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Cardiovascular > Thirteen B > Flashcards

Thirteen B Flashcards

1
Q

Describe the pathophysiology of rheumatic fever.

A

 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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2
Q

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

A

 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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3
Q

Describe the pathophysiology of mitral valve stenosis.

A

 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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4
Q

What are the symptoms of mitral valve stenosis?

A

 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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5
Q

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

A

 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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6
Q

How is rheumatic mitral stenosis diagnosed?

A

 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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7
Q

How is MVS treated?

A

 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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8
Q

Describe some examples of how mitral regurgitation is caused?

A

 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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9
Q

Describe the pathophys of the two different kinds of MR?

A

 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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10
Q

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

A

 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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11
Q

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

A

 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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12
Q

How is MR treated?

A

 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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13
Q

What are some etiologies of aortic stenosis?

A

 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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14
Q

Describe the pathophys of stenosis.

A

 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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15
Q

What are the symptoms and presentation of aortic stenosis?

A

 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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16
Q

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

A

 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

17
Q

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

A

 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)

18
Q

What are the two classifications of etiologies of aortic regurg?

A

 Etiologies can be classified as:

 Disorders/abnormalities of the aortic valve leaflets

 Disorders of the aorta/aortic root

19
Q

Describe various causes of disorders of the aortic valve leaflets.

A

 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

20
Q

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

A

 Aortic aneurysm

 Marfanᾼs syndrome
 Cystic medial necrosis

 Aortic dissection

 Syphilitic aortitis

21
Q

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

A

 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

22
Q

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

A

 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

23
Q

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

A

 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

24
Q

How is AR treated/managed?

A

 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

25
Q

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

A

 Tricuspid regurgitation is frequently encountered

 Typically it is clinically irrelevant

 Commonly seen in pulmonary hypertension

 IV drug users at risk of infective endocarditis

26
Q

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

A

 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

27
Q

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

A

 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

Cardiovascular (15 decks)

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