Shock

Definition

Classification

1. Hypovolemic Shock

• Cause: Loss of blood volume (hemorrhage, burns, vomiting, diarrhea, excessive sweating)
• Hemodynamics: Low CO, high SVR, low CVP, low mixed venous O2 saturation
• Mechanism: Reduced venous return → reduced preload → reduced cardiac output → hypoperfusion

2. Cardiogenic Shock

• Cause: Pump failure - intrinsic (MI, arrhythmia, cardiomyopathy) or extrinsic/obstructive (cardiac tamponade, pulmonary embolism, tension pneumothorax)
• Hemodynamics: Low CO, high SVR, HIGH CVP (backed-up venous pressure), low mixed venous O2 saturation
• Note: Obstructive shock (tamponade, PE) is sometimes listed as its own fourth category

3. Distributive Shock

• Septic shock - dysregulated host response to infection; bacterial endotoxin/gram-positive toxins activate TLRs → TNF, IL-1, IL-6, IL-12 cascade → endothelial activation, vasodilation, microvascular injury, DIC
• Anaphylactic shock - IgE-mediated mast cell degranulation → massive histamine release → vasodilatation
• Neurogenic shock - high spinal cord injury → loss of sympathetic outflow → vasodilatation and bradycardia

4. Endocrine Shock

• Adrenal insufficiency (Addison's, relative insufficiency in sepsis), hypothyroidism (low CO from reduced inotropy + bradycardia), thyrotoxicosis (high-output failure). May combine features of hypovolemic and distributive shock. - Bailey and Love's Short Practice of Surgery, p. 34

Pathophysiology & Stages (Guyton)

Stage 1 - Nonprogressive (Compensated) Shock

1. Baroreceptor reflexes - immediate sympathetic activation within 30 seconds
2. CNS ischemic response - extreme sympathetic discharge when BP < 50 mmHg
3. Renin-Angiotensin-Aldosterone - peripheral vasoconstriction + sodium/water retention (10-60 min)
4. ADH (vasopressin) - arteriole and venous constriction + water retention
5. Adrenal catecholamines - epinephrine/norepinephrine → tachycardia, vasoconstriction
6. Reverse stress-relaxation - blood vessels contract around diminished volume
7. Fluid absorption - interstitial → intravascular shift; thirst; renal conservation (1-48 hours)

Stage 2 - Progressive Shock (Positive Feedback / Vicious Cycles)

• Cardiac depression: Coronary flow falls → myocardial ischemia → further reduced CO
• Vasomotor failure: Brainstem ischemia → vasomotor center fails → vasodilation → catastrophic BP drop (after 10-15 min of severe ischemia)
• Microvascular sludging: Lactic and carbonic acid accumulation → RBC agglutination → capillary obstruction
• Endothelial injury: Activated neutrophils + oxidants + cytokines → capillary leak
• Coagulopathy: Endothelial activation + consumptive coagulopathy → DIC

Stage 3 - Irreversible Shock

• Extensive tissue necrosis, lysosomal enzyme release, depletion of cellular ATP and creatine phosphate
• ATP degrades to adenosine → diffuses out of cells → converted to uric acid → cannot be resynthesized (only ~2%/hour regeneration)
• At this point, even restoration of cardiac output to normal cannot prevent death - Guyton & Hall Medical Physiology, p. 302-304

ATLS Hemorrhagic Shock Classification

Pathogenesis of Septic Shock (in detail)

1. Pro-inflammatory cascade: Microbial PAMPs (LPS, peptidoglycan, M-protein) bind TLRs → NF-κB activation → TNF, IL-1, IL-12, IFN-γ, HMGB1, prostaglandins, PAF → endothelial adhesion molecule upregulation, capillary leak, DIC
2. Counter-regulatory immunosuppression: Th1 → Th2 cytokine shift, IL-10, soluble TNF receptor, lymphocyte apoptosis → septic patients oscillate between hyperinflammatory and immunosuppressed states

• Gram-positive bacteria (most frequent)
• Gram-negative bacteria
• Fungi
• Viral infections (e.g. SARS-CoV-2)

Cellular & Metabolic Consequences

• Anaerobic metabolism → lactic acidosis → base deficit
• The Lethal Triad (in hemorrhagic/traumatic shock): Acidosis + Hypothermia + Coagulopathy - these three feed each other in a destructive cycle
• Hypothermia impairs clotting enzyme function; acidosis worsens coagulopathy; coagulopathy perpetuates hemorrhage
• Large-volume crystalloid resuscitation contributes to the triad (dilutional coagulopathy + heat loss from cold fluids)
• ATP depletion → cell membrane pump failure → cellular swelling (oncotic cell death)
• DIC: Widespread microvascular thrombi form in septic/traumatic shock → consumptive coagulopathy → paradoxical bleeding - Sabiston Textbook of Surgery, p. 571

Organ Effects

Management Principles

General

• Identify and treat the cause - source control is the foundation
• Restore tissue perfusion: target normalization of serum lactate, base deficit, pH, and urine output
• Blood pressure alone is insufficient as an endpoint - occult hypoperfusion can exist with normal vitals

Fluid Resuscitation

• Hemorrhagic shock: Limit crystalloids (avoid resuscitation injury); after 1-2 L crystalloid, switch to blood products. Damage control resuscitation: balanced ratio of PRBCs:FFP:platelets (~1:1:1)
• Septic shock (Surviving Sepsis Campaign): 30 mL/kg IV crystalloid within 3 hours; then reassess with dynamic markers
• Neurogenic shock: Small volumes isotonic crystalloid; vasopressors early (phenylephrine or norepinephrine) to restore vascular tone
• Avoid routine pulmonary artery catheter (no longer recommended)

Vasopressors

• Norepinephrine - first line for septic shock and most distributive shock
• Vasopressin - adjunct in septic shock; add when norepinephrine dose is escalating
• Dopamine - alternative to norepinephrine in selected patients (bradycardic)
• Phenylephrine - pure alpha agonist; useful in neurogenic shock

Specific Treatments

• Cardiogenic shock: Revascularization (PCI for MI), inotropes (dobutamine), mechanical circulatory support (IABP, Impella)
• Septic shock: Antibiotics within 1 hour of recognition, source control, corticosteroids if vasopressor-refractory
• Anaphylactic shock: Epinephrine IM (first line), antihistamines, corticosteroids
• Cardiac tamponade: Pericardiocentesis
• Tension pneumothorax: Needle decompression → chest tube

Acidosis

• Treat the underlying cause of acidosis, not the pH value alone
• Sodium bicarbonate: no proven benefit for metabolic acidosis; rapid infusion may worsen intracellular acidosis (CO2 diffusion); use is controversial and generally reserved for extreme scenarios
• THAM (tromethamine): Alternative buffer; sodium-free, effective during hypothermia, pKa 7.8 - Sabiston Textbook of Surgery, p. 571-572

Key Summary Points

• Shock = inadequate tissue perfusion → cellular hypoxia → lactic acidosis
• Four types: Hypovolemic, Cardiogenic/Obstructive, Distributive (septic/anaphylactic/neurogenic), Endocrine
• Three stages: Compensated (reversible with treatment), Progressive (positive feedback loops), Irreversible (cellular death, ATP depletion)
• The lethal triad in traumatic/hemorrhagic shock: acidosis + hypothermia + coagulopathy
• Septic shock mortality ~40%; first-line treatment = antibiotics + source control + norepinephrine
• Resuscitation endpoints: lactate clearance, base deficit normalization, urine output > 0.5 mL/kg/hr