Step 2 CK · Internal Medicine · Cardiology

Hypertension & Hyperlipidemia

Name: Hypertension & Hyperlipidemia
Creator: Veli Bakalov, MD

Stage it, match the drug to the comorbidity, and tell urgency from emergency

Cardiology·Hypertension & Prevention·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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AHA/ACC 2025 (same categories as 2017): normal < 120/80; elevated 120–129 and < 80; stage 1 130–139 or 80–89; stage 2 ≥140 or ≥90; confirm with ≥2 readings on ≥2 visits.
Drug therapy starts at stage 2 for everyone, with two first-line drugs, preferably in a single pill; at stage 1 it starts with clinical CVD, diabetes, CKD, or PREVENT 10-year CVD risk ≥7.5%, otherwise if BP stays ≥130/80 after 3 to 6 months of lifestyle; first-line agents are a thiazide (chlorthalidone), ACEi/ARB, or dihydropyridine CCB.
ACEi/ARB for diabetes or CKD with proteinuria; ACEi plus β-blocker after MI or with HFrEF; thiazide or CCB first in Black patients without CKD/HF; labetalol, nifedipine, or methyldopa in pregnancy.
Thiazides cause hypokalemia, hyponatremia, hyperglycemia, hyperuricemia, and hypercalcemia; ACE inhibitors cause bradykinin cough/angioedema and hyperkalemia; amlodipine causes edema.
Hypertensive emergency = ≥180/120 with end-organ damage: IV nicardipine, labetalol, clevidipine, or nitroprusside, cutting MAP by no more than 25% in the first hour; urgency (no damage) is lowered gradually with oral drugs.
Aortic dissection is the exception: IV β-blocker first, then rapidly to systolic BP < 120 and heart rate < 60.
Resistant hypertension (uncontrolled on 3 drugs including a diuretic): confirm adherence and technique, screen everyone for primary hyperaldosteronism with the aldosterone-to-renin ratio (even with normal potassium), and add spironolactone.
Statins (2026 ACC/AHA, PREVENT-ASCVD risk): clinical ASCVD, LDL ≥190 mg/dL, diabetes at 40 to 75, or 10-year risk ≥5% at 30 to 79 (reasonable at 3% to <5%); a CAC score helps when the decision is uncertain.
High-intensity statins (atorvastatin 40–80, rosuvastatin 20–40) lower LDL ≥50%; LDL goals are < 100 mg/dL in primary prevention, < 70 at high risk or with ASCVD, and < 55 for very high-risk ASCVD; add ezetimibe or a PCSK9 inhibitor (no fixed order) if needed.

Staging blood pressure and starting therapy

Diagnosis. Use the average of at least two readings on at least two separate visits, measured with proper technique. Home or ambulatory monitoring confirms the diagnosis and exposes white-coat hypertension (high only in the office) and masked hypertension (normal only in the office).

AHA/ACC 2025 categories

Category	Blood pressure (mmHg)	Initial approach
Normal	<120 and <80	Healthy lifestyle
Elevated	120–129 and <80	Lifestyle
Stage 1	130–139 or 80–89	Lifestyle; add a drug now with clinical CVD, diabetes, CKD, or PREVENT 10-year CVD risk ≥7.5%, otherwise if BP stays ≥130/80 after 3 to 6 months
Stage 2	≥140 or ≥90	Lifestyle plus two first-line drugs of different classes for everyone, preferably a single-pill combination

The usual treatment target is below 130/80, and a systolic BP below 120 is encouraged.

Lifestyle is step one. The DASH diet, sodium under 1.5–2.3 g/day, weight loss, aerobic exercise, and limiting alcohol each lower systolic BP by several mmHg; lifestyle alone is first-line for elevated BP and, for 3 to 6 months, for lower-risk stage 1.

First-line drugs. A thiazide (chlorthalidone), an ACE inhibitor or ARB, or a dihydropyridine CCB (amlodipine). Stage 2 starts with two of these classes, ideally combined in one pill. β-blockers are not first-line without a specific indication, and an ACE inhibitor should never be combined with an ARB.

Let the comorbidity pick the drug.

Diabetes or CKD with proteinuria: ACE inhibitor or ARB (renoprotective).
Post-MI or HFrEF: ACE inhibitor plus a β-blocker.
Black patients without CKD or heart failure: thiazide or CCB first, which work better than ACEi/ARB as initial therapy.
Pregnancy: labetalol, nifedipine, or methyldopa; ACE inhibitors and ARBs are contraindicated (teratogenic).

Class side effects. ACE inhibitors cause cough and angioedema (bradykinin-mediated) and hyperkalemia; for ACE-inhibitor cough, switch to an ARB, which does not raise bradykinin. Thiazides cause hypokalemia, hyponatremia, hyperglycemia, hyperuricemia (gout), and hypercalcemia. Dihydropyridine CCBs cause peripheral edema.

Hypertensive urgency vs emergency

Same numbers, different organs

Feature	Urgency	Emergency
Blood pressure	≥180/120	≥180/120
End-organ damage	None	Encephalopathy, stroke, MI, aortic dissection, papilledema, AKI, eclampsia
Treatment	Oral agents; lower gradually over hours to days, outpatient or observation	IV agents in the ICU: nicardipine, labetalol, clevidipine, or nitroprusside
Pace	No rush	Cut MAP by no more than 25% in the first hour

Don't overshoot. Chronically hypertensive vascular beds autoregulate at high pressures, so a rapid drop causes cerebral, renal, and coronary hypoperfusion. After the first hour, if stable, aim for about 160/100–110 over the next 2–6 hours, then normal over the following 24–48 hours. A focused search for organ damage (funduscopic and neurologic exam, troponin and ECG, creatinine and urinalysis) is what separates the two diagnoses.

Exceptions: acute aortic dissection needs rapid lowering to a systolic BP below 120 and a heart rate below 60, with IV β-blockade (esmolol or labetalol) first, before any vasodilator, to reduce aortic shear. Acute ischemic stroke is the opposite: permit high pressures unless BP exceeds 220/120, or 185/110 if thrombolysis is planned.

Resistant and secondary hypertension

Resistant hypertension is BP uncontrolled on three drugs, including a diuretic, at maximal doses, or controlled only with four. First exclude pseudo-resistance: nonadherence, poor measurement technique, and white-coat effect. Then screen every patient for primary aldosteronism with the aldosterone-to-renin ratio, even with normal potassium (2025 AHA/ACC), add spironolactone as the fourth agent, and look for other secondary causes. Young onset, abrupt or severe hypertension, and spontaneous hypokalemia also prompt screening. The 2025 Endocrine Society guideline goes further and advises screening everyone with hypertension for primary aldosteronism.

Secondary causes

Cause	Clues	Screening test
Primary hyperaldosteronism	Most common secondary cause; hypokalemia, metabolic alkalosis, low renin	Plasma aldosterone-to-renin ratio
Renal artery stenosis	Abdominal bruit; creatinine jumps after starting an ACE inhibitor (bilateral disease)	Renal duplex ultrasound, CT or MR angiography
Pheochromocytoma	Episodic headache, sweating, palpitations	Plasma free or 24-hour urine metanephrines
Obstructive sleep apnea	Obesity, snoring, daytime somnolence	Polysomnography
Cushing syndrome	Central obesity, striae, hyperglycemia	Late-night salivary cortisol, 24-hour urine cortisol, or dexamethasone suppression
Coarctation of the aorta	Arm BP higher than leg BP, delayed femoral pulses	Echocardiography or MRI
Thyroid disease	Hyper- or hypothyroid features	TSH

Lipids and statin therapy

Who benefits. The 2026 ACC/AHA guideline estimates 10-year ASCVD risk with the PREVENT-ASCVD equations: low below 3%, borderline 3% to below 5%, intermediate 5% to below 10%, and high 10% or more. Statins are indicated for:

Clinical ASCVD.
LDL ≥190 mg/dL: high-intensity statin regardless of calculated risk.
Diabetes at age 40–75: at least a moderate-intensity statin regardless of calculated risk.
Primary prevention at age 30 to 79: recommended at intermediate or high risk (5% or more, higher intensity at 10% or more) and reasonable at borderline risk. A coronary artery calcium score helps when the decision is uncertain; a score of 0 favors deferring the statin.

Intensity. High-intensity statins (atorvastatin 40–80 mg, rosuvastatin 20–40 mg) lower LDL by ≥50% and are used for ASCVD, LDL ≥190, and other high-risk patients. Moderate-intensity regimens, such as atorvastatin 10–20 mg or rosuvastatin 5–10 mg, lower LDL by 30–50%. Statins inhibit HMG-CoA reductase; recheck a lipid panel after starting to confirm the expected response.

≥50%LDL reduction with a high-intensity statin

<55 mg/dLLDL goal in very high-risk ASCVD (<70 in other ASCVD or high risk, <100 in primary prevention)

≥5%PREVENT-ASCVD 10-year risk at which a statin is recommended

Secondary prevention. Established ASCVD gets a high-intensity statin with an LDL goal below 70 mg/dL, or below 55 mg/dL when risk is very high. If the goal is not met, add ezetimibe or a PCSK9 inhibitor (evolocumab, alirocumab); the 2026 guideline sets no fixed order, so choose by the LDL reduction needed, cost and tolerability. Non-HDL goals are 30 mg/dL above the LDL goals. Combine with aspirin, BP control, and smoking cessation.

Adverse effects are myopathy and transaminitis. Myopathy risk rises with fibrates, especially gemfibrozil; check CK if myalgias develop.