Thirteen B Flashcards by Tim Horrocks

Describe the pathophysiology of rheumatic fever.

 Initial infection with group A ͆-hemolytic streptococcus
causes pharyngitis

 Exaggerated immune response

 Acute rheumatic fever develops 2-4 weeks after initial
infection

 Rheumatic heart valve involvement can take 10-30 years to develop

 Repeated episodes of acute rheumatic fever leads to more severe valvular disease

 Mitral valve is always affected first

 Extremely rare to see aortic/pulmonic/tricuspid involvement

without mitral involvement

 Mitral > Aortic&raquo_space; Tricuspid > Pulmonic

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When do patients become symptomatic with mitral valve stenosis? What are some etiologies?

 Obstruction of normal mitral inflow during diastole

 Abnormal pressure gradient between the left atrium and left ventricle

 The normal mitral valve orifice area is between 4-6 cm2

 Patients typically become symptomatic when the mitral vale orifice area is less than 2 cm2

 Rheumatic heart disease

 Up to 40% of patients with a history of acute rheumatic fever develop mitral stenosis

 Age-related mitral annular calcification

 Mitral calcification in patients with end-stage renal disease

 Congenital mitral stenosis

 Carcinoid syndrome

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Describe the pathophysiology of mitral valve stenosis.

 Obstruction to left ventricular filling

 Chronic elevation in left atrial pressure

 Left atrial enlargement
 Ortner Syndrome (recurrent laryngeal nerve palsy)

 Pulmonary venous hypertension
 Pulmonary venous hypertension results from chronic elevation in left atrial pressure

 Atrial fibrillation
 Left atrial enlargement leads to atrial fibrillation
 Higher risk of forming left atrial thrombi

 Pulmonary arterial hypertension
 Ultimately, changes in pulmonary arterial vasculature can lead to ᾿reactive῀ pulmonary arterial hypertension
 Long-standing pulmonary hypertension affects right
ventricular function
 Right side of the heart was not designed to handle high
pressures
 Right ventricular hypertrophy, dilation and failure

 Decreased cardiac output
 Results from decreased blood flowing into the left ventricle

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What are the symptoms of mitral valve stenosis?

 Exertional dyspnea

 Exercise intolerance

 Signs and symptoms of congestive heart failure

 Palpitations (if there is atrial fibrillation)

 Mitral Facies
 Seen only in severe mitral stenosis
 Mild cyanosis of the lips, cheeks, and malar prominences
 Caused by chronic hypoxemia and low cardiac output

 Ortner Syndrome  Recurrent laryngeal nerve palsy

 Hemoptysis
 Bronchiolar vein rupture

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What physical exam and test findings occur in mitral valve stenosis?

 Low-pitched diastolic murmur

 Best heard with the bell of the stethoscope at the cardiac apex

 Intensity of murmur increases with MS severity

 Timing of OS also correlates with disease severity

 Loud P2 component if there is significant
pulmonary hypertension

 Signs of congestive heart failure
 Elevated JVP
 Pulmonary rales
 Lower extremity edema

 ECG may show:
 Left atrial enlargement (᾿P mitrale῀)
 Atrial fibrillation
 Right atrial enlargement
 Right ventricular hypertrophy

 Chest x-ray may show:
 Left atrial enlargement
 Pulmonary vascular congestion
 Pulmonary arterial dilation
 Right ventricular dilation

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How is rheumatic mitral stenosis diagnosed?

 Echocardiography is the mainstay of diagnosis

 Typical findings from rheumatic mitral stenosis include:
 Calcified mitral valve with diastolic ᾿doming῀
 Left atrial enlargement
 Varying degrees of pulmonary hypertension

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How is MVS treated?

 Medical therapy (non-surgical) is limited

 Patients develop profound dyspnea and pulmonary edema, particularly when tachycardic

 Beta-blockers, non-DHP calcium channel blockers
 Loop diuretics

 Surgical and percutaneous options are available

 Open surgical replacement versus percutaneous balloon
mitral valvuloplasty

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Describe some examples of how mitral regurgitation is caused?

 Rheumatic mitral valve
 Typically causes mitral stenosis
 Shortening of the chordae tendinae and commissural fusion can cause mitral regurgitation

\+ Mitral Valve Prolapse
 AKA ᾿Floppy mitral valve syndrome῀
 Most common cause of isolated MR
 FeMale > male
 Association with connective tissue diseases (marfans

 Infective endocarditis
 Vegetations can damage the surface of the valves
 Leaflet perforation

 Congenital (cleft mitral valve)

\+ Defective Tensor Apparatus
 Rupture of chordae tendinae
 Papillary muscle dysfunction
 Ruptured papillary muscle (associated with acute 
myocardial infarction)

+ Abnormal LA and LV
 Dilated cardiomyopathy
 Alterations in ventricular geometry alter mitral annular geometry

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Describe the pathophys of the two different kinds of MR?

 Acute MR
 Minimally compliant left atrium experiences sudden rise in pressure
 Rapid development of pulmonary edema

 Chronic MR
 Left atrium more compliant
 LA and LV dilate
 Ultimately leads to LV dysfunction

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What are the symptoms and presentation of the two kinds of MR?

 Acute MR
 Symptoms reflect the more acute rise in left atrial pressure
 Sudden onset of dyspnea

 Chronic MR
 Symptoms develop slowly over time
 Exertional dyspnea
 CHF symptoms
 Atrial fibrillation can cause palpitations

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What findings are found in the physical exam for MR? Diagnostic Exam findings?

 Holosystolic murmur

 Typically loudest at the apex

 Radiates to axilla

 In acute settings, an S3 can be heard

 Distinguishing acute from chronic MR (by physical
examination) can be tough

 ECG will show non-specific findings
 Evidence of left atrial enlargement
 Q waves consistent with prior myocardial infarction

 CXR can show pulmonary edema and left atrial enlargement

 Echocardiogram can assess severity and etiology of disease

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How is MR treated?

 Medical management limited

 5-year survival of unrepaired severe MR is 30-45%

 Diuretics for symptomatic relief

 Afterload reducing agents

 Surgical repair/replacement

 Percutaneous options also available

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What are some etiologies of aortic stenosis?

 Age-related calcific degeneration

 Similar risk factors with atherosclerotic vascular disease

 Congenital aortic stenosis

 Bicuspid aortic valve

 Rheumatic aortic stenosis
 Seen in conjunction with rheumatic mitral disease

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Describe the pathophys of stenosis.

 Progressive disease

 Increasing obstruction to left ventricular outflow

 Creates an abnormally elevated systolic pressure
gradient between the left ventricle and aorta

 Pathologic left ventricular hypertrophy leads to impaired
diastolic relaxation of the left ventricle

 Cardiac output becomes heavily dependent upon atrial
contraction to adequately fill the left ventricle during diastole

 Patients who develop atrial fibrillation (loss of atrial
contraction) can become dyspneic and hypotensive

 Elevation of left ventricular pressure leads to elevated left atrial pressure

 Ultimately leads to pulmonary edema

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What are the symptoms and presentation of aortic stenosis?

 Angina due to increased myocardial oxygen demand
 Supply/demand mismatch

 Dyspnea (congestive heart failure) due to pulmonary edema

 Syncope due to reduced cardiac output and reduced cerebral perfusion

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What physical and diagnostic exam findings are there in aortic stenosis?

 Crescendo-decrescendo (diamond-shaped) systolic
ejection murmur heard best at the right upper sternal border

 Intensity of murmur does not necessarily correlate with
disease severity

 Time to peak intensity and S2 quality

 ECG may show LVH, left atrial enlargement

 CXR can reveal pulmonary edema, aortic calcification

 Echocardiogram will show reduced aortic valve leaflet mobility and increased aortic valve pressure gradient

 Left heart catheterization can invasively measure the aortic valve pressure gradient

What is the prognosis for aortic stenosis? How is it managed? Not managed? Treated?

 Long-term survival poor in symptomatic patients with
unoperated valve

 Once symptoms develop, median survival is between 2
to 5 years without surgery

 Medical therapy is limited and consists of symptomatic relief

 Changes in loading conditions (particularly reducing preload) can have disastrous consequences

 Surgical aortic valve replacement is the current gold standard

 Catheter based techniques (valvuloplasty and transcatheter aortic valve replacement)

What are the two classifications of etiologies of aortic regurg?

 Etiologies can be classified as:

 Disorders/abnormalities of the aortic valve leaflets

 Disorders of the aorta/aortic root

Describe various causes of disorders of the aortic valve leaflets.

 Bicuspid aortic valve
 Two of the three leaflets fused
 Abnormal geometry obscures normal valve closure

 Infective endocarditis

 Rheumatic disease
 Typically causes aortic stenosis
 Commissural fusion leads to a central gap in the valve during diastole

 Concomitant aortic stenosis

Describe various causes of disorders of the aorta/aortic root.

 Aortic aneurysm

 Marfanᾼs syndrome
 Cystic medial necrosis

 Aortic dissection

 Syphilitic aortitis

What is the pathophys of the two kinds of aortic regurg?

 Acute vs chronic aortic regurgitation

 Acute AR can lead to a rapid increase in left ventricular
diastolic pressure and cause acute pulmonary edema

 Chronic aortic regurgitation characterized by a widened
aortic pulse pressure

What are the classical presentation and symptoms of the two kinds of AR?

 Acute AR causes an acute/abrupt rise in left ventricular diastolic pressure
 Left ventricle is not able to handle this rapid increase in volume (decreased compliance)
 Acute pulmonary vascular congestion and pulmonary edema causes severe dyspnea
 Frequently a surgical emergency!

 Chronic AR is characterized by a more compliant left ventricle which is able to better handle the increased blood volume
 Eventual development of left ventricular dilation and failure
 Symptoms include exertional dyspnea, fatigue, palpitations

What physical exam finds and diagnostic eval findings are there in AR?

 Decrescendo diastolic murmur

 Heard best in the right upper sternal border, with the patient sitting upright at end-expiration

 Systolic ejection murmur typically heard

 Bounding peripheral pulses (from widened pulse pressure)

 Laterally displaced point of maximal impulse

 Austin-Flint murmur

 ECG can be non-specific
 Inferior STEMI can be seen in cases of aortic dissection causing acute AR
 May show LVH

 CXR with pulmonary edema in acute AR and decompensated chronic AR

 Chest CT can diagnose acute aortic dissection

 Echocardiography can establish cause and severity

How is AR treated/managed?

 Acute AR is typically a surgical emergency

 Patients may present with cardiogenic shock (hypotension, severely reduced cardiac output and reduced end-organ perfusion)

 Treatment of chronic AR includes diuretic therapy for
symptomatic relief

 Anecdotal evidence that ACE-I and dihydropyridine CCBs can be helpful

 Once symptoms of CHF develops or when there is evidence of LV cavity dilation or dysfunction, surgical intervention is indicated

Which right sided valvular disorder is frequently encountered? When is it usually seen? Is it clinically relevant?

 Tricuspid regurgitation is frequently encountered  Typically it is clinically irrelevant  Commonly seen in pulmonary hypertension  IV drug users at risk of infective endocarditis

Describe Carcinoid syndrome. What does it cause? How? What doesn't it usually cause? Why?

 Neuroendocrine tumor typically located in the small bowel or appendix  Secretes serotonin and other vasoactive metabolites  Direct toxic effect on heart valves  Left sided heart valve disease is rare  Serotonin is inactivated in lung parenchyma  Tricuspid regurgitation is common  Tricuspid stenosis can also occur  Scarring of the valve restricts leaflet mobility

What physical exam findings are there in TR? Symptoms? What is the treatment?

 TR murmur is holosystolic, typically loudest at the lower sternal border  Louder with inspiration  Prominent jugular venous pulsations (prominent V-waves)  Pulsatile liver  Symptoms include fatigue and edema  Treatment includes correcting the underlying cause  Diuretic therapy for edema  Rarely, surgical tricuspid valve repair is required