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Cardiovascular System > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

Valve disease stats

A

in children, all 4 valve disease are the same

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2
Q

Presentation of MS

A
  • normal orifice: 4-6 cm2, stenosis: <2 cm2
  • stenosis –> LA works harder to push blood into LV –> backed up pressure in the LA and pulmonary arteries –> increased atrio-ventricular pressure, pulmonary hypertension
  • right sided cardiomegaly or right sided HF, enlarged LA
  • possibly develop tricuspid and pulmonary valve regurg
  • LV pressure and systolic function remains unaffected unless severe
  • dyspnoea
  • haemoptysis
  • systemic emboli (from stagnant blood in enlarged LA)
  • stroke
  • AF, palpitations, angina
  • hoarse voice (compressed laryngeal nerve from enlarged LA)
  • infective endocarditis
  • mitral facies: malar flush (flushed cheeks), central cyanosis
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3
Q

Examination findings in MS

A
  • pulse: should be normal because systolic function is unaffected
  • JVP: raised
  • tapping apex beat + diastolic thrill: should be normal because LV is unaffected
  • RV heave: from right heart hypertrophy
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4
Q

Investigations and findings in MS

A
  • ECG: raised R wave (LV enlargement), raised P wave (AF?)
  • cardiac catheterization: heart block (atria and ventricles contract at the same time)
  • CXR: enlarged LA, prominent pulmonary arteries
  • Echo: fibrosis/scarring of leaflets, elbowing of the anterior leaflet, asymmetrical fusion of leaflets
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5
Q

Treatment of MS

A
  • diuretics: decrease MAP
  • B blockers: reduce bp
  • AF treatment: stores sinus rhythm
  • anticoagulant: decrease embolisation
  • valvotomy: balloon cath, surgery
  • valve replacement
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6
Q

Aetiology of MR

A
  • degenerative disease –> mitral valve prolapse
  • ischaemic heart disease/post infarct
  • dilation of the LV or annulus / cardiomyopathy
  • connective tissue disorders
  • infective endocarditis
  • rheumatic heart disease
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7
Q

Physiology of MR

A
  • severity depends on: contractility, afterload, preload
  • LV compensation (chronic and acute)
  • LA compliance (both increased and reduced)
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8
Q

Presentation of MR

A
  • eccentric LV hypertrophy but decreased CO
  • dyspnoea
  • pulmonary edema
  • right sided heart failure
  • fatigue, exhaustion
  • AF, palpitations
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9
Q

Examination + findings of MR

A
  • pulse: normal (reduced, jerky pulse in severe HF)
  • JVP: raised in severe HF
  • brisk and hyperdynamic apex beat, displaced apex beat
  • RV heave: from forceful contraction of the heart
  • auscultation: soft first heart sound, pansystolic murmur
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10
Q

Investigations + findings of MR

A
  • CXR: cardiomegaly
  • ECG: raised P wave (LA enlargement), raised R wave (from RV heave)
  • CC: not commonly used anymore, too intensive
  • Echo: calcification of mitral annular, gives us clues about LV dimensions and cause of MR
  • CMR: determine regurg volume
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11
Q

treatment of MR

A

ACUTE: (clinical emergency - take into operation, but must stabilize preload and afterload before operation)

  • sodium nitropruside: vasodilator, lower bp
  • dobutamine: vasodilator, increases contractility
  • intra-aortic balloon pump: increased contractility (better perfusion in the heart)

CHRONIC:

  • preserve LV function
  • mitral valve repair/replacement
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12
Q

eccentric vs concentric hypertrophy

A

ECCENTRIC: dilation of the heart chambers
CONCENTRIC: thickening of the ventricular walls (the chamber actually narrows)

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13
Q

effect of increased and reduced LA compliance

A

reduced: increased SV and afterload, increased pulmonary venous return, remodeling of pulmonary vasculature, thickened myocardium, marked rise in pressure
increased: less remodeling, develop AF, marked rise in volume

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14
Q

difference between acute and chronic LV compensation

A

ACUTE: results from acute MR, like valve snapping from infection –> decreased SV –> ventricles have no time to adapt, heart responds to decreased CO by increasing HR –> EDV decreases and LV pressure decreases

CHRONIC: results from chronic MR, like degenerative –> ventricles have time to adapt and slowly dilates in order to hold more EDV in response to slowly decreasing CO –> eccentric LV hypertrophy

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15
Q

aetiology of AS

A
  • degenerative (most common) –> atherosclerosis
  • rheumatic heart disease –> adhesion/fusion of commissures, retraction/stiffening of cusp margins
  • congenital bicuspid aortic valve (most common congenital disorder)
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16
Q

presentation of AS

A
  • normal orafice: 3-4 cm2, stenosis: <1.5-2 cm2
  • pressure gradient between LV and aorta > 50 mmHg
  • LV outflow obstruction –> LV dilation, muscle hypertrophy –> increased EDV, increased LA pressure
  • muscle hypertrophy –> increased O2 demand –> not enough perfusion –> myocardial ischaemia –> LV failure –> decreased SV and CO
  • pulmonary hypertension
  • long asymptomatic phase but life expectancy will drop immediately after onset of symptoms
  • chest pain
  • dyspnoea
  • HF
  • sudden death
  • syncope
17
Q

examination and findings of AS

A
  • pulse: narrow pulse pressure, slow rising pulse
  • JVP: raised
  • RV heave
  • heaving apex beat, displace apex beat
  • systolic thrill
  • systolic murmur (heart over carotid artery)
  • soft S2
18
Q

investigations and findings of AS

A
  • ECG: LV heave, ST elevation, T wave elevation
  • CXR: pulmonary congestion, LV enlargement
  • Echo: calcification
  • CMR (cardiovascular magnetic resonance): to see severity of stenosis
19
Q

treatment of AS

A
  • diuretics
  • b blockers
  • nitrates
  • valve replacement
20
Q

aetiology of AR

A
  • rheumatic fever
  • Marfan’s syndrome (connective tissue disease)
  • hypertension
  • atherosclerosis
  • congenital biscuspid valve
  • infective endocarditis
  • syphillis
  • arthritis
  • aortic dissection
  • myxomatous degeneration (connective tissue disease that presents in their 50s)
21
Q

presentation of AR

A

ACUTE:
- LV cannot cope –> blood backtracks into LA and pulmonary circulation –> pulmonary edema

CHRONIC:

  • long asymptomatic phase (is a slow-progressing disease)
  • exertional dyspnoea, nocturnal dyspnoea
  • arrythmia
  • angina
22
Q

examination + findings of AR

A
  • pulse: wide pulse pressure, waterhammer pulse, visible carotid pulsations (Corrigan’s sign), Capillary pulsations in nail bed (Quimcke’s sign), pistol shots over femoral arteries (Traube’s sign), head nodding with the pulse (Musset’s sign)
  • murmur: diastolic thrill, mid-diastolic murmur (austin-flint murmur), early diastolic, quiet murmur that is heard at the sternal angle when the patient sits forward and holds their expiration
  • third heart sound
  • heaving displaced apex beat
23
Q

investigations and findings of AR

A
  • ECG: ST and T elevation (due to LV strain), strain in AIA, left axis deviation
  • CXR: LV enlargement
  • Echo: AV cusp anatomy, LV function, doppler haemodynamic assessment of regurgitation flow
  • CMR: determine volume of regurg
24
Q

treatment of AR

A
  • vasodilator therapy (the only valve disease where this is useful, will delay surgery by 3-4 years)
  • diuretics
  • ACEI/ARB
  • vasodilators
  • nifedipine (CCB)
  • aortic valve replacement and repair

Cardiovascular System (6 decks)

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