Cardiology Practice Questions

Q: Austin Flint murmur is associated with which condition?

Aortic regurgitation. ***Aortic regurgitation*** - The **Austin Flint murmur** is a **diastolic rumble** heard at the apex, caused by the regurgitant jet of aortic blood interfering with the normal opening of the mitral valve [1]. - This functional **mitral inflow obstruction** is characteristic of severe aortic regurgitation [1]. *A-V Block* - **A-V block** primarily affects the heart's electrical conduction system, leading to irregular or slow heartbeats, and is not directly associated with a specific murmur. - While it can manifest with various cardiac symptoms, it does not produce the characteristic **diastolic rumbling murmur** of Austin Flint. *Mitral stenosis* - **Mitral stenosis** also produces a diastolic murmur (opening snap followed by a low-pitched rumble), but this is due to **structural narrowing of the mitral valve**, not aortic regurgitation [1], [2]. - The murmur in mitral stenosis is often accompanied by an **opening snap**, which is absent in the Austin Flint murmur [2]. *Aortic stenosis* - **Aortic stenosis** typically presents with a **systolic ejection murmur** that radiates to the carotid arteries, due to obstruction of blood flow from the left ventricle to the aorta [2]. - It does not involve a diastolic rumble at the apex related to mitral valve function, which is the hallmark of an Austin Flint murmur.

Q: A patient with new-onset syncope has a blood pressure of 110/95 mmHg and a harsh systolic ejection murmur at the base, radiating to both carotids. What finding may be revealed upon auscultation of the second heart sound at the base?

It is diminished.. ***It is diminished.*** - A **harsh systolic ejection murmur** radiating to the carotids, new-onset syncope, and a narrow pulse pressure (110/95 mmHg) are highly suggestive of **severe aortic stenosis** [1]. - In **severe aortic stenosis**, the aortic valve leaflets are rigid and fail to open properly, causing a significant reduction in the **aortic component of the second heart sound (A2)** due to decreased mobility and calcification [1], [2]. *It is accentuated.* - An **accentuated S2** (specifically A2) would indicate conditions like systemic hypertension or an increased closing pressure of the aortic valve, which is not consistent with severe aortic stenosis. - In **aortic stenosis**, the valve is *stiff* and *calcified*, leading to a weakened rather than an accentuated closing sound [1]. *It is normal in character.* - A **normal S2** would suggest that the aortic valve is functioning adequately or that any stenosis is mild and not significantly impacting valve closure, which contradicts the patient's symptoms and the harsh murmur. - The presence of **syncope** and a **harsh systolic murmur** strongly implies hemodynamically significant valvular disease [1]. *It is widely split due to delayed ventricular ejection.* - A **widely split S2** with delayed ventricular ejection is characteristic of **right bundle branch block** or **pulmonic stenosis**, neither of which fits the clinical picture of a harsh systolic ejection murmur radiating to the carotids. - In severe aortic stenosis, there can be a **paradoxical splitting of S2** (P2 preceding A2) due to prolonged left ventricular ejection time, but a widely split S2 due to delayed right ventricular ejection is incorrect.

Q: Classification of aortic dissection depends on.

Level of aorta affected. The classification of aortic dissection is primarily based on the **segment of the aorta involved**, typically divided into Stanford and DeBakey classifications [1]. This classification helps determine **management strategies** and prognosis based on the affected aortic region (ascending or descending) [1]. Understanding the classification is crucial for guiding **treatment decisions** and predicting outcomes [1]. The classification is more concerned with **anatomical location** rather than the etiology, such as hypertension or collagen disorders [1].

Q: Which of the following ECG findings is most characteristic of acute myocardial infarction?

ST segment elevation. ST segment elevation - **ST segment elevation** on an ECG is the hallmark sign of an **acute, transmural myocardial infarction** (STEMI), indicating full-thickness myocardial injury [1]. - This elevation occurs due to the **ischemic tissue** failing to repolarize normally, leading to a current of injury [1]. *Elevation of S wave* - An elevated S wave, or a deep S wave, is not a typical characteristic of acute myocardial infarction and can be seen in various conditions, including **ventricular hypertrophy**. - It primarily reflects **ventricular depolarization** forces and not myocardial injury [2]. *Prolonged QT interval* - A **prolonged QT interval** indicates delayed ventricular repolarization, which can be associated with an increased risk of **ventricular arrhythmias** (like Torsades de Pointes) but is not a direct sign of acute myocardial infarction. - It can be congenital or acquired due to **medications** or **electrolyte imbalances**. *Prolonged PR interval* - A **prolonged PR interval** indicates a delay in conduction from the atria to the ventricles, known as a **first-degree AV block**. - While it can be associated with underlying cardiac disease, it is not a direct or characteristic sign of **acute myocardial infarction**.

Q: A 60-year-old woman with a history of diabetes mellitus has had left-sided chest pain radiating to the arm for the past 5 hours. Serial measurements of serum creatine kinase-MB levels show an elevated level 24 hours after the onset of pain. Partial thromboplastin time (PTT) and prothrombin time (PT) are normal. Coronary angiography shows occlusion of the left anterior descending artery. Which of the following mechanisms is the most likely cause of thrombosis in this patient?

Damage to endothelium. ***Damage to endothelium*** - Endothelial damage is a critical factor in thrombosis, leading to the exposure of **sub-endothelial collagen** and triggering platelet activation and coagulation cascade [3]. - In the context of **acute coronary syndrome**, such damage often results from **atherosclerosis**, contributing to the formation of thrombosis in coronary arteries [2]. *Decreased antithrombin III level* - While decreased antithrombin III can contribute to thrombosis, it does not directly explain the **acute coronary occlusion** observed in this patient. - This would affect the **inhibition of thrombin** and other coagulation factors, but the mechanism at play here is primarily endothelial damage. *Antibody inhibitor to coagulation* - Antibody inhibitors usually pertain to conditions like **antiphospholipid syndrome**, which is not indicated by the acute presentation and findings in this case. - The normal PT and PTT suggest that there is no significant disruption in coagulation pathways due to antibodies. *Decreased tissue plasminogen activator* - Decreased tissue plasminogen activator (t-PA) would lead to reduced fibrinolysis, but this does not account for the **acute thrombosis** observed in atherosclerosis [1]. - The patient's presentation is more related to the **acute occlusion due to plaque rupture** rather than a deficiency in plasminogen activator [2].

Q: A 36-year-old patient presents to the emergency department with shock. His ECG shows ST elevation in leads II and III and aVF, as well as ST elevation in V4R. On examination, he has raised jugular venous pressure, hypotension, and clear lung fields. What is the most likely cause of shock?

Right ventricular infarction. ***Right ventricular infarction*** - **ST elevation in leads II, III, and aVF** indicates an **inferior myocardial infarction**, which commonly extends to involve the right ventricle. - Involvement of the right ventricle significantly impairs its ability to pump blood, leading to a **preload-dependent state** and **cardiogenic shock**. *Papillary muscle rupture* - While it can cause shock due to **acute mitral regurgitation**, it typically occurs later (2-7 days) post-infarction and might not present immediately with shock in acute MI diagnosis. - The primary ECG finding would still be indicative of the original infarction, but the shock would clinically manifest as signs of severe **mitral regurgitation** (e.g., new murmur, flash pulmonary edema). *Cardiac rupture* - Free-wall rupture can present with **cardiac tamponade** and cardiogenic shock; however, it tends to occur later (within the first week) after an MI, rather than being the immediate cause of shock upon presentation, and the specific combination of right-sided ST elevation with raised JVP and clear lung fields more specifically points to right ventricular infarction. - It also tends to occur later (within the first week) after an MI, rather than being the immediate cause of shock upon presentation. *Septal perforation* - Results in a **ventricular septal defect**, causing a left-to-right shunt and can lead to shock due to **volume overload** and **pulmonary edema**. - It typically manifests as a **holosystolic murmur** and occurs later post-MI (several days), not usually as the initial presentation of shock in acute MI.

Q: A 68-year-old man presents with a syndrome of alcohol withdrawal. His ECG shows a regular narrow complex tachycardia at 150 bpm with characteristic sawtooth waves. What is the most likely diagnosis?

Atrial flutter. ***Atrial flutter*** - The ECG finding of a **regular narrow complex tachycardia at 150 bpm** with characteristic **sawtooth waves** is pathognomonic for **atrial flutter** [1]. - Alcohol withdrawal can trigger atrial arrhythmias due to increased **sympathetic tone** and electrolyte disturbances. *Atrial fibrillation* - Characterized by an **irregularly irregular rhythm** with no distinct P waves, which contrasts with the regular rhythm and sawtooth waves seen [1]. - While common in alcohol withdrawal, the ECG description does not fit atrial fibrillation. *PSVT* - **Paroxysmal supraventricular tachycardia (PSVT)** is typically a regular narrow complex tachycardia, but it **lacks the sawtooth flutter waves** seen in the ECG [2]. - ECG usually shows sudden onset and termination, often with obscured P waves, but not the distinct flutter waves [3]. *VT* - **Ventricular tachycardia (VT)** is generally characterized by a **wide QRS complex** (>0.12 seconds), which is not consistent with a "narrow complex tachycardia" [4]. - While VT can be regular, it originates from the ventricles and would not show atrial sawtooth waves [4].

Q: What type of murmur is most likely associated with a patient presenting with elevated JVP, large v-waves, and a loud systolic murmur?

Tricuspid regurgitation. ***Tricuspid regurgitation*** - **Elevated JVP** with prominent **v-waves** and a **loud systolic murmur** are classic findings for tricuspid regurgitation. [1] The large v-waves are due to blood regurgitating into the right atrium during ventricular systole. - The murmur is typically **holosystolic** and may increase with inspiration (Carvallo's sign). *Functional murmur* - Functional murmurs are generally **benign**, not associated with significant hemodynamic compromise, and rarely present with elevated JVP or prominent v-waves. - They are typically **soft**, early or mid-systolic, and often change intensity with position. *Tricuspid stenosis* - Tricuspid stenosis would cause an **elevated JVP**, but the prominent wave would be an **a-wave** (due to increased right atrial pressure during atrial contraction), not a v-wave. - The murmur associated with tricuspid stenosis is a **diastolic rumble**, not a systolic murmur. [3] *Pulmonary stenosis* - Pulmonary stenosis presents with a **systolic ejection murmur** at the upper left sternal border and can cause elevated JVP due to right ventricular hypertrophy and failure. [2] - However, it typically does not cause prominent **v-waves** in the JVP, as the issue is outflow obstruction from the right ventricle, not regurgitation into the right atrium.

Q: Manifestations of acute aortic dissection include all of the following, except:

Mitral Regurgitation (MR). ***Mitral Regurgitation (MR)*** - **Mitral regurgitation** is not a typical direct manifestation of acute aortic dissection. The mitral valve is anatomically separate from the aorta [3]. - While indirect effects on the heart can occur, direct **MR** is highly unlikely as a primary presentation of acute aortic dissection. *Pericardial effusion* - An acute aortic dissection, especially of the ascending aorta, can rupture into the **pericardial space**, leading to **pericardial effusion** and potentially **cardiac tamponade** [2]. - This occurs due to blood leaking from the dissected aorta into the confines of the pericardium. *AR* - **Aortic regurgitation (AR)** is a common and serious complication of acute aortic dissection when the dissection involves the **aortic root** and disrupts the integrity of the aortic valve leaflets or their support structures [1]. - This can lead to new onset or worsening AR, causing acute heart failure. *AMI* - **Acute myocardial infarction (AMI)** can result from an acute aortic dissection if the dissection flap extends into or compromises the ostium of a **coronary artery**, particularly the right coronary artery [1]. - This occlusion of a coronary artery by the dissecting hematoma or flap leads to **myocardial ischemia** and infarction.

Question 1

Austin Flint murmur is associated with which condition?

Accepted Answer

Aortic regurgitation

Answer

Mitral stenosis

Answer

Aortic stenosis

Answer

A-V Block

Question 2

A 54-year-old man presents after a syncopal episode with no recollection of the event, and bystanders report that he regained consciousness approximately 45 seconds after falling. He has a history of bipolar disorder managed with quetiapine, and recently experienced prostatitis treated with ciprofloxacin. His other medications include lisinopril and hydrochlorothiazide for hypertension, and cyclobenzaprine and a hydrocodone/acetaminophen combination pill for low back pain. On examination, the patient is alert and oriented, with a nonfocal neurological examination and an unremarkable cardiac examination. Electrocardiogram shows nonspecific ST and T wave changes and a prolonged QT interval (QTc of 540 milliseconds). What is the best initial management approach?

Accepted Answer

Admit the patient for telemetry and evaluate for reversible causes of QT prolongation

Answer

Admit for permanent implantable cardioverter-defibrillator (ICD)

Answer

Admit and begin amiodarone infusion

Answer

Refer for genetic counseling

Question 3

A patient with new-onset syncope has a blood pressure of 110/95 mmHg and a harsh systolic ejection murmur at the base, radiating to both carotids. What finding may be revealed upon auscultation of the second heart sound at the base?

Accepted Answer

It is diminished.

Answer

It is accentuated.

Answer

It is normal in character.

Answer

It is widely split due to delayed ventricular ejection.

Question 4

Classification of aortic dissection depends on.

Accepted Answer

Level of aorta affected

Answer

Cause of dissection

Answer

Extent of symptoms

Answer

Percentage of aorta affected

Question 5

Which of the following ECG findings is most characteristic of acute myocardial infarction?

Accepted Answer

ST segment elevation

Answer

Prolonged QT interval

Answer

Prolonged PR interval

Answer

Elevation of S wave

Question 6

A 60-year-old woman with a history of diabetes mellitus has had left-sided chest pain radiating to the arm for the past 5 hours. Serial measurements of serum creatine kinase-MB levels show an elevated level 24 hours after the onset of pain. Partial thromboplastin time (PTT) and prothrombin time (PT) are normal. Coronary angiography shows occlusion of the left anterior descending artery. Which of the following mechanisms is the most likely cause of thrombosis in this patient?

Accepted Answer

Damage to endothelium

Answer

Presence of antibody inhibitors to coagulation factors

Answer

Reduced levels of antithrombin III

Answer

Reduced activity of tissue plasminogen activator (tPA)

Question 7

A 36-year-old patient presents to the emergency department with shock. His ECG shows ST elevation in leads II and III and aVF, as well as ST elevation in V4R. On examination, he has raised jugular venous pressure, hypotension, and clear lung fields. What is the most likely cause of shock?

Accepted Answer

Right ventricular infarction

Answer

Papillary muscle rupture

Answer

Septal perforation

Answer

Cardiac rupture

Question 8

A 68-year-old man presents with a syndrome of alcohol withdrawal. His ECG shows a regular narrow complex tachycardia at 150 bpm with characteristic sawtooth waves. What is the most likely diagnosis?

Accepted Answer

Atrial flutter

Answer

Atrial fibrillation

Answer

PSVT

Answer

VT

Question 9

What type of murmur is most likely associated with a patient presenting with elevated JVP, large v-waves, and a loud systolic murmur?

Accepted Answer

Tricuspid regurgitation

Answer

Functional murmur

Answer

Tricuspid stenosis

Answer

Pulmonary stenosis

Question 10

Manifestations of acute aortic dissection include all of the following, except:

Accepted Answer

Mitral Regurgitation (MR)

Answer

Pericardial effusion

Answer

AR

Answer

AMI

Cardiology — MCQs

Cardiology — MCQs

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