Cardio final: HTN, lipids

What is normal blood pressure?

SBP

What is elevated blood pressure?

SBP 120-129 AND DBP

What is Stage 1 hypertension?

SBP 130-139 OR DBP 80-89 mm Hg.

What is Stage 2 hypertension?

SBP ≥140 OR DBP ≥90 mm Hg.

What BP is considered a hypertensive crisis range?

SBP ≥180 and/or DBP ≥120 mm Hg. The number alone does NOT determine emergency vs severe asymptomatic HTN; assess for acute target-organ damage.

How should hypertension generally be confirmed?

Use the average of ≥2 BP readings on ≥2 separate occasions. Out-of-office/home measurements help confirm the diagnosis because office BP may overestimate or underestimate the patient's usual BP.

What is white-coat hypertension?

Elevated BP in the office but normal BP outside the clinical setting.

What is masked hypertension?

Normal office BP but elevated BP outside the clinical setting.

Why is hypertension often called a silent disease?

Most patients are asymptomatic, and symptoms correlate poorly with BP severity. HTN is often discovered during routine screening.

What symptoms may occur with hypertension?

Headache, blurred vision, dyspnea, chest pain, palpitations, claudication, edema, and dizziness; however, most patients are asymptomatic.

What cardiovascular history should be assessed in a patient with elevated BP?

CAD, HF, stroke/TIA, diabetes, CKD, dyslipidemia, smoking, alcohol use, diet, physical activity, and family history of HTN/premature CVD/DM/dyslipidemia.

What target-organ damage should be assessed in chronic hypertension?

Heart: LVH, angina/MI, prior revascularization, HF. Brain: stroke/TIA. Kidney: ↓GFR, albuminuria/proteinuria, ESRD. Peripheral vascular: PAD/AAA/critical limb ischemia. Eye: hypertensive retinopathy.

What fundoscopic findings may occur with hypertension?

Arteriolar narrowing, copper/silver wiring, exudates, hemorrhages; severe disease may produce papilledema.

What is primary/essential hypertension?

HTN without a single identifiable secondary cause; accounts for ~90-95% of cases. Contributors include sympathetic overactivity, RAAS activation, impaired natriuresis, and sodium/water retention, ultimately increasing systemic vascular resistance.

What is secondary hypertension?

HTN caused by an identifiable, potentially reversible underlying disorder; approximately 5-10% of HTN cases.

When should you suspect secondary hypertension?

Age

What are common secondary causes of hypertension?

Primary aldosteronism, renal parenchymal disease, renal artery stenosis, obstructive sleep apnea, and medications/substances. Other causes include pheochromocytoma, Cushing syndrome, thyroid disease, hyperparathyroidism, and coarctation of the aorta.

What secondary cause is especially important/underdiagnosed in resistant HTN?

Primary aldosteronism.

Primary aldosteronism: classic presentation and screening test?

Resistant HTN + hypokalemia + muscle weakness/cramps. Initial screening test = plasma aldosterone-to-renin ratio (ARR).

Why does primary aldosteronism cause hypertension and hypokalemia?

Excess aldosterone increases renal Na+/water retention → ↑ intravascular volume/BP, while increasing K+ excretion → hypokalemia.

Renal parenchymal disease: clues and evaluation?

↑ creatinine, ↓ eGFR, proteinuria/albuminuria. Evaluate with renal labs/urinalysis and renal ultrasound.

Renal artery stenosis: classic clues?

Resistant HTN, abdominal/renal bruit, flash pulmonary edema, or >30% rise in creatinine after starting an ACE inhibitor.

Renal artery stenosis: initial and further diagnostic testing?

Renal duplex ultrasound is an initial test; CTA or MRA can further evaluate when suspicion is high; arteriography is definitive.

Why can ACE inhibitors markedly increase creatinine in renal artery stenosis?

When renal perfusion is reduced, angiotensin II constricts the efferent arteriole to preserve glomerular pressure. ACE inhibition removes this compensation → GFR can fall → creatinine rises.

Obstructive sleep apnea as a cause of secondary HTN: classic clues and test?

Obesity + loud snoring + witnessed apnea + daytime somnolence. Diagnose with polysomnography/sleep study.

Pheochromocytoma: classic presentation and initial test?

Episodic headache + palpitations + sweating with paroxysmal HTN. Initial screening = plasma free metanephrines.

Cushing syndrome: clues and screening test?

Central obesity, moon facies, purple striae, proximal muscle weakness + HTN. Screening includes 24-hour urinary free cortisol.

Thyroid disease as a cause of HTN: clues and test?

Hyperthyroidism: weight loss, heat intolerance, tremor. Hypothyroidism: weight gain, cold intolerance, constipation. Initial test = TSH.

Hyperparathyroidism: clues and evaluation?

Hypercalcemia with stones/bone pain + HTN; check serum calcium and PTH.

Coarctation of the aorta: classic HTN presentation?

Young patient with upper-extremity hypertension + lower-extremity hypotension and delayed/weak femoral pulses; requires cardiovascular imaging/evaluation.

What lifestyle changes are recommended for hypertension?

Weight loss if overweight, DASH-style diet, sodium restriction, potassium-rich foods when appropriate, regular physical activity, alcohol limitation/avoidance, smoking cessation, and stress reduction.

What sodium restriction is recommended for hypertension?

How much physical activity is recommended for hypertension?

Approximately 90-150 minutes/week of physical activity plus dynamic resistance training.

How is elevated BP (120-129/

Lifestyle modification only: weight loss, DASH diet, ↓ sodium, ↑ physical activity, limit alcohol; recheck in approximately 3-6 months.

How is low-risk Stage 1 HTN treated?

If no DM, CKD, target-organ damage, or sufficiently elevated cardiovascular risk: begin lifestyle modification and reassess in 3-6 months; start medication if BP remains elevated.

What are the major first-line antihypertensive classes?

Thiazide/thiazide-like diuretic, ACE inhibitor or ARB, and calcium channel blocker.

What is a common starting dose of chlorthalidone for hypertension?

Chlorthalidone 12.5 mg daily.

What is a common starting dose of lisinopril for hypertension?

Lisinopril 10 mg daily.

What is a common starting dose of losartan for hypertension?

Losartan 25 mg once daily.

What is a common starting dose of amlodipine for hypertension?

Amlodipine 5 mg daily.

How is Stage 2 HTN generally treated?

Initiate antihypertensive therapy promptly, generally with 2 first-line agents from different classes + lifestyle modification; close follow-up is needed.

When should initial 2-drug therapy be strongly considered?

When BP is ≥20/10 mm Hg above goal.

What are preferred 2-drug combinations for HTN?

ACEi/ARB + CCB OR ACEi/ARB + thiazide-type diuretic.

Why should ACE inhibitors and ARBs generally NOT be combined?

Both suppress the RAAS; combining them increases risk of hyperkalemia, renal dysfunction, and hypotension without sufficient added benefit.

ACE inhibitors: mechanism?

Inhibit ACE → ↓ conversion of angiotensin I to angiotensin II → ↓ vasoconstriction and ↓ aldosterone → ↓ BP.

ACE inhibitors: major adverse effects?

Dry cough, hyperkalemia, increased creatinine/renal dysfunction, hypotension, and angioedema.

ACE inhibitors: major contraindication?

Pregnancy; also avoid after ACE-inhibitor-associated angioedema.

Why do ACE inhibitors cause cough and angioedema?

ACE normally breaks down bradykinin. ACE inhibition increases bradykinin → cough and, rarely, angioedema.

ARBs: mechanism and major advantage over ACE inhibitors?

Block angiotensin II AT1 receptors → ↓ vasoconstriction and aldosterone. They do not increase bradykinin as much, so cough is much less common.

ARBs: major adverse effects/contraindication?

Hyperkalemia, renal dysfunction, hypotension; avoid in pregnancy.

Why monitor creatinine and potassium after starting an ACE inhibitor or ARB?

RAAS blockade can reduce GFR in susceptible patients and decrease aldosterone-mediated K+ excretion → creatinine may rise and hyperkalemia may develop.

Thiazide diuretics: major electrolyte effects?

Can cause ↓Na+, ↓K+, and ↑Ca2+; can also increase uric acid and precipitate gout.

Which thiazide-like diuretic is commonly preferred for hypertension?

Chlorthalidone because of its long duration of action and potency.

Dihydropyridine CCB example and major adverse effect?

Amlodipine; major adverse effect = peripheral edema. May also cause headache/flushing.

Non-dihydropyridine CCB examples and important adverse effects?

Diltiazem and verapamil; ↓HR/AV conduction and may cause bradycardia/AV block. Verapamil commonly causes constipation. Avoid/caution in HFrEF or significant conduction disease.

Are beta blockers first-line for uncomplicated hypertension?

No. They are particularly useful when another indication exists, such as CAD/prior MI, HFrEF, or tachyarrhythmia.

What is resistant hypertension?

BP remains uncontrolled despite 3 antihypertensive medications of different classes, ideally including an appropriate diuretic, OR BP requires ≥4 drugs for control.

Before labeling HTN resistant, what should be considered?

Confirm accurate BP measurement/adherence and evaluate contributing medications/lifestyle factors and secondary causes.

What is the preferred foundational regimen for resistant HTN?

ACEi/ARB + long-acting dihydropyridine CCB + thiazide/thiazide-like diuretic.

What is commonly added as the 4th medication for resistant hypertension?

Spironolactone.

Why is spironolactone effective in resistant hypertension?

It blocks aldosterone; excess/inappropriate aldosterone activity is common in resistant HTN and promotes sodium/water retention.

Spironolactone: important adverse effects?

Hyperkalemia, renal dysfunction, and endocrine effects such as gynecomastia.

What is a hypertensive emergency?

Severe hypertension WITH acute target-organ damage. The presence of acute organ injury—not the BP number alone—defines the emergency.

What acute target-organ damage can occur in hypertensive emergency?

Hypertensive encephalopathy, stroke/ICH, ACS/MI, acute HF/pulmonary edema, aortic dissection, acute kidney injury, or severe retinal injury.

How is hypertensive emergency treated?

Hospital/ICU-level care with titratable IV antihypertensive therapy and close monitoring; BP is reduced in a controlled fashion because overly rapid reduction can compromise organ perfusion.

What is severe asymptomatic hypertension?

Severely elevated BP, often ≥180/120, WITHOUT acute target-organ damage.

How is severe asymptomatic hypertension managed differently from hypertensive emergency?

Do NOT rapidly lower BP with IV medication simply because the number is high. Rest/recheck BP, adjust/initiate oral therapy as appropriate, lower gradually over days to weeks, and arrange close follow-up.

What is the most important distinction in a patient with BP >180/120?

Determine whether acute target-organ damage is present: WITH damage = hypertensive emergency; WITHOUT damage = severe asymptomatic hypertension.

What is the primary lipid treatment target for ASCVD prevention?

LDL-C. Higher LDL-C strongly predicts ASCVD, and lowering LDL reduces cardiovascular events.

What is the major role of LDL?

LDL delivers cholesterol to peripheral tissues; excess LDL can deposit cholesterol in arterial walls → atherosclerotic plaque formation → ASCVD.

What is the major role of HDL?

HDL participates in reverse cholesterol transport, moving excess cholesterol from peripheral tissues toward the liver.

Is HDL a medication treatment target?

No. Higher HDL is associated with lower ASCVD risk, but pharmacologically raising HDL has NOT been shown to reduce ASCVD events.

What do chylomicrons primarily transport?

Dietary triglycerides from the intestine to tissues.

What does VLDL primarily transport?

Triglycerides synthesized/packaged by the liver to muscle and adipose tissue for energy or storage.

What happens to VLDL as triglycerides are removed?

VLDL → IDL → LDL.

What is hyperlipidemia?

Broad term for elevated blood lipids.

What is hypercholesterolemia?

Elevation of LDL-C/cholesterol.

What is hypertriglyceridemia?

Elevation of triglycerides.

What is mixed hyperlipidemia?

Elevation of both LDL-C and triglycerides.

What is dyslipidemia?

Abnormal/imbalanced lipid levels.

Are most patients with dyslipidemia symptomatic?

No. Most have no specific signs or symptoms, which is why screening is important.

What physical exam findings may suggest severe/inherited dyslipidemia?

Xanthelasma, xanthomas, tendinous xanthomas, eruptive xanthomas, and lipemia retinalis with very high triglycerides.

What are common secondary/acquired contributors to dyslipidemia?

Unhealthy diet, poor lifestyle, central obesity, saturated fat/dietary cholesterol intake, uncontrolled diabetes, hypothyroidism, and certain medications.

What is lipoprotein(a), Lp(a)?

An inherited, strongly proatherogenic lipoprotein and ASCVD risk enhancer.

How often should Lp(a) be measured?

At least once in every adult's lifetime.

What does a high Lp(a) suggest clinically?

Increased inherited ASCVD risk and a potential need for more aggressive LDL-C lowering.

At what triglyceride level does pancreatitis become a major concern?

TG ≥500 mg/dL increases pancreatitis risk; extremely high TG, especially >1,000 mg/dL, carries substantial risk.

How are triglycerides 150-499 mg/dL generally managed?

Lifestyle modification + treat secondary causes + focus on LDL/ASCVD risk first, using statin therapy when indicated.

How are triglycerides ≥500 mg/dL managed conceptually?

The immediate treatment priority shifts toward lowering TG to reduce acute pancreatitis risk; fibrate ± prescription omega-3 therapy may be used along with lifestyle/secondary-cause treatment.

What is the foundation of lipid management?

Lifestyle modification.

What is first-line pharmacologic therapy for lowering LDL-C and preventing ASCVD?

Statins.

Statins: mechanism?

Inhibit HMG-CoA reductase → ↓ hepatic cholesterol synthesis → liver increases LDL receptor expression → ↑ LDL removal from circulation.

What LDL reduction defines a high-intensity statin?

Approximately ≥50% LDL-C reduction.

What LDL reduction defines a moderate-intensity statin?

Approximately 30-49% LDL-C reduction.

Which statins/doses are high intensity?

Atorvastatin 40-80 mg daily OR rosuvastatin 20-40 mg daily.

Which statin doses are moderate intensity?

Atorvastatin 10-20 mg; rosuvastatin 5-10 mg; simvastatin 20-40 mg; pitavastatin 1-4 mg; pravastatin 40-80 mg.

Which statins have fewer drug interactions?

Rosuvastatin, pravastatin, and pitavastatin.

What benefits do statins provide beyond LDL reduction?

Plaque stabilization, reduced vascular inflammation/CRP, and improved endothelial function.

What is the most common adverse effect of statins?

Myalgias.

What serious muscle adverse effect can occur with statins?

Rhabdomyolysis, although rare.