1. Lectures from Pathological Physiology
Valvular defects
Lectures from Pathological Physiology
Study materials from Pathological Physiology, school year 2007/2008
Revised
© Oliver Rácz, Eva Sedláková
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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. An old solution TODAY – EARLY
VALVULOPLASTIC INTERVENTION THROUGH CATHETRIZATION
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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: According ro rythm, cardiac frequency, risk of embolisation
Pharmacological cardioversion
Electrical cardioversion and modern methods
Surgical ablation
Catheter Ablation
Suppression of AF by pacing
Internal Atrial cardioverter/Defibrillators
Dissolution of blood clots and monitoring of coagulation !!!
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14. 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. Mitral valve prolapse
Classic description: 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? Increased risk of sudden death?
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17. Prolaps, new data (2009) Prevalence cca 2,4 %
Familiar type, AD, degeneration of valves and annulus fibrosus (young women)
Marfan and other connective tissue diseases
CHD and other pathological conditions of the heart
Increased risk of infectiousus endocarditis and arrhytmias
Migraine ??!!
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18. Aortic stenosis Valvular Causes In addition to valvular also
Hereditary (also cardiomyopathy)
1 % of population has bicuspidal aortic valve
Degeneration, calcification
Postrheumatic
In addition to valvular also
Subvalvular – see hypertrophic cardiomyopathy
Supravalvular – coarctation of aorta
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19. 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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22. 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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23. 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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24. 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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25. The forgotten ventricle*
Often as a „victim“ alebo „bystander“ of overall pathological cardiac or pulmonalry conditions
USG inverstigation is more complicated
Some anatomical, histological and functional specifics (valves, papillar muscles, trabeculisation of the apical part and contraction)
*Šimková a Kaldarárová, Kardiológia pre prax, 8, 2010,
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26. The forgotten ventricle – etiology of pathological conditions
Pressure overload – stenosis of a. pulmonalis, pulmonary HT, pulmonary embolism (acute!)
Volume overload – atrial septum defect, tricuspidal regurgitation
Dysfunction of the myocard - MI, cardiomyopathies
Obstruction of inflow – tricuspidal stenosis, tamponade, constrictive pericarditis
Abusus of some drugs – cocaine, amphetamine
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27. Tricuspidal regurgitation*
Common secondary condition in valvular diseases of the left ventricle, in congenital defects and in left ventricle failure
Primary in inf. endocarditis (i.v. drug users), danger of septic pulmonary embolisation
Prolaps – together with the left side
Ebstein anomaly
*Chňupa P, Kardiológia pre prax 8, 2010, 174 – 180
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