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Cardiorespiratory > Lecture 20: Va;vular Heart Disease > Flashcards

Lecture 20: Va;vular Heart Disease Flashcards

1
Q

what are the valvular heart diseases?

A

Valvular heart diseases can take the form of stenosis, insufficiency (regurgitation), or a combination of the two. These defects are typically acquired as the result of infections, underlying heart disease, or degenerative processes. However, certain congenital conditions can also cause valvular heart diseases. Acquired defects are found primarily in the left heart as a result of higher pressure and mechanical strain on the left ventricle. The type of valvular disease determines the type of cardiac stress and subsequent symptoms. Valvular stenosis leads to a greater pressure load and concentric hypertrophy, while insufficiencies are characterized by volume overload and an eccentric hypertrophy of the preceding heart cavities

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2
Q

what is the concentric hypertrophy?

A

Cardiac remodeling that occurs due to pressure overload and results in increased left ventricular wall thickness. Characterized by sarcomeres duplicating in parallel.

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3
Q

what is the eccentric hypertrophy?

A

A type of cardiac remodeling associated with dilated cardiomyopathy in which sarcomeres duplicate in series, causing muscle fibers to increase in length and width.

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4
Q

how valvular heart diseases are classified?

A
  • -according to
    1) valve involved
  • -Mitral
  • -Tricuspid
  • -Aortic
  • -Pulmonary
    2) nature of lesion
  • -Stenosis – valve opening is narrowed (blood flow through valve is restricted)
  • -Regurgitation – valve is leaking (blood flows in opposite direction to normal flow)
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5
Q

congenital vs acquired valvular heart diseases?

A

1)Congenital
–Heart valve malformation/dysplasia (Bicuspid aortic valve)
–Tetralogy of Fallot
–Ebstein’s anomaly of TV
2)Acquired
–Rheumatic
–Degenerative
–Age related
–Myxomatous change
–Radiation
Rheumatological disorders

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6
Q

what is the rheumatic heart disease (RHD)?

A

A condition of cardiac inflammation and scarring due to an autoimmune reaction following Group A streptococcal infection (i.e., rheumatic fever). More common in children 5–15 years of age and in underdeveloped areas with minimal access to antibiotics. Acutely manifests with pancarditis; chronically, it causes valvular heart disease (e.g. stenosis and/or regurgitation). Most frequently causes mitral and/or aortic valvular dysfunction.

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7
Q

what is the pathophysiology of rheumatic fever?

A

Most commonly accepted mechanism : Group A β-hemolytic streptococcus (Streptococcus pyogenes) (GAS): acute tonsillitis or pharyngitis (“strep throat”) without antibiotic treatment → antibodies develop against streptococcal M protein → cross-reaction of antibodies with nerve and myocardial proteins due to molecular mimicry → type II hypersensitivity reaction → acute inflammatory sequela
Rheumatic fever is not associated with streptococcal skin infections (e.g., erysipelas, impetigo, cellulitis).

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8
Q

does RF develop after streptococcal skin infection?

A

GAS infections of the skin tend to be complicated by poststreptococcal glomerulonephritis rather than rheumatic fever.

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9
Q

how many days after infection does RF develop?

A

2–4 weeks of acute infection

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10
Q

clinical features of acute RF?

A

The symptoms of acute rheumatic fever can be remembered with the JONES criteria, written with a heart-shaped O : J = Joints, ♥ = Pancarditis, N = Nodules, E = Erythema marginatum, S = Sydenham chorea

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11
Q

what are the heart manifestations of acute RF?

A

1) Pancarditis (endocarditis, myocarditis, and pericarditis)
2) Valvular lesions
- –Mitral valve (∼ 65% of cases)
- -Early mitral regurgitation or prolapse
- -Late mitral stenosis: Rheumatic fever is the most frequent cause of mitral stenosis.
- -Mixed mitral stenosis/regurgitation also possible
- –Aortic valve (∼ 25% of cases)
- -Aortic regurgitation
- -Aortic stenosis
- –Tricuspid valve (∼ 10% of cases)
3) Dilated cardiomyopathy due to severe valvular disease, myocarditis

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12
Q

what are the 2 most common valves involved in RF?

A

MV then AV

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13
Q

what is the Jones criteria?

A

Evidence of previous infection with streptococcal upper airway infection and 2 major criteria or 1 major criteria and 2 minor criteria

  • -Major
    1) Polyarthritis
    2) Carditis
    3) Sydenham’s chorea
    4) Erythema marginatum
    5) Subcutaneous nodules
  • -Minor
    1) Fever
    2) Arthralgia
    3) Elevated c-reactive protein or Erythrocyte sedimentation rate
    4) Prolonged PR interval on ECG
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14
Q

what is the most common clinical manifestation of RF?

A
  • -Arthritis
  • -Most common feature: present in 80% of patients
  • -Painful, migratory, short duration,
  • -Usually,>5 joints affected and large joints
  • -Preferred (Knees, ankles, wrists, elbows)
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15
Q

what are the preferred joints in RF?

A

Knees, ankles, wrists, elbows

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16
Q

what is the most serious clinical manifestation of RF?

A
  • -Carditis
  • -Most serious manifestation
  • -May lead to death in acute phase or at later stage
  • -Any cardiac tissue may be affected
  • -Valvular lesion most common: mitral and aortic
  • -Seldom see isolated pericarditis or myocarditis
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17
Q

what is Sydenham’s chorea?

A
  • -Extrapyramidal disorder
  • -Fast, clonic, involuntary movements, Muscular hypotonus, Emotional lability
  • -Usually a late manifestation: months after infection
    • Streptococcal antigens lead to antibody production → antibodies cross-react with structures of the basal ganglia (particularly the striatum) and cortical structures → reversible dysfunction of cortical and striatal circuits
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18
Q

what is the erythema marginatum?

A
  • -Present in 7% of patients
  • -Highly specific to ARF
  • -Cutaneous lesion:
  • -Reddish pink border, pale center, round or irregular shape, often on trunk or abdomen
  • -Location: The trunk and limbs are affected; the face is spared. May rapidly appear and disappear at different locations.
  • -Painless and nonpruritic
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19
Q

name skin manifestation of ARF except for erythema marginatum

A
  • -Firm, non-tender, isolated or in clusters
  • -Most common: along extensor surfaces of joints (Knees, elbows, wrists)
  • -Last a few days only
  • -Occur in 9 - 20% of cases
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20
Q

what is the aortic stenosis?

A

A valvular disease characterized by narrowing of the aortic valve, resulting in obstruction of the outflow of blood from the left ventricle into the aorta during systole.

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21
Q

what are the types of aortic stenosis?

A
  • -Valvular: most common
  • -Supravalvular
  • -Subvalvular
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22
Q

what is the most common valvular lesion in the elderly?

A

aortic stenosis

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23
Q

aortic stenosis severity is defined according to…

A
  • -Size of valve area
  • -Velocity ratio
  • -Pressure gradient across the valve
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24
Q

what is the epidemiology of aortic stenosis?

A
  • -Prevalence of critical aortic stenosis (Helsinki Aging Study)
  • -1-2% in 75-76 yr old
  • -6% in 86 yr old
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25
Q

most patients with AS are symptomatic.T/F

A

False

  • -Most of these patients are asymptomatic. Only 3.4% of individuals ≥ 75 years have severe aortic stenosis, which is typically symptomatic.
  • -Symptoms usually present when the valve area is < 1 cm2 (normal 3–4 cm2) and when the pressure gradient across the stenotic valve is > 40–50 mm Hg.
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26
Q

what are the causes of aortic stenosis?

A
  • -Degenerative calcification of tricuspid valve
  • -Rheumatic heart disease
  • -Congenital calcification of bicuspid valve
  • -Radiation
  • -CTD connective tissue disorder
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27
Q

what are the risk factors of AS?

A
  • -Congenital valve abnormality
  • -Atherosclerosis
  • -Genetic factors
  • -Hypercholesterolaemia
  • -End-stage renal disease
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28
Q

what is the pathophysiology of AS?

A

1) Narrowed opening area of the aortic valve during systole → obstruction of blood flow from left ventricle (LV) → increased LV pressure → left ventricular concentric hypertrophy →
- -Increased LV oxygen demand
- -Impaired ventricular filling during diastole → left heart failure
- -Reduced coronary flow reserve
2) Initially, cardiac output (CO) can be maintained. Later, the decreased distensibility of the left ventricle reduces cardiac output and may then cause backflow into the pulmonary veins and capillaries → higher afterload (pulmonic pressure) on the right heart → right heart failure (see congestive heart failure)

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29
Q

why coronary blood supply to the ventricles is reduced in AS?

A

Impaired ventricular filling during diastole results in a reduced stroke volume; compensatory tachycardia maintains cardiac output but tachycardia is associated with a shortened diastole, thereby reducing the coronary filling time. The hypertrophic LV also compresses the coronary arteries, further reducing the coronary reserve.

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30
Q

what are the common presenting symptoms of AS?

A
  • -Dyspnoea on exertion or decreased exercise tolerance
  • -Exertional dizziness and pre syncope
  • -Exertional angina (Remember mnemonic SAD –Syncope/angina/dyspnoea)
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31
Q

what are the end-stage symptoms of AS?

A
  • -Heart failure
  • -Syncope
  • -Angina
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32
Q

what are the cardiac exam signs of AS?

A
  • -Slow rising pulse – “parvus and tardus”
  • -Apex beat sustained and later in disease displaced
  • -Palpable systolic thrill
  • -S2 soft, Split S2, S4
  • -Early disease – ejection click
  • -Murmur becomes softer as condition progresses due to LV dysfunction-low flow low grade AS
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33
Q

pulse pressure is decreased in AS. T/F

A

True

  • -Small blood pressure amplitude, decreased pulse pressure
  • -increased in AR
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34
Q

describe the murmur of AS

A
  • -Harsh crescendo-decrescendo (diamond-shaped), late systolic ejection murmur that radiates bilaterally to the carotids
  • -Best heard in the 2nd right intercostal space
  • -Hand grip decreases the intensity of the murmur. (Due to increased afterload)
  • -Valsalva and standing from squatting (Decreases preload) decreases or does not change the intensity of the murmur (in contrast to hypertrophic cardiomyopathy) –Loudest on expiration and with leaning forward
  • -Radiating to carotids and apex but not axilla
  • -Accentuated by expiration
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35
Q

leat peaking AS murmur is associated with mild isease.T/F

A

False

  • -Early peaking – mild to moderate AS
  • -Late peaking – severe AS
36
Q

what happens to heart sounds in AS?

A
  • -Soft S2 (S2 is the sound of the aortic and pulmonary valves closing. S2 is softer because the aortic component is delayed, as well as reduced mobility of the aortic valve.)
  • -S4 is best heard at the apex (This is due to decreased compliance of the LV due to LVH)
  • -Early systolic ejection click (The click results from the abrupt stop of the valve leaflets upon opening.)
37
Q

what are the complications of AS?

A
  • -Sudden cardiac death
  • -Arrhythmias
  • -Endocarditis
  • -Heart failure-systolic and diastolic
  • -Associated with calcific coronary disease
  • -Aortic aneursyms
38
Q

what arrhythmias are common in AS?

A
  • -Atrial fibrillation (AF), which is uncommon in isolated AS, often accompanies HF
  • -Ventricular premature beats (VPBs) and nonsustained ventricular tachycardia (NSVT) are common in patients with aortic stenosis
39
Q

what is the Aortic regurgitation (AR)?

A

A valvular disease characterized by incomplete closure of the aortic valve, causing reflux of blood from the aorta into the left ventricle during diastole. On auscultation, characterized by S3 and a high-pitched, decrescendo, early diastolic murmur.

40
Q

what are the causes of AR?

A

1) Chronic
- -Aortic root dilatation
- -Congenital bicuspid valve
- -Rheumatic heart disease
2) Acute
- -Endocarditis
- -Aortic dissection
- -Ruptured cusp
- -Traumatic injury
- -Failed repair

41
Q

what are the symptoms of AR?

A

1) Palpitations
2) Atypical chest pain
3) Symptoms of left-sided heart failure
- -Dyspnoea
- -Orthopnoea
- -Paroxysmal nocturnal dyspnoea

42
Q

what are the cardiac examination signs of AR?

A
  • -Wide pulse pressure
  • -“Waterhammer” pulse/Corrigan pulse
  • -Inferior and lateral displacement of apex beat
  • -Soft S1, variable S2, S3
43
Q

describe the murmur of AR

A

1)High-pitched, blowing, decrescendo early diastolic murmur
–AR due to valvular disease: best heard in the left third and fourth intercostal spaces and along the left sternal border (Erb point)
–AR due to aortic root disease (e.g., aortic dissection): best heard along the right sternal border
Worsens with squatting and handgrip
2)Austin Flint murmur (Rumbling, low-pitched mid-diastolic or presystolic murmur best heard at the apex. It is caused by the regurgitant blood striking the anterior leaflet of the mitral valve, which leads to premature closure of the mitral leaflets.)
3)In more severe stages, possibly a harsh, crescendo-decrescendo mid-systolic murmur that resembles the ejection murmur heard in aortic stenosis

44
Q

S3 or S4 is heard in AR?

A

3 due to volume overload (remember S4 is due to pressure overload: AS,HTN)

45
Q

what happens to pulse pressure in AR?

A
  • -High pulse pressure
  • -Water hammer pulse of peripheral arteries characterized by rapid upstroke and downstroke
  • -Pulsing of carotid arteries with rapid upstroke and downstroke
  • -Visible capillary pulse (Quincke sign)
  • -Nodding of the head with each pulse
46
Q

eccentric or concentric hypertrophy of LV is seen with AR?

A

eccentric

Point of maximal impulse (PMI): displaced inferolaterally, diffuse, and hyperdynamic

47
Q

what re the clinical features of acute AR?

A
  • -Sudden, severe dyspnea
  • -Rapid cardiac decompensation secondary to heart failure
  • -Pulmonary edema
  • -Symptoms related to underlying disease (e.g., fever due to endocarditis, chest pain due to aortic dissection)
48
Q

what re the clinical features of chronic AR?

A

1) May be asymptomatic for up to decades despite progressive LV dilation
2) Palpitations
3) Symptoms of left heart failure
- -Exertional dyspnea
- -Angina
- -Orthopnea
- -Easy fatigability
- -Syncope
4) Symptoms of high pulse pressure (e.g., head pounding, rhythmic nodding, or bobbing of the head in synchrony with heartbeats- de Musset sign)

49
Q

pathophysiology of acute vs chronic AR?

A

1) Acute AR
- -Because LV cannot sufficiently dilate in response to regurgitant blood, LV end-diastolic pressure increases rapidly → pressure transmits backwards into pulmonary circulation → pulmonary edema and dyspnea
- -Decreased cardiac output if severe → cardiogenic shock and myocardial ischemia
2) Chronic AR
- -Initially, a compensatory increase in stroke volume can maintain adequate cardiac output despite regurgitation (compensated heart failure)
- -Over time, increased left ventricular end-diastolic volume → LV enlargement and eccentric hypertrophy of myocardium → left ventricular systolic dysfunction → decompensated heart failure

50
Q

what is the Mitral regurgitation (MR)?

A
  • -A valvular disease characterized by leakage of blood from the left ventricle into the left atrium due to incomplete closure of the mitral valve during systole.
  • -can arise from abnormalities of any part of the mitral valve apparatus including the valve leaflets, annulus, chordae tendineae, and papillary muscles
51
Q

what are the causes of MR?

A
  • -Mitral valve prolapse-degenerative
  • -Infective endocarditis
  • -LV dysfunction with annular dilatation
  • -Rheumatic
  • -Hypertrophic cardiomyopathy
52
Q

what are the signs and symptoms of MR?

A

1) Asymptomatic
2) Left heart failure (usually LVEF is normal till late in disease)
- -Dysnoea
- -Orthopnoea
- -Paroxysmal dyspnoea
3) Pulmonary hypertension
4) Atrial fibrillation
- -Palpitations
- -Embolic phenomena

53
Q

what are the cardiac examination signs of MR?

A

1) Soft S1, Splitting of S2, S3 gallop
2) Murmur
- -Pansystolic
- -Heard best over apex
- -Radiates to axilla
3) Mitral valve prolapse
- -Mid systolic click
- -Late systolic murmur

54
Q

escribe the MR murmur

A
  • -Holosystolic murmur
  • -Radiates to the left axilla and heard loudest over the apex (5th ICS at the left mid-clavicular line)
  • -Intensity increases with increased systemic vascular resistance (hand grip, squatting)
55
Q

primary vs secondary MR?

A

1) Primary MR
- -Degenerative mitral valve disease (mitral valve prolapse, mitral annular calcification, ruptured chordae tendineae)
- -Rheumatic fever
- -Infective endocarditis
2) Secondary (functional) MR
- -Coronary artery disease, prior myocardial infarction causing papillary muscle involvement
- -Dilated cardiomyopathy and left-sided heart failure

56
Q

what is the pathophysiology of MR?

A
  • -Acute MR → ↑ LV end-diastolic volume → rapid ↑ LA and pulmonary pressure → pulmonary venous congestion → pulmonary edema
  • -Chronic (compensated) MR: progressive dilation of the LV (via eccentric hypertrophy) → ↑ volume capacity of the LV (preload and afterload return to normal values) → ↑ end-diastolic volume → maintains ↑ stroke volume (normal EF)
  • -Chronic (decompensated) MR: progressive LV enlargement and myocardial dysfunction → ↓ stroke volume → ↑ end-systolic and end-diastolic volume → ↑ LV and LA pressure → pulmonary congestion, possible acute pulmonary edema, pulmonary hypertension, and right heart strain
57
Q

what are the clinical features of acute vs chronic MR?

A

1) Acute mitral regurgitation
- -Symptoms of left-sided heart failure
- -Signs and symptoms of pulmonary edema
- -Cardiogenic shock
2) Chronic mitral regurgitation: late onset of symptoms
- -(Exertional) dyspnea, dry cough
- -Palpitations
- -Symptoms of left-sided heart failure

58
Q

what is the P mitrale?

A

An electrocardiographic sign of left atrial enlargement (e.g., due to mitral stenosis). Characterized by a biphasic (i.e., “double-humped”) P wave and/or prolongation of the P > 0.10 s (i.e., a wide P wave).

59
Q

what is the mitral stenosis?

A

A valvular disease characterized by obstruction of blood flow from the left atrium into the left ventricle during diastole.

60
Q

what are the causes of MS?

A
  • -Most commonly due to rheumatic fever
  • -Autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis
  • -Congenital
  • -Some conditions may mimic mitral stenosis: bacterial endocarditis of the mitral valve with large vegetation, left atrial myxoma
61
Q

what are the symptoms of MS?

A
  • -Asymptomatic
  • -Dyspnoea
  • -Haemoptysis
  • -Symptoms related to atrial fibrillation/embolic event
  • -Symptoms of pulmonary hypertension and right-sided heart failure
62
Q

what is the pathophysiology of MS?

A
  • -Mitral valve stenosis → obstruction of blood flow into the left ventricle (LV) → limited diastolic filling of the LV (↓ end-diastolic LV volume) → decreased stroke volume → decreased cardiac output (forward heart failure)
  • -Mitral valve stenosis → increase in left atrial pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema → pulmonary hypertension → backward heart failure and right ventricular hypertrophy
63
Q

what are the cardiac examination signs of MS?

A
  • -Low volume pulse
  • -Mitral facies-malar flush
  • -Raised JVP
  • -S1 initially loud then later soft
  • -Loud P2
  • -Opening snap
  • -Diastolic murmur
64
Q

describe the murmur of MS

A

1) Diastolic murmur typically heard best at the 5th left intercostal space at the mid-clavicular line (the apex)
- -Heard loudest when the patient is lying on his/her left side.
2) Loud first heart sound (S1)
3) Opening snap of the mitral valve after S2: A high-frequency, early-to-mid diastolic sound that occurs when leaflet motion suddenly stops during diastole after the stenosed valve has reached its maximum opening
- -Shorter interval between S2 and opening snap indicative of more severe disease, because left atrial pressure is greater than left ventricular end diastolic pressure (LVEDP)

65
Q

examples of right-sided valvular heart diseases?

A

1) Most conditions congenital
2) Tricuspid stenosis
- -Most common cause rheumatic heart disease and carcinoid syndrome
- -Fatigue, dyspnoea ascites, and fluid retention
3) Tricuspid regurgitation
- -Causes pulmonary hypertension or right heart dilatation
- -Endocarditis – IVDU or right heart catheters
4) Pulmonary stenosis
- -Congenital in 95%, rarely carcinoid syndrome
5) Pulmonary regurgitation
- -Significant regurgitation is rare, usually preceded by pulmonary valve intervention in childhood or endocarditis

66
Q

what are the most common causes of tricuspid stenosis?

A

Most common cause rheumatic heart disease and carcinoid syndrome

67
Q

what investigations should be performed in suspected VHDs?

A
  • -ECG
  • -ECHO
  • -Chest x-ray
  • -Cardiac catheterization
  • -TEE-2d and 3d
  • -Cardiac MRI
68
Q

what is the management of VHDs?

A

1) Prophylaxis for endocarditis
2) Treat with progressive deterioration and symptoms
- -Valve repair or replacement
- -Mechanical or tissue
3) Treat complications
4) Address risk factors

69
Q

what is the Infective endocarditis?

A

1) Febrile illness with persistent bacteremia
- -Even if apyrexial
2) Characteristic lesion: Vegetation = microbial infection of the endothelial surface of the heart:
- -Variable in size
- -Amorphous mass of fibrin & platelets
- -Abundant organisms
- -Few inflammatory cells

70
Q

what are the types of IE?

A
  • -Community acquired
  • -Post op surgery
  • -Hospital acquired
  • -Right sided endocarditis
  • -Culture negative
71
Q

list common etiologic agents of IE?

A

1) Streptococci
- -Alpha-hemolytic–Most common
- -Beta-hemolyti –Uncommon
- -Enterococci –Rare
- -Pneumococci–Rare
2) Staphylococci
- -S. aureus–Second most common
- -Coagulase negative–Uncommon, but increasing
3) Gram-Negatives–All Rare
- -Enterics, Pseudomonas species, Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella, Neisseria species
4) Fungi
- -Candida species –Uncommon

72
Q

acute vs subacute IE?

A

1) Acute Bacterial Endocarditis (ABE)
- -Fulminant and severe course
- -Death is not infrequent
- -Organisms: Staphylococcus aureus, Streptococcus pyogenes
2) Subacute Bacterial Endocarditis (SBE)
- -Indolent, slower and less severe course over months
- -Organisms: Streptococcus viridans
- -Streptococcus Viridans is the most common causative organism in native valves!

73
Q

what are the predisposing factors of Native Valve Endocarditis?

A

1)55 - 75% of patients with Native Valve Endocarditis (NVE) have underlying valve abnormalities
–Congenital
–Rheumatic
–Mitral Valve Prolapse
2)Mitral Valve Prolapse – possible predisposing factor
–High prevalence in the population
–2% (new stricter criteria)
–Accounts for 7 – 30% NVE in cases not related to drug abuse or nosocomial infection
3)Rheumatic Heart Disease
–20 – 25% of cases of IE in 1970’s & the ’80s
–7–18% of cases in recently reported series
Mitral site most common “always affected”
4)Congenital Heart Disease
–10 % of cases in young adults
– 8% of cases in older adults
–PDA, VSD, bicuspid aortic valve (esp. in men>60)

74
Q

what is the role of drug abuse in Native valve endocarditis

A

1) Risk is 2 – 5% per patient / year
2) The tendency to involve right-sided valves
- -Distribution in clinical series
- -46 – 78% tricuspid
- -24 – 32% mitral
- - 8 – 19% aortic
3) Underlying valve normal in 75 – 93%
4) S. aureus predominant organism in IVDU

75
Q

what is the most common organism causing IE in IVDUs?

A

S. aureus

76
Q

what are the causes of prosthetic valve endocarditis?

A

–Prosthetic Valve Endocarditis (PVE)
–10 – 30% of all cases in developed nations
–Cumulative incidence
1)1.4 – 3.1% at 12 months
2)3.2 – 5.7% at 5 years
–Early PVE – within 60 days
Nosocomial (S. epidermis predominates)
–Late PVE – after 60 days
Community (same organisms as NVE)

77
Q

early vs late PVE?

A

–Early PVE – within 60 days
Nosocomial (S. epidermis predominates)
–Late PVE – after 60 days
Community (same organisms as NVE)

78
Q

what is the pathophysiology of IE?

A

1) Direct
- -Constitutional symptoms of infection (cytokine)
2) Indirect
- -Local destructive effects of infection
- -Embolization – septic or bland
- -Hematogenous seeding of infection: N.B. may present as local infection or persistent fever, metastatic abscesses may be small, miliary
- -Immune response: Immune complex or complement-mediated

79
Q

what are the clinical features of IE?

A

1) Interval between index bacteremia & onset of symptoms usually < 2 weeks
2) Fever most common sign
3) Murmur present in 80 – 85%
- -Generally indication of the underlying lesion
- -Changing murmur
4) Peripheral Manifestations
- -Less common today
- -Not seen in tricuspid endocarditis ie lung manifestation
5) Systemic Emboli
- -The incidence decreases with effective anti-microbial therapy
6) Neurological Sequelae
- -Embolic stroke 15 – 20% of patients
- -Mycotic aneurysm
- -Cerebritis
7) Congestive Heart Failure
- -Due to mechanical disruption
- -High mortality without surgical intervention
8) Acute Kidney Injury
- -Immune complex-mediated
- -Impaired hemodynamics/drug toxicity

80
Q

what is the most common sign of IE?

A

the fever

81
Q

Janeway lesions vs Osler nodes?

A
  • -Non-tender, small erythematous or hemorrhagic macules or nodules in the palms or soles
  • -Painful, erythmatous nodular lesions
82
Q

what are the causes of kidney injury in IE?

A
  • -Immune complex-mediated

- -Impaired hemodynamics/drug toxicity

83
Q

how IE is diagnosed?

A

1)History and physical - the “old fashioned way”
2)Laboratory studies -
– Microbiology - sustained positive blood cultures
– Other studies - hematologic, rheumatologic, renal
3)Echocardiography
– Transthoracic (reasonable resolution @ < 2-3mm in size) or transoesophageal echocardiography

84
Q

what is the Duke Criteria for the Diagnosis of Endocarditis?

A

1)Definite:
– Pathologic criteria are histologic or culture confirmation of vegetation or emboli.
– Clinical criteria are 2 major, 1 major plus 3 minor or 5 minor criteria
2)Possible:
– 1 major, 1 minor; or 3 minor criteria
3_Rejected:
– Alternate diagnosis, resolution of infection with brief therapy, no pathologic evidence of endocarditis

85
Q

what are the principles of IE therapy?

A

–Bactericidal antibiotics must be used
–Prolonged therapy is necessary (weeks)
–Treatment is best started after multiple sets of blood
cultures have been taken - urgency in the initiation of therapy is required for acute but not subacute endocarditis
–Synergistic combinations of antibiotics are used when available

86
Q

what are the Cardiac Conditions necessitating IE Prophylaxis (dental or respiratory procedures Only)

A

1)Prosthetic Cardiac Valve
2)Previous Infective Endocarditis
3)Congenital Heart Disease (CHD)
• Unrepaired Cyanotic CHD, Including Palliative Shunts and Conduits
• Completely Repaired CHD with Prosthetic Material or Device, whether by Surgery or by Catheter Intervention, during the first 6 months after the procedure
• Repaired CHD with Residual Defects at the Site or Adjacent to the Site of a Prosthetic Patch or Prosthetic Device
4)Cardiac Transplant Recipients who develop Valvulopathy

87
Q

prognosis of IE?

A
  • -In-hospital mortality 18-23%
  • Six month mortality 22-27%
  • Long term morbidity
    1) Heart failure
    2) Stroke

Cardiorespiratory (24 decks)

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