How do I do it?

A 23 yr old primi gravida who was on regular check-up got admitted at 33 weeks of pregnancy with

the complaints of cough for 2 weeks duration. Physician opinion was sought since there was a

murmur on auscultation and her echo revealed MVP of AML, severe MR, adequate LV function, mild

PAH and mild pericardial effusion. Multiple small echogenic structure were attached to the body of

AML, (?? Vegetation). After 2 sets of blood culture she was put on antibiotics and discharged.

She got admitted 3 days later with decreased foetal movements and foetal bradycardia. She was

posted for an emergency section.

Investigations:

Hb 9.3 G%

Platelets : 1,75,000/cmm

TC : 9,100/c mm

ESR: 35/69

LFT: Total bilirubin 0.5

Direct 0.1

Indirect 0.4

Total Protein 6.8

Albumin 4.3

Globulin 2.5

SGPT 6

SGOT 11

ALK PO4 65

Chest X Ray CT 50%

ECG - Normal sinus rhythm.

Problems here are high lighted

Data not available:

NYHA status and Treatment details of previous admission, duration ,drugs (anticoagulants,

vasodilators, anti arrythmics), blood culture report, associated anamolies

The pregnancy is nether uncommon nor a disease. Even though a normal occurrence,

pregnancy does have a lot of physiological changes in all the systems more so in the

cardiorespiratory system. This is to cope with the high BMR and growing fetus.The early

appearence of cardiovascular changes implicates hormonal cause due to estrogen and progestrone.

As pregnancy advances there is increase in the metabolic demand and body mass imparting

significant demand on the cardiovascular system.All these are well tolerated in a healthy female and

child birth is uneventful. The table shows the changes that occur in the CVS in normal pregnancy

Hemodynamic

Parameter

Change During Normal

Pregnancy

Change During Labor

and Delivery Change During Postpartum

Blood volume ↑ 40%-50% ↑ ↓ (auto diuresis)

Heart rate ↑ 10-15 beats/min ↑ ↓

Cardiac output ↑ 30%-50% above baseline ↑ Additional 50% ↓

Blood pressure ↓ 10mmHg ↑ ↓

Stroke volume ↑ First and second

trimesters; ↓ third trimester

↑ (300-

500mL/contraction)

↓

Systemic

vascular

resistance

↓ ↑ ↓

In the presence of cardiac disease this balance is likely to tilt to the adverse side any time during

pregnancy depending upon the specific cardiac disease. As pregnancy advances asymptomatic

cardiac diseases become symptomatic and patients with mild symptoms tend to worsen. Early signs

of cardiac compromise may become apparent in the first trimester and peak at 20 to 24 weeks of

pregnancy when cardiac output reaches a maximum. From 24 weeks onward cardiac output is

maintained at high levels. Cardiac output only begins to decline in the post-partum period. The

Cardiac output returns to prepregnant levels in 4-6wks.

During labor, the sympathetic response to pain, as well as uterine contractions, around 300 and 500

ml of blood is injected into the general circulation with each contraction. Stroke volume rises by an

estimated additional of 50 percent. At the same time, systemic vascular resistance is increased,

exacerbating the additional stress placed on the cardiovascular system. At delivery a predicted blood

loss of between 400 and 800 ml does little to maintain stability in an already compromised

circulatory system

Maternal mortality is high due to critical cardiac events occurring during late pregnancy,

during delivery and immediate post partum. In addition fetal morbidity is also high due to

premature labor , Intra uterine growth retardation and heart disease in the new born .Certain

cardiac lesions warrant avoidance of pregnancy altogether( PPHT, Eisenmengers, Fallots, MVPS

with aortic root dilatation, HOCM) Cardiac diseases complicating pregnancy is the third most

common cause of maternal death. The following table shows the % risk of mortality in various

cardiac disease.

Maternal mortality associated with heart disease in pregnancy

Group 1: Mortality < 1%

Atrial septal defect

Ventricular septal defect

Patent ductus arteriosus

Pulmonary/tricuspid disease

Tetralogy of Fallot, corrected

Bioprosthetic valve

Mitral 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 involvement

Uncorrected Tetralogy of Fallot

Previous myocardial infarction

Marfan syndrome with normal aorta

2B Mitral stenosis with atrial fibrillation

Artificial valve

Group 3: Mortality 25–50%

Primary pulmonary hypertension or Eisenmenger

syndrome

Coarctation of aorta, with valvular involvement

Marfan syndrome with aortic involvement

The mortality is also dependent on the clinical status and the work efficiency of the patient

before pregnancy.The CARPREG( ‘CARdiac disease in PREGnancy’ ) risk score is described in Table

below. In women with congenital heart disease, the CARPREG score may also be associated with a

higher risk of late cardiovascular events post-pregnancy.

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

PERINATAL MANAGEMENT OF PREGNANT PATIENT WITH CARDIAC DISEASE

The general guidelines regardless of the specific cardiac disease are given below:

1. Pre-conceptional counseling- NYHA III and IV are advised corrective cardiac before before

pregnancy. It is advisable for certain cardiac diseases where pregnancy is to be avoided

2. 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)

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

arhythmia

4. Prevention of infection

3. Optimization of Heart rate with pharmacological agents

6. 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.

7. IE prophylaxis -(as per the ACOG guidelines- some of the drugs recommended by

ACC/AHA are not recommended for pregnant patients)

8. 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 atleast

9. 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.

10. Large boluses of Oxytocics should be avoided as they cause profound hypotension.

Ergometrine better avoided. PGF2 alpha and mesoprostol are used cautiously.

11. If planned for Cesarean section choice of anesthetic should be directed to keep the

haemodynamics stable (as near normal SVR, Preload, Afterload as possible)Adequate replacement of

blood loss.

12, All patients with cardiac disease should be kept in High dependency unit and monitored

after the delivery for a minimum period of 72hrs

13. Plan and Advise cardiac surgery in the second trimester if is warranted in the interest

of the mother's well being

Coming to our case _ MVPS is a common valvular disease seen among 2-4% of the general

population .affecting about 17% of young women of child bearing age group. Simple MVPS

pregnancy is well tolerated as the reduced SVR, High blood volume reduce the extent of valve

prolapse. 15% of MVPS cases develop Mitral insufficiency in due course.(esp. in FLAIL VALVE TYPE).

Clinical features: They are asymptomatic but can present with some autonomic features

like palpitation, chest pain, anxiety and fatigue which are usually ignored as functional.

On examination they will have midsystolic 'ejection click' with late systolic crescendo

murmur.If the patient has MR a holosystolic murmur will be heard.

Diagnosis: ECG-usually normal, nonspecific ST,T changes may be seen in Inferior leads. P-

morphology may be biphasic in LAE(in severe MR), Holter monitoring should be performed in

patients with known previous paroxysmal or persistent documented arrhythmia

ECHO: Diagnostic , prolapse of > 2mm beyond mitral annulus denotes MVPS.

M-mode shows sudden posterior movement of posterior mitral leaflet into LA during mid systole

resulting in 'question mark'sign as well as Hammocking of the posterior leaflet into the left atrium.

2D echocardiography is "gold standard" for imaging valve morphology and motion, Leaflet thickness

and mobility, valve calcification, and the appearance of subvalvular and supravalvular structures.

It helps in assessing left ventricular (LV) size and function and for the detection of pericardial

effusion. It can also show the appearance and mobility of the thrombus. Vegetations appear as

mobile linear echo densities attached to valve leaflets.

3D with doppler will show mobility of thrombus.

The severity of the MR is graded as follows

Severe Moderate Mild

Area of MR jet(cms2) >6 3.0- 6.0 <3

Regurgitant fraction(%) >55 30-50 20-30

Pathophysiology of MVPS:

MVPS is a condition where there is a prolapse of the mitral leaflet into the left atrium

during systole due to either elongation or redundancy of the chordae tendinae. This causes the

characteristic mid systolic non ejection click followed by a short crescendo mid-late systolic

murmur.MVPS may be primary or secondary along with conditions like ASD,acute rheumatic

fever,acute MI, Marphans syn, Von Willebrand disease, Graves disease, Kyphoscoliosis,

etc.(connective tissue disorders)

MVPS when it coexists with cardiovascular disease such as HOCM, Marfan’s syndrome,

atrial septal defect,and coronary artery disease the morbidity is high. A benign course is expected in

85% of patients. 15% of patients with MVP progressively develop MR and Pulmonary hypertension

lead to congestive failure

Mitral regurgitation in MVPS can be acute- Acute mitral regurgitation may follow rheumatic

fever,bacterial endocarditis, blunt chest trauma, myocardial ischemia, may also occur in patients

with Marfan’s syndrome.Acute mitral regurgitation imposes a large volume overload on the left

atrium which is noncompliant . Cardiac output decreases, and compensatory peripheral

vasoconstriction aggravates the lesion.Pulmonary congestion ensues, resulting in pulmonary edema.

If the patient survives the acute episode, pulmonary arterial pressures continue to rise, and right

heart failure may develop. In some cases emergency surgery may be necessary.

A rare cause of acute valvular regurgitation during pregnancy is antiphospholipid syndrome.

Marfans syndrome with MVPS needs a special mention .Even though lot of other syndromes have

MVPS as part of their presentation, Marfans carry an additional risk as the aortic root is also

involved. Aortic root diameter should be monitored throughout pregnancy with serial

echocardiograms and if aortic root dilatation occurs, prophylactic β-blockade is advised.

Hypertension should be treated aggressively.Maternal mortality has been reported to be as high as

50% in pregnant patients with aortic root diameter greater than 4.5 cm, aortic regurgitation, left

ventricular dilation, hypertension, or coarctation.

Chronic mitral regurgitation causes less hemodynamic stress on the left ventricle. The left

atrium accommodates the regurgitant blood flow by gradual dilation and increased compliance. Left

atrial dilation predisposes to arrhythmias,peculiarly paroxysmal SVTs are common rather than atrial

fibrillation (which is often seen with Primary MR or MS with MR). Pulmonary hypertension also is

less common in patients with chronic mitral regurgitation than in those with mitral stenosis.

Typically, there is only a modest increase in left atrial pressure. Severe, longstanding mitral

regurgitation leads to increased left atrial pressure and pulmonary congestion.Left ventricle is

chronically volume over loaded.

EF will greatly overestimate systolic function in MR because a portion of the SV is ejected

backwards as mitral regurgitant volume. EF may remain in the normal range despite severe systolic

dysfunction.

Certain conditions which cause an increase in MVProlapse and increase in regurgitation

fraction are

1. Decrease in LVEDV and LVEDP

2. Tachycardia

3. Increase in Pulmonary vascular resistance

Co presence of conditions like Pregnancy induced Hypertension increases the chance of

complications like CCF.

Myocardial oxygen consumption is altered in MR.There is an increase in oxygen

consumption due to the large mass of myocardium . A greater portion of the total workload is

devoted to the generation of volume ejection, which is an energy efficient process.So myocardial

ischemia can occur during extreme tachycardia(dec. Coronary filling) or myocardial depressant

drugs.

MVPS cases can present with complications like Infective Endocarditis, Arrhythmia and CCF.

Infective endocarditis

Infective endocarditis during pregnancy is rare, with an estimated overall incidence of 0.006% (1 per 100 000 pregnancies) and an incidence of 0.5% in patients with known valvular or congenital heart disease.

Aetio pathogenesis

Risk for infective endocarditis is increased by 5-8 times in MVPS due to leaflet redundancy with myxomatous degeneration making them more prone for mechanical damage. mitral regurgitation further increases the risk Generally - the pathognomonic sign is the presence of vegetations which are a mass of platelets,fibrin,micro colonies of micro-organisms and scant inflammatory cells on the mural endocardium where there is denudation of the endothelium due to jets of blood or foreign bodies(catheters, prosthetic valves, ICD)

Types

1. Acute endocarditis- present as fulminant infection, high fever, major embolic events due to hematological spread of seedlings ending mostly fatally.

2. Sub acute endocarditis- It takes an indolent course, structural damage occurring only late, precipitated by embolic events or rupture of mycotic aneurysm

Pathophysiology: Route of infection determines the type of organism causing IE.

Organisms :oral , Skin, URT-route(dental)- viridans streptococci(CoN) staphylococci, HACEK organisms(hemophilus, actinobacillus, cardiobacterium, eikanella, kingella)

Bowel- Strep.bovis

GUT-enterococci

Catheter related: Staph. Aureus(MRSA resistant)

Other causes- HIV, drug abuse(multi organism, Fungal)

NBTE- nonbacterial platelet fibrin thrombus-These are primarily sterile fibro thrombin mass which subsequently serve as nidus for bacterial colonization is commonly seen in MR, MVPS, AR and VSD

NTBE is also seen in hypercoagulable conditions(marantic endocarditis)-malignancy, anti phospholipid antibody syndrome,pregnancy with PIH

Fate of vegetations- The central core has dormant microbes which is beyond the reach of antibiotics makes them remain viable and exacerbate when the host defence mechanisms come down. The superficial proliferative organisms are shed into the blood stream continuously resulting in embolic episodes, bactremia,.

Clinical features: Fever, chills, myalgias, new heart murmurs, splenomegaly, splinter hemorrhages (Osler node,Janeway lesion, Roth spots)

Cardiac: CCF, pericarditis, heart blocks, regurgitant lesions, intracardiac fistulae, embolic transmural infarcts

Investigations: anemia, High ESR, leukocytosis, elevated C-RP.elevated circulating immune complex titer, blood culture, TTE or TEE- useful in suspected IE

Diagnosis-DUKE'S CRITERIA

Major criteria positive blood culture for IE evidence of endocardial involvement Minor criteria predisposition (heart condition or IV drug use) fever of 100.40F or higher vascular or immunologic phenomena microbiologic or echocardiographic evidence not meeting major criteria

Complications

1.Cardiac complications: Ring abscesses with possibility of perforation and fistula formation Suppurative pericarditis. Suppurative pericarditis is a rare life threatening disease, difficult to treat. Heart failure due to acute valve regurgitation is the most common complication, requiring urgent surgery when medical treatment cannot stabilize the patient.

2. Embolic complications- more common with AML vegetations.Vegetations may break loose, and give rise to emboli in brain, spleen, kidneys, and heart (intramural) and lungs. Cerebral and peripheral embolizations are the frequent complications.

3. Renal Complications can arise following Infective endocarditis: 1. Embolic infarcts 2. Focal and diffuse glomerulonephritis 3. Multiple abscesses.

Treatment- Parenteral followed by oral antibiotic after Blood culture sensitivity is recommended for a minimum of two weeks.

Strepto. - 2wk. Penicillin or ceftrixone/gentamycin

Entercocci-ampi/sulbactum.or vancomycin

Staphyococci-vancomycin.aminoglycosides/cefotaxime-6-8 wks for MRSA strains

Fungal- amphoteresin B/flucytosine

Monitor- nephrotoxicity and blood levels when aminoglycosides are used long term

End point- blood culture negative, CRP and ESR return to normal several weeks later.In ECHO vegetations become smaller but does not disappear.

Surgical treatment is required for repair of heart valves and removal of vegetations if medical measures fail or embolic episodes occur.

In our patient who was recently treated for Endocarditis with vegetations persisting in the

AML and a mild pericardial effusion (rheumatic fever or CCF) falls into high risk cardiac condition

who has the highest priority for antibiotic prophylaxis as per the ACC/AHA 2008 guidelines given

below

Antibiotics that can be given during all trimesters of pregnancy are penicillin, ampicillin, amoxicillin,

erythromycin, mezlocillin, and cephalosporins. All of them are included in group B of the Food and

Drug Administration (FDA) classification. Vancomycin, imipenem, rifampicin, and teicoplanin are all

group C drugs. There is a definite risk to the fetus in all trimesters of pregnancy with group D drugs

(aminoglycosides, quinolones, and tetracyclines) and they should therefore only be used for vital

indications. The drugs to be used for IE prophylaxis in Pregnant cardiac patients according to ACOG

2008 guidelines is given

Arrythmias-

Patients with MVPS are more prone for arrhythmia presenting clinically as palpitation and chest pain

. On many occasions this is thought of as functional and ignored. Patients who progress to MR are

prone to arrhythmias like SVT, PAT , Atrial flutter and AF. WPW syndrome, Ventricular tachy

arrhythmias leading to sudden death can also occur in MVPS patients.Episodes of sustained

tachycardia, particularly atrial flutter, are not well tolerated and can cause fetal hypo perfusion in

heart disease. Direct current conversion should be performed to restore sinus rhythm. Digoxin can

be used to control ventricular rate, but has no prophylactic antiarrhythmic effect. β-Blocking agents,

class I antiarrhythmic drugs, and sotalol should be used with caution if the LV or RV function is

impaired . Amiodarone should be used only when other therapy has failed and then at the lowest

effective dose .

SVT s: AV nodal re-entry tachycardia or AV re-entry tachycardia involving an accessory

pathway can be terminated by vagal maneuver or, if that fails, by i.v. adenosine. I.V. s the first drug

of choice if vagal maneuverer fail to terminate an episode of paroxysmal SVT. I.V. Metoprolol. is

recommended if adenosine fails to terminate a tachycardia.

Adenosine 6mg IV bolus repeated with 12 mg iv bolus Can be repeated once.Esmolol 1mg/kg

followed by 50-200g/kg min.followed by 50-200g/kg/hr.

Rapid over drive pacing can be tried after mild sedation . In hemodynamically unstable

patients synchronize cardioversion 50-100J is done.

Atrial flutter: cardio version /rapid atrial pacing, Esmolol-1mg/kg IV bolus,Dilzem

Atrial fibrillation-Digoxin, Verapamil, Beta blocker, Amiodarone, Cardioversion

Anticoagulants are given to patients who have frequent episodes of arrhythmias and patients with

huge LA, Endocarditis with vegetations and PIH.

Warfarin: The use of oral anticoagulants during pregnancy is relatively contraindicated. Warfarin

therapy in the first trimester is associated with an increased incidence of fetal death and birth

defects (“warfarin embryopathy”). Warfarin use later in pregnancy is associated with prematurity

and low birthweight, as well as neonatal cerebral hemorrhage. Despite these risks, warfarin is

sometimes administered in combination with low dose aspirin (80–100 mg/day) to patients with

mechanical valves because of concerns about the efficacy of heparin in preventing systemic

embolism. Warfarin can be used in the postpartum period and appears safe in women who breast-

feed.

Heparin: Heparin, unfractionated (standard, UFH) or low molecular weight (LMWH), is the drug of

choice during pregnancy because it is a large molecule that does not cross the placenta

Perinatal management of Pregnant patients with MVPS

There appears to be no higher risk for obstetric complications or fetal compromise in

patients with MVP. Antibiotic prophylaxis for vaginal delivery is not recommended.General

principles of management of cardiac patients with pregnancy has been dealt with already.The

management of this particular case will be discussed now.

A short recap of the case scenario:

Primi with MVPS with MR, mild PAH with minimal Pericardial effusion

Recently treated for IE

Presenting with diminished fetal movements and fetal bradycardia

So we have a compromised cardiac patient for emergency CS

The outcome of the mother and the baby depend on the expert management of the

patient considering the cardiac condition

Primary goals are,

1. To avoid factors that increase regurgitation fraction- Decrease in Preload, Increase in

heart rate, Increase in after load, decrease in SVR,Myocardial depression

2. Avoid major hemodynamic changes which will affect mother and baby- Aortocaval

compression, PPH and vasodilatation

3. Avoid factors which will precipitate CCF- Increase in airway pressure and PVR

Factors affecting pulmonary vascular resistance (PVR)

Factors decreasing PVR Factors increasing PVR

↑ PaO2 Hypoxia

↓ PaCO2 ↑ PaCO2

Alkalemia Acidosis

Medications: phosphodiesterase III inhibitors (e.g. milrinone),

prostaglandin E1 and I2, isoprenaline, inhaled nitric oxide

Medications: prostaglandin F2-

alpha, nitrous oxide.

Spontaneous ventilation Positive pressure ventilation and

PEEP

Hypothermia

Sympathetic stimulation: pain,

light anesthesia, anxiety

4. Maintain sinus rhythm and treat arrhythmias aggressively if they occur

Anaesthetic plan

Anesthetic technique depend on the urgency of LSCS in the interest of the baby as well as

the mother. The traditional categorization of Cesarean section into ‘elective’ or ‘emergency’ has

limitations for both optimal communication in the clinical setting and for post-delivery audit. A four

tier classification has been proposed and broadly accepted.

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

Our patient fits into category -I

Anesthetic techniques available are

1. Regional anaesthesia ( SA, EA,CSE)

2. General Anaesthesia

3. Field block

Regional anesthesia is an excellent choice for Cesarean section

SA: subarachnoid causes rapid onset of extensive symp. Blockade with intense vasodilation sudden

hypotension and severe tachycardia. This is detrimental to our patient who has high cardiac risk.

EA; 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 the emergency situation. Moreover large volume of

local anesthetic is needed for adequate blockade.Extensive blockade leading to profound

hypotension and insufficient motor blockade may not be ideal for CS.

CSE: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

1. Rapid onset of spinal block

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

3. Spread of spinal anaesthetic can be increased with injection of saline into the epidural space

(compression effect of dural sac)

4. Option for post-op 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 some cardiac conditions

8. Arguably advantageous in pre-eclampsia

9. Advantageous in failed labour epidural, normal dose spinal may lead to a high block

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

11. Airway pressures are not altered and avoids hyperventilation

12. Minimal autonomic blockade , hence no sudden decrease in SVR

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

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

15. Improved microvascular blood flow prevents DVT

16. Offers extended post operative pain relief

17. Allows early ambulation and return of bowel movements

18.Blood loss is relatively less

19.Low incidence of PDPH( Use of whitacre needle, drug in the epidural space prevents CSF leak,

dura is pierced at a different angulation )

20. Epidural and intra thecal opioids are prophylactic against PDPH

Conduct and Intra operative management of CSE:

Single level needle through needle technique is preferred for this patient.

Preparation:

1. All resuscitation equipments and drugs , anaesthesia machine, O2delivery system, Equipments

for GA , Suction apparatus are kept ready

2. Pt. Is given aspiration prophylaxis in the form of 0.3m SODIUM CITRATE 30ml orally, H2

receptor blocker and antiemetic given

3. Transport the pt. To OT with LUD and supplemental O2

4. Record baseline vitals

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

6. Administer IE prophylaxis

7. Monitors- SpO2, ECG(Lead II,V5),IABP,CVP,TTE and urine output

8. Reassure the patient

9. High informed consent is obtained explaining the maternal and fetal risk.

10. Fetal heart rate monitoring

11. Thrombo elasto stockings

12. Adequate Compatible blood

CSE is performed in lateral decubitus position under strict aseptic precautions 'Epidural space is

identified with 16 G tuohy neele using LOR with saline.Spinal needle is introduced through the

Tuohy needle and subarachnoid block is performed.20-30mic,Gm of Fentanyl/5-10Mic.of

Sufentanil along with 2.5 -5mg of 0.5% Bupivacaine is given.This is followed by insertion of

epidural catheter through which 5 ml of 2% Xylocaine without epinephrine is given.

Post operative analgesia is maintained as shown in the table below

Suggested Dosages for Continuous Lumbar Epidural Analgesia

Drug Initial Injection Continuous Infusion

Bupivacaine 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

Sufentanil 10-25 µg in a 10-mL volume 0.03-0.05 µg/mL

If Hypotension occurs- Inj. Ephedrine in 3mg bolus is given IV.

Crystalloids are given according to CVP avoiding fluid over loading

If there tachy arrhythmias inj. Phenyl ephrine -200 mic Gm given IV

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

Arrhythmias should be treated appropriately.

Blood loss should be assessed and replaced accordingly.

Immediate post partum period mandates meticulous care as mortality is very high in these

patients with PAH.

Post operative pain management reduces CV-stress response and prevents DVT.

Myths and Worries about Regional anaesthesia

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

overloading and maintains adequate cardiac output

2. RA is associated with sudden fall in BP:LA 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 does'nt happen with expertise hands

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

negligible with senior anesthesiologists

Controversies about CSE:

1. Risk of epidural catheter through the dural hole

2. Perceived increase in neurotrauma

Contraindications to Regional Anaesthesia

• Active heavy bleeding

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

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

• Thrombocytopaenia

• Systemic sepsis

• Local sepsis at site of insertion

• Patient refusal

As for as the other available technique - General anesthesia is concerned the following are

the advantages in this particular scenario

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

superior hemodynamics.

Anaesthetic Goals:

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

• Maintain LAP high enough to take advantage of the increased preload reserve.

• Avoid pulmonary artery hypertension by treating hypercarbia, hypoxemia, and acidemia.

• 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.

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

Maintain awareness of potential for LV rupture.

Aggressive treatment of arrhythmias if they occur

Avoid profound changes in SVR

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

Adequate analgesia and adequate muscle relaxation guided by Neuro muscular monitoring

Aspiration prophylaxis

Blood loss assessment and prompt replacement

The balance between the myocardial O2 supply and demand should be maintained considering

the fact that pregnancy per se has very limited cardiac reserve.

• The ideal Anesthetic technique at this juncture will be General anesthesia with controlled

ventilation

The other advantages are

1. Rapidly established(category 1 LSCS-FETAL BRADY)

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 Vent/arrhythmias promptly reverted

by cardioversion

9. Intra operative CVP monitoring- concentrating on V-waves which corelate the LV function

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

11. TEE insertion is recommended- Evaluate CO, LVEDV. EF, Emboli, acute rupture of

chordae tendinae, pericardial effusion

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

parturition

13. Effective management of Pulmonary oedema - IPPV with PEEP, liberal use of high dose

morphine

Suggested Technique of General Anesthesia for Cesarean Section

1 Team leader is preferably a senior anesthesiologist with sufficient CT experience apart from

CT surgeon, Neonatologist

2 As there is fetal brady cardia a preterminal rhythm for fetus- intra uterine resuscitation with

High FIO2,BP maintainance, IV fluids, avoid aortocaval compression,no oxytocics, tocolytics

right from admission

3 High risk informed consent and a potential for imminent cardiac surgery,pulmonary

oedema,fetal wastage, cardiac arrest should be obtained.

4. Administer a non particulate antacid -Sodium citrate 0.3 M (30 ml ). Additional agents

such as metoclopramide 10mg or an H2 blocker(ranitidine 50mg IV) should be considered in

patients at high risk for aspiration(unprepared) or failed intubation.Cross matched Blood-

PRBC and FFP 1:1 arranged

5 Patient shifted in semi recumbent posture with LUD and 02 by Venti mask, TED stockings

applied to LL to facilitate Venous return and prevent DVT.

6. Apply routine monitors, including electrocardiography, pulse oximetry, and capnography.In

this case due to recent IE invasive monitors -IBP, CVP are to be established under LA with

strict aseptic precautions

CVP- amplitude of V- is to be monitored which coincides with Ventricular systole

PCWP -risk of rupture of Pulm.artery in PIH , use of it controversial

ECG-lead II and V5-to detect arrhythmias.and MI

TEE after Intubation-monitor CO,LVDEV, severity of MR, movement of the Vegetations

Category I indication: Intra-operative use for endocarditis

CTG- Fetal wellbeing is commonly assessed with cardiotocography. (CTG )

monitoring consists of an external transducer that continuously records fetal

heart rate and uterine contractions

7 Ensure that suction is functioning and that equipment to correct failed intubation is readily

available.

8. Position the patient in a manner to achieve left uterine displacement and optimal airway

position.Establish two peripheral IV lines-Crystalloids at 60-75ml/hr

9. Pre Oxygenate with a high flow of oxygen for 3-5 minutes or 4 vital capacity breaths.

if the fetus is in extremes, airway management with a mask or laryngeal mask airway may be

an acceptable alternative

10

. After the drapes are applied and the surgeon is ready, initiate a rapid-sequence induction

with thiopental, 4.0-5.0 mg/kg, and succinylcholine, 1.0-1.5 mg/kg. Apply cricoid pressure

and continue until correct position of the endotracheal tube is verified and the cuff is

inflated. In hypotensive crises, ketamine, 1.0-1.5 mg/kg, should be substituted for

thiopental.Intubation response is obtunded with IV- Esmolol0.5mg/kg

11

. Ventilate with 50% oxygen and 50% nitrous oxide and a volatile anesthetic(0.33-0.5 MAC) as

necessary. Maintain normocarbia and use muscle relaxation as necessary with either a non

depolarizing muscle relaxant (devoid of histamine release, vagolytic property)

12 Ventilate with PAP<20cms, low rate8-10/min, vT of 8-10ml/kg allowing full expiration

avoiding factors that elevate PVR

13 After delivery, increase nitrous oxide to 70%, discontinue or reduce the volatile anesthetic,

and administer an opioid and a benzodiazepine. Add oxytocin to intravenous

fluids.Opioid(Fentanyl) analgesic can be administered

14 Insert an orogastric tube before completion of surgery.Ensure adequate pain relief -rectal

tramodol/ epidural narcotic/bil.TAP block

15 Reverse neuromuscular blockade as necessary at completion of surgery

16 Extubate when the patient is awake, the anesthesia is adequately reversed, and the patient is

following commands.Patient to be observed in HDU/ICU for 72hrs with invasive monitors

T he table shows the various anesthetic drugs and their action on the cardi vascular system

Choice of the anesthetic should fulfill the anesthetic goals mentioned above ARE HIGH LIGHTED

Cardiovascular effects of commonly used anesthetic and obstetric drugs

Heart rate Blood

pressure SVR

Cardiac

output

Myocardial

contractility Venodilation

Etomidate ↔ ↔ or ↓ ↔ or ↓ ↔ ↔ ↔

Ketamine ↑↑ ↑ ↑ or ↔ ↑ ↑ ↔

Thiopental--

graded ↑ ↓↓ ↔ to ↑ ↓ ↓ ↑

Propofol ↑ or ↔ ↓ ↓↓ ↔ to ↓ ↓ ↑

Succinylcholi

ne

↔ to ↓

with

repeat

doses

↔ to ↑ ↔ to ↑ ↔ ↔ ↔ to ↓

Atracurium ↔ or ↑ ↔ to ↓ ↔ ↔ ↔ ↔ to ↑

Pancuronium ↑ ↑ ↔ to ↑ ↑ ↑ ↔

Rocuronium ↔ or ↑ ↔ ↔ ↔ ↔ ↔

Vecuronium ↔ ↔ ↔ ↔ ↔ ↔

Fentanyl ↓ ↔ to ↓ ↔ ↔ ↔ ↔

Meperidine ↔ or ↑ ↓ ↓ ↓ ↓ ↑

Morphine ↔ or ↓ ↓ ↓ ↓ ↓ ↑

Halothane ↔ or ↑ ↓ ↓ ↔ or ↓ ↓↓ ↓

Isoflurane ↑↑ ↓ ↓↓ ↔ or ↑ ↓ ↓

Sevoflurane ↑ ↓ ↓ ↔ or ↓ ? ↓ ↔

Nitrous oxide ↔ or ↑ ↔ or ↑ ↔ or ↑ ↓ or ↑ ↔ ↔ or ↓

Lidocaine ↔ ↔ ↔ ↑ ↑

↑ if used for

regional

anesthesia

Lidocaine

toxicity ↓ ↓ ↑ ↓ ↓ ↑

Midazolam ↔ or ↑ ↓ ↔ or ↓ ↔ ↔ or ↓ ↔

Ergometrine ↑ ↑↑ ↑ ↑ ↑ ↓

Oxytocin ↔ or ↑

↔ to ↑

(< 10 U)

↓ (> 10 U

bolus

dose)

↔ to ↓ ↔ ↔ ↔ to ↑

Magnesium

sulfate ↔ or ↓ ↓ ↓ ↔ ↔ ↑

Nitroglycerin ↔ ↓↓ ↔ to ↓ ↓ ↔ ↑↑

Terbutaline ↑ ↔ to ↓ ↔ to ↓ ↑ ↔ to ↑ ↑

There is no anesthetic technique which is free of complications.The outcome depends on how well the technique is conducted

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

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

Postoperative management of parturients with cardiac disease In the postoperative period, patients with severe cardiac dysfunction delivered by Cesarean section should be kept in the High Dependent Unit (HDU) / intensive care unit (ICU) for aggressive monitoring of fluid therapy, oxygen saturation and hemodynamics. During the first 24-72 hours significant fluid shift occurs, which may lead to CCF. Adequate post-operative analgesia should be provided in the form of continuous epidural analgesia or patient controlled IV analgesia. Early ambulation to minimize the risk of deep venous thrombosis and paradoxical embolization should be weighed against the risk of cardiovascular stress.

Advise the patient to under go corrective cardiac surgery at an early date

When cardiopulmonary resuscitation is required during pregnancy standard ACLS protocol as per the AHA/ACC guideline of 2010 has to be followed.Important point to note are

1. LUD to be maintained through out CPCR

2. Early definitive airway by only qualified personnel

3. Cesarean section beyond 24 wks for effective maternal resuscitation

4. Cesarean in less than 4min. of arrest for better fetal survival

Conclusion:

Anesthetic management in a pregnant patient with preexisting cardiac disease is a challenge

to even experienced anesthesiologists.A proper understanding of the pathophysiology of the

individual heart disease is essential and management by setting specific goals for each case. The use

of cardiac , obstetric and anesthetic drugs impose a threat to both the mother and the

fetus.Therefore a thorough knowledge of the drug is important.As anesthesiologist our

responsibility extends beyond the delivery room by actively participating in the post partum care of

these critically ill patients.