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HEMODYNAMICS OF AS

HEMODYNAMICS OF AS. Aortic Stenosis. Etiology based on location Supravalvular Subvalvular - Valvular. Congenital Bicuspid Rheumatic Senile degenerative. Pathophysiology.

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HEMODYNAMICS OF AS

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  1. HEMODYNAMICS OF AS

  2. Aortic Stenosis • Etiology based on location • Supravalvular • Subvalvular- • Valvular • Congenital • Bicuspid • Rheumatic • Senile degenerative

  3. Pathophysiology Pressure gradient across the aortic valve increases exponentially (not linearly) with decreasing aortic valve area

  4. Pathophysiology • Increase in afterload • Progressive hypertrophy-Concentric hypertrophy-- II sarcomeres • Decrease in systemic and coronary flow

  5. Compensatory Mechanisms • Adaptive and maladaptive • Progressive worsening of left ventricular outflow obstruction leads to hypertrophy • Compensatory hypertrophy required to maintain wall stress (afterload) • Augmented preload with increased atrial kick preserve LV systolic function

  6. Subendocardial ischemia • Perivascular fibrosis- ECM ellaboration • Large diameter myocytes impairing O2 diffusion • Hgh LVEDP- deccor diastolic perfusion pr • Inc O2 consumption from inc mass and wall stress • Epicardial CAD

  7. ↓ I EF:- 1) NL Contractility increased - Afterload “ mismatch” increased preload- noncompliant vent asynchronous uncoordinated contraction- wall stress 2) decreased contractility- multifactorial ↓ s upply to endocardium ↓ cor flow reserve cytoskeletal abnormalities diastolic dysfunction pathological LVH

  8. In mild AS, intracardiac pressures and CO - normal • As the valve becomes more stenotic- normal at rest, unable to increase CO during exercise • Progressive narrowing of the valve leads to decreased stroke volume and cardiac output even at rest • In moderate to severe AS, patients may develop elevated filling pressures to compensate for the increase in LV end-diastolic pressure • In a minority of patients LV systolic failure occurs- further elevation in intracardiac pressures

  9. the degree to which hypertrophy may go on is limited by the coronary blood flow • The aortic obstruction imposes some limits on the perfusion pressure available for the coronary vessels, and also on the output available for them. • Moreover, the increased systolic resistance to flow in the hypertrophied muscle cuts down on whatever coronary flow normally does occur in systole. • As the obstruction progresses to a critical level, the high afterload “overwhelms” the left ventricle and systolic function begins to decrease. • With continued severe afterload excess, myocyte degeneration and fibrosis occurs and produces irreversible left ventricular systolic dysfunction

  10. Angina • Progressive LV hypertrophy from aortic stenosis leads to increased myocardial oxygen needs • Hypertrophy may compress the coronary arteries • Reduced diastolic filling may result in classic angina, even in the absence of coronary artery disease • 35% presentation • 50% die in 5 years

  11. Syncope • Cardiac output no longer increases with exercise • A drop in systemic vascular resistance that normally occurs with exertion may lead to hypotension and syncope • Rest- arrythmias, av block • 15% presentation • 50% die in 3 years

  12. Heart Failure • Changes in LV function may no longer be adequate to overcome the outflow obstruction • Hypertrophic remodeling leads to diastolic dysfunction • Afterload excess results in decreased ejection fraction – systolic dysfunction • 50% presentation • 50% die in 2 years

  13. There may be a plateau or an anacrotic pulse or a late peaking and small volume pulse, pulsusparvus, and tardus The pulse pressure may be reduced In supravalvular AS, the right brachial and carotid pulsations are of greater amplitude than the left-sided ones

  14. Mask severity High CO & elastic vessels Increased stiffness in elderly AR HTN • Exaggerate severity LV Systloicdysfn MS Hypovolemia

  15. In supravalvular AS- the right brachial pulse and the carotid may be stronger than the left brachial • Coanda effect -properly directed jet , attach to a convex surface instead of moving in a straight line • Obstruction in the supravalvular AS is such that the high-velocity jet is directed towards the right innominate artery

  16. The apex beat is hyperdynamic and sustained due to associated left ventricular hypertrophy. A thrill in the aortic area indicates AS not severity

  17. INTENSITY NL- Pliable, thin valves –BAV without calcification Dec –thickened rigid valves , calcification Severe -the stroke volume is ejected slowly and over a longer period and also leads to poor distension of the aortic root--softer A2 • SPLITTING A2 moves into P2- 1) ↑ LV ejection 2) longer time for LV pr to drop below aortic at end systole Single Paradoxical splitt

  18. S4 • Correlates wit large LV-AO gradient and abnormally elevated LVEDP

  19. AEC • Localises and suggests etiology • sudden cessation of opening motion of abnormal valve leaflets(doming) • Lost with calcification and thickening • High frequency- 40-80 msec after S1 – best heard at apex-constant

  20. MURMUR • Crescendo –decrescendo – shape of the pr diff bet LV-Ao • Site of max intensity and radiation- • Length of the murmur-severity - time to peak intensity- 2nd half • Frequency and pitch- rough ,grunting Harsh- mixed frequency at base – effect of jet to Ao high freq musical- vibfom leaflets with intact commissures , at apex -Gallavardin murmur • Amplitude - generally louder –severe - nonspecific

  21. SEVERITY

  22. Classification of Severity

  23. Doppler data • Peak instantaneous gradient over time • Cath data • Peak to peak data • However, calculated mean P Grd are comparable

  24. AORTIC STENOSIS- (LV-AO)

  25. AVA Pull back hemodynamics : Peak – peak gradient alignment mismatch Distortion of pulse - femoral artery peripheral pulse amplification catheter in LVOT central aorta - pressure recovery Carballo’s sign

  26. Pull back

  27. Schematic representation of the flow and static pressure across the left ventricular (LV) outflow tract, aortic valve, and ascending aorta during systole LVSP = left ventricular systolic pressure; MGnet= transvalvular pressure gradient after pressure recovery MGvc = transvalvular pressure gradient at the venacontracta SAP= systolic aortic pressure SAPvc = systolic aortic pressure at the vena contracta; SV = stroke volume Svi= stroke volume index ZVA= valvulo-arterial impedance.

  28. Doppler derived gradients- using CW doppler @ vena contracta Catheter derived gradients- downstream vena contracta- pressure recovery GRADIENT DERIVED BY CATH IS LOWER THAN DOPPLER DERIVED GRADIENT • Pressure recovery- exaggerated in • Smaller aorta • Stiffer aorta • Hypertension

  29. Hypertension may mask the severity of stenosis, an Presence of stenosis may affect the optimal treatment of hypertension Combination of AS and hypertension- “double-loads” th ventricle Total afterload = the valve obstruction + elevated SVR stenosis severity Underestimated- “recovered” pressure, rather than vencontracta pressure, is rec

  30. Stenotic valve area Torricelli’s law • F = A X V A = F / V A = F / V Cc F- Flow A- Valve area V- Velocity of flow Cc- coefficient of contraction

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