Mitral stenosis and Anesthesia

Case Discussion

Anaesthetic Management of a case of mitral stenosis

G 2P 1L 1 A 0 with 36 weeks gestation with mitral stenosis for

elective caesarean section

Speaker: Dr Bhagirath.S.N

Panelists: Dr Akkamahadevi.P Dr Srinivas.H.T Dr Anil Kumar.M.R

CasePatient details

Name: Mrs. Savitha

Age: 26 years

Sex: female

I.P.No.: 236455

Chief Complaints

G2P1L1A0 with 36 weeks gestation with

Palpitations since 6 weeks

Breathlessness since 4 weeks

Fatigue since 2 weeks

Case………………contd. History of Presenting Illness

Palpitation Breathlessness Fatigue

Intermittent

Associated with exertion

Relieved on rest

6 weeks duration

Gradual in onset

Progressive in nature (NYHA II)

Aggravated on lying down

Relieved on sitting up

4 weeks duration

Feeling of weakness

2 weeks duration

There was no history of haemoptysis or recurrent respiratory infections.

Case………………contd. Past History

No history of similar complaints in previous pregnancy.

History of Rheumatic Heart Disease since 12 years of age. Took treatment in the form of Penicillin injections every 21 days for 8 years till age 20 and then discontinued.

No history of cyanotic spells.

No history of hypertension, Diabetes Mellitus, Tuberculosis, Bronchial Asthma or Epilepsy.

Case………………contd.

No history of similar complaints in the family was noted.

Personal History

Diet: Vegetarian

Appetite: reduced.

Bowel & Bladder: Normal.

Sleep: disturbed.

Habits: None

Family History


A young pregnant female patient, moderately built and nourished

No pallor, icterus, cyanosis, oedema, clubbing

Pulse rate – 90/min; Weight – 58 Kgs

Blood pressure – 110/70 mm of Hg; Height – 155 cms

Respiratory rate – 16/min;

Respiratory System:

Normal Vesicular Breath Sounds heard, No added sounds.

Central Nervous System: Normal. No neurological deficits.

General Physical Examination


Per abdominal examination: Distended. Consistent with pregnancy. No

free fluid. No dilated veins.

Cardiovascular System:

Inspection: No deformity, Engorged superficial veins,

Scars or sinuses. No visible pulsations

Palpation: Apex beat felt in 5th intercostal space medial to left

midclavicular line, absence of left parasternal heave

Auscultation:

S1 S2 Heard. Opening Snap heard near the apex. (after S2)

Low pitched mid-diastolic murmur at apex. (no radiation)


G2P1L1A0 with 36 weeks gestation with Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.

Impression


Hb: 12.0 gm%

Differential count: Neutrophils – 71

Lymphocytes – 24

Monocytes – 02

Eosinophils – 03

Total count – 9, 800

Platelets: 2.73 lakhs/ mm3

PT INR: 1.0

BT: 3’ 00”

CT: 4’ 00”

Investigations


RBS: 99 mg/dl

Urea: 30 mg/dl

Creatinine: 1.1 mg/dl

Na+: 135mEq/l

K+: 4.8mEq/l

Cl-: 104mEq/l

HIV 1 & 2: Not detected

HBsAg: Not detected

Investigations


ECG: Sinus rhythm. Within normal limits. Heart rate: 80/min. Right axis

deviation.

2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic function

No Regional Wall Motion abnormalities

Ejection fraction: 56 %

Mitral Valve Area – 2.0 cms2

Transvalvular Pressure – 8 mm of Hg.

Chest X – Ray: Cardiomegaly. Prominent bronchovascular markings.

Management plan Regional anaesthesia for elective caesarean section

Investigations

Discussion

Causes: -

Palpitations

Tachyarrhythmias, Atrial fibrillation, Atrial kick

Endocrine–Pheochromocytoma, Thyrotoxicosis, Hypogylcemia

High Output states – Anemia, Pyrexia, Aortic Regurgitation, Patent Ductus Arteriosus.

Drugs – Atropine, Adrenaline, Aminophylline, Thyroxine, Caffeine, Tannin, Alcohol

Psychogenic – Prolonged anxiety

Idiopathic

Atrial kick - Palpitations

Discussion

Cardiac causes


Respiratory causes Hematological

Left heart failure

Congenital heart disease

Acquired valvular disease

Bronchial Asthma Severe Anaemia

Acquired valvular disease - Dyspnea

Coronary heart disease

Breathlessness

hypertensive heart disease

Cardiomyopathy

Chronic obstructive lung disease

Chronic restrictive lung disease

Pneumonia

Pulmonary neoplasm/ embolism

Laryngeal/ Tracheal obstruction

Discussion

Past History


Family History Personal History

Rheumatic Heart Disease (RHD)

RHD – Most common cause 40%

More common in females, typically detected in childhood.

Family history of Rheumatic Heart Disease, Congenital Valvular defects may be relevant

Disturbed sleep in Paroxysmal Nocturnal Dyspnoea

Acquired valvular disease - Dyspnea

Recurrent respiratory tract infection indicates pulmonary congestion

RHD,

Female patient,

Childhood history,

disturbed sleep

Discussion

Oedema


Hepatomegaly Mitral Facies

Severe Mitral stenosis ultimately leads to right heart failure.

Seen in right ventricular failure and pulmonary hypertension.

Low Cardiac Output in Mitral Stenosis causes peripheral vasoconstriction producing pinkish purple patches on cheeks. Mitral Flush due to vasodilatation (vascular stasis) is seen

Seen in fair skinned individuals

Acquired valvular disease - DyspneaRHD,

Female patient,

Childhood history,

disturbed sleep

General Physical Examination

Absent here Absent hereEdema & Hepatomegaly absent – mild disease

Discussion

Inspection


No deformity of precordium. – Precordial bulge indicates early onset and longer duration of cardiac disease.


Female patient,

Childhood history,

disturbed sleep

Cardiovascular Examination

Scar marks reveal previous surgeries

Engorged Neck Veins indicate high right heart pressures

Edema & Hepatomegaly absent – mild disease

Discussion

Palpation


Tapping character of the apex beat (palpable S1) is typical.


Female patient,

Childhood history,

disturbed sleep


Palpable diastolic thrill in mitral area best felt in left lateral position in full expiration.

Parasternal heave. (absent here)

If one finds engorged superficial veins look for direction of flow.

Absent Parasternal heave – mild disease


Discussion

Auscultation


S1 is sharp, short, accentuated


Female patient,

Childhood history,

disturbed sleep


Opening Snap after S2

Low pitched mid-diastolic rumbling murmur with presystolic accentuation of Grade IV intensity in mitral area without any radiation

Murmur best heard at cardiac apex with bell of stethoscope in left lateral position at height of expiration Absent

Parasternal heave – mild disease


Absence of click, split, rub or murmur over other areasOpening snap +murmur at apex

Substantiation Atrial kick - Palpitations


Female patient,

Childhood history,

disturbed sleep

Absent Parasternal heave – mild disease


Opening snap +murmur at apex

Childhood history

Female Patient

Rheumatic Heart Disease

Edema & hepatomegaly

absent

Palpitations Dyspnea

Absent parasternal heave – mild disease

Opening Snap + low pitched mid diastolic

murmur

2D – Echo – Mitral Valve 2.0 cms2,, Transvalvular pressure 8 mm of Hg

Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.

Mitral stenosis at a glance

Anatomy

Anatomy

Normal Orifice: 4 – 6 Cms2

4-6 cms2

< 2.5 cms2

1.5- 2.5 cms2

1.0 – 1.5 cms2

< 1.0 cms2

Mild MS – 1.5 – 2.5 Cms2

(Dyspnea on severe exertion)

Moderate MS – 1.0 – 1.5 Cms2

(PND ± pulmonary oedema)

Severe/ Critical- < 1.0 Cms2

(Orthopnea – Class IV)

Symptoms start < 2.5 Cms2

Anatomy

Mitral Valve area is calculated using Gorlin’s Equation:

Area = Cardiac Output/ (DFP or SEP) (HR) 44.3 C √ΔP

DFP = Diastolic Filling Pressure

C = Empirical Constant

SEP = Systolic Ejection Period

ΔP = Pressure Gradient

HR = Heart Rate

Pathophysiology

Decreased LV filling

Increased left atrial pressure and volume

Pulmonary vein pressure

Transudation of fluid into pulmonary interstitial space

Pulmonary compliance

Work of breathing

Progressive Dyspnea

Adaptation Atrial Kick

Adaptation

Lymphatic drainage and thickening of basement membrane

Pulmonary hypertension

Palpitations

Breathlessness Haemoptysis

Pathophysiology

Almost all chambers are shown here , except…

Left Ventricle

So, are we to assume that Left Ventricle

remains unaffected..?

Pathophysiology

The answer is NO. Left Ventricle is affected

Decreased filling ultimately manifests as

1. muscle atrophy

2. Inflammatory myocardial fibrosis

3. Scarring of sub valvular apparatus

4. Abnormal pattern of left ventricle contraction

5. Decreased left ventricular compliance with diastolic dysfunction

6. Right to left shift due to pulmonary hypertension

Aetiology

1. Rheumatic Heart Disease2. Congenital – Parachute Mitral Valve3. Hunter’s Syndrome4. Hurler’s Syndrome5. Drugs – Methysergide6. Carcinoid syndrome7. Amyloidosis8. Mitral annular Calcification9. Rheumatoid Arthritis10. Systemic Lupus Erythematosis11. Infective endocarditis with large vegetations. 12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral

Stenosis (MS) rheumatic origin

Pathology

1. Diffuse thickening of mitral leaflets and subvalvular apparatus.

2. Commissural fusion

3. Calcification of annulus and leaflets

4. Contracture of Chordae and papillary heads

5. Usually develops over 2-3 decades.

Pathological types of Mitral Stenosis

1. Button Hole

2. Fish Mouth

3. Funnel Type

Common symptoms

1. Dyspnoea

2. Orthopnea

3. Paroxysmal Nocturnal Dyspnea

4. Palpitation

5. Fatiguability

6. Haemoptysis

7. Recurrent Bronchitis

8. Cough

9. Chest pain

10. Right hypochondrial Pain (hepatomegaly)

Conditions simulating mitral stenosis

1. Left Atrial Myxoma

2. Cortriatriatum

3. Ball valve thrombus of left atrium

4. Diastolic flow murmurs across normal mitral valve as in VSD,

PDA, severe MR

5. Carey-Coomb’s murmur of mitral valvulitis

6. Tricuspid stenosis

7. Austin-Flint murmur

Complications

1. Acute left heart failure and acute pulmonary edema

2. Pulmonary hypertension

3. Right Ventricular failure

4. Atrial Fibrillation

5. Atrial Flutter

6. Ventricular or atrial premature beats

7. Embolic manifestations

8. Haemoptysis9. Infective Endocarditis10. Recurrent Broncho-pulmonary infections11. Complications arising from enlarged left atrium: Hoarseness of voice – left recurrent laryngeal nerve due to enlarged left atrium (Ortner’s Syndrome) Dysphagia – Oesophageal compression12. Jaundice, Cardiac cirrhosis.

DiagnosisOne needs to assess anatomy of Mitral Valve Leaflet in terms of

1. Thickening

2. Calcification

3. Mobility

4. Extent of involvement and subvalvular apparatus

One also needs to assess extent of stenosis

5. Mitral Valve area

6. Transvalvular pressure gradient Also to be assessed are

7. Cardiac chamber dimension 2. Pulmonary hypertension

3. Ventricular function 4. Associated valvular disease

5. Examination of Left Atrial Thrombus

Diagnosis

Assess extent of calcification

1. Disappearance of Opening snap especially if calcification is more.

Assessment of X-Ray (P-A View)

2. Left Atrial Enlargement – Mitralisation of heart

3. Straightening of Left Heart Border

4. Elevation of Left mainstem Bronchus

5. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary

Vascular Congestion.

6. Kerley’s B lines

Assessment of X-Ray (RAO view)

1. Oesophagus is pushed or curved backward by enlarged left atrium.

DiagnosisAssessment of ECG

1. Broad notched “P” Waves signifying atrial enlargement.

2. Atrial Fibrillation (f- waves replacing p-waves)

3. Right Ventricular Enlargement

2D – Echocardiography Doppler study

4. Chamber Enlargement 1. To know the speed and direction of blood

flow.

5. Valve pathology

6. Valve movement

7. Mitral Orifice

Blood Examination

1. TC and DC 2. ESR

3. ASO Titre

Treatment1. Mild Mitral stenosis – Diuretics

Restriction of physical activity

Salt-restricted diet

2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet)

β- Blockers

Calcium Channel Blockers

Control of heart rate is paramount, because tachycardia impairs left ventricular

filling and further increases left atrial pressure.

3. Anticoagulation – Warfarin to normalise INR

Treatment

4. Surgery if Pulmonary hypertension develops

Percutaneous balloon valvotomy

Surgical commisurotomy

Valve reconstruction

5. Valve replacement

Starr-Edwards ball valve

Bjork-Shiley disc valve

Porcine bio-prosthesis

6. Prophylaxis against recurrence of rheumatic fever

Inj. Benzathine Penicillin 1.2 million units.

Anaesthetic Management

Hemodynamic Parameters

Change in normal pregnancy

Change during Labour & delivery

Change during postpartum

Blood volume Increased by 40 % - 50% Increased Decreased (auto diuresis)

Heart rate Increased by 10 – 15 beats/ min

Increased Decreased

Cardiac Output Increased by 30% - 50 % Additional 50 % Decreased

Blood Pressure Decreased by 10 mm of Hg

Increased Decreased

Stroke Volume Increased in first and second trimester

Increased (300 – 500 ml/contraction)

Decreased

Systemic Vascular Resistance

Decreased Increased Decreased

Maternal mortality associated with heart disease in pregnancyGroup 1: Mortality < 1%

Atrial septal defectVentricular septal defect; PDAPulmonary/tricuspid diseaseTetralogy of Fallot, corrected; Bioprosthetic valveMitral stenosis, NYHA class I and II

Group 2: Mortality 5–15%2A Mitral stenosis NYHA class III–IV; Aortic stenosis

Coarctation of aorta, without valvular involvementUncorrected Tetralogy of FallotPrevious myocardial infarctionMarfan syndrome with normal aorta

2B Mitral stenosis with atrial fibrillationArtificial valve

Group 3: Mortality 25–50%Primary pulmonary hypertension or Eisenmenger syndromeCoarctation of aorta, with valvular involvement

Marfan syndrome with aortic involvement

Mortality: 0 point-5%,1 point-27%,>1 point-75%

CARPREG Score

Anaesthetic ManagementPrinciple involved:

Cardiac Output

Decrease in cardiac output

Hypotension

Tachycardia

Reduced ventricular filling

Vicious cycle

Increased ventricular filling

Trendelenburg's position, Autotransfusion due to uterine contraction

Precipitation of CHF 1

2

3

Anaesthetic ManagementPrinciple involved:

1. Prevent decrease in cardiac output, as hypotension because of this causes

reflex tachycardia, which in turn reduces ventricular filling further

compromising cardiac output.

2. Avoid hypotension for the same reason listed above. If hypotension ensues,

treat with Ephedrine or Phenylephrine.

3. Avoid precipitating Congestive Heart Failure due to factors such as Trendelenburg’s position Autotransfusion due to uterine contraction leading to increased central blood volume. 4. Avoid precipitation of Right Ventricular Failure Hypercarbia Hypoxemia Lung Hyperinflation Increase in lung waterIf Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.

Anaesthetic ManagementPreoperative Medication

1. Decrease anxiety (decreases tachycardia)

2. Drugs used to control heart rate to be continued till day of surgery

3. Hypokalemia if present secondary to diuretic therapy to be addressed

4. If intended surgery is a minor surgery, continue anticoagulant therapy

5. If intended surgery is a major surgery, discontinue anticoagulant therapy. Induction of Anaesthesia

6. Avoid Ketamine – Increases heart rate, blood pressure

7. Avoid Atracurium – Increased histamine release causes hypotension which

manifests as tachycardia.

Anaesthetic ManagementMaintenance of Anaesthesia

1. Drugs should have minimal effects on hemodynamic pattern

2. Balanced anaesthesia with N2O/ Narcotic/ Volatile anaesthetic

3. N2O causes insignificant pulmonary vasoconstriction. It is significant only if

pulmonary hypertension exists. So, one needs to treat pulmonary

hypertension preoperatively.

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

5. Avoid lighter planes of anaesthesia (To avoid tachycardia)

6. Fluid Management:

Avoid Hypervolemia - -> Worsens pulmonary edema

Avoid Hypovolemia - -> Sacrifices already decreased left ventricular filling,

which further decreases Cardiac output. Hypovolemia secondary to

blood loss and vasodilatory effects of anaesthesia ought to be avoided.

Anaesthetic ManagementMonitoring

1. Transesophageal Echocardiography

2. Intra-arterial pressure

3. Pulmonary artery pressure to be monitored

4. Left atrial pressure Principle:

5. Ensure adequacy of cardiac function

intravascular fluid volume

ventilation

oxygenation A word of caution regarding Pulmonary artery pressure monitoring: -When measured too frequently, the risk of pulmonary artery rupture is far too high.

Anaesthetic ManagementPost Operative

1. Assess postoperative risk of pulmonary oedema and right heart failure and

manage accordingly.

2. Avoid pain as pain begets hypoventilation which leads to respiratory acidosis,

hypoxemia which manifests as raised heart rate and pulmonary vascular

resistance.

3. After Major thoracic or abdominal surgery, the decreased pulmonary

compliance and increased work of breathing requires mechanical ventilation.


Category 1 - Immediate threat to life of woman or fetus(baby needs to be removed in 30 min. of making the decision to do LSCS

Category 2 - Maternal or fetal compromise, not immediately life threatening(some time can be spent for resuscitation)

Category 3 - Needing early delivery but no maternal or fetal compromise

Category 4- At a time to suit the woman and maternity team


Anesthetic techniques available are1. Regional anaesthesia (Sub Arachnoid Block, Epidural, Combined Spinal

Epidural)2. General Anaesthesia

Sub Arachnoid Block: subarachnoid causes rapid onset of extensive sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia.

Epidural Block: epidural anaesthesia might not be an ideal technique as it requires slow induction, delay in the onset of action which may not be possible in an emergency situation. Moreover large volume of local anesthetic is needed for adequate blockade.

Combined Spinal Epidural: Combined spinal and epidural will be the technique of choice.CSE offers rapid onset and improved analgesia It offers ability to use low dose spinal with room for post operative analgesia


Why our choice is right..?

1. Rapid onset of spinal block

2. Ability to modify / top-up / prolong anaesthesia with epidural component

3. Spread of spinal anaesthetic can be altered with injection of saline into the

epidural space (compression effect of dural sac)

4. Option for post-operative analgesia

5. Reduces need for conversion to general anaesthetic in event of spinal failure

6. Able to use lower dose spinal and modify if required, potentially reducing

spinal induced hypotension

7. Advantageous in cardiac conditions

8. Arguably advantageous in pre-eclampsia


Why our choice is right..?

9. Can produce a denser block than either technique in isolation

10. Airway pressures are not altered and avoids hyperventilation

11. Minimal autonomic blockade , hence no sudden decrease in Systemic

Vascular resistance

12. Better maintenance of uterine blood flow improving the fetal outcome

13. Auto transfused blood during the third stage of labor is well accommodated

14. Improved microvascular blood flow prevents DVT

15. Allows early ambulation and return of bowel movements


Procedure per se

Preparation:

1. All resuscitation equipments and drugs , anaesthesia machine, O2 delivery

system, Equipments for G.A. , Suction apparatus are kept ready

2. Patient is given aspiration prophylaxis in the form of 0.3ml SODIUM CITRATE

30ml orally, H2 receptor blocker and antiemetic given

3. Record baseline vitals

4. Secure two wide bore cannulae and infuse 60-75ml/hr of crystalloid

5. Administer infective endocarditis prophylaxis

6. Monitors- SpO2, ECG, NIBP, and urine output

7. Reassure the patient

8. Informed consent is obtained explaining the maternal and fetal risk

9. Adequate Compatible blood


Procedure per se

CSE is performed in lateral decubitus position under strict aseptic precautions

Epidural space is identified with 18 G Tuohy needle using LOR with saline. Spinal

needle is introduced through the Tuohy needle and subarachnoid block is

performed.20-30 μg of Fentanyl along with 2.5 -5mg of 0.5% Bupivacaine is given.

This is followed by insertion of epidural catheter through which 3 ml of 2%

Xylocaine with epinephrine is given.

Post operative analgesia is maintained as shown in the table below

Drug Initial Injection Continuous InfusionBupivacaine 10-15 mL of a 0.25%-0.125% solution 0.0625%-0.125% solution at 8-15 mL/hr

Ropivacaine 10-15 mL of a 0.1%-0.2% solution 0.5%-0.2% solution at 8-15 mL/hr

Fentanyl 50-100 µg in a 10-mL volume 1-4 µg/mL


1. If Hypotension occurs- vasopressors are used.

2. After the baby is delivered Oxytocin in minimal dose as slow infusion is given

3. Arrhythmias should be treated appropriately.

4. Blood loss should be assessed and replaced accordingly.

5. Immediate post partum period mandates meticulous care as mortality is very

high in these patients with Pulmonary artery hypertension.

6. Post operative pain management reduces Cardiovascular-stress response and

prevents Deep Vein Thrombosis.


Myths and Worries about Regional anaesthesia

1. Preloading is mandatory and hazardous--CVP guided fluid management

negates overloading and maintains adequate cardiac output

2. Regional Anaesthesia is associated with sudden fall in BP. Local anaesthetic

with Opioid combination intrathecally followed by epidural to titrate the

desired level of block does not produce rapid fall in BP.

3. Delay in performing the actual procedure: this doesnt happen with expert

hands

4. The complications of CSE-like total spinal, LA toxicity, epidural hematoma and

abscess are negligible with senior anesthesiologists


Controversies about CSE:

Risk of epidural catheter through the dural hole

Perceived increase in neurotrauma

Contraindications to Regional Anaesthesia

• Active heavy bleeding

• Uncorrected coagulopathy (e.g. HELLP syndrome (Hemolysis, Elevated

Liver Enzymes, Low Platelets) associated with pre-eclampsia)

• Thrombocytopenia

• Systemic sepsis

• Local sepsis at site of insertion

• Patient refusal


Guidelines for general anaesthesia

General anesthesia has the advantages of speed of induction, control of the airway, and superior hemodynamics.

Anaesthetic Goals:

1. Maintain the heart rate around 80-100 b/min .

2. Maintain Left Atrial Pressure high enough to take advantage of the increased

preload reserve.

3. Avoid pulmonary artery hypertension by treating hypercarbia, hypoxemia, and

acidemia.

4. Aggressively treat pulmonary artery hypertension with vasodilator therapy to

avoid RV failure. If RV failure does occur, inotropic support of the RV and

pulmonary vasodilation may be necessary. The presence of PAH is the major

factor that increase the mortality.



5. Avoid factors which depress the myocardium:(inhalation agents and drugs)

6. Maintain awareness of potential for LV rupture.

7. Aggressive treatment of arrhythmias if they occur

8. Avoid profound changes in SVR

9. Attenuate pressor response(intubation, extubation, light plane of anesthesia)

10. Adequate analgesia and adequate muscle relaxation guided by Neuro

muscular monitoring

11. Aspiration prophylaxis

12. Blood loss assessment and prompt replacement



Other advantages are

1. Rapidly established

2. Better hemodynamic stability

3. Prevention of aspiration as the airway is isolated

4. High FiO2 -which will reduce PVR

5. Ventilation controlled to avoid hypercarbia-which will increase PVR

6. FRC is increased by controlled ventilation

7. Ventilation of atelectatic areas –better V/Q

8. Sinus rhythm can be maintained. In case of SVT and Ventricular arrhythmias

promptly reverted by cardioversion



Other advantages are

9. Peak airway pressure can be kept <20 cms H2O

10. Elective post operative ventilation to tide over the CCF that may be possible

after parturition

11. Effective management of Pulmonary oedema - IPPV with PEEP, liberal use of

high dose morphine



The possible complications that can be anticipated

1. failed intubation

2. Aspiration( more common in unprepared case)

3. Hypoxia and hypocarbia -effect on fetus

4. Hypertensive crisis

5. Arrhythmia-hypoxia, hypercarbia, inhalational agents, Drugs

6. Use of poly pharmacy and anaphylaxis

7. Awareness

8. Uterine atony with inhalation agents



The possible complications that can be anticipated

9. Need for adequate post op. Analgesia

10. Neonatal depression

11. Delayed recovery

12. Anesthetic drug interaction with cerebrovascular drugs(Ca channel blockers

and Magnesium)

13. Increased incidence of PONV

14. Prolonged stay ICU

Outlines of Management

1. Pre-conceptual counseling- NYHA III and IV are advised corrective cardiac before pregnancy. It is advisable for certain cardiac diseases where pregnancy is to be avoided

They have to be registered, interviewed regarding functional difficulties, regular follow ups starting from early pregnancy. It is advisable to manage them in higher centers where multidisciplinary support is available(Multidisciplinary approach: management by a team of specialists apart from obstetricians that includes the cardiologist(failure prevention, arrhythmia management), CT surgeon(emergent cardiac surgery), neonatologist(preterm baby) anesthesiologist(pain relief-epidural, mechanical Ventilation if necessary)

2. Correct factors which will burden the cardiac lesion like anemia, obesity, Hypertension, arrhythmia

3. Prevention of Infection


4. Optimization of Heart rate with pharmacological agents

5. Pregnancy is a hypercoagulable state, which increases the risk of thromboembolic events, especially in the cardiac patient with a prosthetic heart valve, valvular heart disease, or heart failure. Anticoagulant therapy should be considered in these high-risk patients to prevent thromboembolism or thrombus formation.

6. IE prophylaxis -(as per the ACOG guidelines- some of the drugs recommended by ACC/AHA are not recommended for pregnant patients)

7. Monitors- other than the ASA standards recommendation- Advanced monitors like invasive arterial pressure, CVP -, PCWP and TEE are recommended. They should be continued in the post partum period upto 72 hrs at least


8. Planning the mode of delivery-vaginal delivery is better tolerated(less blood loss, less catecholamine), Pain relief during Labor - recommended, shortening the second stage- outlet forceps, episiotomy.

9. Large boluses of Oxytocics should be avoided as they cause profound hypotension. Ergometrine better avoided. PGF2 alpha and mesoprostol are used cautiously.

10. If planned for Cesarean section choice of anesthetic should be directed to keep the haemodynamic stable (as near normal Systemic vascular resistance, Preload, Afterload as possible)Adequate replacement of blood loss.

11. All patients with cardiac disease should be kept in High dependency unit and monitored after the delivery for a minimum period of 72hrs

12. Plan and Advise cardiac surgery in the second trimester if is warranted in the interest of the mother's well being

When to give Infective Endocarditis Prophylaxis..?

How to give Infective Endocarditis Prophylaxis..?

References

Miller’s Anaesthesia , 7th Edition, Vol 1

Clinical Anesthesia by Paul.G.Barash

Morgan’s Clinical Anaesthesiology

Kaplan’s Cardiac Anesthesia

References

Harrison’s Internal Medicine 17th Edn

A Practice of Anesthesiology

by Churchill Wylie

Stoelting’s Anesthesia & co-existing disease

CMDT 2010

References

Bedside Clinics in medicine - Kundu

A Manual of Practical

Medicine by Alagappan

Circulation Journal

References

Indian Journal of Anaesthesiology

Mitral stenosis and Anesthesia

Health & Medicine

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