Shock: Pathophysiology, Classification, and Management

What is Shock?

Shock is a life-threatening condition characterized by systemic hypoperfusion, leading to inadequate oxygen delivery to tissues and cellular dysfunction. It is one of the most common causes of death in surgical and trauma patients. This guide combines the best insights from two authoritative sources to provide a detailed, comprehensive, and reader-friendly overview of shock, covering its pathophysiology, classification, and management.

Shock is a systemic state of low tissue perfusion that disrupts normal cellular respiration. Without adequate oxygen and glucose, cells switch from aerobic to anaerobic metabolism, producing lactic acid and leading to metabolic acidosis. If untreated, shock progresses to cell death, organ failure, and death.

Pathophysiology of Shock

Shock involves complex changes at the cellular, microvascular, and systemic levels:

1. Cellular Level

• Anaerobic Metabolism: Cells deprived of oxygen switch to anaerobic metabolism, producing lactic acid.
• Metabolic Acidosis: Accumulation of lactic acid leads to systemic acidosis.
• Cell Death: Depletion of glucose causes failure of sodium/potassium pumps, cell lysis, and release of intracellular contents (e.g., potassium).

2. Microvascular Level

• Endothelial Damage: Tissue ischemia activates immune and coagulation systems, damaging capillary endothelial cells.
• Capillary Leakage: Damaged endothelium becomes “leaky,” causing tissue edema and exacerbating hypoxia.

3. Systemic Level

• Cardiovascular System: Reduced preload and afterload trigger sympathetic responses (tachycardia, vasoconstriction).
• Respiratory System: Metabolic acidosis increases respiratory rate to compensate.
• Renal System: Reduced perfusion decreases urine output, activating the renin-angiotensin-aldosterone system.
• Endocrine System: Release of vasopressin and cortisol helps retain water and sensitize cells to catecholamines.

Classification of Shock

Shock is classified based on its underlying cause:

1. Hypovolaemic Shock

• Cause: Reduced circulating volume (e.g., hemorrhage, dehydration).
• Stages:
  • Compensated Shock: Tachycardia, cool peripheries, normal blood pressure.
  • Decompensated Shock: Hypotension, decreased urine output, altered mental status.
  • Irreversible Shock: Profound hypotension, anuria, and unconsciousness.

2. Cardiogenic Shock

• Cause: Heart failure (e.g., myocardial infarction, arrhythmias).
• Signs: Cool, pale skin; distended jugular veins; pulmonary edema.

3. Obstructive Shock

• Cause: Mechanical obstruction of cardiac filling (e.g., cardiac tamponade, pulmonary embolism).
• Signs: Reduced preload, hypotension, and distended neck veins.

4. Distributive Shock

• Cause: Vascular dilation and low systemic resistance (e.g., septic shock, anaphylaxis).
• Signs: Warm skin, hypotension, and high cardiac output.

5. Endocrine Shock

• Cause: Hormonal imbalances (e.g., adrenal insufficiency, thyroid disorders).
• Signs: Hypotension, bradycardia, and poor response to catecholamines.

Hemorrhagic Shock: A Detailed Look

Hemorrhagic shock, a subset of hypovolaemic shock, occurs due to significant blood loss. It is the presumed cause of hemodynamic instability in trauma patients.

Stages of Hemorrhagic Shock

1. Class I:
   • Blood loss: Up to 750 mL (≤15% of blood volume).
   • Signs: Normal pulse rate, blood pressure, and urine output.
2. Class II:
   • Blood loss: 750–1,500 mL (15–30% of blood volume).
   • Signs: Tachycardia (>100 bpm), normal blood pressure, decreased pulse pressure, and reduced urine output (20–30 mL/h).
3. Class III:
   • Blood loss: 1,500–2,000 mL (30–40% of blood volume).
   • Signs: Tachycardia (>120 bpm), hypotension, decreased pulse pressure, and significantly reduced urine output (5–15 mL/h).
4. Class IV:
   • Signs: Severe tachycardia (>140 bpm), hypotension, negligible urine output, and altered mental status.
   • Blood loss: >2,000 mL (>40% of blood volume).

Management of Hemorrhagic Shock

1. External Hemorrhage Control:
   • Direct Pressure: Apply firm pressure to the bleeding site.
   • Tourniquet: For extremity hemorrhage when direct pressure fails.
   • Fracture Reduction: Realign fractures to reduce bleeding.
2. Vascular Access:
   • Peripheral Access: Two large-bore IV lines (14 or 16 gauge) in the antecubital fossae.
   • Central Venous Access: 8.5 Fr catheter (e.g., Cordis catheter) placed via the Seldinger technique.
   • Intraosseous Access: Placement of a hollow bore needle into the medullary space of a long bone (e.g., tibia, humerus).
3. Resuscitation:
   • Permissive Hypotension: Maintain systolic blood pressure (SBP) at 80–90 mm Hg to improve survival.
   • Early Blood Product Administration: Prevents dilutional coagulopathy and treats acute traumatic coagulopathy.
   • Tranexamic Acid: Administer early in suspected massive hemorrhage (based on the CRASH-2 trial).
4. Internal Hemorrhage Control:
   • Pelvic Binder: For pelvic fractures.
   • Resuscitative Thoracotomy: For life-threatening thoracic or abdominal hemorrhage.
   • REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta): Minimally invasive technique to control noncompressible torso hemorrhage.

Ischemia-Reperfusion Injury

Restoring circulation after shock can cause further damage due to the release of accumulated acids, potassium, and inflammatory mediators. This leads to:

• Myocardial Depression: Reduced cardiac output.
• Vascular Dilation: Worsening hypotension.
• Multi-Organ Failure: Due to systemic inflammation and endothelial injury.

Monitoring and Resuscitation

1. Minimum Monitoring:
   • ECG, pulse oximetry, blood pressure, and urine output.
2. Advanced Monitoring:
   • Central venous pressure (CVP), invasive blood pressure, and cardiac output.
3. End Points of Resuscitation:
   • Normalize lactate, base deficit, and mixed venous oxygen saturation.
   • Avoid occult hypoperfusion, which increases mortality.

Complications of Shock

1. Multiple Organ Failure:
   • Defined as failure of two or more organ systems.
   • Mortality rate: 60%.
2. Unresuscitatable Shock:
   • Prolonged shock leads to irreversible cell death and organ failure.

Key Takeaways

• Shock is a systemic state of low tissue perfusion with high mortality if untreated.
• Early recognition and classification are critical for effective management.
• Hemorrhagic shock requires immediate hemorrhage control and resuscitation with blood products.
• Monitoring and resuscitation should focus on restoring tissue perfusion and preventing complications.

Keywords:

• Shock pathophysiology
• Hemorrhagic shock management
• Types of shock
• Resuscitation in shock
• Ischemia-reperfusion injury
• Multiple organ failure
• Permissive hypotension
• Tranexamic acid in trauma
• REBOA technique
• Cardiogenic shock treatment