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Cardiology > Valvular Disorders > Flashcards

Valvular Disorders Flashcards

1
Q

What is the problem in cardiac valve disease?

What is the result of this?

Describe the pathophysiology behind the problem?

A

The problem: Structural and/or functional abnormality of the cardiac valve

The result: altered blood flow across the valve

The pathophys: Pressure and volume changes of atria and ventricles (hypertrophy, dilatation and failure)

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2
Q

What are the two types of valvular lesions?

A
  1. Stenosis (scarring and blockage)

2. Regurgitation (insufficiency, incompetence…they leak)

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3
Q

Etiology of valvular disease?

9

A
  1. Rheumatic fever
  2. Infective endocarditis
  3. Functional
  4. Congenital malformations (pediatric/bicuspid)
  5. Aging valve tissue (calcification)
  6. Rupture/dysfunction of the papillary muscles (MI)
  7. Collagen vascular disease
  8. Aortic dissection
  9. Syphilis
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4
Q

Pathology of the Tricuspid Valve

6

A
  1. Regurgitation
  2. Stenosis
  3. Endocarditis
  4. Carcinoid Syndrome
  5. Traumatic Rupture
  6. Ebstein’s Anamoly
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5
Q

Which disease processes cause tricuspid regurgitation?

5

A
  1. Annular dilation (most common right-sided valve disease in the adult)
  2. Rheumatic disease (calcification and fusion)
  3. Carcinoid syndrome
  4. Endocarditis
  5. Ebstein anomaly
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6
Q

Which disease processes cause tricuspid stenosis?

2

A
  1. Rheumatic disease (calcification and fusion)

2. Carcinoid syndrome

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7
Q

Describe the following symptoms involved with each organ system in carcinoid syndrome:

  1. Heart? 2
  2. Liver?
  3. GI? 4
  4. Skin? 2
  5. Respiratory? 3
  6. Retroperitoneal? 2
A

1.

  • pulmonic and tricupid valve thickening and stenosis
  • endocardial fibrosis
  1. heptomegalgy

3.

  • diarrhea
  • cramps
  • nausea
  • vomiting
    • cutaneous flushes
    • apparent cyanosis
    • cough
    • wheezing
    • dyspnea
  3. retroperitoneal and pelvic fibrosis
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8
Q

What is the pathophysiology behind tricuspid regurgitation?

4 steps to result

A
  1. Pulmonary hypertension develops leading to right ventricular dilation… tricuspid annulus dilates
  2. As the annular & ventricular dilation progresses, the chordal papillary muscle complex becomes functionally shortened
  3. This combination prevents leaflet apposition, resulting in valvular incompetence
  4. The pre-load, afterload and RV function also contribute
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9
Q

What is the most common presentation of tricuspid regurgitation due to?

A

The most common presentation of tricuspid regurgitation is functional rather than organic (MS, MR, AS, AI or left-sided failure)
***Process of annular dilatation

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10
Q

Clinical presentation of tricuspid regurgitation

4

A
  1. Clinical presentation (usually need pulmonary hypertension)
  2. Fatigue & weakness related to reduction of cardiac output
  3. DOE and SOB
  4. Right heart failure lead to

ascites, venous engorgement, hepatospenomegaly, pulsatile liver, pleural effusions & peripheral edema (sounds familiar)

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11
Q

In late stages of tricuspid regurgitation what will manifest?
4

A
  1. cachexia
  2. cyanosis
  3. jaundice
  4. A-fib is common
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12
Q

What does right sided heart failure cause?

A
  1. ascites
  2. venous engorgement
  3. hepatospenomegaly
  4. pulsatile liver
  5. pleural effusions &
  6. peripheral edema (sounds familiar)
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13
Q

What will you find on physical exam in tricuspid regurgitation? 3

ECG?

A
  1. Right sided failure
  2. Abnormal pulse in jugular vein
  3. High pitched systolic murmur

RAE (starting to make sense)

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14
Q

What is tricuspid stenosis usually caused by?

A

Most commonly rheumatic, rare isolated stenosis

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15
Q

In tricuspid stenosis pts present with Fatigue, anorexia & malaise related to what?

A

reduction of CO

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16
Q

As the right atrial pressure increases, venous congestion leads to what? 6

Anatomic features are similar to mitral stenosis. How so? 2

The right atrial wall thickens and chamber ______?

Systolic murmur at _____, ___ P waves, ____ on EKG.

A
  1. distention of jugular veins,
  2. edema,
  3. hepatomegaly,
  4. ascites,
  5. pleural effusion, &
  6. peripheral edema
  7. with fusion and shortening of chordae
  8. leaflet thickening
  9. dilates
  10. LLSB
  11. tall
  12. RAE
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17
Q
  1. Infective endocarditis causes what to happen to the tricuspid valve?
  2. Increasing due to rising incidence
  3. What are the four pathological disease processes that endocarditis causes?
  4. How should we treat? 2
  5. Prognosis?
  6. What organism?
A
  1. Tricuspid valve lesion of
  2. IV drug abuse
    • Regurgitation,
    • Conduction Abnormalities,
    • Embolic Events and
    • SEPSIS
  4. Intensive medical Tx (Abx) and maybe valve replacement
  5. Horrible mortality
  6. Staph
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18
Q

What is ebsteins anomaly? 3

A
  1. Atrialization of RV,
  2. sail-like TV,
  3. TR
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19
Q

What does the disease severity depend on for ebsteins anomaly?
4

A
  1. Age at presentation varies from childhood→adulthood and depends on factors such as
  2. severity of TR,
  3. Pulm Vascular resistance in newborn, and
  4. associated abnormalities such as ASD
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20
Q

50% of ebsteins have what? 2

50% will show what on the EKG?

A

50% ASD/PFO

50% EKG evidence of WPW

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21
Q

What will a chest xray show on a pt with ebstens anomaly?

A

Massive cardiomegaly,

mainly due to RAE

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22
Q

Medical Management
of ebsteins anomaly?
3

A
  1. Fluid Restriction
  2. Diuretics
  3. Treat the complications (for example: rhythm disturbances)
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23
Q

Pulmonary Regurgitation has two kinds. What are they?

A

Congenital and Acquired (rare)

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24
Q

Describe the pathphysiology behind congenital pulmonary regurgitation? 3

A
  1. Abnormal cusp number
  2. Abnormal cusp development
  3. NO VALVE (Pulmonary Atresia)
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25
Q

Describe the pathphysiology behind acquired pulmonary regurgitation? 3

A
  1. Pulmonary hypertension (this is what you treat and this is a big deal)
  2. Annular dilation
  3. Structural distortion
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26
Q

What diseases cause acquired pulmonary stenosis?

3

A
  1. Rheumatic heart disease
  2. Carcinoid
  3. Infective endocarditis
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27
Q

If you have a diastolic murmur how is the mitral valve affected?

A

stenosis

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28
Q

Mitral stenosis is primarily a result of what?

A

Primarily a result of rheumatic fever

~ 99% of MV’s @ surgery show rheumatic damage

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29
Q

What are the etiologies of mitral valve stenosis? 6

what are the two most common?

A
  1. Rheumatic heart disease
    –Female
  2. Congenital
    Rare
  3. Carcinoid
  4. SLE
  5. Rheumatoid Arthritis
  6. Amyloid
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30
Q

Mitral Stenosis:
Pathophysiology

Normal valve area?
Mild mitral stenosis?
Moderate?
Severe?

A

Normal valve area: 4-6 cm2

Mild mitral stenosis:
MVA 1.5-2.5 cm2
Minimal symptoms

Mod mitral stenosis
MVA 1.0-1.5 cm2 usually does not produce symptoms at rest

Severe mitral stenosis
MVA less than 1.0 cm2

Pressure Difference

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31
Q

Mitral Stenosis: Natural History

  1. Prognosis?
  2. Onset?
  3. Describe disease progression in later years?
  4. Describe the progression from rheumatic fever symtpoms to the onset of the disease?
  5. How many years before disabling symtpoms?
A
  1. Progressive, lifelong disease,
  2. Usually slow & stable in the early years.
  3. Progressive acceleration in the later years
  4. 20-40 year latency from rheumatic fever to symptom onset.
  5. Additional 10 years before disabling symptoms
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32
Q

Mitral Stenosis: Symptoms

7

A
  1. Fatigue
  2. Palpitations
  3. Cough
  4. SOB (DOE)
  5. Left sided failure
  6. Palpitation
  7. Hoarseness
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33
Q

What causes orthopnea and PND?

A

left sided heart failure

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34
Q

Recognizing Mitral Stenosis: Palpation

3

A
  1. Small volume pulse
  2. Tapping apex-palpable S1
  3. Palpable pulmonic component of S2
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35
Q

Recognizing Mitral
Stenosis: Auscaltation?
2

A
  1. Loud S1- as loud as S2 in aortic area

2. Diastolic murmur: length proportional to severity

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36
Q

Recognizing Mitral
Stenosis: CXR?
2

A
  1. Pulmonary congestion and

2. large LA …if severe RHD can see ring of Ca (annulus)

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37
Q

Mitral Stenosis: Complications

6

A
  1. Atrial dysrhythmias
  2. Systemic embolization (10-25%)
  3. Congestive heart failure (right side)
  4. Hemoptysis
  5. Endocarditis
  6. Pulmonary infections
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38
Q

What is the risk of embolism related to in MS?
3

What is the cause of hemoptysis? 2

A

Risk of embolization is related to, 1. age,

  1. presence of atrial fibrillation,
  2. previous embolic events
  3. Massive: 20 to ruptured bronchial veins (pulm HTN)
  4. Streaking/pink froth: pulmonary edema, or infections (recurrent bronchitis patient)
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39
Q

What is the pathoysiology behind mitral stenosis?

2

A
  1. LA hypertension

2. Limited LV filling and cardiac output

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40
Q

Mitral Stenosis: EKG findings?

4

A

1, LAE

  1. RVH
  2. PVC’s
  3. Atrial flutter and/or fibrillation

LET’S use our necklaces

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41
Q

IN what kind of pts is AFIB increased in frequency?

A

↑ freq. in pts with mod-severe MS for several years

A fib develops in ≈ 30% to 40% of pts w/symptoms

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42
Q

When do symptoms start to appear in MS?

A

Symptoms not apparent until area

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43
Q

Mitral Stenosis:Therapy

3

A
  1. Medical
  2. Balloon valvuloplasty
    - -Effective long term improvement
  3. Surgery
44
Q

Mitral Stenosis:Therapy

  1. What should we use for LHF/RHF?
  2. WHat should we use for rate control in AFIB?
  3. What else do we need to treat AFIB with?
  4. What do we need to treat prophylactically?
  5. WHich is effective for long term improvement?
A
  1. Diuretics for LHF/RHF
  2. Digitalis/Beta blockers/CCB: Rate control in A Fib
  3. Anticoagulation: A Fib
  4. Endocarditis prophylaxis
  5. Balloon valvuloplasty
    - -Effective long term improvement
45
Q

What are the two kinds of mitral stenosis surgical therapy?

A
  1. Mitral commissurotomy

2. Mitral Valve Replacement

46
Q

Mitral Regurgitation:
Etiology?
5

A
  1. Valvular-leaflets
  2. Chordae
  3. Annulus
  4. Papillary Muscles
  5. LV dilatation & functional regurgitation
47
Q

What are the valvular leaflet problems of MR?

3

A
  1. Rheumatic
  2. Endocarditis
  3. Congenital
48
Q

Chordea problems that cause MR? 4

A
  1. Fused
  2. Ruptured
  3. Degenerative
  4. IE
49
Q

Annulus issues that cause MR? 1

A

Calcification, IE (abcess)

50
Q

Papillary muscle issues that cause MR? 3

A

CAD (Ischemia, Infarction, Rupture)

51
Q

MR Etiology: Surgical series

4

A
  1. MVP (20-70%)
  2. Ischemia (40%)
  3. RHD (40%)
  4. Infectious endocarditis (10%)
52
Q

Morphological Patterns
that happen in mitral regurgitation?
4

A
  1. RVD-annular dilatation and leaflet thickening
  2. MVP-leaflet redundancy and thickening
  3. Ischemic papillary muscle dysfunction or chordal rupture
  4. IE-perforation or destruction of cusps or chordae
53
Q

MR Pathophysiology:

  1. Chronic LV volume overload leads to?
  2. Decompensation (increased LV wall tension) leads to?
  3. LVH leads to? Which leads to what?
  4. Backflow leads to what? 3
A
  1. compensatory LVH initially maintaining cardiac output
  2. CHF
  3. annulus dilation which leads to increased MR
    • LAE,
    • Afib,
    • Pulmonary HTN
54
Q

MR Symptoms

8

A

Similar to MS

  1. Dyspnea,
  2. Orthopnea,
  3. PND
  4. Fatigue
  5. Pulmonary HTN,
  6. right sided failure
  7. Hemoptysis
  8. Systemic embolization in A Fib
55
Q 
Recognizing Chronic
Mitral Regurgitation
1. Pulse?
2. Apex? 4
3. Heart sounds? 3
  1. Murmur-Fixed MR? 2
  2. Murmur-Dynamic MR(MVP)? 3
A
  1. brisk, low volume
    • hyperdynamic
    • laterally displaced
    • palpable S3 +/- thrill
    • late parasternal lift 2° to LA filling
    • S 1 soft or normal
    • S 2 wide split (early A2) unless LBBB
    • S 3 / flow rumble if severe
    • pansystolic
    • loudest apex to axilla
    • mid systolic
    • +/- click
    • ↑ upright
56
Q

Recognizing Mitral
Regurgitation
EKG? 5
CXR? 4

A

EKG

  1. LAE
  2. Afib
  3. LVH (50% pts. With severe MR)
  4. RVH (15%)
  5. Combined hypertrophy (5%)

CXR

  1. ↑ LV
  2. ↑↑ LA
  3. ↑ pulmonary vascularity
  4. CHF
57
Q

Etiology of MR that echocardiography would show?

4

A
  1. flail leaflets (chordae/papillary rupture)
  2. thick (RHD)
  3. post movement of leaflets (MVP)
  4. vegetations(IE)
58
Q

How will echocardiography assess severity of MR?

3

A
  1. regurgitant volume/fraction/orifice area
  2. LV systolic function
  3. increased LV/LA size, EF
59
Q
  1. Other names for mitral valve prolapse? 2
  2. Etiology? 4
  3. Pathophysioloy? 2
A
  1. Floppy valve, Barlow’s
    • Congenital
    • Marfan’s syndrome
    • RHD
    • Sequelae of Cardiomyopathy or MI
    • Valve leaflet has redundant tissue
    • Extra tissue balloons into LA, click sound
60
Q
  1. Incidence of Mitral Valve prolapse? 2

2. Clinical presentation? 4

A
  1. Incidence
    - 10-20 % of population
    - F > M, thin young females
Clinical Presentation
-Asymptomatic
Symptomatic
-Palpitations
-Arrhythmias
-Atypical Chest Pain
61
Q

MVP-Physical Exam/Diagnosis

  1. Abnormalities? 2
  2. Auscultation?
  3. EKG?4
  4. Echo?2
A
  1. Abnormalities
    - Skeletal
    - Heart
  2. Auscultation
    - Mid-systolic click
  3. EKG
    -Normal
    Abnormal
    -Arrhythmias: SVT
    -NSST-T changes
    -WPW
  4. ECHO
    - Confirm the diagnosis
    - R/O other abnormalities
62
Q

MVP-Treatment

3

A

Reassurance

SBE prophylaxis

Beta blockers

63
Q

Prognosis of MVP?

A

Usually benign

Rare complications: endocarditid, Progressive MR, Thromboelmbolism, arrhythmias

64
Q

Chronic Mitral Regurgitation
Medical therapy?
3

A
  1. No generally accepted rx in asymptomatic pts

No long term studies suggesting benefit of afterload reduction in absence of hypertension

  1. ACEi if hypertensive
  2. AF requires rate control, anticoagulation and attempt at restoration of SR
65
Q

MR-Treatment

5

A
  1. Low sodium diet
  2. Preload reduction
    - -Diuretics
  3. Afterload reduction
    - -Vasodilators
    - ——-ACE inhibitors, Hydralazine
  4. Digoxin
  5. SBE prophylaxis
66
Q

What is the only effective treatment for mitral valves regurgitation?

What is the best timing for this surgery determined by? 4

A

Mitral Valve Surgery
-valve repair/replacement

  1. Presence/absence of symptoms
  2. Functional state of ventricle
  3. Feasability of valve repair
  4. Presence of Afib/PHTN
67
Q

MV Repair vs. Replacement

5

A
  1. Lower operative mortality
  2. Better late outcome
  3. Preserves sub-valvular apparatus
  4. Curative
  5. Avoids anticoagulation unless atrial fibrillation
68
Q

What is acute mitral regurgitation:

  1. Abrupt volume overload is worse than chronic symptoms why?
  2. Sudden decrease in what?
  3. Sudden increase in what?
  4. How does this affect the pulmonary valve?
  5. This all causes a decrease in forward CO which leads to?
A
  1. Abrupt volume load—no time for adaptation
  2. Sudden ↓ in forward stroke volume
  3. Sudden ↑ in LA volume/pressure →
  4. ↑ PV pressure (pulmonary edema)
  5. Decrease in forward CO…cardiogenic shock
    Call someone….the surgeon

Rapidly fatal if severe

69
Q

Symtpoms of Acute Severe
Mitral Regurgitation 3

What will you find on PE? 5

A
  1. Acute severe dyspnea,
  2. CHF &
  3. hypotension
  4. LV size normal
  5. LV may/may not be hyperdynamic
  6. Loud S1
  7. Systolic murmur
  8. S3 present-may be only abnormality
70
Q

Recognizing Acute Severe
Mitral Regurgitation
What causes it? 3
TEE for diagnosis

A
  1. Chordal or papilllary muscle rupture/tear
  2. Infarction with papillary muscle ischaemia or tear
  3. Infectious endocarditis with leaflet perforation
71
Q

WHat is of Aortic Stenosis

A

Left ventricular outflow obstruction

-LV systolic pressure > aortic pressure

72
Q

In aortic stenosis the LV systolic pressure is greater than in the aorta. WHat sustains this high blood pressure?

What does this eventually result in? 3

A
  1. Concentric left ventricular hypertrophy
    Sustains high LV pressures
    Normalizes wall stress (reduces stress by building muscle)
  2. Eventually results in impaired LV diastolic compliance
  3. LA hypertrophy and enlargement (pressure increases too)
  4. Severe stenosis: Limits ability to increase stroke volume on demand
73
Q

Aortic Stenosis: Etiology

A
  1. Congenital bicuspid aortic valve
  2. Rheumatic aortic valve disease
  3. Calcific (senile) aortic stenosis
74
Q
  1. Describe the onset of aortic stenosis.
  2. “Cardinal” symptoms of severe aortic stenosis? 3
  3. What is it the most common cause of?
  4. How does the LVH act in aortic stenosis?
  5. What kind of arrhythmias could you see? 3
A
  1. Long asymptomatic “latent” period
    • Dyspnea
    • Angina
    • Syncope
  3. Sudden death (most common cause)
  4. Left ventricular dilatation and contractile failure
  5. Arrhythmias
    - Ventricular tachycardia
    - Conduction system disease
    - Atrial fibrillation
75
Q

PP of Aortic Stenosis

  1. LVH leads to?
  2. Progressive left dilation and contractile failure leads to?
  3. Increased wall stress leads to?
A
  1. LVH → diastolic dysfunction
  2. Progressive LV dilation and contractile failure → systolic dysfunction
  3. Increased wall stress → increased myocardial O2 demand, exceeds ability to coronary flow to meet demand
76
Q

PP of Syncope in
Aortic Stenosis
What are the factors that cause syncopal episodes in aortic stenosis pts? 3

A
  1. Fixed cardiac output
  2. Heart block
  3. Ventricular arrhythmias (LVH)
77
Q

How does fixed output cause syncope in aortic stenosis?
3

How does a heart block cause syncope in aortic stenosis?

A
  1. Vasodilation (exercise, vagal stimulation, drug induced),
  2. inability to augment CO,
  3. drop in cerebral perfusion pressure.

Ca++ deposits in aortic ring encroach upon conduction tissue

78
Q 
Key Physical Findings in Severe
Aortic Stenosis:
1. Carotids? 
2. Heart?
3. Lungs?
4. Extremities?
A
  1. may hear transmitted murmur (bruits)
  2. SEM (systolic ejection murmur)
  3. Rales (Failure)
  4. Cold and decreased pulses
79
Q

Diagnostic Studies in Aortic Stenosis:

  1. EKG?
  2. Chest X-Ray?
  3. Echo?
  4. Doppler?
  5. Cath?
A
  1. LVH with repolarization changes “strain pattern”
  2. Aortic root dilation and failure
  3. Aortic valve thickening and restricted motion
  4. Gradient across aortic valve and aortic valve area can be estimated from increased flow velocity across aortic valve
  5. Measure gradient across aortic valve and calculate valve area (less than 1 cm is critical AS), also can look at coronaries
80
Q
  1. Whats the normal valve area?
  2. Circulation affected when valve area is reduced by how much?

State the valve area and gradient for the following levels of severity:

  1. Mild?
  2. Moderate?
  3. Severe?
A

Normal aortic valve area is 3.0 - 4.0 cm2

Circulation affected when valve area is reduced by ~ 75% (i.e. 0.75 - 1.0 cm2)

  1. > 1.5 less than 25 mm Hg
  2. 1.0 - 1.5 25 - 50
  3. less than 1.0 50
81
Q

Treatment of Aortic Stenosis

Mild to moderate that is asymptomatic? 2

Severe, symptomatic aortic stenosis (1 year survival 57%)?
1

Whats the survival rate on severe AS?

A
  1. Close follow up: History and physical exam, serial echocardiograms
  2. Endocarditis prophylaxis
  3. Aortic valve replacement with either mechanical or bioprosthetic valve
    - Ten year survival ~75%
82
Q

Aortic Valve Disease
problems?
4

A 
1. shortness of breath, swelling 
of abdomen
2. history of rheumatic fever
3. history of Laennec’s cirrhosis
4. congenital icthyosis
83
Q

What is aortic insufficiency?

A

Failure of the aortic vavle to close tightly causes back flow of blood into the left ventricle

84
Q

Major Causes of Aortic Regurgitation. 2 Categories?

A
  1. Leaflet Dysfunction

2. Aortic Root Dilation

85
Q

Leaflet dysfunction causes of aortic regurgitation?

10

A
  1. Rheumatic fever
  2. Endocarditis
  3. Trauma
  4. Bicuspid aortic valve
  5. Rheumatoid arthritis
  6. Myxomatous degeneration
  7. Ankylosing spondylitis
  8. Marfan’s syndrome
  9. Fenfluramine-phentermine
  10. Annulo-aortic ectasia
86
Q

Aortic root dilation causes of aortic regurgitation? 9

A
  1. Systemic hypertension
  2. Dissecting aneurysm
  3. Aortitis (syphilis)
  4. Reiter’s syndrome
  5. Ankylosing spondylitis
  6. Ehlers-Danlos
  7. Osteogenesis imperfecta
  8. Pseudoxanthoma elasticum
  9. Marfan’s syndrome
87
Q

Aortic Regurgitation
1. LV faces combined problems with what?

  1. Acute AR results in sudden increase in _______.
  2. What does this lead to? 2
A
  1. pressure and volume load
  2. LVEDP
  3. pulmonary edema and cardiogenic shock
88
Q

Acute Aortic Regurgitation:
Sudden diastolic volume overload without LV dilation leads to?
4

A
  1. Acute elevation in left ventricular diastolic pressure→
  2. pulmonary edema
  3. Acute LV systolic failure →
  4. hypotension
89
Q

How should we treat acute aortic regurgitation?

3

A

Provide

  1. inotropic support,
  2. vasodilator therapy if tolerated,
  3. urgent valve replacement.
90
Q

Pathophysiology of Chronic
Aortic Regurgitation:
1. Slowly progressive what?

  1. Augmented _____ ______ with rapid runoff
  2. Increased ______ pressure with low _________ pressure.
  3. HOw does this affect the pulse pressure?
  4. Progressive left ventricular _______, some hypertrophy
  5. Increased diastolic _______ with maintenance of normal ________ pressures initially
  6. Late systolic failure with reduced ______ _______ and ___.
A
  1. diastolic volume overload
  2. stroke volume
    • systolic
    • diastolic
  4. wide pulse pressure
  5. dilatation
    • compliance
    • diastolic
    • ejection fraction
    • CHF
91
Q
  1. HOw long may the latent phase of AR last?
  2. When do you see decompensation? 2
  3. Reversible or irreversible?
  4. What are the most important predictors of survival after surgery?
A
  1. Latent phase of AR, like AS, may last decades
  2. Decompensation when:
    - -LV systolic function begins to fail
    - -Progressive LV dilatation occurs
  3. Initially this is reversible
  4. LV systolic function and ESD
92
Q

Aortic Insufficiency
Symtpoms? 3

Vital signs indications? 1

A

Symptoms

  1. Angina, Palpitations, CHF symptoms
  2. Fatigue (poor CO)
  3. Poor exercise tolerance

Vital Signs
1. Wide pulse pressure (look at the cheat-cheat at the bottom)

93
Q
  1. What causes an increase in the systolic blood pressure in AI?
  2. Decrease in the diastolic?
A
  1. The force of systolic contraction during aortic insufficiency (AI) elevates the systolic blood pressure (SBP)
  2. the failure of the valve to close decreases the diastolic blood pressure (DBP)
94
Q

Physical Findings in Aortic Regurgitation

5

A
  1. Wide pulse pressure
  2. Bounding pulses
  3. Early diastolic murmur
  4. Systolic murmur at base (similar to aortic stenosis)
  5. Austin Flint murmur: mid to late diastolic “rumble” at apex
95
Q

Where will you hear the early diastolic murmur in AR?

2

A
  1. Upper RSB with root dilation

2. Mid to lower LSB with leaflet dysfunction

96
Q

Some Physical Findings in Severe Chronic Aortic Regurgitation
7

A
  1. deMusset’s sign: Head bob with each systolic pulsation
  2. Corrigans’s pulses: “Pistol shot” pulses over femoral artery
  3. Mueller’s sign: Pulsation of the uvula
  4. Duroziez’s sign: Systolic/diastolic bruit over femoral artery
  5. Quincke’s pulses: Capillary pulsations seen in the nailbeds
  6. Becker’s sign: Pulsation of retinal arteries and pupils
  7. Hill’s sign: Popliteal BP exceeds brachial BP by > 60 mmHg
97
Q

Natural History of Chronic
Aortic Regurgitation
1. Onset?
2. What kind of dysfunction? What does this cause?

  1. Symtpoms associated with this dysfunction? 4
    (two are common, two are rare)
A
  1. Long asymptomatic phase; may be decades long.
  2. Left ventricular systolic dysfunction ( decline in EF)
  3. Symptoms associated with LV dysfunction:
    - Exercise intolerance
    - Dyspnea on exertion
    - Angina (rare)
    - Sudden death (rare)
98
Q

How do we diagnose Aortic Regurgitation:

3 tests and what do they show?

A
  1. EKG – LAE, LVH
  2. Echo 2D/color doppler –test of choice
  3. Cardiac Cath – confirmatory; grades 1-4+ (like MR) as well. Also you see the coronaries.
99
Q

Management of Chronic
Aortic Regurgitation
4

A
  1. Close follow up of left ventricular size and function with serial echocardiograms
  2. Endocarditis prophylaxis
  3. Medical therapy
  4. Aortic valve replacement with mechanical or bioprosthetic valve (don’t wait till it’s too late)
100
Q

What kind of medical therapy for chronic aortic regurgitation?
4

A
  1. Vasodilator therapy: reduces blood pressure→reduces regurgitant fraction
  2. Digoxin (enhance systolic function)
  3. Diuretics (reduce LA pressure)
  4. Do NOT slow heart rate!
101
Q

How often should we do follow up with echocardiograms on:
Mild AR?
Severe AR?

A
  1. Every few years with mild AR, 2. every 6-12 months with severe AR)
102
Q

Valve Replacement Issues
1. Mechanical valve 2

  1. Bioprosthetic valve
  2. Homografts. What procedure?

Age, activity level, and compliance all come into play

4.________________ apparatus preservation with the mitral is important

A
  1. thromboembolism, bleed from anticoagulation (coumadin… the rest of your life)
  2. – limited durability with degeneration (back in 7-10 years)
  3. the Ross procedure
  4. Chordal/subvalvular
103
Q

Where would we hear systolic murmurs?

4

A
  1. Aortic stenosis
  2. Mitral insufficiency
  3. Mitral valve prolapse
  4. Tricuspid insufficiency
104
Q

Where would we hear diastolic murmurs?

2

A
  1. Aortic insufficiency

2. Mitral stenosis

105
Q

TR usually have what sided pathology?

A

left sided

Cardiology (19 decks)

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