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System 01 · ~16% of exam

Cardiovascular

The most heavily tested system. The vast majority of vignettes collapse into five chief complaints: chest pain, dyspnea, palpitations, syncope, and edema. Master these entry points and the pathophysiology follows.

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Chief complaints

BUILD THE DIFFERENTIAL

Vignettes enter through one of these doors. Each complaint lays out the full differential, marks the can't-miss diagnoses, and tells you the next right action for each.

Chest painDyspnea (cardiac)PalpitationsSyncopePeripheral edema
CHIEF COMPLAINT · HIGH-YIELD

Chest pain

The most common can't-miss complaint on the exam. Six killers to exclude before anything else.

Approach

The reflex: is this cardiac, vascular, pulmonary, GI, or musculoskeletal? ECG within 10 minutes and troponin in almost any adult with new chest pain. Tearing pain radiating to the back is dissection. Pleuritic with dyspnea is PE. Pleuritic with fever is pneumonia or pericarditis. Exertional substernal with radiation is ACS. Postprandial burning is GERD. Reproducible with palpation is costochondritis.

The differential
Diagnosis Key features / clues Next step
STEMI / NSTEMI Exertional or at-rest pressure, radiates to arm/jaw, diaphoresis, dyspnea. Risk factors stacked. ECG changes. ECG in 10 min · troponin · aspirin 325 mg chewed. STEMI → cath within 90 min
Aortic dissection Tearing/ripping pain radiating to back, unequal BP between arms, widened mediastinum on CXR, Marfan or uncontrolled HTN. CT angio chest (stable) or TEE (unstable) · esmolol first, then nitroprusside
Pulmonary embolism Pleuritic, dyspnea, tachycardia, recent immobilization or surgery or malignancy, unilateral leg swelling. Wells score → D-dimer if low, CT-PA if intermediate/high · anticoagulate
Tension pneumothorax Sudden, unilateral absent breath sounds, tracheal deviation away, hypotension, distended neck veins. Immediate needle decompression 2nd ICS midclavicular · chest tube after
Cardiac tamponade Beck triad: hypotension, JVD, muffled heart sounds. Pulsus paradoxus > 10 mmHg. Bedside echo · pericardiocentesis
Esophageal rupture (Boerhaave) Severe retrosternal pain after forceful vomiting, subcutaneous crepitus, pleural effusion. Gastrografin esophagram · broad-spectrum antibiotics · surgical consult
Stable angina Predictable exertional pain, relieved by rest or nitro, < 10 minutes. Stress test, exercise ECG if baseline interpretable and can exercise
Pericarditis Pleuritic, positional (worse supine, better leaning forward), friction rub, diffuse ST elevation with PR depression. ECG · echo · NSAIDs + colchicine
GERD Burning, postprandial, worse supine, responds to antacids. Empiric PPI trial · endoscopy if alarm features
Costochondritis Reproducible with palpation of costal cartilage, young patient, normal vitals. NSAIDs · diagnosis of exclusion
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
A 58-year-old man presents with 30 minutes of substernal chest pressure radiating to his left arm, associated with diaphoresis and nausea. BP 146/92, HR 98. ECG shows 2 mm ST elevation in leads II, III, and aVF.
What is the most appropriate next step in management?
Answer › Activate cath lab for primary PCI within 90 minutes. Inferior STEMI. Before PCI: aspirin 325 mg chewed, second antiplatelet (ticagrelor/prasugrel/clopidogrel), heparin. Avoid nitrates until RV infarct is excluded, check right-sided leads V4R. RV infarct is preload-dependent; nitrates drop BP catastrophically.
Pearls
Pearl
Women, diabetics, and the elderly present with atypical ACS: dyspnea, fatigue, epigastric pain, syncope. Have a low threshold for ECG.
Pearl
Troponin peaks at 24 hours and stays elevated 7–10 days. CK-MB clears in 2 days and is useful for detecting reinfarction.
Pearl
If the chest pain is real and the ECG is normal, either the test isn't dispositive yet (serial ECG/troponin) or the pain isn't cardiac. Do not be reassured by a single normal ECG in a patient with ongoing symptoms.
CHIEF COMPLAINT · HIGH-YIELD

Dyspnea (cardiac)

Is this left heart, right heart, pulmonary, or something else entirely?

Approach

Dyspnea is cardiac when orthopnea, PND, elevated JVP, or S3 is present. BNP differentiates cardiac from pulmonary in ambiguous presentations, BNP < 100 makes HF unlikely. CXR shows pulmonary edema. Echo is the next step to characterize EF and valve function.

The differential
Diagnosis Key features / clues Next step
Acute decompensated HFrEF Orthopnea, PND, S3, bilateral crackles, edema, elevated JVP, pink frothy sputum if flash. IV loop diuretic · nitrates · O2 · upright position · BiPAP if distress
Acute valvular failure Sudden dyspnea after MI (papillary rupture → MR) or endocarditis (AR). New loud murmur. Bedside echo · emergent surgical consult
Cardiogenic shock Hypotension, cold extremities, altered mental status, oliguria after large MI or fulminant myocarditis. Pressors (norepinephrine), inotropes (dobutamine), revascularization · IABP/Impella
Tamponade Beck triad, pulsus paradoxus. Echo · pericardiocentesis
HFpEF Same symptoms as HFrEF but EF ≥ 50%. Older, HTN, diabetic, obese female phenotype. Diuretics for symptoms · SGLT2 inhibitor · treat comorbidities
High-output failure Warm extremities, bounding pulses. Anemia, thyrotoxicosis, AV fistula, Paget, beriberi. Treat underlying cause
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
A 72-year-old woman presents with worsening dyspnea over two days. She cannot lie flat. Exam: JVP 12 cm, bibasilar crackles, S3, 2+ pitting edema. BNP 1840. CXR shows cephalization and Kerley B lines.
What is the next best step?
Answer › IV furosemide 40 mg (or 2.5× her home dose if on a loop diuretic). Place upright, supplemental O2, consider BiPAP if in respiratory distress. Echo once stabilized to characterize EF. This is acute decompensated heart failure.
Pearls
Pearl
BNP is elevated in HF but also in renal failure, PE, sepsis, and AFib. It's a ruling-out test (high NPV), not ruling-in.
Pearl
Kerley B lines, cephalization, and bat-wing pulmonary edema on CXR are the radiographic signature of cardiogenic edema.
Pearl
HFrEF mortality-reducing quadruple therapy: ARNI (or ACEi/ARB), beta-blocker, MRA (spironolactone), SGLT2 inhibitor. Memorize this.
CHIEF COMPLAINT · HIGH-YIELD

Palpitations

Stability first. Then: is the rhythm narrow or wide, regular or irregular?

Approach

Unstable (hypotension, altered mental status, chest pain, pulmonary edema) gets synchronized cardioversion. Stable gets an ECG. Four buckets: narrow regular (SVT, sinus, atrial flutter), narrow irregular (AFib, MAT), wide regular (VT, SVT with aberrancy), wide irregular (polymorphic VT, AFib with WPW).

The differential
Diagnosis Key features / clues Next step
Ventricular tachycardia Wide complex regular, structural heart disease or ischemia, AV dissociation, fusion beats, capture beats. Unstable → cardioversion · stable → amiodarone or procainamide
Torsades de pointes Polymorphic VT with long QT baseline. Drugs (fluoroquinolones, antipsychotics, methadone), hypokalemia, hypomagnesemia. IV magnesium 2 g · stop offending drug · correct K · overdrive pacing if refractory
WPW with AFib Irregular, wide complex, very rapid (> 200). Delta wave on baseline ECG. Procainamide or ibutilide. AVOID AV nodal blockers, preferential conduction down accessory pathway → VF
Atrial fibrillation with RVR Irregularly irregular, narrow complex, rate > 100. Palpitations, dyspnea. Rate control (metoprolol, diltiazem) · anticoagulate by CHA2DS2-VASc
SVT (AVNRT) Sudden onset narrow complex tachycardia, rate 150–220, young patient without structural disease. Vagal maneuvers → adenosine 6 mg IV → 12 mg → cardioversion if unstable
Sinus tachycardia Gradual onset, rate usually < 150, identifiable trigger (pain, fever, volume depletion, anxiety, PE, anemia, hyperthyroid). Find and treat the cause
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
A 68-year-old man with HTN presents with palpitations and mild dyspnea for 6 hours. BP 128/76, HR 142, irregular. ECG shows narrow complex tachycardia, irregularly irregular, no discernible P waves.
Next step?
Answer › Atrial fibrillation with rapid ventricular response. Stable, rate control with IV metoprolol or diltiazem. Duration matters: if < 48 hours, cardioversion is an option. If uncertain duration, TEE-guided cardioversion or 3 weeks of anticoagulation first. Start anticoagulation decision based on CHA2DS2-VASc.
Pearls
Pearl
CHA2DS2-VASc: CHF, HTN, Age ≥ 75 (2), Diabetes, Stroke/TIA (2), Vascular disease, Age 65–74, Sex (female). Score ≥ 2 (male) or ≥ 3 (female) → anticoagulate.
Pearl
Adenosine transiently blocks the AV node, breaking reentrant SVTs that use the AV node. It will NOT break AFib or flutter, but will briefly unmask flutter waves, which is diagnostic.
Pearl
Wide complex tachycardia in a patient with known structural heart disease or prior MI is VT until proven otherwise. Treat as VT.
CHIEF COMPLAINT · HIGH-YIELD

Syncope

The fundamental split: cardiac (dangerous) versus reflex or orthostatic (usually benign).

Approach

Cardiac syncope is sudden, no prodrome, exertional, injuries on impact, known heart disease, family history of sudden death. Reflex (vasovagal) has a prodrome (nausea, warmth, tunnel vision), is triggered by emotion or standing, resolves fast. Orthostatic happens on standing, with volume depletion, autonomic dysfunction, or medications.

The differential
Diagnosis Key features / clues Next step
Ventricular arrhythmia Sudden, exertional, known HF or cardiomyopathy, prior MI, family history of SCD. Admit · telemetry · echo · cardiology · consider ICD
Aortic stenosis Exertional syncope in elderly, systolic crescendo-decrescendo murmur radiating to carotids, narrow pulse pressure. Echo · surgical or transcatheter AVR
Hypertrophic cardiomyopathy Young athlete with exertional syncope, family history of SCD, murmur increases with Valsalva. Echo · beta-blocker · activity restriction · ICD if high-risk
Massive PE Dyspnea, pleuritic pain, tachycardia, hypoxia, leg swelling. CT-PA · anticoagulate · thrombolysis if shock
Aortic dissection Tearing back pain, pulse differential. CT angio
Vasovagal syncope Young or healthy patient, prodrome of nausea/warmth/lightheadedness, triggered by pain or emotion, rapid recovery. Reassurance · hydration · counterpressure maneuvers · tilt-table if recurrent unclear
Orthostatic hypotension Syncope on standing, drop > 20 systolic or 10 diastolic, medications, dehydration, autonomic neuropathy. Orthostatic vitals · hydration · medication review · compression stockings · midodrine
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
An 80-year-old man loses consciousness briefly while climbing stairs. Exam: systolic ejection murmur at right upper sternal border radiating to carotids, delayed carotid upstroke, 4/6 intensity.
Most likely diagnosis and next step?
Answer › Severe aortic stenosis. Classic triad: syncope, angina, dyspnea. Next step is transthoracic echo to quantify valve area and gradient. Definitive treatment is surgical or transcatheter aortic valve replacement, once symptomatic, mean survival untreated is 2–3 years.
Pearls
Pearl
Three questions that separate cardiac from benign syncope: (1) Was there a prodrome? (2) Did it happen with exertion? (3) Is there a family history of sudden death or known heart disease?
Pearl
Reflex syncope has a prodrome 90% of the time. Cardiac syncope does not. Treat exertional syncope as cardiac until you've ruled it out.
Pearl
ECG is mandatory in every syncope workup. Look for Brugada pattern, long QT, short QT, WPW, ischemia, LVH.
CHIEF COMPLAINT

Peripheral edema

Unilateral vs bilateral is the first fork. Bilateral is systemic; unilateral is local.

Approach

Bilateral edema: right heart failure, cirrhosis, nephrotic syndrome, hypoalbuminemia, drugs (CCBs, NSAIDs, TZDs), venous insufficiency, lymphedema. Unilateral: DVT, cellulitis, lymphatic obstruction, Baker cyst rupture, compartment syndrome.

The differential
Diagnosis Key features / clues Next step
Deep vein thrombosis Unilateral leg swelling, calf pain, recent immobility or malignancy. Wells score → D-dimer if low, duplex US if high · anticoagulate
Right heart failure Elevated JVP, hepatomegaly, ascites, bilateral lower extremity edema. Often from pulmonary HTN or left heart failure. Echo · BNP · treat underlying cause
Nephrotic syndrome Edema (often periorbital), proteinuria > 3.5 g/day, hypoalbuminemia, hyperlipidemia. UA · urine protein/creatinine · renal biopsy often needed
Cirrhosis Ascites > lower extremity edema, spider angiomata, palmar erythema, caput medusae. RUQ US · LFTs · albumin · coags · MELD
Cellulitis Unilateral, warm, erythematous, tender. Fever. Often preceded by break in skin. Clinical diagnosis · cephalexin or cefazolin · cover MRSA if abscess or risk factors
⚑ = can't-miss diagnosis · rule out first
Pearls
Pearl
D-dimer has value only when pre-test probability is low. Ordering it in a high-probability patient is malpractice, you'll anticoagulate them anyway, and negative D-dimer doesn't rule it out.
Pearl
Bilateral edema with clear lungs and elevated JVP but no orthopnea points to right heart failure, not left.
Pearl
Venous insufficiency produces chronic bilateral edema with stasis dermatitis, brawny hyperpigmentation in gaiter distribution.
✦

Disease deep dives

DEFINITIVE DX

Once you've identified the likely diagnosis from the chief complaint, these pages give you the presentation, workup, management, and exam pearls in depth.

Acute Coronary Syndrome
A spectrum from unstable angina to NSTEMI to STEMI. The question on the exam is almost never the diagnosis, it's the next step.
Heart Failure
Classify by EF (HFrEF vs HFpEF) and acuity (chronic vs decompensated). Treatment diverges meaningfully between the two.
Atrial Fibrillation
Three questions define management: stable or unstable, rate or rhythm control, anticoagulate or not.
Hypertension
Stages, targets, and when to act urgently. The most common chronic diagnosis on the exam.
Aortic Dissection
Tearing pain radiating to the back with unequal arm pressures. Stanford A (ascending) is surgical; B (descending) is medical.
DISEASE DEEP DIVE

Acute Coronary Syndrome

A spectrum from unstable angina to NSTEMI to STEMI. The question on the exam is almost never the diagnosis, it's the next step.

Presentation

Substernal pressure radiating to left arm or jaw, diaphoresis, nausea, dyspnea. Elderly, diabetics, and women often atypical: fatigue, epigastric pain, isolated dyspnea.

Workup
  1. ECG within 10 minutes. Differentiates STEMI (cath lab) from NSTEMI/UA (risk-stratified). Look for ST elevation, Q waves, T-wave inversions.
  2. Troponin. High-sensitivity troponin at 0 and 1–3 hours. Elevated confirms MI. Trend matters.
  3. CXR. Rules out aortic dissection (widened mediastinum), pneumothorax, pulmonary edema.
  4. Echo. Assesses wall motion abnormalities, EF, complications (tamponade, VSD, papillary rupture).
Management
  1. Immediate therapy (MONA-B). Morphine (rare, only for refractory pain), Oxygen (only if SaO2 < 90), Nitrates (avoid in RV infarct or severe AS), Aspirin 325 mg chewed, Beta-blocker (only if no HF/shock).
  2. Dual antiplatelet. Aspirin + P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel in most cases).
  3. Anticoagulation. Unfractionated heparin or enoxaparin until revascularization.
  4. STEMI, primary PCI. Door-to-balloon < 90 minutes. If PCI unavailable within 120 minutes, fibrinolysis within 30 minutes.
  5. NSTEMI/UA, risk stratify. TIMI or GRACE score. High-risk → cath within 24 hours. Low-risk → stress test after medical therapy.
  6. Post-MI medications. Aspirin indefinitely + P2Y12 for 12 months, beta-blocker, high-intensity statin (atorvastatin 80 or rosuvastatin 40), ACEi if EF < 40% or anterior MI, MRA if EF < 40% with HF or DM.
Pearls
Pearl
Right-sided ECG (V4R) for every inferior STEMI. If RV infarct is present → no nitrates. Give IV fluids for preload.
Pearl
Post-MI complications by timeline: minutes (arrhythmia, VFib), hours to days (cardiogenic shock, papillary muscle rupture, VSD, free wall rupture), weeks (Dressler syndrome, LV aneurysm, mural thrombus).
Pearl
New systolic murmur after MI is either papillary rupture (acute MR) or VSD. Both are surgical emergencies.
Classic vignette
Exam-style stem
A 62-year-old man with HTN and smoking presents with 40 minutes of chest pressure. BP 100/70, HR 56. ECG: ST elevation in II, III, aVF. Right-sided V4R shows ST elevation. He received nitroglycerin in the ambulance and became hypotensive.
Answer › Inferior STEMI with RV infarct. Stop nitrates. Bolus IV fluids to restore preload. Activate cath lab for primary PCI.
DISEASE DEEP DIVE

Heart Failure

Classify by EF (HFrEF vs HFpEF) and acuity (chronic vs decompensated). Treatment diverges meaningfully between the two.

Presentation

Dyspnea, orthopnea, PND, fatigue, exercise intolerance. Exam: JVD, S3, bibasilar crackles, peripheral edema, hepatojugular reflux.

Workup
  1. BNP / NT-proBNP. BNP < 100 makes HF unlikely. Elevated in HF but also in PE, AFib, renal failure, sepsis.
  2. ECG + CXR. LVH, prior MI, cephalization, Kerley B lines, cardiomegaly, pleural effusions.
  3. Echo. The defining test. Quantifies EF, chamber size, valve function, wall motion. Determines HFrEF vs HFpEF.
  4. Labs. CBC, BMP, TSH, iron studies, HbA1c. HF can be caused or worsened by anemia, thyroid disease, hemochromatosis, diabetes.
Management
  1. Acute decompensation. IV loop diuretic at 2.5× the home dose, O2 to SpO2 ≥ 92%, upright positioning, BiPAP if in respiratory distress. Add IV nitroglycerin if hypertensive.
  2. HFrEF quadruple therapy. All four reduce mortality. (1) ARNI (sacubitril-valsartan) or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin).
  3. HFrEF devices. ICD if EF ≤ 35% on guideline-directed medical therapy for ≥ 3 months. CRT if QRS ≥ 150 ms with LBBB.
  4. HFpEF. Diuretic for symptoms. SGLT2 inhibitor (empagliflozin, dapagliflozin) is now recommended. Aggressively control HTN, treat AFib, treat obesity.
  5. Lifestyle. Sodium restriction (< 2 g/day), fluid restriction if hyponatremic, daily weights, medication adherence, cardiac rehabilitation.
Pearls
Pearl
NYHA class and EF dictate therapy. Class II–IV + EF < 40% requires full guideline-directed medical therapy. EF ≤ 35% + NYHA II–III on optimal therapy qualifies for an ICD.
Pearl
Start ACEi, beta-blocker, and MRA at low doses and titrate every 2 weeks as tolerated. Do not start beta-blockers during active decompensation.
Pearl
Spironolactone watch: hyperkalemia and gynecomastia. Switch to eplerenone if gynecomastia develops.
Classic vignette
Exam-style stem
A 68-year-old man with prior anterior MI presents with progressive dyspnea on exertion. Echo shows EF 25%. Medications: aspirin, atorvastatin.
Answer › Start guideline-directed medical therapy. ARNI (after ACEi washout of 36 hours) or start with ACEi if ARNI unavailable. Add beta-blocker, MRA, SGLT2 inhibitor. Re-echo in 3 months to reassess EF and ICD candidacy.
DISEASE DEEP DIVE

Atrial Fibrillation

Three questions define management: stable or unstable, rate or rhythm control, anticoagulate or not.

Presentation

Palpitations, dyspnea, fatigue, sometimes syncope or stroke. Many patients are asymptomatic. Exam: irregularly irregular pulse.

Workup
  1. ECG. Irregularly irregular rhythm, no discrete P waves, variable R-R intervals.
  2. Echo. LA size, LV function, valve disease. Rheumatic mitral stenosis defines valvular AFib with different anticoagulation rules.
  3. TSH, BMP, CBC. Rule out hyperthyroidism, electrolyte abnormalities, anemia as triggers.
Management
  1. Unstable → cardioversion. Hypotension, chest pain, pulmonary edema, altered mental status → synchronized DC cardioversion.
  2. Rate control. First-line for most. Beta-blocker (metoprolol) or non-dihydropyridine CCB (diltiazem). Digoxin in HF or refractory cases. Target HR < 110 (lenient) or < 80 (strict if symptomatic).
  3. Rhythm control. Consider in young, symptomatic, or new-onset AFib. Antiarrhythmics (flecainide or propafenone if no structural heart disease; amiodarone, dofetilide, sotalol otherwise). Catheter ablation is increasingly first-line.
  4. Anticoagulation. CHA2DS2-VASc ≥ 2 (male) or ≥ 3 (female) → anticoagulate. DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin. Warfarin required for mechanical valves and moderate-severe mitral stenosis.
  5. Cardioversion safety. If AFib > 48 hours or unknown duration → 3 weeks of anticoagulation before or TEE to exclude LA thrombus, then 4 weeks of anticoagulation after.
Pearls
Pearl
CHA2DS2-VASc memorization: C (CHF), H (HTN), A2 (age ≥ 75, 2 points), D (DM), S2 (stroke/TIA, 2 points), V (vascular disease), A (age 65–74), Sc (sex, female).
Pearl
HAS-BLED assesses bleeding risk but rarely overrides stroke risk. Use it to identify modifiable bleeding factors (BP control, NSAIDs, alcohol).
Pearl
Paroxysmal (self-terminates within 7 days), persistent (> 7 days, requires cardioversion), long-standing persistent (> 1 year), permanent (accepted).
Classic vignette
Exam-style stem
A 72-year-old woman with HTN and DM has palpitations. ECG: AFib at rate 112. BP 132/80. She is asymptomatic at rest.
Answer › Rate control with metoprolol. CHA2DS2-VASc = 4 (female +1, HTN +1, DM +1, age 65–74 +1) → anticoagulate with apixaban. Echo to characterize atrial size and valve function.
DISEASE DEEP DIVE

Hypertension

Stages, targets, and when to act urgently. The most common chronic diagnosis on the exam.

Presentation

Usually asymptomatic. End-organ signs: retinopathy, LVH, proteinuria. Malignant hypertension: headache, visual changes, encephalopathy.

Workup
  1. Confirm diagnosis. Two separate measurements on two separate visits OR ambulatory/home BP monitoring. Avoid white-coat overdiagnosis.
  2. Initial workup. BMP, lipids, glucose or HbA1c, UA, ECG. Looking for end-organ damage and establishing baseline.
  3. Secondary HTN screening. If resistant (3 drugs including diuretic), young onset, or specific features. Renal US/Doppler for renovascular disease, aldo/renin ratio for primary aldosteronism, plasma metanephrines for pheochromocytoma, cortisol for Cushing, polysomnography for OSA.
Management
  1. Stage 1 (130–139/80–89). Lifestyle first. Drug therapy if ASCVD, DM, CKD, or 10-year ASCVD risk ≥ 10%.
  2. Stage 2 (≥ 140/90). Two-drug therapy: thiazide + ACEi/ARB or thiazide + CCB. Target < 130/80.
  3. First-line agents. Thiazide (chlorthalidone > HCTZ), ACEi/ARB, CCB (amlodipine). Beta-blockers are not first-line unless there's a CAD, HF, or arrhythmia indication.
  4. Black patients. Thiazide or CCB first, not ACEi/ARB (less effective as monotherapy).
  5. Special populations. DM or CKD → ACEi/ARB preferred. Pregnancy → labetalol, nifedipine, or methyldopa (avoid ACEi/ARB).
  6. Hypertensive emergency. BP > 180/120 WITH end-organ damage (encephalopathy, AKI, MI, dissection, pulmonary edema). IV therapy (labetalol, nicardipine, nitroprusside, esmolol for dissection). Reduce by no more than 25% in the first hour.
  7. Hypertensive urgency. Same BP, no end-organ damage. Oral therapy with gradual reduction over 24–48 hours.
Pearls
Pearl
ACEi side effects: cough (bradykinin, 10–20%), angioedema, hyperkalemia, acute kidney injury in bilateral renal artery stenosis.
Pearl
Thiazide side effects, the hypers: hypokalemia, hyponatremia, hypercalcemia, hyperglycemia, hyperuricemia, hyperlipidemia.
Pearl
In resistant hypertension, add spironolactone as the fourth agent. Spironolactone is also useful adjunct therapy in primary aldosteronism.
Classic vignette
Exam-style stem
A 55-year-old Black man, BP 158/96 on two visits. No DM, no CKD. Labs unremarkable. 10-year ASCVD risk 14%.
Answer › Stage 2 HTN. Start two-drug regimen. For this patient: thiazide + amlodipine. Reassess in 4 weeks.
DISEASE DEEP DIVE

Aortic Dissection

Tearing pain radiating to the back with unequal arm pressures. Stanford A (ascending) is surgical; B (descending) is medical.

Presentation

Sudden, severe, tearing or ripping pain radiating to the back or interscapular area. Risk factors: uncontrolled HTN, Marfan syndrome, bicuspid aortic valve, pregnancy, cocaine use. Exam: pulse differential > 20 mmHg between arms, new AR murmur (if ascending), neurologic deficits (if carotid or spinal involvement).

Workup
  1. CT angio chest/abdomen. Test of choice in stable patients.
  2. TEE. If unstable or contrast contraindicated.
  3. CXR. Widened mediastinum in 75%, not sensitive enough to rule out.
  4. D-dimer. Useful to rule out if low pretest probability. Elevated in nearly all dissections.
Management
  1. BP and HR control first. IV beta-blocker (esmolol or labetalol) FIRST to reduce shear stress. Target HR < 60, systolic BP 100–120.
  2. Add vasodilator. After beta-blockade, add nitroprusside or nicardipine if BP still elevated. Never give vasodilator first, reflex tachycardia increases shear stress.
  3. Pain control. IV opioids.
  4. Stanford A (ascending). Surgical emergency. Mortality 1–2% per hour untreated.
  5. Stanford B (descending only). Medical management unless complications (rupture, malperfusion, refractory pain, progression).
Pearls
Pearl
Painless dissection in a young patient is Marfan until proven otherwise.
Pearl
Pulse deficit + hypertension + chest or back pain means CT angio stat. Do not anticoagulate, do not thrombolyze, you will kill them if it's a dissection masquerading as ACS.
Pearl
New aortic regurgitation after chest pain means ascending dissection propagating into the aortic valve. OR now.
Classic vignette
Exam-style stem
A 60-year-old man with poorly controlled HTN presents with sudden tearing chest pain radiating to his back. BP right arm 180/100, left arm 140/80. New diastolic murmur.
Answer › Ascending aortic dissection (Stanford A) with AR. IV esmolol first to HR < 60, then nitroprusside. CT angio. Emergent surgical consult.