summarized form of anaesthetic management of a case of valvular heart disease......

1. Anaesthetic management
of Valvular Heart Disease
Presented by :- Dr Ravi shankar sharma
Sanjay gandhi memorial hospital,Rewa

2. Patient details
• Name: Mrs. Savitha ,staff nurse
• Age: 42 years
• Sex: female
• Chief Complaints :-
Large pelvic mass(suspected to be ovarian
cyst),scheduled for excision of mass.
-Palpitations since 6 weeks
-Breathlessness since 4 weeks
-Fatigue since 2 weeks

3. History of Presenting Illness
• Palpitation –Intermittent,
Associated with exertion
Relieved on rest
6 weeks duration
• Breathlessness- Gradual in onset,she can climb
2 flights of stairs without difficulty but feels
breathlessness beyond this point
-Progressive in nature (NYHA II)
-4 weeks duration

4. • Fatigue –
- Feeling of weakness
- 2 weeks duration
h/o rheumatic heart disease since 12 yrs of age,
took T/t in form of penicillin injections every 21
days for 8 years till age 20 and then
discontinued
 h/o normal previous pregnancy 15 year ago
H/o Ballon mitral valvotomy -13 yr ago.
No h/o hypertension, Diabetes mellitus,
tuberculosis ,bronchial asthma or epilepsy

5. • Family history:-
no h/o similar complaints in the family was
noted
• Personal history:-
Vegetarian
Reduced appetite
Normal bladder and bowel movement
Disturbed sleep
No addiction

6. General physical examination
• An elderly female patient , moderately built and
nourished
• No pallor/icterus/cyanosis/oedema/clubbing
• weight-55kgs,
• Height-160cm,
• Pulse-90/min,
• B.P.-110/70 mm of hg
• Respiratory rate-16/min
• JVP:-not raised

7. • Respiratory system:-
B/L equal air entry
Normal vesicular breath sound
No added sounds
• Central nervous system:-
Conscious
Well oriented to time place and person
No neurological deficits

8. • Per abdominal examionation:-
 Distended in the pelvic region
No free fluid
No dilated veins
• Cardiovascular system:-
Inspection: No deformity, smallscar mark
present over the precordium, no engorged
superficial veins , no visible pulsations
Palpation: Apex beat felt in 5th IC space medial
to left mid clavicular line , abesence of
parasternal heave

9. • Auscultation:-
S1 S2 heard,(S1 is short,shrp,accentuated)
Opening snap heard near the apex(after s-2)
Low pitched mid diastolic murmur at apex(no
radiation)

10. Investigations:-
• Hb-12.4 gm%
• TLC-7400 cells/cumm(P-76,L-17,M-4,E-3,B-0)
• Platelet-2.3lac.
• Blood group-B+ve
• BT:-3min.
• CT:-4 min.
• RBS:-94 mg/dl
• Urea:-38 mg/dl
• Creatinine:-1.3mg/dl

11. • Na+:-135 meq/l
• K+:-4.5meq/l
• Cl-: 104meq/l
• HIV 1&2-non reactive
• HbsAg-Non reactive
• ECG:-sinus Rhytm ,H.R.-75/min, Right axis
deviation
• ECHO:-normal left ventricular systolic function
No regional wall motion abnormalities
Ejection fraction-50%
• CXR:-cardiomegaly, prominent Bronchovascular
marking

12. Substantiation
disturbed
sleep
Absent
Parasternal
heave – mild
disease
Edema &
Hepatomegaly
absent – mild
disease
Opening snap
+murmur at
apex
Childhood
history
Female
Patient
Rheumatic
Heart Disease
Edema &
hepatomegaly
absent
Palpitations Dyspnea
Absent parasternal
heave – mild disease
Opening Snap + low
pitched mid diastolic
murmur
2D – Echo – Mitral Valve 2.0 cms2,(theory),
Transvalvular pressure 8 mm of Hg
Mitral Stenosis of Rheumatic Origin without evidence of
congestive cardiac failure.

13. MITRAL STENOSIS
Narrowing of the mitral valve orifice causing
obstruction to blood flow from left atrium to the
left ventricle.

14. Etiology of Mitral Stenosis
1. Rheumatic Heart Disease-M.C. cause
2. Congenital – Parachute Mitral Valve
3. Hunter’s Syndrome
4. Hurler’s Syndrome
5. Drugs – Methysergide
6. Carcinoid syndrome
7. Amyloidosis
8. Mitral annular Calcification
9. Rheumatoid Arthritis
10. Systemic Lupus Erythematosis
11. Infective endocarditis with large vegetations.
12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral
Stenosis (MS) rheumatic origin

15. Pathophysiology
Decreased LV filling
Increased left atrial
pressure and volume
Pulmonary vein pressure
Transudation of fluid into
pulmonary interstitial space
Pulmonary compliance
Work of breathing
Progressive Dyspnea
Adaptation Atrial Kick
Adaptation
Lymphatic drainage and thickening of
basement membrane
Pulmonary hypertension
Palpitations
Breathlessness Haemoptysis

16. Pathophysiology
Almost all chambers are
shown here , except…
Left Ventricle
So, are we to assume
that Left Ventricle
remains unaffected..?

17. Pathophysiology
The answer is NO. Left Ventricle is affected
Decreased filling ultimately manifests as
1. muscle atrophy
2. Inflammatory myocardial fibrosis
3. Scarring of sub valvular apparatus
4. Abnormal pattern of left ventricle contraction
5. Decreased left ventricular compliance with diastolic dysfunction
6. Right to left shift due to pulmonary hypertension

18. Common symptoms
1. Dyspnoea
2. Orthopnea
3. Paroxysmal Nocturnal Dyspnea
4. Palpitation
5. Fatiguability
6. Haemoptysis
7. Recurrent Bronchitis
8. Cough
9. Chest pain
10. Right hypochondrial Pain (hepatomegaly)

19. Mitral Stenosis: Physical Examination
S1 S2 OS S1
• First heart sound (S1) is loud and snapping
• Opening snap (OS)
• Low pitch diastolic rumble at the apex
• Pre-systolic accentuation (esp. if in sinus rhythm)

20. GRADING :-
Normal Orifice: 4 – 6 Cms2
4-6 cms2
< 2.5 cms2
1.5- 2.5 cms2
1.0 – 1.5 cms2
< 1.0 cms2
Mild MS – 1.5 – 2.5 Cms2
(Dyspnea on severe exertion)
Moderate MS – 1.0 – 1.5 Cms2
(PND ± pulmonary oedema)
Severe/ Critical- < 1.0 Cms2
(Orthopnea – Class IV)
Symptoms start < 2.5 Cms2

22. Anatomy
Mitral Valve area is calculated using Gorlin’s Equation:
Area = Cardiac Output/ (DFP or SEP) (HR)
44.3 C √ΔP
DFP = Diastolic Filling Pressure
C = Empirical Constant
SEP = Systolic Ejection Period
ΔP = Pressure Gradient
HR = Heart Rate

23. Cormier’s grading of Mitral valve
anatomy
Echocardiographic group Mitral valve anatomy
Group 1 Pliable non calcified anterior mitral leaflet and mild
subvalvular disease(ie thin chordae>/=10mm long)
Group 2 Pliable non calcified anterior mitral leaflet and severe
subvalvular disease(thickened chordae<10mmlong)
Group 3 Calcification of mitral valve of any extent as assesed by
fuoroscopy ,whatever the state of subvalvular apparatus

24. Diagnosis
One needs to assess anatomy of Mitral Valve Leaflet in terms of
1. Thickening
2. Calcification
3. Mobility
4. Extent of involvement and subvalvular apparatus
One also needs to assess extent of stenosis
1. Mitral Valve area
2. Transvalvular pressure gradient
Also to be assessed are
1. Cardiac chamber dimension 2. Pulmonary hypertension
3. Ventricular function 4. Associated valvular disease
5. Examination of Left Atrial Thrombus

25. Diagnosis
Assess extent of calcification
1. Disappearance of Opening snap especially if calcification is more.
Assessment of X-Ray (P-A View)
1. Left Atrial Enlargement – Mitralisation of heart
2. Straightening of Left Heart Border
3. Elevation of Left mainstem Bronchus
4. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary
Vascular Congestion.
5. Kerley’s B lines
Assessment of X-Ray (RAO view)
1. Oesophagus is pushed or curved backward by enlarged left atrium.

26. Diagnosis
Assessment of ECG
1. Broad notched “P” Waves signifying atrial enlargement.
2. Atrial Fibrillation (f- waves replacing p-waves)
3. Right Ventricular Enlargement
2D – Echocardiography Doppler study
1. Chamber Enlargement 1. To know the speed and direction of blood flow.
2. Valve pathology
3. Valve movement
4. Mitral Orifice
Blood Examination
1. TC and DC 2. ESR
3. ASO Titre

27. Treatment
1. Mild Mitral stenosis – Diuretics
Restriction of physical activity
Salt-restricted diet
2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet)
β- Blockers
Calcium Channel Blockers
Control of heart rate is paramount, because tachycardia impairs left ventricular
filling and further increases left atrial pressure.
3. Anticoagulation – Warfarin to normalise INR 2.5 to 3.0

28. Treatment
4. Surgery if Pulmonary hypertension develops
Percutaneous balloon valvotomy
Surgical commisurotomy
Valve reconstruction
5. Valve replacement
Starr-Edwards ball valve
Bjork-Shiley disc valve
Porcine bio-prosthesis
6. Prophylaxis against recurrence of rheumatic fever
Inj. Benzathine Penicillin 1.2 million units.

29. Anaesthetic Management

30. Anaesthetic Management
Principle involved:
Cardiac Output
Decrease in cardiac output
Hypotension
Tachycardia
Reduced ventricular
filling
Vicious cycle
Increased
ventricular filling
Trendelenburg'
s position,
Autotransfusio
n due to
uterine
contraction
Precipitation of
CHF
1
2
3

31. Anaesthetic Management
Principle involved:
1. Prevent decrease in cardiac output, as hypotension because of this causes
reflex tachycardia, which in turn reduces ventricular filling further
compromising cardiac output.
2. Avoid hypotension for the same reason listed above. If hypotension ensues,
treat with Ephedrine or Phenylephrine.
3. Avoid precipitating Congestive Heart Failure due to factors such as
Trendelenburg’s position
Autotransfusion due to uterine contraction leading to
increased central blood volume.
4. Avoid precipitation of Right Ventricular Failure
Hypercarbia
Hypoxemia
Lung Hyperinflation
Increase in lung water
If Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.

32. Anaesthetic Management
Preoperative Medication
1. Decrease anxiety (decreases tachycardia),also avoide anti- cholinergics.
2. Drugs used to control heart rate to be continued till day of surgery
3. Hypokalemia if present secondary to diuretic therapy to be addressed
4. If intended surgery is a minor surgery, continue anticoagulant therapy
5. If intended surgery is a major surgery, discontinue anticoagulant therapy.
Induction of Anaesthesia
1. Avoid Ketamine – Increases heart rate, Avoide Propofol(fall in blood pressure)
(ETOMIDATE/THIOPENTONE)-Better choice
2. Avoid Atracurium – Increased histamine release causes hypotension which
manifests as tachycardia.(vecuronium-preffered)

33. Anaesthetic Management
Maintenance of Anaesthesia
1. Drugs should have minimal effects on hemodynamic pattern
2. Balanced anaesthesia with Narcotic/ N2O /Volatile anaesthetic(avoide
halothane)
3. N2O causes insignificant pulmonary vasoconstriction. It is significant only if
pulmonary hypertension exists. So, one needs to treat pulmonary
hypertension preoperatively.
4. Cardiac stable muscle relaxants are to be used. (preferably avoid Pancuronium)
5. Avoid lighter planes of anaesthesia (To avoid tachycardia)
6. Fluid Management:
Avoid Hypervolemia - -> Worsens pulmonary edema
Avoid Hypovolemia - -> Sacrifices already decreased left ventricular filling,
which further decreases Cardiac output. Hypovolemia secondary to blood
loss and vasodilatory effects of anaesthesia ought to be avoided.

34. Anaesthetic Management
Monitoring
1. Transesophageal Echocardiography
2. Intra-arterial pressure
3. Pulmonary artery pressure to be monitored
4. Left atrial pressure
Principle:
1. Ensure adequacy of cardiac function
intravascular fluid volume
ventilation
oxygenation
A word of caution regarding Pulmonary artery pressure monitoring: -
When measured too frequently, the risk of pulmonary artery rupture is far too
high.

35. Anaesthetic Management
Post Operative
1. Assess postoperative risk of pulmonary oedema and right heart failure and
manage accordingly.
2. Avoid pain as pain begets hypoventilation which leads to respiratory acidosis,
hypoxemia which manifests as raised heart rate and pulmonary vascular
resistance.
3. After Major thoracic or abdominal surgery, the decreased pulmonary
compliance and increased work of breathing requires mechanical ventilation.

36. Role of regional anaesthesia in MS:-
Regional anaesthesia (Sub Arachnoid Block, Epidural, peripheral nerve blocks)
Sub Arachnoid Block:
-can be used in mild cases of MS only
-sympathetic blockade with intense vasodilatation sudden hypotension and severe
tachycardia should be avoided
Epidural Block: compared with spinal anaesthesia epidural anaesthesia allow
better control of level of sympathectomy and reduction in blood pressure
-can be used as a sole anaesthesia technique in patients with mild to moderate MS
Peripheral nerve blocks : can be used safely
-ASRA guidelines on regional anaesthesia in patient receiving anticoagulation or
thrombolytic theory should be followed

37. The New York Heart Association (NYHA) Grading of
functional capacity of the heart:
CLASS I
No functional limitation of activity Symptoms with extra ordinary
physical work.
CLASS II
Mild limitation of physical activity. Symptoms with ordinary
physical work
CLASS III
Marked limitation of physical activity Symptoms with less than
ordinary physical work
CLASS IV Severe limitation of physical activity Symptoms at rest
Management of pregnancy with MS

38. Prognosis depends on the functional status
v NYHA classes I and II lesions
usually do well during pregnancy and have a
favorable prognosis (mortality rate of <1%).
v NYHA classes III and IV -mortality rate of 5% to 15%.
-These patients should be advised against becoming
pregnant.

40. Why does pregnancy aggravate the symptoms of
Mitral stenosis
I. ↑ in blood volume by 30-50%→↑ in pulmonary capillary hydrostatic
pressure→ ↑ risk of pulmonary oedema
II. ↓in systemic vascular resistance
III. ↑ in HR by 10-20 beats /min→ ↓diastolic filling time of LV
IV. C.O. ↑ by 30-50% after 5th month &returns to normal within 3 days
of delivery
V. Because TPG ↑by square of CO,TPG ↑ significantly →LA pressure
→symptoms
VI. During labour &delivery →sympathetic stimulation →tachycardia →
↑CO
VII. ↑in venous return to heart d/t autotransfuson and IVC compression
→decompensation
VIII. Enlarged atrial dimension predispose to atrial arrythmias including
atrial fibrillation
IX. Also induces changes in haemostasis which contribute to increased
coagulability and thromboembolic stroke

41. Anaesthetic Options
VAGINAL DELIVERY :
 Recommended whenever possible if the haemodynamic condition is
stable at the end of pregnancy
• Epidural anaesthesia is recommended
• Tachycardia, secondary to labour pain, increases flow across the mitral
valve, producing sudden rises in left atrial pressure, leading to acute
pulmonary oedema. This tachycardia is averted by epidural analgesia
without significantly altering the patient haemodynamics.
• LA can be used to provide Perineal anaesthesia
• Caesarean section is indicated for OBSTETRIC REASONS ONLY.

42. When to give Infective Endocarditis Prophylaxis..?

43. Aortic Stenosis
• Aortic stenosis (AS) is narrowing of the aortic
valve resulting in obstruction of blood flow
from the left ventricle to the ascending aorta
during systole.
-Normal aortic
valve area is 2.5
to 3.5 cm²

44. Etiology
• congenital bicuspid aortic valve (2%).
• Rheumatic heart disease.
• Valve Calcification.

45. Pathophysiology:-

46. AS severity
Severity Mean gradient,
mm Hg
Aortic valve
area, cm2
Mild <25 >1.5
Moderate 25-40 1.0-1.5
Severe >40 <1.0
Critical >80 <0.7
Normal aortic valve area is 2.5 to 3.5 cm²

48. Aortic Stenosis: Physical Findings
S1 S2 S1 S2
Mild-Moderate Severe
An early peaking murmur is typical for mild to moderate AS
Late peaking murmur is consistent with severe AS.
Delayed A2
Pulsus Tardus-pulse ie slowly rising to peak and then has a
low down slope

50. Medical Treatment
• Antibiotic prophylaxis is NOT recommended in all pts with AS for
prevention of infective endocarditis.
• Caution with diuretics and vasodilators (reduce preload)
• HTN should be treated cautiously with appropriate
antihypertensives (preload dependence)
• Statins have been studied to see if they cause regression or
delayed progression of leaflet calcification (need more data)
Effective treatments for severe AS:-
1.Surgical replacement of the aortic valve
2.Transcatheter aortic valve replacement (TAVR)

51. Anesthesia concerns:
– Maintain normal sinus rhythm
– Avoide bradycardia or tachycardia
– Watch out for vasodilation(hypotension)Rx-
phenylephrine
– Optimize i/vascular fluid volume to maintain venous
return and left ventricular filling
– Mild to moderate AS may tolerate spinal or epidural
(epidural preferred)
– Spinal and epidural contraindicated in severe AS
– High risk of myocardial ischaemia

52. Pregnancy considerations
Caesarean section:
-General anaesthesia with the aid of invasive haemodynamic
monitoring. Aggressive maintenance of systemic blood
pressure with vasopressors (e.g. phenylephrine).
- Spinal anaesthesia is generally contraindicated.
- vaginal delivery under carefully introduced and limited
epidural analgesia in mild cases

53. Mitral Regurgitation
A portion of the LV volume is ejected back into
LA during systole because of an incompetent
valve.

54. Etiology
ACUTE
– Myocardial ischemia
or infarctions
– Infective
Endocarditis
– Chest trauma
CHRONIC
 Rheumatic fever
 Incompetent valve
 Destruction of mitral valve
annulus

55. Chronic MR: Pathophysiology
Vol load imposed on LA & LV (usually it gradually ↑ over time)
Large total SV (supra normal EF) and normal forward SV
MR begets MR (viscious cycle in which further LV/annular
dilatation ↑ MR
↑ Preload, LV hypertrophy, & reduced or normal afterload (low
resistance LA provides unloading of LV)
↑ LVEDP &↑ LAP
Compensatory dilatation of LA & LV to accommodate vol load at
lower pressure; this helps relieve pul congestion
LV hypertrophy (eccentric) stimulated by LV dilatation (↑ wall
stress- Laplace Law)

56. Chronic MR: Pathophysiology..continue
Reduced forward SV/CO
MR begets MR (viscious cycle in which further LV/annular
dilatation ↑ MR
Pul congestion & pHTN
Contractile
dysfunction
↓ EF, ↑ end-systolic volume ↑ LVEDP/ vol, ↑ LAP
Regurgitant fraction >0.6 -severe mitral regurgitation.

57. Symptoms and signs
Acute phase
C/f of decompensated
congestive heart failure (i.e.
shortness of breath,
pulmonary edema,
orthopnea, and paroxysmal
nocturnal dyspnea),
- decreased exercise tolerance
-Palpitations.
- cardiogenic shock
Chronic phase
• may be asymptomatic,
with a normal exercise
tolerance and no
evidence of heart failure.
• individuals may be
sensitive to small shifts in
their intravascular volume
status, and are prone to
develop volume overload
(congestive heart failure).
MOHAMMAD ALADAM
The symptoms associated with mitral regurgitation are dependent
on which phase of the disease.

58. MITRAL REGURGITATION
Acute Chronic
ECG Normal
P mitrale, AF, Left Ventricular
Hypertrophy
Heart size Normal Cardiomegaly, left atrial enlargement
Systolic murmur
Heard at the base,
radiates to the
neck, spine, or top
of head
Heard at the apex, radiates to the
axilla
Apical thrill May be absent Present
Jugular venous distension Present Absent

59. Chest X Ray-
- Enlarged LA and LV,
-Signs of pulmonary venous hypertension
-RVH
-Mitral calcification (in co existing MS)
Severity of MR evaluated by:
-Color-flow and pulsed-wave Doppler
-Pulmonary artery occlusion pressure waveform
-Cardiac catheterisation
-ECHO-confirms diagnosis ,Also assess mechanism and severity of MR
DIAGNOSIS:-
MILD MODERATE SEVERE
Area of MR jet (cm2) <3 3.0-6.0 >6
MR jet area as percentage of
left atrial area
20–30 30–40 >40
Regurgitant fraction (%) 20–30 30–50 >55

60. • TREATMENT
• Drugs-
Digoxin, diuretics for CHF
Vasodilators ( ACE inhibitors, nitrates) in acute symptomatic MR
Warfarin for AF/Thromboembolism
• Surgery-
-Mitral annuloplasty/valvuloplasty
-Mitral valve repair> replacement
• Patients with an EF <30% or left ventricular end-systolic dimension more
than 55 mm do not improve with mitral valve surgery.

61. • Prevention and treatment of events that decrease CO.
• Improve forward LV Stroke Volume and decrease the regurgitant fraction.
Vasodilatation can improve forward flow- NTG/ nitroprusside infusions.
Useful in PAH as well but not once RVF sets in.
• Preload – maintain or slightly increase
• Maintain or increase HR- Avoid bradycardia
• Decrease in afterload beneficial- Avoid sudden increase in SVR
• Minimize drug-induced myocardial depression
• Avoid hypoxia, hypercarbia and acidosis (all increase PAH)
Anaesthetic goals

62. PREMEDICATION + INDUCTION:-
• Light premedication preferred
• Large dose narcotics induction or
• Opoids + Benzodiazepenes ( Fentanyl + midazolam / sufentanyl+ midazolam)
either continuous or intermittent bolus
• Muscle relaxant
Pancuronium preferred as increased HR desirable
Vecuronium/ Atracurium- depending on basal HR
• MAINTAINENCE
• Volatile anesthetics ( Isoflurane ,sevo, des)
Increase in heart rate and minimal negative inotropic effects. Vasodilatation
desirable.(afterload reduction)
• Nitrous oxide avoided in severe PAH.
• myocardial function is severely compromised--- opioid-based anesthetic
potent narcotics → bradycardia, deleterious in severe MR.

63. MAINTAINENCE cont......
• Mechanical ventilation → maintain near-normal acid-base and respiratory
parameters.
• The pattern of ventilation must provide sufficient time between breaths for
venous return.
• Maintenance of intravascular fluid volume is very important for maintaining left
ventricular volume and cardiac output in these patients.
• Monitoring
• Invasive monitoring- ( CVP, PAC)
Useful in severe MR- detecting the adequacy of CO and the hemodynamic
response to anesthetic and vasodilator drugs
• facilitating intravenous fluid replacement.
• Pulmonary artery occlusion pressure –
-V waveform to assess severity of MR

64. Aortic regurgitation (AR)
Aortic regurgitation (AR) is a diastolic reflux of blood from the
aorta into the left ventricle owing to failure of coaptation of the
valve leaflets during diastole
- d/t aortic valve disease/aortic root dilatation or combination of
both

65. Etiology
Acute AR
• Infective endocarditis
• Prosthetic valve dysfunction
• Aortic dissection
• Trauma
• Systemic hypertension
Chornic AR
• Bicuspid Aortic Valve
• Rheumatic and SLE
• Degenerative
andHypertension
• Anorectic drugs
• Aortitis
• Giant cell arteritis
• Ankylosing spodylitis
• Connective tissue disorders

67. Symptoms:-
Asymptomatic: 10-15 Years
 PALPITATION -( early symptom), head pounding - on exertion,
exertional dyspnoea , orthopnoea , paroxysmal nocturnal dyspnoea
,excessive diaphoresis , angina ,ccf - late
Corrigan pulse or Water hammer pulse or Collapsing pulse ie
Rapid rise and rapid fall ,Bisferiens’s pulse -two peaks in systole
Widened pulse pressure along with dec. diastolic blood pressure
Early diastolic murmur, Austin flint murmur( Soft, low
pitched rumbling mid diastolic murmur)

68. Peripheral Signs of AR
• Lighthouse sign ( blanching of forehead)
• Landolfi’s sign ( alternate dilatation and contraction of iris)
• Becker’s sign (prominent retinal artery pulsations)
• De Musset’s Sign (head bobs with heart beat)
• Corrigan’s sign ( Dancing carotids )
• Muller’s sign (systolic pulsation of uvula)
• Corrigan’s pulse (water hammer pulse)
• Quninckey’s sign (pulsatile nailbed)
• Palfrey’s sign ( pistol shot sounds in radial artery )
• Rosenbach’s sign (pulsations in liver)
• Gerhart’s sign ( pulsations in spleen )
• Traube’s sign (Pistol shot sounds in femoral artery)
• Duroziez murmur (murmur heard over femoral artery) systolic on
proximal compression , diastolic on distal compression
• Hill sign (popliteal systolic pressure – Brachial 20-40 – mild, 40-60 –
mod > 60 mm Hg severe AR)

69. • ECG- shows Lt axis deviation
• CXR- Cardiomegaly ,Hypertrophy and dilatation of LV
• Echo
• Doppler examination-to identify the presence and severity
• AR quantification by Based on
– Color flow Doppler (Jet width and jet area measurement)
– Continuity equation &Regurgitant jet velocity assessment
Treatment:-
Vasodilators , inotropes(improves LV stroke volume
&↓reguirgitant volume
chronic aortic regurgitation (requires surgery)
Long term Rx with nifedipine/hydralazine –delays the need
of surgey
Diagnosis:-

70. Anesthetic considerations
– Maintain normal heart rate (avoide bradycardia)
– Keep SVR low
– Avoid myocardial depression
– GA is usual choice for patient with AR
– Spinal/Epidural well tolerated.
Pregnancy considerations-During labour, epidural
analgesia improves forward flow, and is therefore the
anaesthetic of choice in patient’s requiring an operative
delivery.