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USMLE Step 1 High‐Yield Cardiovascular/Cardiology Topics
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Cardiology
High Yield USMLE Step 1 Notes
Welcome to the Cardiology High-Yield Notes for Step 1.
These are the most commonly tested topics on the exam—ideal for quick review in your last 2 weeks before the exam, when you’re short on time, or when you’re just starting out and want to focus on what is high yield. Created and peer-reviewed by physicians who scored 260+ on Step 1 in a Q&A style to reinforce active learning.
How to use this file
- Read the question ➔ cover the answer ➔ self-quiz before revealing.
- Review the NOTES ➔ they include high-yield details you don’t want to miss.
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- Don’t forget to watch the video lessons that go with this file. Learn more here.
Table of Contents
Anatomy
1. 32 y/o woman with embolic CVA. Bubbles pass from the right to the left atrium during an echocardiogram.
➔ Patent Foramen Ovale
- Note: Can cause paradoxical embolism when right atrial pressure > left atrial pressure. It is due to incomplete fusion of septum primum and septum secundum. Diagnose with bubble study.
- Commonly presents as DVT + arterial emboli, for example, having DVT in the legs plus a stroke.
2. A young man with a varicocele on the left side that appeared after a recent weight loss surgery. What’s the probable cause?
➔ Compression of the left renal vein between the aorta and the superior mesenteric artery
- Note: The left renal vein is long, receives the left gonadal vein, and then passes under the SMA (so between the SMA and the aorta).
Compression of the left renal vein (“nutcracker effect”) after rapid weight loss can cause flank pain, hematuria, and varicocele due to increased venous pressure.
Duodenum can also be compressed, leading to postprandial abdominal pain.
Created with BioRender.com
3. An old man with dysphagia and signs of heart failure. What cardiac chamber enlargement can compress the esophagus?
➔ Left atrium
- Note: The left atrium lies directly anterior to the esophagus.
LA enlargement (e.g., from mitral stenosis or regurgitation) can compress:
- The esophagus → dysphagia
- The left recurrent laryngeal nerve → hoarseness (Ortner syndrome).
The LA is closest to the transesophageal echo (TEE) probe
4. Retrograde flow in the left vertebral artery. Occlusion of which vessel?
➔ Left subclavian artery
- Note: Subclavian Steal Syndrome: Caused by proximal subclavian artery stenosis or occlusion (before vertebral artery origin).
Blood reverses from the contralateral vertebral artery to supply the affected arm. Symptoms during arm exertion:
- Arm claudication (fatigue, pain)
- Vertebrobasilar insufficiency (dizziness, vertigo, syncope)
5. An infant with patent ductus arteriosus. In which vessel would PaO₂ be higher compared to a normal infant?
➔ Pulmonary artery
- Note: An increase in SPO₂ in the right side of the heart indicates a left-to-right shunt.
Normal people: Blood goes IVC ➔ RA ➔ RV ➔ PA without oxygenation.
If SPO₂ in:
IVC < RA ➔ ASD ➔ wide-fixed splitting of S2.
RA < RV ➔ VSD ➔ loud holosystolic murmur, lower left sternal border.
RV < PA ➔ PDA ➔ continuous machinery murmur.
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6. A young man is stabbed in the chest at the left lower sternal border, fourth intercostal space. He is hypotensive and tachycardic. Which cardiac structure is most likely injured?
➔ Right ventricle
- Note: The right ventricle forms the anterior surface of the heart. It is the most exposed cardiac chamber to penetrating trauma
- Injury at the mid-to-lower left sternal border likely hits the RV. It can lead to hemopericardium → tamponade → obstructive shock
Valvular Disorders
7. A middle-aged man presents with exertional dyspnea, bounding peripheral pulses, and visible head bobbing with each heartbeat. What is the most likely finding on cardiac auscultation?
➔ Early diastolic murmur (aortic regurgitation)
- Note: Early diastolic blowing murmur at the left sternal border, caused by backflow of blood from the aorta → LV
- Wide pulse pressure → bounding pulses (“water-hammer”), head bobbing (de Musset sign)
- Associated findings: hyperdynamic precordium, displaced apical impulse
8. A woman with progressive dyspnea undergoes cardiac catheterization. Pulmonary capillary wedge pressure is elevated with normal left ventricular pressures. What is the diagnosis?
➔ Mitral stenosis
Note: PCWP = left atrial pressure. In mitral stenosis and left HF, left atrial pressure (and thus PCWP) increases while left ventricular filling may remain normal.
9. An elderly man with an ejection murmur and left ventricular hypertrophy experiences lightheadedness and chest pain during exertion. S2 sound is decreased. What is the cause of his condition?
➔ Extensive valve calcification with impaired leaflet mobility
- Note: Causes of aortic stenosis: Age-related calcification (>70), bicuspid valve calcification (younger), rheumatic disease (they mention immigrants in the question).
- Exam: Harsh systolic murmur at right-upper sternal border, radiating to carotids (important keyword in question stem); delayed pulses; S4 may be heard due to LV hypertrophy.
10. A woman is hospitalized due to infective endocarditis. On cardiac auscultation, there is a midsystolic click followed by a systolic murmur. What underlying condition predisposed her?
➔ Regurgitant mitral valve prolapse
- Note: The mitral valve is most often involved in infective endocarditis (IE). Mitral valve damage or pathology is a risk factor for IE:
- In developed countries: mitral valve prolapse, while in developing countries: Rheumatic heart disease
11. A woman with a diastolic murmur dies from a stroke. Autopsy reveals thickened mitral valve leaflets with commissural fusion. What condition caused these valve changes?
➔ Rheumatic fever
- Note: This patient has mitral stenosis. Thickened and fused mitral leaflets due to chronic inflammation.
- Commonly involves the mitral valve. The mitral valve is the most common, while the aortic is the second. (Immigrant is a common keyword for rheumatic fever.)
- MS leads to left atrial dilation predisposing to atrial fibrillation, and thereby strokes.
12. An old man with low-grade fever, fatigue, and shortness of breath. A new systolic ejection murmur. Blood cultures: Streptococcus gallolyticus. What additional workup?
➔ Colonoscopy (evaluate for colonic neoplasm)
- Note: This patient has IE, evidenced by fever plus a new murmur. The next step is drawing a blood culture and broad-spectrum antibiotics.
- Culture showing S. gallolyticus (formerly S. bovis) is associated with colon cancer, indicating screening by colonoscopy.
- Note: Colorectal cancer disrupts the mucosal barrier, allowing S. gallolyticus (formerly S. bovis) to enter the bloodstream and seed the heart valves → leading to endocarditis.
- Note: Colonoscopy is indicated to rule out colorectal malignancy.
Infective Endocarditis: Fever, new murmur, splinter hemorrhages, Janeway lesions (Nontender, Embolic phenomenon), Osler nodes (Ouchy/Tender, Immune complex deposition).
| Organism | Associated Conditions |
|---|---|
| Staphylococcus aureus | Prosthetic valves Intravenous drug users |
| Viridans streptococci | Gingival manipulation Respiratory tract incision or biopsy |
| Staphylococcus epidermidis | Prosthetic valves Intravascular catheters |
| Enterococci | Nosocomial urinary tract infections |
| Streptococcus gallolyticus (formerly S. bovis) | Colon carcinoma Inflammatory bowel disease |
| Fungi (e.g., Candida) | Immunocompromised host Intravascular catheters |
NOTE: IV drug users ➔ right-sided infective endocarditis (tricuspid or pulm valves)
13. A 2-month-old boy with poor feeding and sweating during nursing. Cardiac auscultation reveals a holosystolic murmur best heard at the left lower sternal border. What is the most likely cause of his symptoms?
➔ Ventricular septal defect (VSD)
- Note: Left-to-right shunt, pulmonary overcirculation, and left-sided volume overload. Results in heart failure symptoms (poor feeding and tachypnea). Large VSD ➔ softer murmur.
- Over time, if untreated, it can lead to Eisenmenger syndrome: cyanosis.
- Untreated ASD, VSD, PDA ➔ increased blood flow to right heart ➔ right ventricular hypertrophy ➔ increased pressure in right heart ➔ reversal of shunt (becomes right to left) ➔ cyanosis.
14. A pregnant woman with episodes of palpitations. A wide-fixed splitting of S2. What congenital heart condition best explains these findings?
➔ Atrial septal defect (ASD)
- Note: ASD results in a left-to-right atrial shunt, causing right heart volume overload. The keyword is a wide and fixed splitting of S2. If left untreated, it may progress to right heart failure or Eisenmenger syndrome.
15. A 20-year-old woman with a systolic murmur at the apex becomes less prominent with squatting. What is the most likely diagnosis?
➔ Mitral valve prolapse (MVP)
- Note: Myxomatous degeneration of valve leaflets. Auscultation: a midsystolic click followed by a late systolic murmur of mitral regurgitation.
General Rule for Murmurs
↑ Blood in the heart → murmur intensity ↑, ↓ Blood in the heart → murmur intensity ↓.
Exceptions to the Rule:
1. Mitral Valve Prolapse (MVP)
○ Murmur: midsystolic click + late systolic murmur (apex)
○ ↑ with ↓ preload (e.g., Valsalva, standing) → earlier click, louder murmur
○ ↓ with ↑ preload/afterload (e.g., squatting, handgrip)
2. Hypertrophic Cardiomyopathy (HCM)
○ Murmur: crescendo-decrescendo systolic murmur (left sternal border)
○ ↑ with ↓ preload → less LV volume → worsened outflow obstruction
○ ↓ with ↑ preload/afterload → more LV volume → reduced obstruction
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Ischemic Heart Disease and Complications
16. An old man with inferior wall ischemia on myocardial perfusion scan. Which coronary artery is blocked?
➔ Right coronary artery
- Note: V1-4: Anterior wall, left anterior descending.
I, aVL: Lateral wall, left circumflex.
II, III, aVF: Inferior wall, right coronary artery (RCA).
Right MI: RCA, Hypotension, RV is volume-dependent. Avoid β-blockers and Nitroglycerin.
Inferior MI: Typically involves RCA, which supplies the SA and AV node, causing bradycardia and increased vagal tone. Avoid β-blockers and Nitroglycerin.
Created with BioRender.com ECG from ecglibrary.com
17. A patient with irregularly irregular rhythm has an embolic stroke. Where was the origin of the embolus?
➔ Left atrial appendage
- Note: Irregularly Irregular = Atrial Fibrillation, an important risk factor for AF.
Risk of stroke or acute limb ischemia. Long-term anticoagulation based on CHADS₂VASC₂
18. A 65-year-old man with exertional chest pain. ECG and enzymes are normal. What’s the next step?
➔ Exercise stress test (if the patient can’t exercise due to osteoarthritis or obesity, then pharmacological stress test using dobutamine or dipyridamole)
- Note: Chronic stable angina occurs when myocardial oxygen demand exceeds supply. Since oxygen supply is relatively fixed, ischemia occurs with increased demand.
- Stable angina pathophysiology is similar to chronic mesenteric ischemia and intermittent vascular claudication.
19. What is the goal of pharmacologic treatment in stable angina?
➔ Reduce myocardial oxygen demand
| Ischemic Heart Disease | |||||
|---|---|---|---|---|---|
| Type | Cause | ECG | Biomarkers | Diagnosis | Treatment |
| Stable Angina | Fixed atherosclerotic plaque Exertional ischemia | Normal | Normal | Stress Test | Nitroglycerin, β-blockers, CCBs |
| Unstable Angina | Plaque rupture & thrombosis (subtotal occlusion) | Normal or ST-depression | Normal | Clinical + ECG | Heparin, Aspirin, Clopidogrel (Non-emergent revascularization) |
| NSTEMI | Plaque rupture & thrombosis (subtotal occlusion) | ST-depression or normal | Elevated | Clinical + ECG | Heparin, Aspirin, Clopidogrel (Non-emergent revascularization) |
| STEMI | Plaque rupture & thrombosis (total occlusion) | ST-elevation | Elevated | ECG | Emergent revascularization, Heparin, Aspirin, Clopidogrel |
- Note: β-blockers, non-DHP CCBs: ↓ HR & contractility → ↓ O2 demand.
- Nitrates: ↓ preload → ↓ wall stress
- DHP CCBs (e.g., amlodipine): ↓ afterload → ↓ wall stress
20. A patient died following MI, biopsy of his myocardium shows neutrophils in infarcted myocardial tissue. What timeline post-MI?
➔ 1 to 3 days (acute inflammation)
- Note: 4–24 hrs: Necrosis, edema; 1–3 days: Neutrophilic infiltration (fibrinous pericarditis);
3–10 days: Macrophages remove dead cells (risk of rupture)
10–14 days: Granulation tissue and new vessels
2 weeks–2 months: Scar formation with collagen (risk of Dressler syndrome)
21. The patient has a new Mobitz type 1 AV block post-acute coronary syndrome. Which coronary artery is involved?
➔ Right coronary artery
- Note: In myocardial infarction, AV block suggests right coronary artery occlusion, which supplies the AV node in most individuals. Treat with Atropine + revascularization. Avoid β-blockers.
22. An old man has an anterior myocardial infarction but rejects revascularization. Five days later, he becomes hypotensive. A new-onset harsh holosystolic murmur. What is the most likely diagnosis?
➔ Interventricular septum rupture
| Complication | Time | Culprit vessel | Clinical Findings | Echocardiography |
|---|---|---|---|---|
| Papillary muscle rupture/dysfunction | 3–7 days | Right coronary artery (RCA) | Severe pulmonary edema Systolic murmur Cardiogenic shock | Severe mitral regurgitation |
| Interventricular septum rupture | 3–7 days | Left anterior descending (LAD) or RCA | Chest pain Harsh holosystolic murmur + thrill Cardiogenic shock | Left-to-right ventricular shunt |
| Free wall rupture | 3-14 days | LAD | Chest pain, Distant heart sounds, Shock, cardiac arrest | Pericardial effusion with tamponade |
| Left ventricular aneurysm | Up to several months | LAD | Heart failure, angina, and ventricular arrhythmias | Thin & dyskinetic myocardial wall |
23. A patient with left ventricular hypokinesia undergoes CABG. Follow-up shows improved EF. What explains this recovery?
➔ Hibernating myocardium
- Note: Ventricular dysfunction due to chronic low blood flow. It can improve with revascularization.
24. An old man develops sharp chest pain worse on inspiration, 2 days after STEMI, and has a pericardial friction rub. What is the diagnosis?
➔ Fibrinous pericarditis (Self-resolving, treat the pain with high-dose aspirin)
- Note: Acute Pericarditis: caused by viral infections, autoimmune diseases (e.g., SLE), uremia, and post-MI (peri-infarction pericarditis or Dressler syndrome).
- Presents with pleuritic chest pain (chest pain on inspiration), a pericardial friction rub, diffuse ST elevations on ECG, and possible pericardial effusion.
- They might ask you to differentiate between fibrinous pericarditis (3 days after MI, extension of ischemia into pericardium, self-resolving) and Dressler syndrome (> 2 weeks after MI, autoimmune disease, treat with colchicine).
25. A 32-year-old woman with chest pain and ST elevations on ECG. Angiography is normal, but acetylcholine reproduces symptoms. What is the underlying mechanism?
➔ Smooth muscle hyperreactivity (Vasospastic Angina)
- Note: Pathophysiology: Coronary artery smooth muscle hyperreactivity due to endothelial dysfunction → same mechanism as Raynaud phenomenon
- Usually affects patients <50 years old
- Clinical presentation:
○ Recurrent chest pain episodes at rest, pain mimics acute coronary syndrome (ACS) and resolves spontaneously within 15 minutes - ECG findings (during attacks): Transient ST-segment elevations
26. A 58-year-old man with inferior STEMI becomes dizzy and bradycardic (HR 38/min) before PCI. Blood pressure is 70/40 mm Hg. Next step?
➔ Atropine (avoid β-blockers and nitroglycerine)
- Note: Common after inferior wall myocardial infarction due to nodal ischemia and increased vagal tone. It usually resolves with reperfusion, but symptomatic bradycardia requires IV atropine to block vagal influence and raise the heart rate.
Arrhythmias and treatment
27. A man with intermittent palpitations has atrial fibrillation on ECG. Where is the likely source of aberrant electrical activity?
➔ Pulmonary veins
- Note: Atrial Fibrillation: Atrial remodeling from aging, hypertension, and mitral stenosis. Triggered by ectopic foci (often from pulmonary veins); worsened by alcohol or sympathetic stimulation.
- It causes palpitations, dyspnea, fatigue, and irregularly irregular pulse; risk of thromboembolism (e.g., stroke).
- Diagnosis: ECG shows no P waves and irregular R-R intervals; continuous ECG may be needed for paroxysmal AF.
28. A man with palpitations and atrial flutter on ECG. Where is the likely source of aberrant electrical activity?
➔ Inside the right atrium
- Note: Rapid, regular atrial activity and a saw-tooth pattern on ECG.
Reentrant circuit through the cavotricuspid isthmus, the primary target for ablation therapy.
29. A child with bilateral sensorineural hearing loss and a prolonged QT interval. Which ion channel is most likely affected?
➔ Potassium channels
- Note: Jervell and Lange-Nielsen Syndrome: congenital bilateral sensorineural hearing loss and long QT syndrome. Risk of ventricular arrhythmias and sudden death. Caused by mutations in potassium channel genes.
30. An athlete with a low resting heart rate and progressive PR interval lengthening followed by dropped QRS complexes. What is the best next step in management?
➔ Reassurance with no further intervention
- Note: Endurance athletes: increased vagal tone, leading to benign bradycardia and first-degree or Mobitz type I AV block. Incidental finding, no treatment needed.
AV Blocks
First-Degree: PR > 200 ms (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 PR intervals 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 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.
31. A 76-year-old woman with heart failure presents with confusion and yellow vision. ECG shows junctional escape rhythm at 50/min. Which medication is responsible?
➔ Digitalis toxicity
- MOA: Inhibits Na⁺/K⁺ ATPase → ↓ Na⁺ efflux → ↑ intracellular Ca²⁺ → Leads to increased cardiac contractility
- Note: Triggered by: Hypokalemia, ↓ GFR (e.g., renal failure), and Drug interactions: Amiodarone, Verapamil (↑ digoxin levels).
- Presents with: Arrhythmias (most dangerous), GI: (Nausea, vomiting, abdominal pain), Confusion, and Yellow-tinted vision
32. A patient is about to start long-term amiodarone. Which test should be done before starting therapy?
➔ Serum TSH
- Note: Amiodarone can cause hypothyroidism (via decreased hormone synthesis) or hyperthyroidism (via increased synthesis or thyroiditis with hormone release).
33. A 56-year-old man with atrial fibrillation starts dofetilide. Which arrhythmia is he most at risk of developing?
➔ Polymorphic ventricular tachycardia
- Note: Class III antiarrhythmics (Dofetilide, Amiodarone, Sotalol, Ibutilide) block delayed-rectifier potassium currents, prolonging repolarization and the QT interval. They increase the risk of torsades de pointes.
- The only class III antiarrhythmics w/o the risk of torsades ➔ Amiodarone
Congenital and pediatric
34. A 9-day-old preterm infant has a continuous machine-like murmur. Which drug treats this condition?
➔ NSAIDs (Inhibition of cyclooxygenase)
- Note: PDA often affects premature infants and is maintained by elevated PGE2 levels. Treatment includes NSAIDs (eg, indomethacin), which lower PGE2 and close the ductus.
35. A newborn with cyanosis and known tetralogy of Fallot requires immediate stabilization. Which intervention is indicated?
➔ Maintenance of ductus arteriosus patency
- Note: Closure of the ductus arteriosus in severe congenital cyanotic heart diseases can lead to rapid hemodynamic collapse. Prostaglandin E1 infusion is used to maintain ductal patency until definitive surgical or catheter-based intervention.
36. What hemodynamic changes occur in the neonate after birth?
➔ Patent foramen ovale closes. Also Ductus arteriosus closes
- Note: Pulmonary vascular resistance ↓ , while Systemic vascular resistance ↑
- left ventricular output ↑
37. An infant with RR = 55, tiring with feeds, and a holosystolic murmur is found to have ASD and VSD. Which genetic condition is most likely present?
➔ Down syndrome
- Note: ASD + VSD ➔ endocardial cushion defects ➔ associated with Down syndrome
38. A child with tetralogy of Fallot squats during cyanotic episodes to relieve symptoms. What is the physiologic mechanism?
➔ Increasing systemic vascular resistance
- Note: Tetralogy of Fallot: 1) RVOT obstruction, 2) large VSD, 3) overriding aorta, 4) RV hypertrophy.
- Squatting increases systemic vascular resistance, ↓ right-to-left shunting, and ↑ oxygenation by ↑ pulmonary blood flow.
39. A child with prolonged fever, conjunctivitis, cracked lips, and hand/foot edema is at significant risk for what complication?
➔ Coronary artery aneurysm
- Note: Kawasaki: A medium-vessel vasculitis in children under 5.
Fever > 5 days plus: conjunctivitis, mucositis, rash, extremity changes, and cervical lymphadenopathy. - Coronary artery aneurysms, HF, and MI are causes of death. Prevented with aspirin.
40. A 20-month-old boy with recurrent pneumonia, sinusitis, and displaced heart sounds toward the right. What is the most likely diagnosis?
➔ Kartagener syndrome
- Note: A subset of primary ciliary dyskinesia, defective dynein arms, impaired mucociliary clearance, recurrent respiratory infections, and situs inversus (e.g., dextrocardia with rightward point of maximal impulse).
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Cardiomyopathy
41. A young man with exertional syncope has asymmetric septal hypertrophy on echo. Which structures cause the left ventricular obstruction?
➔ Mitral valve leaflet and interventricular septum
- Note: HCM: Asymmetric septal hypertrophy, myocardial disarray, and diastolic dysfunction. Mutation in beta-myosin heavy chain.
- Symptoms vary from asymptomatic to exertional dyspnea or syncope and the risk of sudden cardiac death. A systolic murmur that ↑ when the preload is ↓.
- Treatment BB and CCB (↓HR, which leads to ↑ time for diastole and therefore ↑ preload).
42. An elderly man with dyspnea, peripheral edema, and jugular venous distension. He has LV hypertrophy on echo. Biopsy shows pink deposition. What is the diagnosis?
➔ Senile amyloidosis (Transthyretin deposition)
- Note: A kind of Restrictive Cardiomyopathy: due to infiltrative diseases (amyloidosis or sarcoidosis).
Diastolic heart failure. Cardiac amyloidosis shows pink, amorphous amyloid deposits in the myocardium on histology.
Tips on cardiac chamber sizes in heart diseases:
Pressure overload → Concentric hypertrophy (↑ wall thickness, normal size at first).
Volume overload → Eccentric hypertrophy (↑ chamber size, normal/thinner walls).
| Disease | Chamber Size | Wall Thickness | Notes |
|---|---|---|---|
| Dilated Cardiomyopathy | ↑ All chambers | Normal or ↓ | Systolic dysfunction (↓ EF), causes: alcohol, ischemia, etc. |
| Hypertrophic Cardiomyopathy | ↓ LV chamber | ↑ LV wall (especially septum) | Risk of outflow obstruction, S4 gallop |
| Restrictive Cardiomyopathy | Normal chamber size | Normal wall thickness | Stiff ventricles (↓ compliance), causes: amyloidosis, fibrosis |
| Hypertension & Aortic Stenosis | Normal or ↑ LV chamber (late) | ↑ LV wall (LVH) | Concentric hypertrophy from pressure overload |
| Mitral Regurgitation | ↑ LA, ↑ LV | Normal | Volume overload → dilation |
| Aortic Regurgitation | ↑ LV (massive dilation) | Normal | Volume overload → eccentric hypertrophy |
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43. A young man collapses during exercise and dies. Autopsy reveals Distorted myocardial structure and myofibril disarray. What auscultatory finding would likely have been present before death?
➔ S4
- Note: S4 = diastolic heart failure, LV is stiff or hypertrophied due to chronic HTN or AS. Also, early following MI.
44. A 35-year-old man presents with dyspnea and leg swelling. Two months ago, he had a viral illness. What auscultatory finding is present?
➔ S3
- Note: S3 = Systolic heart failure and dilated LV.
- Causes include infections (viral and Chagas), toxins (alcohol and cocaine), medications (Doxorubicin), sarcoidosis, amyloidosis, and thiamine deficiencies.
45. A young man with a sharp chest pain. Mild upper respiratory symptoms a week ago. ECG shows diffuse ST-segment elevations without reciprocal changes. Most likely cause?
➔ Viral pericarditis
- Note: Viral pericarditis: the most common cause of acute pericarditis, often triggered by respiratory viruses (eg, coxsackievirus, echovirus, influenza).
- Findings: pleuritic chest pain that improves when sitting upright and worsens when lying flat. a pericardial friction rub on auscultation. diffuse ST elevations on ECG.
Differentiating Viral Pericarditis vs Myocarditis
- Pericarditis = chest pain + friction rub + ST elevation without wall motion abnormality.
- Myocarditis = chest pain ± heart failure signs + troponin elevation + LV dysfunction on echo.
46. A 32-year-old woman with worsening shortness of breath and leg swelling. TSH = 0.1. What hemodynamic change?
➔ High cardiac output
- Note: Hyperthyroidism ↑ heart rate and contractility ➔ peripheral vasodilation, ↓ systemic vascular resistance. ➔ high-output heart failure.
- Other scenarios for high-output heart failure: 1) ESRD patients with AV fistula, 2) AV malformation, 3) Paget’s disease of bone.
47. A 70-year-old man with HFrEF (EF 30%). Which diuretic improves survival?
➔ Spironolactone
- Note: Drugs to improve survival in HFrEF: βblockers, ACEi-ARBs, Spironolactone, SGLT2 inhibitors.
- If Spironolactone results in gynecomastia, ➔ Switch to Eplerenone. Both eplerenone and spironolactone can cause hyperkalemia
48. An old man with progressive shortness of breath, orthopnea, bilateral lower extremity swelling, and elevated jugular venous pressure. Most likely mechanism?
➔ Heart failure with reduced ejection fraction (HFrEF)
- Note: HFrEF (Heart failure with reduced ejection fraction): ↓ contractility and ejection fraction. ischemic heart disease or dilated cardiomyopathy.
- HFpEF (Heart failure with preserved ejection fraction): Impaired relaxation (↓ compliance). diastolic dysfunction. due to myocardial hypertrophy.
Differentiating left-sided from right-sided heart failure:
- Left-sided heart failure:
○ Results in pulmonary venous congestion.
○ Symptoms include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema.
○ Physical signs: Bibasilar crackles, S3 heart sound. - Right-sided heart failure:
○ Often occurs secondary to left-sided heart failure (cor pulmonale when isolated).
○ Symptoms include peripheral edema, ascites, and hepatomegaly.
○ Physical signs: Elevated jugular venous pressure, peripheral edema, and congestive hepatomegaly (“nutmeg liver”).
Hypertension
49. A 65-year-old woman treated for hypertension develops bilateral leg swelling. Examination and labs are normal. Which medication was likely prescribed?
➔ Amlodipine side effect
- Note: Dihydropyridine CCBs result in arterial vasodilation. This arterial vasodilation decreases the blood pressure but increases the blood flow to the capillaries. This will cause edema.
- Treat this edema by adding ACEi, which causes venous dilation, so blood can easily flow from capillaries to venules.
Antihypertensive side effects
Thiazides: AKI, hyperuricemia, hyperglycemia, hyperlipidemia, hypercalcemia
ACE inhibitors: Cough, angioedema, hyperkalemia
Calcium channel blockers: Peripheral edema, dizziness
Beta blockers: Bronchospasm, bradycardia, fatigue, sexual dysfunction
50. An old man with a myocardial infarction. Receives medication in ED but develops sudden wheezing and shortness of breath. What is the most likely cause?
➔ Beta-blocker induced bronchospasm
- Note: Beta-blockers, especially non-selective ones (eg, propranolol, nadolol), can block beta-2 adrenergic receptors in the lungs.
- Blocking beta-2 receptors leads to bronchoconstriction, which can cause wheezing, cough, and respiratory distress, particularly in patients with underlying asthma or chronic obstructive pulmonary disease (COPD).
51. A 59-year-old man is started on lisinopril. Compared to no therapy, what changes are expected?
➔ ↑ Renin, ↑ Angiotensin I, ↓ Angiotensin II, ↓ Aldosterone, ↑ bradykinin (super high yield)
- Note: Activation of RAAS: ↑ Renin ➔ ↑ Angiotensin I ➔ ↑ Angiotensin II ➔ ↑Aldosterone
ACEi (captopril, lisinopril) inhibits the conversion of angiotensin I to angiotensin II, leading to a decrease in all downstream effects and an accumulation of upstream components.
ACEi increases bradykinin and can cause cough and angioedema.
52. An old man is receiving an ACE inhibitor for hypertension. Switches to ARB. What changes in renin, angiotensin I, angiotensin II, aldosterone, and bradykinin levels are expected compared to baseline?
➔ Renin↑, Angiotensin I ↑, Angiotensin II ↑, Aldosterone ↓, Bradykinin: No significant change
- Note: RAAS function: Regulates blood pressure via angiotensin II → promotes vasoconstriction and aldosterone → sodium/water retention.
- ACE Inhibitors (e.g., lisinopril):
○ Block conversion of angiotensin I → angiotensin II → vasodilation.
○ Inhibit bradykinin breakdown → ↑ bradykinin → dry cough.
○ ↓ aldosterone → ↓ Na⁺/H₂O reabsorption, vasodilation, ↓ BP - ARBs (e.g., losartan):
○ Block the angiotensin II receptor (AT1), Angiotensin II is still produced, but it can’t act.
○ Do not increase bradykinin → cough usually resolves.
Created with BioRender.com
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Other
53. A man with a pulsatile abdominal mass has a history of hypertension and smoking. What are the primary risk factors?
➔ Smoking and age
- Note: Abdominal Aortic Aneurysm (AAA) risk factors: age >60, smoking, hypertension, male sex, and family history. Inflammation and matrix degradation by macrophages weaken the aortic wall.
- If young, it’s usually in the ascending aorta (associated with connective tissue diseases).
54. A young man with severe headache, vomiting, and sudden death. Autopsy reveals a ruptured cerebral aneurysm. What vascular abnormality is most likely associated?
➔ Coarctation of the aorta
- Note: Coarctation of the aorta ➔ chronic hypertension in the head and upper extremities.
High risk of aortic or cerebral aneurysms, which may lead to dissection of the aorta or hemorrhagic stroke. - In another scenario, they will present a patient with signs of severe hypertension (headache, epistaxis). The patient won’t be able to compete with his friends (due to decreased blood flow to the lower extremities).
55. A man with progressive fatigue, ascites, and bilateral leg swelling. Echocardiography shows thickening of the tricuspid and pulmonic valves. The mitral and aortic valves are normal. Which lab finding would confirm the diagnosis?
➔ Elevated urinary 5-hydroxyindoleacetic acid
- Note: Carcinoid Syndrome: serotonin-secreting tumors. Flushing, diarrhea, and bronchospasm. If metastasis to liver ➔ right-sided heart valve lesions.
- These tumors produce serotonin. But normally, the liver breaks down the serotonin. When the tumor metastasizes to the liver, the produced serotonin bypasses the liver and directly goes to the right heart and causes valve thickening. But the lung breaks down the serotonin, and the left heart is intact
- Diagnose with 5-HIAA in urine and imaging studies. Treat with octreotide and surgery.
56. A hypertensive patient presents with tearing chest pain. BP is significantly different between the upper extremities. What is the underlying event?
➔ Intimal tearing
- Note: Severe and acute (tearing) chest pain + blood pressure differences between limbs or just HTN ➔ Aortic Dissection
- The next step is Beta Blockers.
57. A man in a motor vehicle accident with chest trauma develops hypotension, distended neck veins, and clear lung sounds. What is the most likely diagnosis?
➔ Cardiac tamponade (Blood or fluid in the pericardial space)
- Note: Hypotension, jugular venous distension (JVD), muffled heart sounds, pulsus paradoxus, and low-voltage ECG. Treat with emergent pericardiocentesis
- Pulsus paradoxus: exaggerated drop (>10 mm Hg) in systolic blood pressure during inspiration, typically seen in conditions like cardiac tamponade, asthma, or severe COPD.
- Normal lung sounds rule out pneumothorax
58. A man experiences syncope when buttoning his tight collar/ shaving his neck. Stimulation of which nerve is responsible for this reflex?
➔ Glossopharyngeal
- Note: Afferent: Glossopharyngeal, efferent: Vagus.
Another common scenario can be shaving the neck.
In this patient, the carotid sinus is hypersensitive. Small touch to the carotid area, will result in a large parasympathetic stimulation.
59. A man with prior chest radiation presents with heart failure symptoms. There’s a rise in JVP during inspiration. What’s the diagnosis?
➔ Constrictive Pericarditis
- Note: Occurs after pericarditis, cardiac surgery, radiation, or tuberculosis (immigrant is a keyword). A stiffened pericardium limits diastolic filling, mainly affecting the right heart.
- Elevated JVP, pericardial knock, pulsus paradoxus, and a positive Kussmaul sign.
60. A woman with severe bleeding after a trauma presents with hypotension and tachycardia. What changes are expected in cardiac contractility, baroreceptor firing, and atrial natriuretic peptide release?
➔ Cardiac contractility ↑, baroreceptor firing ↓, and atrial natriuretic peptide release ↓
- Note: Baroreceptors are stretch-sensitive sensors that modulate autonomic output. ↓ Arterial stretch (e.g., from blood loss or standing) → ↓ baroreceptor firing → ↑ sympathetic tone & ↓ parasympathetic tone → ↑ heart rate, contractility, and vasoconstriction → helps maintain blood pressure.
- ↓ Atrial stretch during hypovolemia → ↓ ANP secretion → promotes volume retention.
61. An elderly patient with septic shock receives norepinephrine for hypotension. What is the most likely intracellular response in cardiac muscle cells?
➔ ↑ cAMP (β1-2 agonists and glucagon ↑ cAMP)
- Note: Key Autonomic Receptor: α1: ↑ IP3 → vasoconstriction, urethral constriction, pupillary dilation
α2: ↓ cAMP → CNS sympatholytic, ↓ insulin, and intestinal motility
β1: ↑ cAMP → ↑ heart rate, contractility, and renin release
β2: ↑ cAMP → vasodilation, bronchodilation
M2: ↓ cAMP → ↓ heart rate and contractility
M3: ↑ IP3 → bronchoconstriction, ↑ insulin and intestinal motility, bladder contraction, pupillary constriction, vasodilation
62. A 50-year-old woman presents with septic shock. What are the measurements?
➔ ↓ PCWP, ↑ Cardiac index, ↓ Systemic Vascular Resistance (same as anaphylaxis)
- Note: Systemic vasodilation, low central venous and wedge pressures, high cardiac output, and elevated mixed venous oxygen saturation due to impaired oxygen extraction.
Hemodynamic Changes in Different Shocks
| Parameter | Hypovolemic | Cardiogenic | Obstructive | Distributive |
|---|---|---|---|---|
| CVP (central venous pressure) | ↓ | ↑ | ↑ | ↓ |
| PCWP (pulmonary capillary wedge pressure) | ↓ | ↑ | ↓ | ↓ |
| Cardiac Index (LV output) | ↓ | ↓ | ↓ | ↑ (early) / ↓ (late) |
| SVR (systemic vascular resistance) | ↑ | ↑ | ↑ | ↓ |
| SvO₂ (mixed venous oxygen saturation) | ↓ | ↓ | ↓ | ↑ |
63. A 62-year-old man with recent cardiac catheterization presents with painful, mottled skin on his feet, acute kidney injury, and eosinophilia. What is the most likely diagnosis?
➔ Cholesterol crystal embolism
- Note: Cholesterol embolism is a complication of vascular procedures, where cholesterol crystals from disrupted plaques embolize to small arteries. It typically presents with livedo reticularis, AKI, eosinophilia, and low complement levels.
- Common scenarios: surgeries involving the aorta, cardiac catheterization.
- Keywords are livedo reticularis (Net-like reddish-blue skin discoloration), blue toe syndrome, Needle shaped cholesterols on.
64. During an autopsy, yellow streaks are found on the aorta. Microscopy shows abundant lipid-laden cells. What is the predominant cell type in these lesions?
➔ Macrophages
- Note: 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.
- Plaque inflammation increases elastase and causes plaque instability.
🏁 Final Thoughts
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Disclaimer
Version 1.0 May 2025. No part of this document may be reproduced or distributed without written permission. For personal study only. Medical information herein is for educational purposes and does not constitute clinical advice. Always confirm with current guidelines and your institution’s policies.
Prefer a narrative review instead of Q&A style? Scroll down to the section below for high-yield concepts in paragraph format (they cover the same concepts).
Narrative Format
High-Yield Cardiology Topics
High‐yield facts on Cardiovascular/Cardiology that most frequently appear on the USMLE Step 1. Focus on these Heart Development, Heart Anatomy, Ischemic Heart Disease (IHD) and Cardiovascular pharmacology.
Table of Contents
- Heart Development
○ Key Embryonic Structures and Their Derivatives
○ ATRIUM
○ VENTRICLE - Fetal Circulation
○ Key shunts - Heart Anatomy
- High Yield Heart Sounds & Murmurs
○ SPLITTING OF S2
○ Systolic Murmurs
○ Diastolic Murmurs
○ Continuous Murmur
○ Effects of Maneuvers on Murmurs - Myocardial Action Potential
- Baroreceptors
- Congenital Right-to-Left Shunts
- Congenital Left-to-Right Shunts
- Hypertension
○ Hyperlipidemia Signs - Atherosclerosis
- Arteriosclerosis
○ Aortic Aneurysms - Ischemic Heart Disease (IHD)
○ MI evolution - AV blocks
- Dilated Cardiomyopathy (DCM)
○ Hypertrophic cardiomyopathy (HCM) - Infective Endocarditis
○ RHEUMATIC FEVER - Aortic Dissection
- Cardiovascular pharmacology
- Antiarrhythmics
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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.
Created with BioRender.com
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.
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)
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. - 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.
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
Congenital Right-to-Left Shunts
Early cyanosis (“blue babies”). Require urgent surgical intervention or maintenance of PDA.
- Truncus arteriosus: Failure to divide into pulmonary trunk and aorta; associated with VSD.
- Transposition of Great Arteries: Aorta leaves RV, pulmonary trunk leaves LV → separation of systemic and pulmonary circulation. Requires a shunt (e.g., VSD, PDA) for survival.
CXR: “Egg on a string.”
- Tricuspid Atresia: Absence of tricuspid valve, hypoplastic RV; requires ASD and VSD/PDA.
- 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.
- 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.
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
- Xanthomas: Lipid-laden histiocytes in skin, especially eyelids (xanthelasma).
- Tendinous Xanthoma: Lipid deposits in tendons, especially Achilles tendon.
- 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.
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.
| Ischemic Heart Disease | |||||
|---|---|---|---|---|---|
| Type | Cause | ECG | Biomarkers | Diagnosis | Treatment |
| Stable Angina | Fixed atherosclerotic plaque, exertional ischemia | Normal | Normal | Stress Test | Nitroglycerin, β-blockers, CCBs |
| Unstable Angina | Plaque rupture & thrombosis (subtotal occlusion) | Normal or ST-depression | Normal | Clinical + ECG | Heparin, Aspirin, Clopidogrel (Non emergent revascularization) |
| NSTEMI | Plaque rupture & thrombosis (subtotal occlusion) | ST-depression or normal | Elevated | Clinical + ECG | Heparin, Aspirin, Clopidogrel (Non emergent revascularization) |
| STEMI | Plaque rupture & thrombosis (total occlusion) | ST-elevation | Elevated | ECG | Emergent revascularization, Heparin, 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.
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)
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
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.
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.
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
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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.
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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