Regarding the pathophysiology of different types of shock, all of the following statements are correct EXCEPT:

Explanation

## Pathophysiology of Shock Types ### Classification by Mechanism | Shock Type | Primary Defect | Mechanism | Compensation | |---|---|---|---| | Cardiogenic | Pump failure | ↓ CO, ↑ LVEDP | SNS activation, vasoconstriction | | Hypovolemic | ↓ Circulating volume | ↓ Preload, ↓ CO | SNS activation, fluid shift, vasoconstriction | | Distributive (Septic) | Vasodilation + ↑ permeability | NO-mediated, endotoxin | Initially maintained CO, later ↓ CO | | Obstructive | Impaired venous return | Tension pneumothorax, PE, tamponade | SNS activation | ### Why Option 4 is Incorrect **Key Point:** Anaphylactic shock is a **distributive** shock, NOT a hemorrhagic/hypovolemic shock. **High-Yield:** The primary mechanism in anaphylactic shock is: 1. **Massive mast cell degranulation** → release of histamine, tryptase, leukotrienes 2. **Vasodilation** (especially arteriolar) → decreased systemic vascular resistance 3. **Increased capillary permeability** → fluid extravasation into interstitium 4. **Bronchoconstriction** and laryngeal edema → airway compromise The hemoglobin concentration is **normal** in anaphylaxis; the shock results from distributive failure (vasodilation + capillary leak), not from loss of circulating RBCs. **Clinical Pearl:** Anaphylaxis can progress to true hypovolemic shock if massive fluid shifts occur, but the *primary* defect is distributive, not hemorrhagic. ### Correct Statements (Options 1, 2, 3) - **Option 1 (Cardiogenic):** Correct — pump failure is the hallmark; CO falls acutely. - **Option 2 (Septic):** Correct — LPS-induced NO production causes vasodilation and increased vascular permeability. - **Option 3 (Hypovolemic):** Correct — sympathetic compensation (tachycardia, vasoconstriction) is a hallmark early response. [cite:Robbins 10e Ch 4]