Cardiology Practice Questions

Q: True about VSD is all except -

Pulmonary Oligemia in chest x-ray. ***Pulmonary Oligemia in chest x-ray*** - **Ventricular Septal Defects (VSDs)** with a significant left-to-right shunt typically cause **pulmonary plethora** (increased pulmonary vascular markings) due to increased blood flow to the lungs, not oligemia. - **Pulmonary oligemia** (decreased pulmonary vascular markings) is seen in conditions with reduced pulmonary blood flow, such as severe pulmonary stenosis or tetralogy of Fallot [2]. *Small hole closes spontaneously* - Many **small, restrictive VSDs**, particularly those in the muscular septum, close spontaneously within the first few years of life. - This spontaneous closure is observed in up to 30-50% of VSDs, making it a common outcome for smaller defects. *Defect is usually in membranous part* - The **membranous portion of the interventricular septum** is the most common site for VSDs, accounting for approximately 80% of all defects [1]. - VSDs in this region are often referred to as perimembranous VSDs [1]. *Endocarditis is a common complication* - Patients with VSDs, especially those with smaller or moderate defects where there is a turbulent flow and high-velocity jet, are at an increased risk of developing **infective endocarditis**. - The turbulent blood flow at the site of the VSD can damage the endocardial lining, making it more susceptible to bacterial colonization.

Q: Swan Ganz catheter is used for what ?

Pulmonary capillary pressure. ***Pulmonary capillary pressure*** - A Swan-Ganz catheter, when properly wedged, measures the **pulmonary capillary wedge pressure (PCWP)**, which is an indirect estimate of the left atrial pressure [1] and, consequently, the **left ventricular end-diastolic pressure (LVEDP)** or **preload**. - This measurement helps in assessing left heart function and fluid status [1]. *saturation in mixed venous blood* - While a Swan-Ganz catheter can measure **mixed venous oxygen saturation (SvO2)** from the distal port positioned in the pulmonary artery, this is not its primary or most unique diagnostic application. - SvO2 reflects the balance between oxygen delivery and consumption, providing insights into overall tissue perfusion and oxygen utilization. *LV filling pressure* - The Swan-Ganz catheter does not directly measure the **left ventricular (LV) filling pressure**. Instead, it estimates it indirectly via the **pulmonary capillary wedge pressure (PCWP)**, which is typically a good surrogate for LVEDP [1]. - Direct measurement of LV filling pressure would require a catheter to be placed within the left ventricle. *Pulmonary artery occlusion pressure* - **Pulmonary artery occlusion pressure (PAOP)** is the technical term for the pressure measured when the balloon at the tip of the Swan-Ganz catheter is inflated, occluding a branch of the pulmonary artery [1]. This pressure is synonymous with the **pulmonary capillary wedge pressure (PCWP)**. - Therefore, while the Swan-Ganz catheter measures PAOP, PCWP is a more common and direct description of the physiological parameter being assessed, which represents the pulmonary capillary pressure.

Q: During your preoperative assessment, a 28-year-old woman complains of dyspnea on exertion. Upon auscultation of her heart, you notice a mid-diastolic rumbling murmur. This murmur is most characteristic of which valvular lesion?

Mitral stenosis. ***Mitral stenosis*** - A **mid-diastolic rumbling murmur** is the classic auscultatory finding in **mitral stenosis**, caused by turbulent blood flow across a narrowed mitral valve during ventricular filling [1], [4]. - The associated **dyspnea on exertion** is due to increased left atrial pressure and pulmonary congestion resulting from the stenotic mitral valve [1]. *Aortic regurgitation* - Characterized by a **diastolic decrescendo murmur**, best heard at the left sternal border, not a rumbling mid-diastolic murmur. - Often presents with a **wide pulse pressure** and peripheral signs like head bobbing (De Musset's sign) or pulsating nail beds (Quincke's sign). *Aortic stenosis* - Typically produces a **systolic ejection murmur** that **radiates to the carotids**, best heard at the right upper sternal border. - Main symptoms include **dyspnea**, **angina**, and **syncope** on exertion [2]. *Mitral regurgitation* - Presents with a **holosystolic murmur** that **radiates to the axilla**, indicating continuous backflow of blood into the left atrium during systole. - Can lead to **dyspnea** and **fatigue** due to decreased forward cardiac output and pulmonary congestion [3].

Q: Infective endocarditis is not seen in –

ASD. Atrial septal defect (ASD) is generally considered a low-risk lesion for infective endocarditis because the pressure gradient across the defect is low, leading to less turbulent flow and less endothelial damage. While IE very rarely occurs, it is not common cause for IE. Generally the risk of infective endocarditis in an uncomplicated ASD is comparable to the general population. Tetralogy of Fallot (TOF) is a cyanotic congenital heart disease characterized by four defects (pulmonary stenosis, VSD, overriding aorta, right ventricular hypertrophy) that create turbulent flow, significantly increasing the risk of infective endocarditis. The abnormal anatomy and high flow jets in TOF predispose the heart valves and endocardium to damage, making them fertile ground for bacterial adherence and infection. Ventricular septal defect (VSD) involves an abnormal opening between the ventricles, causing a high-pressure, high-velocity jet of blood flow [1]. This turbulent flow leads to endothelial damage, particularly on the right ventricular side of the defect or the tricuspid valve, creating a nidus for bacterial colonization and infective endocarditis [1]. Mitral regurgitation (MR), especially due to degenerative valve disease or rheumatic heart disease, creates turbulent backward flow into the left atrium during systole. This chronic turbulent flow can cause endothelial injury on the mitral valve leaflets or the atrial wall, increasing the susceptibility to bacterial adherence and subsequent infective endocarditis.

Q: Which of these acyanotic congenital heart diseases is associated with volume overload?

Ventricular septal defect. ***Ventricular septal defect*** - A **ventricular septal defect (VSD)** causes a left-to-right shunt, leading to increased blood flow to the **pulmonary circulation** and the left side of the heart [1]. - This increased blood flow results in a **volume overload state** for the left atrium and left ventricle [1]. *Aortic stenosis* - **Aortic stenosis (AS)** is characterized by an obstruction to outflow from the left ventricle, leading to **pressure overload** on the left ventricle, not volume overload. - While prolonged AS can cause left ventricular hypertrophy, it doesn't primarily cause the type of volume overload seen with shunts. *None of the options* - This option is incorrect because **ventricular septal defect** is a specific acyanotic congenital heart disease that causes significant volume overload [1]. - **VSDs** are a classic example of conditions leading to increased pulmonary blood flow and chamber dilation due to shunting [1]. *Coarctation of aorta* - **Coarctation of the aorta** is a narrowing of the aorta, primarily causing **pressure overload** in the left ventricle due to increased resistance to systemic blood flow. - It does not cause a shunt or increased pulmonary blood flow, thus not leading to volume overload in the same way as VSD.

Q: Causes of wide fixed splitting of second heart sound include all except:

Ebstein anomaly. ***Ebstein anomaly*** - Ebstein anomaly is characterized by a **downward displacement of the tricuspid valve leaflets** into the right ventricle. - While it can cause wide splitting of S2 due to **right ventricular dysfunction** and prolonged RV ejection, the splitting is typically not fixed. *Right bundle branch block* - This condition causes a **delay in right ventricular depolarization**, leading to a prolonged right ventricular ejection time. - The delayed closure of the **pulmonary valve (P2)** relative to the aortic valve (A2) results in wide splitting of the second heart sound. *Total anomalous pulmonary venous return* - This condition involves all four **pulmonary veins connecting abnormally to the systemic venous circulation**. - It leads to an **obligate left-to-right shunt** at the atrial level, causing a chronic right ventricular volume overload and wide fixed splitting of S2 due to prolonged RV ejection time. *Atrial septal defect* - An **atrial septal defect (ASD)** results in a **left-to-right shunt**, increasing blood flow through the right ventricle and pulmonary artery [2]. - This increased flow prolongs **right ventricular ejection time**, leading to a physiologically fixed and wide splitting of the second heart sound [1][2].

Q: Neurocardiagenic syncope, the least useful investigation is -

Carotid duplex scan. ***Carotid duplex scan*** - This investigation evaluates for **carotid artery stenosis** and **atherosclerotic disease**, which is not relevant to neurocardiogenic syncope pathophysiology. - Neurocardiogenic syncope is a **reflex-mediated condition** involving inappropriate vasodilation and/or bradycardia, not mechanical vascular obstruction [2]. *Carotid sinus massage* - Relevant as a **provocative test** that can help identify reflex-mediated syncope by assessing **baroreflex sensitivity** [2]. - Can induce **bradycardia** or **hypotension** similar to neurocardiogenic syncope, making it diagnostically useful. *Echocardiography* - Essential for ruling out **structural heart disease** such as **valvular abnormalities**, **hypertrophic cardiomyopathy**, or **impaired ventricular function**. - Crucial in the **differential diagnosis** of syncope to distinguish cardiac causes from neurocardiogenic syncope [1]. *Orthostatic blood pressure recording* - While it may be normal in neurocardiogenic syncope, it remains a **fundamental, first-line investigation** in all syncope evaluations [3]. - Important to rule out **orthostatic hypotension** and should always be performed as part of basic syncope workup [1].

Q: Eisenmenger syndrome-True are All except ?

RV & LV walls come back to normal size. ***RV & LV walls come back to normal size*** - In **Eisenmenger syndrome**, there is **irreversible pulmonary hypertension** and **ventricular hypertrophy** due to chronic volume and pressure overload. - The right ventricle (RV) undergoes significant hypertrophy and dilatation to pump against increased pulmonary vascular resistance, and the left ventricle (LV) may also be affected due to the shift in the ventricular septum and changes in preload and afterload conditions. Therefore, these chambers **do not revert to normal size**. *Dilatation of central pulmonary artery* - This is a characteristic finding in **pulmonary hypertension**, which is a hallmark of Eisenmenger syndrome. - The central pulmonary arteries **dilate** due to the increased pressure, while more distal arteries constrict. *Peripheral pruning of pulmonary arteries* - In Eisenmenger syndrome, there is **progressive remodeling** of the pulmonary vasculature, leading to **narrowing and obliteration** of the smaller arteries. - This "pruning" effect means the distal pulmonary arteries become less visible on imaging. *Pulmonary veins are not distended* - **Eisenmenger syndrome** is primarily a condition of the **pulmonary arteries**, characterized by increased pressure and resistance. - The pulmonary veins which carry oxygenated blood to the left atrium, typically **do not become distended** as the primary issue is arterial and not a post-capillary or left-sided heart failure problem that would cause venous congestion.

Q: About carey coombs murmur which is false –

Can be associated with AR. *Carey Coombs murmur can be associated with AR* - The Carey Coombs murmur is caused by inflammation and thickening of the mitral valve in **acute rheumatic fever**, leading to increased flow velocity across the valve during diastole [3]. - It is **not directly associated with aortic regurgitation (AR)**; instead, AR can occur concurrently as part of the overall rheumatic heart disease aetiology, but the murmur itself is mitral in origin [1], [3]. *Mid-diastolic murmur* - The Carey Coombs murmur is indeed a **mid-diastolic murmur**, heard at the apex [2]. - This timing is due to the turbulent flow of blood across the inflamed **mitral valve** during the middle part of ventricular diastole [2]. *Seen in rheumatic fever* - The Carey Coombs murmur is a classic sign specifically associated with **acute rheumatic fever** [3]. - It results from inflammation of the mitral valve causing relative **mitral stenosis** and turbulence during diastole. *Low pitched murmur* - This murmur is typically described as **low-pitched and rumbling**, heard best with the bell of the stethoscope [2]. - Its low pitch is characteristic of turbulent flow caused by relative mitral stenosis [2].

Question 1

True about VSD is all except -

Accepted Answer

Pulmonary Oligemia in chest x-ray

Answer

Small hole closes spontaneously

Answer

Defect is usually in membranous part

Answer

Endocarditis is a common complication

Question 2

Swan Ganz catheter is used for what ?

Accepted Answer

Pulmonary capillary pressure

Answer

saturation in mixed venous blood

Answer

LV filling pressure

Answer

Pulmonary artery occlusion pressure

Question 3

During your preoperative assessment, a 28-year-old woman complains of dyspnea on exertion. Upon auscultation of her heart, you notice a mid-diastolic rumbling murmur. This murmur is most characteristic of which valvular lesion?

Accepted Answer

Mitral stenosis

Answer

Aortic regurgitation

Answer

Aortic stenosis

Answer

Mitral regurgitation

Question 4

Infective endocarditis is not seen in –

Accepted Answer

ASD

Answer

TOF

Answer

VSD

Answer

MR

Question 5

Which of these acyanotic congenital heart diseases is associated with volume overload?

Accepted Answer

Ventricular septal defect

Answer

Aortic stenosis

Answer

None of the options

Answer

Coarctation of aorta

Question 6

Which of the following statements is false about ostium secundum ASD?

Accepted Answer

Narrow splitting of the second heart sound is a feature of ostium secundum ASD.

Answer

A prominent shunt murmur is often heard in ostium secundum ASD.

Answer

Fixed splitting of the second heart sound is a feature of ostium secundum ASD.

Answer

Left axis deviation in ECG is commonly seen in ostium secundum ASD.

Answer

Right axis deviation in ECG is commonly seen in ostium secundum ASD.

Question 7

Causes of wide fixed splitting of second heart sound include all except:

Accepted Answer

Ebstein anomaly

Answer

Right bundle branch block

Answer

Total anomalous pulmonary venous return

Answer

Atrial septal defect

Question 8

Neurocardiagenic syncope, the least useful investigation is -

Accepted Answer

Carotid duplex scan

Answer

Carotid sinus massage

Answer

Echocardiography

Answer

Orthostatic blood pressure recording

Question 9

Eisenmenger syndrome-True are All except ?

Accepted Answer

RV & LV walls come back to normal size

Answer

Dilatation of central pulmonary artery

Answer

Peripheral pruning of pulmonary arteries

Answer

Pulmonary veins are not distended

Question 10

About carey coombs murmur which is false –

Accepted Answer

Can be associated with AR

Answer

Mid-diastolic murmur

Answer

Seen in rheumatic fever

Answer

Low pitched murmur

Cardiology — MCQs

Cardiology — MCQs

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