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In acute aortic syndromes, shear stress from tachycardia and contractility must be blunted before vasodilation. Esmolol (short-acting β-blocker) rapidly reduces heart rate and dP/dt, providing immediate anti-impulse therapy. Once heart rate is controlled (~60 bpm), a vasodilator such as nicardipine or nitroprusside can titrate systolic blood pressure to ~100–120 mmHg, balancing perfusion with a reduction in wall stress. Initiating nitroprusside first (A) can trigger reflex tachycardia and increased shear. Nicardipine alone (C) similarly risks reflex tachycardia. Withholding labetalol due to HR <60 (D) ignores the need for careful HR/pressure control—esmolol’s titratability is preferred. CCP-C practice: analgesia (e.g., fentanyl) to reduce sympathetic surge, continuous arterial BP monitoring if available, careful titration, and communication with receiving cardiothoracic team. Watch for hypotension that may compromise end-organ perfusion; adjust targets based on neuro status and overall hemodynamics.