Unilateral leg swelling, calf tenderness (may be absent—embolized)

Obstructive Shock: Cardiac Tamponade

History:

• Trauma (penetrating chest injury)
• Recent cardiac surgery
• Malignancy (lung, breast, lymphoma)
• Renal failure (uraemic pericarditis)
• Acute MI (free wall rupture—sudden deterioration 3-7 days post-MI)

Examination:

• Beck's triad (classic but present in only 30%): Hypotension, elevated JVP, muffled heart sounds
• Pulsus paradoxus: SBP drops > 10 mmHg on inspiration (exaggerated normal physiology)
• Tachycardia
• Kussmaul's sign: JVP rises on inspiration (constriction or tamponade)
• Reduced cardiac dullness on percussion
• Dyspnoea, orthopnoea (patients may sit upright leaning forward for relief)

Obstructive Shock: Tension Pneumothorax

History:

• Trauma (rib fractures, penetrating chest injury)
• Iatrogenic: Post-central line insertion, post-positive pressure ventilation
• Spontaneous (tall, thin young males; emphysema patients)

Examination:

• Respiratory distress, severe dyspnoea
• Tracheal deviation AWAY from affected side (late sign)
• Hyperresonance to percussion on affected side
• Absent or markedly reduced breath sounds ipsilaterally
• Elevated JVP (venous return obstruction)
• Hypotension, tachycardia
• Cyanosis, hypoxia

Clinical diagnosis: Do NOT wait for CXR—immediate needle decompression if clinical suspicion high.

Red Flags Requiring Immediate Intervention

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Clinical Examination

Structured ABCDE Approach to the Patient in Shock

Examination of the shocked patient follows the resuscitation-focused ABCDE approach, allowing simultaneous assessment and intervention:[15]

A - Airway

Assessment:

• Is the airway patent? Can the patient speak in full sentences?
• Stridor, gurgling, snoring suggest obstruction
• Anaphylaxis: Lip, tongue, or pharyngeal swelling (angioedema)

Action: If compromised, secure with head-tilt/chin-lift, airway adjuncts (oropharyngeal/nasopharyngeal airway), or definitive airway (endotracheal intubation) if GCS less than 8 or threatened airway.

B - Breathing

Assessment:

• Respiratory rate: Tachypnoea (> 20) is common in shock (metabolic acidosis compensation); bradypnoea (less than 10) suggests respiratory fatigue or CNS depression
• Work of breathing: Accessory muscle use, intercostal recession
• Oxygen saturation: SpO₂ less than 90% indicates hypoxia
• Auscultation:
  • "Bilateral crackles: Pulmonary oedema (cardiogenic shock)"
  • "Unilateral reduced sounds: Pneumothorax, consolidation"
  • "Wheeze: Anaphylaxis, bronchospasm"
  • "Bronchial breathing: Pneumonia (septic shock)"
• Percussion: Hyperresonance (pneumothorax), dullness (effusion, consolidation)

Action: High-flow oxygen (15 L/min via non-rebreather mask) to all shocked patients initially. Continuous SpO₂ monitoring. Consider non-invasive ventilation (CPAP for cardiogenic pulmonary oedema) or mechanical ventilation if respiratory failure.

C - Circulation

Vital signs:

• Blood pressure: SBP less than 90 mmHg or MAP less than 65 mmHg defines shock (use invasive arterial line for continuous monitoring in ICU)
• Pulse: Rate (tachycardia > 100, except neurogenic with bradycardia), rhythm (irregular—AF, VT), character (thready/weak in hypovolaemic/cardiogenic; bounding in early septic)
• Pulse pressure: Narrow (less than 25 mmHg) in hypovolaemic/cardiogenic; wide in septic
• Capillary refill time: Press nail bed for 5 seconds; > 3 seconds to refill indicates poor perfusion

Skin assessment:

• Temperature: Cold and clammy (hypovolaemic, cardiogenic, late septic); warm and flushed (early septic, anaphylactic, neurogenic)
• Colour: Pale (anaemia, vasoconstriction), flushed (vasodilation), cyanotic (hypoxia), mottled (severe shock—livedo reticularis)
• Moisture: Diaphoresis (shock, sympathetic activation) vs. dry (neurogenic shock)

Jugular venous pressure (JVP):

• Low/flat (even when supine): Hypovolaemic shock
• Elevated: Cardiogenic, obstructive (PE, tamponade, tension pneumothorax), RV failure
• Position patient at 45° for accurate assessment; measure vertical height from sternal angle (normal less than 3-4 cm)

Cardiac auscultation:

• Heart sounds: Muffled (tamponade), distant (obesity, emphysema)
• Murmurs: New systolic murmur post-MI suggests VSD or acute MR
• S3 gallop: Volume overload, heart failure
• Pericardial rub: Pericarditis (may precede tamponade)

Peripheral pulses:

• Central vs. peripheral: Presence of radial/pedal pulses; absent peripheral but present central suggests severe vasoconstriction
• Asymmetry: Aortic dissection (check all four limbs)

Fluid status:

• Oedema: Sacral, pedal (heart failure, fluid overload)
• Ascites: Liver failure, malignancy, tamponade physiology

Action: Establish large-bore IV access (×2 cannulae, ≥18G) or intraosseous if IV access impossible. Begin fluid resuscitation (unless cardiogenic). Continuous cardiac monitoring (ECG telemetry). Consider arterial line for invasive BP monitoring and frequent blood gas sampling.

D - Disability (Neurological Assessment)

Assessment:

• Glasgow Coma Scale (GCS): Score less than 13 suggests significant cerebral hypoperfusion or alternative pathology (intracranial haemorrhage, hypoglycaemia)
• AVPU: Alert / responds to Voice / responds to Pain / Unresponsive
• Pupils: Size, symmetry, reaction to light (dilated unreactive may indicate cerebral hypoxia; asymmetric suggests intracranial pathology)
• Blood glucose: Hypoglycaemia mimics shock and worsens outcomes (check in all patients)

Action: Protect airway if GCS less than 8. Treat hypoglycaemia (IV dextrose if less than 4 mmol/L). Avoid sedatives that may worsen hypotension. If focal neurology or asymmetric pupils, consider CT head to exclude haemorrhage.

E - Exposure

Full-body examination:

• Remove all clothing to identify:
  • "Bleeding sources: Wounds, haematomas"
  • "Rashes: Purpura (meningococcal sepsis, DIC), urticaria (anaphylaxis)"
  • "Abdominal distension: Haemoperitoneum, AAA, bowel obstruction"
  • "Flank/periumbilical bruising: Retroperitoneal haemorrhage (Grey Turner's sign, Cullen's sign)"
  • "Surgical scars: Recent surgery (bleeding, infection)"

Temperature:

• Fever (> 38°C): Septic shock, though may be absent in immunosuppressed or elderly
• Hypothermia (less than 36°C): Severe sepsis, hypovolaemic shock with prolonged exposure, end-stage shock

Action: Maintain normothermia (warming blankets if hypothermic; avoid hyperthermia which increases metabolic demand). Identify and control external bleeding. Maintain dignity (cover patient after examination).

Special Examination Techniques

Passive leg raise test (fluid responsiveness assessment):

• Patient supine; raise legs to 45° for 60 seconds
• Monitor blood pressure, pulse pressure variation, or cardiac output (if available)

• 10% increase in stroke volume/cardiac output predicts fluid responsiveness

• Useful to avoid fluid overload in uncertain cases[9]

Pulsus paradoxus (tamponade):

• Inflate BP cuff above systolic pressure; slowly deflate
• Note pressure when first Korotkoff sound heard (systole on expiration)
• Continue deflating until sounds heard throughout respiratory cycle (systole on inspiration and expiration)
• Difference > 10 mmHg = pulsus paradoxus (suggests tamponade or severe asthma)

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Investigations

Immediate Bedside Tests

Laboratory Investigations

Essential blood tests:

Arterial blood gas parameters in shock:

Imaging

Chest X-ray (CXR): Essential in all shocked patients

Bedside echocardiography (POCUS—Point-of-Care Ultrasound): Increasingly standard in shock assessment[11]

CT imaging (once stabilized):

Haemodynamic Monitoring (ICU)

Invasive arterial line:

• Continuous beat-to-beat BP measurement (more accurate than non-invasive cuff in shock)
• Arterial blood gas sampling
• Pulse pressure variation (PPV) and stroke volume variation (SVV) to assess fluid responsiveness (> 12-15% variation predicts fluid responsiveness in mechanically ventilated patients)[9]

Central venous pressure (CVP) monitoring:

• Trends more useful than absolute values
• Very low CVP (less than 5 mmHg) suggests hypovolaemia
• Elevated CVP (> 12 mmHg) suggests cardiogenic or obstructive shock, or fluid overload
• Limitations: Poor predictor of fluid responsiveness; influenced by ventricular compliance, intrathoracic pressure

Pulmonary artery catheter (PAC) (Swan-Ganz):

• Direct measurement of cardiac output, PCWP, SVR, mixed venous oxygen saturation
• Differentiates shock types definitively (see haemodynamic profiles table in Pathophysiology)
• Use declined due to lack of mortality benefit and complication risk; reserved for complex cases (e.g., cardiogenic shock requiring mechanical support decisions)

Less invasive cardiac output monitoring:

• Oesophageal Doppler
• Pulse contour analysis (PiCCO, LiDCO)
• Echocardiography

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Management

Immediate Resuscitation: The First 15 Minutes

Time-critical actions follow the ABCDE approach:[15]

A - Airway

• Secure airway if compromised (GCS less than 8, obstructed airway, respiratory failure)
• Call anaesthetics for intubation if required
• Caution: Induction agents (propofol, thiopentone) cause vasodilation and worsen hypotension; use reduced doses, have vasopressors ready

B - Breathing

• High-flow oxygen: 15 L/min via non-rebreather mask to all shocked patients (target SpO₂ 94-98%; 88-92% in COPD)
• Treat tension pneumothorax: Needle decompression (14-16G cannula, 2nd intercostal space, midclavicular line), then chest drain
• Consider CPAP for cardiogenic pulmonary oedema

C - Circulation

Vascular access:

• Two large-bore IV cannulae (≥18G, ideally 16G or 14G for rapid fluid resuscitation)
• Site: Antecubital fossa (larger veins) preferred over hand/wrist
• If IV access impossible: Intraosseous (proximal tibia, humeral head) in extremis

Fluid resuscitation (type-dependent—see below):

• Crystalloid (0.9% saline or Hartmann's) preferred first-line
• Rapid boluses (500 mL over 10-15 minutes), reassess, repeat
• Blood products if haemorrhagic shock (activate major haemorrhage protocol if > 4 units anticipated)

Monitor and reassess:

• Continuous ECG, SpO₂, non-invasive BP (5-minute intervals minimum)
• Urinary catheter: Hourly urine output target ≥0.5 mL/kg/hr
• Arterial line for continuous BP and frequent blood gases (ICU)

Blood tests:

• Venous or arterial blood gas (lactate, pH, base excess, glucose)
• FBC, U&E, LFT, coagulation, troponin, CRP
• Group & Save / crossmatch (if bleeding)
• Blood cultures before antibiotics (if sepsis suspected)

D - Disability

• Check GCS, pupils, blood glucose
• Treat hypoglycaemia immediately (IV 10% dextrose 100-200 mL or 50 mL 50% dextrose)
• Avoid sedatives unless intubating

E - Exposure

• Full examination to identify bleeding, rashes, sources of infection
• Keep patient warm (hypothermia worsens coagulopathy and outcomes)

Type-Specific Management

Hypovolaemic Shock

Haemorrhagic shock:[13]

Fluid resuscitation:

• Permissive hypotension until definitive haemostasis: Target SBP 80-90 mmHg (avoid aggressive fluid that disrupts clot formation and causes dilutional coagulopathy)
• Exception: Traumatic brain injury—maintain MAP ≥80 mmHg for cerebral perfusion
• Crystalloid (Hartmann's or 0.9% saline): Initial bolus 500-1000 mL rapidly
• Blood products (if ongoing bleeding or Hb less than 70 g/L):
  • Activate major haemorrhage protocol if massive bleeding
  • "Balanced resuscitation: Red cells : FFP : Platelets = 1:1:1 ratio"
  • "Tranexamic acid: 1 g IV over 10 minutes (within 3 hours of injury in trauma; reduces mortality)[18]"
  • Target Hb > 70 g/L, platelets > 75 × 10⁹/L (> 100 if ongoing bleeding), fibrinogen > 1.5 g/L

Haemorrhage control:

• External bleeding: Direct pressure, haemostatic dressings, tourniquets (pre-hospital)
• GI bleeding: Urgent endoscopy (variceal band ligation, clip/inject bleeding ulcer); consider balloon tamponade (Sengstaken-Blakemore) for variceal bleeding as bridge to definitive therapy
• Postpartum haemorrhage: Uterotonic agents (oxytocin, ergometrine, carboprost), uterine massage, balloon tamponade, surgical options (hysterectomy)
• Trauma: Damage control surgery (pack and stabilize, definitive repair later); interventional radiology (embolization for pelvic fracture bleeding, solid organ injury)
• Ruptured AAA: Emergency open or endovascular aneurysm repair (EVAR)

Non-haemorrhagic hypovolaemia:

• Aggressive fluid resuscitation: 20-30 mL/kg crystalloid bolus (1-2 L in 70 kg adult) rapidly
• Reassess after each bolus: HR, BP, capillary refill, urine output, lactate
• Continue boluses until haemodynamic improvement
• Consider 4-5% albumin if large volumes required (> 3-4 L crystalloid)
• Address underlying cause: Anti-emetics, anti-diarrhoeals, insulin (DKA), source control

Cardiogenic Shock

Key principle: Avoid aggressive fluids (worsen pulmonary oedema); optimize preload, contractility, and afterload.[10]

Fluid management:

• Small fluid challenges only if signs of hypovolaemia (flat JVP, no pulmonary oedema)
• 250 mL bolus over 10-15 minutes, reassess (JVP, lung auscultation, oxygen saturations)
• Stop if JVP rises, crackles develop, or SpO₂ drops
• Consider diuretics (furosemide 40-80 mg IV) if pulmonary oedema

Vasopressors and inotropes (ICU, via central line):

Reperfusion for acute MI:

• STEMI: Immediate primary PCI (percutaneous coronary intervention) preferred; thrombolysis if PCI unavailable
• Early revascularization reduces mortality from > 80% to 40-50%[10]

Mechanical circulatory support (specialist centres):

• Intra-aortic balloon pump (IABP): Inflates in diastole (increases coronary perfusion), deflates in systole (reduces afterload); no longer first-line but may assist
• Impella: Percutaneous LV assist device; unloads LV and augments cardiac output
• VA-ECMO (veno-arterial extracorporeal membrane oxygenation): Full cardiopulmonary support; bridge to recovery or transplant

Treat arrhythmias:

• VT/VF: Immediate DC cardioversion
• Bradycardia: Atropine, temporary pacing
• AF with rapid rate: Rate control (beta-blockers, digoxin)

Mechanical complications (post-MI):

• Acute severe MR (papillary muscle rupture): Surgical mitral valve replacement
• VSD: Surgical repair
• Free wall rupture: Emergency surgery (high mortality)

Distributive Shock: Septic Shock

Surviving Sepsis Campaign Guidelines (2021)—Hour-1 Bundle:[7]

1. Measure lactate: Repeat in 2-4 hours if initial > 2 mmol/L
2. Obtain blood cultures before antibiotics: ≥2 sets (aerobic + anaerobic)
3. Administer broad-spectrum antibiotics within 1 hour: Mortality increases 7.6% per hour delay[14]
4. Begin rapid fluid resuscitation: 30 mL/kg crystalloid if hypotensive or lactate ≥4 mmol/L
5. Apply vasopressors if hypotensive during or after fluid resuscitation: Target MAP ≥65 mmHg

Antibiotic selection (local guidelines vary—examples):

De-escalate antibiotics once culture and sensitivities available.

Source control:

• Drain abscesses (percutaneous or surgical)
• Remove infected devices (lines, catheters)
• Surgical debridement (necrotizing fasciitis, intra-abdominal sepsis)
• Time-critical: Initiate within 6-12 hours of diagnosis

Fluid resuscitation:

• 30 mL/kg crystalloid (2-3 L in 70 kg adult) within first 3 hours[7]
• Reassess after each bolus; stop if signs of fluid overload (pulmonary oedema)
• Use dynamic measures (passive leg raise, pulse pressure variation) to guide further fluids[9]

Vasopressors (if MAP less than 65 despite fluids):

• Noradrenaline: First-line, 0.05-0.5 mcg/kg/min via central line (peripheral if central access delayed)
• Vasopressin: Add if high-dose noradrenaline required (0.03-0.04 units/min)
• Target MAP ≥65 mmHg (higher in chronic hypertension)

Adjunctive therapies:

• Corticosteroids: Hydrocortisone 50 mg IV 6-hourly if refractory shock despite fluids and vasopressors (reduces time to shock resolution)[7]
• Consider IVIG: Necrotizing fasciitis, toxic shock syndrome (inhibit toxin-mediated damage)

Distributive Shock: Anaphylactic Shock

Immediate management:[19]

1. IM adrenaline: 0.5 mg (0.5 mL of 1:1000) into anterolateral thigh; repeat every 5 minutes if no response
   • Dose: Adults and children > 12 years: 0.5 mg; 6-12 years: 0.3 mg; less than 6 years: 0.15 mg
2. Remove trigger: Stop drug infusion, remove stinger
3. High-flow oxygen: 15 L/min
4. IV fluid resuscitation: 500-1000 mL crystalloid rapid bolus (profound vasodilation causes relative hypovolaemia)
5. Lie patient flat, elevate legs: Improve venous return

If refractory to IM adrenaline:

• IV adrenaline infusion: 0.05-0.5 mcg/kg/min (high-risk—requires continuous monitoring, ICU)

Adjuncts:

• Antihistamines: Chlorphenamine 10 mg IV (H1 blocker), ranitidine 50 mg IV (H2 blocker)—relieves urticaria, pruritus but do NOT treat shock
• Corticosteroids: Hydrocortisone 200 mg IV—may prevent biphasic reaction (symptom recurrence 6-12 hours later)
• Bronchodilators: Salbutamol nebulizers if wheeze persists

Special considerations:

• Patients on beta-blockers: May not respond to adrenaline (beta effects blocked); consider glucagon 1-2 mg IV (bypasses beta receptors)
• Pregnant patients: Adrenaline safe in pregnancy; priority is maternal resuscitation (fetal survival depends on maternal survival)

Observation: Minimum 6 hours (biphasic reactions occur in 20%); 12-24 hours if severe or slow response.

Discharge:

• Prescribe adrenaline auto-injector (EpiPen 0.3 mg for adults; 0.15 mg for children)
• Allergy clinic referral for identification and desensitization if appropriate
• Medical alert bracelet

Distributive Shock: Neurogenic Shock

Principles: Restore vascular tone and heart rate (lost sympathetic innervation).[3]

Fluid resuscitation: Cautious (risk of fluid overload as vasoconstriction recovers)

• 500 mL crystalloid boluses, reassess frequently

Vasopressors: Often required

• Noradrenaline: First-line (restores vascular tone)
• Target MAP ≥85 mmHg (higher than other shock to ensure spinal cord perfusion)

Bradycardia: May require atropine or pacing (sympathetic denervation → unopposed vagal tone)

Spinal immobilization and definitive care: Neurosurgical input, spinal MRI, consider surgery (spinal decompression, stabilization)

Obstructive Shock: Massive Pulmonary Embolism

Immediate:

• Oxygen, IV access, fluid resuscitation (500-1000 mL cautiously—avoid RV overload)
• Anticoagulation: Unfractionated heparin bolus (80 units/kg IV) then infusion (18 units/kg/hr)

Reperfusion therapy (if shock/RV dysfunction):[11]

• Thrombolysis: Alteplase 50 mg IV over 2 hours (or 10 mg bolus + 90 mg over 2 hours)
  • "Indications: Haemodynamically unstable PE (SBP less than 90 mmHg), cardiac arrest from PE"
  • "Contraindications: Active bleeding, recent surgery/trauma, intracranial pathology"
• Surgical embolectomy: If thrombolysis contraindicated or failed
• Catheter-directed therapy: Percutaneous thrombectomy (specialist centres)

Vasopressors: If hypotensive despite fluids

• Noradrenaline preferred (avoid excessive fluids which worsen RV strain)

Obstructive Shock: Cardiac Tamponade

Definitive treatment: Pericardiocentesis (drainage of pericardial fluid)

Temporizing measures (while arranging pericardiocentesis):

• Fluid resuscitation: Increase preload to maintain cardiac output (unusual—fluids help in tamponade)
• Avoid positive pressure ventilation: Worsens venous return and cardiac output

Pericardiocentesis:

• Echocardiography-guided (safest): Identify effusion, guide needle
• Subxiphoid approach: 16-18G needle inserted inferior to xiphoid, directed toward left shoulder, aspirate while advancing
• Confirmation: Aspirate non-clotting blood (pericardial blood defibrinated vs. cardiac chamber puncture which clots)
• Drain insertion: Leave pigtail catheter for ongoing drainage

Surgery (pericardial window or pericardiectomy) if recurrent or malignant effusion.

Obstructive Shock: Tension Pneumothorax

Immediate needle decompression (clinical diagnosis—do NOT wait for imaging):

• Site: 2nd intercostal space, midclavicular line on affected side
• Technique: Large-bore cannula (14-16G), insert just above 3rd rib (avoid neurovascular bundle below ribs), advance until rush of air, remove needle and leave plastic cannula
• Immediate relief: Hypotension and respiratory distress improve

Definitive: Chest drain (large-bore, 28-32 Fr) inserted in "safe triangle" (5th intercostal space, mid-axillary line, bordered by anterior edge latissimus dorsi, lateral edge pectoralis major, base at 5th ICS)

Underwater seal drainage: Connect to bottle; observe for air bubbling (confirms air leak) and lung re-expansion on CXR.

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Monitoring and Reassessment

Continuous monitoring:

• ECG (arrhythmias)
• SpO₂ (oxygenation)
• Blood pressure (invasive arterial line preferred in ICU)
• Urine output (hourly via catheter)
• Temperature

Serial measurements (every 1-2 hours initially):

• Lactate: Target ≥10% reduction per hour, normalize (less than 2 mmol/L) within 6 hours[8]
• Arterial blood gas: pH, base excess (track acidosis resolution)
• Urine output: Target ≥0.5 mL/kg/hr (35 mL/hr in 70 kg adult)

Clinical endpoints of resuscitation:

• MAP ≥65 mmHg (or higher target if chronic hypertension)
• Lactate clearance (≥10% reduction/hour)
• Urine output ≥0.5 mL/kg/hr
• Improved mental status
• Warm peripheries, capillary refill less than 3 seconds
• Central venous oxygen saturation (ScvO₂) > 70% (if central line placed)

Fluid balance: Positive balance expected in resuscitation phase (first 24 hours), but aim for neutral/negative balance once stabilized (avoid fluid overload complications).

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Complications

Shock itself is a complication of underlying disease, but inadequately treated or prolonged shock leads to further complications:[2]

Acute Organ Dysfunction

Multi-Organ Dysfunction Syndrome (MODS)

Definition: Dysfunction of ≥2 organ systems requiring intervention to maintain homeostasis.[2]

Epidemiology: Develops in 30-50% of shock patients; mortality 60-80% if ≥3 organs fail.

Scoring systems: SOFA (Sequential Organ Failure Assessment) score tracks daily organ dysfunction (0-4 points per organ system—respiratory, cardiovascular, hepatic, coagulation, renal, neurological).

Management: Supportive care for each failing organ; treat underlying shock.

Infection and Sepsis

• Nosocomial infections: ICU patients at high risk (ventilator-associated pneumonia, catheter-related bloodstream infections, catheter-associated UTIs)
• Prevention: Strict asepsis, early removal of invasive devices, antimicrobial stewardship

Thromboembolic Complications

• Deep vein thrombosis / pulmonary embolism: Immobility, hypercoagulable state
• Prevention: Pharmacological VTE prophylaxis (LMWH) unless contraindicated (active bleeding); mechanical prophylaxis (compression stockings, intermittent pneumatic compression)

Critical Illness-Related

• ICU-acquired weakness: Polyneuropathy/myopathy from critical illness, prolonged mechanical ventilation, corticosteroids
• Delirium: Common (30-80% ICU patients); managed with reorientation, avoid sedatives, treat precipitants
• Stress ulceration: GI bleeding from gastric/duodenal ulcers; prevented with PPI (pantoprazole 40 mg IV daily)
• Pressure ulcers: Immobility; prevent with frequent repositioning, pressure-relieving mattresses

Post-Intensive Care Syndrome (PICS)

Survivors of critical illness may experience long-term sequelae:[15]

• Physical: Muscle weakness, fatigue, reduced exercise tolerance, chronic pain
• Cognitive: Memory impairment, reduced attention span, executive dysfunction
• Psychological: PTSD, anxiety, depression

Management: ICU follow-up clinics, rehabilitation (physiotherapy, occupational therapy), psychological support.

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Prognosis & Outcomes

Mortality by Shock Type

Mortality varies significantly by etiology, severity, and timeliness of treatment:[6]

Prognostic Factors

Adverse prognostic indicators:

• Persistent lactic acidosis: Lactate > 4 mmol/L after 6 hours of resuscitation—mortality > 50%[8]
• Delayed treatment: Each hour delay in septic shock antibiotic administration increases mortality 7.6%[14]
• Age > 65 years: 2-3 times higher mortality across all shock types
• Comorbidities: Chronic kidney disease, cirrhosis, immunosuppression, malignancy
• Multi-organ failure: Mortality increases exponentially (1 organ 20-30%; 2 organs 40-50%; ≥3 organs 60-80%)
• Refractory shock: Requiring high-dose vasopressors (e.g., noradrenaline > 0.5 mcg/kg/min)

Favorable prognostic indicators:

• Rapid lactate clearance: ≥10% reduction per hour, normalization within 6 hours[8]
• Early source control: Sepsis with drainage of abscess, haemorrhage with surgical control
• Young age, no comorbidities
• Single-organ dysfunction (vs. MODS)

Long-Term Outcomes

Survivors of severe shock face increased long-term mortality and morbidity:

• 1-year mortality: 10-20% higher than age-matched controls (recurrent sepsis, cardiovascular events)
• Chronic kidney disease: 20-30% of AKI survivors develop CKD; some require long-term dialysis
• Heart failure: Cardiogenic shock survivors at risk of recurrent heart failure
• Cognitive impairment: Equivalent to mild Alzheimer's disease in some ICU survivors
• Reduced quality of life: Physical disability, unemployment, psychological disorders (PTSD, depression)[15]

Quality Indicators and Bundles

Surviving Sepsis Campaign: Adherence to Hour-1 Bundle (lactate, cultures, antibiotics, fluids, vasopressors) reduces mortality by 20-30%.[7]

Early goal-directed therapy (EGDT): While specific protocol (Rivers protocol) not superior to standard care in later trials, principles (early recognition, prompt resuscitation, source control) remain essential.[4]

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Evidence & Guidelines

Major International Guidelines

1. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063-e1143. PMID: 34605781

   • Comprehensive sepsis and septic shock management; Hour-1 Bundle; fluid resuscitation targets; vasopressor selection; source control.

2. Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419-2432. PMID: 29083953

   • CULPRIT-SHOCK trial: In cardiogenic shock with multivessel disease, culprit-lesion-only PCI superior to multivessel PCI; informs revascularization strategy.

3. Resuscitation Council UK. Advanced Life Support Guidelines. 2021.

   • UK standard for management of cardiac arrest and peri-arrest conditions including shock.

4. National Institute for Health and Care Excellence (NICE). Sepsis: recognition, diagnosis and early management. NG51. 2016 (updated 2024).

   • UK guidance on sepsis recognition and management in all healthcare settings.

Landmark Trials and Evidence

5. Rivers E, Nguyen B, Havstad S, et al. Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock. N Engl J Med. 2001;345(19):1368-1377. PMID: 11794169

   • Landmark trial demonstrating mortality reduction with structured early resuscitation protocol in septic shock (absolute mortality reduction 16%); established EGDT concept.

6. Vincent JL, De Backer D. Circulatory Shock. N Engl J Med. 2013;369(18):1726-1734. PMID: 24171518

   • Comprehensive review of shock pathophysiology, classification, and management principles.

7. Seymour CW, Gesten F, Prescott HC, et al. Time to Treatment and Mortality during Mandated Emergency Care for Sepsis. N Engl J Med. 2017;376(23):2235-2244. PMID: 28528569

   • Large observational study (49,000 patients): Each hour delay in antibiotic administration associated with 7.6% increased odds of mortality; emphasizes urgency of sepsis treatment.

8. Hernández G, Ospina-Tascón GA, Damiani LP, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock: The ANDROMEDA-SHOCK Randomized Clinical Trial. JAMA. 2019;321(7):654-664. PMID: 30772908

   • Capillary refill time-targeted resuscitation non-inferior to lactate-targeted; validates clinical perfusion assessment alongside lactate monitoring.

9. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl Starch 130/0.42 versus Ringer's Acetate in Severe Sepsis. N Engl J Med. 2012;367(2):124-134. PMID: 22738085

   • 6S trial: Hydroxyethyl starch increased mortality and AKI vs. crystalloid in sepsis; colloids no longer recommended in septic shock.

10. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock. N Engl J Med. 2012;367(14):1287-1296. PMID: 22920912

    • IABP-SHOCK II trial: IABP did not reduce mortality in cardiogenic shock; shifted practice toward alternative mechanical support (Impella, ECMO).

11. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603. PMID: 31504429

    • European guidelines on PE management including massive PE with shock; thrombolysis indications, risk stratification.

12. Bakker J, Nijsten MW, Jansen TC. Clinical use of lactate monitoring in critically ill patients. Ann Intensive Care. 2013;3(1):12. PMID: 23587445

    • Reviews lactate as a biomarker in shock; lactate clearance predicts outcomes; serial measurements guide resuscitation.

13. American College of Surgeons Committee on Trauma. ATLS Advanced Trauma Life Support Student Course Manual. 10th edition. 2018.

    • Standardized approach to trauma resuscitation including haemorrhagic shock classification and management.

14. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789. PMID: 20200382

    • Noradrenaline superior to dopamine (fewer arrhythmias, lower mortality in cardiogenic shock subgroup); established noradrenaline as first-line vasopressor.

15. Pearse RM, Harrison DA, MacDonald N, et al. Effect of a perioperative, cardiac output-guided hemodynamic therapy algorithm on outcomes following major gastrointestinal surgery: a randomized clinical trial and systematic review. JAMA. 2014;311(21):2181-2190. PMID: 24842135

    • Goal-directed fluid therapy reduces complications in high-risk surgery; principle applies to shock resuscitation.

16. Angus DC, van der Poll T. Severe Sepsis and Septic Shock. N Engl J Med. 2013;369(9):840-851. PMID: 23984731

    • Comprehensive review of septic shock pathophysiology, epidemiology, and management.

17. Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med. 2011;183(7):847-855. PMID: 21097695

    • Pharmacology and clinical use of vasopressors and inotropes in different shock types.

18. CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23-32. PMID: 20554319

    • Tranexamic acid within 3 hours of injury reduces mortality in trauma with haemorrhagic shock.

19. Resuscitation Council UK. Emergency treatment of anaphylactic reactions: Guidelines for healthcare providers. 2021.

    • UK standard for anaphylaxis management including anaphylactic shock.

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Patient & Family Information

What is Shock?

Shock is a medical emergency where your body is not getting enough blood flow to deliver oxygen and nutrients to your vital organs (brain, heart, kidneys). Without enough oxygen, your organs cannot work properly and may be damaged. Shock is life-threatening and requires immediate hospital treatment.

Shock is not the same as the emotional feeling of being "shocked" or upset, although severe illness or injury can cause both.

What Causes Shock?

There are several causes:

Loss of blood or fluids:

• Severe bleeding from injury, surgery, or internal bleeding (e.g., stomach ulcer)
• Severe dehydration from vomiting, diarrhoea, or burns

Heart problems:

• Heart attack (the heart muscle is damaged and cannot pump effectively)
• Abnormal heart rhythms
• Heart failure (the heart is too weak to pump blood)

Severe infection (sepsis):

• Bacterial, viral, or fungal infections spread through the bloodstream
• The body's response to infection causes blood vessels to widen, reducing blood pressure

Severe allergic reaction (anaphylaxis):

• Allergies to foods (peanuts, shellfish), medications (penicillin), or insect stings
• Causes sudden drop in blood pressure and difficulty breathing

Blockages:

• Blood clot in the lungs (pulmonary embolism)
• Fluid around the heart (cardiac tamponade)
• Collapsed lung under pressure (tension pneumothorax)

What Are the Symptoms?

• Feeling faint, dizzy, or confused
• Rapid heartbeat (pounding in your chest)
• Rapid, shallow breathing
• Cold, clammy, pale, or bluish skin
• Sweating
• Nausea or vomiting
• Reduced or no urine output
• Loss of consciousness in severe cases

Call 999 immediately if you or someone else has these symptoms, especially after injury, severe illness, or allergen exposure.

How is Shock Treated?

Shock is treated in hospital, often in the Intensive Care Unit (ICU). Treatment depends on the cause:

General treatments:

• Oxygen: Given through a mask or nasal tubes to help your body get more oxygen
• Intravenous (IV) fluids: Fluids given directly into your veins through a drip to increase blood volume and blood pressure
• Medications to raise blood pressure: If fluids alone do not improve blood pressure, medications called vasopressors are given through a drip
• Monitoring: Continuous monitoring of heart rate, blood pressure, oxygen levels, and urine output

Specific treatments based on cause:

• Bleeding: Stop the bleeding (surgery, endoscopy, blood transfusions)
• Heart attack: Medications to dissolve clots, procedures to open blocked arteries (angioplasty)
• Severe infection (sepsis): Antibiotics given urgently (within 1 hour), draining any abscesses or infected fluid
• Severe allergic reaction (anaphylaxis): Adrenaline injection into the muscle, antihistamines, steroids
• Blood clot in lungs: Blood thinners, sometimes clot-dissolving medications
• Fluid around heart or collapsed lung: Procedures to drain fluid or release pressure

What is the Outlook?

The outlook depends on:

• Cause of shock: Some types respond better to treatment than others
• How quickly treatment is started: Early treatment greatly improves survival
• Your age and overall health: Older patients and those with other medical problems may have a harder time recovering
• Severity: Shock affecting multiple organs has a higher risk of death

With prompt treatment, many people recover fully. However, shock is serious and can be fatal, especially if treatment is delayed.

Recovery and Rehabilitation

If you survive severe shock requiring ICU admission, recovery may take weeks to months. You may experience:

• Weakness and fatigue
• Difficulty concentrating or remembering things
• Emotional changes (anxiety, low mood)
• Reduced fitness and muscle strength

Rehabilitation with physiotherapy, occupational therapy, and psychological support can help you recover. Many hospitals have ICU follow-up clinics to support recovery.

Prevention

Preventing shock depends on the cause:

• Injury prevention: Wear seatbelts, use protective equipment, prevent falls
• Manage chronic conditions: Take medications for heart disease, diabetes, high blood pressure as prescribed
• Recognize infections early: Seek medical attention for worsening infections (e.g., pneumonia, urinary tract infections)
• Allergy awareness: If you have severe allergies, carry an adrenaline auto-injector (EpiPen), avoid known allergens, wear a medical alert bracelet
• Hydration: Drink enough fluids, especially in hot weather or if vomiting/diarrhoea

When to Seek Help

Call 999 immediately if:

• You or someone else has symptoms of shock (faint, rapid heartbeat, cold clammy skin, confusion)
• Severe bleeding that cannot be stopped with pressure
• Difficulty breathing, chest pain, or suspected heart attack
• Signs of severe infection with confusion, very high or very low temperature, rapid breathing
• Severe allergic reaction (swelling of lips/tongue, difficulty breathing, rash)

Resources

• UK Sepsis Trust: sepsistrust.org – Information on recognizing and preventing sepsis
• British Heart Foundation: bhf.org.uk – Information on heart attack and heart failure
• Anaphylaxis Campaign: anaphylaxis.org.uk – Allergy and anaphylaxis information
• NHS: nhs.uk/conditions/shock – General information on shock
• Intensive Care Society: ics.ac.uk – Information for families of ICU patients

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References

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3. Standl T, Annecke T, Cascorbi I, et al. The nomenclature, definition and distinction of types of shock. Dtsch Arztebl Int. 2018;115(45):757-768. PMID: 30573009

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11. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603. PMID: 31504429

12. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789. PMID: 20200382

13. American College of Surgeons Committee on Trauma. ATLS Advanced Trauma Life Support Student Course Manual. 10th edition. Chicago, IL: American College of Surgeons; 2018.

14. Seymour CW, Gesten F, Prescott HC, et al. Time to treatment and mortality during mandated emergency care for sepsis. N Engl J Med. 2017;376(23):2235-2244. PMID: 28528569

15. Pearse RM, Harrison DA, MacDonald N, et al. Effect of a perioperative, cardiac output-guided hemodynamic therapy algorithm on outcomes following major gastrointestinal surgery: a randomized clinical trial and systematic review. JAMA. 2014;311(21):2181-2190. PMID: 24842135

16. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(9):840-851. PMID: 23984731

17. Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med. 2011;183(7):847-855. PMID: 21097695

18. CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23-32. PMID: 20554319

19. Resuscitation Council UK. Emergency treatment of anaphylactic reactions: Guidelines for healthcare providers. London: Resuscitation Council UK; 2021.

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Last updated: 2026-01-08
Version: 2.0 (Gold Standard)
Contributors: MedVellum Medical Education Team
Peer review: Emergency Medicine, Intensive Care Medicine consultants