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Cardiology Syllabus

Medical Specialization. The full Cardiology syllabus: 7 chapters, 22 topics and 68 sub-topics, with 50 flashcards written against it.

7Chapters
22Topics
68Sub-topics
50Flashcards

Cardiology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Cardiology, not a summary of it.

  1. Introduction to Cardiology

    2 topics
    • History of Cardiology
      • Early Discoveries
      • Modern Advancements
    • Basic Cardiac Anatomy and Physiology
      • Heart Chambers
      • Cardiac Cycle
      • Electrical Conduction System
  2. Cardiac Pathophysiology

    3 topics
    • Ischemic Heart Disease
      • Pathogenesis
      • Clinical Manifestations
      • Diagnosis
      • Management
    • Heart Failure
      • Types of Heart Failure
      • Pathophysiology
      • Clinical Features
      • Diagnostic Approaches
      • Treatment Options
    • Cardiomyopathies
      • Dilated Cardiomyopathy
      • Hypertrophic Cardiomyopathy
      • Restrictive Cardiomyopathy
      • Arrhythmogenic Right Ventricular Cardiomyopathy
  3. Diagnostic Techniques in Cardiology

    4 topics
    • Electrocardiography (ECG)
      • Basic Principles
      • Interpretation of Normal ECG
      • ECG Changes in Cardiac Pathologies
    • Echocardiography
      • Types of Echocardiography
      • Indications
      • Interpretation
    • Cardiac Catheterization
      • Procedure
      • Indications and Contraindications
      • Complications
    • Advanced Imaging Techniques
      • Cardiac MRI
      • Cardiac CT
  4. Cardiac Pharmacology

    4 topics
    • Antianginal Drugs
      • Nitrates
      • Beta-Blockers
      • Calcium Channel Blockers
    • Heart Failure Medications
      • ACE Inhibitors
      • ARBs
      • Diuretics
      • Aldosterone Antagonists
    • Antiarrhythmic Drugs
      • Classification
      • Mechanisms of Action
      • Clinical Use
    • Anticoagulants and Antiplatelets
      • Warfarin
      • Direct Oral Anticoagulants (DOACs)
      • Aspirin
      • P2Y12 Inhibitors
  5. Interventional Cardiology

    3 topics
    • Percutaneous Coronary Intervention (PCI)
      • Indications
      • Techniques
      • Complications
    • Structural Heart Interventions
      • Transcatheter Aortic Valve Replacement (TAVR)
      • Mitral Valve Repair
      • Left Atrial Appendage Occlusion
    • Electrophysiological Interventions
      • Catheter Ablation
      • Pacemakers
      • Implantable Cardioverter-Defibrillators (ICDs)
  6. Preventive Cardiology

    3 topics
    • Risk Factors
      • Modifiable Risk Factors
      • Non-Modifiable Risk Factors
    • Lifestyle Modifications
      • Diet
      • Exercise
      • Smoking Cessation
    • Pharmacological Prevention
      • Statins
      • Antihypertensives
      • Antidiabetic Drugs
  7. Cardiac Surgery

    3 topics
    • Coronary Artery Bypass Grafting (CABG)
      • Indications
      • Techniques
      • Postoperative Care
    • Valve Surgery
      • Types of Valve Surgery
      • Indications
      • Complications
    • Congenital Heart Disease Surgery
      • Common Procedures
      • Postoperative Management

Cardiology flashcards

The complete Cardiology deck: 50 questions with worked answers.

  1. Who is often called the "father of modern cardiology" and what 1628 work founded the field of circulation?

    William Harvey, in his 1628 work "De Motu Cordis" (An Anatomical Study of the Motion of the Heart and Blood), first correctly described systemic blood circulation and the heart as a pump.

  2. Who invented the first electrocardiograph and won the 1924 Nobel Prize for it?

    Willem Einthoven developed the string galvanometer ECG (~1903) and defined the waves P, Q, R, S, T. He received the Nobel Prize in Physiology or Medicine in 1924.

  3. Name the four chambers of the heart and the valve guarding each outflow/inflow on the left side.

    Chambers: right atrium, right ventricle, left atrium, left ventricle. Left side: mitral (bicuspid) valve between LA and LV; aortic valve between LV and aorta.

  4. Trace the normal path of the cardiac conduction system.

    SA node (pacemaker) $\to$ atria $\to$ AV node $\to$ Bundle of His $\to$ right and left bundle branches $\to$ Purkinje fibers $\to$ ventricular myocardium.

  5. State the formula for cardiac output and give a typical resting value.

    $$CO = HR \times SV$$ where HR is heart rate and SV is stroke volume. Typical resting value is about $5\ \text{L/min}$ (e.g., $70\ \text{bpm} \times 70\ \text{mL}$).

  6. Define ejection fraction and give the formula and normal range.

    Ejection fraction is the fraction of end-diastolic volume ejected per beat: $$EF = \frac{SV}{EDV} = \frac{EDV - ESV}{EDV} \times 100\%.$$ Normal is roughly $55\text{–}70\%$.

  7. What are the three main determinants of stroke volume?

    Preload (end-diastolic ventricular stretch/filling), afterload (resistance the ventricle ejects against), and contractility (inotropy, intrinsic myocardial force).

  8. State the Frank-Starling law of the heart.

    Within physiological limits, increased ventricular end-diastolic volume (preload/stretch) increases the force of contraction and thus stroke volume, allowing the heart to match output to venous return.

  9. What supplies the majority of the left ventricle's blood, and which artery is the "widow-maker"?

    The left coronary artery (via LAD and left circumflex) supplies most of the LV. The proximal left anterior descending (LAD) artery is nicknamed the "widow-maker."

  10. Distinguish stable angina from unstable angina.

    Stable angina: predictable chest pain on exertion, relieved by rest/nitrates, fixed atherosclerotic stenosis. Unstable angina: new-onset, at rest, or accelerating pain from plaque rupture/thrombus; an acute coronary syndrome without troponin elevation.

  11. Differentiate NSTEMI from STEMI on ECG and pathology.

    STEMI: complete coronary occlusion causing transmural ischemia with ST-segment elevation. NSTEMI: partial occlusion causing subendocardial infarction with ST depression/T-wave inversion; both have elevated troponin (distinguishing them from unstable angina).

  12. Which cardiac biomarker is most specific for myocardial infarction and what is its time course?

    Cardiac troponin (I or T) is the most specific/sensitive. It rises within 3–6 hours of infarction, peaks around 12–24 hours, and remains elevated for 7–14 days.

  13. Define heart failure and distinguish HFrEF from HFpEF by ejection fraction.

    Heart failure is the inability of the heart to pump/fill adequately to meet metabolic demand. HFrEF (reduced EF): $EF \leq 40\%$ (systolic dysfunction). HFpEF (preserved EF): $EF \geq 50\%$ (diastolic dysfunction). EF $41\text{–}49\%$ is "mildly reduced."

  14. Contrast the typical symptoms of left-sided versus right-sided heart failure.

    Left-sided: pulmonary congestion — dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema. Right-sided: systemic congestion — peripheral/pedal edema, jugular venous distension, hepatomegaly, ascites.

  15. What are the NYHA functional classes of heart failure?

    Class I: no limitation of activity. Class II: slight limitation, symptoms on ordinary activity. Class III: marked limitation, symptoms on less-than-ordinary activity. Class IV: symptoms at rest, unable to do any activity without discomfort.

  16. Which natriuretic peptide is used to diagnose heart failure and what does elevation indicate?

    BNP (B-type natriuretic peptide) and NT-proBNP. They are released by ventricular myocytes in response to wall stretch/stress; elevated levels support a diagnosis of heart failure and correlate with severity.

  17. List the three main types of cardiomyopathy and their defining feature.

    Dilated (DCM): ventricular dilation with systolic dysfunction. Hypertrophic (HCM): asymmetric septal/ventricular hypertrophy, often causing outflow obstruction. Restrictive (RCM): stiff, non-compliant ventricle with impaired diastolic filling.

  18. What is the classic genetic and clinical concern of hypertrophic cardiomyopathy (HCM)?

    HCM is usually autosomal dominant, caused by sarcomeric protein gene mutations (e.g., beta-myosin heavy chain, MYBPC3). It is a leading cause of sudden cardiac death in young athletes due to LV outflow obstruction and arrhythmias.

  19. What is Takotsubo cardiomyopathy?

    Takotsubo (stress-induced or "broken heart") cardiomyopathy is transient LV apical ballooning triggered by emotional/physical stress and catecholamine surge, mimicking MI but with normal coronary arteries; usually reversible.

  20. On a standard ECG, what do the P wave, QRS complex, and T wave represent?

    P wave: atrial depolarization. QRS complex: ventricular depolarization (atrial repolarization is hidden within it). T wave: ventricular repolarization.

Show the other 30 Cardiology flashcards
  1. State the standard ECG paper speed and voltage calibration, and the duration/amplitude of one small box.

    Standard speed is $25\ \text{mm/s}$ and calibration $10\ \text{mm/mV}$. One small box (1 mm) = $0.04\ \text{s}$ horizontally and $0.1\ \text{mV}$ vertically; one large box (5 mm) = $0.20\ \text{s}$.

  2. Give the normal durations of the PR interval and the QRS complex.

    Normal PR interval: $0.12\text{–}0.20\ \text{s}$ (3–5 small boxes). Normal QRS duration: $< 0.12\ \text{s}$ (less than 3 small boxes).

  3. How do you quickly estimate heart rate from an ECG using large boxes?

    $$HR \approx \frac{300}{\text{number of large boxes between two R waves}}$$ (the 300-150-100-75-60-50 rule). Alternatively, $HR = \frac{1500}{\text{small boxes between R waves}}$.

  4. What ECG finding defines first-degree AV block versus complete (third-degree) AV block?

    First-degree AV block: prolonged PR interval $> 0.20\ \text{s}$, every P conducts. Third-degree (complete) block: complete AV dissociation—P waves and QRS are independent with no relationship (atrial rate faster than escape ventricular rate).

  5. What is echocardiography and what is its main advantage?

    Echocardiography uses ultrasound to image cardiac structure and function in real time. Advantages: non-invasive, no ionizing radiation, portable, assesses chamber size, wall motion, valves, ejection fraction, and (with Doppler) blood flow.

  6. Contrast transthoracic (TTE) with transesophageal (TEE) echocardiography.

    TTE: probe on the chest wall, non-invasive, first-line but limited by body habitus/lungs. TEE: probe in the esophagus, semi-invasive, gives superior posterior-structure images (left atrium, appendage, valves, prosthetic valves, endocarditis, aortic dissection).

  7. What does Doppler echocardiography add, and what equation relates pressure gradient to velocity?

    Doppler measures blood flow velocity and direction (valve gradients, regurgitation, stenosis). The simplified Bernoulli equation estimates pressure gradient: $$\Delta P = 4v^{2}$$ where $v$ is peak velocity in m/s and $\Delta P$ in mmHg.

  8. What is cardiac catheterization and what is the gold-standard diagnostic use of coronary angiography?

    Cardiac catheterization threads a catheter through a peripheral artery/vein into the heart/coronaries. Coronary angiography (injecting contrast) is the gold standard for visualizing coronary artery anatomy and stenoses.

  9. In cardiac catheterization, what is fractional flow reserve (FFR) and its ischemia threshold?

    FFR is the ratio of maximal blood flow (pressure) distal to a stenosis versus proximal (normal), measured under hyperemia: $FFR = \frac{P_{distal}}{P_{aorta}}$. A value $\leq 0.80$ indicates a hemodynamically significant lesion warranting revascularization.

  10. Name two access sites for cardiac catheterization and the preferred one.

    The radial artery (wrist) and the femoral artery (groin). Radial access is now preferred for coronary procedures due to fewer bleeding/vascular complications and earlier ambulation.

  11. Compare cardiac MRI and cardiac CT in their primary strengths.

    Cardiac MRI: gold standard for tissue characterization (fibrosis/scar via late gadolinium enhancement), myocardial viability, and precise volumes/function; no radiation. Cardiac CT (CTA): excellent for coronary anatomy/calcium scoring, fast, but uses radiation and iodinated contrast.

  12. What is a coronary artery calcium (CAC) score used for?

    CAC scoring (via CT, Agatston score) quantifies coronary calcification to refine atherosclerotic cardiovascular disease risk. A score of 0 indicates very low risk; higher scores indicate greater plaque burden and event risk.

  13. What is myocardial perfusion imaging (nuclear SPECT/PET) used to assess?

    It uses radiotracers with stress and rest imaging to detect reversible ischemia (perfusion defect on stress that normalizes at rest) versus fixed defects (scar/infarct), assessing functional significance of coronary disease and viability.

  14. What are the three main classes of antianginal drugs and their unifying goal?

    Nitrates, beta-blockers, and calcium channel blockers. All reduce myocardial oxygen demand (and/or improve supply) to relieve the imbalance between demand and supply that causes angina.

  15. By what mechanism do nitrates (e.g., nitroglycerin) relieve angina?

    Nitrates release nitric oxide (NO), which activates guanylate cyclase, raising cGMP and causing vascular smooth muscle relaxation—primarily venodilation, reducing preload and myocardial oxygen demand; also coronary vasodilation.

  16. How do beta-blockers reduce anginal symptoms?

    By blocking $\beta_1$ adrenergic receptors, they lower heart rate, contractility, and blood pressure, decreasing myocardial oxygen demand; the slower heart rate also prolongs diastole, improving coronary perfusion.

  17. What are the four pillars (guideline-directed medical therapy) of HFrEF treatment?

    1) ARNI (or ACE inhibitor/ARB), 2) Beta-blocker, 3) Mineralocorticoid receptor antagonist (MRA, e.g., spironolactone), and 4) SGLT2 inhibitor. Together they reduce mortality and hospitalization in HFrEF.

  18. What is the mechanism and toxicity concern of digoxin in heart failure?

    Digoxin inhibits the $\ce{Na+/K+}$-ATPase, raising intracellular calcium to increase contractility (positive inotrope) and slowing AV conduction. It has a narrow therapeutic index; toxicity is worsened by hypokalemia and causes arrhythmias, nausea, and visual disturbances.

  19. How do loop diuretics like furosemide help heart failure, and what electrolyte must be monitored?

    Loop diuretics inhibit the $\ce{Na+/K+/2Cl-}$ cotransporter in the thick ascending limb of Henle, causing potent diuresis that relieves congestion/edema. Potassium must be monitored (risk of hypokalemia).

  20. State the Vaughan-Williams classification of antiarrhythmic drugs.

    Class I: sodium channel blockers (Ia, Ib, Ic). Class II: beta-blockers. Class III: potassium channel blockers (prolong repolarization, e.g., amiodarone). Class IV: non-dihydropyridine calcium channel blockers (verapamil, diltiazem).

  21. Which antiarrhythmic is class III but has properties of all four classes, and what are its major toxicities?

    Amiodarone. Toxicities include pulmonary fibrosis, thyroid dysfunction (hypo/hyper), hepatotoxicity, corneal deposits, blue-gray skin, and QT prolongation.

  22. What is the first-line drug for terminating acute paroxysmal supraventricular tachycardia (PSVT) and its mechanism?

    Adenosine. It transiently activates $A_1$ receptors, hyperpolarizing AV nodal tissue and briefly blocking AV conduction to interrupt the reentry circuit; it has a very short half-life (seconds).

  23. Contrast the mechanisms of warfarin, heparin, and direct oral anticoagulants (DOACs).

    Warfarin inhibits vitamin K epoxide reductase, reducing factors II, VII, IX, X. Heparin potentiates antithrombin to inhibit thrombin (IIa) and Xa. DOACs directly inhibit either factor Xa (rivaroxaban, apixaban) or thrombin (dabigatran).

  24. How do aspirin and clopidogrel differ in their antiplatelet mechanisms?

    Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1), blocking thromboxane $A_2$ synthesis. Clopidogrel irreversibly blocks the platelet $P2Y_{12}$ ADP receptor, inhibiting ADP-mediated platelet aggregation.

  25. What lab test monitors warfarin therapy and what is a typical target range for most indications?

    The INR (International Normalized Ratio), derived from the prothrombin time. The typical therapeutic target is $2.0\text{–}3.0$ (higher, $2.5\text{–}3.5$, for mechanical mitral valves).

  26. What is percutaneous coronary intervention (PCI) and the role of a drug-eluting stent?

    PCI uses a catheter with a balloon to dilate a stenosed coronary artery (angioplasty), usually deploying a stent. Drug-eluting stents release antiproliferative agents (e.g., sirolimus, everolimus) to reduce neointimal hyperplasia and in-stent restenosis.

  27. What is the target "door-to-balloon" time for primary PCI in STEMI, and why does it matter?

    The target door-to-balloon time is $\leq 90$ minutes. Rapid reperfusion limits infarct size ("time is muscle"), preserving myocardium and improving survival.

  28. What structural heart intervention is TAVR/TAVI and who is it for?

    Transcatheter aortic valve replacement/implantation delivers a prosthetic aortic valve via catheter (usually transfemoral) for severe symptomatic aortic stenosis. Originally for high/prohibitive surgical risk, now also for intermediate and low-risk patients.

  29. What does catheter ablation treat and by what mechanism?

    Catheter ablation treats arrhythmias (e.g., atrial fibrillation, SVT, flutter, VT) by delivering radiofrequency energy or cryoablation to destroy the abnormal electrical focus or reentry pathway. Pulmonary vein isolation is the cornerstone for atrial fibrillation.

  30. Classify the major cardiovascular risk factors into non-modifiable versus modifiable.

    Non-modifiable: age, male sex, family history/genetics, ethnicity. Modifiable: hypertension, dyslipidemia (high LDL), diabetes mellitus, smoking, obesity, physical inactivity, and unhealthy diet. Lifestyle changes plus statins, BP control, and smoking cessation reduce risk.

Cardiology syllabus FAQ

What is in the Cardiology syllabus?

The Cardiology syllabus is split into 7 chapters: Introduction to Cardiology, Cardiac Pathophysiology, Diagnostic Techniques in Cardiology, Cardiac Pharmacology, Interventional Cardiology, Preventive Cardiology and Cardiac Surgery. Together they contain 22 topics and 68 sub-topics.

How many chapters and topics are in the Cardiology syllabus?

7 chapters and 22 topics, broken down further into 68 sub-topics. The largest chapter is Diagnostic Techniques in Cardiology, with 4 topics.

Are there Cardiology flashcards?

Yes — 50 question-and-answer flashcards, printed in full on this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.