how do i do it? disease compli… · in the presence of cardiac disease this balance is likely to...
TRANSCRIPT
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.