Hemodynamics II Flashcards

1
Q

What does aortic stenosis mimic in its pathology?

A

Hypertensive heart disease

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2
Q

What are the 3 main causes of Aortic Stenosis?

A
  1. Congenital anomalous bicuspid valve
  2. Senile dgeneration
  3. Chronic rheumatic disease
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3
Q

What percent reduction in size of the valve is required before increase LV pressure is needed to push a normal stroke volume during systole?

A

50%

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4
Q

What is the result of Aortic stenosis?

A

Concentric Left ventricular hypertrophy with a reduction in compliance

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5
Q

What is the early pathology of the valve in Aortic stenosis?

A

Thickening with lipid deposition and inflmmation with macrophages and lymphocytes followed by fibrosis

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6
Q

What is the late pathology of the valve in aortic stenosis?

A

Nodular heaped up calcifications in the mid portion of each cusp protruding into the sinuses of the Valsalva

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7
Q

What are the symptoms of Aortic stenosis?

A
  1. Angina Pectoris (fr myocardial ischemia)
  2. Syncope
  3. Dyspnea
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8
Q

When do symptoms of calcific aortic stenosis usually occur?

A

With exertion

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9
Q

What are the signs of Aortic stenosis?

A
  1. Crescendo-Decrescendo systolic mumur
  2. Weak delayed pulse
  3. An atrial gallop
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10
Q

What does the onset of symptoms indicate?

A

High probability of death within 5 years

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11
Q

What is the treatment for Aortic stenosis?

A

Surgical valve replacement

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12
Q

What is Mitral regurgitation?

A

The ejection of a portion of the left ventricular stroke volume backward into the left Atrium due to incompetence of the Mitral valve

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13
Q

What subset of the population is most prone to mitral valve regurgitation?

A

There is an increase in incidence with age

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14
Q

What is the most common cause of Mitral regurgitation?

A

Mitral valve prolapse

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15
Q

What is the second most common cause of Mitral regurgitation?

A

Ischemic heart disease

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16
Q

What are the pathophysiological consequences of Mitral regurgitation?

A
  1. Reduced forward ejection fraction
  2. Increased left Atrial volume and pressure
  3. volume related stress on the left ventricle because the added left atrial volume gets returned to it
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17
Q

How can one determine if Mitral regurgitation is acute?

A

Left Atrial pressure is raised

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18
Q

What separates chronic from acute mitral regurgitation?

A

In chronic mitral regurgitation left atrial dilation allows it to hold extra volume with less elevated pressure

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19
Q

What causes Flash pulmonary edema?

A

Ruptured papillary muscle (due to MI or infective endocarditis) causes sudden mitral regurgitation the resulting increased left Atrial pressure transmitted backwards to pulmonary circulation causes rapid pulmonary congestion and edema

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20
Q

With the increased ejection fraction to the L atrium in acute mitral regurgitation what is the symptom?

A

Dyspnea

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21
Q

What is the symptom with CHRONIC mitral regurgitation?

A

Fatigue

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22
Q

What is the sign of Mitral regurgitation?

A

An apical holosystolic (pansystolic) murmur which sometimes has a harsh quality

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23
Q

What may also be present in severe chronic Mitral regurgitation

A

A ventricular gallop

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24
Q

What happens to end diastolic volume in cases of chronic Mitral regurgitation?

A

The end diastolic volume increases to accommodate for what is loss to back flow into the L Atrium

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25
Q

What is decompensation related to Mitral regurgitation?

A

The drop in end distolic volume and stroke volume and left atrial pressure.(change from all being very high to very low if mitral regurge is survived long enough)

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26
Q

What is decompensation associated with?

A

The onset of symptoms.

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27
Q

What drug class is very helpful with chronic Mitral regurgitation?

A

ACE inhibitors

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28
Q

What percent reduction of the normal forward stoke volume of 100ml is associated with the clinical symptoms of heart failure?

A

25% reduction to 75ml

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29
Q

What is Mitral valve prolapse?

A

A billowing / balloning of the mitral valve into the left Atrium during systole

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30
Q

What is the incidence of Mitral valve prolapse in the united states?

A

It is the most common valvular disease with a slight female predominance.

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31
Q

With what connective tissue disease is MVP associated?

A

Marfan’s syndrome and Ehlers-Danlos

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32
Q

What is the state of the chordae tendinae in MVP?

A

Can be attenuated, elongated, and vulnerable to rupture.

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33
Q

What is the microscopic pathology in MVP?

A

Degeneration and attenuation of the outer zona fibrosa of the valve and expansion of the inner zona spongiosa with myxomatous tissue

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34
Q

What are the symptoms of MVP

A

Usually asymptomatic but patients may experience chest pain or palpitation due to associated arrhythmias

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35
Q

What are the signs of MVP?

A

A mid systolic CLICK as well as a late systolic mumur

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36
Q

How is MVP diagnosed?

A

By physical exam

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37
Q

How is a diagnosis of MVP confirmed

A

Via echocardiography

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38
Q

Complications are common with MVP true or false?

A

False

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39
Q

What are some rare but possible complications of MVP?

A
  1. Regurgitation (most common)
  2. Endocarditis (rare)
  3. Rupture of Chordae
40
Q

What is Rheumatic heart disease?

A

An inflammation of the endocardium, myocardium, and epicardium following group A beta-hemolytic strepyococcal pharyngitis

41
Q

What is the criteria used for diagnosing Rheumatic heart disease?

A

Jones criteria

42
Q

What subset of the population is most affected by Rheumatic fever?

A

Children, 2-3 weeks after strep throat

43
Q

What is the cause of Rheumatic heart disease?

A

Caused by molecular mimicry; bacterial M protein resembles proteins in human tissue (heart antigens)

44
Q

What does the gross pathology of Rheumatic heart disease look like?

A

Tiny (1-2mm) verrucous (wartlike) vegetations lined up on the line of valve closure along with fibrinous pericarditis

45
Q

What is the microscopic pathology of Rheumatic fever

A
  1. Fibrin &
  2. Platelet thrombi on valves
  3. Aschoff bodies which are foci of fibrinoid necrosis with histocytes and Anitschkow cells
46
Q

What are the signs of acute rheumatic heart disease?

A

Various systolic and diastolic murmurs and a pericardial friction rub.

47
Q

What is the treatment for acute Rheumatic heart disease?

A

Asprin, penecillin and supportive care

48
Q

What is the most likely progression from acute Rheumatic fever?

A
  1. Mitral Stenosis

2. Aortic regurgitation and stenosis 25%

49
Q

What are the causes of Chronic Rheumaatic heart disease?

A
  1. Recurrent carditis
  2. Severe carditis
  3. Carditis at an early age
50
Q

What is the pathology of rheumatic mitral stenosis?

A
  1. A slitlike fishmouth or round buttonhole stenosis with fibrous thickening and rgidity of valves with or without calcification.
  2. There is a fusion of commissures, along with thickening, retraction and fusion of chordae and sometimes MacCallum patches
51
Q

What are the common complications of Mitral stenosis?

A
  1. L Atrial hypertension
  2. L Atrial dilation
  3. Atrial fibrillation
  4. L Atrial thrombus formation
  5. Pulmonary Hypertension
  6. R Ventricular hypertrophy
  7. Right heart failure
52
Q

What are MacCallum patches?

A

Maplike areas of atrial endocardial thickening and fibrosis usually seen in chronic rheumatic heart disease mitral stenosis.

53
Q

What are the possible cause of Aortic regurgitation?

A
  1. insufficiency of a congenitally anomalous bicuspid valve
  2. Endocarditis (inflammation)
  3. Chronic Rheumatic valve deformation
54
Q

WHat medical emergency can also cause Aortic regugitation?

A

Dilation of the aortic valve ring can occur by aortic aneurysm or dissection

55
Q

What are the complications of Acute Aortic regurgitation?

A
  1. Increased diastolic L ventricular pressure
  2. Increased Left Atrial pressure
  3. Pulmonary congestion and edema manifested by dyspnea
56
Q

If Aortic regurgitation is severe what is the best therapy?

A

Surgical valve replacement

57
Q

What is the effect of Chronic Aortic regurgitation?

A

Causes dilation of the L ventricle with increased muscle mass yielding increased compliance and less elevated left ventricular diastolic pressure.

58
Q

What happens to volumes and pressure in Chronic Aortic regurgitation?

A

Stroke volume increases to compensate for the volume of blood flowing back into the L Ventricle. End diastolic pressure would rise slightly.

59
Q

What are the symptoms of decompensated aortic regurgitation?

A
  1. Fatigue
  2. Decreased excercise tolerance
  3. Dyspnea
60
Q

What are the signs of Aortic regurgitation?

A
  1. Diastolic decrescendo some times with a blowing quality
  2. A hyperdynamic bounding
  3. Rapidly collapsing pulse (Corrigan pulse)
  4. Head Bobbing with each pulse (de Musset sign)
61
Q

What is characteristic of Aortic regurgitation?

A

A wide pulse pressure due to increased systolic and decreased diastolic pressure from the abnormally large amount of blood ejected into the Aorta in systole and back leak into the left ventricle in diastole

62
Q

WHat is the treatment for symptomatic Aortic regurgitation?

A

Aortic valve replacement

63
Q

What kind of therapy is required for patients who have undergone valve replacement?

A

Lifelong anticoagulant therapy

64
Q

What is Libman-Sacks endocarditis?

A

An autoimmune inflammation of heart valves that occurs as part of SLE

65
Q

What does Libman-Sacks endocarditis usually occur with?

A

Pericarditis

66
Q

What is the Gross pathology of Libman-Sacks endocarditis?

A

Small to medium verrucous, berrylike or flat vegetations, commonly on multiple valves, most commonly mitral and tricuspid on either or both sides

67
Q

What is the microscopic pathology of Libman-Sacks endocarditis?

A

Necrotic debris fibrinoid material, degenerating leukocytes, fibroblasts and hema

68
Q

What is marantic endocarditis?

A

A common non-bacterial thrombotic endocarditis

69
Q

What disease predisposes about 75% of its patients to marantic endocarditis?

A

Malignant tumors especially adenocarcinomas especially mucinous adenocarcinomas and also patients with DIC, chronic sepsis and Swan Ganz right heart Catherization

70
Q

What is the pathology of Marantic endocarditis?

A

small (1-5mm) fibrin and platelet thrombi, most commonly on the atrial side of the mitral valve, usually on the line of the valve closure

71
Q

Where is the second most common site of the fibrin and platelet thrombi in marantic endocarditis?

A

The ventricular side of the Aortic valve

72
Q

Why do the fibrin and platelet thrombi form at those two sites?

A

Due to the high resting pressure on those 2 valves

73
Q

What are the complications of marantic endocarditis?

A
  1. Systemic Emboli (Kidneys, spleen, brain, gut and heart)

2. Infection

74
Q

What subset of patients does Infective endocarditis generally affect?

A

Adults

75
Q

What areas of the heart does nfective endocarditis generally affect?

A

The valves rather than the endocardium

76
Q

What is the pathogenisis of infective endocarditis?

A
  1. Valvular endothelial injury
  2. Platelet and Fibrin deposition
  3. Microbial seeding
  4. Microbial multiplication
77
Q

What are the appropriate therapies for infective endocarditis?

A

IV antibiotics and/or surgery

78
Q

What are the 2 types of infective endocarditis?

A
  1. Acute Bacterial
  2. Subacute Bacterial
    - Native Valve
    - Prosthetic valve
79
Q

What organism is generally responsible for acute bacterial endocarditis?

A

Highly virulent such as Staph aureus

80
Q

What organisms are generally responsible for Sub-acute bacterial endocarditis?

A

Viridians Streptococci

81
Q

What side of the heart is most likely to be affected by infective endocarditis?

A

The Left side 75%

82
Q

What valve is most likely to be affected by infective endocarditis?

A

Mitral valve

83
Q

What valve is least likely to be affected by infective endocarditis?

A

Pulmonic

84
Q

What microorganism is most likely to cause PVE prosthetic valve Endocarditis (common in IV drug users)?

A

Coagulase negative Staph epidermis which is rare in NVE

85
Q

What type of infective endocarditis is most common in IV drug users?

A

Acute and commonly on the Tricuspid valve

86
Q

What do the majority of patients with infective endocarditis have?

A

A predisposing heart disease such as MVP, congenital disease, prosthetic valve, degenerative disease, rheumatic fever or previous endocarditis

87
Q

What are some of the portals of entry for organisms causing infective endocarditis

A

Central venous caterterization, dental procedures, gingivitis, endoscopy, shaving etc

88
Q

What makes a bug suitable for causing infective endocarditis?

A

Ability to adhere to blood clot

89
Q

What substance is known to facilitate adherence of organisms to blood clots

A

Dextran (a cell wall component) prominent id Strep mutans

90
Q

Which micro organisms are more prominent in infective endocarditis in rural settings?

A

Viridians Strep

91
Q

What is the pathology of infective endocarditis?

A

Large (up to 3cm) friable vegetations that are some combination of tan, grey, red or brown located on the line of valve closure

92
Q

What are the consequences of infective vegetations on tissue?

A

Destructive, may cause perforation of a valve, adjacent abscess, fibrotic scarring and calcification.`

93
Q

What is the microscopic pathology of infective endocarditis vegetations?

A
  1. Fibrin
  2. Platelets
  3. Masses of organisms sometimes with necrosis and neutrophils
94
Q

What is the most common symptom of infective endocarditis?

A

Fever experienced by 80% of patients

95
Q

What are the common physical signs of infective endocarditis??

A
  1. Fever
  2. Heart mumur
  3. Splenomegaly
  4. Petechiae
96
Q

What are the common laboratory findings in infective endocarditis?

A
  1. Elevated ESR (mean 57 mm/hr)
  2. Circulating immune complexes
  3. Anemia
  4. Proteinuria
97
Q

How does one make a diagnosis of infective endocarditis?

A
  1. Continuos low grade bacteremia

2. Transthoracic echocardiograph but Transesophageal echocardiography has >90%