CVS Week 5 Flashcards
Topic 1: Murmurs
* TLO 5.1.1: Describe why murmurs occur
- 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.
- TLO 5.1.2: Describe how murmurs are affected by inspiration, expiration, Valsalva and isometric handgrip manoeuvre
- 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.
- TLO 5.1.3: Describe why and when S3 and S4 heart sounds occur
- 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.
- TLO 5.1.4: Familiarize yourself with murmurs associated with the pathologies involving the left and right-side valve lesions.
Left-Sided Lesions
1. Aortic Stenosis (AS)
- Timing: Systolic
- Maximal Intensity: Right upper sternal border
- Radiation: Carotid arteries
- Characteristics: Harsh, crescendo-decrescendo
-
Aortic Regurgitation (AR)
- Timing: Diastolic
- Maximal Intensity: Left upper sternal border
- Radiation: Down the left sternal border
- Characteristics: High-pitched, blowing, decrescendo
-
Mitral Stenosis (MS)
- Timing: Diastolic
- Maximal Intensity: Apex
- Radiation: None
- Characteristics: Low-pitched, rumbling, often with an opening snap
-
Mitral Regurgitation (MR)
- Timing: Systolic
- Maximal Intensity: Apex
- Radiation: Axilla
- Characteristics: High-pitched, blowing, holosystolic (pansystolic)
-
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
-
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)
-
Tricuspid Stenosis (TS)
- Timing: Diastolic
- Maximal Intensity: Left lower sternal border
- Radiation: None
- Characteristics: Low-pitched, rumbling, increases with inspiration
-
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
Topic 2: Aortic Stenosis (AS)
* TLO 5.2.1: Define AS and explain epidemiology.
- 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.
Topic 2: Aortic Stenosis (AS)
* TLO 5.2.2: Discuss the causes and explain the pathophysiology of AS.
- 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.
Topic 2: Aortic Stenosis (AS)
* TLO 5.2.3: Discuss the clinical features of AS.
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.
Topic 2: Aortic Stenosis (AS)
* TLO 5.2.4: Discuss the diagnosis of AS.
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.
Topic 3: Mitral Stenosis (MS)
* TLO 5.3.1: Define and explain epidemiology of MS.
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.
Topic 3: Mitral Stenosis (MS)
* TLO 5.3.2: Discuss the causes and explain the pathophysiology of MS.
- 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.
Topic 3: Mitral Stenosis (MS)
* TLO 5.3.3: Discuss the clinical features of MS.
- 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.
Topic 3: Mitral Stenosis (MS)
* TLO 5.3.4: Discuss the diagnosis of MS.
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
Topic 3: Mitral Stenosis (MS) (Continued)
* TLO 5.3.4: Discuss the diagnosis of MS.
- 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.
Topic 3: Mitral Stenosis (MS) (Continued)
* TLO 5.3.5: Outline the management of MS.
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).
Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.1: Define and explain epidemiology of AR.
- 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.
Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.2: Discuss the causes and explain the pathophysiology of AR.
- 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.
Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.3: Discuss the clinical features of AR.
- 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.
Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.4: Discuss the diagnosis of AR.
- 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.
Topic 4: Aortic Regurgitation (AR)
* TLO 5.4.5: Outline the management of AR.
- 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.
Topic 5: Mitral Regurgitation (MR)
* TLO 5.5.1: Define and explain epidemiology of MR.
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.
Topic 5: Mitral Regurgitation (MR)
* TLO 5.5.2: Discuss the causes and explain the pathophysiology of MR.
- 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.
Topic 5: Mitral Regurgitation (MR)
* TLO 5.5.3: Discuss the clinical features of MR.
- 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.
Topic 5: Mitral Regurgitation (MR)
* TLO 5.5.4: Discuss the diagnosis of MR.
- 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.
Topic 5: Mitral Regurgitation (MR)
* TLO 5.5.5: Outline the management of MR.
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
