Shock: Definition and Classification

Definition of Shock

• Shock is a widespread process that impairs tissue perfusion causing cellular, metabolic, and hemodynamic alterations.

Classification of Shock

• Hypovolemic shock: results from fluid loss, either external or internal.
• Cardiogenic shock: occurs due to the heart's inability to pump effectively.
• Distributive shock: causes blood maldistribution within the body, further categorized into:
  • Septic shock: arises from infection entering the body.
  • Anaphylactic shock: caused by severe allergic reactions.
  • Neurogenic shock: results from the loss of sympathetic nerve function

Stages of Shock

• Initial stage: decreased cardiac output leads to anaerobic metabolism, producing lactic acid.
• Compensatory stage: sympathetic nervous system activation increases heart rate, vasoconstriction, and redirects blood to vital organs. This involves neural, hormonal, and chemical responses.
• Progressive stage: compensatory mechanisms fail, leading to organ dysfunction like cardiovascular, central nervous system, pulmonary, renal, and gastrointestinal impairments.
• Refractory stage: shock becomes unresponsive to treatment, leading to multiple organ dysfunction syndrome (MODS) and eventual death.

Pathophysiology of the Compensatory Stage

• Neural response: increased heart rate, contractility, and vasoconstriction to redirect blood.
• Hormonal response: Includes:
  • Renin response: causes vasoconstriction, aldosterone, and ADH release.
  • Anterior pituitary stimulation: releases ACTH, leading to glucocorticoid release.
  • Adrenal medulla stimulation: releases epinephrine and norepinephrine, reinforcing compensatory mechanisms.
• Chemical response: hyperventilation, resulting in respiratory alkalosis.

Pathophysiology of the Progressive Stage

• Cardiovascular system: Myocardial hypoperfusion causes dysfunction. Ventricular failure occurs.
• Central nervous system: Cerebral hypoperfusion causes SNS failure, cardiac and respiratory depression, and thermoregulatory failure.
• Pulmonary system: Pulmonary capillary membrane permeability, microemboli, and vasoconstriction lead to acute lung injury (ALI) and ventilatory failure.
• Renal system: Renal vasoconstriction causes renal hypoperfusion resulting in acute kidney injury (AKI).
• Gastrointestinal system: Splanchnic vasoconstriction and hypoperfusion impair gut function. Enteric bacteria release into the bloodstream, exacerbating shock.

Assessment and Diagnosis

• Mean arterial pressure (MAP) less than 60 mmHg and systolic BP less than 90 mmHg.
• Tachycardia or bradycardia.
• Altered mental status.
• Elevated serum lactate, arterial base deficit, serum bicarbonate, and reduced central or mixed venous oxygen saturation.

Medical Management

• Focus on restoring tissue perfusion through:
  • Improving pulmonary gas exchange: Ensuring adequate oxygenation through airway management, supplemental oxygen, and mechanical ventilation.
  • Adequate cardiac output and hemoglobin: Using fluids (crystalloids, colloids, or blood products) and medications like vasoconstrictors, vasodilators, inotropes, and anti-dysrhythmics.

Hypovolemic Shock

• Occurs due to inadequate intravascular volume, leading to decreased tissue perfusion and shock syndrome.
• Types:
  • Absolute hypovolemia: external fluid loss (blood, plasma, etc).
  • Relative hypovolemia: vasodilation reduces effective circulating volume.

Pathophysiology of Hypovolemic Shock

• Causes: Loss of circulating fluid volume, reduced venous return, lowered preload, decreased CO, inadequate cellular oxygen supply, and ineffective tissue perfusion.

Clinical Manifestations of Hypovolemic Shock

• Initial stage: fluid loss up to 15% (750 ml), compensatory mechanisms maintain CO, appears asymptomatic.
• Compensatory stage: fluid loss of 15-30% (750-1500 mL), CO drops, leading to:
  • Increased heart rate (more than 100 bpm).
  • Increased respiratory rate (20-30 bpm).
  • Respiratory alkalosis and hypoxemia (low PaCO2 and low PaO2).
  • Decreased urine output (20-30 ml/h).
  • Pale and cool skin with delayed capillary refill.
  • Flat jugular veins.
• Progressive stage: fluid loss of 30-40% (1500-2000 mL), compensatory mechanisms fail, resulting in:
  • Heart rate exceeding 120 bpm, dysrhythmias, and myocardial ischemia..
  • Respiratory distress.
  • Respiratory and metabolic acidosis, hypoxemia (high PaCO2, low bicarbonate, low PaO2).
  • Oliguria.
  • Ashen, cold, and clammy skin with marked delayed capillary refill.
  • Lethargy due to declining cerebral perfusion.
• Refractory stage: fluid loss exceeding 40% (2000 mL), compensatory mechanisms collapse, leading to:
  • Severe tachycardia and hypotension.
  • Absent peripheral pulses and capillary refill.
  • Cyanotic and diaphoretic skin.
  • Unresponsiveness, and multiple organ system failure manifestations.

Hemodynamic Parameters in Hypovolemic Shock

• Reduced CO and cardiac index.
• Decreased preload (reduced CVP, RAP, PAOP).
• Increased afterload (elevated SVR).
• Lowered MAP.

Management of Hypovolemic Shock

• Focus on addressing the cause of hypovolemia and restoring circulatory volume.
• Methods include:
  • Stopping fluid loss.
  • Administering fluids (crystalloids, colloids, blood products).
  • Monitoring for fluid overload.

Explore the critical concepts surrounding shock, including its definition, classification into hypovolemic, cardiogenic, and distributive types, and the stages of shock. Learn how tissue perfusion and metabolic alterations affect the body in this essential medical overview.