Cardiology Practice Questions

Q: Which condition is characterized by a 'hockey-stick' appearance on echocardiography?

Mitral stenosis. The **'hockey-stick' appearance** is a classic echocardiographic hallmark of **Mitral Stenosis (MS)**, specifically seen in rheumatic etiology [1]. **1. Why Mitral Stenosis is correct:** In rheumatic mitral stenosis, the leaflets undergo commissural fusion and thickening. During diastole, the high pressure in the Left Atrium attempts to push the mitral valve open [1]. While the tips of the leaflets are restricted and fused, the mid-portions of the **Anterior Mitral Leaflet (AML)** remain relatively mobile. This results in **diastolic doming** of the AML, which resembles the shape of a hockey stick when viewed in the Parasternal Long Axis (PLAX) view [1]. **2. Why other options are incorrect:** * **Mitral Incompetence (Regurgitation):** Characterized by poor coaptation, prolapse, or flail leaflets, but does not exhibit the specific restricted doming seen in MS [2]. * **Aortic Stenosis:** Associated with a "bicuspid" appearance or heavy calcification of the aortic cusps, often showing restricted opening (systolic doming in bicuspid valves), but not the 'hockey-stick' sign. * **Aortic Regurgitation:** May show "fluttering" of the anterior mitral leaflet due to the regurgitant jet hitting it, but not the characteristic doming of MS [3]. **High-Yield Clinical Pearls for NEET-PG:** * **M-Mode Echo in MS:** Shows a "Square root sign," decreased E-F slope, and paradoxical anterior movement of the Posterior Mitral Leaflet (PML). * **Auscultation:** Loud S1, Opening Snap (OS), and a Mid-diastolic rumbling murmur [1]. * **Severity:** The interval between S2 and the Opening Snap (S2-OS gap) is inversely proportional to the severity of MS (shorter gap = more severe). * **Most common cause:** Rheumatic Heart Disease.

Q: A patient in CCU on day 2 of PCI procedure has the following rhythm. BP=90/60mmHg. Which is the next best step for management of this patient?

Pacemaker. ***Pacemaker*** - The patient has **complete (third-degree) AV block** post-PCI with hemodynamic compromise (BP 90/60 mmHg), requiring urgent **temporary pacemaker** insertion. - **AV block** following PCI is a mechanical complication that needs **electrical support**, not antiarrhythmic medications. *Lignocaine* - Used for **ventricular arrhythmias** like VT/VF, not for **bradyarrhythmias** or conduction blocks. - Would worsen the situation by potentially causing further **cardiac depression** and hypotension. *Amiodarone* - Primarily used for **tachyarrhythmias** and has **negative chronotropic effects** that would worsen bradycardia. - Can further **suppress AV conduction** and is contraindicated in complete heart block. *Synchronized cardioversion* - Used for **tachyarrhythmias** with hemodynamic instability, not for **bradyarrhythmias**. - The patient has **slow heart rate with AV dissociation**, not a fast rhythm requiring cardioversion.

Q: A 56-year-old man presents with severe chest pain and difficulty in breathing. An immediate ECG was taken. What diagnosis does the ECG suggest?

Atrial fibrillation. ***Atrial fibrillation*** - Characterized by **absent P waves** and an **irregularly irregular rhythm** on ECG, which fits with chest pain and dyspnea presentation. - Shows a **fibrillatory baseline** with chaotic atrial activity and variable ventricular response rates. *Ventricular fibrillation* - Presents as **chaotic, disorganized waveforms** without identifiable QRS complexes on ECG. - Would cause **immediate cardiac arrest** and unconsciousness, not chest pain with maintained consciousness. *Acute pulmonary embolism* - ECG typically shows **sinus tachycardia** or the classic **S1Q3T3 pattern** (deep S in lead I, Q wave and inverted T in lead III). - Does not produce the **irregularly irregular rhythm** characteristic of atrial fibrillation. *Second degree heart block* - Shows **dropped QRS complexes** with either progressive PR prolongation (Mobitz I) or intermittent non-conducted P waves (Mobitz II). - Maintains **regular P waves** and organized atrial activity, unlike the chaotic pattern in atrial fibrillation.

Q: Troponin-T is preferable to CPK-MB in the diagnosis of acute myocardial infarction in all of the following situations except:

Reinfarction after 4 days. **Explanation:** The diagnosis of Acute Myocardial Infarction (AMI) relies heavily on the kinetics of cardiac biomarkers. The core concept here is the **duration of elevation** in the bloodstream. [1] **Why Option C is correct:** Troponin-T (TnT) remains elevated in the blood for **10–14 days** after an initial MI. If a patient suffers a second heart attack (reinfarction) 4 days after the first, Troponin levels will still be high from the initial event, making it impossible to distinguish a new rise. In contrast, **CK-MB** returns to baseline within **48–72 hours**. Therefore, if CK-MB levels rise again after 4 days, it specifically indicates a new, acute reinfarction. **Why the other options are incorrect:** * **A. Bedside diagnosis:** Point-of-care Troponin tests are highly sensitive and specific for cardiac muscle, making them the gold standard for rapid bedside triage. * **B. Post-CABG:** During cardiac surgery, skeletal muscle trauma is common. CK-MB is present in small amounts in skeletal muscle and can be falsely elevated. Troponins are more cardio-specific and better for detecting perioperative MI. [1] * **D. Small infarcts:** Troponins are significantly more sensitive than CK-MB; they can detect "micro-infarctions" that do not cause a detectable rise in CK-MB. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Marker:** Myoglobin (rises in 1–3 hours), but it is non-specific. * **Most Specific Gold Standard:** Cardiac Troponin I or T. * **Marker for Reinfarction:** CK-MB (due to its short half-life). * **Kinetics of Troponin:** Rises in 3–6 hours, peaks at 12–24 hours, stays elevated for up to 2 weeks.

Q: A female patient presents with short stature and a history of wearing socks even in the summer season. Physical examination reveals icy cold toes with cyanosis. What is the likely underlying condition?

Coarctation of the aorta. **Explanation:** The clinical presentation of **short stature**, **icy cold toes**, and **cyanosis** (specifically differential cyanosis/ischemia) is a classic description of **Coarctation of the Aorta (CoA)**. [1] **1. Why Coarctation of the Aorta is correct:** CoA involves a narrowing of the aorta, typically distal to the origin of the left subclavian artery. This leads to high blood pressure in the upper extremities and significantly reduced perfusion to the lower extremities. The "history of wearing socks in summer" is a classic clinical clue indicating **intermittent claudication** and chronic coldness of the feet due to poor arterial supply. Short stature is frequently associated with CoA because it is a hallmark feature of **Turner Syndrome (45,XO)**, where CoA is the most common cardiovascular malformation (occurring in ~15-20% of cases). [2] **2. Why other options are incorrect:** * **Hyperparathyroidism:** Typically presents with "stones, bones, abdominal groans, and psychic overtones" due to hypercalcemia; it does not cause localized lower limb ischemia. * **Neurofibromatosis (NF-1):** While NF-1 can be associated with renal artery stenosis (causing hypertension), it does not typically present with short stature and cold toes as primary features. * **Multiple Myeloma:** A plasma cell dyscrasia presenting with bone pain, anemia, and renal failure in older adults; it has no association with the pediatric/syndromic presentation described. **Clinical Pearls for NEET-PG:** * **Radio-femoral delay:** The most important physical sign of CoA. [1] * **Rib Notching:** Seen on X-ray due to collateral circulation through intercostal arteries (usually ribs 3-8). * **Figure-of-3 sign:** Seen on Chest X-ray (pre-stenotic dilation, indentation, and post-stenotic dilation). * **Turner Syndrome:** Always screen these patients for CoA using echocardiography. [2]

Q: Which of the following arrhythmias is most likely to be heritable?

Long QT syndrome. **Explanation:** **Long QT Syndrome (LQTS)** is the most likely heritable arrhythmia among the options. It is a prototypical **channelopathy** [3] caused by mutations in genes encoding cardiac ion channels (primarily potassium and sodium) [1]. It follows distinct inheritance patterns: * **Romano-Ward Syndrome:** Autosomal dominant (most common; no deafness). * **Jervell and Lange-Nielsen Syndrome:** Autosomal recessive (associated with sensorineural deafness). These mutations lead to delayed ventricular repolarization, predisposing patients to *Torsades de Pointes* and sudden cardiac death [1], [2]. **Analysis of Incorrect Options:** * **Short QT Syndrome:** While also a heritable channelopathy, it is **extremely rare** compared to the prevalence of Long QT Syndrome. In the context of NEET-PG, LQTS is the classic representative of inherited arrhythmias. * **Ventricular Ectopy:** Most commonly caused by acquired factors such as electrolyte imbalances (hypokalemia), myocardial ischemia, caffeine, or stress. It is rarely a primary genetic condition. * **WPW Syndrome:** While familial clusters exist (associated with PRKAG2 mutations), the vast majority of cases are **sporadic** and occur due to the persistence of an embryological remnant (Bundle of Kent) [4] rather than a clear Mendelian inheritance pattern. **High-Yield Clinical Pearls for NEET-PG:** * **LQTS Type 1:** Triggered by exercise/swimming (KCNQ1 mutation). * **LQTS Type 2:** Triggered by auditory stimuli/emotion (KCNH2 mutation). * **LQTS Type 3:** Occurs during sleep/rest (SCN5A mutation). * **Drug of Choice:** Beta-blockers (Propranolol/Nadolol) are the mainstay, except in LQTS3 where they are less effective. * **ECG Hallmark:** QTc >440ms in men or >460ms in women [1].

Q: A young male with acute myeloid leukemia was treated with induction chemotherapy. Two months later, he presents with bilateral pedal edema and dyspnea on exertion, as well as paroxysmal nocturnal dyspnea. Which of the following is the most likely cause of his current symptoms?

Dilated cardiomyopathy. **Explanation:** The clinical presentation of bilateral pedal edema, dyspnea on exertion, and paroxysmal nocturnal dyspnea (PND) in a patient previously treated for Acute Myeloid Leukemia (AML) strongly suggests **congestive heart failure (CHF)** [1]. The most likely cause is **Dilated Cardiomyopathy (DCM)** secondary to **Anthracycline-induced cardiotoxicity**. Anthracyclines (e.g., Doxorubicin, Daunorubicin) are the backbone of AML induction therapy. They cause dose-dependent, irreversible myocardial damage through the formation of iron-anthracycline complexes and free radicals, leading to lipid peroxidation of the cardiomyocyte membranes. This results in ventricular dilatation and impaired systolic function (reduced ejection fraction). **Why other options are incorrect:** * **Restrictive Cardiomyopathy:** Usually associated with infiltrative disorders like amyloidosis or post-radiation fibrosis. While some chemo agents cause this, anthracyclines characteristically lead to a dilated phenotype. * **Hypertrophic Cardiomyopathy:** This is typically a genetic condition (mutations in sarcomeric proteins) and is not a known complication of chemotherapy. * **Pericardial Fibrosis:** This leads to constrictive pericarditis, often seen after chest radiation or chronic inflammation, rather than as a direct result of standard AML induction chemotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Doxorubicin Toxicity:** The risk increases significantly once the cumulative dose exceeds **450–550 mg/m²**. * **Monitoring:** Baseline and periodic **Echocardiography or MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF) [2]. * **Prevention:** **Dexrazoxane** (an iron chelator) can be used to reduce free radical formation and protect the myocardium in high-risk patients. * **Histology:** Look for "myofibrillar loss and cytoplasmic vacuolization" on endomyocardial biopsy.

Q: Which of the following is not an indicator of chronic congestive heart failure?

Siuin. In the context of chronic congestive heart failure (CHF), clinicians rely on specific biomarkers to assess myocardial stress, systemic inflammation, and ongoing injury. **Why "Siuin" is the correct answer:** The term **"Siuin"** is not a recognized medical biomarker or clinical indicator for heart failure. It appears to be a distractor or a typographical error in the question source. In medical examinations, identifying the "nonsense" term among established clinical markers is a key test-taking skill. **Analysis of Incorrect Options:** * **Brain Natriuretic Peptide (BNP):** This is the gold-standard biomarker for CHF [1]. It is released by the ventricles in response to increased wall tension and volume overload [1]. It has a high negative predictive value for excluding heart failure. * **CRP (C-Reactive Protein):** Chronic CHF is increasingly recognized as a pro-inflammatory state. Elevated CRP levels are common in heart failure patients and serve as an indicator of systemic inflammation and poor long-term prognosis. * **Troponin:** While primarily used for acute coronary syndromes [2], chronic low-level elevations of Troponin (especially high-sensitivity Troponin) are frequently seen in chronic CHF. This indicates ongoing subclinical cardiomyocyte necrosis or "leakage" due to wall stress and is a marker of disease severity [2]. **High-Yield Clinical Pearls for NEET-PG:** * **BNP vs. NT-proBNP:** NT-proBNP has a longer half-life and is more stable than BNP. * **The "Rule Out" Value:** BNP <100 pg/mL or NT-proBNP <300 pg/mL effectively rules out acute heart failure [1]. * **Neprilysin Inhibitors (ARNI):** Patients on Sacubitril/Valsartan will have **elevated BNP** levels (as the drug prevents its breakdown), so **NT-proBNP** must be used instead to monitor these patients.

Question 1

True regarding atrial fibrillation?

Accepted Answer

Digoxin treatment

Answer

Increased thromboembolism

Answer

Anticoagulant not required

Answer

Aspirin given

Question 2

Which condition is characterized by a 'hockey-stick' appearance on echocardiography?

Accepted Answer

Mitral stenosis

Answer

Mitral incompetence

Answer

Aortic stenosis

Answer

Aortic regurgitation

Question 3

Which of the following statements about blood pressure measurement is INCORRECT?

Accepted Answer

Diastolic blood pressure is indicated by the fourth Korotkoff sound.

Answer

Cuff width should be 40% of arm circumference.

Answer

Using a small cuff will measure spuriously elevated Diastolic blood pressure.

Answer

Monkenberg sclerosis can cause pseudohypertension.

Question 4

A patient in CCU on day 2 of PCI procedure has the following rhythm. BP=90/60mmHg. Which is the next best step for management of this patient?

Accepted Answer

Pacemaker

Answer

Lignocaine

Answer

Amiodarone

Answer

Synchronized cardioversion

Question 5

A 56-year-old man presents with severe chest pain and difficulty in breathing. An immediate ECG was taken. What diagnosis does the ECG suggest?

Accepted Answer

Atrial fibrillation

Answer

Ventricular fibrillation

Answer

Acute pulmonary embolism

Answer

Second degree heart block

Question 6

Troponin-T is preferable to CPK-MB in the diagnosis of acute myocardial infarction in all of the following situations except:

Accepted Answer

Reinfarction after 4 days

Answer

Bedside diagnosis of MI

Answer

Postoperatively after CABG

Answer

Small infarcts

Question 7

A female patient presents with short stature and a history of wearing socks even in the summer season. Physical examination reveals icy cold toes with cyanosis. What is the likely underlying condition?

Accepted Answer

Coarctation of the aorta

Answer

Hyperparathyroidism

Answer

Neurofibromatosis

Answer

Multiple myeloma

Question 8

Which of the following arrhythmias is most likely to be heritable?

Accepted Answer

Long QT syndrome

Answer

Short QT syndrome

Answer

Ventricular ectopy

Answer

WPW Syndrome

Question 9

A young male with acute myeloid leukemia was treated with induction chemotherapy. Two months later, he presents with bilateral pedal edema and dyspnea on exertion, as well as paroxysmal nocturnal dyspnea. Which of the following is the most likely cause of his current symptoms?

Accepted Answer

Dilated cardiomyopathy

Answer

Restrictive cardiomyopathy

Answer

Hypertrophic cardiomyopathy

Answer

Pericardial fibrosis

Question 10

Which of the following is not an indicator of chronic congestive heart failure?

Accepted Answer

Siuin

Answer

CRP

Answer

Brain natriuretic peptide

Answer

Troponin

Cardiology — MCQs

Cardiology — MCQs

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