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Aortic Insufficiency Diagnosis and Management
- 2. KARAGANDA STATE MEDICAL UNIVERCITY STUDENT INDIVIDUAL WORK SUBJECT- Propaedeutics Topic – Aortic Insufficiency SUBMITTED BY – GODARA MOTI LAL GROUP NO. 3003
- 4. 49 WM sent for “transplant” evaluation from local cardiologist HPI – DOE x 6mos-1year, insidious onset, also with L sided Chest tightness when tired/stressed and occasionally awakens him at night, last 1- 2hrs and relieved with anxiolytics. Occasional lightheadedness after taking Coreg. Denies PND, Orthopnea, cough, pre/syncope. Former maintenance worker, now on medical leave. Pt states trying to remain active (walking/ swimming) but limited by dyspnea
- 5. PMHx: • Chronic LBP • Obesity • OSA/ CPAP • Depression/Anxiety • Basal Cell Carcinoma Social: • no alcohol, cocaine, tobacco or drugs; married with 1 teenage son Meds (at presentation) • Carvedilol 50 bid, Celebrex, Lasix, ASA, anxiolytic, hydrocodone, Combivent MDI
- 6. PE: HR 65 BP 170/67 HNT: jvp est 10cm, CV: nl S1/2, + S3, no S4; PMI displaced laterally to ant ax; 3/6 diastolic decrescendo m USB Resp: basilar rales Abd: obese, no ascites/masses Ext: tr edema, distal pulses brisk
- 7. Lab: • Chem 142 110 / 14 H/H 16.6/ 46 4.4 / 27 1.4 TSH, LFT, FLP, WBC/PPC, Coags nl ECG: NSR, PRWP, nl axis, no ischemia
- 8. Etiology Physical Examination Assessing Severity Natural History Prognosis Timing of Surgery © Continuing Medical Implementation …...bridging the care gap
- 9. Any conditions resulting in incompetent aortic leaflets Congenital • Bicuspid valve Aortopathy • Cystic medial necrosis • Collagen disorders (e.g. Marfan’s) • Ehler-Danlos • Osteogenesis imperfecta • Pseudoxanthoma elasticum Acquired • Rheumatic heart disease • Dilated aorta (e.g. hypertension..) • Degenerative • Connective tissue disorders E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis ) • Syphilis (chronic aortitis) Acute AI: aortic dissection, infective endocarditis, trauma © Continuing Medical Implementation …...bridging the care gap
- 10. Dyspnea, orthopnea, PND Chest pain. • Nocturnal angina >> exertional angina • ( diastolic aortic pressure and increased LVEDP thus coronary artery diastolic flow) With extreme reductions in diastolic pressures (e.g. < 40) may see angina © Continuing Medical Implementation …...bridging the care gap
- 11. Quincke’s sign: capillary pulsation Corrigan’s sign: water hammer pulse Bisferiens pulse (AS/AR > AR) De Musset’s sign: systolic head bobbing Mueller’s sign: systolic pulsation of uvula Durosier’s sign: femoral retrograde bruits Traube’s sign: pistol shot femorals Hill’s sign:BP Lower extremity >BP Upper extremity by • > 20 mm Hg - mild AR • > 40 mm Hg – mod AR • > 60 mm Hg – severe AR © Continuing Medical Implementation …...bridging the care gap
- 12. Widened pulse pressure • Systolic – diastolic = pulse pressure High pitched, blowing, decrescendo diastolic murmur at LSB Best heard at end-expiration & leaning forward Hands & Knee position S1 S2 S1 © Continuing Medical Implementation …...bridging the care gap
- 13. Apex: • Enlarged • Displaced • Hyper-dynamic • Palpable S3 • Austin-Flint murmur Aortic diastolic murmur • length correlates with severity (chronic AR) • in acute AR murmur shortens as Aortic DP=LVEDP • in acute AR - mitral pre-closure © Continuing Medical Implementation …...bridging the care gap
- 14. Assess severity by impact on peripheral signs and LV • peripheral signs = severity • LV = severity • S3 • Austin -Flint • LVH • radiological cardiomegaly © Continuing Medical Implementation …...bridging the care gap
- 17. Asymptomatic %/Y Normal LV function (~good prognosis) • Progression to symptoms or LV dysfunction < 6 • Progression to asymptomatic LV dysfunction < 3.5 • 75% 5-year survival • Sudden death < 0.2 Abnormal LV function • Progression to cardiac symptoms 25 Symptomatic (Poor prognosis) • Mortality > 10 TX: Medical Surgery BEFORE LV dysfunction © Continuing Medical Implementation Bonow RO…, .e..bt riadgl,in Jg AtheC cCare. g1a9p 98;32:1486.
- 18. ACC/AHA Class I • Symptomatic patients with preserved LVF (LVEF >50%) • Asymptomatic patients with mild to moderate LV dysfunction (EF 25-49%) • Patients undergoing CABG, aortic or other valvular surgery ACC/AHA Class II a • Asymptomatic patients with preserved LVEF but severe LV dilatation (EDD>75 mm or ESD > 55mm) © Continuing Medical Implementation …...bridging the care gap
- 19. ACC/AHA Class II b • Patients with severe LV dysfunction (EF < 25%) • Asymptomatic patients with normal systolic func-tion at rest (EF >0.50) and progressi ve LV dilata-tion when the degree of dilatation is moderatelysevere (EDD 70 to 75 mm, ESD 50 to 55 mm). ACC/AHA Class III • Asymptomatic patients with normal systolicf unction at rest (EF >0.50) and LV dilatation when the degree of dilatation is not severe (EDD <70 mm, ESD <50 mm). © Continuing Medical Implementation …...bridging the care gap
- 20. Etiology Pathophysiology History / Physical Findings Natural History Diagnosis Management
- 21. Aortic Root • Age related dilatation • Medial degeneration/ Marfans • Dissection • HTN • Other ( osteogenesis imperfecta, Reiters, syphilitic aortitis, Bechet, psoriatic arthritis, relapsing polychondritis, UC arthritis, AS, giant cell arteritis Aortic Valve • Rheumatic • Calcific degeneration • Congenital (Bicuspid, VSD) • Myxomatous degeneration • Endocarditis • Structural degeneration of Bioprosthetic valve • Other (SLE, AS, Takayasu, Whipple, Crohns)
- 22. increased LV EDV addition of new sarcomeres in series/ elongation of myocytes and myocardial fibers (Eccentric Hypertrophy) enlarged chamber/ increased wall stress is stimulus for concentric hypertrophy dilatation and hypertrophy with resultant recruitment of preload reserve allow compensation and maintenance of LV systolic function may be asymptomatic for decades until decompensated state develops, wall thickening unable to keep pace with hemodynamic load, increased interstitial fibrosis and decreased compliance symptoms of CHF ensue
- 23. CO at rest may approach 25 L/min in severe AI with little increase in EDP very large EDV (Cor Bovinum) Braunwald 6th ed
- 26. DOE, Orthopnea, PND • usually after 4th / 5th decade and significant cardiomegaly and LV dysfxn Angina pectoris • develops later, nocturnal sxs prominent; often with diaphoresis due to HR slowing with arterial DBP falling to low levels Palpitations / Head pounding • especially in supine position, pounding of heart against chest wall • tachycardia from stress/exertion may precipitate and cause extreme discomfort for pt From Braunwauld. Cardiovascular Dz, 6th ed.
- 27. de Musset sign – head bobbing with heartbeat Corrigan pulse – “water hammer” pulse Bisferiens pulse – brach/ fem arteries Hill sign – popliteal > brachial by 60mmHg Traube sign – “pistol shot sounds” over fem artery Duroziez sign – sys m when femoral artery compressed proximally and diastolic m when compressed distally Quincke sign – capillary pulsations Apical impulse - diffuse, hyperdynamic and displaced inf/lat systolic thrill – base/suprasternal notch / carotid arteries
- 28. Diastolic murmur • high frequency, sitting up, leaning forward • duration > intensity correlates with severity • mild AR – early diastole, hi pitched blowing • severe AR – holodiastolic, rough • musical (“cooing dove”) – eversion/perforation of Ao cusp • Primary valve dz – heard best LSB 3-4 intercostal • Ao Root dz – heard best RSB Austin Flint murmur • mid-late diastolic apical rumble – severe AR Wide Pulse Pressure Systolic flow murmur (/thrill)
- 29. Mortality rate for severe AI+CHF sxs > 20-50%/yr2 Bonow, et al. JACC Nov 1988 2Aronow , et a. Am J Cardiol 1994; 74: 286. l
- 31. 2D/ M-Mode • AV/ Ao Root anatomic abnormalities • LV dimension / sphericity • AMVL – fluttering, reverse doming • increased EPSS Doppler • Color Flow Mapping • Continuous Wave • Flow reversal in desc Ao (100% sens 97% spec for severe AI) Limitations – What is severe AI?
- 32. AMVL fluttering Color Flow – top mild, bottom moderate
- 33. Vasodilators • goal is to reduce SBP, improve forward SV, reduce regurgitant volume Uses • severe AR + sxs/ LV dysfxn • short term hemodynamic improvement in pt with symptomatic AR before AVR • prolong compensated phase of asymptomatic patients • No indication for asymptomatic pt with mild AI and normal LV fxn Studied in AI • Nifedipine, Hydralizine, ACEI, Nipride, Prazosin • Children/ severe AR – ACEI reversed LV dilatation/wall stress • avoid (-) inotrope in LV dysfxn
- 34. Rx CHF – diuretics, aldactone, dig avoid vigorous exertion if symptomatic AI control diastolic BP (increases regurg) avoid BB - prolong diastole, increase AR
- 35. Goal is to intervene before irreversible LV systolic dysfxn ensues • initially reversible, mainly due to afterload excess – full recovery in LV size/fxn possible • with progressive chamber dilatation, decreased myocardial contractility >> afterload excess as cause of LV dysfxn. • associated with worse recovery of LV fxn and increased mortality
- 36. Indications for AVR (Severe AR)1 • Sxs (NYHA III-IV) regardless of LV fxn • Sxs (NYHA II) with evidence of progressing LV dysfxn ( LV ESD ~ 55, LV EF <50-55%) • Angina (CHA Class II or higher) w or w/o CAD • mild-mod LV dysfxn (EF 25-49%) regardless of sxs • mod-sev AR and undergoing CABG or other valvular surgery Predictors of Postoperative Prognosis • LV systolic function • LV End Systolic Size ( LV ESD) 1 Bonow, et al. Circulation 1998;98:1949-84
- 37. Asymptomatic, nl LV size/fxn Asymptomatic, ESD >55 EF < 50-55% • serial exam/ measurements q 2-4 mos Symptomatic, mild-mod LV dysfxn Symptomatic, severe LV dysfxn • Hi surgical risk, but worse with med Rx (mortality 20-50%) • individualize
- 38. Preload kept high immediate postop period to fill dilated LV temporary IABP use may be necessary until LV fxn improves early post op
- 39. Ao Root disease • annuloplasty or other valve sparing surgery possible if pure Ao Root dz Primary AV disease • valve replacement
- 40. Figure 46-42 Repair of the aortic valve in patient with severe AR. Conduit tailoring in the supravalvular position. The conduit is cut to replace three (left), two (middle), or one (right) individual sinuses. The aortic aneurysm is replaced and the valve is spared. (From David TE, Feindel CM, Bos J: Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 109:345, 1995.) Braunwauld 6th ed
- 41. Figure 29-15 A. Björk-Shiley Monostrut mechanical prosthesis. B. Sorin Allcarbon monoleaflet mechanical prosthesis. C. Medtronic-Hall mechanical prosthesis. D. Omnicarbon mechanical prosthesis. Figure 29-16 A. Carpentier-Edwards Supra-annular Edmunds. Cardiac Surgery in the Adult. Ch 29 porcine bioprosthesis. B. Hancock II porcine bioprosthesis. C. Hancock modified orifice porcine bioprosthesis. D. St. Jude Medical Bioimplant porcine bioprosthesis.