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HealthConsider > Blog > Health > Shock Clinical Guide
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Shock Clinical Guide

Last updated: August 29, 2025 4:18 am
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Shock Clinical Guide

Introduction

Shock is a life-threatening syndrome characterized by inadequate tissue perfusion and oxygen delivery, leading to cellular hypoxia, metabolic derangements, and multi-organ dysfunction. It represents a common final pathway in critical illness and injury, with prompt recognition and targeted interventions critical to reducing morbidity and mortality. This guide outlines the classification, pathophysiology, clinical assessment, diagnostic evaluation, and evidence-based management strategies for shock.

Contents
  • Shock Clinical Guide
    • Introduction
    • Classification and Pathophysiology
    • Clinical Assessment
      • Initial Evaluation (ABCDE Approach)
      • Hemodynamic Monitoring
    • Diagnostic Workup
    • Initial Management
      • Fluid Resuscitation
      • Vasoactive Agents
      • Source Control and Specific Therapies
    • Supportive Care
    • Monitoring and Titration
    • Advanced Therapies
    • Prognosis and Disposition
    • Conclusion

Classification and Pathophysiology

Shock is traditionally categorized into four major types based on etiology and hemodynamic profiles:

  1. Hypovolemic Shock
  2. Etiology: Acute blood loss (trauma, hemorrhage), fluid depletion (dehydration, diuretics).
  3. Pathophysiology: Reduced preload → decreased stroke volume → lowered cardiac output → inadequate tissue perfusion.

  4. Cardiogenic Shock

  5. Etiology: Myocardial infarction, acute valvular dysfunction, cardiomyopathy, arrhythmias.
  6. Pathophysiology: Primary pump failure → elevated filling pressures → pulmonary and systemic congestion despite adequate intravascular volume.

  7. Distributive Shock

  8. Etiology: Sepsis (most common), anaphylaxis, neurogenic.
  9. Pathophysiology: Systemic vasodilation and capillary leak → relative hypovolemia, maldistribution of blood flow, and decreased systemic vascular resistance (SVR).

  10. Obstructive Shock

  11. Etiology: Cardiac tamponade, tension pneumothorax, massive pulmonary embolism.
  12. Pathophysiology: Mechanical obstruction to ventricular filling or ejection → impaired cardiac output.

Clinical Assessment

Initial Evaluation (ABCDE Approach)

  • Airway: Assess patency; prepare for intubation if compromised.
  • Breathing: Measure respiratory rate, oxygen saturation, and work of breathing; administer supplemental oxygen or ventilatory support.
  • Circulation: Rapid assessment of pulse rate, blood pressure, capillary refill, skin perfusion, and peripheral pulses.
  • Disability: Evaluate mental status (AVPU/GCS) for cerebral hypoperfusion.
  • Exposure: Look for bleeding, rash (anaphylaxis), abdominal distension (obstruction).

Hemodynamic Monitoring

  • Invasive: Arterial line for real-time blood pressure, central venous catheter for CVP trends, and pulmonary artery catheter in complex cases.
  • Noninvasive: Echocardiography (cardiac function, pericardial effusion), ultrasound-based cardiac output monitoring.

Diagnostic Workup

  • Laboratory Studies: CBC (hemoglobin, infection), electrolytes, renal and liver panels, lactate (tissue hypoxia), arterial blood gas, coagulation profile, biomarkers (troponin, proBNP).
  • Imaging: Chest radiograph, focused echocardiography (RUSH exam), ultrasound for fluid status and pericardial tamponade.
  • Electrocardiogram: Identify arrhythmias, ischemia.

Initial Management

Fluid Resuscitation

  • Hypovolemic/Distributive Shock: Administer isotonic crystalloids (30 mL/kg bolus within first 3 hours in septic shock); monitor response and avoid fluid overload.
  • Colloids: Reserved for specific indications (e.g., hypoalbuminemia); no mortality benefit over crystalloids.

Vasoactive Agents

  • Distributive Shock (Septic): Norepinephrine is first-line to maintain mean arterial pressure (MAP) ≥65 mm Hg; add vasopressin or epinephrine if needed.
  • Cardiogenic Shock: Inotropes (dobutamine) to augment contractility; cautious vasopressor use (norepinephrine) to support perfusion.
  • Obstructive Shock: Relieve obstruction (needle decompression, pericardiocentesis) before initiating vasoactives.

Source Control and Specific Therapies

  • Septic Shock: Early broad-spectrum antibiotics within one hour, identify and control infection source (drainage, debridement).
  • Hemorrhagic Shock: Rapid hemorrhage control (surgery, interventional radiology), massive transfusion protocols (ratio-based packed RBC:plasma:platelets).
  • Anaphylactic Shock: Epinephrine intramuscularly, adjunct H1/H2 blockers, corticosteroids.

Supportive Care

  • Oxygen Delivery: Maintain hemoglobin ≥7–9 g/dL; consider transfusion thresholds in active bleeding or ischemia.
  • Ventilation: Lung-protective strategy (ARDSnet) if respiratory failure coexists.
  • Stress Ulcer and DVT Prophylaxis: Proton-pump inhibitors and low-molecular-weight heparin unless contraindicated.

Monitoring and Titration

  • Perfusion Targets: Normalize lactate levels, maintain urine output ≥0.5 mL/kg/hr, and preserve mental status.
  • Organ Function: Serial renal, hepatic, and coagulation studies to detect evolving organ dysfunction.

Advanced Therapies

  • Mechanical Circulatory Support: Intra-aortic balloon pump (IABP), extracorporeal membrane oxygenation (ECMO) in refractory cardiogenic or septic shock with cardiac failure.
  • Renal Replacement Therapy: Initiate for severe acute kidney injury, volume overload, or refractory acidosis.

Prognosis and Disposition

  • Risk Stratification: Utilize scoring systems (SOFA, APACHE II) to estimate severity and guide ICU admission.
  • Disposition: Patients with persistent hemodynamic instability or multi-organ failure require ICU care; respond to initial resuscitation may allow step-down to intermediate care.

Conclusion

Management of shock demands a systematic, protocol-driven approach: rapid classification, targeted resuscitation, source control, and supportive measures. Employing evidence-based guidelines, multidisciplinary collaboration, and continuous reassessment optimizes patient survival and minimizes complications in critically ill populations.

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