Brief Introduction

1. AORTIC REGURGITATION -
PATHOPHYSIOLOGY
Dr Kunwar Sidharth Saurabh

2. TYPES
AORTIC
REGURGITATION
ACUTE AORTIC
INSUFFICIENCY
CHRONIC
AORTIC
REGURGITATION

3. ETIOLOGY

6. PATHOPHYSIOLOGY
• VOLUME LOAD – COMPENSATORY
MECHANISMS
– LV END DIASTOLIC VOLUME INCREASES TO
ACCOMMODATE REGURGITANT VOLUME
– ALONG WITH INCREASE IN CHAMBER
COMPLIANCE
– HENCE, THERE IS NO INCREASE IN DIASTOLIC
FILLING PRESSURE

7. Cont..
– INCREASE IN EDV  INCREASE TOTAL STROKE
VOLUME
– HENCE, FORWARD STROKE VOLUME MAINTAINED
WITHIN NORMAL RANGE
– ALSO, ADAPTATION TO VOLUME OVERLOAD IS BY
NEW SARCOMERES CAUSING “ECCENTRIC LV
HYPERTROPHY”

8. Cont..
LV PRELOAD INCREASES
PRELOAD AT SACRCOMERE LEVEL IS
NEAR NORMAL
CONTRACTILE FUNCTION PRESERVED
ENHANCED TOTAL STROKE VOLUME

9. Cont..
AUGMENTED
CHAMBER
VOLUME
INC SYSTOLIC
WALL STRESS AND
AFTERLOAD
AFTERLOAD INCREASE IN STIMULUS FOR CONCENTRIC
HYPERTROPHY

10. Cont..
• THUS “AR – CHRONIC” IS A CONDITION OF
COMBINED
– VOLUME OVERLOAD
– PRESSURE OVERLOAD
• HENCE THERE IS BOTH –
– ECCENTRIC HYPERTROPHY
– CONCENTRIC HYPERTROPHY

11. POINTS TO NOTE -
• DUE TO COMPENSATORY PROCESSES-
– PATIENT MAY REMAIN ASYMPTOMATIC FOR
DECADES
– AFTER LOAD REDUCTION THERAPY HAS
POTENTIAL TO REDUCE DEGREE OF
REGURGITATION VIA –
• REDUCES AFTERLOAD AND COMPENSATORY
DILATATION AND HYPERTROPHY

12. Cont..
• In some patients  compensatory process
cannot be maintained for long
• Results in LV systolic dysfunction
• Symptoms of dyspnoea and fatigue often
develops at this transition point.
• Process is mostly insiduos

13. IMPORTANT TO NOTE
LV SYSTOLIC
DYSFUNCTION
AFTERLOAD
MISMATCH
REVERSIBLE
AVR CAUSES
COMPLETE
REVERSAL
IMPAIRED
MYOCARDIAL
CONTRACTILITY
IRREVERSIBLE

14. NATURAL HISTORY
• It can be divided into -
– Patients with normal LV systolic function
– Patients with LV systolic dysfunction

15. With normal LV Systolic function
• These patients remain asymptomatic for
decades.
• Charecterised by very gradual rate of
deterioration to symtoms.
• Likelihood of developing symptoms – 4.3%/yr
• Average mortality rate – 0.2%/yr

16. Cont ..
• Most important aspect of evaluation – detailed
history.
• However, 25% pt may decompensate without
significant history.
• Implies the importance of noninvasive evaluation.
• Factors associated with high risk –
– Age
– Lved - >50mm – 19% , 40-50mm – 6%, <40mm -nil
– LVes

17. With LV systolic dysfunction
• Much more aggressive natural history.
• Become candidate for operation because of
symptoms, within a few years.
• If asymp  symptomatic , require operation
within 2-3 years.

18. Clinical presentation
• Absence of complications, asymptomatic for
decades
• May have some episodes of orthostatic dizziness
• May be aware of increased vigor of contraction of
lv while lying down or audible heart tones.
• May have anginal pain –
– Low aortic diastolic pressure and inc myocardial
demands
– Atherosclerosis
– Luetic

19. Cont ..
• CHF – Most common symptom
• LV failure precedes RV failure.
• Decreased exercise tolerance, dyspnoea.
• Orthopnea , PND
• Dyspnoea may be releived with eventual RV
failure without TR.
• Palpitations – usually not due to arrythmia

20. Cont ..
• Complications which may worsen porgnosis –
– Infectious endocarditis
– Ostial narrowing
– Co-existing CAD
– Atrial or ventricular arrythmias

21. Physical Findings
• DBP low.
• Kortokoff sounds may be heard even when the
cuff pressure reaches zero
• Wide pulse pressure.
• Sinus tachycardia.
• Apical impulse is displaced to left and below its
usual location
• Murmur – soft, blowing, holodiastolic,
decresendo

22. Cont ..
• Duration of murmur related to severity.
• Systolic ejection murmur may be present.
• Carotid thrill is present in considerable
number of patients.
• Austin Flint Murmur – late diastolic rumbling
murmur

23. Peripheral signs.
• Corrigans Pulse - water hammer pulse
• Mayne’s sign – fall in DBP >20mmhg on raising
arm

24. De musset sign, Muller’s Sign

25. Lighthouse Sign – Blanching of
forehead

26. Ashrafian Sign- pulsatile pseudo-
proptosis

27. Landolfi Sign – Pupillary Contraction

28. Beckers sign

29. Quinckie’s sign

30. Signs in Lower extremities

31. Rosenbach Sign

32. Gerhardts sign – pulsating spleen

33. Shileys Sign – Pulsating Cervix

34. INVESTIGATIONS
• ECG –
– LEFT VENTRICULAR PREPONDERANCE
– SMALL Q, TALL R, ISOELECTRIC ST SEG. AND
UPRIGHT T – DIASTOLIC OVERLOAD
– ST DEPRESSION, T INVERSION – SYSTOLIC
OVERLOAD
– AR SEC. TO INFLAMTORY PROCESS – BLOCKS,
LONG PR ETC

35. CXR
• CARDIOMEGALY
• “BOOT SHAPED”
• PROMINENT ASCENDING AORTA
• EGG SHELL LINEAR CALCIFICATION ALONG
ASCENDING AORTA – LUETIC
• CALCIFICATION – RHD, BICUSPID, UNICUSPID
• LVF – PULMONARY VASCULAR
REDISCTRIBUTION

36. CXR

37. ECHO
• IN ABSENCE OF MITRAL DISEASE – BROAD
BAND OF (3-4MM) DIASTOLIC FLUTTER (20-
70HZ) OR VIBRATION OF ANTERIOR MITRAL
LEAFLET.
• MITRAL VALVE CLOSURE PRIOR TO QRS.
• DIALATED AORTIC ROOT
• LVED, LVES DIMENSIONS, EF
• DOPPLER TECHNIQUE

41. CARDIAC CATH
• HAEMODYNAMIC MEASUREMENTS
• WITH SEVERE DECOMPENSATION – LT
VENTRICULAR END DIASTOLIC AND AORTIC
DIASTOLIC PRESSURES EQUALISE
• LEFT VENTRICULOGRAPHY –
– INC EDV
– ECCENTRIC LVH
– REDUCED CONTRACTILE FUNCTION
– ABNORMAL END SYSTOLIC VOLUME AND END
SYSTOLIC PRESSURE RELATIONSHIP

42. CONT..
• MORE ACCURATE METHOD – CALCULATE
REGURGITANT FRACTION
• REGURG FRACTION = TOTAL CO FROM LEFT
VENTRICULOGRAM – FORWARD CO BY FICK
TECHNIQUE
– MILD TO MOD- <0.50
• SEVERE - >0.50

43. THERAPY
• MOST IMPORTANT DETERMINANT –
– PREOP LV SYSTOLIC FUNCTION
– OTHERS –
– FRACTIONAL SHORTENING
– END SYSTOLIC DIMENSIONS

44. ROLE OF VASODILATOR THERAPY
• REDUCE REGURGITANT VOLUME HENCE –
– REDUCE LVed, WALL STRESS, AFTERLOAD
• MAINLY DRUGS USED ARE –
– SNP
– HYDRALAZINE
– NIFEDIPINE
• RATIONALE – BENEFICIAL HAEMODYNAMICS SHOULD
TRANSLATE TO PROLONGATED COMPENSATED PHASE
• MAY RESULT ONLY AS “COSMETIC EFFECT”
• EVEN SLIGHTLY DEPRESSED LV FUNCTION NECESSITATE AVR
• REMEMBER, ITS NOT AN ALTERNATIVE TO AVR

45. INDICATION FOR AVR
• AVR, ONLY IF THE DEGREE IS SEVERE
• LV DYSFUNCTION – AVR
• CO EXISTING CONDITION – AVR
• ONSET OF TRUE CARDIAC SYMPTOMS EVEN
MILD – AVR
• A DEC IN EF DURING EXERCISE IS A VERY NON
SPECIFIC FINDING.