CCS Integrated Cases

CCS case: outpatient management of newly diagnosed hypertension

Clinical Overview and When to Suspect Hypertension

— Normal: <120/<80

— Elevated: 120–129/<80

— Stage 1 HTN: 130–139 or 80–89

— Stage 2 HTN: ≥140 or ≥90

— Hypertensive urgency: ≥180/≥120 without target-organ damage; emergency if damage present

— Do not diagnose on a single office reading unless ≥180/120 or with end-organ damage

— Confirm with out-of-office measurement: ambulatory BP monitoring (ABPM, gold standard) or home BP monitoring (HBPM) over ≥7 days

— Average ≥2 readings on ≥2 separate occasions

— Asymptomatic adult with elevated office BP at routine visit

— New headache, epistaxis, or visual changes in middle-aged adult

— Incidental finding on pre-employment, pre-op, or insurance physical

— Workup of LVH on ECG, microalbuminuria, or unexplained CKD

— Screen all adults ≥18; annually if ≥40 or at increased risk (overweight, Black race, family hx)

— Every 3–5 years if 18–39 with normal BP and no risk factors

— ~half of US adults meet criteria under 2017 thresholds

— Onset <30 or >55, resistant HTN, abrupt worsening, hypokalemia, abdominal bruit, episodic spells

— Common causes: primary aldosteronism, renovascular disease, OSA, CKD, thyroid disease, pheochromocytoma, Cushing, drug-induced (NSAIDs, OCPs, stimulants, decongestants)

— Seated 5 min, back supported, feet flat, arm at heart level, no caffeine/exercise/smoking 30 min prior, appropriate cuff size, average of 2 readings

Board pearl: White-coat HTN (elevated in office, normal at home) and masked HTN (normal in office, elevated at home) both require ABPM or HBPM to identify — masked HTN carries CV risk similar to sustained HTN and must be treated.

Definition (ACC/AHA 2017, still current for Step 3):

Diagnosis requires confirmation:

When to suspect on a CCS case:

Epidemiology and screening (USPSTF Grade A):

Secondary HTN — suspect when:

Proper measurement technique (frequently tested):

Presentation Patterns and Key History

— 52-year-old presents to your office for routine physical. BP 148/92 today; previous visit 6 months ago 144/88. Asymptomatic. BMI 31. Father had MI at 60.

— Headache (especially occipital, AM), blurred vision, chest pain, dyspnea, focal neuro deficit, hematuria, flank pain

— These flip the case from outpatient to ED triage

— Duration of elevated readings, prior diagnoses, family history of HTN/CVD/stroke/CKD

— Lifestyle: dietary sodium, alcohol (>2 drinks/d in men, >1 in women), tobacco, physical activity, weight trajectory

— Sleep: snoring, witnessed apnea, daytime sleepiness, neck circumference (OSA screen with STOP-BANG)

— Medications: NSAIDs, oral/intranasal decongestants, stimulants, OCPs, glucocorticoids, SNRIs, erythropoietin, herbal (licorice, ephedra), cocaine/amphetamines

— Symptoms of secondary causes: episodic palpitations/sweating/headache (pheo), muscle weakness/cramping (hyperaldo), heat intolerance/weight loss (hyperthyroid), proximal weakness/striae (Cushing)

— Age, sex, race, total/HDL cholesterol, diabetes, smoking, treated HTN

— Calculate 10-year ASCVD risk using Pooled Cohort Equations

CCS pearl: On the CCS interface, after obtaining BP and history, order home BP log as a first action for any new elevated reading <180/120 — this both confirms diagnosis and avoids treating white-coat HTN. Schedule a follow-up visit at 2–4 weeks with the log.

Key distinction: Stage 1 HTN (130–139/80–89) is treated pharmacologically only if ASCVD ≥10%, DM, CKD, or clinical CVD; otherwise lifestyle alone first. Stage 2 always gets drug + lifestyle.

Typical CCS opening:

Most patients are asymptomatic — HTN is the "silent killer." Symptoms suggest either severe HTN or a complication.

Symptoms that should prompt urgency/emergency workup:

Key history elements (must obtain on the CCS history screen):

ASCVD risk inventory (essential for Stage 1 treatment decision):

Physical Exam Findings and Hemodynamic Assessment

— BP in both arms at first visit; inter-arm difference >15 mmHg suggests subclavian stenosis or aortic disease

— HR, RR, SpO2, weight, height, BMI, waist circumference

— Recheck BP after 5 min seated rest; if elevated, repeat in opposite arm and in standing position (orthostatics in elderly/diabetic)

— Body habitus (central obesity → metabolic syndrome, Cushing)

— Moon facies, buffalo hump, purple striae → Cushing

— Sweating, tremor, anxious → pheo or hyperthyroid

— Fundoscopy for hypertensive retinopathy (AV nicking, copper/silver wiring, hemorrhages, exudates, papilledema)

— Thyromegaly, JVD

— Carotid bruits (atherosclerotic burden)

— Displaced/sustained PMI (LVH), S4 gallop (stiff LV), murmurs (AR widens pulse pressure; AS in elderly)

— Radio-femoral delay → coarctation (especially in young patient with HTN)

— Abdominal bruit (renovascular HTN, especially lateralizing)

— Palpable kidneys (PCKD)

— Striae, central adiposity

— Diminished/delayed femoral pulses (coarctation)

— Lower-extremity edema (HF, CKD, CCB-related)

— Skin: neurofibromas/café-au-lait (NF1 → pheo, RAS)

Step 3 management: A young adult (<30) with HTN, diminished femoral pulses, and upper-extremity HTN → order echocardiogram and CT/MR angiogram of the aorta for coarctation. Refer to cardiology/cardiothoracic surgery.

Board pearl: Hypertensive emergency on exam = severely elevated BP plus evidence of acute target-organ damage (papilledema, neuro deficit, chest pain, pulmonary edema, AKI, hematuria) → ED, IV antihypertensives, NOT an outpatient case anymore.

Vitals on arrival:

General appearance:

Head/Neck:

Cardiac:

Pulmonary: crackles suggest LV dysfunction/HF

Abdomen:

Extremities:

Neuro: baseline cognitive screen, focal deficits

Diagnostic Workup — Initial Labs

— BMP: Na, K, Cl, HCO3, BUN, creatinine, glucose, calcium

— CBC (baseline)

— Lipid panel (fasting or non-fasting)

— HbA1c (screen for DM, drives treatment threshold)

— TSH (thyroid as secondary cause)

— Urinalysis with urine albumin-to-creatinine ratio (UACR) — screens for CKD/hypertensive nephrosclerosis

— ECG — baseline for LVH, prior MI, conduction disease

— K+ low (<3.5) before any diuretic → suspect primary aldosteronism; order aldosterone:renin ratio

— K+ high → consider CKD, will guide RAAS inhibitor choice

— Creatinine/eGFR → defines CKD stage, drug dosing, drug selection

— UACR ≥30 mg/g → CKD; ACEi/ARB becomes preferred first-line

— Glucose/A1c ≥6.5% → diabetic HTN target and ACEi/ARB preferred

— ECG LVH (Sokolow-Lyon, Cornell) → end-organ damage already present, reinforces treatment urgency

— Order BMP, CBC, lipid panel, HbA1c, TSH, UA with UACR, 12-lead ECG

— Order home BP monitoring log (AM and PM readings × 7 days)

— Schedule follow-up visit in 2–4 weeks

— Advance clock to that follow-up

CCS pearl: Do not order renal artery duplex, plasma metanephrines, aldosterone/renin, or 24-hr cortisol on every patient. Order these only when history/exam/initial labs raise suspicion for secondary HTN — random secondary workup is penalized as low-yield.

Board pearl: Echocardiogram is not routine in newly diagnosed HTN — order only if symptoms of HF, murmur, or ECG suggests LVH/prior MI.

Baseline labs for every newly diagnosed HTN patient (AHA/ACC):

Why each test matters on CCS:

Ordering sequence on CCS interface (Day 0, office visit):

Calculate ASCVD 10-yr risk at the follow-up visit using lipids + BP + demographics

Diagnostic Workup — Confirmatory and Secondary HTN Studies

— ABPM (preferred, USPSTF): 24-hour readings; daytime average ≥130/80 confirms HTN; allows detection of nocturnal non-dipping (CV risk marker), white-coat, and masked HTN

— HBPM: ≥2 readings AM and PM × 7 days, discard day 1, average remaining; ≥130/80 confirms

— Onset <30 or sudden onset/worsening, resistant HTN (≥3 drugs incl. diuretic), severe HTN, target-organ damage out of proportion, suggestive clues on history/exam, hypokalemia, drug-resistant

— Primary aldosteronism (most common secondary cause): plasma aldosterone:renin ratio (ARR); ratio >20 with aldo >15 ng/dL → confirmatory salt-loading test, then adrenal CT and adrenal vein sampling

— Renovascular HTN: renal artery duplex US first-line; CTA/MRA if duplex inconclusive; fibromuscular dysplasia in young women, atherosclerotic in older

— Pheochromocytoma: plasma free metanephrines (high sensitivity) or 24-hr urine metanephrines; then CT/MRI adrenals; MIBG if extra-adrenal suspected

— Cushing syndrome: 1 mg overnight dexamethasone suppression, late-night salivary cortisol, or 24-hr urinary free cortisol

— OSA: STOP-BANG screen → polysomnography

— Thyroid: TSH already done at baseline

— Coarctation: echo + CT/MR angiography

— CKD: eGFR, UACR, renal US

— Echocardiogram for HF symptoms or ECG LVH

— Carotid duplex if bruit or TIA symptoms

— Fundoscopy for retinopathy

— Repeat UACR annually

Key distinction: Aldosterone:renin ratio, not random aldosterone alone, screens for primary aldosteronism. Hold MRAs (spironolactone, eplerenone) ≥4 weeks before testing; ACEi/ARB/diuretics can usually be continued with interpretation caveats; beta-blockers raise the ratio (false positive).

Confirming the diagnosis (out-of-office BP):

When to pursue secondary HTN workup (any of):

Targeted secondary workup:

End-organ damage assessment (when indicated):

Risk Stratification and First-Line Management Logic

— Normal (<120/80): lifestyle counseling, recheck annually

— Elevated (120–129/<80): lifestyle interventions, recheck 3–6 months

— Stage 1 (130–139/80–89):

— Stage 2 (≥140/≥90): lifestyle + 2 drugs (usually from different classes), reassess in 1 month

— Older guidelines used <140/90 — use the newer target on Step 3

— Frail elderly with high fall risk: individualize, often <140/90 acceptable

— DASH diet: ↓BP ~11 mmHg

— Weight loss: ~1 mmHg per kg lost

— Aerobic exercise 90–150 min/wk: ↓5–8 mmHg

— Sodium <1500 mg/d (definitely <2300): ↓5–6 mmHg

— Potassium 3500–5000 mg/d (unless CKD): ↓4–5 mmHg

— Alcohol limit (≤2 drinks/d men, ≤1 women): ↓4 mmHg

— Tobacco cessation (CV risk, not BP per se)

— Thiazide diuretic (chlorthalidone preferred over HCTZ for longer half-life and outcomes data)

— ACE inhibitor (lisinopril)

— ARB (losartan, valsartan)

— Dihydropyridine CCB (amlodipine)

— DM with albuminuria, CKD, HF → ACEi/ARB

— Post-MI, HF → beta-blocker + ACEi/ARB

— Black patients without HF/CKD → thiazide or CCB first

— Osteoporosis → thiazide (Ca retention)

CCS pearl: On follow-up 2–4 weeks after starting therapy, recheck BMP (K+, creatinine) for any ACEi/ARB or diuretic, and reassess BP. Titrate every 2–4 weeks until at goal.

Treatment threshold algorithm (ACC/AHA 2017):

Without ASCVD risk: lifestyle only, reassess 3–6 months

With clinical ASCVD, DM, CKD, or 10-yr ASCVD risk ≥10%: lifestyle + 1 drug

BP goal: <130/80 mmHg for most adults, including DM, CKD, post-stroke, CAD, HF (per 2017 ACC/AHA; SPRINT-supported)

Lifestyle interventions (DASH-PLUS):

First-line drug classes (any of four, equal weight):

Compelling indications dictate choice:

Pharmacotherapy — First-Line Drug Regimens

— Lisinopril 10 mg daily, titrate to 40 mg

— OR losartan 50 mg daily, titrate to 100 mg (use if ACEi cough)

— OR amlodipine 5 mg daily, titrate to 10 mg

— OR chlorthalidone 12.5–25 mg daily

— Typical combos: ACEi/ARB + CCB (lisinopril + amlodipine) OR ACEi/ARB + thiazide (lisinopril + chlorthalidone)

— Never combine ACEi + ARB — increased AKI, hyperkalemia, no benefit

— Single-pill combinations improve adherence

— ACEi: dry cough (10–20%), angioedema (higher in Black patients), hyperkalemia, AKI (esp. bilateral RAS), teratogenic

— ARB: similar to ACEi but minimal cough; still teratogenic, hyperkalemia

— Thiazide (chlorthalidone/HCTZ): hypokalemia, hyponatremia, hyperuricemia/gout flare, hyperglycemia, hypercalcemia, ED

— CCB (amlodipine): peripheral edema (dose-dependent), flushing, gingival hyperplasia

— Non-DHP CCB (diltiazem, verapamil): bradycardia, AV block, constipation — avoid in HFrEF

— Add the third class from the ACEi/ARB + CCB + thiazide trio

— Spironolactone 25–50 mg/d is the preferred 4th drug for resistant HTN (PATHWAY-2 trial); monitor K+

— Beta-blockers are NOT first-line for uncomplicated HTN — reserve for CAD, HF, arrhythmia, post-MI

— Hydralazine, clonidine, minoxidil for refractory cases

Board pearl: ACE inhibitor–induced cough resolves within 1–4 weeks of stopping; angioedema requires permanent discontinuation of ACEi and avoidance of all ACEi lifelong — ARB usually tolerated but use cautiously.

Step 3 management: For a Black patient without HF/CKD, start with thiazide or CCB, not ACEi monotherapy (less effective; higher angioedema risk).

Stage 1 with indication (single-drug start):

Stage 2 (start 2 drugs from different classes):

Class adverse effects to memorize:

Second-line / add-on agents (when 2-drug combo inadequate):

Resistant HTN definition: BP above goal despite 3 drugs at max tolerated doses including a diuretic, OR controlled requiring ≥4 drugs.

Expanded Pharmacology — Titration, Combinations, Resistant HTN

— Visit 1 (Day 0): diagnose, lifestyle, start drug(s), order baseline labs, give home BP log

— Visit 2 (Week 2–4): review log, recheck BP, recheck BMP, titrate up or add second agent if not at goal

— Visit 3 (Week 6–8): continue titration; consider third agent

— Once at goal: follow-up every 3–6 months

— Confirm adherence (most common reason for "resistance")

— Confirm proper BP technique and out-of-office readings

— Review for drugs raising BP (NSAIDs, decongestants, OCPs, alcohol)

— Add the missing class from ACEi/ARB + CCB + thiazide

— If still not at goal on 3 drugs → screen for secondary HTN AND add spironolactone

— Chlorthalidone (longer t½, more potent) preferred over HCTZ for outcomes

— Amlodipine + ACEi combo reduces ACEi-related and CCB-related edema vs either alone (ACCOMPLISH trial favored amlodipine + benazepril over HCTZ + benazepril)

— Spironolactone in resistant HTN: watch for gynecomastia in men (switch to eplerenone) and hyperkalemia (especially with ACEi/ARB and CKD)

— Loop diuretics replace thiazides when eGFR <30 (thiazides lose efficacy)

— NSAIDs blunt antihypertensive effect of nearly all classes and worsen AKI with ACEi/ARB/diuretic ("triple whammy")

— Verapamil + beta-blocker → high-grade AV block

— ACEi/ARB + K-sparing diuretic or K-supplement → hyperkalemia

— Grapefruit juice ↑ amlodipine levels

— Once-daily dosing, single-pill combinations, generics, 90-day fills, pill organizers, automated refills

CCS pearl: When BP fails to respond despite escalation, order ABPM to rule out white-coat effect and confirm true resistant HTN — avoid stacking drugs on a patient who is actually controlled outside the office.

CCS titration cadence (typical case flow):

Add-on logic when not at goal on 2 drugs:

Specific drug pearls (high-yield):

Drug–drug interactions / pitfalls:

Adherence strategies:

Special Populations — Elderly and Renal/Hepatic Impairment

— Goal still <130/80 in non-institutionalized, ambulatory adults (SPRINT included ≥75 subgroup with benefit)

— Individualize for frailty, polypharmacy, fall risk, life expectancy — accept <140/90 in frail

— Check orthostatics before and after each titration

— Start low and go slow; thiazides and CCBs often well tolerated

— Beware of isolated systolic HTN — common in elderly due to arterial stiffness; treat with thiazide or CCB

— Avoid alpha-blockers as first-line (ALLHAT: ↑HF risk), avoid centrally acting agents (sedation, falls)

— Goal <130/80; <120 SBP considered for selected CKD per KDIGO 2021

— ACEi or ARB is first-line if UACR ≥30 mg/g (albuminuric CKD or DM with albuminuria) — slows progression

— Tolerate creatinine rise up to 30% and K+ up to ~5.5 after ACEi/ARB initiation; if higher, reduce dose or stop

— eGFR <30: switch thiazide → loop diuretic (furosemide, torsemide)

— Avoid spironolactone if K+ >5 or eGFR <30

— Monitor BMP within 1–2 weeks of any RAAS change

— Most antihypertensives metabolized hepatically; reduce dose of labetalol, metoprolol, amlodipine, losartan in severe cirrhosis

— Avoid non-selective beta-blockers (propranolol, nadolol) for HTN alone in cirrhosis — used for variceal prophylaxis with different dosing

— Spironolactone is the preferred diuretic in cirrhotic ascites (also lowers BP)

— Pre-dialysis BP poorly correlates with CV outcomes; home BP preferred

— Volume management is primary; antihypertensives second

— Beta-blockers (atenolol dialyzable), ACEi/ARB caution

Step 3 management: A 78-year-old with HTN, eGFR 35, UACR 250 mg/g → start losartan, recheck K+ and Cr in 1–2 weeks, accept Cr rise ≤30%. Add amlodipine if not at goal.

Board pearl: Bilateral renal artery stenosis (or RAS in a solitary kidney) is the classic ACEi/ARB contraindication — expect acute creatinine rise >30% as the giveaway.

Older adults (≥65):

CKD:

Hepatic impairment:

Dialysis patients:

Special Populations — Pregnancy and Younger Demographics

— Categories: chronic HTN (pre-pregnancy or <20 wks), gestational HTN (≥20 wks, no proteinuria), preeclampsia (≥20 wks + proteinuria or end-organ damage), preeclampsia superimposed on chronic HTN

— Severe-range BP in pregnancy: ≥160/110 → treat acutely (IV labetalol, IV hydralazine, or PO nifedipine immediate-release)

— Chronic HTN BP target in pregnancy (CHAP trial, ACOG 2022): treat to <140/90; improves outcomes without increasing SGA

— Safe agents: labetalol, nifedipine ER, methyldopa, hydralazine

— Contraindicated: ACEi, ARB, direct renin inhibitors (teratogenic — renal dysgenesis, oligohydramnios), and spironolactone (antiandrogen)

— Counsel women of reproductive age on contraception before starting ACEi/ARB; transition to labetalol or nifedipine when planning pregnancy

— BP can peak 3–6 days postpartum

— Lactation-compatible: labetalol, nifedipine, enalapril, captopril (ACEi acceptable while nursing despite teratogenicity)

— Continue monitoring for at least 12 weeks postpartum; persistent HTN beyond → diagnose chronic HTN

— Pediatric BP thresholds use age/sex/height percentiles; adolescents ≥13 use adult thresholds

— Aggressively pursue secondary causes in young patients — renovascular (FMD in young women), coarctation, primary aldo, OCP-induced, substance use (cocaine, stimulants, anabolic steroids, energy drinks)

— OCP-induced HTN: stop OCP, reassess in 2–3 months

— Highly prevalent in resistant HTN; CPAP modestly lowers BP (~2–3 mmHg)

— Screen with STOP-BANG; refer for polysomnography

Key distinction: Preeclampsia with severe features (BP ≥160/110, AKI, transaminitis, thrombocytopenia, pulmonary edema, neuro symptoms) requires hospitalization, magnesium for seizure prophylaxis, and delivery as definitive treatment — distinct from outpatient chronic HTN management.

Hypertension in pregnancy:

Postpartum:

Adolescents and young adults:

OSA-associated HTN:

Complications and Adverse Outcomes

— Cardiac:

— Cerebrovascular:

— Renal:

— Vascular:

— Ophthalmic:

— Hyperkalemia from ACEi/ARB/MRA → arrhythmia

— Hyponatremia/hypokalemia from thiazide → falls, arrhythmia

— Orthostatic hypotension → falls, hip fractures (especially elderly)

— AKI from ACEi/ARB + NSAID + diuretic triple whammy

— Angioedema (airway emergency) from ACEi

— Gout flare from thiazide

— BP ≥180/120 plus acute end-organ damage

— Hospital admission, IV agent: nicardipine, labetalol, clevidipine, esmolol; nitroprusside for select cases

— Lower MAP by ~10–20% in first hour, then 5–15% over next 23 hours

— Exception: aortic dissection (target SBP <120, HR <60 with esmolol then nicardipine), ischemic stroke (permissive HTN unless thrombolysis), hemorrhagic stroke (SBP <140 per AHA)

CCS pearl: If BP ≥180/120 in clinic without symptoms (urgency) — re-measure properly, address pain/anxiety, restart/intensify oral regimen, and follow up in 24–72 hours. Do not send to ED; do not give clonidine or nifedipine to crash the pressure (risk of stroke from rapid drop).

Target-organ damage from uncontrolled HTN:

LVH → diastolic dysfunction → HFpEF

Accelerated atherosclerosis → CAD, MI

Atrial fibrillation (LA enlargement)

Eventually HFrEF

Ischemic stroke (most common HTN-related event)

Intracerebral hemorrhage (Charcot-Bouchard microaneurysms, basal ganglia)

Lacunar infarcts, vascular dementia

Hypertensive encephalopathy in severe acute rise

Hypertensive nephrosclerosis → CKD → ESRD (2nd leading cause after DM)

Albuminuria precedes eGFR decline

Aortic dissection (HTN is #1 risk factor)

Aortic aneurysm

PAD

Hypertensive retinopathy (Keith-Wagener-Barker grades I–IV)

Grade IV (papilledema) = emergency

Treatment-related complications (drug-specific):

Hypertensive emergency (must escalate immediately):

When to Escalate Care — Inpatient Triage and Consults

— BP ≥180/120 with any of: chest pain, dyspnea, neuro deficit, severe headache with visual change, oliguria, hematuria, papilledema, back/abdominal pain (dissection), pregnancy-related severe HTN

— Suspected aortic dissection (asymmetric pulses, inter-arm BP diff, tearing pain) — order CT angiography stat

— Suspected pheochromocytoma crisis (severe HTN, headache, sweating, palpitations, pallor)

— Nephrology: eGFR <30 declining rapidly, UACR >300, refractory hyperkalemia, suspected renovascular disease, resistant HTN with CKD

— Cardiology: suspected HFrEF/HFpEF, resistant HTN, complex CAD, arrhythmia, suspected coarctation

— Endocrinology: confirmed or strongly suspected primary aldosteronism, pheochromocytoma, Cushing syndrome

— Sleep medicine: STOP-BANG ≥3 with daytime symptoms or resistant HTN → polysomnography

— Vascular surgery / interventional radiology: confirmed atherosclerotic RAS with refractory HTN/flash pulmonary edema; FMD with significant stenosis

— Ophthalmology: retinopathy grade III–IV

— Maternal-fetal medicine: chronic HTN in pregnancy, preeclampsia

— Most newly diagnosed HTN: outpatient management throughout

— Move location to ED only when meeting hypertensive emergency criteria

— Admit if pregnancy + severe HTN, dissection, pulmonary edema, neuro emergency, acute renal failure

— Call clinic if home BP consistently ≥160/100

— Go to ED if BP ≥180/120 with symptoms, chest pain, neuro change, severe headache, dyspnea

Step 3 management: Resistant HTN on 4 agents including spironolactone — re-confirm adherence, repeat ABPM, screen for OSA and primary aldosteronism, and refer to HTN specialist/nephrology. Consider renal denervation only in highly selected centers (not first-line).

CCS pearl: Don't over-consult on a CCS clock — most uncomplicated HTN cases stay in your office. Consults are scored when clinically indicated, not as a hedge.

Send to ED / admit immediately:

Specialty consults — outpatient referral pathways:

CCS disposition thresholds:

Patient self-monitoring escalation rules (write into discharge instructions):

Key Differentials — Causes of Elevated BP Within "Hypertension Category"

— No identifiable cause; multifactorial (genetic + lifestyle)

— Diagnosis of exclusion after ruling out secondary causes when indicated

— Primary aldosteronism (most common secondary cause, ~10% of HTN, higher in resistant)

— Renovascular HTN

— CKD-related HTN: volume overload + RAAS activation; ACEi/ARB + diuretic mainstay

— Obstructive sleep apnea: 30–80% in resistant HTN; CPAP modestly helps

— Drug-induced (very high yield):

— Endocrine: Cushing syndrome, hyperthyroidism, hyperparathyroidism (hypercalcemia), acromegaly

— Pheochromocytoma: classic triad of headache, palpitations, sweating; paroxysmal HTN; rule of 10s

— Coarctation of aorta: upper-extremity HTN, lower-extremity hypotension, radio-femoral delay, rib notching on CXR

Key distinction: Renal parenchymal disease (intrinsic CKD) is the most common secondary cause overall, but primary aldosteronism is the most common endocrine/correctable secondary cause and is massively underdiagnosed — screen liberally in resistant HTN.

Primary (essential) hypertension — 90–95% of cases

Secondary causes — same-category (sustained HTN):

Hypokalemia (only ~30%, so don't require it), metabolic alkalosis, suppressed renin, elevated aldo

ARR screening → confirmatory testing → adrenal CT, AVS

Treatment: adrenalectomy (unilateral adenoma) or MRA (bilateral hyperplasia)

Atherosclerotic RAS (older, diffuse atherosclerosis) vs fibromuscular dysplasia (young women, "string of beads" on imaging)

Clues: abdominal bruit, AKI on ACEi/ARB, asymmetric kidney size, flash pulmonary edema

Treatment: medical management first; angioplasty for FMD or refractory atherosclerotic disease

NSAIDs, COX-2 inhibitors

Oral contraceptives, estrogens

Glucocorticoids, mineralocorticoids

Stimulants: cocaine, amphetamines, methylphenidate

Decongestants: pseudoephedrine, phenylephrine

SNRIs (venlafaxine), MAOIs

Erythropoietin

Licorice (mimics aldosterone), ephedra

Alcohol, chronic NSAID use

Key Differentials — Mimickers and Out-of-Category Considerations

— White-coat hypertension: elevated in office, normal at home/ABPM (~15–30% of "HTN")

— Masked hypertension: normal in office, elevated at home (~15%)

— Pseudohypertension (elderly): non-compressible calcified arteries; Osler's sign (palpable radial pulse despite occluded cuff)

— Acute pain, anxiety, full bladder, recent caffeine/tobacco: transient elevation; recheck after rest

— Hypertensive emergency vs urgency — covered earlier; emergency = end-organ damage

— Posterior reversible encephalopathy syndrome (PRES): HTN + headache, seizure, visual change, occipital lesions on MRI; treat by controlled BP lowering

— Thrombotic microangiopathy: HTN + hemolytic anemia + thrombocytopenia + AKI → TTP/HUS/scleroderma renal crisis

— Scleroderma renal crisis: sudden severe HTN + AKI in patient with scleroderma; ACEi is treatment of choice (one place ACEi is started despite rising creatinine)

— Preeclampsia: new HTN ≥20 wks gestation + proteinuria/end-organ damage

— Withdrawal syndromes: alcohol, opioid, benzodiazepine, clonidine rebound

— HTN + hypokalemia → primary aldo, Liddle, Cushing, licorice

— HTN + hyperkalemia → Gordon syndrome (pseudohypoaldo type II), CKD

— HTN + headache/palpitations/sweating → pheochromocytoma

— HTN + central obesity/striae → Cushing

— HTN + AKI on ACEi → bilateral RAS

— HTN + hypocalcemia in young patient → consider Gitelman/Bartter mimicry (usually hypotensive though)

Board pearl: Clonidine withdrawal causes severe rebound HTN within 18–36 hours of abrupt cessation — always taper. Treat acute rebound with resumed clonidine (or phentolamine if severe), not beta-blockers alone (unopposed alpha effect).

Conditions causing transient or pseudo-HTN that aren't true sustained HTN:

Don't treat with drugs; monitor with annual ABPM/HBPM; ~50% develop sustained HTN within 10 years

CV risk equal to sustained HTN

Treat with same algorithm

Suspect when treatment causes symptoms but office BP remains high; consider intra-arterial measurement

Conditions presenting like HTN but really another diagnosis:

"HTN plus" syndromes — pattern recognition:

Secondary Prevention and Long-Term Plan

— Lipids: statin per ACC/AHA — moderate intensity if 10-yr ASCVD ≥7.5%, high intensity if ≥20%, clinical ASCVD, LDL ≥190, or DM with risk factors

— Diabetes screening: A1c at baseline and at least every 3 years (annually if prediabetes); target A1c <7% individualized

— Aspirin: not routinely recommended for primary prevention (USPSTF 2022); shared decision in 40–59 with ≥10% risk and low bleeding risk; yes for secondary prevention (prior MI, stroke, PAD)

— Smoking cessation: ask, advise, assess, assist, arrange; varenicline, bupropion, NRT

— Weight loss: GLP-1 agonist (semaglutide, tirzepatide) if BMI ≥30 or ≥27 with comorbidity; bariatric surgery if BMI ≥40 or ≥35 with comorbidity

— Alcohol moderation, sodium restriction, DASH diet, exercise

— Influenza annually

— Pneumococcal per age/comorbidity

— COVID-19, RSV (≥60 shared decision), shingles ≥50, Tdap

— Colorectal 45–75, mammography, cervical, lung CT if heavy smoker, prostate shared decision

— Review for BP-elevating drugs and deprescribe when possible (NSAIDs!)

— Generic, 90-day, single-pill combos

— Med reconciliation at every visit

— Validated home BP cuff (upper-arm, oscillometric, cuff-size correct)

— Daily BP log for first months, then weekly when stable

— DASH meal planning resources

— Pedometer/wearable goal: ≥7,500 steps/day or 150 min moderate exercise/wk

Step 3 management: Newly diagnosed HTN in a 55-year-old smoker with LDL 145, A1c 6.2, ASCVD 18% → start antihypertensive AND moderate-to-high-intensity statin, intensive smoking cessation counseling + pharmacotherapy, lifestyle counseling. Address all levers, not just BP.

ASCVD risk reduction is the goal — HTN control is only one lever.

Concurrent risk-factor management at every visit:

Vaccinations (preventive care during HTN visits):

Cancer screening reminders (use the HTN follow-up as touchpoint):

Medication stewardship:

Self-management toolkit:

Follow-Up, Monitoring Parameters, and Counseling Cadence

— Week 0: Diagnose, baseline labs/ECG, start therapy or lifestyle, HBPM log, ASCVD calc

— Week 2–4: Recheck BP, review HBPM log, recheck BMP if on RAAS/diuretic, titrate

— Week 4–8: Further titration; add agent if not at goal

— At goal: Follow-up every 3–6 months

— Annually: Repeat BMP, lipid panel, A1c, UACR, weight; reassess ASCVD risk; medication reconciliation

— ECG: repeat only if symptoms or change in exam

— ABPM/HBPM: annually or when treatment effect unclear

— ACEi/ARB/MRA/diuretic: BMP at 1–2 weeks after start or dose change, then 6–12 months when stable

— Tolerate creatinine rise ≤30% and K+ ≤5.5 after RAAS initiation

— Stop/reduce if K+ >5.5 or Cr rise >30%

— Annual UACR in DM, CKD, baseline microalbuminuria

— Statin: lipids 4–12 weeks after start, then 3–12 months

— Home BP technique: seated 5 min, feet flat, arm at heart level, no caffeine 30 min prior, 2 readings 1 min apart, AM and PM, record in log

— Medication adherence: same time daily, pair with routine (brushing teeth), pill organizer

— Side effects to report: dizziness, syncope, cough, swelling, muscle cramps, sexual dysfunction

— When to seek urgent care: BP ≥180/120, chest pain, neuro symptoms, severe headache

— Refer to cardiac rehab if comorbid CAD/post-MI/HF

— Otherwise, community exercise programs, supervised gym, walking programs

— Registered dietitian for DASH counseling

— Tobacco quitline 1-800-QUIT-NOW

— Mental health screening (PHQ-9, GAD-7) — depression worsens adherence

CCS pearl: Schedule the next visit before ending the current encounter; failure to set follow-up is a frequently scored omission. Post-discharge handoff after any hospitalization: PCP visit within 7–14 days, med reconciliation, BP log, lab follow-up.

Visit cadence on CCS clock:

Lab monitoring rules:

Patient counseling at each visit:

Cardiac rehabilitation / structured exercise:

Behavioral support:

Ethical, Legal, and Patient Safety Considerations

— Stage 1 HTN with borderline ASCVD risk is a shared decision zone — discuss absolute risk reduction, NNT, side effects, lifestyle alternative; document discussion

— Statin and aspirin decisions especially require shared decision-making — patient values matter

— Document ASCVD risk percentage and treatment offered/accepted in the chart

— Polypharmacy in elderly: fall risk from orthostatic hypotension → check orthostatics, deprescribe when possible, use Beers Criteria to avoid clonidine, alpha-blockers as first-line

— Triple whammy: ACEi/ARB + diuretic + NSAID → AKI; counsel against OTC NSAIDs at every visit

— Pregnancy teratogen alert: Every woman of reproductive age on ACEi/ARB/MRA needs contraception counseling; switch to labetalol/nifedipine when pregnancy planned or confirmed

— ACEi angioedema: life-threatening, requires permanent class avoidance and clear documentation as drug allergy

— Potassium monitoring: ACEi/ARB + spironolactone + K-supplement combo is a sentinel error — verify K before refills

— Post-hospital discharge: PCP visit within 7–14 days, especially after HTN-related event (stroke, MI, HF)

— Medication reconciliation at every transition — compare admission list, hospital list, and discharge list

— Avoid the common error of continuing transient inpatient antihypertensives (e.g., a clonidine started inpatient) indefinitely

— HTN control rates lower in Black, Hispanic, low-income, and uninsured populations

— Address SDOH: pharmacy access, healthy food access, BP cuff cost, language

— Use 90-day generic refills, $4 lists, patient assistance programs

— Not applicable to most HTN; however, DMV reporting in some states required if recurrent syncope from medications affects driving safety

— Document driving counseling after syncope or symptomatic orthostasis

— HEDIS / CMS: controlled BP <140/90 (some metrics still use <140/90) in HTN patients — measured for value-based care

Step 3 management: Before any ACEi/ARB refill for a 32-year-old woman, document contraception in the chart and counsel on teratogenicity — this is both a safety and a medicolegal item commonly tested.

Informed consent and shared decision-making:

Patient safety pearls:

Transitions of care:

Health systems and equity:

Mandatory reporting / legal:

Quality measures:

High-Yield Associations and Rapid-Fire Clinical Facts

— Normal <120/80, Elevated 120–129/<80, Stage 1 130–139/80–89, Stage 2 ≥140/90, Crisis ≥180/120

— Goal <130/80 for almost everyone

— CAD/post-MI → beta-blocker + ACEi/ARB

— HFrEF → ACEi/ARB or ARNI + beta-blocker + MRA + SGLT2i

— CKD with albuminuria → ACEi/ARB

— DM → ACEi/ARB (if albuminuria) or any first-line

— Stroke history → thiazide + ACEi

— BPH → alpha-blocker (add-on)

— Migraine → beta-blocker or CCB

— Osteoporosis → thiazide

— Black patients without HF/CKD → thiazide or CCB

— Pregnancy → labetalol, nifedipine, methyldopa

— ACEi + ARB

— Non-DHP CCB + beta-blocker (AV block)

— Triple K-retainers (ACEi + ARB + MRA)

— Aldosterone:renin ratio for primary aldo

— Plasma free metanephrines for pheo

— 1 mg dexamethasone suppression for Cushing

— Renal Doppler for RAS

— Polysomnography for OSA

— Echo for HF or LVH on ECG

— ABPM gold standard for diagnosis

— ≥30 mg/g UACR = albuminuria (significant)

— eGFR <30 → switch thiazide to loop

— Cr rise ≤30% on ACEi/ARB is acceptable

— Spironolactone 25–50 mg for resistant HTN

— Sodium <1500 mg/d goal

— ASCVD ≥10% triggers Stage 1 drug therapy

— Young woman + abdominal bruit → FMD

— Older man + AKI after starting lisinopril → bilateral RAS

— Resistant HTN + hypokalemia → primary aldosteronism

— Episodic HTN + headache/sweating/palpitations → pheo

— Upper > lower extremity BP + radio-femoral delay → coarctation

— Severe HTN + scleroderma → renal crisis → ACEi

— HTN + central obesity + striae → Cushing

— Severe HTN + papilledema → hypertensive emergency

Board pearl: SPRINT trial supports SBP <120 (intensive) in high-CV-risk non-diabetic adults, BUT ACC/AHA chose <130/80 as the practical goal to balance benefit and harm. Use <130/80 on exams.

BP thresholds (memorize cold):

First-line classes: thiazide, ACEi, ARB, dihydropyridine CCB — not beta-blockers for uncomplicated HTN

Compelling indications cheat sheet:

Avoid combos:

Tests to remember:

Numbers that show up on tests:

Classic vignettes:

Board Question Stem Patterns

— "62-year-old, BP 134/82 in office today and 132/84 two weeks ago. ASCVD 7%. No DM/CKD. Next step?"

— Answer: Lifestyle modification, recheck 3–6 months (Stage 1 without compelling indication)

— Same patient, ASCVD 12% or has DM → Start single agent (ACEi, ARB, thiazide, or CCB) + lifestyle

— BP 156/94 confirmed → Two-drug therapy (e.g., lisinopril + amlodipine) + lifestyle

— First-line should be thiazide or CCB, not ACEi monotherapy

— ACEi or ARB first-line regardless of stage

— On lisinopril + amlodipine + HCTZ at max doses, BP still 150/92 → Add spironolactone (PATHWAY-2); also confirm adherence and screen for secondary HTN/OSA

— HTN + K 3.2 not on diuretic → Aldosterone:renin ratio

— Cr rose from 1.0 to 1.8 two weeks after starting lisinopril → Bilateral renal artery stenosis suspected; renal artery duplex

— Cough → switch to ARB. Angioedema → stop ACEi permanently; ARB possible but cautious

— 28-week-pregnant patient with BP 150/95, currently on lisinopril → Stop lisinopril, switch to labetalol or nifedipine

— BP 210/130 + papilledema + AKI → ED, IV nicardipine or labetalol, reduce MAP 10–20% in first hour

— Confirmed pheo before adrenalectomy → alpha-blocker first (phenoxybenzamine), then beta-blocker; never beta-blocker first (unopposed alpha)

— Office BP elevated, ABPM normal → No drug, annual reassessment

— 80-year-old, BP 145/85, ambulatory, no falls → Goal <130/80; start single agent

Key distinction: When the stem includes chest pain, neuro deficit, dyspnea, papilledema, or AKI with severely elevated BP, the answer is inpatient/ED with IV antihypertensives, not outpatient titration.

Stem 1 — Threshold/diagnosis:

Stem 2 — Stage 1 with risk:

Stem 3 — Stage 2 initial:

Stem 4 — Black patient without HF/CKD:

Stem 5 — Diabetic with albuminuria:

Stem 6 — Resistant HTN:

Stem 7 — Hypokalemia clue:

Stem 8 — AKI after ACEi:

Stem 9 — ACEi cough/angioedema:

Stem 10 — Pregnancy:

Stem 11 — Hypertensive emergency:

Stem 12 — Pheochromocytoma management order:

Stem 13 — White-coat:

Stem 14 — Older adult:

One-Line Recap

Newly diagnosed hypertension is a longitudinal outpatient diagnosis confirmed with out-of-office BP, treated to <130/80 with lifestyle plus 1–2 first-line agents (ACEi/ARB, thiazide, or DHP CCB) chosen by compelling indications, with structured 2–4 week titration visits, baseline and follow-up metabolic monitoring, and integrated ASCVD risk reduction.

Board pearl: Hypertension is treated as a lifelong cardiovascular risk syndrome, not a number — score every CCS case on BP control PLUS lifestyle counseling, lab monitoring, secondary cause screening when indicated, and timely follow-up.

Diagnose with ABPM or HBPM — never on a single office reading unless ≥180/120 or with end-organ damage; rule out white-coat and identify masked HTN.

Treatment thresholds: Stage 1 (130–139/80–89) → lifestyle alone unless ASCVD ≥10%/DM/CKD/CVD; Stage 2 (≥140/90) → lifestyle plus two-drug therapy from different first-line classes.

First-line drugs are thiazide, ACEi, ARB, or DHP CCB; compelling indications override (ACEi/ARB for albuminuric CKD or DM; beta-blocker for CAD/HF; labetalol/nifedipine in pregnancy; thiazide/CCB for Black patients without HF/CKD); spironolactone is the preferred fourth agent for resistant HTN after confirming adherence and screening for secondary causes (especially primary aldosteronism and OSA).

CCS workflow: baseline BMP/CBC/lipids/A1c/TSH/UA-UACR/ECG, home BP log, 2–4 week titration cadence, BMP within 1–2 weeks of any RAAS/diuretic change, follow-up every 3–6 months once at goal, and concurrent management of lipids, glucose, weight, smoking, and aspirin (secondary prevention only) at every visit.