## Discriminating Feature: Cardiovascular Stability **Key Point:** Etomidate is the ONLY induction agent that maintains cardiovascular stability (minimal change in BP and HR), whereas ketamine causes sympathomimetic stimulation with increased heart rate and blood pressure. ### Comparison Table: Etomidate vs Ketamine | Feature | Etomidate | Ketamine | | --- | --- | --- | | **Cardiovascular effect** | Minimal (stable BP/HR) | Sympathomimetic (↑BP, ↑HR) | | **Airway reflexes** | Preserved | Preserved | | **Analgesia** | Absent | Present (potent) | | **Dissociation** | No | Yes (characteristic) | | **Muscle tone** | Decreased | Increased (muscle rigidity) | | **Respiratory depression** | Mild | Mild–moderate | | **Emergence phenomena** | Rare | Common (hallucinations, dysphoria) | | **Adrenal suppression** | YES (single dose) | No | ### Why Cardiovascular Stability Matters **High-Yield:** Etomidate's hemodynamic stability makes it the agent of choice in: - Hypovolemic patients - Septic shock / hemodynamic instability - Critically ill ICU patients - Cardiogenic shock - Elderly with poor cardiac reserve **Clinical Pearl:** Ketamine's sympathomimetic effects (catecholamine release) are beneficial in hypovolemia but problematic in hypertensive patients or those with coronary artery disease. **Warning:** Single-dose etomidate causes transient adrenal suppression (↓ cortisol for 4–8 hours), which is clinically significant in septic shock. Ketamine does NOT suppress adrenal function. ### Mechanism of Cardiovascular Stability Etomidate's preservation of sympathetic tone and lack of direct myocardial depression result in: - No change or minimal decrease in systolic BP - Maintained or slightly increased HR - Preserved cardiac output Ketamine's sympathomimetic effect (via catecholamine release and CNS stimulation) causes: - Increased systolic and diastolic BP - Tachycardia - Increased myocardial oxygen demand [cite:Gupta & Rao Anesthesia 3e Ch 8]
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