Viva Questions of Mitral Stenosis

MITRAL STENOSIS

 

Q.1 What are the characteristics of  Mitral stenosis?

- Dysnea

- H/O Rheumatic fever

- JVP normal or raised

- Pulsus parvus

- Tapping apex

- Diastolic shock

- Diastolic thrill

- Heart sounds- Loud S1, Loud P2, OS- may/ may not be present

- Murmur- middiastolic murmur with a presystolic accentuation heard over

the apex, best heard with the bell of the stethoscope,

with the patient in left lateral position & breath held in expiration.

 

Q.2 What are the symptoms of MS ?

• Shortness of breath, especially with exertion or in lying down position


• Fatigue mainly during increased physical activity


• Swollen feet or legs


• Palpitations


• Dizziness


• Heavy coughing, sometimes with blood-tinged sputum


• Chest discomfort


• Severe headache or symptoms of stroke

 

Q.3 When should percussion be avoided ?

Percussion should not be done if thrombus is present

 

Q.4 Are there any procoagulation abnormalities in MS ?

Procoagulation abnormalities in mitral stenosis are changes in platelet activity; increased concentration of fibrinopeptide A, thrombin-antithrombin III complex, and D-dimer; and changes in fibrinolytic activity.

These changes have most obvious effects in the left atrium, probably originate in the left atrium or hypertensive pulmonary circulation

Atrial fibrillation worsens them

Anticoagulation and PBV reduce hypercoagulability

 

Q.5 Which murmurs are best heard in expiration and in inspiration ?

Inspiration increase right-sided heart murmurs

Expiration increase left-sided heart murmurs

 

Q.6 Explain pathophysiology of MS

The normal MV orifice area is approximately 4-6 cm². As the orifice size decreases, the pressure gradient across the mitral valve increases to maintain adequate flow and this leads to increase in left atrial pressure. Increase in LA pressure leads to LA dilatation which causes distortion of nerve tracts in the myocardium to give rise to atrial fibrillation.Also, the dilated LA stagnates blood which cause clot formation and subsequent thromboembolism.

Increase in LA pressure is transmitted backwards giving rise to pulmonary venous hypertension first, later causing pulmonary arterial hypertension.

Pulmonary hypertension develops due to  1) retrograde transmission of LA pressure 2) pulmonary arteriolar constriction 3) interstitial edema  4) obliterative changes in the pulmonary vascular bed (intimal hyperplasia and medial hypertrophy).

Increased pulmonary arterial pressure is back transferred to RV causing right ventricular hypertrophy and then dilation.This leads to tricuspid annular dilatation and functional  tricuspid regurgitation develops.This may cause right heart failure leading to elevated jugular venous pressure, liver congestion, ascites, and pedal edema.

MS is a relatively fixed cardiac output state.Left ventricular end-diastolic pressure and cardiac output are usually normal in isolated mitral stenosis. As MS becomes severe, cardiac output becomes subnormal at rest and fails to increase during exercise.

 

Q.7 Explain the pressure volume loop in MS

Pressure-volume loop measurements by cardiac catheterization constitute a highly reliable method for the direct beat-to-beat functional analysis of the heart

PV loops are measured using conductance micromanometer tipped catheters

Mitral stenosis impairs left ventricular filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume (reduced width of PV loop) by the Frank-Starling mechanism and a fall in cardiac output.

Reduced ventricular filling and reduced aortic pressure decrease ventricular wall stress (afterload), which may result in a small decrease in ventricular end-systolic volume; however, this is not sufficient to offset the reduction in end-diastolic volume. Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume (shown as the width of the loop) decreases.

 

Q.8 What is the mechanism of haemoptysis ?

Pulmonary apoplexy – Sudden increase in LA pressure leads to rupture of bronchial & pulmonary veins

Bronchitis – sputum blood straked

Pulmonary edema

             Pulmonary infarction

 

Q.9 What is Wilkin’s Score ?

 

Assessment of mitral valve anatomy according to the Wilkins score (Boston score).

 

       Leaflet mobility

       1.Highly mobile valve with restriction of only the leaflet tips

        2. Middle portion and base of leaflets have reduced mobility

        3. Valve leaflets move forward in diastole mainly at the base

 4. No or minimal forward movement of the leaflets in diastole

Valvular thickening

1. Leaflets near normal (4–5 mm)

2. Mid-leaflet thickening, marked thickening of the margins

3. Thickening extends through the entire leaflets (5–8 mm)

4. Marked thickening of all leaflet tissue (>8–10 mm)

        Subvalvular thickening

1. Minimal thickening of chordal structures just below the valve


2. Thickening of chordae extending up to one third of chordal length


3. Thickening extending to the distal third of the chordae


4. Extensive thickening and shortening of all chordae extending down to the papillary muscle

Valvular calcification

       1. A single area of increased echo brightness

       2. Scattered areas of brightness confined to leaflet margins

       3. Brightness extending into the mid-portion of leaflets

       4. Extensive brightness through most of the leaflet tissue

 

Q. What is Cormier Score ?

Group 1 - Pliable non calcified anterior mitral leaflet and mild subvalvular disease ( thin chordae > 10 mm long )

Group 2 - Pliable non calcified anterior mitral leaflet and severe subvalvular disease ( thin chordae < 10 mm long )

Group 3 - Calcification of mitral valve of any extent by fluoroscopy whatever the state of the subvalvular apparatus.

 

Q. Which chamber fails first in MS ?

LA – RV – RA

 

Q. Which ventricle fails first in MS ?

Right Ventricle

Left Ventricle never fails in MS unless is associated with MR,AR,AS,HTN,IHD,CMP.

 

Q. What are the characteristic findings in physical examination ?

Presence of mitral facies (pinkish-purple patches on the cheeks) indicate chronic severe MS (reduced CO & vasoconstriction).

Jugular venous distension may be seen.

 

Q. What findings are sought during palpation in MS ?

The arterial pulses are reduced in volume due to the decreased SV

Pulses may be irregular in AF

Tapping apex beat that is not displaced

Left parasternal heave - presence of RVH due to pulmonary HTN

P2 may be palpable in the 2^nd left intercoastal space.

 

Q. What are the various types of AF ?

Paroxysmal AF – Terminates within 7 days of onset

Persistent AF – Remains >7 days

Long standing AF - >12 months duration

Permanent AF

Non valvular AF

 

Q. What are the recommendations for Anticoagulation for Atrial Fibrillation (AF) in Patients With VHD?

 Recommendations for Anticoagulation for Atrial Fibrillation (AF) in Patients With VHD are -

I B-NR - Anticoagulation with a vitamin K antagonist (VKA) is indicated for patients with rheumatic mitral stenosis (MS) and AF.

MODIFIED: VKA as opposed to the direct oral anticoagulants (DOACs) are indicated in patients with AF and rheumatic MS to prevent thromboembolic events.

 

I C-LD - Anticoagulation is indicated in patients with AF and a CHA2DS2-VASc score of 2 or greater with native aortic valve disease, tricuspid valve disease, or MR. 

NEW: Post hoc subgroup analyses of large RCTs comparing DOAC versus warfarin in patients with AF have analyzed patients with native valve disease other than MS and patients who have undergone cardiac surgery. These analyses consistently demonstrated that the risk of stroke is similar to or higher than that of patients without VHD. Thus, the indication for anticoagulation in these patients should follow GDMT according to the CHA2DS2-VASc score.

 

IIa C-LD - It is reasonable to use a DOAC as an alternative to a VKA in patients with AF and native aortic valve disease, tricuspid valve disease, or MR and a CHA2DS2VASc score of 2 or greater.

NEW: Subgroup analyses have demonstrated that DOACs, when compared with warfarin, appear as effective and safe in patients with VHD as in those without VHD.

 

Q. LV is small in MS but is it normal ?

Although the LV is small and underfilled in Mitral Stenosis,the myocardium is not normal



•    Mechanical block &  myocardial insufficiency.



•    Myocardial mechanical performance is responsible for  LV dysfunction in MS.   



•    Filling is limited at higher heart rates as it prohibits adequate diastolic filling and limit cardiac output and stroke work.Thisfailure to increase stroke work in MS is due to abnormal LV function.



•    Impairment may be localised to posterior ventricular wall,selective atrophy of posterior wall of LV due to fibrosis downward from PML involving chordae and immobilised adjacent muscle can occur.



•    Adherence of scarred,shortened ALPM to contagious ventricular wall can cause poor contraction in anterior wall.





Intrinsic Myocardial Function may be impaired due to –



      Papillary muscle ischaemia and fibrosis extending into myocardium



      Severe PHTN and PA dilatation compresses left main artery causing ischaemia  



      Atrial fibrillation causing coronary embolism leading to myocardial ischaemia



      LV dysfunction secondary to RV dysfunction.

 

Q. What are the pressure symptoms?

- Hoarseness of voice

- Dysphagia

 

Q.What are the reasons for dysphagia?

Due to pressure on esophagus by

- arch/ descending thoracic aortic aneurysm

- aberrant Rt. Subclavian artery- dysphagia lusoria

- LA enlargement

- Rt. Aortic arch

 

Q.What are the reason for hoarseness (Otner’s syndrome)?

Due to compression on the left recurrent laryngeal nerve by

- Dilated LA

- Tracheobronchial LN

- Enlarged PA

- Arch aorta or proximal descending thoracic aortic aneurysm

      - Aneurysm of ductal ampulla

 

Q. What is the incidence of valvar affection of RHD ?

     MV- 70-80%,

      MV + AV- 20- 25%

Only AV- 5- 8%

TV- 30- 50% (autopsy)

 

Q. What are the auscultatory findings in MS ?

Auscultation: Heart sounds

The S1 is accentuated because of a wide closing excursion of the mitral leaflets.

The degree of loudness of the S1 depends on the pliability of the MV.

The intensity of the S1 ↓ as the valve becomes more fibrotic, calcified, and thickened.

The S2 is initially normal but, with the development of PHTN, P2 becomes ↑ in intensity .

Opening Snap -

 An OS of the MV is heard at the apex when the leaflets are still mobile .

OS is a high frequency sound that results from a stenotic mitral valve that can open only partially during the rapid filling phase of mid diastole. OS occurs 80-90msec after S2 at the beginning of mid diastole.

As the MS progresses and LAP is ↑, the OS occurs earlier after S2 or A2. Thus, the shorter the A2-OS interval, the more severe the MS.

Low-pitched diastolic rumble that is most prominent at the apex.

Duration and not intensity of MDM correlate with severity of MS

It reflects the transvalvular gradient and the duration of blood flow across the valve.

The ↑ in atrial pressure after atrial contraction, results in an increase in the loudness of the murmur, termed "presystolic accentuation" .

The murmur is best heard at cardiac apex with bell of stethoscope ,in left lateral position,at the height of expiration and after doing mild exercise.

 

Q. How to assess severity of MS ?

Symptoms – Occur MVA < 1 sq cm

Proximity of A2 – Opening snap ( A2 – Aortic valve closure)

Longer duration of MDM

Echo features

 

Q. What investigations are done before anesthesia planning ?

Routine Blood Investigations – Hb, CBC, Platelets,PT INR, LFTs, KFTs, TFTs

BSL, Urine examination

Specific Investigations – CXR, ECG, Echo, Angiography

 

Q. Discuss CXR findings in MS -

1.Mitralisation of heart - Straightening of left heart border

2.Enlarged LA: Double density shadow- Heart in heart appearence

3.Splaying of carina (left main bronchus is lifted by enlarged LA)

4.Prominent upper zone pulmonary veins

5.Kerley B lines (indicating fluid collection in the interlobular septa)

6.Pulmonary HTN – Dilated pulmonary arteries at hilum with peripheral pruning

 7.Bat wing appearance of Pulmonary edema

 8.MV Calcification

9.Pulmonary hemosiderosis

10.Sickling of oesophagus as it is pushed backwards by LA enlargement – RAO oblique

11.Obliteration of retrosternal space in left lateral view  - Right ventricular hypertrophy

 

Q. What are Kerley lines ?

Kerley A lines (arrows) are linear opacities extending from periphery to the hila;

they are caused by distention of anastomotic channels between peripheral and central lymphatics.

Pulmonary venous pressure > 30mmHg

Kerley B lines (white arrowheads) are short horizontal lines situated perpendicularly to the pleural surface at the lung base;

they represent edema of the interlobular septa.

Occur when pulmonary venous pressure 20-30mmHg

Kerley C lines

Short lines which do not reach the pleura (i.e. not B or D lines) and

do not course radially away from the hila (i.e. not A lines).

Kerley’s C lines (black arrowheads) are reticular opacities at the lung base,

representing Kerley’s B lines en face. These  suggest cardiogenic pulmonary edema.

             Kerley D lines

Kerley D lines are exactly the same as Kerley B lines, except

that they are seen on lateral chest radiographs in the retrosternal air gap.

 

 

Q. What are the findings in Echo Report of Mitral Stenosis ?

1. RHD


2. Dilated chambers


3. Wilkins Score


4. Thromboembolism importance


5. Pulmonary Hypertension


6. LA smoke


7. Biventricular function


8. LAA clot


9. Associated MR

 

Q. What are the complications of MS ?

1. Thromboembolism


2. Pulmonary hypertension


3. Atrial fibrillation


4. RVF

 

Q. How is Pulmonary Hypertension classified ?

According to Mean PAP -

Mild PAH - < 30 mmHg

Moderate PAH- 30-50mmHg

Severe PAH- >50 mmHg

 

Q. Discuss treatment of MS -

           1) Mild MS - Diuretics to control pulmonary congestion

            Restriction of physical activity

            2) If in atrial fibrillation -

Digoxin

Beta Blockers

Calcium Channel Blockers

3) Anticoagulation - warfarin to normalise INR 2.5 - 3

Anti failure measures

Rheumatic prophylaxis

Infective endocarditis prophylaxis

4) Surgery if pulmonary hypertension develops -

Percutaneous balloon valvotomy

Surgical commisurotomy

Valve reconstruction

5) Valve Replacement

6) Prophylaxis against recurrence of rheumatic fever

 

Q. What are the Anaesthesia Goals in MS ?

According to the Cardiac Grid -

Rate – Avoid tachycardia

Rhythm – preferred is sinus rhythm, if patient is in atrial fibrillation avoid fast ventricular rate.

Contractility - controlled ventricular response

Preload – normal or increased

Afterload – normal

PVR – No pulmonary vasoconstriction :

          Avoid hypoxia,hypercarbia,acidosis

 

Q. How to optimize anticoagulants ?

Warfarin stopped 5 days before surgery

LMWH started – stopped 12 hours prior

UFH started – stopped 4-6 hours prior

Start Warfarin 12-24 hours postoperatively

 

Q. Discuss Preoperative Management -

1. Decrease anxiety (decreases tachycardia),also avoid anticholinergics.


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. Minor surgery - continue anticoagulant therapy


5. Major surgery - discontinue anticoagulant therapy.

 

Q. Discuss Induction of Anaesthesia -

Avoid Ketamine – Increases heart rate, Avoid Propofol(fall in blood pressure)

(ETOMIDATE/THIOPENTONE)-Better choice

Avoid Atracurium – Increased histamine release causes hypotension

which manifests as tachycardia.(vecuronium- choice)

 

Avoid any stimulus which can increase PVR including: nitrous oxide, adrenaline, dopamine, protamine, serotonin,

thromboxane A2, prostaglandins such as PGF2alpha and PGE2, hypoxia, hypercarbia,

acidosis, PEEP and lung hyperinflation, cold, anxiety and stress. 

If PVR is increased it can be reduced by: hypocarbia (via hyperventilation), nitric oxide, morphine, glyceryl trinitrate,

sodium nitroprusside, tolazoline, prostacycline (PGI2), isoprenaline, and aminophylline.

 

Q. What care should be taken during induction in MS?

All sedative premedicants decrease vascular tone by decreasing sympathetic activity which can lead to decrease in systemic arterial pressure as well as RV preload.

Heavy premedication is poorly tolerated in these patients.

- No tachycardia allowed -Pulmonary oedema can occur

- No fast administration of fluids even if hypotension develops – can lead to Pulmonary oedema

Avoid sympathetic stimulation

 

Q. How does control of heart rate benefit ?

The control of the heart rate provides sufficient diastolic period for the emptying of LA which keeps the mean LA pressure low and avoids the complications of increased LA pressure such as pulmonary venous congestion

sufficient diastolic interval provides time for LV filling which helps maintaining CO

 

Q. How is tachycardia  deleterious in MS ?

Tachycardia decreases diastolic period hence decreases diastolic filling. This leads to increase in LA pressure, sudden increase of which can lead to pulmonary edema.

 

Q.What is the importance of sinus rhythm ?

Sinus rhythm has atrial kick which normally accounts for 15-20 % of LV filling which is lost in atrial fibrillation.

In MS – accounts for 30% of LV filling

In MR – accounts for 35% of LV filling

In AS – accounts for 40 % of LV filling

In HOCM – accounts for 75 % of LV filling

 

Q. What are the extra precautions to be taken during induction ?

Etomidate is considered the most cardio-stable induction agent for these patients.

The CO is subnormal and preferentially distributed to well-perfused areas like heart, brain, liver, and kidney.

Circulation is slow so the volume of distribution is decreased and the drugs are distributed to well-perfused areas. Hence, small anesthetic dose is required, also their effect is delayed.

Large doses given rapidly can cause hemodynamic collapse due to vasodilation due to suppression of sympathetic drive,decrease in RV preload and myocardial depression.



 

Q. Discuss Maintenance of Anaesthesia -

1. Avoid lighter planes of anaesthesia


2. Drugs should have minimal effects on hemodynamics


3. Balanced anaesthesia with Opoid/ N₂O /Volatile anaesthetic agent


4. N₂O causes insignificant pulmonary vasoconstriction except in pulmonary hypertension.Treat pulmonary hypertension preoperatively.


5. Cardiac stable muscle relaxants are to be used. (preferably avoid Pancuronium)


6. Fluid Management

 

Q. What are the monitoring modalities  intraoperatively ?

1. Transesophageal Echocardiography


2. Intra-arterial pressure


3. Pulmonary artery pressure


4. Left atrial pressure

Q. Discuss myocardial protection during cardiopulmonary bypass in MS.

Systemic hypothermia and cold crystalloid or blood cardioplegia are done for myocardial protection.

At the end of the surgical procedure, the patient is warmed to 35°C rectal temperature or 36–37°C nasopharyngeal temperature.

 

Q. Discuss importance of de-airing.

The heart is meticulously de-aired before removal of aortic clamp.

After removing cross clamp, the arterial inflow is maintained at nearly 1.5 L/min/m ² and

the LA  vent is run at approximately 25 revolutions per min until myocardial tone returns and contractions are resumed.

The aortic root needle inserted for the administration of cardioplegia is usually

left open or actively vented for letting out released air.

This prevents systemic and coronary artery air embolism.

 This residual air can cause embolism of the right coronary artery because

of its anatomical position and the Trendelenburg position at the time of aortic clamp release.

Air emboli in the RCA circulation result in ST-segment elevation in ECG leads II, III, and aVF (inferior leads).

RCA air embolism is most damaging in the presence of RV hypertrophy and PAH.

Coronary air emboli during CPB are managed by continuing CPB and administration of intravenous inotropic agents.

Pulsatile blood flow, partial aortic clamp application, and/or increased blood pressure and

force of myocardial contraction help facilitate transit of gaseous emboli through the coronary circulation.

The patients with RV hypertrophy and dilation may develop RV dysfunction due to inappropriate

increases in its preload, afterload, and decreased myocardial perfusion

 

Q. How is weaning from CPB done ?

ABG, serum potassium, hematocrit are optimized

Lung recruitment done manually

Ventilator started

             Pacing done if required

Monitors re-calibrated

Inotrope - epinephrine infusion, 0.05 - μg/kg/min 10–15 min before weaning

      Inj Milrinone in PAH can be given

 

Q. How is RV dysfunction treated ?

Pulmonary vasodilators (nitroglycerin and sodium nitroprusside) along with milrinone or levosimendan can be started.

The patients with RV hypertrophy and dilation may develop RV dysfunction due to inappropriate increases in

its preload, afterload, and decreased myocardial perfusion hence these parameters need to be optimized.

 

Q. What are the reasons of difficulty in weaning this patient from CPB ?

CPB-induced inflammatory response

myocardial dysfunction due to

myocardial ischemia during aortic clamp

inadequate myocardial protection

myocardial edema

preexisting myocardial dysfunction

paravalvular leak

Prosthesis dysfunction

Conduction block

iatrogenic damage to circumflex artery

 

Q. what are the problems of large LA post CPB ?

1) Deairing

2) Higher chances of thromboembolism

5) Persistence of atrial fibrillation

 

Q. When is CPB reinstituted ?

If slowing of the heart occurs or distention of the LV or RV initially inotropic support is increased,

circulatory support by intra-aortic balloon pump is considered.

       If residual lesion( in case of repair),paravalvular leak,prosthetic valve dysfunction,

       circumflex artery injury is suspected CPB should be reinstituted.

 

Q. Discuss Postoperative management -

Assess postoperative risk of pulmonary oedema and right heart failure

Avoid pain as pain leads to tachycardia

Postoperative hypoventilation leads to respiratory acidosis and hypoxemia

which manifests as raised pulmonary vascular resistance.

 

Q. Discuss role of regional anaesthesia in MS -

Spinal Anaesthesia:

• can be used in mild cases of MS only


• sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia should be avoided

 

            Epidural Block: allows better control of level of sympathectomy and reduction in blood pressure

          -can be used in 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

 

Q. What is the anaesthetic importance of  severe pulmonary hypertension ?

            Pulmonary hypertensive crisis

RV failure

Stretch PFO – may open causing paradoxical embolism

 

Q. Why does pregnancy aggravate the symptoms of mitral stenosis ?

Increase  in blood volume by 30-50% lead to increase in pulmonary capillary hydrostatic pressure which increases the risk of pulmonary oedema

• Decrease in SVR


• Increase in HR by 10-20 beats /min lead to decrease in diastolic filling time of LV


• CO increases by 30-50% after 5^th month


• PG when increased significantly causes increase in LA pressure


• During labour &delivery →sympathetic stimulation →tachycardia → ↑CO


• ↑in venous return to heart due to autotransfuson and IVC compression →decompensation


• Enlarged atrial dimension predispose to atrial arrythmias including atrial fibrillation


• Also induces changes in haemostasis which contribute to increased coagulability and thromboembolic stroke

 

Q.What is the prognosis of pregnant patient with MS ?

Prognosis depends on the functional status

NYHA classes I and II lesions usually do well during pregnancy and have a favorable prognosis (mortality rate of <1%).

NYHA classes III and IV -mortality rate of 5% to 15%. These patients should be advised against   becoming pregnant.

 

Q. What are the Anaesthesia options for these patients ?

VAGINAL DELIVERY :

           Recommended whenever possible if the haemodynamic condition is stable at the end of pregnancy

            Epidural anaesthesia is recommended as tachycardia is averted by epidural analgesia

            LA can be used to  provide  Perineal anaesthesia

Caesarean section is indicated for OBSTETRIC REASONS ONLY.

With preemptive epidural bolus of bupivacaine gradually titrated 15 min before the patient beared down to deliver,

the expansion of the venous circuit allowed blood volume to accumulate without causing much fluid shift into the lungs.

Minimum of an arterial line and CVP monitoring for symptomatic mitral stenosis for

strict blood pressure control and fluid management.

 Pulmonary Artery Catheter should be used in MS with - multiple vulvular abnormalities, cardiac arrhythmia,

maternal hypertension, severe pulmonary hypertension

  

Q. Why is this case not of LA myxoma?

LA myxoma has constitutional symptoms, postural syncope, tumor plop, changing

murmur in different positions.

 

Q. If murmur is not heard in MS what will you do?

- Make patient walk  – Auscultate again

- Left lateral decubitus

- Bell of stethoscope

- Breath hold in expiration

 

Q. What are the causes of thromboembolic episode in SR with MS?

- Transient AF

Calcific valve

- Infective endocarditis

- LA myxoma

LA clot

 

Q. What are the causes of mitral stenosis?

- Rheumatic heart disease

Calcification

Congenital – Parachute Mitral valve, double orifice mitral valve, supra mitral ring

Hunter’s syndrome

Hurler’s syndrome

Lutembacher’s syndrome

Mucopolysaccharidosis

Fabry's disease

systemic lupus erythematosus

Rheumatoid arthritis

Methysergide therapy

 

Q. How does a patient of MS improve spontaneously?

In MS, symptoms may get reduced and patient may have a feeling  improved condition when occurs -

1) Development of TR

2) Development of PH

3) Development of precapillary stenosis (secondary MS)

 

Q. Rheumatic valvulitis produce which distinct pathological changes ?

- Commissural fusion

- Fibrosis of leaflet with stiffening & retraction

- Fusion & shortening of chordae

 

Q. What is “Auscultatory Triad” in MS?

- Apical diastolic rumble – Blood flow through stenotic orifice

- Loud S1 –Thickening of Mitral leaflets

- Opening snap

 

Q. How will assess severity of MS?

 A) According to Valve area & Symptoms

Normal Mitral valve area is 4-6cm2

Valve area     Symptoms

> 2.5 cm2     None

1.5-2.5cm2 (Mild MS)   Dyspnoea on severe exertion

1-1.5cm2(Moderate MS)   PND ± Pulmonary oedema

<1.0 cm2 (Severe/critical MS)  Orthopnoea (Class IV)

 

 B)  Severity of MS is on A2- OS interval

Mild MS (LAP ≈ 15 mm Hg) 0.08- .12 sec   

Moderate MS (LAP ≈ 20 mm Hg) 0.04- 0.08 sec

Severe MS (LAP ≈ 25 mm Hg) < 0.04 sec   

 

C) According to gradient across Valve

Normal valve mean gradient is 0 mmHg.

Severity    Mean gradient

Mild MS    <5 mmHg

Moderate MS   5-15mmHg

Severe MS    > 15mmHg

 

D) Duration of diastolic murmur is directly proportional to severity.

 

Q. Which Conditions simulate MS ?

-LA myxoma

- Cortritriatum

- Ball valve thrombus in LA

- Diastolic flow murmur across normal valve in VSD, PDA, Severe MR

-Carey coomb’s murmur of mitral valvulitis

 

 Q. What are the features of pulmonary venous congestion in MS?

- Pulmonary vascular markings

- Upper & lower lobe pulmonary vein congestion

- Peribronchial cuffing

- Pulmonary oedema

- Kerley’s A,B,C lines

- Hemosiderosis

 

Q. Prominent aortic knuckle in MS is in which conditions ?

MS with -

- AR

- HTN

 

Q. What will be the ECG findings in MS?

- Sinus rhythm or AF

- Left artial enlargement – P mitrale “M” shaped P in Lead II ,Biphasic P in V1

- RVH

RAE in ECG of MS if associated TR

 

 

Q. What are the TEE views to assess MS ?

1.  MID ESOPHAGEAL VIEWS :-

• Midesophageal 4 chamber view.


• Midesophageal mitral commissural view.


• Midesophageal 2 chamber view.


• Midesophageal long axis view.

1. TRANSGASTRIC VIEWS :-

• Transgastric  basal short axis view.


• Transgastric 2 chamber view.

 

Q. What is Pressure Half Time ?

It is the time taken for the diastolic pressure difference between LA and LV to decrease to half of the initial value.

MVA = 220/Pressure half time (msec)

Normal : 40-70 msec

Mild MS :  70-150 msec

Moderate MS :  150-200 msec 

Severe MS : 220 msec

 

Q.What is Deceleration time  ?

It is the time taken for the diastolic pressure difference between LA and LV to decrease to the initial value.

MVA (cm2)= 759/DT.

PHT=0.29 X DT.

 

Q. What is LA smoke?

Whirling of stagnated blood in  dilated LA produce echodensity called as LA smoke or SEC (Spontaneous echo contrast)

Large amount of LA smoke is called as ‘Tornado’ sign

 

Q. What are the indications for cath in MS ?

- No correlation between ECG, Echo & CxR.

- Evaluate PA pressure

- LV systolic function

- AR Status – not able to quantitate on Echo

- Age > 40,Angina on exertion – for coronary angiography

 

Q. What are the other modalities of treatment?

- Balloon Valvuloplasty ( PBMV/PTMC)

- Surgery ( CMV/CMC,OMC,MVR)

 

Q. What are the indications of PBMV ?

Pliable, noncalcific valve with mild – moderate subvalvar pathology, No MR

Wilkins’s Echo score < 9

 

 Q. What are the contraindications for PBMV ?

- Other valve disease/ Coronary artery disease needs surgery

- LA/LV thrombus

- Thickened atria septum  

- Moderate MR

- Calcification of mitral valve

- Recurrent thromboembolic events

 

Q. What is the importance of Wilkins’s score?

Score

4-8 – Young patient with loud OS –Excellent candidate for BMV, good long term result

9-12 –Less likely to achieve lasting improvement with BMV, Greater potential for

restenosis, better for OMV/MVR

≥ 13 Poor result of Mitral valve repair – Usually requires MVR

 

Q.  During BMV why a pigtail is kept in the aorta?

To avoid damage to the NCC during septal puncture.

 

Q. How to calculate size of Inoue balloon for BMV?

Size of balloon= {height (cm)/ 10} + 10

 

Q. What are the contraindications of CMV?

- Calcium in the valve

- LA/LAA clot

- MR++

- AR++

 

Q. What are the indications of OMV?

- Calcium in valve

- LA/LAA clot

- MR

 

Q. What are the approaches for CMV?

- Anterolateral thoracotomy

- Posterolateral thoracotomy

 

Q. What are the problems of a high profile valve in the mitral position?

1) LVOT obstruction

2) Hemolysis

3) Increased thromboembolism

 

Q. Which valves are high profile valve?

- Starr-Edwards

- Bioprosthetic valve

 

Q. Which valves are low profile valves?

- St.Jude

- Medtronic Hall

- Omniscience

- Carbomedics

- TTK Chitra

 

 Q. What are the Ten commandments of prosthetic heart valves ?

By Harken 

1) It must not propagate emboli

2) It must be chemically inert & not damage blood elements

3) It must close promptly (< 0.05 sec)

4) It must offer no resistance to physiologic flow

5) It must remain closed during the appropriate phase of cardiac cycle

6) It must have lasting physical & geometric features

7) It must be inserted in a physiologic site- generally the normal anatomic site

8) It must be capable of permanent fixations

9) It must not annoy the patient

10) It must be technically practical to insert.

 

 

Q. What are the problems after MVR for MR  ?

1) In MR, LV is pumping into low pressure LA & post MVR now has to pump in aorta

2) In MVR, when the valve is excised, a portion of the LV is excised.

3) MR/MS is associated with elevated PAP.

 

Q. What are the Survival rates post valve replacement ?

Survival rates are better for AVR than for MVR/ DVR.

10 year survival, in general, for

AVR = 65%

MVR= 55%

DVR= 55%

-Late mortality is higher for regurgitant lesions.

-Late mortality is higher for rheumatic/ ischemic valve replacement in comparison with

degenerative diseases.

 

Predictors of mortality are:

1) age > 65 years

2) LV dysfunction

3) NYHA 4 at time of surgery

4) Coronary artery disease

5) Ventricular arrhythmias

 

 

Q. Discuss changes in PAH post valve replacement

Regressive changes in PAH occur within first few days after

surgery & are generally complete 6 months postoperatively.

 Full normalization is rarely achieved.

 

Q. What is rheumatic fever?

Definition: It is an acute non suppurative immune mediated inflammatory disease,

usually in children, that follows a few weeks after pharyngitis caused by group A β

hemolytic streptococci. 

 

(Students appearing for exams are expected to read about Rheumatic fever , Infective endocarditis in detail)

 

Q. What are the Recommendations for Antithrombotic Therapy for Patients with Prosthetic Heart Valves ?

I A - Anticoagulation with a VKA and INR monitoring is recommended in patients with a mechanical prosthetic valve.

I B - Anticoagulation with a VKA to achieve an INR of 2.5 is recommended for patients with a mechanical bileaflet or

currentgeneration single-tilting disc AVR and no risk factors for thromboembolism.

I B - Anticoagulation with a VKA is indicated to achieve an INR of 3.0 in patients with a mechanical AVR and additional

risk factors for thromboembolic events (AF, previous thromboembolism, LV dysfunction, or hypercoagulable conditions) or

an oldergeneration mechanical AVR (such as ball-incage)

I B - Anticoagulation with a VKA is indicated to achieve an INR of 3.0 in patients with a mechanical MVR

I A - Aspirin 75 mg to 100 mg daily is recommended in addition to anticoagulation with a VKA in patients

with a mechanical valve prosthesis.

IIa B - Aspirin 75 mg to 100 mg per day is reasonable in all patients with a bioprosthetic aortic or mitral valve

IIa B-NR - Anticoagulation with a VKA to achieve an INR of 2.5 is reasonable for at least 3 months and for as

long as 6 months after surgical bioprosthetic MVR or AVR in patients at low risk of bleeding

 MODIFIED: LOE updated from C to B-NR. Anticoagulation for all surgical tissue prostheses was combined into 1 recommendation,

with extension of the duration of anticoagulation up to 6 months. Stroke risk and mortality rate are lower in patients

who receive anticoagulation for up to 6 months after implantation of a tissue prosthesis than in those who have do not have anticoagulation.

Anticoagulation for a tissue prosthesis is also supported by reports of valve thrombosis for patients undergoing

bioprosthetic surgical AVR or MVR, a phenomenon that may be warfarin responsive.

II b B-R - A lower target INR of 1.5 to 2.0 may be reasonable in patients with mechanical On-X AVR and

no thromboembolic risk factors (209).

NEW: A lower target INR was added for patients with a mechanical On-X AVR and no thromboembolic

risk factors treated with warfarin and lowdose aspirin. A single RCT of lower- versus standard-intensity anticoagulation

in patients undergoing On-X AVR showed equivalent outcomes, but the bleeding rate in the control group was unusually high.

IIb B-NR -  Anticoagulation with a VKA to achieve an INR of 2.5 may be reasonable for at least 3 months after TAVR in patients at low risk of bleeding.

NEW: Studies have shown that valve thrombosis may develop in patients after TAVR, as assessed by

multidetector computerized tomographic scanning. This valve thrombosis occurs in patients who received antiplatelet

therapy alone but not in patients who were treated with VKA.     

II b C - Clopidogrel 75 mg daily may be reasonable for the first 6 months after TAVR in addition to life-long aspirin 75 mg to 100 mg daily. 

III: Harm B - Anticoagulant therapy with oral direct thrombin inhibitors or anti-Xa agents should not be used in patients with mechanical valve prostheses.

 

Q. What are the Recommendations for Bridging Therapy for Prosthetic Valves ?

I C - Continuation of VKA anticoagulation with a therapeutic INR is recommended in patients with mechanical

heart valves undergoing minor procedures (such as dental extractions or cataract removal) where bleeding is easily controlled. 

I C - Temporary interruption of VKA anticoagulation, without bridging agents while the INR is subtherapeutic,

is recommended in patients with a bileaflet mechanical AVR and no other risk factors for thrombosis who are undergoing invasive or surgical procedures. 

IIa C-LD - Bridging anticoagulation therapy during the time interval when the INR is subtherapeutic preoperatively

is reasonable on an individualized basis, with the risks of bleeding weighed against the benefits of thromboembolism prevention,

for patients who are undergoing invasive or surgical procedures with a 1) mechanical AVR and any thromboembolic risk factor, 2) oldergeneration mechanical AVR, or 3) mechanical MVR.

MODIFIED: COR updated from I to IIa, LOE updated from C to CLD. RCTs of bridging anticoagulant therapy versus no bridging therapy

for patients with AF who do not have a mechanical heart valve have shown higher risk of bleeding without a change in incidence of thromboembolic events.

This may have implications for bridging anticoagulation therapy for patients with prosthetic valves. 

IIa C - Administration of fresh frozen plasma or prothrombin complex concentrate is reasonable in patients with mechanical valves

receiving VKA therapy who require emergency noncardiac surgery or invasive procedures.

 

 

References –

 Mitral Stenosis Y Chandrashekar, Stephen Westaby,Jagat Narula. The Lancet Volume 374,Issue 9697, Volume 374,10–16 October 2009, Pages 1271–1283

Praveen Kumar Neema,Mukul Chandra Kapoor. Anesthetic management of a patient with mitral stenosis undergoing mitral valve repair/replacement

MAMC Journal of Medical Sciences, a publication of Maulana Azad Medical College 2016 vol 2;2,94-98

2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease 

A Report of the American College of Cardiology/American Heart Association  Task Force on Clinical Practice Guidelines 

Satyasai Notes of Cardiac Surgery.