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DR.

MOUNICA
MODERATOR-DR AJAY SIR
 Definition:- An acquired or congenital disorder of cardiac valve characterised by
stenosis(obstruction) or regurgitation(backward flow) of blood
 Stenosis – narrowing of the orifice
 Regurgitation –abnormal reversal of blood flow

 MITRAL VALVE –BICUSPID VALVE OR LEFT ATRIOVENTRICULAR VALVE

 AORTIC VALVE – THREE LEAFLETS OR SEMILUNAR VALVE


 MITRAL resembles BISHOPS MITRE
 MITRE-GREEK WORD MEANS HEAD BAND OR TURBAN
 Mitral Annulus
 Mitral Leaflets
MITRAL
 Chordae Tendineae SUB VALVULAR VALVE MITRAL VALVE
COMPLEX
 Papillary Muscles APPARATUS
 Left Ventricular Wall
 Left Atrium

 Chordae tendinae VALVULAR


APPARATUS
 Valve leaflets

 Fibrous annulus
TENSOR APPARATUS
 Papillary muscles
 RHEUMATIC –ALMOST ALL CASES IN ADULTS
 Mitral annular calcification and congenital –rare
 Female;male=2;1
 Latency period of 20to30 years exist between initial rheumatic
fever and the disease process

 NORMAL MITRAL VALVE AREA 4TO6CM²

 patients – asymptomatic till valve area reaches 2cm².


NORMAL HEART CHAMBER PRESSURES
 CLINICAL FEATURES

 Symptoms of mitral stenosis include:

 Due to decreased CO:


Easy fatiguability
Syncope
 Due to increased LAP
Pulmonary congestion- Dyspnea, orthopnea
Hemoptysis
Pulmonary edema
 Due to LA enlargement
Ortners syndrome= HOARSNESS OF VOICE
 due to compression of LEFT recurrent laryngeal nerve
Atrial Fibrillation (30-40%)- more common in older patients
 Due to PAH, RV hypertrophy, RVF
Chest pain, ascites, edema

 Causes of death- CHF, systemic embolism, pulmonary embolism,


infection
 Inspection-
-Mitral facies- Pinkish purple patches on
cheeks+ peripheral cyanosis in lips, tip of
nose and cheeks.
-Malar flush
Rarely seen in India

-Raised JVP, ascites,pedal edema when


RHF develops

 Palpation-
-Pulse – Regular, low volume, all peripheral pulses palpable.
-Left parasternal heave when RV hypertrophy develops
-Atrial fibrillation- irregular pulse
-Hepatomegaly- in RHF
-Tapping apex beat not displaced
-Diastolic thrill at cardiac apex with patient in lateral recumbent
position
ON AUSCULTATION
• Opening snap
• Rumbling diastolic murmur best heard at
apex radiating to the axilla
• Loud P2 component of S2: pulmonary
hypertension
• Severity: distance between OS & aortic
component of S2
• Closer OS to S2 more severe the stenosis
• Calcification of valve: OS disappears
 MEASURES THE GRADIENT AND VALVE AREA
 RIGHT VENTRICULAR ASSESSMENT
 LA ENLARGEMENT
 Routine investigations like Hb, TLC, DLC, RFT etc
 L.F.T. for assessing hepatic dysfunction d/t RVF
 A.B.G.-- severe pulmonary symptoms
 Serum Electrolytes
 Coagulation profile
 Blood grouping
 Blood sugar
 Esr,aso titre
 Chest X-ray- straightening of lt heart border, cardiomegaly,
double shadow
 ECG- P mitrale(LAH),Rt axis deviation,RVH, AF
 Echocardiography (TEE)
 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
Straightening
of Left Heart
Border
 Anatomically moderate MS can become functionally severe.
 Increased incidence of pulmonary congestion, AF.
 High risk of maternal and fetal mortality and morbidity
 Regular echocardiographic followup recommended
SURGERIES

Percutaneous balloon dilatation


Closed mitral valvotomy
Mitral commissurotomy
Mitral valve replacement
 Systolic function - contract and eject blood
 Contractility - intrinsic ability of myocardium to contract and
generate force
 Preload - load placed on myocardium before contraction -
diastolic volume and filling pressure
 After load - load placed on myocardium during contraction -
systolic volume and generated pressure
HEMODYNAMIC GOALS
HEMODYNAMIC GOALS AVOID MONITOR INTERVENTION
1.SINUS RHYTHM • AVOID ATRIAL 5 LEAD ECG • MANAGE NEW
FIBRILLATION ONSET AF OR
• AVOID SVT,HEART RATE
TACHYARRHYTHMI CONTROL
A • CARDIOVERSION –IF
APPROPRIATE
2.SLOW TO NORMAL HR (50 – 70) • AVOID • 5 LEAD ECG • PREVENT PAIN
TACHYCARDIA • PULSE OXIMETRY INDUCED
• AVOID SEVERE WITH VISIBLE TACHYCARDIA BY
ENSURING ADEQUATE
BRADYCARDIA WAVEFORM
ANESTHETIC DEPTH
AND EFFECTIVE
ANALGESIA
• MANAGE
TACHYCARDIA
RELATED
HYPOTENSION WITH
PHENYL EPHRINE OR
NORADRENALINE
• HR – SLOWED WITH
BETA BLOCKERS
HEMODYNAMIC GOALS AVOID MONITOR INTERVENTION
3.MAINTAIN • AVOID INTRA ARTERIAL BP • ADMINISTER
AFTERLOAD HYPOTENSION VASOCONSTRICTOR
• AVOID TO MANAGE
SYMPATHECTOMY HYPOTENSION
(SPINAL ANAESTHESIA)

4.ADEQUATE PRELOAD • AVOID • CLINICAL COURSE • MANAGEMENT OF


HYPERVOLEMIA AND OXYGENATION PULMONARY EDEMA
• AVOID • DEVELOPMENT OF • TREAT HYPOXEMIA
HYPOVOLEMIA PULMONARY EDEMA WITH 100% O2
• ASSESS CLINICAL PEEP,IF NECESSARY
RESPONSE TO FLUID INTUBATION AND
BOLUSES CONTROL
VENTILATION
• MAINTAIN
INTRAVASULAR
VOLUME STATUS
• RAPID
RESUSCITATION FOR
HEMORRHAGE
HEMODYNAMIC GOALS AVOID MONITOR INTERVENTION

5.MAINTAIN RV AVOID DOSES OF HEMODYNAMICS • IF INOTROPIC


CONTRACTILITY DRUGS THAT CAUSES SUPPORT NEEDED-
MYOCARDIAL MILRINONE /
DEPRESSION DOBUTAMINE USED
• LOW DOSE OF
NORADRENALINE

6.MINIMIZE PVR • AVOID HYPOXEMIA • PULSE OXIMETRY • MINIMIZE RISK OF


• AVOID HYPERCARBIA • CAPNOMETRY HYPOXEMIA,HYPERCA
RBIA – BY O2
SUPPORT
• ENSURING
CONTROLLED
VENTILATION – IF
INTUBATED
 Assessment of
1. Severity of cardiac disease
2. Degree of impaired myocardial contractility
3. Presence of associated major organ disease (hepatic, renal &
pulmonary)
4. Compensatory mechanisms for maintaining cardiac output
(↑sympathetic activity, cardiac hypertrophy)
5. Prosthetic heart valves
6. Drug therapy
 Management of Patients on warfarin
◦ Emergency surgery
 Discontinue warfarin
 Give vitamin K 0.5 – 2.0 mg IV
 FFP 15 ml/kg repeat if necessary
 Accept for surgery if INR <1.5
◦ Elective surgery
 Stop 3 days preoperatively
 monitor INR daily
 Give heparin when INR <1.5
 Management of Patients on Heparin
◦ Emergency surgery
 Consider reversal with IV protamine 1 mg
for every 100 IU of heparin
◦ Elective Surgery
 Stop heparin 6 hours prior to surgery
 Check INR, accept for surgery if INR <1.5
 Restart heparin in post-op as soon as
possible
If patient is on LMWH, we rarely need to stop
it.
Monitoring
Asymptomatic • Symptomatic pts or major surgery
• Standard non-invasive – Standard non-invasive
– ECG, – Serial ABG
– HR – Invasive monitoring
• IBP
– NIBP
• CVP/PAC
– Pulse-oxymetry
• Echocardiography (TTE/TEE)
– Capnograph • Cardiac catheterization
– Temperature

Use of invasive monitoring depends on complexity of operative


procedure and physiological impairment produced by MS
 Narcotics, benzodiazepine -- To decrease anxiety & any
associated likelihood of adverse circulatory responses
produced by tachycardia

CLASS DRUG DOSE MG/KG ROUTE

BZPs DIAZEPAM 0.1-0.15 PO,IM


LORAZEPAM 0.03 – 0.06 PO,IM
MIDAZOLAM 0.03 – 0.07 IM

OPIOIDS MORPHINE 0.2 IM


MEPERIDINE 1.0 – 1.5 IM
 Anticholinergics- avoided as they increase heart rate

 Diuretics- Evaluate fluid status ,


Check electrolytes on day of surgery ,
Withold on night before surgery if massive fluid shifts expected in
surgery.
 Drugs to control AF ( Digoxin, beta blockers, CCB) –
Continue in perioperative period

 Watch serum potassium- in patients receiving digoxin and


diuretics

 Current ACC/AHA guidelines do not recommend


endocarditis antibiotic prophylaxis for patients with
isolated mitral stenosis undergoing surgical procedures.
 No ideal general anesthetic

 An opioid is a better choice than a volatile agent for induction.


Because volatile agent can produce undesirable vasodilatation,
or precipitate junctional rhythm with loss of effective atrial
kick.

 IV agents – except ketamine because of sympathetic


stimualtion. (Should be double diluted and given slowly)

 Etomidate best for hemodynamic stabilty


• A nitrous/narcotic anesthetic or a balanced anesthetic that
includes low concentrations of a volatile anesthetic

• SEVOFLURANE - IDEAL

• halothane- can be used as it decreases HR and has least


vasodilating properties

• N2O can evoke acute increase in pulm. vascular resistance


hence best avoided in PAH

• Muscle relaxants: Avoid Pancuronium as it induces


tachycardia.
• Vecuronium and rocuronium ideal
 Prevent hypothermia

 Judicious Fluid therapy


Avoid hypervolemia--Worsens pulmonary edema
Avoid Hypovolemia - -decreases Cardiac output.

 Intra operative tachycardia:


◦ Deepening Anaesthesia with an opioid excluding
meperedine.
◦ β-blocker: esmolol or propanolol.

◦ GIVE HEPARIN AND MONITOR APTT


 Phenylephrine is preferred over ephedrine as a vasopressor
because it lacks β agonist activity.

 Treatment of acute Hypertension and afterload reduction with


potent vasodilators should be undertaken only with full
hemodynamic monitoring.
 Atrial fibrillation:
◦ IV β- blocker.
◦ Digoxin useful when more sustained but not immediate control of
heart rate is needed.

 Sudden SVT may lead to hemodynamic instability and require


cardioversion.

 REVERSAL – SLOWLY TO AVOID TACHYCARDIA ASSOCIATED


WITH ANTICHOLINERGICS
Post-operative
Management Complication
• Monitoring • Pulmonary congestion/edema
• Oxygen • Thrombo-embolism
• Pain relief: multimodal including • Heart failure
neuroaxial opioids
• Intravenous fluids
• Anticoagulants
 Vaginal delivery recommended whenever possible
 Epidural analgesia helps in reducing sympathetic stimulation
 Use of forcep/vacuum to shorten delivery time
 Epidural ---for LSCS
 Spinal avoided in severe MS d/t uncontrolled hypotension
DRUGS TIME

WARFARIN INR < 1.5 (STOP 4 TO 5 DAYS PRIOR TO


PROCEDURE)

HEPARIN FULL DOSE IV aPTT<40

LOVENOX FULLL DOSE WAIT 24 HOURS

LOVENOX PROPHYLACTIC DOSE WAIT 12 HOURS

HEPARIN PROPHYLACTIC DOSE >5000 sq aPTT <40

HEPARIN PROPHYLACTIC DOSE 5000 bid/tid WAIT 1 HOUR

NSAIDS NOW
Agent Intrathecal Epidural

Morphine 0.25-0.5 mg 5 mg

Meperidine 10-15 mg 50-100 mg

fentanyl 12.5-25 µg 50-150 µg

sufentanil 3-10 µg 10-20 µg

53
•SAB is best avoided.

•Careful epidural anaesthesia in NYHA class 1 and 2


patients

•General anaesthesia in NYHA class 3 and 4 patients


Aortic Stenosis
 AORTIC VALVE – THREE LEAFLETS ONLY
 AORTIC ROOT –
COMPONENTS
1.SINUSES OF VALSALVA
2.INTER LEAFLET TRIANGLES
3.SINO TUBULAR JUNCTION
4.LEAFLET ATTACHMENTS
5.ANNULUS

LOOKS LIKE
3 PRONGED
CORONET
 1.Obstruction To LV Outflow
 2.Intraventricular Systolic Pressure And Wall Tension
Increase
 3.Concentric Hypertrophy
 4.Decreased LV Compliance
 5.Reliance On Atrial Contribution
 1.ANGINA
 Imbalance Between Supply And Demand
 Elevated Lvedp Decrease Perfusion Pressure
 Myocardial Hypertrophy Increases Demand

 2.SYNCOPE WITH EXERTION


 Inability To Increase Co To Meet Metabolic Demands
 Decrease In Cerebral Perfusion Pressure

 3.CONGESTIVE HEART FAILURE


 ELEVATED LVEDP => ELVATED LAP => PULMONARY VENOUS
CONGESTION
➢ Pulse – usualy Regular, thready/ low volume,
Atrial fibrillation- irregular pulse(show associated mitral
valve disease)
 Peripheral pulse rises slowly to a delayed sustained peak
_pulsus parvus et tardus .
 apex beat displaced laterly
Systolic thrill at base of heart
 Carotid thrill
 Blood pressure -low SBP ,narrow pulse pressure
 Harsh late systolic murmur (2nd intercostal space at base of
heart) radiating to carotids.
 Second heart sound is soft or absent
 Paradoxical spliting of S2
CHEST XRAY
• POST STENOTIC
DILATATION- calcified calcifications in
aortic the region of the
PROMINENT , left
aortic valve
valve ventricle
DILATED,ASCENDING leaflets
is
AORTA enlarged

• CALCIFIC AORTIC VALVE

• CARDIOMEGALY
ECG CHANGES
ECG SHOWING LEFT
VENTRICULAR HYPERTROPHY
AND LEFT ATRIAL DELAY

DUE TO PRESSURE OVERLOAD


ST DEPRESSION
T WAVE INVERSION

LEADS 1,AVL,V5,V6
 Showing Thickened,calcified,immobile Aortic Valve
Cusps
 Left Ventricular Hypertrophy
 Aortic Gradients
❖ NO definitive medical treatment for aortic stenosis.
❖ Some recent retrospective trial demonstrated slowing of
disease progression in patient receiving statin therapy.
❖ Restriction of physical activity.
❖ Angina treated with calcium blockers and/or beta-blockers.
❖ Any hypertension is treated aggressively, but caution must be
taken in administering beta-blockers.

❖ Nitrates are contraindicated due to their potential to cause


profound hypotension in aortic stenosis
The main goals are:
▪ Maintain sinus rhythm
◦ sinus tachy- decreases diastolic time for myocardial perfusion
◦ sinus brady- limits CO in pts with fixed stroke volume
▪ Maintain adequate intraventricular volume (preload)
▪ b/c of dec. LV compliance and inc. LVEDP & LVEDV, preload augmentation is
needed for a normal stroke volume

▪ Maintain systemic vascular resistance (SVR; afterload)


▪ Patients with severe aortic stenosis have a fixed cardiac output.
– They cannot compensate for falls in systemic vascular resistance which
result in severe hypotension, myocardial ischaemia and a downward spiral
of reduced contractility causing further falls in blood pressure and
coronary perfusion.
 very rare valvular abnormality occurring due to the narrowing of the
tricuspid valve
• Palpitations
• A fluttering discomfort in the chest or neck
• Swelling in the legs
• Cold skin
• Fatigue
• Discomfort in the abdominal area, specifically the right upper quadrant.
 Medical:Salt restriction, digitalization, diuretics•
 Surgical therapy- valvuloplasty/ valve replacement
 Anaesthetic goal: Maintain preload & control HR
 • Isolated from the other three heart valves by the
infundibulum.
 • Pulmonary valvular disease is usually congenital
 • Stenosis > regurgitation
 • Congenital pulmonary stenosis is usually treated with
balloon valvuloplasty.
 Maintain right ventricular preload, left ventricular afterloadand
right ventricular contractility.

 Avoid hypothermia, hypercarbia, acidosis,hypoxia and high


ventilatory pressures.

 Spinal anaesthesia may be associated with an uncontrolled


reduction in right ventricular preload and should therefore be
avoided in cases

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