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Presentation valvular heart disease.pptx
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- 2. Aortic stenosis Mostcommon valve lesion among adult patients with chronic valvular heart disease. Causes: Congenital (bicuspid, unicuspid) Degenerative calcific disease Rheumatic fever Radiation
- 3. Pathogenesis Endothelial dysfunction lipid accumulation inflammatory cell activation cytokine release Fibrocalcific response (calcium hydroxyapatite crystals deposition)
- 4. Pathophysiology Lv outflowobstruction produces systolic pressure gradient between the LV and aorta. Sudden severe obstruction – Lv dilatation and stroke volume reduction Gradual- Lv concentric hypertrophy( adaptive mechanism) Laplace law(S=Pr/h) A large transaortic valve pressure gradient present for long term without reduction in cardiac output or LV dilation Later this hypertrophy becomes maladaptive, systolic function declines because of afterload,diastolic function progress which leads to irreversible myocardial fibrosis.
- 5. Symptoms Exertional dyspnoea(increasedpulmonary capillary pressures) Angina pectoris(imbalance between oxygen demand and supply) Syncope(decline in arterial pressure or low cardiac output status)
- 6. Physical findings: Rhythm- regular,if AF present – associated mitral valve disease Hypertension – older adults Carotid arterial pulse rises slowly to a delayed peak( pulsus parvus et tarsus) Thrill palpable over left carotid artery Lv impulse displaced laterally Double apical impulse Systolic thrill
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- 9. Auscultation Congenital BAVdisease- early systolic ejection sound Paradoxical splitting of S2 Audible S4 at the apex Mid ejection systolic murmur –low pitched , rough and rasping in character, especially loudest at the base of the heart(2nd Right ICS) Transmitted upward along the carotid arteries Transmitted downward along the apex of the heart(Gallavardin effect)
- 10. Laboratory examination ECG: Leftventricular hypertrophy(severe AS) LV strain ( ST depression and T wave inversion ) in lead 1 and aVL and in left precordial leads
- 11. Echocardiogram Thickening,calcification, andreduced systolic opening of the valve leaflets and Lv hypertrophy. Eccentric closure of aortic valve cusps- Congenital bicuspid valve Valve gradient and aortic valve – Doppler measurement of trans aortic velocity Lv dilatation and reduced systolic shortening – Lv impairment Useful for identifying coexisting valvular abnormalities, differentiating valvular abnormalities from other forms of Lvot obstruction and measuring aortic root and proximal ascending aortic dimensions.
- 12. Chest X ray No or little cardiac enlargement Hypertrophy without dilatation- rounding of cardiac apex in frontal projection and slight backward displacement in lateral view Frontal view- dilated proximal ascending aorta seen along the upper right heart border
- 13. Medical management Severe As-avoid strenuous physical activity and competitive sports Avoid dehydration and hypovolemia – not to reduce CO ACE inhibitors and beta blockers ( used for HT and CAD) – safe for asymptomatic patients with preserved LV systolic function Nitroglycerin – relieved Anginal pain in CAD patients Endocarditis prophylaxis – restricted to As patients with a prior history of endocarditis
- 14. Surgical treatment Indications: Severe AS(valvearea: <1 cm2 or 0.6/m2 body surface area) who are asymptomatic those who exhibit LV systolic dysfunction (EF<50%) AS due to BAV disease Aneurysmal root or ascending aorta( max dimension >5.5 cm)
- 16. Aortic Regurgitation Aortic regurgitationmay be caused by primary valve disease , aortic root disease or their combination.
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- 19. Symptoms Acute severeAR- elevation of Lv diastolic pressure associated with elevation of LA and PA wedge pressures – pulmonary Edema and cardiogenic shock Chronic AR –long latent period, asymptomatic (10-15 yrs) Palpitation on lying down – early complaint Sinus tachycardia during exertion , premature ventricular contraction – palpitation and head pounding
- 20. Exertional dyspnoea-symptoms of diminished cardiac reserve Orthopnea Paroxysmal nocturnal dyspnoea Diaphoresis Anginal chest pain even in the absence of CAD Congestive hepatomegaly and ankle edema – develop late in the course
- 21. Physical findings Chronic severeAR – jarring of the entire body and bobbing motion of head with each systole. Abrupt distension and collapse of the larger arteries – easily visible Identify condition predisposing to AR like Bicuspid valve Infective endcarditis Marfan syndrome Ankylosing spondylitis
- 22. Arterial pulse Waterhammer pulse which collapses suddenly as arterial pressure falls rapidly during late systole and diastole ( Corrigan’s pulse) Quince’s pulse – capillary pulsation (alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail Traube sign- booming pistol shot sound heard over femoral arteries Duroziez’s sign- to and fro murmur of femoral artery when lightly compressed with stethoscope Widened pulse pressure (both systolic hypertension and lowering diastolic pressure)
- 23. Palpation Chronic severeAR- Heaving Lv impulse displaced laterally and inferiorly Palpable diastolic thrill along left sternal border Palpable systolic thrill along suprasternal notch and transmitted upward along the carotid arteries Bisferiens carotid arterial pulse- two systolic waves separated by a trough
- 24. Auscultation Severe AR-A2(aortic valve closure sound) – absent BAV disease- systolic ejection sound is audible and occasionally S4 may be heard Chronic AR- high pitched , blowing , decrescendo distolic murmur, heard in third intercostal space along left sternal border AR by primary valvular disease- louder diastolic murmur along the left sternal border AR by aneurysmal dilation of aortic root- louder diastolic murmur along the right sternal border
- 25. Isolated AR– mid – systolic ejection murmur heard at the base of the heart and transmitted along the carotid arteries Severe AR -Austin flint murmur – soft , low- pitched, rumbling mid to late diastolic murmur This murmur is produced by diastolic displacement of anterior leaflet of mitral valve by AR stream and not associated with mitral valve obstruction These features are intensified by strenuous and sustained hand grip – augers systemic vascular resistance and increases Lv afterload
- 26. Ecg Chronic severeAR- signs of LV hypertrophy Lv strain ( ST segment depression and T wave inversion in leads 1 , aVL, V5 and V6 Left axis deviation QRS prolongation
- 27. Echocardiogram Chronic AR-increased Lv size and normal systolic function until decline in myocardial contractility Regurgitant jet produces rapid , high frequency diastolic fluttering of the anterior mitral leaflet Useful in determining the cause of AR like dilation of the aortic annulus and root, aortic dissection or primary leaflet pathology Severe AR – central jet width assessed by color flow Doppler imaging exceeds 65% of the Lv outflow tract width, regurgitant volume is > 60ml/beat and there is diastolic flow reversal in the proximal portion of the descending thoracic aorta
- 28. Chest X ray Chronic severe AR- downward and leftward displacement of apex ( frontal projection ) Posterior displacement of Lv and encroaches on the spine in the left anterior oblique and lateral projection Aneurysmal dilation of aorta may be noted in lateral view if AR is caused by primary aortic root disease
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- 32. Treatment Acute Aorticregurgitation : Acute severe AR – respond to iv diuretics and vasodilators ( sodium nitroprusside)- for short term Intra aortic balloon counterpulsation is contraindicated Beta blockers are avoided in order not to reduce the cardiac output or slow the heart rate , allowing time for LV diastolic filling Surgery is the treatment of choice
- 33. Chronic Aortic regurgitation Symptomsonset or Lv systolic dysfunction – indication for surgery Medical treatment with diuretics and vasodilators (ACE inhibitors,ARBs , dihydropyridine CCB or hydralazine – temporary measure Cardiac arrhythmias and infections – treated promptly Syphillic aortitis –full course of penicillin therapy Beta blockers and ARB losartan – useful in retarding the rate of aortic root enlargement in patients with Marfan’s syndrome and aortic root dilation.
- 34. Surgical treatment Indication forAortic valve replacement : Severe AR in symptomatic patients irrespective of Lv function Also carried out in severe AR in asymptomatic patients with progressive Lv dysfunction ( LVEF<55%), Lv end systolic dimension >50 mm or Lv diastolic dimension of >65mm.