PracticeVideosBlogFlashcardsEspañol
All Practice Exams

Free Practice Questions for Adult Cardiology Fellowship

Exam-style questions and explanations by OpenExamPrep.

✓ No registration✓ No credit card
100+ Questions
100% Free

Loading practice questions...

Same family resources

Explore More Saudi Board Specialty Exams

Continue into nearby exams from the same family. Each card keeps practice questions, study guides, flashcards, videos, and articles in one place.

Saudi Board Anesthesia Final Written Exam (SCFHS)

Practice Questions120 questions

Saudi Board Emergency Medicine Final Written Exam (SCFHS)

Practice Questions114 questions

Saudi Board Dermatology Final Written Exam (SCFHS)

Practice Questions113 questions

Saudi Board Orthopedic Surgery Final Written Exam (SCFHS)

Practice Questions110 questions

Saudi Board Diagnostic Radiology Final Written Exam (SCFHS)

Practice Questions100 questions

Saudi Board Family Medicine Final Written Exam (SCFHS)

Practice Questions100 questions
Exam Review

Key Facts: Adult Cardiology Fellowship Exam

80-120

Official written MCQ range

SCFHS Adult Cardiology Blueprint

70%

Standard passing score (min 65%)

SCFHS Fellowship Written Exam Regulations

20%

Largest blueprint domain: CAD

SCFHS Adult Cardiology Blueprint

Not published

Official exam fee

SCFHS Examination Regulations

Saudi Fellowship Final Examination - Adult Cardiology (SCFHS). One paper of 80–120 single-best-answer MCQs. Up to 10% additional unscored items may be added. Duration is not stated in the written blueprint. The standard pass mark is 70%; when the initial pass rate is below 70%, SCFHS lowers the score one mark at a time toward a 70% pass rate or a 65% score, whichever comes first. A separate final clinical examination follows the written examination.

Sample Adult Cardiology Fellowship Practice Questions

Try these sample questions to review concepts for the Adult Cardiology Fellowship exam. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1During the ventricular action potential, phase 0 rapid depolarization is primarily mediated by which ion channel and inward current?
A.Inward-rectifier Kir2.1 channels carrying a resting potassium current (IK1)
B.L-type Cav1.2 channels carrying a slow inward calcium current (ICa,L)
C.Voltage-gated Nav1.5 channels carrying a rapid inward sodium current (INa)
D.T-type Cav3.1 channels carrying a transient inward calcium current (ICa,T)
Explanation: Phase 0 depolarization in working ventricular myocytes is driven by the opening of voltage-gated Nav1.5 sodium channels, which generate the rapid inward sodium current (INa). This massive inward positive charge rapidly shifts membrane potential from approximately -90 mV to +20 mV. This current is the primary target of Class I antiarrhythmic medications.
2In cardiac excitation-contraction coupling, which mechanism triggers the release of the bulk of calcium from the sarcoplasmic reticulum into the cytosol?
A.Inositol 1,4,5-trisphosphate (IP3) receptor stimulation on the nuclear envelope
B.Calcium-induced calcium release via opening of ryanodine receptor 2 (RyR2)
C.Direct mechanical pulling on sarcoplasmic reticulum channels by the T-tubule membrane
D.Passive diffusion through unphosphorylated phospholamban tetramers
Explanation: Cardiac excitation-contraction coupling depends on calcium-induced calcium release (CICR). Depolarization activates sarcolemmal L-type calcium channels (Cav1.2), producing a modest influx of extracellular calcium that binds to and activates ryanodine receptor 2 (RyR2) on the junctional sarcoplasmic reticulum, triggering a massive release of stored intra-sarcoplasmic calcium into the cytosol to activate troponin C.
3According to the Law of Laplace, which therapeutic intervention produces the greatest reduction in left ventricular peak systolic wall stress?
A.Reducing systolic pressure and cavity radius while increasing wall thickness
B.Increasing end-diastolic volume while decreasing left ventricular wall thickness
C.Increasing systemic vascular resistance while maintaining end-systolic volume
D.Increasing heart rate while maintaining stroke volume and mean arterial pressure
Explanation: According to Laplace's Law, wall stress (sigma) is directly proportional to intraventricular pressure (P) and cavity radius (r), and inversely proportional to twice the wall thickness (2h): sigma = (P * r) / (2 * h). Consequently, reducing systolic pressure and cavity radius while increasing wall thickness yields the greatest reduction in peak systolic wall stress and myocardial oxygen demand.
4On a left ventricular pressure-volume loop, what change is observed following the intravenous administration of an inotropic agent such as dobutamine?
A.A widening of the loop purely due to an increase in end-diastolic volume without changing end-systolic volume
B.A rightward shift of the end-diastolic pressure-volume relationship (EDPVR) slope
C.A leftward and steeper shift of the end-systolic pressure-volume relationship (ESPVR) slope (Ees)
D.A downward and rightward shift of the end-systolic elastance line
Explanation: End-systolic elastance (Ees), represented by the slope of the end-systolic pressure-volume relationship (ESPVR), is a load-independent index of left ventricular myocardial contractility. Positive inotropes such as dobutamine increase contractility, shifting the ESPVR slope upward and to the left, which results in a smaller end-systolic volume at any given afterload.
5A newborn is diagnosed with persistent truncus arteriosus. Abnormal development and migration of which embryonic cell population is the primary cause of this defect?
A.Lateral plate splanchnic mesoderm forming the primary heart field
B.Neural crest cells responsible for septation of the conotruncus
C.Endocardial cushions of the atrioventricular canal
D.Secondary heart field cells forming the sinus venosus
Explanation: Conotruncal septation defects—including persistent truncus arteriosus, tetralogy of Fallot, and transposition of the great arteries—stem from abnormal migration or differentiation of cardiac neural crest cells. These cells migrate from the neural tube into the pharyngeal arches and cardiac outflow tract to form the spiral aorticopulmonary septum that divides the truncus into the aorta and pulmonary trunk.
6Under normal physiological conditions, coronary blood flow is maintained at a relatively constant level across a mean arterial pressure range of 60 to 140 mmHg. Which phenomenon best accounts for this regulatory plateau?
A.Passive elastic recoil of the epicardial coronary conductance arteries during systole
B.Continuous reflex variation in sympathetic alpha-1 adrenergic coronary vasoconstriction
C.Coronary autoregulation governed by local metabolic factors and myogenic vascular tone
D.Retrograde venous flow from the Thebesian veins during left ventricular ejection
Explanation: Coronary autoregulation maintains near-constant myocardial perfusion across perfusion pressures between 60 and 140 mmHg. This is mediated by microvascular resistance alterations driven by myogenic responses (Bayliss effect) and local metabolic vasoactive mediators including adenosine, nitric oxide, hydrogen ions, and interstitial carbon dioxide, ensuring myocardial oxygen delivery precisely matches demand.
7An endomyocardial biopsy demonstrates patchy non-caseating granulomatous inflammation with multinucleated giant cells and CD4+ T lymphocytes, accompanied by surrounding fibrosis and preserved myocyte architecture outside the granulomas. What is the most likely diagnosis?
A.Cardiac sarcoidosis
B.Giant cell myocarditis
C.Acute lymphocytic viral myocarditis
D.Eosinophilic (hypereosinophilic) myocarditis
Explanation: Cardiac sarcoidosis is histologically characterized by non-caseating granulomas composed of epithelioid histiocytes, multinucleated Langhans giant cells, and CD4+ T lymphocytes with interstitial fibrosis. Giant cell myocarditis, in contrast, demonstrates widespread active myocyte necrosis and degeneration intimately mixed with multinucleated giant cells without well-formed discrete granulomas.
8In a patient experiencing acute hypovolemic shock, unloading of high-pressure carotid sinus baroreceptors triggers reflex compensatory responses through which neural pathway?
A.Decreased efferent traffic along the phrenic nerve resulting in secondary vagal withdrawal
B.Increased afferent firing along the vagus nerve (CN X), stimulating the rostral ventrolateral medulla
C.Direct sympathetic stimulation of carotid chemoreceptors activating the sympathetic trunk
D.Reduced glossopharyngeal afferent firing to the NTS, disinhibiting sympathetic outflow
Explanation: Carotid sinus baroreceptors fire tonically in proportion to arterial pressure via the glossopharyngeal nerve (CN IX) to the nucleus tractus solitarius (NTS). A sudden reduction in arterial stretch decreases afferent inhibitory input to the NTS, which disinhibits the rostral ventrolateral medulla (RVLM), triggering systemic sympathetic discharge (vasoconstriction, tachycardia, and increased contractility) while decreasing efferent vagal tone.
9At the cellular level, the Frank-Starling mechanism relates increased myocardial end-diastolic sarcomere length up to 2.2 micrometers to greater force generation primarily through which mechanism?
A.Phosphorylation of troponin I by protein kinase A accelerating cross-bridge detachment
B.Increased total quantity of calcium released per twitch from the sarcoplasmic reticulum
C.Increased myofilament calcium sensitivity and optimized actin-myosin cross-bridge geometry
D.Opening of stretch-activated sodium channels causing prolonged action potential duration
Explanation: The Frank-Starling law operates at the sarcomere level by length-dependent activation. As sarcomere length increases toward an optimal 2.2-2.3 micrometers, lateral interfilament lattice spacing decreases, which brings myosin heads closer to actin filaments and markedly enhances the affinity of troponin C for calcium, producing greater active force without necessarily altering the total calcium transient.
10During physical examination of the jugular venous pulse (JVP), cannon 'a' waves are observed. Which clinical condition is classic for this physical finding?
A.Severe tricuspid regurgitation with right ventricular volume overload
B.Complete atrioventricular block with atrioventricular dissociation
C.Severe pulmonary hypertension with sinus rhythm
D.Constrictive pericarditis with rapid early diastolic ventricular filling
Explanation: Cannon 'a' waves are tall, irregular venous pulsations produced when the right atrium contracts against a closed tricuspid valve, classic in AV dissociation such as complete heart block, ventricular tachycardia, or ventricular pacing. Regular cannon 'a' waves can also occur in junctional tachycardia or 1:1 retrograde AV conduction.

About the Adult Cardiology Fellowship Exam

This resource is an independent English-language MCQ study adaptation created by OpenExamPrep for fellows preparing for the Saudi Fellowship Final Written Examination in Adult Cardiology. It is a subspecialty fellowship qualification under SCFHS, distinct from the core Internal Medicine residency board exam. The written examination tests ten core cardiology domains across 80-120 MCQs, followed by a separate clinical OSCE and structured oral exam. OpenExamPrep is an independent educational platform and is not affiliated with, approved by, or endorsed by SCFHS.

Exam sponsor: Saudi Commission for Health Specialties (SCFHS). The requirements and fees below concern the certification or admission exam, separate from our free practice resources.

Assessment

One paper of 80–120 single-best-answer MCQs. Up to 10% additional unscored items may be added. Duration is not stated in the written blueprint.

Time Limit

Not published by SCFHS

Passing Score

70% (lowered to minimum 65% if pass rate under 70%)

Exam / Certification Fees

Not published by SCFHS

Exam sponsor website

Reported exam pass rate: Not published by SCFHS. SCFHS publishes no candidate pass rate. The blueprint instead sets the passing score at 70% and, if fewer than 70% of candidates pass before final approval, lowers that score one mark at a time until a 70% pass rate is reached or the score reaches 65%, whichever comes first; it is never lowered below 65%. Exam sponsor website

Fees, eligibility, and exam policies can change. Confirm them with the exam sponsor before applying or paying.

Our practice resources: topics covered

We aim to reflect publicly available exam outlines and topic information in our study resources. Coverage, format, and difficulty may differ from the actual exam, and we cannot guarantee that every detail is accurate or current. Confirm exam requirements, fees, and policies with the official exam sponsor.

20%

Coronary Artery Diseases

Chronic coronary syndromes, STEMI/NSTEMI, cardiogenic shock, invasive angiography, intravascular imaging, and revascularization strategies.

17%

Valvular Diseases

Aortic stenosis and regurgitation, mitral stenosis and regurgitation, tricuspid and pulmonic disease, prosthetic valve dysfunction, and endocarditis.

13%

Cardiomyopathies and Heart Failure

HFrEF, HFpEF, hypertrophic cardiomyopathy, dilated/infiltrative cardiomyopathies, myocarditis, and mechanical circulatory support.

9%

Basic Sciences, Cardiac Pathology and Physiology

Cardiac embryology, cellular electrophysiology, myocardial mechanics, pressure-volume relationships, and vascular biology.

9%

Cardiac Arrhythmia

Supraventricular tachycardia, atrial fibrillation/flutter, ventricular arrhythmias, channelopathies, syncope, and pacemaker/ICD/CRT indications.

7%

Clinical Examination

Jugular venous pulse analysis, heart sounds, murmurs, dynamic maneuvers, and bedside hemodynamic evaluation.

7%

Cardiac Pharmacology

Antiarrhythmics, inotropes, vasopressors, antiplatelets, anticoagulants, GDMT neurohormonal modulators, and drug interactions.

7%

Adult Congenital Heart Disease, Pericardial and Systemic Diseases

Adult congenital heart disease (shunt lesions, repaired tetralogy, Eisenmenger physiology, coarctation), pericardial disease (acute and recurrent pericarditis, effusion, tamponade, constriction) and the cardiac manifestations of systemic disease (amyloidosis, sarcoidosis, connective tissue and endocrine disorders).

6%

Aortic Disease and Heart Disease in Pregnancy

Thoracic aortic aneurysm, acute aortic syndromes, genetic aortopathies, maternal hemodynamics, and cardiac management during pregnancy.

5%

Systemic and Pulmonary Hypertension

Primary and secondary systemic hypertension, hypertensive emergencies, pulmonary arterial hypertension, and right ventricular strain.

Preparing for the Adult Cardiology Fellowship Exam

What You Need to Know

  • Passing score: 70% (lowered to minimum 65% if pass rate under 70%)
  • Assessment: One paper of 80–120 single-best-answer MCQs. Up to 10% additional unscored items may be added. Duration is not stated in the written blueprint.
  • Time limit: Not published by SCFHS
  • Exam / certification fees: Not published by SCFHS Official sources

Using Our Practice Resources

  • Work through all 100 available questions
  • Review every answer and explanation
  • Track weak areas and revisit them
  • Use our AI tutor for tough concepts

Adult Cardiology Fellowship: Suggested Study Strategy

1Prioritize high-yield core areas: coronary artery disease (20%), valvular heart disease (17%), and heart failure/cardiomyopathy (13%) account for 50% of the blueprint.
2Master cardiac pressure-volume loops and Wiggers diagrams, especially relating dynamic murmur changes and acute valvular lesions to hemodynamic profiles.
3Carefully study the 2024 ESC and ACC/AHA guidelines for chronic coronary syndromes, acute coronary syndromes, valvular heart disease, and heart failure.
4Practice interpreting hemodynamic tracings from right heart catheterization, such as constrictive pericarditis versus restrictive cardiomyopathy and pulmonary hypertension subtyping.
5Review maternal cardiology risk stratification under the modified WHO classification and management of aortopathy in bicuspid aortic valve and Marfan syndrome.

Frequently Asked Questions

What is the official title and nature of this cardiology credential?

The examination is officially titled the Saudi Fellowship Final Examination - Adult Cardiology, awarded by the Saudi Commission for Health Specialties (SCFHS). It is a specialized 3-year fellowship taken after completing an Internal Medicine residency, rather than an initial residency board.

What is the format and duration of the final written exam?

One paper of 80–120 single-best-answer MCQs. Up to 10% additional unscored items may be added. Duration is not stated in the written blueprint.

What passing score is required by SCFHS for the adult cardiology written paper?

The official passing score is 70%. If the overall cohort passing rate falls below 70%, the cut score may be lowered one mark at a time to reach a 70% cohort pass rate, but it is never lowered below 65%.

Is there a clinical examination in addition to the written examination?

This bank is an independent English-language MCQ study adaptation for the written examination. It does not simulate or replace the separate mandatory final clinical/practical assessment. Consult the specialty clinical blueprint for its station formats and any structured oral or OSCE components.

What are the most heavily weighted subjects on the cardiology written blueprint?

Coronary Artery Diseases represents 20% of the blueprint, Valvular Diseases represents 17%, and Cardiomyopathies and Heart Failure accounts for 13%, together comprising half of the examination.

Is this practice resource affiliated with or endorsed by SCFHS?

No. This practice question bank is an independent educational study aid created by OpenExamPrep and is neither endorsed by nor affiliated with the Saudi Commission for Health Specialties.