What are the causes and management of shock?

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Causes and Management of Shock

Classification of Shock by Etiology

Shock results from inadequate blood flow and oxygen delivery to meet tissue metabolic demands, with four primary categories: hypovolemic (most common in children), distributive (most common in adults, particularly septic shock), cardiogenic, and obstructive. 1, 2, 3

Hypovolemic Shock

  • Hemorrhagic causes: Trauma, gastrointestinal bleeding, surgical blood loss 1, 3
  • Non-hemorrhagic causes: Severe dehydration, burns, third-spacing of fluids 3, 4
  • Hemodynamic pattern: Decreased cardiac index, elevated systemic vascular resistance (compensatory vasoconstriction), decreased central venous pressure, decreased pulmonary capillary wedge pressure 5, 4

Distributive Shock

  • Septic shock: Most common form of distributive shock in adults, caused by overwhelming infection with inflammatory mediator release 1, 2, 3
  • Anaphylactic shock: Severe allergic reaction with massive histamine release 3
  • Neurogenic shock: Spinal cord injury causing loss of sympathetic tone 5, 2
  • Hemodynamic pattern: Normal or increased cardiac index (early stages), markedly decreased systemic vascular resistance (pathological vasodilation), normal or decreased central venous pressure, normal or decreased pulmonary capillary wedge pressure 5, 2

Cardiogenic Shock

  • Acute myocardial infarction: Most common cause, occurring in 5-12% of AMI cases, typically with >40% loss of left ventricular myocardium 1, 6, 7
  • Mechanical complications: Acute mitral regurgitation, ventricular septal rupture, free wall rupture 6, 7
  • Acute decompensation of chronic heart failure 1, 6
  • Myocarditis, cardiomyopathy, arrhythmias 6, 3
  • Hemodynamic pattern: Decreased cardiac index (<2.2 L/min/m²), elevated systemic vascular resistance (compensatory), elevated central venous pressure (>15 mmHg), elevated pulmonary capillary wedge pressure (>15 mmHg) 1, 5, 7

Obstructive Shock

  • Pulmonary embolism: Massive PE causing right ventricular failure 2, 3
  • Tension pneumothorax: Mediastinal shift compromising venous return 3, 8
  • Cardiac tamponade: Pericardial fluid restricting cardiac filling 2, 3
  • Hemodynamic pattern: Elevated central venous pressure, decreased cardiac output, variable systemic vascular resistance 5, 2

Diagnostic Approach to Shock

Clinical Recognition Criteria

  • Hypotension: Systolic blood pressure <90 mmHg for >30 minutes, or mean arterial pressure <60 mmHg 1, 7
  • Signs of end-organ hypoperfusion (must be present for shock diagnosis): 1, 7
    • Altered mental status (decreased mentation, confusion) 1
    • Cold extremities, livedo reticularis (except distributive shock with warm extremities) 1, 5
    • Urine output <30 mL/h or <0.5 mL/kg/h 1, 6
    • Elevated lactate >2 mmol/L 1, 7
    • Acute liver injury (bilirubin ≥1.3 mg/dL) or acute kidney injury 5, 6

Hemodynamic Differentiation Algorithm

Step 1: Assess cardiac index and systemic vascular resistance 5

  • If cardiac index <2.2 L/min/m² with elevated SVR → Consider cardiogenic or hypovolemic shock 5
  • If cardiac index normal/elevated with decreased SVR → Distributive shock 5

Step 2: Assess filling pressures 5

  • If PCWP >15 mmHg and CVP >15 mmHg → Cardiogenic shock 1, 5
  • If PCWP <15 mmHg and CVP <10 mmHg → Hypovolemic shock 5
  • If CVP >15 mmHg with normal PCWP → Consider obstructive shock (PE, tamponade) 5

Step 3: Calculate additional hemodynamic markers for cardiogenic shock 1, 5

  • Cardiac power output <0.6 W indicates severe cardiogenic shock 1, 5
  • Shock index (HR/systolic BP) >1.0 suggests significant hemodynamic compromise 1
  • Pulmonary artery pulse index <1.0 with CVP >15 mmHg indicates right ventricular shock 1

SCAI Classification for Cardiogenic Shock Staging

  • Stage A (At Risk): Normal hemodynamics, normotension, no hypoperfusion 5, 6
  • Stage B (Beginning): Relative hypotension without hypoperfusion 5
  • Stage C (Classic): Hypotension with hypoperfusion requiring intervention 5
  • Stage D (Deteriorating): Failing to respond to initial interventions 5
  • Stage E (Extremis): Cardiac arrest, refractory hypotension requiring CPR or ECMO 5, 6

Management Principles by Shock Type

Hypovolemic Shock Management

  • Immediate fluid resuscitation: Crystalloids (normal saline or lactated Ringer's) as first-line therapy 3, 4
  • Blood products: For hemorrhagic shock, initiate massive transfusion protocol with 1:1:1 ratio of packed red blood cells, fresh frozen plasma, and platelets 3
  • Source control: Stop bleeding through surgical intervention, endoscopy, or interventional radiology as indicated 3, 8
  • Avoid excessive fluid: Monitor for fluid tolerance to prevent volume overload complications 4

Distributive (Septic) Shock Management

  • Early fluid resuscitation: 30 mL/kg crystalloid within first 3 hours 3, 4
  • Vasopressor therapy: Norepinephrine as first-line agent to maintain mean arterial pressure ≥65 mmHg 6, 9
  • Source control: Identify and treat underlying infection, remove infected devices, drain abscesses 3, 8
  • Antimicrobial therapy: Broad-spectrum antibiotics within first hour of recognition 3

Cardiogenic Shock Management Algorithm

Step 1: Immediate revascularization for AMI-related shock 7

  • Percutaneous coronary intervention (PCI) if coronary anatomy suitable 6, 7
  • Emergency coronary artery bypass grafting (CABG) if PCI unsuitable or failed 7
  • Consider fibrinolysis if PCI would be delayed >120 minutes in STEMI 7

Step 2: Hemodynamic support 7

  • Vasopressor: Norepinephrine as first-line to maintain mean arterial pressure 6, 7, 9
  • Inotropic support: Dobutamine 2-20 μg/kg/min as first-line inotrope when signs of low cardiac output persist despite adequate blood pressure 1, 7, 9
  • Avoid routine intra-aortic balloon pump: Not indicated for routine use as it has not shown mortality benefit 7

Step 3: Respiratory support 7

  • Non-invasive positive pressure ventilation for pulmonary edema with respiratory rate >25 breaths/min or SaO2 <90% 7
  • Endotracheal intubation if unable to achieve adequate oxygenation 7
  • Critical pitfall: Positive pressure ventilation decreases left ventricular afterload but reduces right ventricular preload, potentially worsening right ventricular failure 1

Step 4: Mechanical circulatory support for refractory shock 1, 5, 7

  • Refractory shock criteria: Cardiac power output <0.6 W, cardiac index <2.2 L/min/m², persistent hypoperfusion despite two vasopressors at adequate doses 5
  • Device options: Percutaneous ventricular assist devices, extracorporeal membrane oxygenation (ECMO) 6, 7
  • Timing: Apply mechanical circulatory support within 1 hour from first weaning attempts to prevent complications 5
  • Contraindications: Anoxic brain injury, irreversible end-organ failure, prohibitive vascular access, DNR status 5

Step 5: Multidisciplinary shock team approach 1, 7

  • Team-based management associated with improved 30-day mortality 7
  • Transfer to tertiary center with 24/7 cardiac catheterization and mechanical circulatory support capability 7

Obstructive Shock Management

  • Tension pneumothorax: Immediate needle decompression followed by chest tube placement 3, 8
  • Cardiac tamponade: Emergent pericardiocentesis or surgical pericardial window 3, 8
  • Massive pulmonary embolism: Systemic thrombolysis, catheter-directed therapy, or surgical embolectomy 3, 8

Critical Monitoring Parameters

Hemodynamic Targets

  • Mean arterial pressure: ≥65 mmHg 7, 4
  • Cardiac index: >2.0-2.2 L/min/m² 1, 5, 7
  • Pulmonary capillary wedge pressure: <20 mmHg in cardiogenic shock, 15-18 mmHg optimal for myocardial infarction with pump failure 5, 7
  • Lactate: Trending toward normalization (<2 mmol/L) 1, 7

Invasive Monitoring Indications

  • Pulmonary artery catheter: Consider for refractory shock, unclear shock etiology, or guiding mechanical circulatory support decisions 1, 7, 4
  • Arterial line: Recommended for all shock states requiring vasopressors for accurate continuous blood pressure monitoring 7, 4
  • Central venous pressure monitoring: Helpful for assessing right-sided filling pressures and differentiating shock types 5, 4

Common Pitfalls and Caveats

Diagnostic Pitfalls

  • Tachycardia is non-specific: Can result from shock, pain, anxiety, or fever—must be interpreted with other clinical signs 1
  • Capillary refill time limitations: Influenced by ambient temperature, site, age, and lighting—use in combination with other perfusion markers 1
  • Late-stage septic shock mimics cardiogenic shock: Septic shock can develop myocardial depression, but primary hemodynamic pattern remains distributive with decreased SVR 5
  • Dynamic hemodynamic changes: Parameters change rapidly as shock progresses or responds to treatment, requiring continuous reassessment 5, 2

Management Pitfalls

  • Excessive fluid in cardiogenic shock: Worsens pulmonary edema and right ventricular failure—target euvolemia, not hypervolemia 7, 4
  • Inadequate fluid in distributive shock: Vasopressors without adequate volume resuscitation worsens tissue hypoperfusion 4
  • Right ventricular infarction: Avoid volume overload as it worsens hemodynamics despite hypotension 7
  • Delayed mechanical circulatory support: Prolonged medical optimization in refractory cardiogenic shock increases complications and mortality 5
  • Positive pressure ventilation in right ventricular failure: Can decrease venous return and worsen right ventricular shock—use lowest effective PEEP 1

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

The Intensivist's Perspective of Shock, Volume Management, and Hemodynamic Monitoring.

Clinical journal of the American Society of Nephrology : CJASN, 2022

Guideline

Hemodynamic Differentiation of Shock Types

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Cardiogenic Shock Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Management of Cardiogenic Shock

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Shock: aetiology, pathophysiology and management.

British journal of nursing (Mark Allen Publishing), 2022

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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