Key Points
            - Use the highest‑yield diagnostic test early; do not let testing delay time‑critical therapy.
- Set objective targets and reassess frequently.
- Plan definitive source control or disease‑specific therapy when indicated; document follow‑up and patient education.
                                        Algorithm
            - Confirm true emergency with organ injury; set target reduction (usually 20–25% MAP in 1 h).
- Choose agent(s) based on syndrome (dissection needs rapid HR/BP control; pregnancy uses labetalol/hydralazine).
- Admit to ICU; address precipitant; transition to oral regimen once stable.
                                        Clinical Synopsis & Reasoning
            BP with acute target‑organ injury (encephalopathy, ACS, APE, aortic dissection, AKI). Reduce MAP by ~20–25% in the first hour (except aortic dissection/ischemic stroke with unique targets) using IV agents (nicardipine, clevidipine, labetalol). Identify/ treat precipitating cause and avoid rapid overcorrection.
                                        Treatment Strategy & Disposition
            Stabilize ABCs. Initiate guideline‑concordant first‑line therapy with precise dosing and continuous monitoring. Escalate to advanced/procedural interventions based on explicit failure criteria. Define ICU, step‑down, and ward disposition triggers; involve specialty teams early.
                                        Epidemiology / Risk Factors
            - Risk varies by comorbidity and precipitants; see citations for condition‑specific data.
                                        Investigations
            
              
                | Test | Role / Rationale | Typical Findings | Notes | 
|---|
                
                  | Neuro exam, ECG/troponin, BMP/UA, CXR | Target‑organ evaluation | Identify end‑organ involvement | — | 
| CT head (neurologic symptoms) and CTA chest (tearing pain) | Rule out ICH/dissection | Imaging‑driven targets | — | 
| Urine tox/medication review | Etiology | Sympathomimetics, MAOIs, nonadherence | — | 
                
              
             
                                        High-Risk & Disposition Triggers
            
              
                | Trigger | Why it matters | Action | 
|---|
                
                  | Acute target-organ damage (encephalopathy, ACS, APE, aortic dissection) | End-organ injury | ICU; IV titratable agents; specific targets | 
| Pregnancy (severe preeclampsia/eclampsia) | Maternal/fetal risk | Obstetric pathway; Mg; labetalol/hydralazine | 
| Stroke (ischemic/ICH) | BP nuance | Follow stroke-specific targets | 
| Renal failure or pheochromocytoma crisis | Special therapy | Nicardipine/clevidipine; α-blockade then β | 
| Medication nonadherence or stimulant use | Precipitant | Counsel and treat tox | 
                
              
             
                                        Pharmacology
            
              
                | Medication/Intervention | Mechanism | Onset | Role in Therapy | Limitations | 
|---|
                
                  | Nicardipine or Clevidipine infusion | Arterial vasodilators | Minutes | Preferred in neuro/renal syndromes | Titrate with arterial line | 
| Labetalol bolus/infusion | α/β‑blocker | Minutes | Useful in many scenarios | Avoid in asthma/CHF decompensation | 
| Nitroprusside/Nitroglycerin (selected) | Vasodilators | Minutes | For APE/HTN emergencies with ischemia | Cyanide risk (nitroprusside) | 
                
              
             
                                        Prognosis / Complications
            - Outcome depends on timeliness of diagnosis and definitive therapy; monitor for complications.
                                        Patient Education / Counseling
            - Provide red‑flag education, adherence guidance, and explicit return precautions; arrange timely specialty follow‑up.
                  
        
                  References
                      - AHA scientific statement on hypertensive emergencies — Link