Cardiovascular

USMLE STEP 1, ULTRA‐HIGH‐YIELD.

Ischemic Heart Disease.

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Contents
01 Heart Development

02 Fetal Circulation

03 Heart Anatomy
04 High Yield Heart Sounds & Murmurs

05 Myocardial Action Potential

06 Baroreceptors

07 Congenital Right-to-Left Shunts

08 Congenital Left-to-Right Shunts

09 Hypertension
10 Atherosclerosis

11 Arteriosclerosis
12 Ischemic Heart Disease (IHD)
13 AV blocks
14 Dilated Cardiomyopathy (DCM)

15 Infective Endocarditis

16 Aortic Dissection

17 Cardiovascular pharmacology
18 Antiarrhythmics
Heart Development

Left-right polarity and beating spontaneously by week 4 of development.

Defect in left-right dynein causes dextrocardia, as seen in Kartagener syndrome (Primary Ciliary
Dyskinesia)(Classic findings: Situs inversus, chronic sinusitis, bronchiectasis, infertility).

KEY EMBRYONIC STRUCTURES AND THEIR DERIVATIVES:

Cardinal veins → Superior and inferior vena cava (SVC & IVC).

Endocardial cushion → Atrial septum, membranous interventricular septum, and AV valves.

Truncus arteriosus → Ascending aorta and pulmonary trunk.

How it is tested: A kid with chronic sinus infections and recurrent pneumonia. Heart sounds are
heard on the right side (Dextrocardia). What’s the diagnosis or which one is the underlying defect?
Answer: Kartagener Syndrome (Primary Ciliary Dyskinesia), due to defective dynein motor proteins

A 3-month-old infant with poor feeding, failure to thrive, and loud holosystolic murmur best heard at
the left lower sternal border (VSD). On physical examination there's epicanthal folds, upslanting
palpebral fissures and single palmar crease. This anomaly most likely originates from which
structure? Answer: Endocardial cushions. Remember, Endocardial cushions disorder is associated
with Down’s syndrome.

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ATRIUM

Failure of septum primum and secundum to fuse leads to Patent Foramen Ovale:

Seen in 25% of the population.

Risk of paradoxical emboli in right-to-left shunting conditions (e.g., during straining, atrial septal
defect).

VENTRICLE

Muscular ventricular septum forms first; gap = interventricular foramen.

Ventricular Septal Defect (VSD) is the most common congenital cardiac anomaly.

Typically occurs in the membranous septum.

How it is tested: A 32-year-old woman with embolic CVA. The patient has signs of left leg DVT.
Echocardiography with bubble study reveals a right-to-left shunt at the level of atria. What caused
the patient’s disorder? Answer: Paradoxical embolism due to patent foramen ovale.

Remember, PFO is caused by failure of fusion of septum primum and septum secundum.

Fetal Circulation

KEY SHUNTS:

1. Ductus venosus: Blood bypasses hepatic circulation to enter IVC.

2. Foramen ovale: Shunts oxygenated blood from RA → LA.

1st breath → ↓ pulmonary resistance → ↑ Pulmonary flow to the left atrium → ↑ LA pressure →
closure of foramen ovale.

3. Ductus arteriosus: Shunts blood from pulmonary artery to descending aorta, bypassing lungs.
↑ O₂ → ↓ Prostaglandins → closure of ductus arteriosus (ligamentum arteriosum).
o NSAIDs (↓ prostaglandin) close a patent ductus arteriosus (PDA).
o Prostaglandins keep PDA open (e.g., in cyanotic heart defects).

How it is tested: A neonate with continuous machine-like murmur (PDA). What’s the appropriate
pharmacologic treatment? Answer: Indomethacin (an NSAID)

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Heart Anatomy

Left Atrium (LA): Most posterior part of the heart. Best assessed with transesophageal echo.

Enlargement (e.g., mitral stenosis) can lead to:

o Dysphagia (compression of esophagus).
o Hoarseness (compression of left recurrent laryngeal nerve – Ortner syndrome).

Right Ventricle (RV): Most anterior part of the heart and most commonly injured in penetrating
trauma in that area.

Left Ventricle (LV): Forms 2/3 of the inferior (diaphragmatic) cardiac surface.

How it is tested: An old man with an irregularly irregular pulse (Atrial Fibrillation) presents with
progressive difficulty swallowing. CT scan reveals an enlarged cardiac silhouette. Which chamber is
responsible? Answer: Left Atrium (Remember, AF originates from pulmonary veins and left atrium.
left atrial enlargement predisposes to AF)

High Yield Heart Sounds & Murmurs

SPLITTING OF S2:

Physiologic splitting: Delay in P2 during inspiration.

Wide, fixed splitting: Highly suggestive of Atrial Septal Defect (ASD).

Paradoxical splitting: Seen in Aortic Stenosis due to delayed closure of A2.

SYSTOLIC MURMURS:

Aortic Stenosis (AS): Crescendo-decrescendo murmur best heard at right upper sternal border.
Radiates to the carotids. Delayed and diminished carotid pulse (pulsus parvus et tardus).
Bicuspid aortic valve (younger patients)
Age-related calcification (elderly)

Hypertrophic Cardiomyopathy (HCM): Crescendo-decrescendo murmur best heard at mid-left

sternal border.
Increases with Valsalva & standing (↓ preload).
Decreases with squatting & handgrip (↑ afterload & preload).

Mitral Regurgitation (MR): Holosystolic murmur best heard at apex, radiates to axilla.
Causes: Mitral valve prolapse, ischemic heart disease, infective endocarditis.

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 Mitral Valve Prolapse (MVP): Midsystolic click followed by late systolic murmur.
Increases with Valsalva & standing (↓ preload).
Decreases with squatting (↑ preload).

Ventricular Septal Defect (VSD): Holosystolic murmur best heard at left 3rd-4th intercostal
spaces.
Smaller defects cause a louder murmur.

DIASTOLIC MURMURS:

Aortic Regurgitation (AR): Early diastolic decrescendo murmur

Wide pulse pressure, bounding pulses, head bobbing .

Mitral Stenosis (MS): Opening snap followed by diastolic rumble best heard at apex.
↑ Severity = ↓ interval between S2 & opening snap.

CONTINUOUS MURMUR:

Patent Ductus Arteriosus (PDA): Machinery murmur heard at left infraclavicular area.
Associated with congenital rubella, prematurity.

How it is tested: A 35-year-old man presents with syncope, angina, and exertional dyspnea. Cardiac
auscultation reveals a crescendo-decrescendo murmur at the right upper sternal border. What is the
most likely diagnosis? Answer: Aortic stenosis due to bicuspid valve.

A young athlete collapses during exercise. Physical exam reveals a crescendo-decrescendo murmur at
the left lower sternal border that increases with Valsalva and decreases with squatting. What is the
most likely diagnosis? Answer: Hypertrophic cardiomyopathy (HCM)

EFFECTS OF MANEUVERS ON MURMURS:

↑ Preload (Squatting, Passive leg raise): ↑ most murmurs except MVP & HCM.
↓ Preload (Valsalva, Standing): ↑ MVP & HCM, ↓ most murmurs.
↑ Afterload (Handgrip): ↑ regurgitant murmurs (MR, AR, VSD), ↓ HCM & AS.

Myocardial Action Potential

Key differences from skeletal muscle:

Plateau phase due to Ca²⁺ influx and K⁺ efflux.

Ca²⁺ influx trigger’s sarcoplasmic reticulum to release Ca²⁺ (Ca²⁺-induced Ca²⁺ release).

Electrical coupling through gap junctions.

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Pacemaker Action Potential. Occurs in SA and AV nodes:

Phase 0: Depolarization via voltage-gated Ca²⁺ channels.

Phase 3: Repolarization due to activation of K⁺ channels.

Phase 4: Spontaneous diastolic depolarization via If (“funny current”) channels:

Mixed Na⁺ and K⁺ inward current.

ANP: Released by atrial myocytes in response to ↑ atrial tension.

BNP: Released by ventricular myocytes in response to ↑ ventricular tension.

Both lead to vasodilation, ↑ Na+ excretion, and diuresis.

BNP is used to diagnose heart failure (high negative predictive value → If it’s negative in the
question, definitely rule out heart failure).

How it is tested: A young patient is presented with hemorrhagic shock. Which of the following is true
about cardiac contractility, baroreceptor firing, and ANP? Answer: ↑, ↓, ↓

Baroreceptors

Respond to ↑ BP
Aortic arch: Afferent and efferent: vagus.

Carotid sinus: Afferent: Glossopharyngeal, efferent: Vagus.

Hypotension: ↓ stretch → ↓ nerve firing → ↑ sympathetic → ↑ HR, BP, contractility.

Carotid massage: ↑ stretch → ↑ parasympathetic tone → slower SA firing → ↓ HR.

Cushing reflex: ↑ ICP → hypertension, bradycardia, respiratory depression.

Very High Yield: Pulmonary capillary wedge pressure (PCWP) is evaluated via pulmonary arteries
but is an estimate of left atrial pressure. Elevated in mitral stenosis and heart failure.

How it is tested: An old patient with several episodes of syncope when buttoning a shirt collar.
Which afferent sensory nerve is responsible? Answer: Glossopharyngeal

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Congenital Right-to-Left Shunts

Early cyanosis (“blue babies”). Require urgent surgical intervention or maintenance of PDA.

1. Truncus arteriosus: Failure to divide into pulmonary trunk and aorta; associated with VSD.

2. Transposition of Great Arteries: Aorta leaves RV, pulmonary trunk leaves LV →

104s;.kpjeparation of systemic and pulmonary circulation. Requires a shunt (e.g., VSD, PDA) for
survival.

CXR: “Egg on a string.”

3. Tricuspid Atresia: Absence of tricuspid valve, hypoplastic RV; requires ASD and VSD/PDA.

4. Tetralogy of Fallot:
Pulmonary infundibular stenosis (key for prognosis).

RV hypertrophy (boot-shaped heart on CXR).

Overriding aorta.

VSD.

“Tet spells”: Cyanosis exacerbated by crying or fever, improved by squatting (↑SVR, ↓ right-to-
left shunting)

TOF is the most common congenital heart disease in DiGeorge syndrome.

5. Total Anomalous Pulmonary Venous Return (TAPVR):

Pulmonary veins drain into right heart circulation; requires ASD and PDA to maintain CO.

Congenital Left-to-Right Shunts

Not cyanotic at birth. If left untreated → pulmonary HTN → reversal to right-to-left shunt →
Eisenmenger: Later cyanosis, clubbing, polycythemia.

Coarctation of Aorta: upper extremity HTN, delayed and weak femoral pulse, Rib notching on CXR.
Associated with Turner Syndrome

Ebstein anomaly: Downward displacement of the tricuspid valve (Tricuspid regurgitation) +

Atrialization of the right ventricle. Associated with prenatal lithium exposure.

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How it is tested: A cyanotic newborn. SPO2 = 65%. Chest x-ray reveals an “egg on a string”
appearance (they may tell you this term or show you a picture). Which of the following is the best
initial intervention? Answer: Prostaglandin E1 (Keeps ductus arteriosus open).

A 10-year-old boy is evaluated for hypertension. BP in right arm = 170/90, but in lower left leg =
100/60. What’s the diagnostic finding on chest X-ray? Answer: Rib notching.

Hypertension

If Hypertension is in young patients without risk factors or resistance to treatment, look for
secondary causes:

· Renal artery stenosis (Fibromuscular dysplasia if young or atherosclerosis if old):

Abdominal bruit and rise of BUN/Cr (especially after starting ACEi/ARB)

· Primary Hyperaldosteronism
Adrenal adenoma or hyperplasia, Hypokalemia, metabolic alkalosis, aldosterone/renin > 20

· Obstructive sleep apnea

Obese patient, Loud snoring, periods of apnea, Daytime somnolence.

How it is tested: A 26-year-old woman with hypertension. She has been taking captopril and
amlodipine since one month ago. Current BP = 160/95. Physical examination reveals an abdominal
bruit. What’s the level of renin and aldosterone, respectively? Answer: Elevated, Elevated. (The
patient has renal artery stenosis, which is activating the RAAS.

HYPERLIPIDEMIA SIGNS:

1. Xanthomas: Lipid-laden histiocytes in skin, especially eyelids (xanthelasma).

2. Tendinous Xanthoma: Lipid deposits in tendons, especially Achilles tendon.

3. Corneal Arcus: Lipid deposits in cornea (arcus senilis in the elderly).

Atherosclerosis

Endothelial dysfunction → lipid accumulation → foam cells (Macrophages) → fatty streaks →

smooth muscle migration (PDGF) → vascularization inside the plaque and growth (TGF-β) → fibrous
plaque (collagen) → complex atheroma.

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Arteriosclerosis

Hyaline: Thickening of vessel walls due to plasma protein leakage into media. Seen in HTN,
diabetes. Homogeneous pink color under LM

Hyperplastic: "Onion-skinning” of smooth muscle proliferation. Seen in severe HTN.

AORTIC ANEURYSMS:

Thoracic: risk factors: HTN, bicuspid aortic valve, Marfan syndrome, tertiary syphilis.
It can cause aortic regurgitation.

Abdominal: risk factors: Smoking > age.

Pulsating abdominal mass, hypotension, back pain.

How it is tested: A 72-year-old man with a history of smoking presents with a pulsatile abdominal
mass. What is the most important risk factor? Answer: Smoking.

Ischemic Heart Disease (IHD)

1. Stable Angina: Exertional chest pain, relieved by rest.

ECG: Normal, Biomarkers: Normal. Diagnosis: Stress Test.
Treatment; nitroglycerin, β-blockers, and CCBs.

The following 3 IHDs are Acute coronary syndromes:

2,3,4. Unstable Angina, NSTEMI, STEMI

All ACSs are caused by plaque rupture and thrombosis, requiring antithrombotic (Heparin) and
antiplatelet (Aspirin, Clopidogrel) drugs.

Unstable angina/NSTEMI: Subtotal occlusion, subendocardial ischemia (infarction in NSTEMI), non-

emergent revascularization, ECG normal or ST-depression.
High yield: NSTEMI has infarction, so Biomarkers are elevated.

STEMI: Total occlusion, transmural infarction (Elevated biomarkers), ECG ST-elevation, emergent
revascularization.

V1, V2, V3, V4: Anterior wall, left anterior descending artery.
I, aVL → Lateral wall, left circumflex artery.
II, III, aVF → Inferior wall, right coronary artery.

Right MI: Hypotension, RV is volume-dependent. Give IV isotonic fluids. Avoid: Nitroglycerin

(Vasodilation ↓ Venous Return).
Inferior MI: Vagal stimulation, Bradycardia. Use Atropine for bradycardia. Avoid β-blockers.

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Ischemic Heart Disease.

Type Cause ECG Biomarkers Diagnosis Treatment

Stable Fixed atherosclerotic

Normal Normal Stress Test Nitroglycerin, β-blockers, CCBs
Angina plaqueexertional ischemia

Unstable Plaque rupture & Normal or ST- Heparin, Aspirin, Clopidogrel (Non
Normal Clinical + ECG
Angina thrombosis(subtotal occlusion) depression emergent revascularization)

Plaque rupture & ST-depression or Heparin, Aspirin, Clopidogrel (Non

NSTEMI Elevated Clinical + ECG
thrombosis(subtotal occlusion) normal emergent revascularization)

Plaque rupture & Emergent revascularization, Heparin,

STEMI ST-elevation Elevated ECG
thrombosis(total occlusion) Aspirin, Clopidogrel

How it is tested: A 58-year-old man with acute chest pain. BP = 110/75. ECG shows ST elevations in
leads II, III, and aVF. 5 minutes after starting the treatment, BP = 90/55. Which drug was
contraindicated in this patient? Answer: Nitroglycerin. (Inferior MI, nitrates are contraindicated)

MI EVOLUTION

0-24 hours: Arrhythmia, Heart failure, Cardiogenic shock.

1-3 days: Time of Acute Inflammation (Neutrophil). Fibrinous pericarditis (Self-limiting).

3-14 days: Time of phagocytosis (Macrophages). Macrophages will cause a lot of ruptures:

Posteromedial papillary muscle rupture: mitral regurgitation.

Ventricular free wall and septal rupture
Ventricular pseudoaneurysm (A kind of free wall rupture that is contained by adherent pericardium/
scar tissue).
Weeks to months: True aneurysm and Dressler syndrome (Autoimmune fibrinous pericarditis)

How it is tested: 5 days after a STEMI, an old man presents with acute dyspnea and hypotension.
Cardiac auscultation reveals a new holosystolic murmur at the apex. What’s the problem? Answer:
Papillary muscle rupture resulting in mitral regurgitation.

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Atrial Fibrillation: Irregularly irregular, no discrete P wave.

Rate control: β-blockers, non-dihydropyridine Ca²⁺ channel blockers.

Anticoagulation based on stroke risk (CHA₂DS₂-VASc score).

A 72-year-old man with irregularly irregular pulse. HR = 170/min, BP = 100/70. What’s the best next
step? Answer: Rate control (β-blockers, Non-dihydropyridine CCB)

Congenital Long QT Syndrome: K+ channel mutations

Jarvell and Lange-Nielsen: Deafness, autosomal dominant.

Romano-Ward: No deafness, autosomal recessive.

AV blocks

First-Degree: PR > 200ms (5 small squares). Benign. Avoid β-blockers.

Second-Degree:
Mobitz I (Wenckebach): Progressive PR lengthening, eventually dropped QRS.
Mobitz II: Dropped QRS without PR change.

When in doubt, check the PRs before and after the dropped QRS. If the PR before the dropped QRS is
longer, it’s Mobitz I. If they are equal, it’s a Mobitz II.

Third-Degree (Complete): Atria and ventricles beat independently.

RR: Regular. PP: Regular. No apparent association between R and P.

Mobitz II and Third- degree generally require a pacemaker.

Dilated Cardiomyopathy (DCM)

Causes:
Alcohol (reversible with withdrawal), cocaine, Trastuzumab (reversible), doxorubicin
(irreversible), Chagas disease (Trypanosoma cruzi), Beriberi (B1 deficiency), and peripartum.

Most common gene: TTN gene(Encodes for Titin protein which anchors myosin to Z- discs)

HYPERTROPHIC CARDIOMYOPATHY (HCM)

Concentric hypertrophy (sarcomeres in parallel)

Most common gene: Myosin-binding protein C, β-myosin heavy chain. Autosomal dominant.
Very Helpful: S3 → LV is dilated (systolic dysfunction)
S4 → LV is stiff and non-compliant (Diastolic dysfunction)

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How it is tested: A patient with alcohol use disorder presents with dyspnea and lower extremity
edema. Cardiac auscultation reveals S3. What’s the definitive treatment for this patient? Answer:
Alcohol cessation.

Beck’s triad for cardiac tamponade includes distended neck veins, hypotension, and distant heart
sounds.

Pulsus paradoxus: A decrease in systolic blood pressure by more than 10 mmHg during inspiration.

Infective Endocarditis

Fever, new murmur, splinter hemorrhages, Janeway lesions (Nontender, Embolic phenomenon),
Osler nodes(Ouchy/Tender, Immune complex deposition).

Common associations:
Prosthetic valves: S. epidermidis

IV drug use: S. aureus, affecting tricuspid valve.

Colon cancer: S. gallolyticus (bovis).

Culture negative: Coxiella, Bartonella.

How it is tested: A 60-year-old presents with dyspnea, fever, and a systolic murmur. Blood cultures
are positive for S. Bovis. After treating the current condition, what’s the best additional workup?
Answer: Colonoscopy to rule out colonic cancer.

RHEUMATIC FEVER

Post-GAS pharyngitis (type II hypersensitivity)

Aschoff bodies (granulomas), Anitschkow cells (macrophages with wavy nuclei) Valve involvement:
Mitral > Aortic. Regurgitation in acute and stenosis in chronic. Immigration is an important key for
USMLE. JONES criteria- Joints(Migratory polyarthritis), Carditis, Nodules, Erythema Marginatum,
Syndenham chorea

Aortic Dissection

Longitudinal intimal tear forming a false lumen in the aorta.

Treatment: β-blockers, vasodilators, surgery.

Risk Factors: Hypertension (most common), bicuspid aortic valve, Marfan syndrome, Ehlers-Danlos
syndrome.
Symptoms: Tearing chest pain radiating to the back, asymmetric BP, mediastinal widening on CXR.
Complications: Organ ischemia, aortic rupture, stroke.

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Cardiovascular pharmacology

Nitrates: Vasodilate via ↑ NO → ↑ cGMP → smooth muscle relaxation.

Adverse Effects: Reflex tachycardia (prevented with β-blockers), hypotension, flushing,

headache.

“Monday disease”: Loss of tolerance over the weekend in industrial exposure → tachycardia,
dizziness upon re-exposure.

Contraindicated in right ventricular infarction, hypertrophic cardiomyopathy, and concurrent

PDE-5 inhibitor use.

Hydralazine: ↑ cGMP → smooth muscle relaxation.

Clinical Use: Severe hypertension, heart failure (combined with nitrates).

Safe during pregnancy.

Adverse Effects: Reflex tachycardia, drug-induced lupus (anti-histone antibodies).

How it is tested: A 40-year-old woman being treated for hypertension develops a fever, joint pain,
and a malar rash. ANA: +, anti-histone antibodies = +. What’s responsible? Answer: Hydralazine.
Remember, Kidney is less commonly affected in drug induced lupus as compared to SLE.

Antianginal Therapy: ↓ O2 demand by ↓ preload, afterload, heart rate, or contractility.

Nitrates: ↓ preload, BP, and O2 demand.

β-Blockers: ↓ BP, heart rate, contractility, and preload.

Ranolazine: Inhibits late-phase inward Na+ → ↓ diastolic wall tension and O2 demand.

Digoxin

Inhibits Na+/K+-ATPase → indirect inhibition of Na+/Ca2+ exchanger → ↑ intracellular Ca2+ →

positive inotropy. Stimulates vagus nerve → ↓ HR.

Clinical use: HF (↑ contractility), atrial fibrillation (↓ HR).

Toxicity predisposed by renal failure and hypokalemia. Yellow vision.

Antidote: anti-digoxin Fab fragments, Normalize electrolytes.

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How it is tested: A 78-year-old woman being treated for AF presents with nausea and complains of
yellow vision. Which electrolyte abnormality increased the risk of developing these symptoms?
Answer: Hypokalemia.

Antiarrhythmics

Class I (Sodium Channel Blockers)

Class IA: Quinidine, procainamide, disopyramide.

↑ AP duration.
Use: Both atrial and ventricular arrhythmias.

Adverse Effects: Torsades de pointes, SLE-like syndrome(procainamide).

Class IB: Lidocaine, mexiletine.

Preferentially affects ischemic tissue.
Use: Acute ventricular arrhythmias, post-MI.

Adverse Effects: CNS depression.

Class IC: Flecainide, propafenone.

Use: SVT; last resort in VT.
Contraindicated structural heart diseases(Heart failure, MI)

Class II (β-Blockers): Metoprolol, propranolol, esmolol, atenolol, carvedilol.

Mechanism: ↓ SA and AV nodal activity by ↓ cAMP → ↓ slope of phase 4 depolarization.

↑ PR interval

Clinical Use: SVT, rate control for atrial fibrillation and flutter.

Adverse Effects: Bradycardia, AV block, asthma exacerbation, dyslipidemia, vasospasm.

Class III (Potassium Channel Blockers): Amiodarone, ibutilide, dofetilide, sotalol.

Mechanism: ↑ AP duration, ERP, QT interval.

Clinical Use: Atrial fibrillation, flutter, VT.

Amiodarone: Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism.

Sotalol: Torsades de pointes.

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Class IV (Calcium Channel Blockers): Verapamil, diltiazem.

Mechanism: ↓ conduction velocity, ↑ ERP, ↑ PR interval.

Clinical Use: SVT, rate control in atrial fibrillation.

Adverse Effects: Constipation, gingival hyperplasia, flushing, bradycardia.

How it is tested: A 65-year-old man with a history of atrial fibrillation develops cough and dyspnea.
Pulmonary function tests reveal restrictive lung disease with fibrosis. What’s responsible? Answer:
Amiodarone.

A patient is taking amlodipine for hypertension treatment. He comes to the office complaining of
lower extremity edema. What’s the best next step? Answer: Add captopril.

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