1. Lectures from Pathological Physiology
Valvular defects
Lectures from Pathological Physiology
Study materials from Pathological Physiology, school year 2007/2008
Revised 2011
© Oliver Rácz, Eva Sedláková
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2.
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3.
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4. Valvular dysfunction - introduction
Stenosis – block of flow; regurgitation – backward flow
For pathological physiology the hemodynamics is the most important. It helps to understand heart failure also in other diseases.
Symptoms. auscultation (murmurs), USG – see internal propedeutics.
In the past mostly a consequence of rheumatic fever, today this is changing:
degenerative processes of valves
hereditary causes ( mitral valve prolapse, pulmonary, stenosis)
inflammation
secondary dilatation (cardiomyopathies, papillary muscle dysfunction)
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6. Mitral stenosis 10 – 20 years after febris rheumatica
From 1st symptoms to decompensation: 5 – 10 years
Often in combination with other valvular defects (aortic insufficiency)
25 years after f. rh 33 % NYHA III, 50 % NYHA IV
Narrowing of the ostium from 4 – 6 to 1 cm2 and less
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7. Mitral stenosis
Pressure gradient between left atrium and ventricle – first only during exercise, later also in rest
Left ventricle is intact – not involved in compesation
Postcapillary pulmonary hypertension. Over 30 mmHg danger of pulmonary oedema
Overload of right ventricle
Symptoms of left heart failure without dysfunction of left ventricle
3 typical complications – atrial fibrillation, thrombus formation and the danger of embolisation
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8. Grades of mitral stenosis
norm
mild
middle
severe
Area of ostium (cm2)
4-6
2-4
1-2
< 1
gradient (mm Hg)
< 5
5-12
12-20
> 20
Pressure t1/2 (ms)
< 60
60-100
> 200
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10.
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11. A short diversion towards atrial fibrillation
A common dysrythmic condition
Different forms – paroxysmal, recurrent, etc... and according to hemodynamics (with or without tachycardia)
Dg. also without ECG – pulsus irregularis et inaequalis - why?
In the past – mitral stenosis
Today – age, sex (m > w)
60 y. cca 1 %, 80 y. up to 6 %
Thyreotoxicosis
Cardiac disease in general
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13. Atrial fibrillation Management rythm, cardiac frequency, embolisation
Farmacological cardioversion
Electrical cardioversion and modern methods
Surgical ablation
Catheter Ablation
Suppression of AF by pacing
Internal Atrial cardioverter/Defibrillators
Dissolution of blodd clots and monitoring of coagulation
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14. Mitral regurgitation& mitral valve prolapse
Classic description: Mitral insufficiency after f.rheumatica, or ventricle dilatation. Valve prolapse with acute regurgitation after necrosis of papillary muscles or as a part of inherited diseases of collagen (m. Marfan, Ehlers-Danlos) RARE
New view: Small regurgitation due to mitral valve prolapse visible on USG – usually without hemodynamic consequences and symptoms.
COMMON AD disease? Altered histological structure of valves?
Arrhytmias, migraine???
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15. Mitral regurgation Hemodynamics
Regurgitation from LV back into left atrium during systole.
Volume overload of LV (to get 5 liters into circulation the heart pumps and more).
Excentric hypertrophy of LV compensates the hemodynamic disorder.
Symptoms (except murmurs, ECG and X ray) are similar to stenosis (left heart failure, pulmonary oedema, complications).
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16.
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17. Aortic stenosis In addition to valvular also Causes
subvalvular and supravalvular forms
Causes
Hereditary (also cardiomyopathy)
1 % of population has bicuspidal aortic valve
Degeneration, calcification
Postrheumatic
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18. Aortic stenosis Hemodynamics Pressure gradient between LV and aorta
Pressure overload of LV (as in hypertension)
Concentric hypertrophy, well compensated for a long time, diastolic dysfunction. Finally decompensation and left heart failure
Pulsus parvus et tardus – insufficient perfusion of tissues, especially of heart muscle
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20. Grades of aortal stenosis
Norm
mild
middle
severe
Area of ostium (cm2)
2-3
> 1,5
1,0-1,5
< 1,0
gradient (mm Hg)
< 50
50-70
> 70
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22. Aortic insufficiency Mostly postrheumatic
Hemodynamics: Regurgitation in diastole, volume overload of LV.
High systolic and low diastolic pressure – disadvantegous for heart muscle perfusion.
Pulsus celer et altus
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23. Overview of hemodynamics of valvular defects
Disorder
Timing
Overload
Notes
M.Sten.
A ÞV
Diastole
not of LV !
fibrillation
embolisation
M.Ins.
A ÜV
Systole
volume
„exercise“
Ao. Sten.
V Þ Ao
pressure
pulsus !
Ao. Ins
V Ü Ao
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