Valvular heart diseases are commonly encountered in anesthesia management. Each valvular needs different approach.

1. ANESTHESIA IN VALVULAR
SURGERY
Tenzin Yoezer
Resident
KGUMSB

2. DEFINITION
•An acquird or congenital disorder of cardiac valve
characterized by stenosis (obstruction) or
regurgitation (backward flow) of blood

3. INTRODUCTION
• Anesthetic management during periop period is based on likely effects of drug
induced changes in:
• Cardiac rhythm
• HR
• Preload
• Afterload
• Myocardial contraliltiy
• Systemic BP
• SVR
• PVR

4. BASIC CARDIOLOGY TERMS
• Systolic function – contract & ejection blood
• Contractiltiy – intrinsic ability of myocardium to contract & generate force
• Preload – laod placed on myocardium before contraction – diastolic volume & filling
pressure
• Afterload - load placed on myocardium during contraction – systolic volume and
generated pressure

5. EVALUATION OF VALVULATR PATIENT
• Preop assessment :
• Severity of cardiac disease
• The degree of impaired myocardial contractiltiy
• Presence of assocaited major organ system disease

6. EVALUATION OF VALVULATR PATIENT
• current drug therapy
• Presence of secondary effects on pulmonary, renal & hepatic function
• Presence of concimitant CAD

8. PHYSICAL FINDINGS
• Signs of CHF:
• S3 gallop
• Pulmonary rales
• Elevated JVP
• Hepatojugular reflux
• Pedal oedema
• Specfc to individual valvular lesions:
• Murmur- character, systolic/diastolic,
location, intensiy, grade, radiation
• Neurologic deficits secondary to
embolic phenomena

9. INVESTIGATIONS
• Tailored to pt & procedure:
• ECG – LVH, RVH, arrythmias, ischemia
• CXR- cardiac size, pulmonary vascular
congestion, oedmea
• Echo
• Cadiac catherization to identify:
• Coexisting CAD
• Sevrity of stenosis/regurgitation
• Intracardiac shunts
• Clincal & echo discrepancies

10. INVESTIGATIONS
• Serum electrolytes
• RFT
• Cagulation profile
• ABG – significant pulmonary symptoms

11. ENDOCARDITIS
PROPHYLAXIS

12. CLASS 1 RECOMMEDNATION
(HIGH TO MODERATE RISK)
• Prostehis valves/history of IE
• Complex cyanotic CHD
• Surgically constructed systemic-pulmonary shutns or conduits
• Congenital cardiac valve malformations – bicuspid aortic valve
• History of surical repair
• Hypertrophic cardiomyopathy with resting/latent obstruction
• MVP with auscultaory evidence of valvular regurgitation & or thickened leaflets on
echo

13. CLASS II RECOMMEDNATION ( LOW RISK –
PROPHYLAXIS NOT RECOMMENDED
• Isolated secumdum ASD
• >6 onths after successful surgical or percutanesou reair of AD, VSD< PDA
• MVP witout MR or thickened leaflets on echo
• Physiological heart murmur
• Echo e/o physiological MR with ansensceof murmur withstructurally normal valves
• Echo e/o physiologic TR or Pr with absence of murmur and strcuturaly normal valves

15. PROSTHETIC VALVES

16. PROSTHETIC VALVE
• Bioprostehtic
• mechanical
• Bioprosthetic valves:
• Hetergeneous graft made form animal tissue
• Low thrombogenic potential
• Do not need systemic anticoagulation
• Aspirin is recommendaed

17. PROSTHETIC VALVE
• Mechanical valves:
• Longer lastinf
• Need for lifelong anticogualtion 0 warfarin therapy
• Aspirin is usually combined with warfarin in mechanical heart valves
• Aspirin allergy - clopidogrel

18. PATIENTS WITH PROSTHETIC VALVE
UNDERGOING SURGICAL PROCEDURES
• Complete history & physica examination
• Type of valve inserted
• Ausculation – high-pitched, crisp opening & closing sounds
• Bioprsothetic valves do not have special ausculatatory characteristics
• Onset of new murmurs/change in quality of murmurs
• Problems with vavle/endocarditis

21. AORTIC VALVE

22. AORTIC VALE
• 3 semilunar AV:
• left (posterior),
• right (anterior)
• non-coronary cusp
• Functions:
• to permit unimpeded LV systolic ejection
• to prevent regurgitation of the LV stroke
volume during diastole.
• Normal adult AV orifice area = 2-4 cm ( 3-4
by Miller 9th edition)

23. AORTIC STENOSIS
• Defined as fixed obstruction to systolic
LV outflow
• Severe = area < 1cm2 or mean gradient
> 40mmhg
• c/f:
• Asymtomatic for many years
• Classic traid – angina, syncope,
breathlessness
• Sudden cardiac death

24. SIGNS OF AORTIC STENOSIS
• Slow-rising crotid pulse
• Narrow pulse pressure
• Heaving apex beat (LVpressure overload)
• Ejection systolic murmur aortic area
• Signs of pulmonary venous congestion

25. DIANOSIS
• ECG – LVH, Tall R & S wave, T inversion(strain) in anterior leads
• CXR – ascending aorta dialation (post-stenotic)
• Echo + doppler – assess severity of AS:
• Aortic valve area
• Transvalvular pressure gradient
• LVH
• Valve thickening/calcification
• Mobility of leaflet
• Bicuspid valve
• Systolic/diastolic dysfunction

27. PATHOLOGY
• Degenerative – calcification, stiffness, thickening
• Age related - > 70 years
• Associated with MV annular calcification
• Chronic RHD
• Congenital – bicuspid

28. PATHOPHYSIOLOGY
• Fixed obstruction to LV ejectin – chronic
LV pressure pverload and increased wall
tension (laplace law) – compensatory
concentric LVH – diastolic dysfuction
• Almost always associated with some
degree of AR
• Produces both systolic and diastolic LV
dysfunction

31. TREATMENT
• Asymptomatic – medical management
• Symptomatic – AV replacement
• Coronary revascularization – pt with both AS & CAD
• Percutaneous aortic ballon valvotomy – adolescents & young with
congenital/rheumatic etiology

32. INDICATIONS FOR AV REPLACEMNT
• Severe AS with any classic symptoms
• Severe AS undergoing CABG
• Severe AS undergoing surgeries on aorta/ other heart valves

33. ANESTHETIC
GOALS IN AS

34. KEY NOTES
• Tachycardia, severe bradycardia and vasodilatation are poorly tolerated in AS.
• Hypotension should be treated early in AS to prevent haemodynamic collapse.
• Avoid vasodialtors to treat introp HTN
• Deliberate ‘nodal’ A-V pacing can be used in extreme circumstances to treat
hypertension following AVR for AS.

35. INDUCTION OF ANESTHESIA
• GA preferred over RA due to risk of HYPOTENSION
• Induction drugs – etomidate, opioids, midazolam
• Ketamine – avoid
• Thiopentone – decreases preload
• Propofol - hypotension

36. MAINTENACE OF ANESTHESIA
• N2O/ volatile/ opioid or opioids alone
• Marked LV dysfunction – N2O + Opioids or high dose of opioids alone
• Fentanyl (10-25mcg/kg) or sufentanil (2-5mcg/kg
• NMB – minimal hemodynamic effect

37. PREGNANCY CONSIDERATION
• CS –
• GA with invasive monitoting
• SA is CI
• VD –
• careful epidural anlgeisa
• Maintence of with vasopressor like phenyephrine

38. AORTIC REGURGITATION

39. AORTIC REGURGITATION
• Defined as diastolic leakage across the AV, which causes LV volume overload
• C/F: depends on acute or chronic
• Acute AR – acute pulmonary oedmea, tachycardia, poor perfusion
• Chronic AR – asymptomatic, breathlessness on exertion, angina ( less common)

40. SIGNS
• Collapsing pulse
• Increased pulse pressure
• Bounding peripheral pulse
• Capillary pulsation in nail beds
• Femoral bruit
• Murmurs – early diastolic murmur, systolic murmur(increased SV), Austin flint murmur(Soft
mid-diastolic)
• Displaced, heaving apex beat(volume overload)
• 4th heart sound
• Crepitation

42. PATHOLOGY

43. PATHOPHYSIOLOGY
• Chnonic AR – increase LVEDV – eccentric
LVH(increase radius)
• Acute AR – diastolic and pressure overload in
normal sized, non-compliant LV
• Acute rise of LVEDV – reduces CPP – early
clossure of MV – requires higher LA filling
pressure

44. PATHOPHYSIOLOGY
• Magnitude of regurgitant volume depends on:
• Tiem availabe for regurgitant flow to ccur- determined by HR
• Pressure gradient across the aortic valve – dependent on SVR
• Thus, magnitude of regurgitant is decreased by tachycardia & peripheral
vasodialtion
• Pulse pressure is proportional to the SV & aortic elastance, increased SV increases
systolic pressure---- systolic HTN increases afterload

45. TREATMENT
Medical therapy
• Asymptomatic pts with normal LV fucntion
• Afterload reductions by:
• Vasodialtors
• Nifedipine
• ACEI
• hydralazine
Surgical therapy
• Acute AR:
• Vasodilaors(Nitroprusside)
• Course of antibiotics
• Valve replacemnt/repair
• Chronic AR:
• AV repair
• AV prosthesis

46. AORTIC VALVE SURGERY
• J-shaped upper (mini) sternotomy
• A-V conduction abnormalities are common after AV replacement.
• Epicardial pacing and close monitoring after ICU discharge are considered
mandatory.

48. INDUCTION OF ANESTHESIA
• Stavle pt – thiopental/etomidate
• A;ternative – high dose narcotic & benzodiazepam
• Critically ill with acute AR:
• Require inotropic & vasodilatory support prior to induction of anesthesia

49. MAINTENACE OF ANESTHESIA
• Sever LV dysfucntion – N2O = volatile &/opioid
• Iso, Des & Sevo
Bradycardia & myocardial depression – N2O/BZD, high-dose narcotic
NMB – pancuronium (tachyacrdia)
Treat bradycaida promptly with aropine (0.4 to 0.8mg)
Ephedrine –poor choice because increase in afterload hypotension not treated routinely with
vasopressors
RA – well tolerated

50. PREGNANCY CONSIDERATIONS
• Avoidance of aortocaval compression
• EA & anesthesia decreases afterload – preferred for VD/CS
• During labour – ealry adminstration of EA prevents pain-associated increase SVR ---
prevents acute LV volume overload
• Bradycardia not tolerated – treat promptly

51. MITRAL VALVE
DIESASE

52. MITRAL VALVES
• Normal adult area = 4-6 cm2
• 2 leaflets – AML & PML
• Carpentier classification of leaflets
• Chordae tendinate

53. MITRAL STENOSIS
• Defined as a valve area of < 2 cm2
• Severe or critical when the valve area is < 1 cm2
• Secondary to rheumatic fever (most common)
• Elderly – heavy calcification
• Rarely – congenital, rheumatoid arthritis
• Pure MS is less common than mixed stenosis and regurgitation, as a result of the
fixed orifice.

54. Mitral valve-
diagrammatic
representation with
haemodynamic
changes
LA- Left atrial pressure, PA- pulmonary arterial pressure, CO- cardiac output. 9th edition Miller

55. CLINICAL FEATURES
• Exertional dyspnoea – commonest due to pulmonary congestion
• Fatigue – low CO
• Odema, ascites - RHF
• Haemoptysis –pulmonary congestion, pulmonary embolism
• Cough – pulmonary congestion
• Chest pain - PHTN
• New onset AF
• Perpiheral embolic events – stroke, ischaemic limb
• Primarily affects female

56. SIGNS
• Mitral face
• AF
• Signs of PHTN:
• Loud 1st heart sound, opening snap
• Loud P2
• Low-pitched rough rumbling mid-diastollic murmur with presystolic ascentuation
• Signs of raised pulmonary capillary pressure:
• Crepitations, pulmonary oedema, effusion

57. SIGNS
• ECG – tall peaked P wave in II, upright in V1, RAD, RVH
• CXR:
• Straightening of upper left cardiac border
• Prominence of main pulmonary arteries
• Dilatation of upper lobe pulmonary veins
• Posterior displacement of esophagus by enlarged LA
• Kerley-B lines

58. ECHO
• Assessment of mitral valve anatomy :
• degree of thickening,
• calcification,
• Mobility
• Involvemnt of subvalvular apparatus
• Cardiac chamber dimensions
• Pulmonary HTN
• Thrombus
• Other valvular involvement

59. PATHIPHYSIOLOGY
• Fixed MV obsruction –creates pressure
gradient across MV – increase LAP – LA
hypertophy, AF, PHT,TR
• Depressed LV systolic function due to
myocaardial fibrosis and chronic
underloading
• Transduction of fluid into pulmonary
interstitial space – reduced pulmonary
compliance - increased WOB – progressive
dyspnea on exertion

61. MANAGEMENT OF MS
• Minor symptoms – medical treatment
• Diuretics – decrease pulmonary congestion
• Digoxin, B-blockers, CCB – control ventricular rate in AF
• Anticoagulants – redcues risk of embolism
• Antiotic prophylaxis – IE
• Definite Rx: surgical
• Severe symptoms (NYHA III/IV)
• Symptomatic despite medical Rx
• PHTN > 50 mmHg
• Surgery - ballon valvuloplasty, mitral valvotomy, MV replacement

62. SURGERY OF MS
• Percutaneous transeptal ballon valvotomy
• - non-calcified, pliable leaflets
• Valvotomy
• Palliative procedure
• Recurrence is common
• Valvular calcification
• Thickened fibrotic leaflets
• Subvalvular fusion

64. PREOP MEDICATION
• Low dose opioid or benzodiazaepam
• Avoid sendation – sensitve to small dose of narcotics & hypnotics
• Drugs for HR control
• Diuretic-induced hypokalaemia – treat preoperatively
• Anticoagulation – decide according to surgery

65. CHOICE OF SNETHESIA
• GA
• Epidural :
• Decreases afterload

66. MAINTENCANCE OF ANESTHESIA
• Low conc volatile, opioids, nitrous oxide
• Avoid N2O in PHTN
• Cardiostabel muscle relaxants
• Reversla – slowly to prevent drug-induced tacycardia by anticholinergic
• Intraoperative fluids – careful tititration- avoid fluid overload

67. INDUCTION OF ANESTHESIA
• Avoid ketamine – increases HR
• Intubation & muscle relaxation by cardiastable muscle relaxant – VECURONIUM
• Avoid relaxants with histamine release
• Short acting B-blockers for rate control eg, Esmolol

68. MONITORING
• Asymptomatic without evidence of pulmonary congestion
• - routine monitors
• Symptomatic and undergoing major surgery:
• CVP
• TEE
IBP
PAC
• LAP
ABG

69. TROUBLE SHOOTING
• Hypotension is usually associated with Tachycardia
• Consider DC cardioversion if tachycardia os due to acute
onset AF
• Sinus tachycardia – IV fluid, phenylephrine, esmolol
• External CPR is unlikely to be succesful in severe MS
• - cardiac massage and emergency CPB

70. POSTOPERATIVE MANAGEMENT
• Risk of pulmonary oedmea & RVF
• Continue cardiovascular monitoring
• Adeqaute postop pain
• (pain – hypoventilation – respiratory acidosis & hypoxemia – increase HR & PVR)
• IV Opioids or epidural
• Decreased pulmonary compliance & increased WOB - MV

71. INTERACTION WITH PREGNANCY
• Expandned blood volume in pregnancy – increased risk of pulmonary congestion &
oedema
• Anemia leding to tachycadrdia
• Physiologic tachycardia in pregancy :
• Decrease left ventricular filling time
• Increase left atrial & pulmonary arterial pressure

72. INTERACTION WITH PREGNANCY
• Vaginal delivery:
• Early admission
• Invasive blood pressure monitoring
• Small top-ups for epidural
• Avoid fluid overload
• CS – avoid spinal anesthesia
• Careful EA – NYHA I & II
• GA for NYHA III & IV
• Bolus oxytocin & Methergine CI – risk of systemic hypotension & pulmonary HTN
• Brief period of postop ventilation may required in some cases

73. MITRAL REGURGITATION

74. MITRAL REGURGITATION
• Mitral apparatus has 6 pry
components:
1. LA wall
2. Annulus of MV
3. Mitral valve leaflets
4. Condae tendinae
5. Papillary muscle
6. Wall of LV
• Anormailities or dysfunction in any
component can result in valve
incompentence

75. MITRAL REGURGITATION
• Classified as organic (intrinsic valvular disease) or functional (related to non-valvular
components of mitral apparatus)
• Acute MR is usually due to rupture or ischaemia of a papillary muscle or
rupture of the chordae tendinae.
• Posterior papillary muscle dysfunction is more common than anterior
papillary dysfunction, because the former is supplied by a single coronary
artery whereas the latter is supplied by two coronary arteries.

76. MITRAL REGURGITAION – AETOLOGY
Acute
• Endocarditis
• Papillary muscle rupture (post MI)
• Trauma Chordal rupture
• Leaflet flail (MVP)
Chronic
• Myxomatous (MVP)
• Rheumatic fever
• Endocarditis (healed)
• Mitral annular calcification
• Congenital (cleft, AV canal)
• Ischemic (LV remodeling)
• Dialated cardiomyopathy

77. MITRAL REGURGITATION
• Severity of MR is assessed in the context of acute or chronic
• Carpentier classification:
• Type 1 MR – normal leaflet motion & annular dilatation
• Type II MR - excessive motion of the margin of the leaflet & most
common
• Type III MR – restricted motion of mitral leaflet
• Type IIIa – due to fibrosis of subvalvular apparatus
• Type IIIb – due to tethering of leaflet to the ventricular wall as a result
of remodeling

78. Miller 9th edition
p1777

79. PATHOPHYSIOLOGY
Acute MR
• Sudden increase in LAP – increased
LVEDP- acute pulmonary oedmea
• Balance b/n demand and supply
interrupted – high risk of
subendocardial isachemia
• Chronic MR
• LV volume overload – increase LVEDV

80. MITRAL REGURGITATION
• Fraction of LV Svthat regurgitate back into LA depends on:
1. Size of mitral valve orifice
2. Heart size- which determiens duration of ventricular ejection
3. Pressure gradiet across theMV
• Such gradient are related to LV compliance & impedance of LV ejection into the aorta

81. CLINICAL FEATURES
Acute MR:
• Acute LV failure
• Pulmonary oedmea
Chronic MR:
• Exertional dyspnea
• Fatigue
• Symptomsworsens following onset of AF

82. SIGNS
• Atrial fibrillation/fluuter
• Cardiomegaly
• Apical pansystolic murmur +/- thrill
• Sodt S1, apical S3
• Signs of pulmonary venous congestion – crepitation
• Signs of PHTN & RHF

84. Miller 9th edition, p1778

85. MANAGEMENT OF MR
Medical
• Diuretics
• Vasodialtors, ACEI
• Digoxin – AF
• Anticoagulant – AF
• Antibiotic prophylaxis
Surgical
• Valvuloplasty
• -moderate to severe symptoms
• Regurgitan volume 30 – 60%

86. SURGERY OF MR

88. INDUCTION OF ANESTHESIA
• With IV drugs
• Dose adjustment to prevent increase SVR & decrease HR
• Muscle relaxant – pancuronium (modest increase in HR)

89. MAINTENACE OF ANESTHESIA
• Volatile anesthetics cautiously– isoflurane, desflurane, sevoflurane
• Severely compromised myocardium – opioid-based anesthetic preferred
• -minimal myocardial depression
• Mechanical ventilation – adjusted to maintain near-normal acid-base & respiratory
parameter
• Pattern of ventilation – provide sufficient time btween breaths for venous return

90. PREGNANCY CONSIDERATION
• No specific recommendations for management of MR during labour & delivery
• Prior to labour - symptoms managed with diuretics & vasodialtors
• Labour & CS – regional anesthesia well tolerated
• NYHA class 3 & 4 - may require GA

92. POSTOP MX SPECIFIC TO MV REPLACEMENT
• Anticoagulation
• If in sinus rhythm after surgery:
• Long-term anticoagulation not necessary (Evidence for use
of antiplatelet therapy weak )
• If in AF after surgery:
• Anticoagulation indicated at the level determined by AF as
the primary indication

93. POSTOP MX SPECIFIC TO MV REPLACEMENT
• Dysrhythmias
AF is the most common dysrhythmia –
• particularly in the elderly
• Onset is often accompanied by hypokalaemia/ hypomagnesaemia
• Amiodarone has replaced digoxin as first-line therapy
• Amiodarone continued until at least the first outpatient clinic visit

94. POSTOP MX SPECIFIC TO MV REPLACEMENT
•Infection:
• The risk of bacterial endocarditis is lower following MV repair than
MV replacement.
• Changes in international guidelines since the last edition mean that
antibiotic prophylaxis is no longer recommended before dental,
genitourinary and GI surgery.

95. MITRAL VALVE PROLAPSE

96. MV PROLAPSE
• Prolapse of one or both mitral leaflets into LA during systole with or without MR
• Most common form of valvular heart disease
• Common in young women
• Associated:
• Marfan syndrome
• Rheumatic carditis
• Myocarditis
• Thyrotoxicosis
• SLE

97. MV PROLAPSE
• May be anatomical or functional
• Anatomical :
• Redundant & thickened leaflets
• Connective disease
• Elderly men
• Functional:
• Normal appearing leaflet/ mild bowing only

98. CLINCIAL FEATURES
• Anxiety
• Orthostatic symptoms
• Palpitations
• Dysnpea
• Fatigue
• Atypical chest pain
• Cardiac dysrhythmias
• Older men with anatomical MVP can present with mild to moderate CHF

99. SIGNS
• Midsystolic click +/- systolic murmur
• (in the absence of symptoms doesn’t warrant cardio consulatation)
• S3 gallop,
• Midsystolic/holosystolic murmur
• Basal creps

100. COMPLICATIONS
• Cerebral embolic events
• IE
severe MR requirng surgery
• Dysrhythmias
• Sudden death

101. PREOPERATIVE EVALUATION
• Functional disease from those with MR
• B-blockers to control dysrhthmias
• anticoagulants

102. ANESTHETIC MANAGEEMNT
• Periop factors which increase LV emptying & decrease filling are avoided:
• Increase sympathetic activity
• Decrease SVR
• Upright posture
• hypovolemia

103. SELCTION OF ANESTHETIC TECHNIQUE
• Most MVP have normal LV function
• Tolerate all forms of GA & RA
• GA – volatile anesthetic induced myocardial depression is beneficial
• RA – maintain adeqate intravasular volume to prevent fall in SVR

104. INDUCTION OF ANESTHESIA
• With IV drugs – avoid signifcant & prolong decrease SVR
• Etomidate – choice for induction in hemodynaically significant MVP
• Ketamine avoided –
• increase sympathetic NS activity
• increases MVP & MR

105. MAINTENANCE OF ANESTHESIA
• Volatile /N2O/ opioid – titrate dose to maintain SVR
• 0.5 MAC of Iso, Des,& Sevo – decreases regurgitation fraction
• Muscle relaxants – Vec/Pancuronium
• Proper fluid balance
• Vasopressor – alpha agonist (phenylephrine)

106. MONITORING
• Haemodynamically signifcant MVP (MR/LV dysfunction
• - invasive monitoring

107. HYPERTROPHIC OBSTRUCTIVE
CARDIOMYOPATHY

108. HOCM
• Can lead to:
• Valvular insufficency (MR)
• LV outflow tract (LVOT) obstruction
• Autosomal dominant
• Mutated gene – hypertrophy of segment of the ventricle
• Common cause of sudden death in young adults

109. HOCM
• Generally, inotropic agent should not be used
• Thick, hypertrophied ventricles has reduced compliance
• Very load sensitive – thus, maintain preload and afterload (reduce worsen the
obstruction, increase –decreases trans-outflow tract gradient leading to SAM)
• Vasoconstrictors such as phenylephrine & vasopressin administered
• Obstruction is exacerbated by hypercontractile & tachycardia ( Rx- beta-blocker)

110. TRICUSPID VALVE

111. TRICUSPID VALVE
•3 unequal membranous leaflets – anterior (usually
largest), septal and posterior
•A saddle-shaped annulus
•The chordae tendinae
•The papillary muscles

112. TRICUSPID STENOSIS
• Fiixed obstruction to RV filling due to TV orifice narrowing
• Normal area -= 7-9 cm2
• Clinically significant symptoms develop - < 2 cm2
• Similar to MS
• In TS – congestion is in RA & systemic circuit, whereas MS – congestion is in LA &
pulmonary circuit
• Common of rheumatic origin

113. • Isolated TS is rare, 5 to 10% is associated with MS
• If pure TS – assocaited with carcinoid or congenital
• Non-rheumatic casues are rare
• - congenital atresia or stenosis, SLE, endomyocardial fibroelastosis, carcinoid syndroe,
prosthetic-valve endocarditis, pacemaker led infection or adhesions

114. • Some degree of TR is always present
• Minimal rise in gradient across the valve (>4mmHg) can lead to rise in RA pressure –
systemic congestion --- decrease CO
• When both TS & MS present, MS develops first with pulmonary congestion &
dyspnea--- then when TS develops, sysmptoms are relieved

115. ASSESSMENT
• Assocaited MS present
• If already diagnoised – medications on
• Electroltye imabalce – salt restricytion & diuretics
• Features of RHF
• Severe hepatic congestion with cirrhosis, jaundice, malnutrition, anasacra
• Speneomegaly
• Raised JVP – large q wave
• P-pulmonale in ECG (V1 or V5)

116. CLINICAL PRESENTATION
• Long asymptomatic period
• Isolated TS – dypsnea, fatigue, peripheral oedmea, hepatomegaly,
ascites
• Left lower sternal edge- opening snap & high pitched, mid-diastolic
murmur
• CVP – dominant a-wave & slow y decent
• ECG – tall peaked P-waves in II, III & aVF

118. SURGERY
• TV surgery is usually performed with other valve procedures
• Isolated TV surgery – dtermined by severity of symptoms
and degree of stenosis
• Surgery preferred over percutenous ballon valvotomy
• Biological preferred

119. TRICUSPID REGURGITATION
• Retrograde blood flow from RV into RA during systole
• 70% - mild or physiological
• Significant TR/ secondary TR – secondary to RV dialatation, dialatation of tricuspid
annulus
• -carries poor prognosis
• Pry TR – rare. (Ebstein’s anomaly, infective endocarditis, rheumatic heart dis- ease,
carcinoid syndrome and iatrogenic damage from surgery, endocardial biopsies,
catheter placements and pacemaker leads)

120. CLINICAL PRESENTATION
• Isolated TR – asymptomatic
• Dyspnea
• Fatigue
• Exercise intolerance
• Features of systemic venous HTN
• Pansystolic murmer
• CVP – prominet cv-wave, absent x-descent, sharp y-descent
• ECG – RV dysfunction, RAD, tall P waves, RBBB,, AF

122. SURGERY
• Indicated for severe TR
• Done for left sided valves
• Ring annuloplasty
• Usually need large bioprsothetic valve

123. PULMONARY VALVE

124. PULMONARY VALVE
• PV separates the RVOT from main PA
• 3 cusp
• Seprated from other 3 heart valves by infundibulum
• Normal adult orifice area = 2 cm2
• PV disease Usually congenital
• Stenosis > regurgitation

125. PULMONARY STENOSIS
• Types:
• Subvalvular
• Valvular
• Supravalvular
• Proximal pulmonary stenosis

126. PATHOLOGY
• Congenital – eg Noonans syndrome, rubella, Williams syndrome
• Physiological – Neonates
• Acquired – rare
• - carcinoid syndrome, RHD, external compression by tumour or sinus of valsava
aneurysm

127. CLINICAL PRESENTATION
• Adults – asymptomatic systolic murmur
• Children :
• Moderate to severe – exertional dyspnea
• Features are of those of systemic venous congestion & RV failure
• Features of severe PS:
• Prominent a-wave
• Precordial thrill
• Paraternal heave

129. PULMONARY REGURGITATION
• Retrograde blood flow from the PA into the RV during diastole
• Mild PR – physiological
• PR is frequent findings in normal hearts
• Pathological PR – annular dilaation secondary to PHT

130. PATHOLOGY
• Secondary to PHT
After surgical intervention for PS
Complication of ToF
Infective endocarditis
Carcinoid syndrome
CTD – Marfan syndrome
Congenital – extremely rare

131. CLINICAL PRESENTATION
• PR is well tolerated – remains asymptomatic for many
years
• As diseases progress – RHF features
• Parasternal heave
• Soft diastolic murmur at lef upper stenal adge
• Loud P2
• With PHT – high pitched early diastolic murmur (Graham
Steel)

133. THANK YOU

134. REFERENCES
• Miller’s text book 9th edition
• Kaplan’s textbook of cardiac anestehsia
• Practicalapproach to caridac anesthesia (Henseley & Martin)
• Stoeltings textbook of Coexisting diseases)
• Upto date