ANAESTHESIA FOR PATIENT

WITH MITRAL STENOSIS

SANCON 2016
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Contents
SYMPTOMS .........................................................................................................................................4
HISTORY ..............................................................................................................................................9
CCF IN MITRAL STENOSIS..................................................................................................................10
RHEUMATIC FEVER ...........................................................................................................................11
INFECTIVE ENDOCARDITIS ................................................................................................................15
CLINICAL EXAMINATION ...................................................................................................................19
X-RAY FINDINGS: ..............................................................................................................................23
ECG FINDINGS: ..................................................................................................................................24
INVESTIGATIONS: ..............................................................................................................................25
ECHO FINDINGS: ...............................................................................................................................26
ANATOMY OF MITRAL VALVE: ..........................................................................................................27
CAUSES OF MS: .................................................................................................................................28
PATHOPHYSIOLOGY ..........................................................................................................................28
PRE-OP ASSESSMENT AND OPTIMISATION: .....................................................................................31
MEDICAL MANAGEMENT OF MS: .....................................................................................................34
SURGICAL MANAGEMENT ................................................................................................................38
Percutaneous balloon mitral valvotomy.......................................................................................39
Open Commissurotomy(OMC)......................................................................................................40
Closed commissurotomy(CMV) ....................................................................................................40
PROSTHETIC VALVES .........................................................................................................................41
Recommendations for Prosthetic Valve Choice............................................................................41
Anticoagulation for Prosthetic valves ...........................................................................................42
ANAESTHETIC MANAGEMENT ..........................................................................................................43
Goals of anaesthetic management ...............................................................................................43
Regional anesthesia in mitral stenosis..........................................................................................45
ANAESTHETIC MANAGEMENT OF PREGNANT PATIENT WITH MS ...................................................45
Physiological changes during pregnancy ......................................................................................45
Obstetric management of pregnant patient with MS ......................................................................48
MS patient with pregnancy subjected for Caesarian section ...........................................................48
Anticoagulation of Pregnant Patients with Mechanical Valves ........................................................50

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Anesthesia for PBMV in pregnancy...................................................................................................51
CARDIOPULMONARY BYPASS ...........................................................................................................52
Cardiopulmonary bypass circuit....................................................................................................52
Sequence of events to go on cardiopulmonary bypass ................................................................57
Circuit Selection and Priming ........................................................................................................57
Anticoagulation.............................................................................................................................58
Cannulation...................................................................................................................................58
Initiation and Maintenance of Cardiopulmonary Bypass .............................................................59
Myocardial protection ..................................................................................................................60
Weaning and Termination of Cardiopulmonary Bypass ...............................................................62
Annexure...........................................................................................................................................66

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SYMPTOMS
DYSPNOEA:

What is dyspnoea?

Abnormal uncomfortable awareness of one’s own breathing.

How will you grade the dyspnoea?

NYHA Classification: The New York Heart Association Classification

There are 4 components- Dyspnoea, palpitations, fatigue & angina
(Presently followed is the 7th edition of NYHA, laid down in 1994)

NYHA I: In a patient with heart disease with no limitation of physical activity. Ordinary
physical activity does not cause dyspnoea, palpitations, fatigue or angina. (More than
Accustomed activity)

NYHA II: In a patient with heart disease with mild limitation of physical activity.
Comfortable at rest but ordinary physical activity causes dyspnoea, palpitations, fatigue or
angina. (On accustomed activity)

NYHA III: In a patient with heart disease with moderate limitation of physical activity.
Comfortable at rest but less than ordinary physical activity causes dyspnoea, palpitations,
fatigue or angina. (Less than Accustomed activity)

NYHA IV: In a patient with heart disease with marked limitation of physical activity.
Symptoms present at rest & increase on exertion. (At rest)

Roizen’s classification of dyspnoea

Grade 0: No dyspnoea while walking on the level at normal pace.

Grade I: I am able to walk as far as I like, provided I take my time

Grade II: Specific street block limitation – I have to stop for a while after one or two blocks

Grade III: Dyspnoea on mild exertion – I have to stop and rest going from the kitchen to the
bathroom

Grade IV: Dyspnoea at rest

Functional status
Functional status is a reliable predictor of perioperative and long-term cardiac events. It is
often expressed in terms of metabolic equivalents (METs), where 1 MET is the resting or
basal oxygen consumption of a 40–year-old, 70-kg man. In the perioperative literature,

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functional capacity is classified as excellent (>10 METs), good (7 METs to 10 METs),
moderate (4 METs to 6 METs), poor (<4METs)
One MET is defined as 1 kcal/kg/hour and is roughly equivalent to the energy cost of sitting
quietly.
One MET also is defined as oxygen uptake in ml/kg/min with one MET equal to the oxygen
cost of sitting quietly, equivalent to 3.5 ml/kg/min.

Energy requirements for common activities

1 MET Eat, dress
↓ Walk indoors
↓ Walk a block or two on level ground
↓ Do light housework
4 METS Climb a flight of stairs
↓ Run a short distance
↓ Do heavy housework, e.g., scrubbing
↓ Golf, bowling, dancing
10 METSSwimming, skiing, singles tennis, running

What is Orthopnoea?

Dyspnoea in lying down position & relieved in sitting position corresponds to NYHA grade
IV

What is the Mechanism of orthopnoea?

In the recumbent position there is decreased pooling in the lower limbs & abdomen

Blood is displaced from extrathoracic compartment to thoracic compartment

Failure of LV pump to pump blood

Increased pulmonary venous congestion & capillary pressure

Interstitial edema

1) Decrease in lung compliance

2) Increase in airway pressure Dysnpoea
3) Ventilation perfusion mismatch
It occurs rapidly, within1-2 minutes of lying down & is relieved on sitting

What is Platypnea?

It is dyspnoea which occurs only in the upright position

Causes:
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1. Left atrial thrombus
2. Left atrial tumors – Myxomas
3. Pulmonary arterio-venous fistula.
What is Paroxysmal Nocturnal Dyspnoea (PND)?
Attacks of dyspnoea which occur at night and awaken the patient from sleep. It occurs 2-5
hours after the onset of sleep and takes 10-30 minutes for recovery after assuming the upright
posture.
What is the mechanism of PND?
Mechanism of PND is similar to that of orthopnea.
However, a fall in PaO2 and a decreased sympathetic support to left ventricular function
during sleep also contribute to the development of PND.
It is a symptom of minimal left ventricular dysfunction.

1) Slow absorption of extracellular fluid from the dependent areas & resultant increase in
blood volume
2) Elevation of diaphragm
3) Decrease LV adrenergic support during sleep
4) Depression of respiratory centre during sleep
5) Transient nocturnal arrhythmias.

What are the causes of PND?

1. Ischemic heart disease

2. Valve diseases
3. Hypertension
4. Cardiomyopathy
5. Atrial fibrillation
6. Rarely in atrial tumours.

PND is the earliest symptom of left heart failure.

HEMOPTYSIS:

What is Hemoptysis?

Definition: Expectoration of blood. Ranges from streaky sputum to gross hemoptysis.

Types:
i) True- tracheobronchial & alveolar
ii) False- oral/ nasopharyngeal

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What are the causes of hemoptysis in a patient with MS/ LVF ?

1) Pulmonary apoplexy/ sudden haemorrhage- profuse, rarely life threatening, due to rupture
of dilated thin walled bronchial veins caused by acute rise in left atrial pressure. (This is not
seen generally due to chronicity which causes the vein walls to become thick)- stops on own

2) Blood stained sputum associated with PND.

3) Pink frothy sputum seen in pulmonary edema due to rupture of alveolar capillaries.
4) Pulmonary infarction- due to PA embolism.
5) Following chronic bronchitis due to edematous bronchial mucosa.

CHEST PAIN:

What are the causes of chest pain?

Ischemic cardiac Non ischemic cardiac Non cardiac

Coronary artery Pericarditis Pulmonary

disease(decreased supply) embolism
LVH/RVH (increased Dilatation of PA Plueral
demand)
Dissection of aorta Oesophageal

Skeletal muscle

Chest pain in Mitral stenosis is seen 10 to 20%. Cause could be thromboembolism, pulmonary
hypertension or CAD.

PALPITATIONS:

What is Palpitation?

Awareness of beating of one’s own heart. It is due to following cardiac physiological

alterations:

1) change in heart rate

2) change in rhythm &
3) augmentation of contractility

Other causes of palpitations are:

- Thyrotoxicosis
- Hypoglycemia
- Fever

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- Drugs
-Anemia

SYNCOPE:

What is Syncope?

An association of -
 Generalized weakness of muscles with a loss of postural tone
 Inability to stand upright &
 Loss of consciousness

What are the cardiac causes of syncope?

- Decreased cardiac output:

- LVOT obstruction- AS, hypertrophic subaortic stenosis
- Obstruction to pulmonary blood flow- severe PS/ pulmonary atresia, cyanotic spell,
pulmonary embolism
- Myocardial- massive MI
- Pericardial- tamponade
- Arrhythmias:
- Bradyarrythmias
- Tachyarrhythmia
- Others
CNS- embolism/ hypoperfusion
- LA thrombus, arch aorta aneurysm with thrombus
- LA myxomas
- Vegetations
- Carotid artery stenosis, vasovagal, rupture of IC aneurysm due to hypertension.

What are the pressure symptoms?

- Hoarseness of voice (compression of recurrent laryngeal nerve by dilated PA or enlarged

LA)
It is called Ortner’s syndrome.
- Dysphagia (compression of esophagus)

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HISTORY
What will you ask for H/O Congestive cardiac failure?

- Exertional breathlessness
- Oedema feet & puffiness of face
- Distension of abdomen
- Pain in the right upper abdomen
- Anorexia, nausea & vomiting
- Chest pain (15% of cases of CCF) due to RVH
- Oliguria & nocturia (due to fluid retention with redistribution at night)

What will you ask for H/O Thromboembolic episode?

1) CNS- loss of consciousness

- transient (TIA)
- prolonged with neurological deficit
- Convulsions

2) Other organs:
- hematuria
- abdominal pain
- limb pain
- coronary pain

What are the sources of embolism from the heart?

1) Thrombus
2) Vegetations
3) Myxomas
4) Paradoxical embolism
5) Plaques (rarely)
Tendency for embolisation is directly related to:
- age,
- size of LAA
- atrial fibrillation

Tendency for embolisation is inversely related to:

- Cardiac output.

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CCF IN MITRAL STENOSIS

Mitral stenosis can present with pulmonary edema or right heart failure.

1) Patients with MS generally present with pulmonary edema

It is associated with precipitating factors like onset of AF or tachycardia due to infection,

anemia, non adherence to diuretic therapy, pregnancy and exercise.

 Clinical features:
Tachypnea
Tachycardia
Palpitations,
B/L coarse crepts,
Pink frothy sputum,
Low cardiac output(due to reduced LV filling)

 Management:

High-flow oxygen is recommended in patients with a capillary oxygen saturation<90%.

IV loop diuretic is recommended to improve breathlessness and relieve congestion.

Non-invasive ventilation (e.g. CPAP) should be considered in dyspnoeic patients with

pulmonary oedema and a respiratory rate >20 breaths/min to improve breathlessness and
reduce hypercapnia and acidosis. (Non-invasive ventilation can reduce blood pressure).

Symptoms, urine output, renal function, and electrolytes should be monitored regularly
during use of i.v. diuretic.

Inotropic agents can be used if the the patient is hypotensive (systolic blood
pressure<85mmHg)

Opiates such as morphine may be useful in some patients with acute pulmonary oedema as
they reduce anxiety and relieve distress associated with dyspnoea

Control of atrial fibrillation with rapid ventricular response has to be done with any of the
following agents: Metoprolol, Esmolol, Diltiazem, Digoxin.
If the patient is unstable, immediate cardioversion is indicated with anticoagulation.
2) Patients with severe PH present with right heart failure.

 Clinical features: breathlessness, pedal edema, raised JVP, tender hepatomegaly,

ascites, fatigue
 Management: Treatment of pulmonary-induced RV failure is to address the correction
of a primary pulmonary etiology and a decrease in RV afterload via specific
pulmonary artery dilators.

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In patients with severe, hemodynamically compromising RV failure, inotropic therapy is
administered, using dobutamine (2-5 mcg/kg/min), dobutamine and inhaled nitric oxide, or
dopamine alone. Milrinone is preferred if the patient has tachycardia or is on beta-blockers.

RHEUMATIC FEVER
What will you ask for H/O Rheumatic fever?
Ask for h/o sore throat followed by fleeting arthritis, involuntary movements, and nodules
under skin.

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
hemolytic
streptococci. Beta

Reason for increased prevalence in developing nations is not known.

Believed to be due to
- Increased urbanization (due to increased droplet infection)
- Overcrowding

Causative agent is group A
hemolytic streptococci however in 1/3rd of the patients

there is no h/o sore throat or blood culture yield e/o streptococcal infection.

Describe the pathogenesis

 Acute rheumatic fever results from immune responses to group A streptococci, which
happen to cross-react with host tissues.
 Antibodies directed against the M proteins of streptococci have been shown to cross-
react with self antigens in the heart.
 During acute RF, focal inflammatory lesions are found in various tissues.
 Distinctive lesions occur in the heart, called Aschoff bodies which consist of foci of
lymphocytes (primarily T cells), occasional plasma cells, and plump activated
macrophages called Anitschkow cells (pathognomonic for RF).
 Diffuse inflammation and Aschoff bodies may be found in any of the three layers of
the heart, causing pericarditis, myocarditis, or endocarditis (pancarditis).
 Inflammation of the endocardium and the left-sided valves typically results in
fibrinoid necrosis within the cusps or along the tendinous cords.
 The cardinal anatomic changes of the mitral valve in chronic RHD are leaflet
thickening, commissural fusion and shortening, and thickening and fusion of the
tendinous cords

Prevention of rheumatic fever

Secondary prevention of rheumatic fever is class I indication in patients with rheumatic heart
disease, specifically mitral stenosis

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Secondary Prevention of Rheumatic Fever (AHA 2014 guidelines)

Agent Dosage
Penicillin G benzathine 1.2 million units IM every 4 wk
Penicillin V potassium 250 mg orally BID
Sulfadiazine 1 g orally once daily
Macrolide or azalide antibiotic (for patients varies
allergic to penicillin and sulfadiazine)

Duration of Secondary Prophylaxis for Rheumatic Fever (AHA 2014 guidelines)

Type
Duration After Last Attack

Rheumatic fever with carditis and residual 10 y or until patient is 40 y of age(whichever

heart disease(persistent VHD) is longer)

Rheumatic fever with carditis but no residual 10 y or until patient is 21 y of age(whichever

heart disease(no valvular disease) is longer)

Rheumatic fever without carditis 5 y or until patient is 21 y of age(whichever

is longer)

What are the clinical features of rheumatic fever?

Acute RF typically appears 10 days to 6 weeks after an episode of pharyngitis caused by

group A streptococci in about 3% of infected patients.
It occurs most often in children between ages 5 and 15, but first attacks can occur in middle
to later life
The predominant clinical manifestations are

1) Arthritis: It is a fleeting arthritis affecting large joints with no residual deficit. Generally
affected joints are;
- knee
- ankle
- elbow
- wrist
Each joint remains inflamed for 1-7 days & complete episode lasts for about 3 weeks.

Rarely affected joints are:

- shoulder
- hip
- Small joints.

2) Subcutaneous nodules:
#considered pathognomic of rheumatic fever.
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They are:
- less than 2 cm diameter
- freely mobile overlying skin
- Site: Over bony prominences especially skull, galae aponeurotica.
For examining for these nodules, ask the patient to squat & keep the elbows on the knees &
wrists folded beneath the chin. Now palpate the shin, extensor aspect of elbow, occiput &
mid back, i.e., over & around the spine & scapula.

3) Erythema marginatum: These are;

- Rapidly evolving small macules
papules
large circles with raised & well defined edges
which blanch on pressure.
- Disappear within few hours.
- Site; trunk, limbs. Very rare on the face.

4) Chorea (St. Vitus dance): These are;

- Characterized by involuntary, non repetitive, jerky movements which decrease during sleep
and increase with anxiety.
- In children any gender, but post puberty mainly in girls,
- The patient becomes irritable & produces jerky movements, grimacing involuntarily & has
slurred speech.
- Generally seen along with carditis or nodules.
#clinical examination: when child is asked to extend the arms there is tendency to flexion of
wrist & hyperextension of the fingers.

5) Carditis: It is essentially a pancarditis.

50% of cases of rheumatic fever have carditis.

Endocarditis-
¾ th of patients developing carditis have a new murmur which may be
- apical pan systolic murmur; due to myocarditis (the commonest murmur)
- apical mid diastolic murmur, Carrey Coombs murmur,
- PA systolic murmur, due to fever, anemia.

Myocarditis-
- Important feature of myocarditis is progressive dilatation of LA & LV.

Pericarditis- 2 types
- acute fibrinous
- effusion

Pericarditis is associated with severe forms of carditis

#CCF occurs in 10% of patients with rheumatic carditis.

#Prolongation of PR interval is temporary but may persist for months (reason is not known)
# Rheumatic fever may lick the joints but certainly bites the heart.
# Rheumatic fever mainly affects the left side of the heart (reason unknown)

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What is Jones criteria?

Original- T. Duckett Jones (Australia) in 1944

Current- 4th edition of Jones criteria, updated in 1992.
Major Minor Evidence of streptococcal
infection in the form of-
Carditis Clinical- ASLA + or >166 TODD
units or >200IU/ml
Polyarthitis Fever Throat culture +
Subcutaneous nodules Arthralgia H/0 scarlet fever
Erythema marginatum H/o rheumatic fever or RHD
Chorea Investigations-
Presence of acute phase
reactants (CRP, ESR,
leuckocytosis)
Prolongation of PR interval

How do you diagnose rheumatic fever by modified Jones criteria?

- 2 major criteria + e/o streptococcal infection, or

- 1 major & 2 minor criteria + e/o streptococcal infection.

If there is no supporting e/o streptococcal infection then the diagnosis of rheumatic fever
should not be accepted, except in 2 conditions:
- Only signs of chorea, or
- Only signs of carditis.

This is because the infection may have occurred few months back & hence the antibody titres
may have returned to normal.

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INFECTIVE ENDOCARDITIS
What is infective endocarditis?

Definition: Infective endocarditis (IE) is a serious infection characterized by colonization or

invasion of the heart valves or the mural endocardium by a microbe.

IE has been classified on clinical grounds into acute and subacute forms.

This subdivision reflects the range of the disease severity , which are determined in large part
by the virulence of the infecting microorganism and whether underlying cardiac disease is
present.

Acute infective endocarditis is typically caused by infection of a previously normal heart

valve by a highly virulent organism that produces necrotizing, ulcerative, destructive lesions.
These infections are difficult to cure with antibiotics and usually require surgery.

Subacute IE , the organisms are of lower virulence. These organisms cause insidious
infections of deformed valves that are less destructive. The disease may pursue a protracted
course of weeks to months, and cures are often produced with antibiotics.

Areas of affectation:

- Tends to occur in high pressure areas thus more on the left side.

- Areas where the blood flows through a narrow orifice from high to low pressure, E.g. distal
to a coarctation, VSD on the RV side, PDA on the PA side.

#Endocarditis is rare in low flow states, e.g. ASD.

#Endocarditis occurs more frequently in Regurgitant lesions than stenotic lesions & is
characteristically on the atrial surface of MV & ventricular surface of AV.

What you will ask in history of infective endocarditis?

-Pyrexia
-Petechial haemorrhages
-Tender finger pads
-Prolonged treatment with high doses of penicillin
-Hemoptysis
-Haematuria
-Hemiplegia

What is the diagnostic Criteria for Infective Endocarditis?

Dukes criteria for diagnosis of IE

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Diagnosis by the Duke Criteria, requires either pathologic or clinical criteria; if clinical criteria are used, 2 major, 1 major + 3
minor, or 5 minor criteria are required for diagnosis

What are the Clinical features of Infective endocarditis?

1) Constitutional features of infection,

2) Local destruction of valves
3) Embolisation of vegetation leading to
- Infarction
- Infection

4) Other area of infection due to persistent bacteraemia

5) Immune reactions.

Thus symptoms of IE are:

- onset after ≈ 2 weeks of precipitating event
- gradual onset with mild fever & malaise if the organism is of low virulence (streptococcus)
or acute onset with high fever if the organism is of high pathogenecity ( staph)
- Fever- low or high is present in all patients with IE. (#except in elderly, congenital heart
disease, fungal IE)
- fever is generally low grade (< 39.4 C)
- arthralgia & arthritis
- symptoms of embolisation are:
- Hematuria
- Hematemesis
- Limb ischemia

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- Worsening of symptoms/ CCF- due to leaflet destruction

What are the Signs of IE?

- Constitutional- fever

- Local destruction resulting in –

i) new murmur
ii)change in pre-existing murmur
iii)CCF

- Splenomegaly & petechie ≈ 30% of patients with long duration. Petechie are usually seen
on conjunctiva, palate, buccal mucosa, upper extremity.

- Roth spots- retinal haemorrhages with clear centre.

-Osler nodes- tender nodules on fingers/ toe pads- believed to be due to deposition of immune
complexes

-Jane way lesions- seen in acute endocarditis- are small haemorrhages with nodular character
seen on palm & soles.

-Clubbing- long standing disease.

-Embolization- especially pulmonary emboli are seen with- IV drug abusers with Rt. sided IE
& - Lt. sided IE with Lt.→ Rt. shunt.

-Mycotic aneurysm

-CNS manifestation- due to embolization& cerebral abscess

-Glomerulonephritis- due to immune complexes & embolisation

D/D:
- Acute rheumatic fever
- Myxomas

Prophylaxis against IE in a patient with a prosthetic valve

Procedures not requiring antibiotic prophylaxis are

- Dental picking
- Upper GI scopy
- Primary bronchoscopy
- Clean surgery- E.g. Elective caesarean section
- Shedding of primary tooth
- IUCD insertion

Recommendations regarding Infective endocarditis (ESC 2015 guidelines)

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1. A prosthetic heart valve or who have had a heart valve repaired with prosthetic
material.
2. A history of endocarditis.
3. A heart transplant with abnormal heart valve function
4. Certain congenital heart defects including:
o Cyanotic congenital heart disease (birth defects with oxygen levels lower than
normal), that has not been fully repaired, including children who have had a
surgical shunts and conduits.
o A congenital heart defect that's been completely repaired with prosthetic
material or a device for the first six months after the repair procedure.
o Repaired congenital heart disease with residual defects, such as persisting
leaks or abnormal flow at or adjacent to a prosthetic patch or prosthetic device.

Recommendations regarding Infective endocarditis (AHA 2014 guidelines)

Prophylaxis against IE is reasonable for the following patients at highest risk for adverse
outcomes from IE before dental procedures that involve manipulation of gingival tissue,
manipulation of the periapical region of teeth, or perforation of the oral mucosa Class IIa
(Level of Evidence: B):
_ Patients with prosthetic cardiac valves;
_ Patients with previous IE;
_ Cardiac transplant recipients with valve regurgitation due to a structurally abnormal
valve; or
Patients with congenital heart disease with:
- Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits;
- Completely repaired congenital heart defect repaired with prosthetic material or device,
whether placed by surgery or catheter intervention, during the first 6 months after the
procedure;
-Repaired congenital heart disease with residual defects at the site or adjacent to the site
of a prosthetic patch or prosthetic device.

No prophylaxis is required in which cardiac lesions?

1) ASD- unoperated or operated

2) MV prolapse
3) Coronary artery disease/ post CABG

Classification of postoperative IE

Early < 60 days postoperative

Late > 60 days postoperative
Early is due to intraoperative or immediate postoperative contamination.
Mechanical > Bioprosthetic > Homograft IE is more in the early period
However in the late period, IE is equal in all the kinds of valves.

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CLINICAL EXAMINATION
What is mitral facies?

Plethoric cheeks punctuated by bluish patches (venocapillary stasis caused by low cardiac
output)

Pulse in mitral stenosis?

Regular (sinus rhythm) or irregular (AF)

Types of irregular pulses

Regularly irregular Irregularly irregular

Sinus arrhythmia Atrial fibrillation
Pulsus bigeminus Multifocal atrial tachycardia
Pulsus alternans Frequent PVCs
1st and 2nd degree heart block

Other Types of pulses

Condition Characteristics
Aortic stenosis Pulses parvus et tardus

Aortic Bisferiens pulse

regurgitation

Hypertrophic Double peaked waveform

cardiomyopathy

Systolic left Pulses alternans

ventricular
failure

Cardiac Pulses paradoxus

tamponade

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Intra aortic IABP trace
balloon pump

Hypovolemia Systolic variation

JVP IN MS?

 Elevated with RV failure, associated TS or ASD

 Prominent a wave with PH or TR
 Absent a wave - AF
 Diminished or absent x descent – AF/TR
 Prominent v waves-RVF/TR
 Rapid y descent- RVF/TR
 Slow y descent- TS

How do you measure JVP?

 Patient is in semi reclining position. Neck muscles have to be relaxed. By shining a
beam of light across skin over the internal jugular vein exposes the top of the
oscillating venous column.
 Horizontal lines are placed at the top of the venous column and the sternal angle.
 Vertical distance in centimeters between the two horizontal lines gives the JVP which
reflects mean RA pressure.
 Normal JVP is not more than 4cm from sternal angle which corresponds to RA
pressure of 9cm.
 RA is approximately 5cm below sternal angle(4+5=9)

What is type of apex impulse seen in MS?

 Tapping apex beat is seen in MS
 Apex beat is impalpable, is replaced by short systolic tap, palpable equivalent of
aloud S1.
 Shortened outward movement of the apex during systole due to reduced ventricular
filling during diastole gives apex beat its sharp , short and tapping nature in mitral
stenosis.

What are the types of apex beat?

1. Tapping
2. Hperdynamic
3. Heaving
4. Absent/feeble

Hyperdynamic /hyperkinetic
 It is forceful and ill sustained.
 There is increase in amplitude and duration of excursion of the apical impulse but it is
ill sustained. Duration of excursion is < 50% of systole.
 It is seen in volume overloaded conditions and eccentric LVH.
 Cardiac –AR, MR, VSD, PDA, BT shunt, systemic arteriovenous fistula.

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 Non cardiac- Anemia, Beri beri, Thyrotoxicosis, Pregnancy

Heaving /sustained apex beat

 It is forceful and sustained.
 There is increase in amplitude and also sustained increase in the duration of excursion
of apical impulse. It is > 50% of systole.
 It is seen in pressure overload conditions and concentric LVH.
 Causes- AS, systemic hypertension, HOCM

What is pulse deficit?

 The difference between the radial pulse rate and the heart rate counted by auscultation
is defined as pulse deficit. Pulse deficit of more than 6 /min is diagnostic of atrial
fibrillation.
 In tachyarrhythmias, the diastole is shortened and subsequently systolic stroke volume
is sufficient to cause opening of the aortic valve therefore, the arterial pulse will be
non existent inspite of the cardiac contraction. RAs diastole becomes longer in
subsequent cardiac cycles , the stroke volume gadually increases and arterial pulse is
felt.

What other sound is palpable?

Palpable opening snap occurs in early diastole with pliable valve.

Is parasternal heave present in mitral stenosis?

It can be present in right ventricular hypertrophy.

Grading of parasternal heave

It is felt with the heal of the hand in the left parasternal area

Grade I (Mild)
 Light objects like pencil or scale kept along parasternal region may make it obvious.
 It disappears with the application of mild counter pressure.
 It is ill sustained <1/3 of systole.
 Can be seen in children and young adults, thin chest wall and pectus excavatum.

Grade II ( Moderate)
 Obvious lift can be made out.
 It disappears /diminishes with moderate counter pressure.
 Not well sustained. >50% of systole but not through systole.
 Seen in mild to moderate PH( MS,VSD, PDA), RV volume overload( ASD, VSD)
and moderate to severe mitral regurgitation.

Grade III( Severe)

 Very prominent parasternal lift.
 Well sustained. Present through systole.
 Seen in moderate to severe PS, severe MS, large PDA, VSD.
 Note: there is no parasternal heave in RVH due to TOF as it decompresses through
VSD.
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What is diastolic shock?

-Palpable second heart sound

-Loud P2: Pulmonary hypertension

Can we see thrill in MS?

Yes, diastolic (presystolic) thrill in apical area. It indicates mobile and non calcified valve.
It is absent in mild MS, severe calcified MS, severe RVF.

What are the auscultatory findings in MS?

-Loud S1

-Attenuated S1 (Immobility of valve due to calcification)

-P2 loud: Pulmonary hypertension (Severe MS)

-Opening snap

-Diastolic murmur (at the apex)

Why is S1 loud in MS?

It is due to thickened but mobile leaflets. Presystolic gradient between LA and LV prevents
reclosure of the mitral leaflets but kept wide open at the end diastole. Delayed MV closure at
a higher LV pressure at a time when there is a more rapid rise of LV pressure increases the
velocity of valve closure.

What are the signs of PAH?

Loud P2

Prominent ‘a’ wave in JVP

What is opening snap?

High pitched, loud snapping or clicking sound, best heard just inside the apex beat. Interval
between S2 and OS determines severity. S2-OS is often mistaken foe wide split of S2. S2 is
loudest in S2-OS ,while in split S2 it is the last of the two components i.e, P2 is loudest.

Opening snap is absent in?

a) Mild mitral stenosis

b) Calcified mitral valve
c) MS with associated MR

Differential diagnosis of mid diastolic murmur?

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-MS

-Atrial myxoma

-Ball valve thrombosis

-Flow across TV in ASD

-Austin flint murmur

Describe the MDM of MS

 -It is a decrescendo diastolic filling rumble occurring in the first rapid filling phase.
 -It is low pitched rough rumbling in character.
 -Intensity of MDM correlates poorly with severity but length of the murmur does.
 -It is well localised, best heard just medial to apex in left lateral position during
expiration with bell of the stethoscope.
- It is introduced with prominent OS, associated with Loud S1, presystolic
accentuation and a diastolic thrill.
 -Left lateral position, hand grip exercise, amyl nitrate inhalation – Enhance MDM
 -Valsalva maneuver –Diminishes the murmur.

Grades of murmur
I Faintest that can be heard with difficulty
II Faint but easily heard
II I Moderately loud without a thrill
IV Loud with a palpable thrill
V Very loud but still need stethoscope (thrill present)
VI Heard without a stethoscope

X-RAY FINDINGS:
What is the characteristic X ray finding in MS?

-Normal or slightly increased CT ratio

- Left atrial enlargement

-Double atrial shadow

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- Straightening of left heart border: Due to Prominent PA & LAA

- Splayed carina
- Small Aortic knob
-Enlarged pulmonary conus
-Moustache/Antler sign: Prominence of upper veins/ cephalisation of pulmonary blood flow
occurs when pulmonary venous pressure rises to 13 -18mmHg. This is because interstitial
edema occurs in the lower lobes first which restricts further blood flow and is now directed
upward.
- Kerley’s B line – Dense, short horizontal line seen in Costophrenic angle –Pulmonary
venous pressure 18 mmHg.
- Kerley’s A line – straight, dense lines up to 4 cm length running towards the hilum –
Pulmonary venous pressure > 30mmHg
- Mitral valve calcification
- Pulmonary hemosiderosis – Parenchyma ossification

-Lower lobe collapse due to compression of left lower lobe bronchus

- Pulmonary edema- fluffy shadows, batwing appearance in the inner two third of lung.

- Posterior displacement of barium filled esophagus

- Radiographically right atrial enlargement is considered when it bulges >5.5 cm to right of

midline or when RA border occupies more than 3 intercostal spaces.

ECG FINDINGS:
What will be the ECG findings in MS?

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- SR/AF
- Left atrial enlargement – P mitrale “M” shaped P in Lead II , Biphasic P in V1
- RVH- Tall R wave, small S wave, increased R/S ratio in V1 ( Due to PH)

-Right axis deviation

ECG showing atrial fibrillation

Absent P waves
Irregular heart rate.

INVESTIGATIONS:
1. HB% : HB% is important investigationfor patient with MS
*Patient can be anaemic in case of history of severe hemoptysis
*There can be possibility of nutritional anaemia

2. COMPLETE BLOOD COUNT: To rule out leucocytosis and to rule out active infection

3. ESR:To rule out active rheumatic fever.

4. ASO TITRE:

5. BLOOD GROUPING AND CROSSMATCHING: To keep blood ready for

surgical intervention.

6. Can be deranged in patients with CCF or severe right heart failure.

7. RFT:Can be deranged in patients with CCF.Serum electrolytes might be deranged if

patient is on diuretics.

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8. BLOOD SUGAR: To rule out other co morbidities like DM.

9. COAGULATION PROFILE: Sometimes patients can be on anticoagulants, if they

are in AF and if LFT is deranged targeted anticoagulation is INR between 1.5-2.5.

10. X-RAY CHEST

11.ECG

12.ECHOCARDIOGRAPHY

ECHO FINDINGS:
What you would like to see on Echo in MS?

- Morphology of Mitral valve- Pliability, MVA, Subvalve, MVGr

- Ventricular function
- LA & LAA clot
- Other valve

Mitral valve area assessment by Echocardiography

1. Pressure half time

2. Continuity equation
3. Planimetry of valve orifice
4. PISA analysis

TEE in MS

# Transesophageal echocardiography is indicated in patients before percutaneous mitral

balloon valvotomy to rule LA/LAA thrombus.

Intraoperatively to reassess the valve and for post operative assessment.

# Stress echocardiography and cardiac catheterization might be helpful in those cases in

which there is a discrepancy between the severity of symptoms and baseline
echocardiographic findings. To rule out CAD.

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ANATOMY OF MITRAL VALVE:

Describe the anatomy of mitral valve

 The mitral valve is bicuspid and consists of a large anterior leaflet and a smaller
posterior leaflet.
 The anterior leaflet covers about two thirds of the surface area of the valve.
 The posterior leaflet is C-shaped and wraps around the anterior leaflet accounting for
about two thirds of the circumference of the valve.
 The leaflets join at the anterolateral and posteromedial commissures.
 The posterior leaflet is further divided anatomically into three scallops whereas the
anterior leaflet does not have scallops per se.
 The mitral valve attaches to two papillary muscles, anterolateral and posteromedial,
through chordae tendinae.
 Each papillary muscle sends off chordae tendinae to both mitral leaflets.
 There are three types of chordae tendinae.
-First-order (or primary) chordae attach to the edge of the leaflets
-Second-order (or secondary) chordae attach to the body of the leaflets
-Third-order (or tertiary) chordae attach to the base of the posterior leaflet.

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Carpentier classification

Posterior leaflets:P1, P2, P3 where P1 is laterally oriented and P3 medially

Anterior leaflets: A1,A2,A3 orientation same as posterior leaflets

CAUSES OF MS:
What are the causes of mitral stenosis?

- Rheumatic heart disease

- Congenital – Parachute Mitral valve
- Hunter’s syndrome
- Hurler’s syndrome
- Lutembacher’s syndrome

-SLE

-Rheumatoid arthritis

-Malignant carcinoid

-Fabry disease

-Whipple disease

-Methysergide therapy

Diseases manifesting like MS?

-Cor tritriatum

-Large LA Neoplasms

-Pulmonary venous obstruction

PATHOPHYSIOLOGY
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Pathophysiology of MS

 Normal Mitral valve area is 4-6cm2

 A decades-long asymptomatic period characterizes the initial phase of rheumatic MS.
 Symptoms rarely appear until the normal mitral has been reduced to 2.5 cm2 or
 less.
 When the mitral valve area reaches 1.5 to 2.5 cm2, symptoms usually occur only in
association with exercise or other conditions such as fever, pregnancy, or AF, that
lead to increases in heart rate or cardiac output.
 After the mitral valve area decreases to less than 1.5 cm2, symptoms may develop at
rest

Valve area Symptoms

>2.5 cm2 None

1.5-2.5 cm2 (Mild) Dyspnoea on severe exertion
1-1.5 cm2 (Moderate) PND +/- Pulmonary edema
<1 cm2 (Severe/ critical MS) Orthopnoea

Symptoms get precipitated by clinical events associated with increased cardiac output and
consequent increased flow across the valve.

Obstructed flow across the mitral valve is associated with pressure gradient across the valve,
more the severe the MS, greater is the gradient.
Obstructed mitral valve inflow leads to secondary increase in LAP which leads to
 LA enlargement leading to onset of AF and ultimately thromboembolic episodes.
 Passive increase in pulmonary venous and arterial pressures, longstanding pulmonary
venous hypertension leads to pulmonary arterial hypertension secondary to changes in
medial and intimal layers of pulmonary arteries and arterioles. Increase in pulmonary
artery pressures leads to RV overload causing hypertrophy and dysfunction.
 Decreased flow across the mitral valve causes decreased ventricular filling and hence
low stroke volume.

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Patients with MS commonly report dyspnea as their initial symptom, reflective of increased
LA pressure and pulmonary congestion
Patients may report palpitations that signal the onset of AF.
Systemic thromboembolization occurs in 10% to 20% of patients with MS

Pressure volume loops

Normal pressure volume loop

 Phase 1 depicts left ventricular filling

 Phase 2 depicts isovolumetric contraction

 Phase 3 shows left ventricular ejection

 Phase 4 shows isovolumetric relaxation.

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 MVO stands for opening of the mitral valve (MV) and represents left ventricular
end-systolic volume and early diastolic pressure.

 MVC is closure of the MV and the end of diastolic pressure (LVEDP) and volume
(left ventricular end-diastolic volume [LVEDV]).

 AVO represents the opening of the aortic valve and coincides with systemic, aortic
diastolic pressure.

 AVC is the closure of the aortic valve and represents left ventricular end-systolic
pressure and volume,coinciding with the dicrotic notch in the aortic pressure tracing

The P-V loop is shifted to left in MS. It results in diminished left ventricular preload reserve.
LVEDV and LVEDP are reduced with an accompanying decline in SV.

What are the causes of LV dysfunction in MS?

 Posterobasal regional wall motion abnormalities as a consequence of thickening and

calcification of the mitral apparatus.
 Vasoconstriction in response to diminished cardiac output may impair LV ejection
 Afterload can also be increased due to inadequate wall thickness (Laplace law)
 RV dysfunction due to PH can lead to LV dysfunction.
 Rheumatic myocarditis

PRE-OP ASSESSMENT AND OPTIMISATION:

What is the targeted heart rate in MS patients? Why?
Patients with MS tolerate tachycardia particularly poorly due to decline in the diastolic period
that accompanies tachycardia.

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The flow rate across the stenotic valve must increase to maintain left ventricular filling in a
shorter diastolic period.
As the valve area remains constant, the pressure gradient between the LA and LV increases
by the square of the increase in the flow rate, according to the Gorlin formula, in which PG is
the transvalvular pressure gradient:

Valve area = Transvalvular flow rate/Constant * √PG

Tachycardia necessitates a significant increase in the transvalvular pressure gradient and may
precipitate feelings of breathlessness in awake patients.
HR of 60-80 is acceptable in Mitral stenosis.

In patients with AF, it is the increased ventricular rate that is most deleterious, rather than the
loss of atrial contraction. Although coordinated atrial activity is always preferable, the
primary goal in treating patients with MS and AF should be control of the ventricular
rate.

How can you assess mitral valve area?

a) During catheterisation using Gorlin equation

.
b) Echocardiography:

i) Two dimensional planimetry of valve orifice,

ii) Continuity equation, and
iii) PISA analysis.

Other invaluable information obtained during an echocardiographic study includes the size
and function of the ventricle and an estimation of the PAP.

c) Doppler derived measurements of the gradient, pressure half time and deceleration time.

How will assess severity of MS?

A) According to Valve area & Symptoms

Normal Mitral valve area is 4-6cm2

>2.5 cm2 None

1.5-2.5 cm2 (Mild) Dyspnoea on severe exertion
1-1.5 cm2 (Moderate) PND +/- Pulmonary edema
<1 cm2 (Severe/ critical MS) Orthopnoea

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

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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 > 15 mm Hg

Grading of MS

Mild Moderate Severe

Mean pressure <6 5-10 >10
gradient(mmHg)
Pressure half ≤100 100-200 >220
time(ms)
Mitral valve >1.5 1.0-1.5 <1.0
area(cm2)
Systolic pulmonary <30 30-50 >50
artery
pressure(mmHg)

Stages of MS - 2014 AHA/ACC Valvular Heart Disease Guideline

What are the features of pulmonary venous congestion in MS?

- Pulmonary vascular markings

- Upper & lower lobe pulmonary vein congestion

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- Peribronchial cuffing
- Pulmonary oedema
- Kerley’s A,B,C lines
- Hemosiderosis

MEDICAL MANAGEMENT OF MS:

What is the medical treatment in MS?

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- Anti cardiac failure measures

- Treatment of AF and anticoagulation
- Rheumatic prophylaxis
- Infective endocarditis prophylaxis

Medical treatment is directed toward alleviating pulmonary congestion with diuretics,

treating atrial fibrillation, and anti-coagulating patients who are at increased risk of arterial
embolic events.

Tachycardia is typically poorly tolerated in patients with MS and can lead to an acute
deterioration as diastolic filling time may be inadequate.

Heart rate control can be beneficial in patients with MS and atrial fibrillation and fast
ventricular response (Class IIa).

Heart rate control may also be considered for patients with MS in normal sinus rhythm and
symptoms associated with exercise (Class IIb).

AF in MS is multifactorial nature. It is likely that persistent rheumatic inflammation and left

atrial fibrosis contribute in addition to left atrial size and left atrial hypertension as causes of
AF in MS.

Treatment of AF

A) Control of ventricular rate

B) Maintainence of sinus rhythm

C) Anticoagulation

Drugs for rate control

Beta blockers, calcium channel blockers, digoxin and ivabradine have been used to
control ventricular rate.

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Note on digoxin use

Digoxin is not usually first-line therapy for ventricular rate control in patients with AF,
despite its common use.

Onset of action requires >1 hour and the effect does not peak until approximately 6 hours
after initial administration hence, not an optimal agent when rapid rate control is desired.

Digoxin may be combined with beta blockers or nondihydropyridine calcium channel

blockers to improve ventricular rate control during exercise.

It has been used in HF as one of the few rate control agents that does not have negative
inotropic effects.

Adverse effects of digoxin include AV block, ventricular arrhythmias, and, infrequently,

aggravation of sinus node dysfunction.

Dose adjustment is required in patients with renal dysfunction, the elderly, and in the
presence of drugs that reduce its excretion, such as amiodarone, propafenone, or
nondihydropyridine calcium channel blockers. Therefore, periodic assessment of serum
levels is warranted in many patients.

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Drugs to maintain sinus rhythm

The following antiarrhythmic drugs are recommended in patients with AF to maintain sinus
rhythm, depending on underlying heart disease and co morbidities Amiodarone , Dofetilide,
Dronedarone,Flecainide, Propafenone, and Sotalol.

An attempt to restore sinus rhythm with direct current electrical cardioversion or

antiarrhythmic drugs may be considered in hemodynamically unstable patient.

Prevention of thromboembolism

 With AF or atrial flutter for ≥48 h, or unknown duration, anticoagulate with warfarin
for at least 3 wk before and 4 wk after cardioversion I B .

 With AF or atrial flutter for >48 h or unknown duration, requiring immediate

cardioversion, anticoagulate as soon as possible and continue for at least 4 wk I C.

 With AF or atrial flutter <48 hrs and high stroke risk, IV heparin or LMWH, or factor
Xa or direct thrombin inhibitor, is recommended before or immediately after
cardioversion , followed by long term anticoagulation.

 Following cardioversion of AF, long term anticoagulation should be based on

thromboembolic risk.

Anticoagulation (vitamin K antagonist [VKA] or heparin) is indicated in patients with

1) MS and AF (paroxysmal, persistent, or permanent),

2) MS and a prior embolic event, or
3) MS and a left atrial thrombus (Class I).

Anticoagulation may also be considered if the left atrium is markedly dilated (5.0-5.5 mm)
or if there is spontaneous contrast on echocardiography (Class IIb).

-Antibiotic therapy is important for the secondary prevention of rheumatic carditis, de-novo
rheumatic valvular disease or worsened rheumatic valvular disease.

-Patients with a history of rheumatic fever are at high risk of recurrence.

-Long-term secondary prophylaxis, preferentially with penicillin, is therefore recommended

for all patients with a history of rheumatic fever, rheumatic carditis or rheumatic valve
disease.

- The duration of prophylaxis depends on a number of factors, including time since the last
attack, the age of the patient, the extent of cardiac involvement, and the patient's risk of
exposure to streptococcal infections.

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Routine antibiotic prophylaxis for endocarditis is no longer recommended for patients

with MS.

SURGICAL MANAGEMENT
What are the other modalities of treatment?

- Balloon Valvuloplasty (PBMV/PTMC)

- Surgery (CMV/CMC, OMC, MVR)

INDICATIONS FOR INTERVENTIONS - 2014 AHA/ACC Valvular Heart

Disease Guidelines

 PMBC is recommended for symptomatic patients with severe MS (MVA _1.5 cm2,
stage D) and favorable valve morphology in the absence of contraindications I A
 Mitral valve surgery is indicated in severely symptomatic patients (NYHA class
III/IV) with severe MS (MVA _1.5 cm2, stage D) who are not high risk for surgery
and who are not candidates for or failed previous PMBC I B
 Concomitant mitral valve surgery is indicated for patients with severe MS (MVA _1.5
cm2, stage C or D) undergoing other cardiac surgery I C

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Percutaneous balloon mitral valvotomy

 During BMV, a large balloon is introduced across the mitral valve via either the
transseptal or retrograde route.
 Inflation of the balloon fractures the rheumatic fusion of the valve leaflets at the
commissures, dramatically improving leaflet excursion and orifice area.
 Successful BMV is usually defined as a postprocedure mitral valve area of >1.5
cm2 with no more than moderate mitral regurgitation.
 Sixty-five percent of patients are free of restenosis 10 years after the procedure.
 Suitability for BVM is determined by valve morphology and the amount of mitral
regurgitation present.
 The Wilkins score gives a rough guide to the suitability of the mitral valve’s
morphology for BMV.
 This scoring system assigns a point value from 1 to 4 for each of (1) valve
calcification, (2) leaflet mobility, (3) leaflet thickening, and (4) disease of the
subvalvular apparatus.
 In general, patients with a score of <9 and less than moderate mitral
regurgitation have the best outcomes.
 Before BMV, a transesophageal echocardiogram is performed in all patients to look
for the presence of clot (an obvious risk for embolization) in the left atrium or left
atrial appendage.

What are the indications of PBMV?

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

Wilkins’s Echo score < 9

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Contraindications for PBMV

- Other valve disease/ Coronary artery disease which needs surgery

- LA/LV thrombus

- Moderate MR
- Dense Calcification of mitral valve
- Recurrent thromboembolic events

Anesthetic considerations: Generally it is done under light sedation.

Open Commissurotomy(OMC)

Recent emphasis on mitral valve conservation may lead to increased use of this procedure,
wherein the surgeon, under direct vision, may be able to provide relief of obstruction in
patients thought not to be BMV candidates because of poor valve morphology. Exactly what
percentage of patients would likely have a bad outcome with BMV yet a good outcome with
open commissurotomy is unknown but probably is small. However, when the valve can be
conserved, it avoids the risks inherent to prosthetic valves and also avoids the need for
anticoagulation in patients in sinus rhythm.

Closed commissurotomy(CMV)

Arterial line is placed in right radial artery. After induction central line is placed and
inotropes connected.

Patient is positioned in right lateral decubitus position.

Anterolateral incision is made over the interspace through which apical impulse is palpated.

Pericardium is opened anterior to phrenic nerve.

Purse –string sutures are taken lateral and superior to LV apex and around the tip of left
atrial appendage.

Inciscion is made in the appendage to accommodate surgeons right index finger snuggly.

Surgeon’s right index finger is insinuated through the appendage into the left atrium and
passed directly to the mitral valve..

After valve evaluation , pressure is applied with the exploring finger against anterolateral
commissure. Pliable stenotic valve opens up sometimes with this maneuver alone. Usually
Tubbs dilator is required.

Tubbs dilator is inserted through a small stab wound in the center of the LV apical purse
string suture.

Guided by the intraatrial finger and the setscrew on the dilator positioned so that maximal
opening is 2.5 cm, the dilator is passed through the valve.

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The dilator blades are opened for 5 to 6 seconds only, ensuring that each blade is against a
leaflet and not commissure. Heart is allowed to fully recover completely between dilations.

Successive dilatations are performed starting with 2.5cm and maximum of 4cm.

After procedure index finger is removed , tubbs dilator is removed the purse strings sutures
tied snuggly.

Close monitoring of hemodynamics during dilation and post dilation is required.

Valve area is assessed by TEE.

Anesthetic considerations for OMC/CMV are similar to MVR. Patients undergoing CMV
can be extubated after few hours of ventilation and hence dose of opioids should be titrated.

PROSTHETIC VALVES
Mechanical valves Bioprosthetic valves

Bileaflet Stented bioprostheses

Monoleaflet Stentless bioprostheses

Caged ball valves Percutaneous bioprostheses

Recommendations for Prosthetic Valve Choice

1. Choice of valve intervention and prosthetic valve type should be a shared decision process
(I C)

2. A bioprosthesis is recommended in patients of any age for whom anticoagulant therapy is

contraindicated, cannot be managed appropriately, or is not desired (I C)

3. A mechanical prosthesis is reasonable for AVR or MVR in patients <60 y of age who do
not
have a contraindication to anticoagulation (IIa B)

4. A bioprosthesis is reasonable in patients >70 y of age (IIa B)

5. Either a bioprosthetic or mechanical valve is reasonable in patients between 60 y and 70 y

of age (IIa B)

6. Replacement of the aortic valve by a pulmonary autograft (the Ross procedure), when
performed by an experienced surgeon, may be considered in young patients when VKA
anticoagulation is contraindicated or undesirable (IIb C)

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Anticoagulation for Prosthetic valves

 Anticoagulation with a VKA (Vitamin K antagonist) and INR monitoring is

recommended in patients with a mechanical prosthetic valve. (Class I)
 Anticoagulation with a VKA is indicated to achieve an INR of 3.0 in patients with a
mechanical MVR (Class I)

Bridging Therapy for Prosthetic Valves

 The management of patients with mechanical heart valves in whom interruption of

anticoagulation therapy is needed for diagnostic or surgical procedures should take
into account the type of procedure, risk factors, and type, location, and number of
heart valve prosthesis.
 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.
 Temporary interruption of VKA anticoagulation, without bridging agents while the
INR is subtherapeutic is done in pts with bileaflet mechanical AVR and no other risk
factors for thrombosis who are undergoing invasive or surgical procedures.
 Bridging anticoagulation with either intravenous UFH or subcutaneous LMWH is
recommended for 1) mechanical AVR and any thromboembolic risk factor, 2) older
generation mechanical AVR, or 3) mechanical MVR.
 Patients at high risk of thrombosis include all patients with mechanical MVR or
tricuspid valve replacements and patients with an AVR and any risk factors for
thromboembolism.

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 Such risk factors include AF, previous thromboembolism, hypercoagulable condition,
older-generation mechanical valves, LV systolic dysfunction (LVEF <30%), or >1
mechanical valve.
 When interruption of VKA therapy is needed, VKA is stopped 2 to 4 days before the
procedure (so the INR falls to <1.5 for major surgical procedures) and restarted as
soon as bleeding risk allows, typically 12 to 24 hours after surgery.
 Bridging anticoagulation with intravenous UFH or subcutaneous LMWH is started
when INR is <2.0 (usually about 48 hours before surgery) and stopped 4 to 6 hours
(for intravenous UFH) or 12 hours (for subcutaneous LMWH) before the procedure.
 When LMWH is used, therapeutic weight-adjusted doses are given twice daily.

ANAESTHETIC MANAGEMENT
Goals of anaesthetic management
a) Prevent tachycardia

 Avoidance of tachycardia begins in the preoperative period.

 Anxiety-induced tachycardia may be treated with small doses of narcotics or
benzodiazepines.
 However, excessive sedative-induced hypoventilation can result in hypoxemia or
hypercarbia, which aggravates pulmonary hypertension,
 Large doses of premedication can reduce the already limited left ventricular preload.
 Control of the ventricular rate remains the primary goal in managing patients with AF
 Cardioversion should not be withheld from patients with atrial tachyarrhythmias who
become hemodynamically unstable.

b) Maintenance of left ventricular preload

 Appropriate replacement of blood loss and prevention of excessive anesthetic-induced

venodilation help preserve hemodynamic stability intraoperatively.
 Avoid exacerbation of pulmonary vascular congestion.

c) Avoid factors that aggravate pulmonary hypertension and impair right ventricular
function

 Meticulous attention to arterial blood gas results allows appropriate adjustment of

ventilatory parameters.
 Vasodilator therapy in patients with pulmonary hypertension generally is ineffective
because the venodilation produced further limits left ventricular filling and does not
improve cardiac output. The only MS patients who may benefit from vasodilator
therapy are those with
 Concomitant mitral regurgitation
 Severe pulmonary hypertension
 Right ventricular dysfunction in whom pulmonary vasodilation can facilitate
transpulmonary blood flow and improve left ventricular filling.

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Preload: normal or increased

Afterload: normal
Goal: controlled ventricular response
Avoid: tachycardia, pulmonary vasoconstriction

Preoperative medication

 Appropriate monitoring and supplemental oxygen therapy should be considered for

patients receiving preoperative narcotics or benzodiazepines.
 Medications taken by the patient before surgery to control heart rate, such as digitalis,
β-blockers, calcium-receptor antagonists, or amiodarone, should be continued in the
perioperative period.
 Additional doses of β-blockers and calcium-receptor antagonists may be required
intraoperatively, particularly to control the ventricular rate in patients with AF.

Monitoring:
 Invasive hemodynamic monitoring allows the anesthesiologist to maintain adequate
preload while avoiding excessive fluid administration that could aggravate pulmonary
vascular congestion.
 Placement of an arterial catheter facilitates timely recognition of hemodynamic
derangements.
 PACs can be invaluable in the management of patients with significant MS.
 Even though the PCWP overestimates left ventricular filling and the pulmonary
artery diastolic pressure may not accurately reflect left-heart volume in patients
with pulmonary hypertension, examination of trends and responses to
intervention can be more readily assessed.
 TEE used to assess ventricular filling and function.
 Invasive monitoring depends on the severity and type of the surgery.

Induction:

Cardiostable drug Etomidate in doses of 0.3 to 0.5 mg/kg is ideal for induction along with
Fentanyl 2 to 5 mcg/kg. Vecuronium or Rocuronium can be used to facilitate intubation.
Lignocaine 1 to 2mg/kg or Esmolol 500 mcg/kg can be used for the pressor response control
which is most important in Mitral stenosis patient. Drugs causing tachycardia and
hypotension are avoided.

For cardiac surgery, Narcotic-based anesthetics often are helpful in avoiding intraoperative
tachycardia. However, these patients may be receiving other vagotonic drugs, and that
profound bradycardia is possible in response to large doses of narcotics. The selection of a
muscle relaxant such as pancuronium may help prevent the unwanted bradycardia associated
with high-dose narcotics.

Maintainence – can be done using oxygen air or nitrous oxide, opioids, isoflurane and
vecuronium. Nitrous oxide is avoided in PH. Light planes of anesthesia which cause
sympathetic stimulation are to be avoided.

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Post operative management – risk of developing pulmonary edema and right heart failure
continues in the post op period. Pain and hypoventilation cause tachycardia and increase in
pulmonary vascular resistance. Hence, good post op pain relief is important in these
patients. Patients undergoing major surgeries might require post op ventilation.

RV dysfunction probably poses a greater challenge in treating patients with MS than does LV
dysfunction. Management of RV dysfunction includes optimizing acid-base balance and
using hypocapnia, hyperoxia, and possibly vasodilators to decrease PVR ( milirinone).

Regional anesthesia in mitral stenosis

Regional anesthesia can be given with epidural and spinal in mild to moderate mitral stenosis
who are in NYHA class I and II.

It requires close hemodynamic monitoring

Hypotension can be managed by vasopressors like phenylephrine and titrated fluid

supplementation.

It is contraindicated in patients on anticoagulation and in severe mitral stenosis

Post operative monitoring is important pereferably in ICU set up.

ANAESTHETIC MANAGEMENT OF PREGNANT

PATIENT WITH MS
Physiological changes during pregnancy

Both tachycardia and increase in cardiac output are detrimental for MS patients.
The cardiac output increases from the fifth week of pregnancy and reaches its maximum
levels by 32 weeks.

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 SANCON 2016
Cardiac decompensation and pulmonary oedema may occur in pregnant women during the
second or third trimester. The risk of maternal death is greatest during labour and during the
immediate post-partum period.

Haemodynamics during labour

Stage of labour Percentage of change Cardiac output

Latent phase 10%Increase

Active phase 25%Increase

Expulsive phase 40%Increase

Medical management:
Immediate post-partum 75–80%Increase
1. Bed rest, oxygen therapy and diuretics.
2. Beta-adrenergic receptor
Heart rate blockade with All
Propranolol or atenolol
stages Increase
3. Atrial fibrillation requires aggressive treatment with digoxin and beta blockers to revert it
to sinus rhythm. CVPCardioversion should be All
performed if pharmacologic therapy fails to control
stages Increase
the ventricular response.
4. Anticoagulation to prevent systemic embolization, Standard therapy during pregnancy
would be

 SC/IV heparin for up to 12 weeks antepartum (aPTT 1.5–2.5-times of normal)

 Warfarin from 12 to 36 weeks (maintain INR 2.5–3.0)
 SC/IV heparin after 36 weeks

Surgical management:

1. If mitral stenosis is diagnosed before pregnancy, mitral commissurotomy is preferred.

2. During pregnancy, the second trimester is the preferred period for any invasive procedure.
Percutaneous valvuloplasty using the balloon technique has become the accepted treatment
for patients with severe symptomatic mitral stenosis.

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 SANCON 2016

 Valve replacement is reasonable for pregnant patients with severe MS (mitral valve
area <1.5 cm2, stage D) and valve morphology not favorable for percutaneous mitral
balloon commissurotomy only if there are refractory NYHA class IV HF symptoms.

 Valve operation during pregnancy is high risk, with a 30% to 40% fetal
mortality rate and up to 9% maternal mortality rate.

 Surgery for MS during pregnancy should be reserved for those with refractory NYHA
class IV HF symptoms that are not responsive to medical therapy.

 The operation needs to be carefully planned with a Heart Valve Team of cardiologists,
cardiovascular anesthesiologists, surgeons, and obstetricians specializing in high-risk
obstetrics to determine optimal timing and sequence of therapies.
 High pump flows and normothermic perfusion should be used to protect the fetus
during cardiopulmonary bypass, with the shortest pump time possible.

 Continued monitoring of the fetus should be performed

 There is no ideal time during pregnancy to perform open heart surgery, so timing is
based on the combination of the clinical status of the mother and the fetus.

 The period between the 20th and 28th weeks of pregnancy appears to be safest for
the fetus in terms of risk of malformation and premature delivery.

 If the mother can carry the fetus to full maturity, a combined cesarean section
followed by cardiac surgery can be planned.

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 SANCON 2016

Obstetric management of pregnant patient with MS

1. Vaginal delivery under epidural anaesthesia is recommended unless obstetrically
contraindicated. Caesarean section is indicated for obstetric reasons only.

2. Labour analgesia: 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.

3) Monitoring: Invasive cardiac monitoring like radial artery cannulation and pulmonary
catheter are beneficial in assessing the cardiac output, pulmonary artery pressure and for
guiding fluid and drug therapy, especially in NYHA III and IV patients. Sudden drops in
systemic vascular resistance (SVR) in the presence of a fixed cardiac output can be prevented
by small bolus doses of phenylephrine, with volume expansion when necessary.

4) Combined spinal–epidural analgesia during labour using intrathecal fentanyl 25 μg

produces good analgesia without major haemodynamic changes during the first stage of
labour.
During the second stage of labour, only the uterine contractile force should be allowed rather
than the maternal expulsive effort that is always associated with the valsalva maneuver.
Therefore, the second stage of delivery should be cut short by instrumentation.
Supplementary analgesia for instrumentation with slow epidural boluses of fentanyl and a
low concentration of bupivacaine reduces SVR and the cardiac pre-load.
Low spinal anaesthesia for vaginal instrumental delivery has also been used with good
results in these patients.
5) Foetal heart rate monitoring should be carried out during all stages of labour.
Supplemental oxygen administration with pulse oximetry monitoring to minimize increases
in pulmonary vascular resistance and maintenance of left uterine displacement for good
venous return are mandatory.
Supplementary epidural anaesthesia can be maintained throughout the immediate post-partum
period and the catheter left in situ could provide anaesthesia for immediate or post-partum
tubal sterilization.

MS patient with pregnancy subjected for Caesarian

section
The goals for the anaesthetic management of patients with mitral stenosis are:

(1) maintenance of an acceptable slow heart rate,

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(2) immediate treatment of acute atrial fibrillation and reversion to sinus rhythm,

(3) avoidance of aortocaval compression,

(4) maintenance of adequate venous return,

(5) maintenance of adequate SVR and

(6) prevention of pain, hypoxaemia, hypercarbia and acidosis, which may increase
pulmonary vascular resistance.

Regional anaesthesia has proved to be a safe technique in cardiac patients presenting for
caesarean section. Epidural and spinal anaesthetic techniques are attractive options in mild
and moderate mitral stenosis.

Advantages of epidural analgesia:

It can be administered in incremental doses and that the total dose could be titrated to the
desired sensory level.

Slower onset of anaesthesia, allows the maternal cardiovascular system to compensate for the
occurrence of sympathetic blockade, resulting in a lower risk of hypotension and decreased
uteroplacental perfusion.

Segmental blockade spares the lower extremity “muscle pump,” aiding in venous return, and
also decreases the incidence of thromboembolic events. Invasive haemodynamic monitoring,
judicious intravenous administration of crystalloid and administration of small bolus doses of
phenylephrine maintain maternal haemodynamic stability.

Contraindications

1. Patients on anticoagulation

2. Severe mitral stenosis.

Disadvantages of General anaesthesia:

1) Increased pulmonary arterial pressure and tachycardia during laryngoscopy and tracheal
intubation.
2) The adverse effects of positive-pressure ventilation on the venous return may ultimately
lead to cardiac failure.
Tachycardia, inducing drugs like atropine, ketamine, pancuronium and meperidine,
should be totally avoided.
A beta-adrenergic receptor antagonist and an adequate dose of opioid like fentanyl should be
administered before or during the induction of general anaesthesia.
Esmolol has a rapid onset and short duration of action, better choice in controlling
tachycardia however foetal heart rate should be monitored.

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 SANCON 2016
Modified rapid sequence induction using etomidate, remifentanyl and
succinylcholine/rocuronium is an ideal choice in tight stenosis with pulmonary hypertension.
Maintenance of anaesthesia can be carried out with oxygen and air, isoflurane, opioids and
vecuronium.
With associated severe pulmonary hypertension, nitrous oxide can be omitted. At this
juncture, invasive haemodynamic monitoring is an inevitable guide.
After delivery of the foetus, oxytocin 10–20 u in 1,000 ml of crystalloid should be
administered at a rate of 40–80 mu/min.
An infusion of oxytocin can lower the SVR as well as elevate the pulmonary vascular
resistance, resulting in a drop in cardiac output. Care must be taken during its administration.
Methylergonovine produces severe hypertension, tachycardia and increased pulmonary
vascular resistance hence avoided.

Anticoagulation of Pregnant Patients with Mechanical

Valves
 Warfarin is recommended in pregnant patients with a mechanical prosthesis to
achieve a therapeutic INR in the second and third trimesters
 Discontinuation of warfarin with initiation of intravenous UFH(with an activated
partial thromboplastin time [aPTT] >2 times control) is recommended before planned
vaginal delivery in pregnant patients with a mechanical prosthesis.
 Low-dose aspirin (75mgto 100 mg) once per day is recommended for pregnant
patients in the second and third trimesters with either a mechanical prosthesis or
bioprosthesis.
 Continuation of warfarin during the first trimester is reasonable for pregnant patients
with a mechanical prosthesis if the dose of warfarin to achieve a therapeutic INR is 5
mg per day or less after full discussion with the patient about risks and benefits
 Dose-adjusted continuous intravenous UFH (with an aPTT at least 2 times control)
during the first trimester is reasonable for pregnant patients with a mechanical
prosthesis if the dose of warfarin is greater than 5 mg per day to achieve a therapeutic
INR

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Anticoagulation of Pregnant Patients With Mechanical Valves

Anesthesia for PBMV in pregnancy

 It is best done in awake state with minimal dose of opioids to avoid fetal
bradycardia and apnea in the pregnant patient. Small doses of propofol can be
supplemented.
 General anesthesia is usually avoided due to aspiration risks and difficult airway. It
also helps minimize fetal exposure to anesthetic drugs.
 Procedure is usually done after 14 - 20 wks of gestation.
 Anti aspiration prophylaxis is given
 Wedging of right lumbar region is done to avoid supine hypotension syndrome.
 Abdominal lead shielding is done.
 Radiation exposure time is cut down to minimum.

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CARDIOPULMONARY BYPASS

Cardiopulmonary bypass circuit

 CPB circuit consists of tubings (cannulae) that drain venous and return arterial blood;
an oxygenator, where gas exchange occurs; and a mechanical pump that provides
systemic perfusion.
 The initiation of CPB involves the drainage of venous blood to the CPB machine.
 This is accomplished by placing a large-bore cannula (dualstage or single cannula)
into the right atrium.
 The cannulae are snared to preventing systemic venous blood from entering the heart.
 During CPB, the rate of venous drainage is passive and depends on proper placement
of appropriately sized cannulae, intravascular volume status, and hydrostatic pressure
gradient (the difference in height between the right atrium and the venous reservoir).
 From the venous reservoir, blood enters the oxygenator/heat exchanger unit, where it
is oxygenated, carbon dioxide is removed, and the blood is warmed/cooled.
 The now-oxygenated blood is returned to the arterial circulation via a large “arterial”
cannula.
 Arterial cannulae may be placed in the ascending aorta, femoral, or axillary arteries.
 Other functions provided by the CPB machine include delivery of cardioplegia,
cardiotomy suction (which scavenges shed blood from the surgical field), and vents to
decompress the LV/aspirate air from the heart during de-airing procedures.
 Venting prevents ventricular distention that may lead to myocardial ischemia.
 Common vent sites include the LV via a cannula placed in the left superior pulmonary
vein (or, rarely, the LV apex) or the aortic root.
 In addition to providing cardiopulmonary support, CPB circuits contain filters for the
removal of bubbles and debris, in-line blood gas monitors, and volatile agent
vaporizers.

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 SANCON 2016
 Warning monitors are placed in key locations of the CPB circuit. These monitors are
used to detect low blood levels in the venous reservoir/ oxygenator (to prevent
entrainment of air to the arterial side of the circuit), high systemic line pressure (to
diagnose possible arterial cannula obstruction/aortic dissection; both cause elevated
line pressure), and bubbles.

Blood Tubings

 The tubing used to connect the various components and conduct blood into and out of
the patient’s vascular system is medical-grade polyvinyl chloride.
 The blood-tubing interface is untreated polyvinyl chloride.
 The newer generation of polyvinyl chloride tubing has surface coatings and other
modifications that significantly alter the bioreactivity of the surface.
 These coatings have been shown to reduce plasma levels of markers of subclinical
coagulation, attenuate the increase of cytokines and other inflammatory markers, and
shorten intubation times.

Venous and arterial cannulas

 The venous cannula can be either a single stage (one opening at the end), a two-stage
(an opening at the end and a “basket” opening in the right atrium), or a three-stage
(one opening and two center baskets). Placement is made with the end opening
directed into the IVC.
 Intracardiac repairs are usually completed with bicaval cannulation with two venous
cannulas separately inserted into the IVC and SVC.

 Arterial cannulas- Arterialized blood is returned to the patient from the CPB circuit
through an arterial cannula placed either in the ascending aorta, in the femoral artery
or more recently the axillary artery has also been used.
 The size of the cannula is chosen to minimize the pressure drop across the cannula at
the patient's calculated flow rate

Venous Reservoirs

 Blood reservoirs may be collapsible plastic bags or clear plastic hard-shelled

containers.
 Hard-shelled reservoirs include an integral filtration mechanism with a screen and
depth filters through which blood must pass before leaving the outlet of the vessel. It
functions as the cardiotomy reservoir for debubbling and filtration of suctioned or
vented blood
 Hard-shelled reservoirs have integrated positive- and negative-pressure release valves,
which are necessary for the application of vacuum to the reservoir to augment venous
drainage.
 If vacuum-assisted venous drainage is employed, the vacuum pressure in the reservoir
should be maintained at the minimum necessary, and entrainment of air from the
surgical field into the venous line should not be permitted.
 Reservoir pressures in excess of 60 mm Hg have been shown to increase microbubble
 counts measured in the circuit’s arterial infusion line dramatically
 Determination of volume status is more precise with a hard-shell reservoir than with a
soft-bag reservoir due to the presence of gradations on the outside of the reservoir.
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 SANCON 2016
 Soft-bag venous reservoirs require a separate hard-shell cardiotomy reservoir to be
used for the collection and transfer of suctioned and vented blood to the venous
reservoir.
 The advantage of a soft-bag venous reservoir is absence of an air-blood interface and
its collapsible function so that large volumes of air cannot be pumped if it is emptied.
Pumps

 There are currently two types of blood pumps used in the CPB circuit: roller and
kinetic (centrifugal)

Roller pumps

The method of action is for fluid to move via the compression of tubing placed in between
rollers and a horseshoe-shaped backing plate or raceway.

Each pump has two roller heads configured 180 degrees apart to maintain continuous roller
head contact with the tubing.

There is a small depression in the backing plate when the rollers are both in the raceway to
prevent over-occlusion of the tubing.

The revolutions per minute (rpm) for roller pumps used for arterial blood flow typically range
from 50 to 150 rpm, depending on the pump head tubing internal diameter (ID).

Flow from a systemic roller pump increases or decreases linearly with rpm.

The total pump output is displayed in milliliters or liters per minute on the pump control
panel.

Roller pumps also are used to deliver cardioplegic solution, remove blood and air from heart
chambers or great vessels(vent) and suction shed blood from the operative field.

Their occlusive nature, is capable of generating extremely high positive and negative pressure
and are also able to pump massive quantities of air.

Kinetic or centrifugal pump

They operate on a principle of constrained vortex that moves fluid by the action of rapidly
rotating cones or a series of vanes on an impeller, which create negative pressure by the
centrifugal action of the rotating core.

Due to the spinning action imparted to the blood, the highest positive pressure is located most
distant to the center axis of rotation and propels fluid forward through the outlet connector.

Kinetic pumps are both preload sensitive (dependent upon fluid entering the pump inlet) and
afterload sensitive (will not move forward when the downstream resistance is high).

Being nonocclusive, they are unable to generate extremely high or low pressure.

Centrifugal pumps will not pump blood if they become filled with air

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When the pump’s revolutions per minute are reduced to below a critical threshold, there will
be retrograde flow from patient to arterial line.

Comparison of roller and centrifugal pumps

Advantages Disadvantages
Roller Predictable pump flow based on Can pump large quantities of air
pump speed
Can overpressurize lines, causing
Capable of pulsatile flow connector/tubing disruptions
CentrifugalCannot pump large quantities of Output not necessarily indicated by pump
air speed

Cannot overpressurize lines Not capable of pulsatile flow

Roller pump and centrifugal pumps

Oxygenators

 Provide a mechanism for CO2 removal and O2 transfer.

 Membrane oxygenators are used nearly universally for CPB.

 Current adult membrane oxygenators have a large surface area, approximately 1.5 to
4.5 m2, which is either fan folded, coiled, or configured as capillary tubes.

 Blood passes through the oxygenator as a thin film, minimizing the diffusion distance
for gases in the blood and thereby maximizing gas exchange

 Types of membrane oxygenators 1) Hollow-fiber membranes 2) Microporous sheets

3) Nonporous membrane oxygenators.

 Membrane oxygenators independently control the exchange of CO2 and O2.

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 SANCON 2016
 This is accomplished through the use of the ventilating circuit, which consists of an
air to oxygen blender and a flow meter.

 The degree of oxygenation is a function of the fraction of inspired oxygen (FIO2) of a

mixture of medical grade air and oxygen, with higher oxygen tensions occurring with
increased FIO2.

 The flow of gas is controlled by a flow meter and is termed the “sweep rate.”

 Similar to ventilation, higher flow rates reduce Paco2, and lower flow rates retain more
CO2.

 Because of the relatively high resistance to blood flow through most membrane
oxygenators, blood must be drawn from the venous reservoir and actively pumped
through the oxygenator

 The major disadvantage of microporous membrane oxygenators is the length of use;

the U.S. Food and Drug Administration has approved these for CPB procedures of 6
hours or less.

Heat exchangers

 Heat exchangers are an integral part of the oxygenator and are located proximal to
the membrane module of the oxygenator.

 Water is circulated through the heat exchanger from a separate cooler/heater with
the temperature adjusted to either cool or warm the blood.

 Perfusate temperature should not be less than 12°C to 15°C when cooling nor
greater than 37°C to 37.5°C when warming.

 Gradients of no more than 6°C are maintained throughout the entire CPB circuit,
cooler/heater water bath, and the patient.

Arterial Line Filter

 . These filters are placed in the arterial line as the last component through which
blood passes before it returns to the patient.
 With pore sizes of 20 to 40 μm, arterial line filters increase the patient’s safety by
removing particulate and gaseous microemboli.

Arterial line pressure monitor

 The most common form of CPB arterial pressure monitoring uses electronic
transducers, which are located close to the arterial line filter.

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 SANCON 2016
 These transducers can be used in conjunction with aneroid-type gauges that display
phasic pulsations with aortic cannulation, which indicates that the aortic cannula is
not overtly obstructed or wedged in an inappropriate location.

 This monitor is extremely important for detecting obstructions to flow in the arterial
line caused by the presence of an inadvertent clamp, kinking, or occlusion of the line.

Temperature sensors

 The temperature of the blood in the venous and systemic flow lines is continuously
monitored during CPB, and arterial blood temperature should never exceed 37.5°C.

 The temperature is measured by either thermocouple or thermistor and is displayed on

the CPB console.

 Cardioplegic solution temperature is measured at the heat exchanger and is adjusted

according to myocardial requirements and stage of the operation. Generally during
warm induction and during the final dose of cardioplegia, temperatures are near or at
37°C, while other cardioplegia doses are between 4°C and 10°C.

Anesthesia vaporizer

 An anesthesia vaporizer is usually placed in the ventilating gas line to the oxygenator.

 This vaporizer typically is the same as those found on anesthesia machines.

 Isoflurane is the agent usually used because of its low blood solubility and its
prominent vasodilating effect.

 The vaporizer should not be located directly above the oxygenator or other plastic
components of the CPB circuit because anesthetic liquid that spills onto these devices
while the vaporizer is being filled can cause damage or cracking.
Sequence of events to go on cardiopulmonary bypass
 Circuit selection and priming
 Anticoagulation
 Cannulation
 Initiation and maintenance of CPB
 Myocardial protection
 Weaning and termination from CPB

Circuit Selection and Priming

 The highest blood flow that may be necessary during the procedure is calculated.

 The highest blood flow is approximately 2.4 to 3.0 L/minute/m2 or 60 to 70

mL/kg/minute.

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 SANCON 2016
 The calculated flow is then compared with the rated flow for the components of the
ECC circuit. This flow rating represents the highest blood flow rate at which the
component can perform its function within the acceptable range of hydraulic forces
(pressure and shear stress) without causing an unacceptable amount of blood trauma.

 Priming is done by balanced electrolyte solution, blood or cryo poor plasma to de-air
the circuit completely.

 This prime volume is the main cause of the hemodiluion associated with CPB.

 Drugs that may be added to the prime solution

-To attenuate the dilutional effect of CPB -albumin, heparin, bicarbonate

-To discourage edema formation or encourage diuresis of the prime fluid - mannitol.
Anticoagulation

 Anticoagulation is done by Heparin before cannulation to achieve ACT of 480s.

 Heparin dosing may be based on the patient’s weight (300 to 400 units/kg) or
determined by a dose-response curve.

 Heparin dose-response curves are determined in vitro by measuring the ACT of the
patient’s blood at baseline (without heparin) and after a known concentration of
heparin (2.5 units/mL) is added.

 By graphing the ACT in seconds against the blood concentration of heparin, one can
extrapolate the blood concentration of heparin needed to achieve a target ACT
acceptable for CPB.

 Most patients need circulating blood heparin concentrations between 1.5 and 3.0
units/mL to achieve an ACT of 480 seconds.
Cannulation

 Arterial cannula is placed before venous cannulation to supplement fluids if required.

The arterial cannula returns oxygenated blood from the pump to the aorta, It is placed
in ascending aorta about 3 to 4 cm above the aortic valve. The alternative sites are the
axillary or femoral artery.

 Potential complications are associated with aortic cannulation including embolization

of air or atheromatous debris, inadvertent cannulation of aortic arch vessels, aortic
dissection, and other vessel wall injury.

 Epiaortic ultrasound imaging can be used as a guide to selection of cross-clamping

and cannulation sites to prevent embolisation of atheromatous debris.

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 Cannula malposition can looked for by checking for unilateral blanching of the face,
gently palpating carotid artery pulses for new unilateral diminution, and by measuring
blood pressure in both arms to check for new asymmetries.

 Assessments of CBFs can be made more reliably with the use of near-infrared
spectroscopy cerebral oximetry.

 Aortic dissection can be detected by decreasing mean pressures, decreased venous

return, increasing line pressures, and bluish discolouration of aorta.

 Venous cannulation can be done by a single cannula inserted in the right atrium, with
openings to admit right atrial and inferior vena caval (IVC) blood, or by separate
cannulas inserted in the superior and inferior venae cavae. Femoral venous
cannulation is done for redo surgeries and minimal access surgeries. The femoral
cannula extends the entire length of the IVC and rests with its openings in the right
atrium.

 Superior vena caval obstruction is detected by venous engorgement of the head and
neck, conjunctival edema, and increased SVC pressure.

 IVC obstruction is far more insidious, presenting only as decreased filling pressures
and lowered venous return to the bypass circuit.

 Cardioplegia cannula is placed in the ascending aorta below the aortic arterial
cannula. Aortic cross clamp is applied between the aortic and cardioplegia cannula.

 Vent cannula is placed to prevent LV distension and hence myocardial ischemia. It

can be placed in the pulmonary artery, pulmonary veins, left atrium, left ventricle and
the aortic root.

Initiation and Maintenance of Cardiopulmonary Bypass

 Before initiating CPB, the anesthesiologist should maintain adequacy of the depth of
anesthesia and muscle relaxation to prevent patient movement that could result in
dislodgment of bypass circuit cannulae and prevent shivering due to hypothermia that
is induced.

 CPB may be initiated by removing the clamps on the venous line between the venous
cannula and the reservoir.

 The patient’s blood then passively drains into the ECC.

 The arterial pump on the CPB machine begins to infuse the mixture of prime solution
and autologous blood into the patient through the arterial cannula.

 Evaluating the performance of the venous and arterial cannulas is very important
during the initial seconds of CPB.

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 The pressure in the arterial line of the ECC should be maintained at less than 300 mm
Hg to prevent excessive trauma to the formed elements of the blood.

 Venous cannula position is evaluated mainly by examining the patient’s

hemodynamics.

 CVP and PAP should decrease to 0 mm Hg

 Arterial blood pressure should reach a normal mean pressure of 50 to 90 mm Hg and

is nonpulsatile.

 Once full flow has been achieved, the function of the heart and lungs will have been
completely transferred to the CPB machine; the anesthesiologist then can turn off the
ventilator, and hypothermia of the patient can be initiated.

 If full flows are not achieved position of venous cannulae has to be checked.

 The initiation of CPB is often associated with a period of hypotension, which can be
managed with the administration of an α-agonist (e.g., phenylephrine) into the venous
reservoir of the ECC circuit

 Acutely reduced cerebral oximetry values on CPB initiation may provide the first
indication of poor SVC drainage or selective perfusion of a single aortic head vessel.
Recheck cannula position.

 While CPB is maintained, the adequacy of perfusion is continuously evaluated by

monitoring hemodynamic variables.

 Blood flow from the arterial pump can be manipulated across a range of 1.6 to 3.0
L/minute/m2 to deliver an arterial blood pressure of 50 to 90 mm Hg and SvO2
greater than 65%.

 Any hypotension or hypertension that occurs despite adequate flow and SvO2 can be
treated by adjusting the patient’s SVR with vasoconstrictors or vasodilators

 Arterial blood gas samples should be taken at least every 30 minutes

-To assess the performance of the oxygenator and
-To look for development of acidosis
-To monitor proper anticoagulation status.

 Urine output is also monitored during CPB as an indicator of perfusion flow and
pressure.

Myocardial protection

 The most common method of myocardial protection used is that of intermittent

hyperkalemic cold cardioplegia and moderate systemic hypothermia.

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 The beneits of hypothermia are a reduction in metabolic rate and oxygen
consumption, preservation of high-energy phosphate substrates, and a reduction in
excitatory neurotransmitter release.

 For each degree Centigrade reduction in temperature, there is an 8% reduction in

metabolic rate, so that at 28°C there is an approximate reduction in metabolic rate of
50%.

 Moderate systemic hypothermia can be achieved with either passive or active cooling.

 Most patients undergoing cardiac surgery are actively cooled and then rewarmed
using a heat exchanger.

 The fundamental concept of cold cardioplegia is that a cold solution (10 to 15°C) of
either blood or crystalloid with a supranormal concentration of potassium
(>20mmol/L) is injected into the coronary arteries or veins to induce diastolic
electrical arrest.

 Advantages of blood cardioplegia are its potential oxygen carrying capacity, inherent
buffering ability, scavenging of free radicals, delivery of nutrients.

 Optimal composition of cardioplegia is subject of research. It should be hyperosmolar

(limit edema), alkalotic and have low calcium.

 Additives used are aspartate and glutamate, insulin and glucose, adenosine,
magnesiem, L-arginine, N-acetylcysteine, nicorandil.

 The temperature at which cardioplegia is administered can be divided into cold (5-
10C), tepid (27-30C) and warm (37-38C). Low temp help in ischemic protection.
Warm plegia has to be a continuous administration. When given only at the end of
procedure it is called hot shot.

 Cardioplegia may be employed via an anterograde, a retrograde, or a combination of

the two routes.

 Anterograde cardioplegia solution is injected via the aortic root following aortic
cross-clamp and into the native coronaries.

 Retrograde cardioplegia is employed for myocardial protection by the placement of a

catheter inside the coronary sinus.

 Depending on the time required for surgical repair, multiple injections of cardioplegia
may be necessary to wash out metabolic by-products, add new high-energy and
oxygen-carrying substrates, and maintain hypothermic diastolic arrest.

 LV distention and lack of rapid electrical arrest may be evidence of poor myocardial
protection and the possibility of difficulty in separation from CPB.

 TEE is particularly helpful in diagnosing ventricular distention and its relief by

venting or manual decompression of the LV.
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Weaning and Termination of Cardiopulmonary Bypass

C V P
Cold Ventilation Predictors
Conduction Vaporizer Protamine
Calcium Volume expanders Pressure
Cardiac output Visualization Pressors
Cells Pacer
Coagulation Potassium

The major objectives in preparing for termination of CPB can be remembered with the aid of
the mnemonic CVP

 Before weaning and termination, the patient should be rewarmed and the heart de-
aired.

 Regular cardiac electrical activity should be confirmed and supported with a

pacemaker if necessary.

 Ventilation of the lungs must be resumed and laboratory values confirmed and
corrected if needed.

 By slowly reducing venous drainage to the ECC and transfusing volume from the
reservoir to the patient, normal filling volume can be returned to the heart.

 As the CO is returned to normal, flow from the arterial pump of the heart and lung
machine is decreased and eventually terminated.

 Immediately after the termination of CPB, the patient is often hemodynamically

supported by volume replacement with the blood remaining in the ECC, frequently
supplemented with vasopressors or inotropic agents

 When the patient is hemodynamically stable, protamine can be administered to

reverse the anticoagulatory effect of heparin.

 All cannulas should be removed before the action of heparin is fully reversed, and the
blood remaining in the ECC should be salvaged by centrifugation or hemofiltration
for return to the patient by the anesthesiologist.

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 Protamine inactivates heparin by irreversibly binding with the strongly acidic heparin
molecule to form a stable salt with no anticoagulant effects.

 Usually 1 to 1.3 mg of protamine for every 100 units of heparin given.

 Protamine should be administered slowly over a period of 5 to 10 minutes to reduce

the risk of hypotension.

 After protamine administration, ACTs should return to baseline.

 An increased ACT may indicate residual heparin or may be the result of a coagulation
deficiency that necessitates additional laboratory tests, such as coagulation panel tests,
heparin assays, platelet function analysis, thromboelastography, or any combination
of these investigations.

Pre bypass checklist

On bypass checklist

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Preparation for separation from bypass checklist

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Annexure
2014 AHA /ACC GUIDELINES FOR VALVULAR HEART DISEASE FOR NON-
CARDIAC SURGERY
Class 1
It is recommended that patients with clinically suspected moderate or greater degrees of
valvular stenosis or regurgitation undergo preoperative echocardiography if there has been
either
1) No prior echocardiography within 1 year or
2) A significant change in clinical status or physical examination since last evaluation.
(Level of Evidence: C)
2. For adults who meet standard indications for valvular intervention (replacement and repair)
on the basis of symptoms and severity of stenosis or regurgitation, valvular intervention
before elective noncardiac surgery is effective in reducing perioperative risk.
Class IIb

1. Elevated-risk elective noncardiac surgery using appropriate intraoperative and

postoperative hemodynamic monitoring may be reasonable in asymptomatic patients with
severe mitral stenosis if valve morphology is not favorable for percutaneous mitral balloon
commissurotomy. (Level of Evidence: C)

References:

1. R. Algappan, Manual of practical medicine 3rd edition

2. 2015 ESC Guidelines for the management of infective endocarditis

3. Miller’s Anesthesia, 8th edition

4.2014 AHA/ACC guidelines for non cardiac surgery

5.2014 AHA/ACC Valvular Heart Disease Guideline

6. Kaplan Cardiac anaesthesia 6th edition

7. Mitral Valve Disease: Stenosis and Regurgitation Cleveland clinic 2014

8. Contemporary Reviews in Cardiovascular Medicine. Modern Management of Mitral

StenosisCirculation.2005; 112: 432-437
9. Indian J Anaesth. 2010 Sep-Oct; 54(5): 439–444.

10. Clinical examination in cardiology. B.N. Vijay Raghawa Rao

11. Clinical anesthesia. 7th edn. Paul. G. Barash

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12. Pathological basis of diseases. 8 th edn. Robbins and Cotran

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