Hypertensive Emergencies & Acute Aortic Syndromes

Triage & Dual-Arm Hemodynamics: Place on cardiac monitor, pulse oximetry, and cycle NIBP on both upper extremities simultaneously. Place two 18G IV cannulae (leave right radial wrist free for arterial line) [1,2].

Fentanyl: 1 mcg/kg IV bolus (50–100 mcg in an 80 kg adult) over 2 min; repeat 25–50 mcg q5min PRN pain/sympathetic surge [1].

Blunt pain-driven catecholamine surge to immediately reduce ventricular contractility ( ) and shear stress on the aortic intimal tear; detect inter-arm SBP differential greater than 20 mmHg [1,2].

Point-of-Care Diagnostics: Perform 12-lead ECG (evaluate for inferior STEMI from RCA ostial dissection or LVH strain) and Bedside POCUS (Parasternal Long Axis [PLAX], Suprasternal Notch, Subxiphoid, Abdominal Aorta) [1,2].

Esmolol (First-Line Anti-Impulse in AAS): Load 500 mcg/kg (0.5 mg/kg; 40 mg for 80 kg) IV over 1 min, then start continuous infusion at 50 mcg/kg/min (24 mL/hr of 10 mg/mL solution for 80 kg), titrating by 50 mcg/kg/min q4min (Max 300 mcg/kg/min) [1,2].

Mandatory β-blockade BEFORE vasodilators in AAS. Reduces HR to < 60 bpm and lowers left ventricular impulse ( max), arresting false-lumen propagation [1,2].

Invasive Hemodynamic Monitoring: Insert radial 20G arterial line in the limb with the blood pressure reading (typically the right radial artery unless innominate artery is dissected) [1,2].

Alternative β-Blocker (Labetalol): 20 mg IV slow push over 2 min, followed by 40–80 mg IV q10min (Max cumulative 300 mg), OR infusion at 2 mg/min (120 mg/hr) [1,3].

Avoid under-reading true central aortic root pressure caused by subclavian/innominate branch compromise; combined α1/β blockade lowers SVR and simultaneously [1,3].

Afterload Reduction (Vasodilator Phase): Initiate IV dihydropyridine calcium channel blocker if SBP > 120 mmHg HR < 60 bpm is achieved in AAS, OR as immediate first-line monotherapy in non-aortic hypertensive emergencies (e.g., Encephalopathy, AKI) [3,4].

Nicardipine: Start at 5 mg/hr IV (50 mL/hr of standard 0.1 mg/mL concentration); increase by 2.5 mg/hr (25 mL/hr) every 5 min to max 15 mg/hr (150 mL/hr) [3].
Clevidipine: 1–2 mg/hr IV, double q90s (Max 32 mg/hr) [3].

Selective arteriolar L-type Ca²⁺ channel blockade lowers Systemic Vascular Resistance (SVR) without venous pooling or reflex tachycardia (once β-blocked). AAS Target: SBP 100–120 mmHg. Non-AAS Target: Reduce MAP by 15–25% in Hour 1 [1,3].

Definitive Vascular Imaging & Surgical Activation: Transport with portable monitor and infusion pumps to ECG-Gated CT Angiography (CTA) of the Chest, Abdomen, and Pelvis (non-contrast + arterial + delayed phases). Alert Cardiothoracic Surgery for Stanford Type A [1,2].

Flash Pulmonary Edema (SCAPE) Override: High-dose Nitroglycerin 400–800 mcg (0.4–0.8 mg) IV bolus over 2 min + infusion starting at 100–200 mcg/min + BiPAP/CPAP (10/5 cmH₂O) [3,5].

Non-contrast CT identifies crescentic high-attenuation Intramural Hematoma (IMH); CTA maps the primary intimal tear, true vs. false lumen, and visceral branch malperfusion [1,2].