Shock

Types / Classification

1. Cardiogenic Shock

• Mechanism: Failure of myocardial pump - low cardiac output despite adequate blood volume
• Causes:
  • Intrinsic myocardial damage: MI, myocarditis
  • Ventricular arrhythmias
  • Extrinsic compression: cardiac tamponade
  • Outflow obstruction: pulmonary embolism
• Characterized by: low CO, high SVR (compensatory), elevated filling pressures (PCWP), cool/clammy skin

2. Hypovolemic Shock

• Mechanism: Inadequate blood/plasma volume leading to low cardiac output
• Causes: Hemorrhage, vomiting, diarrhea, burns, trauma, third-spacing
• Most commonly studied form; basis for ATLS classification

3. Septic Shock (Distributive)

• Mechanism: Dysregulated host response to infection causing peripheral vasodilation and maldistribution of blood flow
• Sepsis = life-threatening organ dysfunction from dysregulated host response to infection
• Septic shock = subset with profound circulatory, cellular, and metabolic abnormalities + greater mortality than sepsis alone
• Most commonly triggered by: gram-positive bacteria > gram-negative bacteria > fungi
• Hemodynamics: high CO (early), low SVR, warm/flushed skin ("warm shock")

4. Neurogenic Shock (Distributive)

• Loss of sympathetic vascular tone after spinal cord injury or high spinal anesthesia
• Acute vasodilation leads to hypotension and tissue hypoperfusion
• Characterized by bradycardia (unlike other shock types) + hypotension

5. Anaphylactic Shock (Distributive)

• IgE-mediated hypersensitivity reaction
• Systemic vasodilation + increased vascular permeability
• Bronchospasm, urticaria, angioedema accompanying hypotension

6. Obstructive Shock

• Obstruction to cardiac output despite normal pump and volume: massive PE, tension pneumothorax, cardiac tamponade

ATLS Classification of Hemorrhagic Shock

Note: These classes were arbitrarily generated and not rigorously validated. Children compensate with large blood loss (showing mainly tachycardia until a tipping point), while elderly patients decompensate earlier.

Stages of Shock

Stage 1: Nonprogressive (Compensated)

• Baroreceptor reflexes activated
• Catecholamine + ADH release
• Renin-angiotensin-aldosterone axis activation
• Generalized sympathetic stimulation
• Result: Tachycardia, peripheral vasoconstriction, renal fluid conservation
• Skin: cool, pale (cutaneous vasoconstriction shunts blood to heart and brain)
• Exception: Septic shock may initially cause warm, flushed skin from vasodilation

Stage 2: Progressive

• Aerobic respiration replaced by anaerobic glycolysis → lactic acid accumulation
• Metabolic lactic acidosis blunts vasomotor response → arterioles dilate
• Blood pools in microcirculation → worsening cardiac output
• Endothelial anoxic injury → risk of DIC
• Vital organs begin to fail

Stage 3: Irreversible

• Severe widespread cell injury with lysosomal enzyme leakage
• Myocardial contractile function worsens (increased NO synthesis)
• Ischemic bowel allows intestinal flora to enter circulation → superimposed bacteremic shock
• Renal failure from ischemic tubular injury (ATN)
• Downward spiral culminating in death despite best therapeutic interventions

Pathogenesis of Septic Shock

• Microbial PAMPs engage TLRs, G-protein-coupled receptors, C-type lectin receptors
• Trigger massive proinflammatory cytokine (TNF, IL-1, IL-6, IL-12) and anti-inflammatory (IL-10, TGF-β) responses simultaneously

• Cytokines loosen tight junctions → protein-rich edema throughout body
• Upregulated NO and vasoactive mediators (C3a, C5a, PAF) → systemic vasodilation and hypotension
• Microvascular dysfunction: heterogeneous capillary flow, loss of autoregulation → oxygen delivery/need mismatch

• Increased tissue factor on monocytes and endothelium
• Decreased anticoagulant factors (TFPI, thrombomodulin, protein C)
• Increased PAI-1 → impaired fibrinolysis
• Neutrophil extracellular traps (NETs) promote coagulation
• → Systemic thrombin activation → DIC in up to 50% of patients

• Insulin resistance and hyperglycemia (cytokines + stress hormones suppress insulin, induce gluconeogenesis)
• Elevated blood glucose, triglycerides, and lactate
• Hyperglycemia suppresses neutrophil bactericidal activity
• Adrenal insufficiency (from DIC causing adrenal necrosis = Waterhouse-Friderichsen syndrome, or suppressed synthesis)
• Lactic acidosis from reduced oxidative phosphorylation

• Hypotension + interstitial edema + microvascular dysfunction + small vessel thrombosis
• Mitochondrial damage from oxidative stress impairs oxygen utilization
• High cytokines/mediators diminish myocardial contractility → ARDS, ATN, hepatic failure

Morphologic Changes (Organs Affected)

Lactate in Shock

• Traditionally viewed as a byproduct of anaerobic metabolism (oxygen debt marker)
• Current evidence shows lactate is also an active metabolite / energy shuttle - transferred between tissues and oxidized as fuel in heart, brain, liver, and kidney
• Elevated lactate in shock can result from: anaerobic glycolysis, high adrenergic state, and impaired hepatic clearance
• Lactate remains a key clinical marker of injury severity and resuscitation adequacy, despite evolving understanding of its role
• Base deficit is a complementary marker

Prognosis

Key Concepts (Summary)

• Shock = systemic tissue hypoperfusion → cellular hypoxia → organ failure
• Three major types: cardiogenic, hypovolemic, septic (+ neurogenic, anaphylactic, obstructive)
• Evolves through: nonprogressive → progressive → irreversible stages
• Septic shock: endothelial injury + vasodilation + DIC + metabolic derangements
• ATLS classifies hemorrhagic shock in 4 classes based on blood loss and clinical signs
• Organs most vulnerable: brain, heart, kidneys, adrenals, GI tract
• Lactate and base deficit are key clinical markers of shock severity