Eduovisual
Cardiovascular
Hypertensive emergency vs urgency: outpatient and inpatient triage
— Hypertensive emergency: SBP >180 and/or DBP >120 mmHg plus acute target-organ damage (TOD) — brain, heart, kidneys, retina, aorta, placenta
— Hypertensive urgency: SBP >180 and/or DBP >120 mmHg without acute TOD — asymptomatic or with mild headache/anxiety
— Absolute BP number matters less than rate of rise and presence of end-organ injury; a chronically hypertensive patient may tolerate 220/120 while a previously normotensive eclamptic at 160/110 is in emergency
— Neuro: encephalopathy, confusion, seizure, focal deficit, severe headache → think hypertensive encephalopathy, ICH, ischemic stroke, PRES
— Cardiac: chest pain, dyspnea, pulmonary edema → ACS, acute LV failure, aortic dissection
— Renal: AKI, hematuria, new proteinuria → acute hypertensive nephrosclerosis, scleroderma renal crisis
— Ocular: papilledema, flame hemorrhages, exudates (grade III/IV retinopathy)
— Obstetric: BP ≥160/110 after 20 wks → preeclampsia with severe features/eclampsia
— Catecholamine surge: pheochromocytoma, cocaine/methamphetamine, MAOI–tyramine, clonidine withdrawal
— Step 1: confirm BP in both arms with correct cuff size, repeat after 5 min rest
— Step 2: targeted symptom screen + focused exam + ECG, urinalysis, BMP, troponin, CXR
— Step 3: if any TOD → ICU-level care, IV agents, arterial line; if no TOD → outpatient/urgency pathway
Step 3 management: Asymptomatic severe hypertension found in clinic (e.g., 198/118) does not require ED referral if reliable follow-up exists — restart/uptitrate oral therapy and recheck within days. ED transfer is reserved for symptoms, suspected TOD, pregnancy, or no follow-up. Sending every elevated BP to the ED is a common board-trap overtreatment error and exposes patients to overly rapid lowering.
— Neurologic: thunderclap headache + neck stiffness → SAH; gradual confusion + visual changes + seizures → hypertensive encephalopathy or PRES; sudden focal deficit → ischemic stroke or ICH
— Cardiopulmonary: crushing substernal pain → ACS; tearing interscapular or anterior chest pain radiating to back → aortic dissection; orthopnea, pink frothy sputum → flash pulmonary edema (often with renal artery stenosis)
— Renal: flank pain, oliguria, foamy urine
— Obstetric: RUQ pain, scotomata, brisk reflexes in 2nd/3rd trimester
— Autonomic surge: palpitations, diaphoresis, tremor, episodic — pheochromocytoma; recent cocaine/meth/MDMA; missed clonidine doses
— Missed doses of clonidine, beta-blockers, or short-acting antihypertensives → rebound surges
— NSAIDs, decongestants (pseudoephedrine), oral contraceptives, glucocorticoids, stimulants (ADHD meds), VEGF inhibitors (bevacizumab), calcineurin inhibitors, erythropoietin
— Recreational: cocaine, methamphetamine, MDMA, synthetic cathinones, PCP
— Herbals: licorice (apparent mineralocorticoid excess), ephedra, yohimbine
— Recent MAOI + tyramine-rich food
— Known HTN duration, prior BP averages, last echo (LVH), baseline creatinine, prior strokes
— Snoring/witnessed apneas → OSA; episodic spells → pheo; young woman with abdominal bruit → fibromuscular dysplasia
Board pearl: A patient with SBP 230 who walked in for a med refill and feels fine has urgency, not emergency — abrupt IV lowering risks watershed stroke and acute kidney injury. Conversely, a pregnant woman at 165/108 with a headache is an emergency despite "lower" numbers, because the rate of rise and gravid physiology mean she is one seizure away from eclampsia.
— Measure BP in both arms; >20 mmHg SBP difference suggests aortic dissection or subclavian stenosis
— Use appropriately sized cuff (bladder 80% of arm circumference); undersized cuff falsely elevates
— Confirm with manual auscultation if oscillometric reading is extreme
— Orthostatics if symptoms suggest volume depletion or autonomic surge
— Neuro: mental status, cranial nerves, motor/sensory, reflexes, gait; papilledema and flame hemorrhages, cotton-wool spots, hard exudates on fundoscopy = grade III/IV hypertensive retinopathy → emergency
— Cardiac: S4 (LVH), S3 (failure), new murmur of aortic regurgitation (dissection extending to root), pulse deficits
— Pulmonary: rales, frothy sputum (acute pulmonary edema)
— Vascular: abdominal bruit (renovascular HTN), radio-femoral delay (coarctation in young patient), diminished femoral pulses
— Abdomen: flank tenderness, palpable kidneys (PKD)
— Skin/endocrine: café-au-lait, neurofibromas (pheo/NF1), moon facies (Cushing), thyroid mass
— Distinguish vasoconstricted/high-SVR (cool extremities, MAP-driven afterload disease) from hyperdynamic/sympathetic-surge (warm, tachycardic, tremor)
— Volume status: JVP, lung exam, edema — pulmonary edema with HTN often reflects diastolic failure from chronic LVH, not volume overload, and responds rapidly to afterload reduction (nitroglycerin) more than diuresis alone
Key distinction: Grade III/IV retinopathy = automatic emergency category even without other symptoms because microvascular injury is already occurring. Always look at the fundus before discharging a severely hypertensive patient. A normal exam plus normal labs in an asymptomatic patient strongly supports the urgency pathway and outpatient management.
— BMP/CMP: creatinine (AKI), potassium (hypokalemia → primary aldo; hyperkalemia → CKD), bicarbonate
— Urinalysis with microscopy: hematuria, proteinuria, RBC casts (acute hypertensive nephrosclerosis vs glomerulonephritis)
— CBC: schistocytes suggest hypertensive thrombotic microangiopathy or scleroderma renal crisis
— ECG: LV strain, ischemia, prior infarct, LVH by voltage
— Troponin: if any chest pain, dyspnea, or ECG change
— CXR: pulmonary edema, widened mediastinum (dissection), cardiomegaly
— Pregnancy test in any woman of reproductive age — changes the entire pathway
— Neurologic symptoms → non-contrast head CT first (ICH vs ischemic stroke); MRI for PRES (parieto-occipital vasogenic edema)
— Chest/back pain with pulse differential or widened mediastinum → CT angiography of chest/abdomen for dissection; TEE if unstable
— Dyspnea + edema → BNP, bedside echo for EF, valvular pathology
— Suspected renal: renal ultrasound for size asymmetry (renovascular), kidney biopsy rarely acutely
— More limited: BMP, UA, ECG; targeted history; usually no imaging unless red flags
— Do not routinely order CT head for asymptomatic SBP 200
CCS pearl: On a CCS case, when you click "BP 220/130" the initial orders should be: IV access, continuous telemetry, BMP, CBC, troponin, UA, ECG, CXR, urine pregnancy (if applicable), and fundoscopic exam. Then move the clock 15–30 minutes and re-evaluate — do not start IV antihypertensives until you have confirmed TOD status, except in dissection, eclampsia, pulmonary edema, or active stroke where treatment begins immediately.
— Renovascular: renal Doppler US, CTA or MRA renal arteries — atherosclerotic (older, smokers) vs fibromuscular dysplasia (young women, "string of beads")
— Primary aldosteronism: plasma aldosterone-to-renin ratio (PAC/PRA); hypokalemia + metabolic alkalosis is a clue but only ~30% are hypokalemic
— Pheochromocytoma: plasma free metanephrines (highest sensitivity) or 24-hr urinary metanephrines; CT/MRI adrenals if positive; MIBG for extra-adrenal
— Cushing: 24-hr urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression
— Coarctation: echo, CT/MRI aorta — young patient, leg claudication, rib notching
— OSA: polysomnography — obese, snoring, daytime somnolence, refractory HTN
— Thyroid: TSH
— Renal parenchymal: UA, eGFR, renal US
— Drug-induced: review meds and toxicology screen
— Dissection: CTA chest/abdomen/pelvis is first-line; MRA if contrast contraindicated; TEE bedside if hemodynamically unstable
— Stroke: CT first, then CTA head/neck if candidate for thrombectomy; MRI for posterior circulation
— PRES: MRI shows symmetric posterior white matter vasogenic edema
— Eclampsia: workup is clinical + labs (CBC for hemolysis, LFTs, LDH, uric acid, urine protein/Cr)
Board pearl: A 32-year-old woman with severe HTN, hypokalemia, and abdominal bruit = fibromuscular dysplasia until proven otherwise — confirm with CTA or catheter angiography. Conversely, a 65-year-old smoker with diffuse atherosclerosis, flash pulmonary edema, and a rising creatinine on ACE inhibitor = bilateral atherosclerotic renal artery stenosis. Both cause secondary HTN but the demographics and intervention differ.
— Step 1: SBP >180 or DBP >120? If no → standard HTN management
— Step 2: Any acute TOD? → EMERGENCY pathway
— Step 3: No TOD? → URGENCY pathway
— Reduce MAP by no more than 20–25% in the first hour
— Then to ~160/100–110 over the next 2–6 hours
— Gradually to near-normal over 24–48 hours
— Exceptions where you go faster/lower:
· Aortic dissection: SBP <120 and HR <60 within 20 minutes
· Ischemic stroke not getting tPA: treat only if >220/120; if eligible for tPA, lower to <185/110
· ICH: target SBP 130–140 (per INTERACT/ATACH-2 — avoid going below 130)
· Eclampsia/severe preeclampsia: SBP <160, DBP <110
· Pheochromocytoma: alpha-block first, never beta-block alone
— No IV agents, no rapid lowering
— Reinstate or uptitrate oral therapy (e.g., long-acting amlodipine, lisinopril, or labetalol)
— Brief observation (1–2 hours) for symptom development
— Discharge with follow-up within 1–7 days
— Address adherence, NSAIDs, dietary sodium, missed clonidine
— Chronically hypertensive patients have right-shifted cerebral autoregulation
— Rapid drop → watershed stroke, MI, blindness, AKI
— Short-acting oral nifedipine and sublingual captopril are contraindicated
Step 3 management: In a clinic patient with BP 210/115, no symptoms, normal exam, normal UA — give one dose of their home medication (or start one if newly diagnosed), observe 1 hour, recheck, arrange follow-up in 3–7 days. Sending to ED for parenteral therapy is overtreatment and the wrong answer on the test.
— Esmolol or labetalol IV first (HR <60) → then nitroprusside or nicardipine for SBP <120
— Never start vasodilator first → reflex tachycardia worsens shear stress
— Phentolamine (alpha-blocker) or benzodiazepines + nitroglycerin/nicardipine
— Avoid pure beta-blockers (unopposed alpha → worse vasoconstriction). Labetalol is controversial; many experts allow it after alpha coverage
— Nicardipine or clevidipine IV infusion (titratable, no reflex tachy)
— Labetalol acceptable; avoid nitroprusside in prolonged use (cyanide/thiocyanate toxicity, increased ICP)
— Nitroglycerin IV (preload and afterload) + loop diuretic
— Add nicardipine or clevidipine if needed
— Avoid beta-blockers acutely, avoid hydralazine (reflex tachy)
— Nitroglycerin + beta-blocker (metoprolol or esmolol) once stable
— Avoid hydralazine
— Labetalol or nicardipine IV; target <185/110 before tPA, <180/105 for 24 h after
— Nicardipine or clevidipine, target SBP 130–140
— IV labetalol, IV hydralazine, or PO immediate-release nifedipine
— Plus magnesium sulfate for seizure prophylaxis
— Captopril (ACE inhibitor) — paradoxically the right drug even with rising creatinine
Key distinction: Nitroprusside = fast, broad, but cyanide toxicity with prolonged use (>24–48 h) or renal failure; nicardipine/clevidipine = cleaner titration, preferred in most modern protocols. Fenoldopam = dopamine-1 agonist, preserves renal blood flow — useful in AKI emergencies.
— Resume or uptitrate the patient's existing regimen if non-adherent
— Add a long-acting agent based on comorbidities:
· Amlodipine 5–10 mg PO — fast onset (~24 h peak), well tolerated, works in CKD
· Lisinopril 10–20 mg PO — preferred in diabetes, CKD with proteinuria, HFrEF (check K+, Cr at 1–2 weeks)
· Losartan 50–100 mg PO — ACEi-intolerant
· Labetalol 200 mg PO — good in pregnancy, post-partum
· Chlorthalidone 12.5–25 mg PO — long-acting thiazide, first-line for primary HTN
· Hydrochlorothiazide 25 mg PO — acceptable alternative
— Sublingual nifedipine immediate-release — precipitous drops, strokes, MIs — contraindicated
— Sublingual captopril — unpredictable, not recommended
— IV agents — no role in true urgency
— Cocaine/meth intoxication with HTN but no TOD: benzodiazepines first, then nitroglycerin or phentolamine if needed
— Clonidine withdrawal: restart clonidine; if not possible, labetalol
— MAOI–tyramine crisis: phentolamine
— Choose drug class by comorbidities:
· Black patient without CKD/HF → thiazide or CCB
· Diabetes/CKD with albuminuria → ACEi or ARB
· HFrEF → ACEi/ARB/ARNI + beta-blocker + MRA
· Post-MI → beta-blocker + ACEi
· Pregnancy → labetalol, nifedipine ER, methyldopa
— Most patients need 2 drugs if BP >20/10 above goal
— Reinforce adherence, sodium <2.3 g/day, DASH diet, exercise 150 min/week, weight loss, alcohol limit, smoking cessation
Step 3 management: A reasonable urgency discharge: amlodipine 5 mg PO daily + chlorthalidone 12.5 mg daily, with PCP visit in 5–7 days and home BP log (twice daily). Document teaching, medication list, and closed-loop follow-up — the Step 3 favorite phrase.
— Higher baseline cerebral autoregulation set point → even more vulnerable to rapid lowering
— Start lower, go slower; first-hour MAP reduction closer to 15–20%
— Watch for orthostasis, falls, syncope — leading iatrogenic harms
— Preferred initial PO agents: thiazide (chlorthalidone), CCB (amlodipine), ACEi if no significant CKD
— SPRINT-style intensive control (SBP <120) appropriate in community-dwelling, low fall risk elderly, but not in frail/institutionalized
— Avoid alpha-blockers as first-line in elderly (orthostasis); avoid centrally acting agents (clonidine, methyldopa) outside specific niches
— ACEi or ARB first-line if albuminuria (UACR >30) — accept up to 30% creatinine rise and mild K+ increase
— Stop ACEi/ARB if Cr rises >30% or K+ >5.5 despite mitigation (dietary, loop diuretic, patiromer)
— Add loop diuretic when eGFR <30 (thiazides lose efficacy below ~30)
— Target BP <130/80 in CKD per KDIGO 2021
— In renovascular disease (bilateral RAS): ACEi/ARB can precipitate AKI — monitor closely or avoid
— Treat the BP and the kidneys recover (usually)
— Fenoldopam or nicardipine preferred; avoid nitroprusside (thiocyanate accumulates)
— Labetalol undergoes hepatic metabolism — reduce dose
— Nicardipine, clevidipine — generally safe
— Esmolol — safe (RBC esterase metabolism), short half-life
— Methyldopa — hepatotoxic, avoid in liver disease
— BP often volume-dependent; ultrafiltration is the primary "antihypertensive"
— Avoid aggressive pharmacologic lowering between sessions; risk of intradialytic hypotension
Board pearl: A 78-year-old with SBP 210 and no symptoms — do not aim for 120 in the ED. Reduce to ~160s acutely, restart home meds, and let outpatient titration achieve a goal of <130/80 over weeks, accepting individualized targets if frailty or orthostasis emerges.
— Severe-range BP: ≥160/110 sustained for >15 minutes = emergency, treat within 30–60 min
— First-line acute agents: IV labetalol, IV hydralazine, or PO immediate-release nifedipine 10 mg
— Magnesium sulfate for seizure prophylaxis in preeclampsia with severe features and eclampsia (loading 4–6 g IV, then 1–2 g/h)
— Definitive treatment = delivery if ≥37 wks, or earlier with severe features uncontrolled
— Avoid in pregnancy: ACEi, ARB, direct renin inhibitors, nitroprusside (cyanide to fetus)
— Chronic HTN in pregnancy: labetalol, nifedipine ER, methyldopa
— Postpartum HTN can persist 6 wks; close follow-up at 7–10 days
— Defined by percentile (≥95th = HTN; ≥99th + 5 mmHg with symptoms = emergency)
— Secondary causes dominate in children: renal parenchymal disease, coarctation, renovascular, endocrine
— IV agents: nicardipine, labetalol, esmolol; oral nifedipine, amlodipine
— Lower BP by ≤25% in first 8 hours, normalize over 24–48 hours
— Always evaluate for coarctation (4-extremity BPs) and renovascular causes
— Cocaine, methamphetamine, MDMA, synthetic cathinones: benzodiazepines first; phentolamine or nicardipine if persistent; avoid unopposed beta-blockade (debated for labetalol)
— Clonidine withdrawal: restart clonidine, then taper
— MAOI + tyramine: phentolamine
— Sympathomimetic OTC abuse (pseudoephedrine, ADHD stimulants): discontinue + supportive
— Anabolic steroids and erythropoiesis-stimulating agents: counsel discontinuation
Key distinction: A pregnant patient at 162/112 with a headache requires immediate parenteral lowering within 30–60 minutes plus magnesium — this is not a "let's observe" scenario. Conversely, a non-pregnant patient with the same number and no symptoms is urgency, not emergency.
— Brain: ischemic stroke, ICH (basal ganglia, thalamus, pons, cerebellum), hypertensive encephalopathy, PRES, cognitive decline
— Heart: ACS/MI, acute LV failure with pulmonary edema, demand ischemia, arrhythmia from LVH
— Aorta: dissection (Stanford A or B), rupture, malperfusion syndromes
— Kidney: acute hypertensive nephrosclerosis with rising Cr, hematuria; chronic accelerated CKD
— Eye: grade IV retinopathy with permanent visual loss, optic atrophy
— Microvascular: thrombotic microangiopathy with schistocytes, MAHA, thrombocytopenia — mimics TTP
— Pregnancy: eclampsia, abruption, HELLP, stroke (leading cause of maternal mortality from HTN)
— Overshoot hypotension from too-rapid lowering → watershed cerebral infarcts (parietooccipital "man in the barrel"), AKI, blindness, MI in coronary-stented patients
— Reflex tachycardia with hydralazine or pure vasodilators — dangerous in dissection or ACS
— Cyanide/thiocyanate toxicity with prolonged nitroprusside (>24–48 h) especially in renal failure — altered mental status, lactic acidosis, almond breath; treat with hydroxocobalamin, sodium thiosulfate
— Beta-blocker monotherapy in cocaine/pheo → unopposed alpha → worse HTN and coronary spasm
— ACEi-induced AKI in bilateral RAS
— Sublingual nifedipine catastrophes — strokes, MI
— Progressive LVH, diastolic dysfunction with HFpEF, CKD progression, dementia (vascular)
CCS pearl: If your patient's BP drops from 230/130 to 130/80 in 30 minutes in your CCS case, expect a complication — order a neuro check and recheck Cr at 6 hours; the scoring rubric penalizes overly aggressive lowering. Aim for the MAP -20–25% in 1 hour target and document it.
— Need for continuous IV antihypertensive infusion
— Arterial line for beat-to-beat monitoring (especially dissection, post-tPA stroke, ICH)
— Active TOD requiring close monitoring (encephalopathy, pulmonary edema, AKI, dissection)
— Post-thrombolysis BP management
— Eclampsia or HELLP requiring magnesium and parenteral antihypertensives
— Hypertensive urgency that requires observation due to comorbidities (recent MI, CKD, pregnancy without severe features)
— Acute symptomatic HTN improving on oral therapy but not yet at goal
— Substance-induced HTN under observation
— Asymptomatic
— Normal initial workup (BMP, UA, ECG)
— Reliable follow-up within 1 week
— Has a pharmacy access and understanding of regimen
— No high-risk features (pregnancy, recent stroke, dissection history)
— Cardiology/CT surgery: aortic dissection (type A → emergent OR; type B → medical unless complicated)
— Neurology: stroke, ICH, PRES
— Nephrology: AKI, suspected renovascular disease, scleroderma renal crisis
— OB: any preeclampsia/eclampsia
— Endocrine: suspected pheochromocytoma, primary aldosteronism, Cushing
— Vascular surgery: symptomatic renal artery stenosis being considered for revascularization (rarely indicated — CORAL trial)
— Toxicology/Poison Control: sympathomimetic intoxication, MAOI crisis
— Tertiary center transfer if no CT surgery for type A dissection, no neurointervention for LVO stroke, no MFM for severe preeclampsia <34 weeks
Step 3 management: Build the disposition logic into your answer — "admit to ICU, arterial line, nicardipine infusion, cardiology and CT surgery consults" for type A dissection is a complete CCS response. Naming consults explicitly is rewarded.
— Long-standing poorly controlled HTN, medication non-adherence, recent NSAID/decongestant
— Most common scenario in middle-aged adults
— Atherosclerotic RAS: older smoker, flash pulmonary edema, ACEi-induced AKI, abdominal bruit
— Fibromuscular dysplasia: young woman, "string of beads" on angiography, may also have carotid/vertebral involvement → headache, TIA
— Workup: renal Doppler, CTA/MRA; revascularization rarely beats medical therapy (CORAL)
— Resistant HTN + hypokalemia (only 30%) + metabolic alkalosis
— PAC/PRA ratio >20–30 with PAC >15 ng/dL
— Adrenal CT, AVS to lateralize
— Paroxysmal HTN, palpitations, headache, diaphoresis ("5 P's")
— Associated MEN2, NF1, VHL, SDH mutations
— Plasma free metanephrines; alpha-block (phenoxybenzamine) before beta-block before surgery
— Truncal obesity, striae, easy bruising, glucose intolerance
— 24-h urinary free cortisol, late-night salivary cortisol
— Young patient, leg claudication, rib notching, upper-extremity HTN with lower-extremity hypotension
— Obese, snoring, daytime somnolence, refractory HTN; polysomnography → CPAP
— NSAIDs, OCPs, glucocorticoids, decongestants, stimulants, cyclosporine/tacrolimus, EPO, VEGF inhibitors, MAOI + tyramine, cocaine/meth
Board pearl: Resistant HTN (BP above goal despite 3 drugs including a diuretic, or controlled on 4+) is the trigger to launch a secondary HTN workup — screen for aldosteronism, renovascular disease, OSA, pheo, and Cushing in approximately that order of prevalence.
— High BP is often protective (maintains penumbra)
— Treat only if >220/120 (or >185/110 if tPA candidate)
— Lowering more aggressively → infarct expansion
— Target SBP 130–140 (INTERACT-2, ATACH-2)
— Avoid <130 (does not improve outcomes, may harm)
— Maintain SBP <160 to reduce rebleeding
— Nicardipine preferred; nimodipine PO for vasospasm prevention (does not lower BP much)
— HTN + bradycardia + irregular respirations
— Treat the ICP, not just the BP; lowering BP can worsen cerebral perfusion
— Postoperative, post-procedural, urinary retention, severe pain
— Treat the cause (analgesia, bladder catheter, anxiolysis) first
— Often resolves without antihypertensives
— Office BP elevated, ambulatory normal
— Confirm with home or 24-h ambulatory BP monitoring before escalating therapy
— HTN + tachycardia + hyperthermia + AMS — manage with PTU, beta-blocker, steroids
— HTN with autonomic instability, hyperreflexia/clonus (serotonin) or rigidity (NMS)
— Spinal cord injury at or above T6, triggered by bladder/bowel distension
— Sit patient upright, remove trigger, then nitrates or nifedipine
— A surgical/nursing emergency unique to SCI
Key distinction: A patient with SBP 200 and a focal deficit at hour 2 of an ischemic stroke who is not receiving tPA: do not aggressively lower BP. Treat only if >220/120 and even then by ≤15% in 24 h. This is a classic Step 3 trap — well-meaning aggressive treatment causes infarct expansion.
— General: <130/80 for most adults
— CKD: <130/80
— Diabetes: <130/80
— Age ≥65, community-dwelling: SBP <130 (SPRINT)
— Pregnancy: <140/90 (CHAP trial supports lowering threshold to 140/90 with chronic HTN)
— Frail/limited life expectancy: individualize, often <150/90 acceptable
— Thiazide-type (chlorthalidone preferred), ACEi, ARB, dihydropyridine CCB
— Avoid: alpha-blockers as monotherapy, beta-blockers as monotherapy (unless compelling indication like HFrEF, post-MI, AFib, migraine)
— HFrEF: ARNI/ACEi/ARB + beta-blocker + MRA + SGLT2i
— Post-MI: beta-blocker + ACEi
— CKD with albuminuria: ACEi or ARB + SGLT2i
— Diabetes with albuminuria: ACEi or ARB + SGLT2i + finerenone
— Stroke: thiazide + ACEi (PROGRESS trial)
— Pregnancy: labetalol, nifedipine ER, methyldopa
— Black patients without CKD/HF: thiazide or CCB first-line
— Most patients with stage 2 HTN (≥140/90) need 2 drugs initially, often as a fixed-dose combination to improve adherence (e.g., lisinopril/HCTZ, amlodipine/benazepril)
— DASH diet, sodium <1500–2300 mg/day
— Weight loss (1 mmHg/kg)
— Aerobic exercise 150 min/wk + resistance 2x/wk
— Alcohol ≤2 drinks/day men, ≤1 women
— Smoking cessation
— Stress reduction, adequate sleep, treat OSA
— Statin if ASCVD risk ≥7.5–10%
— Aspirin only for secondary prevention (not primary in most)
— A1c, lipids annually
Step 3 management: Discharge after a hypertensive urgency: lisinopril 20 mg + amlodipine 5 mg + chlorthalidone 12.5 mg (if needed), DASH counseling, home BP cuff, log twice daily, PCP follow-up in 1 week, BMP at 1–2 weeks if on ACEi/diuretic.
— Hypertensive emergency: clinic visit within 1 week of hospital discharge; reassess BP, medication tolerance, end-organ recovery (Cr, neurologic status, vision)
— Hypertensive urgency: clinic visit within 3–7 days for asymptomatic patient discharged from ED
— Newly diagnosed HTN started on therapy: recheck in 2–4 weeks, titrate every 2–4 weeks until at goal
— Validated upper-arm oscillometric cuff (not wrist)
— Twice daily (AM and PM), 2 readings 1 min apart, for 7 days
— Average readings; goal home BP <130/80
— Patient logs improve adherence and engagement
— ACEi/ARB or diuretic: BMP at 1–2 weeks after initiation or dose change (K+, Cr)
— Annual: CMP, lipid panel, A1c, UACR, ECG every 2–3 years
— Screen for new TOD: microalbuminuria, LVH on ECG/echo, retinopathy
— Single biggest cause of recurrent crises is non-adherence
— Address cost (use generics, $4 lists), pill burden (fixed combos), side effects (cough → ARB; edema → reduce CCB; ED → switch off beta-blocker or thiazide)
— Pharmacy synchronization, 90-day refills, pill organizers
— Teach red flags: severe headache, chest pain, shortness of breath, vision changes, focal weakness → return to ED
— Refer to dietitian, cardiac rehab if indicated, smoking cessation counseling, exercise prescription
— Treat OSA aggressively if suspected — CPAP reduces nocturnal HTN
— BP uncontrolled on 3 drugs including a diuretic, or controlled on ≥4 → refer to HTN specialist, screen for secondary causes, consider 24-h ABPM to exclude white coat
Board pearl: A patient repeatedly returning with BP 200/110 despite multiple meds — check adherence first (pill counts, pharmacy refill records, ask non-judgmentally), then assess for white coat, then secondary causes. Empiric uptitration without confirming adherence guarantees iatrogenic harm when the patient eventually takes everything.
— A patient with asymptomatic SBP 220 who declines ED transfer can refuse if they have decisional capacity — document capacity assessment, risks/benefits discussed, agreed-upon outpatient plan, and signed AMA if applicable
— Do not coerce admission; do arrange next-day follow-up and provide return precautions in writing
— Emergency consent doctrine applies in true emergency with altered patient (e.g., encephalopathy) — proceed with stabilization; obtain consent from surrogate when available
— For elective workup (CT angiography with contrast, kidney biopsy), confirm renal function and document iodinated contrast risk
— Highest-risk window is hospital-to-home and ED-to-clinic
— Use closed-loop handoff: scheduled appointment before discharge, written medication list, teach-back about red flags, BP cuff in hand
— Med reconciliation must capture every dose change; discontinued and added drugs explicitly noted
— Post-discharge phone call within 48 h reduces readmission
— Pregnant patient with preeclampsia who declines admission — engage OB, social work, consider involuntary hold only if imminent danger to fetus is jurisdiction-dependent; generally autonomy prevails
— Suspected intimate partner violence presenting with stress-induced HTN — screen privately, document, offer resources, mandatory report only if jurisdiction requires (varies)
— Pediatric severe HTN with suspected non-adherence due to caregiver neglect — CPS report if criteria met
— Never write for sublingual nifedipine IR — outside standard of care
— Verify pregnancy status before starting ACEi/ARB; teratogenicity (2nd/3rd trimester especially)
— Avoid potassium-sparing diuretic + ACEi/ARB without monitoring (hyperkalemia)
— Beta-blocker withdrawal can precipitate rebound HTN/angina — taper, do not stop abruptly
— Repeat ED visits for asymptomatic severe HTN reflect care fragmentation — link patient to PCP, address SDoH (transportation, cost), use community pharmacy programs
Step 3 management: Document "capacity intact, risks of refusal explained including stroke, MI, death; patient verbalized understanding; agreed to follow-up with PCP in 3 days; return precautions given" when discharging against initial recommendation. This protects the patient and the clinician and is a frequent ethics-scenario answer.
— SBP >180 or DBP >120 = crisis threshold
— Lower MAP by ≤25% in first hour (emergency)
— Aortic dissection: SBP <120 in 20 min
— ICH: SBP 130–140
— Stroke (no tPA): treat only if >220/120
— Stroke (tPA candidate): <185/110 before, <180/105 after
— Preeclampsia severe: ≥160/110 — treat within 30–60 min
— Pregnancy chronic HTN: target <140/90 (CHAP)
— General adult goal: <130/80
— Nitroprusside: cyanide/thiocyanate, avoid >24–48 h, contraindicated in renal failure & pregnancy
— Nicardipine/clevidipine: clean titration, modern first-line
— Esmolol: short half-life, hepatic esterase, safe in liver disease
— Labetalol: alpha + beta blocker, useful broadly, hepatic metabolism
— Hydralazine: reflex tachycardia, avoid in dissection/ACS
— Phentolamine: pheo, cocaine, MAOI crisis
— Fenoldopam: preserves renal perfusion
— Sublingual nifedipine IR: never
— Young woman + HTN + abdominal bruit = FMD
— Older smoker + flash pulmonary edema + Cr rises on ACEi = bilateral atherosclerotic RAS
— Episodic HTN + headache + palpitations + diaphoresis = pheo
— Resistant HTN + hypokalemia = primary aldosteronism
— Tearing chest pain + BP differential = dissection
— Pregnant + headache + BP 165/110 + brisk reflexes = severe preeclampsia
— Schistocytes + AKI + HTN = TMA / scleroderma renal crisis
— SCI patient + HTN + bradycardia + flushing above lesion = autonomic dysreflexia
— Grade III/IV retinopathy = automatic emergency
— Symmetric posterior white matter edema on MRI = PRES
— Widened mediastinum on CXR = dissection
— "String of beads" renal angiogram = FMD
Key distinction: Emergency = TOD present, IV drugs, ICU. Urgency = no TOD, oral drugs, outpatient follow-up. The single most testable concept is recognizing that the BP number alone never defines the category — the presence or absence of acute organ injury does.
— "55-year-old man at clinic for med refill, BP 212/118, no symptoms, normal exam." Wrong answers: send to ED, IV labetalol, sublingual nifedipine. Right answer: restart/uptitrate oral therapy, observe briefly, follow-up in 3–7 days.
— "Tearing chest pain radiating to back, BP 200/110 right arm, 160/90 left arm, widened mediastinum on CXR." Right answer: IV esmolol/labetalol first to HR <60, then nitroprusside/nicardipine to SBP <120; CTA chest; CT surgery consult.
— "32-week pregnant woman, BP 168/112, headache, 3+ proteinuria, hyperreflexia." Right answer: IV labetalol or hydralazine, magnesium sulfate, OB consult, plan delivery.
— "Acute left-sided weakness, last known well 90 minutes ago, BP 198/108, NIHSS 12." Right answer: lower BP to <185/110 with IV labetalol/nicardipine, then tPA.
— "30-year-old with chest pain after cocaine, BP 220/115, HR 130." Right answer: benzodiazepines first, nitroglycerin, phentolamine if needed; avoid metoprolol alone.
— "Episodic headaches, palpitations, BP 220/120, adrenal mass." Right answer: alpha-block with phenoxybenzamine first, then beta-block, then surgery.
— "Patient given IV labetalol, BP fell from 220/120 to 110/60 over 30 min, now confused." Right answer: iatrogenic watershed hypoperfusion; stop infusion, give fluids.
— "Discharged from ED yesterday after BP 195/110, asymptomatic, given lisinopril and amlodipine." Right answer: PCP follow-up within 1 week, BMP at 1–2 weeks, home BP log.
— "BP 165/100 on lisinopril, amlodipine, HCTZ; K+ 3.2." Right answer: screen for primary aldosteronism with PAC/PRA ratio.
CCS pearl: When the stem ends with "What is the next best step?" and the BP is severe, the presence or absence of TOD is your single discriminator. Read the symptoms, exam, and labs carefully before reaching for any drug — the answer is often observation and oral therapy, not IV escalation.
The bottom line: Hypertensive crisis is triaged by the presence (emergency → IV agents in the ICU with MAP -20–25% per hour, organ-specific targets) or absence (urgency → oral agents with close outpatient follow-up) of acute end-organ damage — not by the BP number itself.
— Dissection: SBP <120 in 20 min (beta-block first)
— ICH: SBP 130–140
— Ischemic stroke without tPA: treat only if >220/120
— Pre-tPA: <185/110
— Severe preeclampsia: <160/110 + magnesium
— All others: ≤25% MAP reduction in first hour