CVS Oral Exam 3 - Week 5-8

Question 1

Week 5

MURMURS

Answer 1

1. Definition: Murmurs are abnormal heart sounds caused by turbulent blood flow.
2. Causes: Narrowed or leaky valves, high blood flow states, or heart defects.
3. Inspiration Effect: Right-sided murmurs get louder.
4. Expiration Effect: Left-sided murmurs get louder.
5. Valsalva Effect: Straining makes most murmurs quieter, except HCM and MVP.
6. Handgrip Effect: Louder murmurs from leaky valves, quieter murmurs from narrow valves.

Question 2

Week 5

HEART SOUNDS

Answer 2

1. S3 Sound: Happens after S2; normal in young people but abnormal in heart failure.
2. S4 Sound: Happens before S1; always abnormal, linked to stiff ventricles.

Question 3

Week 5

VALVE LESIONS

Answer 3

1. Aortic Stenosis: Systolic murmur, harsh sound heard at the right chest, radiates to neck.
2. Aortic Regurgitation: Diastolic blowing sound, heard at left chest, radiates down.
3. Mitral Stenosis: Diastolic rumble with snap, heard at heart apex.
4. Mitral Regurgitation: Constant, high-pitched murmur at heart apex, radiates to armpit.

Question 4

Week 5

AORTIC STENOSIS (AS)

Answer 4

1. What is it: Narrow valve stops blood from leaving the heart.
2. Symptoms: Chest pain, fainting, shortness of breath.
3. Treatment: Surgery for severe cases.

Question 5

Week 5

MITRAL STENOSIS (MS)

Answer 5

1. What is it: Narrow valve blocks blood from the atrium to the ventricle.
2. Symptoms: Difficulty breathing, fatigue, and coughing blood.
3. Treatment: Balloon procedure or surgery.

Question 6

Week 5

AORTIC REGURGITATION (AR)

Answer 6

1. What is it: Valve doesn’t close properly, letting blood flow backward.
2. Symptoms: Pounding heartbeat, tiredness, and breathlessness.
3. Treatment: Medications or valve surgery.

Question 7

Week 5

MITRAL REGURGITATION (MR)

Answer 7

1. What is it: Blood flows backward from the ventricle to the atrium.
2. Symptoms: Fatigue, heart palpitations, and breathing problems.
3. Treatment: Valve repair or replacement.

Question 8

Topic 1: Murmurs
* TLO 5.1.1: Describe why murmurs occur

Answer 8

• Murmurs are abnormal heart sounds produced by turbulent blood flow across heart valves or within the heart chambers. This turbulence can arise from:
• Stenosis: Narrowing of a valve orifice restricts forward blood flow, increasing velocity and causing turbulence as blood squeezes through.
• Regurgitation (Insufficiency): Leaky valves allow backward flow of blood when the valve should be closed, creating turbulence as blood flows against the pressure gradient.
• High flow states: Increased cardiac output or blood volume can overwhelm normal valve function, leading to relative turbulence (e.g., in pregnancy or anemia).
• Structural abnormalities: Defects like ventricular septal defects (VSDs) or atrial septal defects (ASDs) create abnormal flow patterns and turbulence.

Question 9

• TLO 5.1.2: Describe how murmurs are affected by inspiration, expiration, Valsalva and isometric handgrip manoeuvre

Answer 9

• These maneuvers alter preload and afterload, affecting the intensity and characteristics of murmurs:
• Inspiration:
  o Increases venous return to the right side of the heart.
  o Increases the intensity of right-sided murmurs (tricuspid stenosis/regurgitation, pulmonic stenosis/regurgitation).
  o May slightly decrease the intensity of left-sided murmurs due to reduced left ventricular filling.
• Expiration:
  o Increases venous return to the left side of the heart.
  o Increases the intensity of left-sided murmurs (mitral stenosis/regurgitation, aortic stenosis/regurgitation).
  o May slightly decrease the intensity of right-sided murmurs.
• Valsalva Maneuver (Forced expiration against a closed glottis):
  o Phase I (Strain): Increases intrathoracic pressure, briefly increasing aortic pressure and decreasing venous return. Most murmurs decrease.
  o Phase II (Continued Strain): Decreased venous return leads to decreased preload and cardiac output. Most murmurs decrease further.
  o Phase III (Release): Intrathoracic pressure drops, but venous return is still reduced. Most murmurs remain soft.
  o Phase IV (Overshoot): Increased venous return and increased cardiac output. Most murmurs return to baseline or increase transiently.
  o Exceptions:
   Hypertrophic Cardiomyopathy (HCM) murmur: Increases in intensity during the strain phase (II) due to decreased left ventricular volume and increased outflow obstruction.
   Mitral valve prolapse (MVP) murmur: The click moves earlier and the murmur lengthens during the strain phase (II) due to decreased left ventricular volume causing earlier prolapse.
• Isometric Handgrip Maneuver (Sustained forceful squeezing of the hand):
  o Increases systemic vascular resistance (afterload).
  o Increases the intensity of regurgitant murmurs (mitral regurgitation, aortic regurgitation, tricuspid regurgitation) because the increased afterload makes it harder for blood to be ejected forward, increasing backward flow.
  o Decreases the intensity of stenotic murmurs (aortic stenosis, mitral stenosis) because the increased afterload reduces forward flow across the narrowed valve.
  o HCM murmur: Decreases in intensity due to increased afterload reducing the outflow gradient.
  o MVP murmur: The click moves later and the murmur shortens due to increased left ventricular volume delaying prolapse.

Question 10

• TLO 5.1.3: Describe why and when S3 and S4 heart sounds occur

Answer 10

• S3 (Ventricular Gallop):
  o Timing: Occurs early in diastole, shortly after S2, during the rapid ventricular filling phase.
  o Mechanism: Caused by the sudden deceleration of blood as it rushes from the atria into a volume-overloaded or overly compliant ventricle. Think of it like a “sloshing” sound.
  o Physiological: Can be normal in young adults and well-trained athletes.
  o Pathological: Often associated with heart failure (increased ventricular volume), mitral or tricuspid regurgitation (increased preload), and high output states.
• S4 (Atrial Gallop):
  o Timing: Occurs late in diastole, just before S1, coinciding with atrial contraction.
  o Mechanism: Caused by the forceful atrial contraction ejecting blood into a stiff, non-compliant ventricle. The ventricle resists filling, creating vibration.
  o Always pathological: Associated with conditions that increase ventricular stiffness, such as left ventricular hypertrophy (due to hypertension or aortic stenosis), acute myocardial infarction, and restrictive cardiomyopathy.

Question 11

• TLO 5.1.4: Familiarize yourself with murmurs associated with the pathologies involving the left and right-side valve lesions.

Answer 11

Left-Sided Lesions
1. Aortic Stenosis (AS)
- Timing: Systolic
- Maximal Intensity: Right upper sternal border
- Radiation: Carotid arteries
- Characteristics: Harsh, crescendo-decrescendo

2. Aortic Regurgitation (AR)
   
   • Timing: Diastolic
   • Maximal Intensity: Left upper sternal border
   • Radiation: Down the left sternal border
   • Characteristics: High-pitched, blowing, decrescendo
3. Mitral Stenosis (MS)
   
   • Timing: Diastolic
   • Maximal Intensity: Apex
   • Radiation: None
   • Characteristics: Low-pitched, rumbling, often with an opening snap
4. Mitral Regurgitation (MR)
   
   • Timing: Systolic
   • Maximal Intensity: Apex
   • Radiation: Axilla
   • Characteristics: High-pitched, blowing, holosystolic (pansystolic)
5. Mitral Valve Prolapse (MVP)
   
   • Timing: Systolic
   • Maximal Intensity: Apex
   • Radiation: Variable
   • Characteristics: Mid-systolic click followed by a late systolic murmur

Right-Sided Lesions (Generally less intense and affected by respiration)
6. Pulmonic Stenosis (PS)
- Timing: Systolic
- Maximal Intensity: Left upper sternal border
- Radiation: Left shoulder and neck
- Characteristics: Harsh, crescendo-decrescendo

7. Pulmonic Regurgitation (PR)
   
   • Timing: Diastolic
   • Maximal Intensity: Left upper sternal border
   • Radiation: Down the left sternal border
   • Characteristics: High-pitched, blowing, decrescendo (Graham Steell murmur in pulmonary hypertension)
8. Tricuspid Stenosis (TS)
   
   • Timing: Diastolic
   • Maximal Intensity: Left lower sternal border
   • Radiation: None
   • Characteristics: Low-pitched, rumbling, increases with inspiration
9. Tricuspid Regurgitation (TR)
   
   • Timing: Systolic
   • Maximal Intensity: Left lower sternal border
   • Radiation: Right sternal border, may have pulsatile liver
   • Characteristics: Blowing, holosystolic, increases with inspiration

Question 12

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.1: Define AS and explain epidemiology.

Answer 12

• TLO 5.2.1: Define AS and explain epidemiology.
• Definition: Aortic stenosis (AS) is the narrowing of the aortic valve orifice, obstructing blood flow from the left ventricle into the aorta during systole.
• Epidemiology:
  o The most common valvular heart disease in the elderly.
  o Prevalence increases with age.
  o Significant AS affects approximately 2-7% of individuals over 65 years old.
  o The incidence is rising due to the aging population.

Question 13

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.2: Discuss the causes and explain the pathophysiology of AS.

Answer 13

• TLO 5.2.2: Discuss the causes and explain the pathophysiology of AS.
• Causes:
  o Degenerative Calcification (Senile): Most common cause in older adults (>70 years). Progressive calcification and fibrosis of the valve leaflets restrict their movement.
  o Congenital Bicuspid Valve: Present in 1-2% of the population. These valves often become stenotic earlier in life (50-70 years) due to abnormal wear and tear and calcification.
  o Rheumatic Heart Disease: Less common in developed countries. Inflammation from rheumatic fever can cause leaflet fusion and thickening, leading to stenosis. Often associated with mitral valve disease.
• Pathophysiology:
  1. Obstruction to Outflow: Narrowed aortic valve increases resistance to left ventricular ejection.
  2. Left Ventricular Hypertrophy (LVH): To overcome the increased resistance, the left ventricle hypertrophies concentrically (increased wall thickness without chamber dilation) to maintain stroke volume and cardiac output.
  3. Increased Left Ventricular Pressure: The pressure gradient across the aortic valve increases.
  4. Diastolic Dysfunction: The thickened, less compliant left ventricle can lead to impaired relaxation and filling during diastole, increasing left atrial pressure.
  5. Symptoms Develop: Eventually, LVH can no longer compensate, leading to decreased cardiac output and symptoms, especially during exertion.
  6. Late Stages: Can progress to left ventricular dilation and systolic dysfunction, heart failure, and increased risk of sudden cardiac death.

Question 14

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.3: Discuss the clinical features of AS.

Answer 14

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.3: Discuss the clinical features of AS.
* The classic triad of symptoms (often occurring late in the disease course) is:
* Angina: Chest pain due to increased myocardial oxygen demand from LVH and reduced coronary perfusion pressure.
* Syncope: Fainting or near-fainting, often exertional, due to transient decrease in cerebral blood flow from the inability to increase cardiac output.
* Dyspnea: Shortness of breath due to increased left atrial pressure and pulmonary congestion from diastolic dysfunction and eventually systolic dysfunction.
* Other clinical features may include:
* Fatigue and exercise intolerance: Due to limited cardiac output reserve.
* Palpitations: From arrhythmias.
* Sudden cardiac death: Can occur, especially with severe AS.
* Physical Exam Findings:
o Harsh, systolic ejection murmur: Heard best at the right upper sternal border, radiating to the carotid arteries.
o Weak and delayed carotid upstroke (pulsus parvus et tardus): Reflects slow ejection of blood.
o Narrow pulse pressure: Due to reduced stroke volume.
o S4 heart sound: Due to forceful atrial contraction against a stiff ventricle.
o Thrill: Palpable vibration over the aortic area.

Question 15

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.4: Discuss the diagnosis of AS.

Answer 15

Topic 2: Aortic Stenosis (AS)
* TLO 5.2.4: Discuss the diagnosis of AS.
* Cardiac Auscultation: The characteristic systolic murmur is the initial clue.
* Echocardiogram: The primary diagnostic tool. It can:
o Assess aortic valve morphology and mobility.
o Measure the aortic valve area.
o Determine the pressure gradient across the aortic valve (mean and peak).
o Evaluate left ventricular size, wall thickness, and function.
o Identify other valvular abnormalities.
* Electrocardiogram (ECG): May show signs of left ventricular hypertrophy (increased QRS voltage, ST-T wave changes), but can be normal even in severe AS.
* Chest X-ray: May show post-stenotic aortic dilation and calcification of the aortic valve in later stages.
* Cardiac Catheterization: Considered when echocardiography is inconclusive or to assess coronary artery disease in patients undergoing valve intervention. It directly measures aortic valve gradient and can assess coronary anatomy.
* CT Angiography: Can be used to assess the aortic valve calcium score, which can help in risk stratification, particularly in asymptomatic patients.
* TLO 5.2.5: Outline the management of AS.
* Management depends on the severity of AS and the presence of symptoms:
* Asymptomatic Severe AS:
o Close observation: Regular clinical and echocardiographic follow-up (typically every 6-12 months).
o Avoidance of strenuous activity: May precipitate syncope or sudden death.
o Treatment of associated conditions: Hypertension, hyperlipidemia.
* Symptomatic Severe AS:
o Aortic Valve Replacement (AVR): The definitive treatment.
 Surgical AVR (SAVR): Traditional open-heart surgery with replacement of the diseased valve with either a mechanical or bioprosthetic valve.
 Mechanical valves: More durable but require lifelong anticoagulation with warfarin.
 Bioprosthetic valves: Less durable (typically 10-20 years) but generally do not require long-term anticoagulation (may need short-term). Choice depends on age, lifestyle, and comorbidities.
 Transcatheter Aortic Valve Implantation (TAVI): A less invasive procedure where a prosthetic valve is delivered via a catheter, typically through the femoral artery. Preferred for elderly patients, those with significant comorbidities, or those deemed high-risk for SAVR.
* Medical Management: No effective medical therapy to treat AS itself. Medications are used to manage associated symptoms like heart failure (diuretics, ACE inhibitors/ARBs, beta-blockers) and atrial fibrillation (rate/rhythm control, anticoagulation).
* Balloon Aortic Valvuloplasty: A temporary palliative measure for patients who are not candidates for AVR or as a bridge to surgery. High rates of restenosis limit its long-term utility.

Question 16

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.1: Define and explain epidemiology of MS.

Answer 16

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.1: Define and explain epidemiology of MS.
* Definition: Mitral stenosis (MS) is the narrowing of the mitral valve orifice, obstructing blood flow from the left atrium to the left ventricle during diastole.
* Epidemiology:
o The most common cause is rheumatic heart disease, so its prevalence is higher in regions with a history of untreated streptococcal pharyngitis (rheumatic fever).
o Incidence has decreased significantly in developed countries due to widespread antibiotic use.
o More common in women than men.
o Symptoms typically appear years to decades after the initial episode of rheumatic fever.

Question 17

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.2: Discuss the causes and explain the pathophysiology of MS.

Answer 17

• TLO 5.3.2: Discuss the causes and explain the pathophysiology of MS.
• Cause:
  o Rheumatic Heart Disease: The overwhelming majority of cases are due to the sequelae of acute rheumatic fever. Repeated episodes of inflammation lead to thickening, fibrosis, and calcification of the mitral valve leaflets, chordae tendineae, and commissures (the points where the leaflets meet). This results in fusion of the leaflets and a narrowed, fish-mouth-like orifice.
  o Rare causes include congenital mitral stenosis, carcinoid heart disease, and left atrial myxoma.
• Pathophysiology:
  1. Obstruction to Inflow: Narrowed mitral valve impedes blood flow from the left atrium to the left ventricle during diastole.
  2. Increased Left Atrial Pressure: To maintain adequate left ventricular filling, the left atrium must generate higher pressures to push blood through the stenotic valve.
  3. Left Atrial Enlargement: Chronic pressure overload leads to dilation of the left atrium.
  4. Pulmonary Hypertension: Elevated left atrial pressure is transmitted back to the pulmonary veins and capillaries, causing pulmonary venous congestion and eventually pulmonary arterial hypertension (both passive and reactive).
  5. Right Ventricular Hypertrophy: In response to pulmonary hypertension, the right ventricle hypertrophies to pump blood against the increased resistance in the pulmonary circulation.
  6. Decreased Cardiac Output: As the stenosis worsens and left ventricular filling is compromised, cardiac output decreases, especially during exercise.
  7. Increased Risk of Atrial Fibrillation: Left atrial enlargement and stretching increase the risk of atrial fibrillation, which can further impair left ventricular filling and increase the risk of thromboembolism.

Question 18

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.3: Discuss the clinical features of MS.

Answer 18

• TLO 5.3.3: Discuss the clinical features of MS.
• Symptoms are often related to pulmonary congestion and reduced cardiac output:
• Dyspnea: Shortness of breath, initially exertional and progressing to orthopnea (difficulty breathing when lying flat) and paroxysmal nocturnal dyspnea (sudden shortness of breath at night).
• Fatigue and exercise intolerance: Due to limited cardiac output reserve.
• Palpitations: Often due to atrial fibrillation.
• Hemoptysis: Coughing up blood, usually due to rupture of small pulmonary veins from high pulmonary pressure.
• Chest pain: Less common than in aortic stenosis, may occur due to pulmonary hypertension or associated coronary artery disease.
• Systemic embolization: Thrombi can form in the enlarged left atrium, especially in the presence of atrial fibrillation, and embolize to various organs (e.g., brain, causing stroke).
• Physical Exam Findings:
  o Loud S1: Due to forceful closure of the mitral valve leaflets, which are held open longer by the pressure gradient.
  o Opening snap: A high-pitched sound occurring after S2, due to the sudden opening of the stiff mitral valve leaflets. The interval between S2 and the opening snap correlates with the severity of stenosis (shorter interval = more severe stenosis).
  o Low-pitched, rumbling diastolic murmur: Heard best at the apex in the left lateral decubitus position, often with bell of the stethoscope. May be preceded by an opening snap.
  o Accentuated P2: If pulmonary hypertension is present.
  o Signs of right heart failure: In advanced stages, such as jugular venous distension (JVD), peripheral edema, hepatomegaly.
  o Mitral facies: Pinkish or purplish patches on the cheeks due to chronic low cardiac output and vasoconstriction.

Question 19

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.4: Discuss the diagnosis of MS.

Answer 19

Topic 3: Mitral Stenosis (MS)
* TLO 5.3.4: Discuss the diagnosis of MS.
* Cardiac Auscultation: The characteristic diastolic murmur and opening snap are highly suggestive.
* Echocardiogram: The primary diagnostic tool. It can:
o Assess mitral valve morphology, thickness, and mobility.
o Measure the mitral valve area.
o Determine the pressure gradient across the mitral valve.
o Evaluate left atrial size and the presence of left atrial thrombus.
o Assess for pulmonary hypertension.
o Evaluate other valvular abnormalities.
* Electrocardiogram (ECG): May show left atrial

Question 20

Topic 3: Mitral Stenosis (MS) (Continued)
* TLO 5.3.4: Discuss the diagnosis of MS.

Answer 20

• TLO 5.3.4: Discuss the diagnosis of MS.
• Electrocardiogram (ECG): May show left atrial enlargement (P mitrale - broad, notched P wave in leads II) and atrial fibrillation. Right ventricular hypertrophy may be seen in advanced stages.
• Chest X-ray: May reveal left atrial enlargement (straightening of the left heart border, double density shadow), pulmonary venous congestion (Kerley B lines), and pulmonary artery enlargement.
• Cardiac Catheterization: Rarely needed for diagnosis but can be used to assess the severity of stenosis (pressure gradient) and evaluate for concomitant coronary artery disease, especially before surgical intervention.

Question 21

Topic 3: Mitral Stenosis (MS) (Continued)
* TLO 5.3.5: Outline the management of MS.

Answer 21

Topic 3: Mitral Stenosis (MS) (Continued)
* TLO 5.3.5: Outline the management of MS.
* Management focuses on symptom relief, preventing complications, and addressing the underlying stenosis:
* Medical Management:
o Diuretics: To manage pulmonary congestion.
o Beta-blockers or Calcium Channel Blockers: To control heart rate, especially in atrial fibrillation, allowing for more diastolic filling time.
o Anticoagulation (Warfarin or Direct Oral Anticoagulants - DOACs): Essential in patients with atrial fibrillation or a history of thromboembolism due to the high risk of stroke.
o Antibiotic prophylaxis: Against infective endocarditis in high-risk situations (e.g., dental procedures).
* Percutaneous Mitral Balloon Valvuloplasty (PMBV): The preferred treatment for symptomatic severe MS with favorable valve morphology (non-calcified, pliable leaflets without significant subvalvular fusion). A balloon catheter is inserted into the femoral vein, advanced to the mitral valve, and inflated to widen the stenotic orifice.
* Surgical Intervention: Considered for patients with:
o Severe MS unsuitable for PMBV (e.g., heavily calcified valve, significant subvalvular disease).
o Failed PMBV with recurrent stenosis.
o Concomitant cardiac conditions requiring surgery (e.g., other valve lesions, coronary artery disease).
o Mitral Valve Repair: If possible, preferred over replacement, especially in younger patients. Involves techniques like commissurotomy (surgical separation of fused leaflets), chordal shortening or lengthening, and leaflet repair.
o Mitral Valve Replacement: If repair is not feasible, the diseased valve is replaced with either a mechanical or bioprosthetic valve (choice depends on age, lifestyle, and risk of thromboembolism).

Question 22

Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.1: Define and explain epidemiology of AR.

Answer 22

• TLO 5.4.1: Define and explain epidemiology of AR.
• Definition: Aortic regurgitation (AR), also known as aortic insufficiency, is the backward flow of blood from the aorta into the left ventricle during diastole due to incomplete closure of the aortic valve.
• Epidemiology:
  o Prevalence increases with age.
  o Causes vary by age group and geographic location.
  o In developed countries, common causes include aortic root dilation and bicuspid aortic valve.
  o Rheumatic heart disease is a less common cause but still significant in some regions.

Question 23

Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.2: Discuss the causes and explain the pathophysiology of AR.

Answer 23

• TLO 5.4.2: Discuss the causes and explain the pathophysiology of AR.
• Causes: Can be due to abnormalities of the aortic valve leaflets or the aortic root:
  o Valve Leaflet Abnormalities:
   Congenital bicuspid valve.
   Rheumatic heart disease (often with aortic stenosis and mitral valve disease).
   Infective endocarditis (can cause valve perforation or destruction).
   Trauma.
   Fenestrations (holes) in the leaflets.
  o Aortic Root Abnormalities (causing annular dilation and preventing proper leaflet coaptation):
   Hypertension (chronic).
   Marfan syndrome and other connective tissue disorders (e.g., Ehlers-Danlos syndrome).
   Aortic dissection.
   Ankylosing spondylitis and other inflammatory conditions.
   Syphilis (tertiary).
   Aortitis (inflammation of the aorta).
• Pathophysiology:
  1. Backward Flow: During diastole, blood leaks back from the high-pressure aorta into the lower-pressure left ventricle.
  2. Increased Left Ventricular Volume (Volume Overload): The left ventricle receives blood from both the left atrium (normal filling) and the aorta (regurgitant flow), leading to an increase in end-diastolic volume.
  3. Left Ventricular Eccentric Hypertrophy: In response to the chronic volume overload, the left ventricle dilates and undergoes eccentric hypertrophy (increased chamber size with proportionally less increase in wall thickness) to accommodate the increased blood volume and maintain stroke volume.
  4. Increased Stroke Volume: The total stroke volume ejected by the left ventricle is increased to compensate for the regurgitant volume and maintain forward cardiac output.
  5. Decreased Diastolic Aortic Pressure: The leakage of blood back into the left ventricle causes a fall in diastolic aortic pressure.
  6. Wide Pulse Pressure: The combination of increased systolic pressure (due to increased stroke volume) and decreased diastolic pressure results in a widened pulse pressure.
  7. Left Atrial Enlargement and Pulmonary Congestion (Late): Over time, chronic volume overload can lead to left ventricular dysfunction, increased left ventricular end-diastolic pressure, left atrial enlargement, and eventually pulmonary congestion and heart failure.

Question 24

Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.3: Discuss the clinical features of AR.

Answer 24

• TLO 5.4.3: Discuss the clinical features of AR.
• Symptoms may remain absent for a long time due to compensatory LV dilation. When they appear, they often indicate significant regurgitation and LV dysfunction:
• Chronic AR:
  o Often asymptomatic for years.
  o Palpitations: Awareness of a forceful heartbeat, especially when lying down.
  o Exertional dyspnea and fatigue: Due to decreased cardiac reserve.
  o Angina: Less common than in AS, may occur due to increased myocardial oxygen demand and reduced diastolic coronary perfusion pressure.
  o Orthopnea and paroxysmal nocturnal dyspnea: In later stages with LV dysfunction and pulmonary congestion.
• Acute AR (e.g., from endocarditis or aortic dissection):
  o Sudden onset of severe heart failure symptoms: Severe dyspnea, pulmonary edema, hypotension, cardiogenic shock.
  o Less time for LV dilation: Leads to a rapid increase in left ventricular pressure.
• Physical Exam Findings:
  o Wide pulse pressure: A hallmark of chronic AR.
  o Bounding peripheral pulses (Corrigan’s pulse or water-hammer pulse): Rapid rise and fall due to the large stroke volume and rapid diastolic runoff.
  o Quincke’s sign: Pulsation of the nail beds with light pressure.
  o De Musset’s sign: Head bobbing with each heartbeat.
  o Müller’s sign: Pulsation of the uvula.
  o Austin Flint murmur: A low-pitched mid-diastolic rumble heard at the apex, caused by the regurgitant jet impinging on the anterior mitral valve leaflet, functionally narrowing the mitral orifice. This murmur does not indicate mitral stenosis.
  o High-pitched, blowing diastolic murmur: Heard best at the left upper sternal border (for valvular AR) or right upper sternal border (for aortic root dilation), often radiating down the left sternal border.
  o Systolic ejection murmur: May be present due to increased stroke volume across the aortic valve.
  o S3 heart sound: May be heard with significant LV dilation and dysfunction.

Question 25

Topic 4: Aortic Regurgitation (AR) * TLO 5.4.4: Discuss the diagnosis of AR.

Answer 25

* TLO 5.4.4: Discuss the diagnosis of AR. * Cardiac Auscultation: The characteristic high-pitched diastolic murmur is key. * Echocardiogram: The primary diagnostic tool. It can: o Assess aortic valve morphology and coaptation. o Quantify the severity of regurgitation (color Doppler, vena contracta width, pressure half-time). o Evaluate left ventricular size, function, and wall thickness. o Assess the aortic root size and identify any dilation or dissection. o Look for associated valvular abnormalities. * Electrocardiogram (ECG): May show signs of left ventricular hypertrophy (increased QRS voltage) but can be normal. * Chest X-ray: May show cardiomegaly (left ventricular enlargement) and aortic dilation. * Cardiac Catheterization: Not routinely used for diagnosis but can be helpful in assessing the severity of AR, evaluating coronary artery disease before surgery, and measuring aortic root dimensions. * MRI or CT Angiography: Can be used to assess aortic root anatomy and dilation in more detail, especially in suspected aortic root disease.

Question 26

Topic 4: Aortic Regurgitation (AR) * TLO 5.4.5: Outline the management of AR.

Answer 26

* TLO 5.4.5: Outline the management of AR. * Management depends on the severity of AR, the presence of symptoms, and the underlying cause: * Medical Management: o Vasodilators (ACE inhibitors, ARBs, calcium channel blockers): Reduce afterload, which can decrease the regurgitant volume and improve forward flow. Particularly important in chronic asymptomatic severe AR and in patients with hypertension. o Beta-blockers: May be useful in Marfan syndrome to reduce aortic root dilation and slow progression. o Diuretics: To manage heart failure symptoms. o Digoxin: For symptom control in heart failure with reduced ejection fraction. o Antibiotic prophylaxis: Against infective endocarditis in high-risk situations. * Surgical Intervention (Aortic Valve Replacement - AVR): The definitive treatment for symptomatic severe AR and for asymptomatic severe AR with evidence of progressive LV dilation or dysfunction. o Mechanical valves: More durable, require lifelong anticoagulation. o Bioprosthetic valves: Less durable, generally do not require long-term anticoagulation (may need short-term). o Aortic Root Repair or Replacement: May be necessary in patients with significant aortic root dilation (e.g., Marfan syndrome, aortic aneurysm). This can be done concurrently with AVR. * Management of Acute AR: Requires urgent intervention, often surgical AVR, due to the rapid development of heart failure. Preload reduction (diuretics, nitrates) and afterload reduction (nitroprusside) may be used as temporizing measures.

Question 27

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.1: Define and explain epidemiology of MR.

Answer 27

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.1: Define and explain epidemiology of MR. * Definition: Mitral regurgitation (MR), also known as mitral insufficiency, is the backward flow of blood from the left ventricle into the left atrium during systole due to incomplete closure of the mitral valve. * Epidemiology: o Common valvular heart disease. o Prevalence increases with age. o Causes vary depending on the population and age group. o In developed countries, common causes include mitral valve prolapse, ischemic heart disease, and degenerative mitral valve disease. o Rheumatic heart disease is a less common cause but still prevalent globally.

Question 28

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.2: Discuss the causes and explain the pathophysiology of MR.

Answer 28

* TLO 5.5.2: Discuss the causes and explain the pathophysiology of MR. * MR can be classified as primary (due to intrinsic abnormalities of the mitral valve apparatus) or secondary (functional, due to left ventricular dilation or dysfunction): * Primary MR (Organic): o Mitral Valve Prolapse (MVP): The most common cause in developed countries. One or both mitral valve leaflets prolapse (bulge) into the left atrium during systole due to myxomatous degeneration of the valve tissue. o Rheumatic Heart Disease: Causes thickening, fibrosis, and shortening of the leaflets and chordae tendineae, leading to incomplete coaptation. o Infective Endocarditis: Can damage the valve leaflets or chordae. o Ruptured Chordae Tendineae: Can occur spontaneously or due to trauma or ischemia, leading to a flail leaflet. o Papillary Muscle Dysfunction or Rupture: Usually due to myocardial infarction, affecting valve support. o Congenital Abnormalities: Cleft mitral valve. o Calcification of the Mitral Annulus: Can prevent proper leaflet closure. * Secondary MR (Functional): o Left Ventricular Dilation: In conditions like heart failure due to ischemic cardiomyopathy or dilated cardiomyopathy, the mitral annulus (the ring supporting the valve) dilates, preventing proper leaflet coaptation even if the leaflets themselves are normal. o Left Ventricular Remodeling: Changes in LV geometry can tether the papillary muscles, pulling on the chordae and restricting leaflet closure. * Pathophysiology: 1. Backward Flow: During systole, blood leaks back from the high-pressure left ventricle into the lower-pressure left atrium. 2. Increased Left Atrial Volume and Pressure: The left atrium receives blood from both the pulmonary veins (normal filling) and the left ventricle (regurgitant flow), leading to increased volume and pressure. 3. Left Atrial Enlargement: Chronic pressure and volume overload cause dilation of the left atrium. 4. Increased Pulmonary Venous Pressure: Elevated left atrial pressure is transmitted back to the pulmonary veins and capillaries, causing pulmonary congestion. 5. Left Ventricular Volume Overload: The left ventricle has to pump a larger total volume (forward flow plus regurgitant flow) to maintain adequate forward cardiac output, leading to increased end-diastolic volume. 6. Left Ventricular Eccentric Hypertrophy: Chronic volume overload leads to left ventricular dilation and eccentric hypertrophy. 7. Decreased Forward Cardiac Output (Late): Over time, the left ventricle may become unable to compensate, leading to decreased forward cardiac output and heart failure symptoms. 8. Increased Risk of Atrial Fibrillation: Left atrial enlargement increases the risk of atrial fibrillation.

Question 29

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.3: Discuss the clinical features of MR.

Answer 29

* TLO 5.5.3: Discuss the clinical features of MR. * Symptoms depend on the severity and chronicity of the regurgitation: * Acute MR (e.g., ruptured chordae, papillary muscle rupture): o Sudden onset of severe heart failure symptoms: Severe dyspnea, pulmonary edema, hypotension, cardiogenic shock. * Chronic MR: o May be asymptomatic for years. o Exertional dyspnea and fatigue: Due to decreased cardiac reserve and pulmonary congestion. o Palpitations: Especially if atrial fibrillation develops. o Orthopnea and paroxysmal nocturnal dyspnea: In later stages with LV dysfunction and pulmonary congestion. o Weakness and lightheadedness: Due to reduced forward cardiac output. * Physical Exam Findings: o Holosystolic (pansystolic) murmur: High-pitched, blowing, heard best at the apex, radiating to the axilla. May be softer in acute MR. o Loud S3: Often present in significant MR due to rapid ventricular filling from the increased atrial volume. o Soft S1: May be present if leaflet closure is impaired. o Widely split S2: Due to early aortic closure from reduced LV ejection time. o Signs of left atrial enlargement: Prominent V waves in the jugular venous pulse (if in sinus rhythm). o Signs of pulmonary hypertension and right heart failure: In advanced stages.

Question 30

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.4: Discuss the diagnosis of MR.

Answer 30

* TLO 5.5.4: Discuss the diagnosis of MR. * Cardiac Auscultation: The characteristic holosystolic murmur is the primary clue. * Echocardiogram: The cornerstone of diagnosis. It can: o Identify the mechanism of MR (e.g., prolapse, flail leaflet, annular dilation). o Assess the severity of regurgitation (color Doppler, vena contracta width, regurgitant volume and fraction, pulmonary venous flow reversal). o Evaluate left atrial and left ventricular size and function. o Assess for pulmonary hypertension. o Identify associated valvular abnormalities. * Electrocardiogram (ECG): May show left atrial enlargement (P mitrale) and atrial fibrillation. Left ventricular hypertrophy may be seen in chronic severe MR. * Chest X-ray: May reveal left atrial and left ventricular enlargement, and pulmonary venous congestion. * Cardiac Catheterization: Not routinely used for diagnosis but can be helpful in assessing the severity of MR, evaluating pulmonary artery pressures, and assessing coronary artery disease before surgery.

Question 31

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.5: Outline the management of MR.

Answer 31

Topic 5: Mitral Regurgitation (MR) * TLO 5.5.5: Outline the management of MR. * Management depends on the severity and chronicity of MR, the presence of symptoms, and the underlying cause: * Medical Management: o ACE inhibitors or ARBs: Reduce afterload, which can decrease the regurgitant volume and improve forward flow, especially in chronic MR. o Diuretics: To manage pulmonary congestion. o Beta-blockers: May be used for rate control if atrial fibrillation is present. o Anticoagulation (Warfarin or DOACs): Indicated for atrial fibrillation or a history of thromboembolism. o Treatment of underlying conditions: Management of heart failure, hypertension, or ischemic heart disease. o Antibiotic prophylaxis: Against infective endocarditis in high-risk situations. * Surgical or Percutaneous Intervention: Considered for symptomatic severe primary MR and for asymptomatic severe primary MR with evidence of progressive LV dilation or dysfunction. For secondary MR, management focuses on the underlying heart failure, and intervention on the mitral valve may be considered in select symptomatic patients despite optimal medical therapy. o Mitral Valve Repair: Generally preferred over replacement when feasible, especially in primary MR. Repair techniques include leaflet resection, annuloplasty (ring placement to reduce annular size), and chordal repair or replacement. Repair offers better long-term outcomes and avoids the need for lifelong anticoagulation in most cases. o Mitral Valve Replacement: Used when repair is not possible. Can be with a mechanical or bioprosthetic valve (choice depends on age, comorbidities, and risk of thromboembolism). o Percutaneous Mitral Valve Repair (e.g., MitraClip): A

Question 32

🔹 Topic 1: Introduction to Myocardial Ischaemia Q1: What is myocardial ischaemia?

Answer 32

A1: A condition where the heart muscle receives insufficient oxygen due to reduced coronary blood flow.

Question 33

Q2: What are the determinants of myocardial oxygen demand?

Answer 33

A2: Heart rate, contractility, wall tension, and myocardial metabolic activity.

Question 34

Q4: What characterizes Prinzmetal’s angina?

Answer 34

A4: Occurs at rest due to coronary artery spasm with transient ST elevation.

Question 35

Q3: What are the main causes of myocardial ischaemia?

Answer 35

A3: Atherosclerosis, coronary artery spasm, thrombosis, embolism, anemia, and hypotension.

Question 36

Q6: What ECG changes are seen in angina?

Answer 36

A6: ST depression, T wave inversion (stable/unstable); transient ST elevation (Prinzmetal’s).

Question 37

Q5: How is stable angina different from unstable angina?

Answer 37

A5: Stable angina is predictable and exertional; unstable angina is unpredictable and occurs at rest or with minimal exertion.

Question 38

Q7: How is angina managed?

Answer 38

A7: Lifestyle changes, nitrates, beta-blockers, calcium channel blockers, antiplatelets, and possible PCI/CABG.

Question 39

Q9: Describe the pathogenesis of atherosclerosis.

Answer 39

A9: Endothelial injury → lipid accumulation → inflammation → foam cells → fibrous plaque.

Question 40

🔹 Topic 2: Atherosclerosis Q8: List modifiable and non-modifiable risk factors for atherosclerosis.

Answer 40

A8: Modifiable: smoking, hypertension, hyperlipidemia, diabetes. Non-modifiable: age, sex, genetics.

Question 41

Q12: What therapies help prevent atherosclerosis?

Answer 41

A12: Lifestyle modification and statins, antihypertensives, antidiabetics.

Question 42

Q10: What are the microscopic features of an atherosclerotic plaque?

Answer 42

A10: Lipid core, fibrous cap, inflammato cells, neovascularization.

Question 43

Q11: How does plaque rupture differ from erosion in causing MI?

Answer 43

A11: Rupture exposes core, causing thrombosis; erosion exposes endothelium, also triggering clotting.

Question 44

🔹 Topic 3: Lipids and Heart Disease Q13: What are major lipid types?

Answer 44

A13: Triacylglycerols, phospholipids, cholesterol (esters).

Question 45

Q14: What are the main lipoproteins?

Answer 45

A14: Chylomicrons, VLDL, LDL, HDL.

Question 46

Q17: How is LDL linked to atherosclerosis?

Answer 46

A17: Oxidized LDL promotes endothelial injury, inflammation, and plaque formation.

Question 47

Q16: What are apolipoproteins?

Answer 47

A16: Protein components of lipoproteins that help in lipid transport and receptor binding.

Question 48

Q15: What is the function of LDL?

Answer 48

A15: Transports cholesterol to tissues; contributes to atherosclerosis.

Question 49

Q18: Name three types of lipid-lowering agents and their mechanisms.

Answer 49

A18: Statins (HMG-CoA reductase inhibitors), ezetimibe (cholesterol absorption inhibitor), PCSK9 inhibitors (increase LDL receptor recycling).

Question 50

🔹 Topic 4: Ischaemic Heart Disease (IHD) Q21: What is the global significance of MI?

Answer 50

A21: It is one of the leading causes of death worldwide.

Question 51

Q20: How do high triglycerides affect heart disease?

Answer 51

A20: Associated with increased cardiovascular risk; treated with fibrates, niacin, omega-3s.

Question 52

Q19: What role does HDL play in heart protection?

Answer 52

A19: Removes cholesterol from tissues and ha anti-inflammatory effects.

Question 53

Q22: List the risk factors for MI.

Answer 53

A22: Smoking, diabetes, hypertension, hyperlipidemia, obesity.

Question 54

Q23:* What is the pathophysiology of MI?

Answer 54

A23: Plaque rupture → thrombosis → occlusion → myocardial necrosis.

Question 55

Q27: What cardiac biomarkers are used in MI?

Answer 55

A27: Troponin I/T (most specific), CK-MB (for reinfarction).

Question 56

Q24: What are typical symptoms of MI?

Answer 56

A24: Chest pain, dyspnea, diaphoresis, nausea, fatigue.

Question 57

Q28: What imaging modalities are used in MI?

Answer 57

A28: Echocardiogram, coronary angiography, cardiac MRI, CT.

Question 58

Q25: What are the ECG features of NSTEMI and STEMI?

Answer 58

A25: NSTEMI: ST depression/T inversion. STEMI: ST elevation, new LBBB, Q waves.

Question 59

Q26: How is MI diagnosed on ECG?

Answer 59

A26: ST elevation (STEMI), ST depression/T wave inversion (NSTEMI), serial changes.

Question 60

Q29: Describe the histology of a myocardial infarct.

Answer 60

A29: Coagulative necrosis, neutrophil infiltration, granulation tissue, fibrosis.

Question 61

Q30: What are key investigations in IHD?

Answer 61

A30: ECG, troponins, echocardiography, angiography.

Question 62

Q33: What is the mechanism of nitrates?

Answer 62

A33: Vasodilation, reduces preload and myocardial oxygen demand.

Question 63

Q32: What is the mechanism of aspirin in MI?

Answer 63

A32: Inhibits thromboxane A2 to reduce platelet aggregation.

Question 64

🔹 Topic 6: Management of MI Q31: What is the initial medical management of MI?

Answer 64

A31: MONA: Morphine, Oxygen, Nitrates, Aspirin + beta-blockers, anticoagulants, statins.

Question 65

🔹 Topic 7: Complications and Lifestyle Q36: List complications of MI.

Answer 65

A36: Arrhythmias, heart failure, myocardial rupture, mural thrombus, aneurysm, Dressler’s syndrome

Question 66

Q34: How do beta-blockers help in MI?

Answer 66

A34: Reduce heart rate and contractility, lowering oxygen demand.

Question 67

Q35: What are interventional treatments for MI?

Answer 67

A35: PCI (primary treatment for STEMI), thrombolysis, CABG.

Question 68

Q37: What lifestyle changes are recommended post-MI?

Answer 68

A37: Smoking cessation, regular exercise, heart-healthy diet, weight loss, adherence to medications.

Question 69

Question: What is the correct diagnosis based on the ECG findings? Answer: The correct answer is B. Inferior and posterior ST-elevation myocardial infarction (STEMI).

Answer 69

Explanation: - Inferior ST-elevation: The ECG shows ST-segment elevation in leads II, III, and aVF, which strongly suggests an infarction affecting the inferior wall of the heart, typically due to occlusion of the right coronary artery (RCA). - Reciprocal changes: Leads V1-V4 show ST-segment depression, which is reciprocal to the ST elevation seen in inferior leads and is characteristic of a posterior infarction. This often indicates involvement of the posterior descending artery

Question 76

Topic 1: Embryological Development of the Heart 2. Q: What is the embryonic origin of the heart?

Answer 76

A: The heart develops from the cardiogenic mesoderm, a region of splanchnic mesoderm.

Question 77

Topic 1: Embryological Development of the Heart 3. Q: What contributes to outflow tract septation?

Answer 77

A: Neural crest cells.

Question 78

Topic 1: Embryological Development of the Heart 4. Q: What contributes to the epicardium and coronary vessels?

Answer 78

A: Proepicardial cells.

Question 79

Topic 1: Embryological Development of the Heart 5. Q: What is the primary pacemaker of the heart?

Answer 79

A: Sinoatrial (SA) node.

Question 80

Topic 1: Embryological Development of the Heart 6. Q: What structures form the heart’s conduction system?

Answer 80

A: AV node, His bundle, Purkinje fibers.

Question 81

Topic 2: Septation of the Heart 1. Q: How is the AV canal partitioned?

Answer 81

A: Endocardial cushions grow and fuse, dividing the AV canal into right and left AV canals.

Question 82

Topic 2: Septation of the Heart 2. Q: How does atrial septation occur?

Answer 82

A: Septum primum forms first, leaving the foramen primum. Foramen secundum forms before closure, and the septum secundum develops alongside it.

Question 83

Topic 2: Septation of the Heart 3. Q: What completes ventricular septation?

Answer 83

A: The interventricular septum, endocardial cushions, and bulbus cordis.

Question 84

Topic 2: Septation of the Heart 4. Q: What structures give rise to heart valves?

Answer 84

A: Endocardial cushions.

Question 85

Topic 3: Embryological Development of Blood Vessels 1. Q: What does the aorta develop from?

Answer 85

A: Aortic sac and dorsal aortae.

Question 86

Topic 3: Embryological Development of Blood Vessels 3. Q: Where do coronary arteries originate from?

Answer 86

A: Epicardium and endothelium.

Question 87

Topic 3: Embryological Development of Blood Vessels 2. Q: How do aortic arches contribute to the major arteries?

Answer 87

A: They remodel into the adult arterial pattern.

Question 88

Topic 3: Embryological Development of Blood Vessels 4. Q: What are the early venous systems?

Answer 88

A: Cardinal veins (embryo drainage), vitelline veins (yolk sac), umbilical veins (placental oxygenated blood).

Question 89

Topic 3: Embryological Development of Blood Vessels 5. Q: How do lymphatic channels form?

Answer 89

A: Endothelial sacs arise from veins.

Question 90

Topic 4: Circulation in Utero 1. Q: What is the primary site of fetal oxygenation?

Answer 90

A: Placenta, not lungs.

Question 91

Topic 4: Circulation in Utero 2. Q: What shunts bypass the fetal lungs?

Answer 91

A: Foramen ovale and ductus arteriosus.

Question 92

Topic 4: Circulation in Utero Q: What is the fetal blood flow pathway?

Answer 92

A:Oxygenated blood from placenta via umbilical vein Bypasses liver via ductus venosus Right atrium → foramen ovale → left atrium Right ventricle → ductus arteriosus → aorta Deoxygenated blood exits via umbilical arteries.

Question 93

Topic 4: Circulation in Utero Q: What happens to fetal shunts at birth?

Answer 93

A: They close due to circulatory pressure changes.

Question 94

Topic 5: Congenital Heart Defects 2. Q: Examples of left-to-right shunts?

Answer 94

A: PDA, VSD, ASD, PFO.

Question 95

Topic 5: Congenital Heart Defects 1. Q: What is a congenital heart defect?

Answer 95

A: A structural heart abnormality present at birth.

Question 96

Topic 5: Congenital Heart Defects 3. Q: Examples of right-to-left shunts?

Answer 96

A: Tetralogy of Fallot, TGA.

Question 97

Topic 5: Congenital Heart Defects 4. Q: Examples of obstructions?

Answer 97

A: Coarctation of aorta, pulmonary stenosis, aortic stenosis.

Question 98

Topic 6-8: Congenital Heart Diseases 1. Q: What causes Patent Ductus Arteriosus (PDA)?

Answer 98

A: Failure of the ductus arteriosus to close.

Question 99

Topic 6-8: Congenital Heart Diseases 1. Q: What murmur is heard in PDA?

Answer 99

A: Continuous "machinery-like" murmur.

Question 100

Topic 6-8: Congenital Heart Diseases 2. Q: How is PDA managed?

Answer 100

A: Indomethacin (prostaglandin inhibitor), surgery.

Question 101

Topic 6-8: Congenital Heart Diseases 1. Q: What defines Tetralogy of Fallot?

Answer 101

A: VSD, overriding aorta, pulmonary stenosis, RV hypertrophy.

Question 102

Topic 6-8: Congenital Heart Diseases 2. Q: What defines Transposition of Great Arteries (TGA)?

Answer 102

A: Aorta from RV, pulmonary artery from LV (separate circuits).

Question 103

Topic 6-8: Congenital Heart Diseases 3. Q: What is Coarctation of the Aorta?

Answer 103

A: Aortic narrowing causing hypertension in upper body.

Question 104

Topic 9: Cardiovascular Changes in Pregnancy 1. Q: Why does the CV system change in pregnancy?

Answer 104

A: To meet fetal needs and increase blood volume.

Question 105

Topic 9: Cardiovascular Changes in Pregnancy 2. Q: What happens to cardiac output in pregnancy?

Answer 105

A: ↑ 30-50%.

Question 106

Topic 9: Cardiovascular Changes in Pregnancy 3. Q: What happens to plasma volume in pregnancy?

Answer 106

A: ↑ 40-50%, leading to hemodilution.

Question 107

Topic 9: Cardiovascular Changes in Pregnancy 4. Q: What ECG shift occurs?

Answer 107

A: Right axis shift due to uterus pushing the diaphragm up.

Question 108

Topic 9: Cardiovascular Changes in Pregnancy 5. Q: What is pre-eclampsia?

Answer 108

A: Hypertension + proteinuria after 20 weeks gestation.

Question 109

Topic 9: Cardiovascular Changes in Pregnancy 6. Q: What are key risk factors for pre-eclampsia?

Answer 109

A: Nulliparity, multiple gestation, obesity, HTN, diabetes.

Question 110

A 28-year-old woman in her second trimester of pregnancy attends her routine prenatal check-up. The physician explains the cardiovascular changes occurring during pregnancy. Which of the following best encapsulates why these changes occur and what they entail? Question 1Answer a. Pre-eclampsia is characterized by reduced cardiac output and plasma volume, necessitating reduced physical activity during pregnancy b. Right axis shift on ECG and decreased cardiac output as adaptive mechanisms to increased intra-abdominal pressure c. Decreased plasma volume and increased red cell mass to prepare the body for potential blood loss during delivery d. Increased cardiac output and plasma volume due to hormonal influences that accommodate fetal growth and placental demands e. Vasodilation and decreased heart rate to reduce the risk of developing pre-eclampsia

Answer 110

d. Increased cardiac output and plasma volume due to hormonal influences that accommodate fetal growth and placental demands During pregnancy, hormonal changes (particularly increases in progesterone) lead to vasodilation, which, along with the demands of the growing fetus and placenta, necessitates an increase in cardiac output and plasma volume. This adaptation ensures adequate blood supply to the uterus and supports fetal development

Question 111

Which portion of the fetal heart tube, listed below, has the greatest contribution to the adult right atrium? Question 2Answer a. Primitive ventricle b. Outflow tract c. Bulbus cordis d. Sinus venosus e. Truncus arteriosus

Answer 111

d. Sinus venosus The sinus venosus forms the smooth venous part of the right atrial wall

Question 112

The fetus relies entirely on the maternal circulation for nutrients and oxygen. Which of the following statements about the fate of most of the blood entering the fetal circulation from the placenta is true? Question 3Answer a. It passes through the pulmonary arteries b. It enters the fetus via the umbilical arteries c. It passes through the left ventricle d. It passes through the right atrium e. It enters the pulmonary circulation via the ductus arteriosus

Answer 112

d. It passes through the right atrium Blood flows directly through the ductus venosus into the inferior vena cava, bypassing the liver then enters the right atrium

Question 113

Blood may be shunted between the pulmonary and systemic circulations in some congenital heart defects. These are classified as cyanotic or acyanotic depending on the direction of the shunt. What is a cyanotic congenital heart defect? Question 4Answer a. Atrial septal defect (ASD) b. Patent ductus arteriosus (PDA) c. Transposition of great vessels d. Ventricular septal defect (VSD) e. Coarctation of the aorta

Answer 113

c. Transposition of great vessels Transposition of great vessels in which the aorta and pulmonary artery are transposed and the output from the left and right ventricles are reversed, leading to cyanosis

Question 114

A 32-year-old woman with an ostium secundum ASD presents for follow-up after a 4-year absence from your clinic. You previously advised her to undergo catheter-based closure of her ASD, but she declined because she was feeling well. She has not been seen by a physician since her last office visit with you. Over the past year she has experienced a significant functional decline with progressive weakness, dizziness, and shortness of breath. She also reports headaches, blurry vision, and epistaxis. Her vital signs are as follows: blood pressure 90/68 mmHg, pulse 110 bpm, respirations 22 per minute, and room air oximetry 78%. She has perioral cyanosis. Examination reveals a loud and palpable second heart sound with III/VI holosystolic murmur at the left sternal border. Her lungs are clear, and her extremities are cool with marked digital clubbing. Laboratory data include a normal basic metabolic panel, hemoglobin 21 g/dL, and hematocrit 65%. Her echocardiogram reveals marked right-sided chamber enlargement with severe right ventricular systolic dysfunction with severe tricuspid regurgitation and an estimated right ventricular systolic pressure of 120 mmHg. There is a large secundum ASD with laminar flow from right to left. She agrees to hospitalization for additional diagnostic testing and management. Which of the following treatment choices is not appropriate for this patient? Question 5 a. Phlebotomy b. Oral contraceptive therapy c. Right-heart catheterization with trial of pulmonary vasodilator therapy d. Percutaneous ASD closure e. Advanced heart failure consultation to discuss eligibility for heart and lung transplantation

Answer 114

d. Percutaneous ASD closure

Question 115

All of the following untreated congenital heart defects are associated with a risk for Eisenmenger syndrome except _____ Question 6Answer a. Tetralogy of Fallot b. VSD c. PDA d. ASD e. Bicuspid aortic valve

Answer 115

e. Bicuspid aortic valve Bicuspid aortic valve is an isolated valvular abnormality that is not associated with left-to-right shunting. All of the remaining diagnoses have shunting as a key hemodynamic feature and may result in Eisenmenger syndrome

Question 116

A 2-year-old child presents with failure to thrive and breathlessness. On examination there is a continuous machine-like murmur. Which of the following conditions is most likely present in this patient? Question 7Answer a. Patent ductus arteriosus b. Patent foramen ovale c. Ventricular septal defect (VSD) d. Tetralogy of Fallot e. Cardiomyopathy

Answer 116

a. Patent ductus arteriosus Left-to-right shunt with blood passing back from the aorta down the patent ductus to the pulmonary artery. At age 2–3 years old patients develop harsh blowing machinery murmur in the region of the pulmonary artery

Question 117

The fetus has a different circulatory pattern from the newborn. Of the following statements about the fate of most of the deoxygenated blood returning from the head and neck of the fetus in the fetal circulation, which is correct? Question 8Answer a. It enters the right atrium via the inferior vena cava b. It is returned to the placenta via the umbilical veins c. It passes through the left ventricle d. It passes through the pulmonary circulation e. It passes through the right ventricle

Answer 117

e. It passes through the right ventricle Blood enters the right ventricle via the tricuspid valve

Question 118

Which of the following is not a feature of tetralogy of Fallot (ToF)? Question 9Answer a. Right ventricular hypertrophy b. Aortic dilatation c. Pulmonic stenosis d. Rightward displacement of the aorta e. Ventricular septal defect

Answer 118

b. Aortic dilatation Aortic dilatation is not a feature of tetraolgy of Fallot, all the other answers are a feature

Question 119

A newborn undergoes significant physiological changes immediately after birth. Which of the following best describes an anatomical change in the fetal cardiovascular system that occurs at birth, why it happens, and the outcome of this change? Question 10Answer a. The pulmonary artery dilates significantly to increase systemic blood flow and maintain higher blood pressure b. Constriction of the ductus arteriosus triggered by increased oxygen levels, redirecting blood away from the lungs c. The aorta constricts at the site of the ductus arteriosus to maintain higher pressure in the upper body d. Persistence of the umbilical vein to supplement nutrition until breastfeeding is established e. Closure of the foramen ovale due to pressure changes in the atria, preventing blood mixing and ensuring lung passage

Answer 119

e. Closure of the foramen ovale due to pressure changes in the atria, preventing blood mixing and ensuring lung passage After birth, increased left atrial pressure from lung function initiation closes the foramen ovale, stopping the direct atrial blood flow and directing blood through the lungs for oxygenation

Question 120

A 4-year-old child presents with a murmur found on routine examination. The mother notes that the child is otherwise fit and well but did have difficulty in feeding as a baby. On examination there is a pansystolic murmur, a parasternal heave and a laterally displaced apex beat. Which of the following conditions is most likely affecting this patient? Question 11 a. Tetralogy of Fallot b. Ventricular septal defect (VSD) c. Coarctation of the aorta d. Cardiomyopathy e. Patent ductus arteriosus

Answer 120

b. Ventricular septal defect (VSD) VSDs have a pansystolic murmur with thrills and heaves. May be associated with other cardiac and valve defects

Question 121

A 9-year-old girl has recently been diagnosed with Turner syndrome. Her mother is concerned as the child has episodes of dizziness and shortness of breath. On examination all observations are normal, however on palpation of the radial pulses they are found to be asynchronous. On palpation of the right radial and the femoral pulse, there is also a radio-femoral delay present. Which of the following conditions is most likely present in this patient? Question 13Answer a. Coarctation of the aorta b. Tetralogy of Fallot c. Patent ductus arteriosus d. Ventricular septal defect (VSD) e. Cardiomyopathy

Answer 121

a. Coarctation of the aorta Narrowing of the aorta after birth which causes overload of the left ventricle and heart failure; femoral pulses are weak. Radio-femoral delay will be seen due to narrowing of aorta after the branching of the arteries supplying the upper limbs. Often associated with Turner syndrome in females

Question 122

A 2-year-old child has been brought in by his mother. She is concerned as he can ‘go blue’ whilst running and playing which is improved when the child crouches down and squats. She was told that he had a murmur when he was a baby. On examination: The child is small for his age, observations all normal, clubbing of the fingers, pansystolic murmur. Investigations: CXR – ‘boot-shaped heart’ with large right ventricle and small pulmonary artery. Given the history, examination and investigation findings what is the most likely diagnosis in this patient? Question 12 a. Tetralogy of Fallot b. Eisenmenger's syndrome c. Transposition of the great arteries d. Patent ductus arteriosus e. Coarctation of the aorta

Answer 122

a. Tetralogy of Fallot This is the most common congenital cause of blue baby; a right-to-left shunt is present