2. Introduction
CARDIAC disease in pregnancy remains an
important etiology of maternal ,fetal morbidity and
mortality.
Mitral stenosis is the most commonly acquired valve
lesion encountered in pregnant women and is almost
invariably caused by RHD.
Pregnancy and the peripartum period worsen
symptoms of cardiac disease.
3. Presenting Complaints
A 37 year old woman presented at 28 weeks
gestational age with inability to lie and became
dyspneic even when speaking (class IV).
Had complete placenta previa, possible placenta
accreta.
4. Past History
Patient complained of dyspnea with moderate exertion
before pregnancy( class II )
Past medical history – No history of TB, DM
, HTN, Asthma,convulsion,chest pain
Drug history – no history of any drug allergy.
Family history- not significant
6. Clinical examination
Physical examination revealed an arterial blood pressure of
102/60 mmHg,
Regular heart rate of 108 beats/min,
Respiratory rate of 22 breaths/min.
There were diastolic(grade 2) and holosystolic( grade 3)
apical murmurs.
The patient’s lungs were clear to auscultation
bilaterally, and she had mild pedal edema.
Her symptoms improved with heart rate control
using 25 mg metoprolol orally twice daily.
7. Investigation
Electrocardiogram showed
sinus tachycardia and left
atrial enlargement.
Transthoracic
echocardiogram revealed
moderate to severe mitral
stenosis, moderate to severe
mitral regurgitation, and
moderate pulmonary
hypertension with estimated
pulmonary artery systolic
pressure of 54 mmHg. There
was moderate tricuspid
regurgitation.
Left and right ventricular
systolic function were
normal.
PROVISIONAL DIAGNOSIS-
PREGNANCY WITH MS
8. Management
Cesarean section was planned at 36 weeks
gestational age in a cardiac operating room with
cardiopulmonary bypass capabilities on standby.
9. Prophylaxis against acid aspiration, 30 ml sodium
bicitrate was administered orally in the holding area.
Patient was positioned in the left uterine displacement
Initial systemic arterial blood pressure was 125/65
(mean 76)mmHg. Her heart rate was 105 beats/min.
Remifentanil (0.2 ǔgm/kg/min) was started to
attenuate the sympathetic response to laryngoscopy
and intubation.
10. Induction
Etomidate, and Succinylcholine was used for relaxant administered in
a rapid sequence fashion.
Maintenance
Remifentanil infusion(0.05– 0.1ug /kg/min),
Low level of Isoflurane(less than 0.5 minimum alveolar
concentration),
Vecuronium for muscle relaxant.
Higher doses of inhalational agents were avoided to prevent uterine
atony.
Depth of anesthesia was monitored using bispectral index values
from 40–60 were maintained during the intraoperative period.
The patient was ventilated using 100% oxygen to maintain
normocarbia.
11. Intra op monitoring by TEE ,Colour doppler
Three-dimensional ultrasound reconstruction of the
mitral valve showed significant commissural
fusion(mitral valve area 1.4cm2).
Cesarean section was performed without
complications.
After delivery, 40 U oxytocin was administered
intravenously in 2 hr.
12. Initially monitored in the operating room
after extubation to ensure normocarbia and stable
pulmonary artery pressures.
Then transferred to the cardiac care unit for postoperative
monitoring.
The patient was discharged from the cardiac care
unit on postoperative day 1 and from the hospital on
postoperative day 5.
She underwent mitral valve repair and tricuspid
valve annuloplasty 4 months later.
13. Heart disease with pregnancy
Epidemiology - incidence of cardiac disease in
pregnant
0.2% to 3% of pregnancies are complicated by maternal heart
disease in developed countries
Heart diseases are still the second most common non obstetrical
cause of maternal mortality
Rheumatic heart disease accounts for majority of cases (~ 75%) in
India while congenital heart disease are most common in developed
countries
-- Mitral stenosis is the most commonly acquired valve lesion
in pregnant women and is almost caused by RHD.
14. .
RHD
Highly prevalent in developing countries.
India, the prevalence of RHD is 6:1,000 ( school-
aged children)
Carditis occurs in 30–80% of patients with acute
rheumatic fever, and at least 60% of untreated patients
develop chronic RHD.
15. Physiological changes - Consideration In Pregnancy
The most important changes in cardiac function occurs in
the first 8 weeks of pregnancy with maximum changes at 28
weeks
↓ Vascular resistance
↓ Blood pressure
↑ Heart rate ↑ Stroke volume ↑ CO
↑ Blood volume 30% - 50%
16. The fall in the peripheral resistance is about 20-30% at
21-24 weeks & returns to normal at term. This fall is due to
1. The trophoblastic erosion of endometrial vessels,
the placental bed serves as a large arteriovenous shunt
causing lowered systemic vascular resistance
2. There is physiological vasodilatation which is believed to
be secondary to endothelial prostacyclin and circulating
progesterone.
3 .Anemia decreases blood viscosity with resultant decrease
in systemic vascular resistance.
20. Risk of haemodynamic stress
At the time of labor and delivery, pain and anxiety
increase catecholamine release with resultant
increases in heart rate, arterial blood pressure, and
cardiac output.
Auto-transfusion of up to 500 ml with each
contraction , increases preload and, hence cardiac
output.
After delivery, there is an additional increase in venous
return as a result of auto-transfusion from the
contracting uterus as well as from the loss of foetal
compression of the inferior vena cava.
21. Features in Pregnancy which can
mimic cardiac disease
1. Dyspnoea - due to hyperventilation, elevated
diaphragm.
2. Pedal Edema
3. Cardiac impulse- Diffused and shifted laterally due to
elevated diaphragm.
4. Jugular veins may be distended and JVP raised.
5. Systolic ejection murmurs along the left sternal
border occur in 96% of pregnant women and are
believed to be caused by increased flow across the
aortic and pulmonary valves.
22. Criteria to diagnose cardiac disease
during pregnancy:
1.Presence of diastolic murmurs.
2.Systolic murmurs of severe intensity (grade III)
3.Unequivocal enlargement of heart (X-ray)
4.Presence of severe arrythmias, atrial fibrillation
or flutter .
23. Risk of cardiovascular complications during
pregnancy
Risk of
cardiovascular
complications
during pregnancy
High risk
Low risk Intermediate risk
of
of of
complications
complications (≤ 1%) complications (5-15%)
or death (≥25%)
24. Low risk of complications (≤ 1%):
Corrected tetralogy of fallot
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Mild pulmonic or tricuspid valve disease
Mitral stenosis (NYHA class I, II)
Mild regurgitant valve lesion
Bioprosthetic valve
Compensated heart failure (NYHA class I, II)
25. Intermediate risk of complications (5-15%):
Mechanical valve prosthesis
Aortic stenosis (mild to moderate)
Mitral stenosis with atrial fibrillation
Mitral stenosis (NYHA class III, IV)
Uncorrected cyanotic congenital heart disease
(tetralogy of fallot)
Uncorrected coarctation of the aorta
Previous myocardial infarction
26. High risk of complications or death (≥25%):
Pulmonary hypertension (severe)
Eisenminger syndrome
Marfan disease with aortic root involvement
Peripartum cardiomyopathy
Severe aortic stenosis
NYHA class IV heart failure
27. The indications for Termination of
pregnancy
1. Eisenmenger’s syndrome.
2. Marfan’s syndrome with aortic involvement
3. Pulmonary hypertension.
4. Coarctation of aorta with valvular involvement.
Termination should be done before 12
weeks of pregnancy.
28. The New York Heart Association (NYHA) Grading of
functional capacity of the heart:
No functional limitation of activity Symptoms with extra
CLASS I ordinary physical work.
Mild limitation of physical activity. Symptoms with ordinary
CLASS II physical work
Marked limitation of physical Symptoms with less than
CLASS III activity ordinary physical work
CLASS IV Severe limitation of physical Symptoms at rest
activity
29. Prognosis depends on the functional status
NYHA classes I and II lesions
usually do well during pregnancy and have a
favorable prognosis (mortality rate of <1%).
NYHA classes III and IV -mortality rate of 5% to
15%.
These patients should be advised against
becoming pregnant.
35. Signs of Mitral Stenosis
Palpation:
Small volume pulse
Tapping apex-palpable S1
Palpable S2
Atrial fibrillation
Signs of raised pulmonary capillary pressure
Crepitations, pulmonary oedema, effusions
Signs of pulmonary hypertension
RV heave, loud P2
Auscultation:
Loud S1
S2 to OS interval inversely proportional to severity
Diastolic rumble: length proportional to severity
In severe MS with low flow- S1, OS & rumble may be inaudible
36. Mitral Stenosis: Physical Examination
S1 S2 OS S1
• First heart sound (S1) is loud and snapping
• Opening snap (OS)
• Low pitch diastolic rumble at the apex
• Pre-systolic accentuation (esp. if in sinus rhythm)
37. Mitral Stenosis:
Complications
Atrial dysrrhythmias
Systemic embolization (10-25%)
◦ Risk of embolization is related to, age, presence of atrial
fibrillation, previous embolic events
Congestive heart failure
Pulmonary infarcts (result of severe CHF)
Hemoptysis
◦ Massive: 20 to ruptured bronchial veins (pulmonary HTN)
◦ Streaking/pink froth: pulmonary edema, or infection
Endocarditis
Pulmonary infections
39. Mitral stenosis:CXR
The cardiac size is Unequivocal
1. the left atrial appendage is
prominent (LAA).
2. Main pulmonary artery
(MPA) segment is just outside
the left border, indicating
pulmonary hypertension.
3. The enlargement of left
pulmonary artery (LPA) and
right pulmonary artery (RPA)
are just modest, if at all.
4. The horizontal fissure is
visible, indicating collection of
edema fluid in the fissure.
5.The aortic knuckle (Ao) is also
seen well.
40. Mitral Stenosis:ECG
LAE
RVH
Premature contractions
Atrial flutter and/or fibrillation
freq. in pts with mod-
severe MS for several years No P waves .
A fib develops in 30% to
rhythm is irregularly irregular
40% of patients with
symptoms right ventricular hypertrophy.
Right axis deviation and deep S
waves in the lateral leads.
Combination of atrial fibrillation
and right ventricular hypertrophy
suggests mitral stenosis.
41. Mitral Stenosis: Role of
Echocardiography
Diagnosis of Mitral Stenosis
Assessment of hemodynamic severity
◦ mean gradient, mitral valve area, pulmonary artery
pressure
Assessment of right ventricular size and function.
Assessment of valve morphology to determine
suitability for percutaneous mitral balloon valvuloplasty
Diagnosis and assessment of concomitant valvular lesions
Reevaluation of patients with known MS with changing
symptoms or signs.
43. Mitral Stenosis:Therapy
Medical
Diuretics for LHF/RHF
Anticoagulation: In Atrial Fibrillation
AF requires aggressive treatment with digoxin and β-blockers . If
pharmacotherapy fails, cardioversion should be performed. After
cardioversion bed rest in left lateral position and diuretics should
be given to ameliorates pulmonary oedema.
Endocarditis prophylaxis
β -blockers used to prevents tachycardia.
Propanolol can be administered without any adverse effect on
foetus or neonate
Atenolol should be avoided in the early stages of pregnancy
and only given with caution in the later stages because of its
association with fetal growth retardation
44. Surgical management
» Before pregnancy- if significant MS is recognised before pregnancy :
Surgery is recommended
Mitral commisurotomy Mitral valve replacement –
is preferred Bioprosthetic valve is preferred
» During pregnancy-
1. Palliative Mitral Valvotomy : temporarily delays progression of MS and may
enable successful completion of pregnancy. Best time is in 2nd trimester.
2. Mitral commisurotomy : in case of severe symptoms it can be performed at
any stage of gestation.
3. Balloon Mitral Valvuloplasty : it is safe and effective in women with pliable
valve .This circumvents open heart surgery and risks of anaesthesia and
surgery for mother and foetus.
45. Anaesthetic Goals:
Prevention of pain
Avoid tachycardia (diastolic filling time further
decreased)
Events that increase the pulmonary vascular resistance like
hypoxaemia, hypercarbia and acidosis should be avoided
Avoid increases in blood volume (result in pulmonary
edema)
Avoid rapid and severe drop in SVR (compensatory
increase in HR can lead to further decompensation)
Immediate treatment of acute atrial fibrillation
46. The main principles of management with regard
to valvular heart disease in Pregnancy
• Early identification of the disease, and the assessment of the severity of the
lesion.
• High-risk lesions, for either mother or fetus, should be managed in a high
care environment where invasive monitoring is possible, both pre- and post
delivery.
• Regional anaesthesia techniques in labour are an attractive option, and
may be employed with good outcomes in many patients.
• Carefully titrated epidural anaesthesia for labour is associated with less
sympathetic blockade than spinal or epidural anaesthesia for caesarean
delivery.
• Severe mitral or aortic stenosis, or any valvular heart condition associated
with pulmonary oedema or heart failure, are contraindications to
regional anaesthesia.
47. Anaesthetic Options
VAGINAL DELIVERY :
The role of the anaesthesiologist begins by providing good labour
analgesia.
Epidural anaesthesia is recommended, unless obstetrically
contraindicated.
Caesarean section is indicated for OBSTETRIC REASONS ONLY.
Tachycardia, secondary to labour pain, increases flow across the mitral
valve, producing sudden rises in left atrial pressure, leading to acute
pulmonary oedema. This tachycardia is averted by epidural analgesia
without significantly altering the patient haemodynamics.
48. Mitral stenosis : Regional
Anaesthesia
I stage of labour : MS does not change management-adequate
analgesia is essential to minimize tachycardia. Epidural analgesia is
effective. Adequate hydration should be maintained. Intrathecal opioid
such as Fentanyl 25 μg produces good analgesia without major
haemodynamic changes.
II stage of labour : Minimize maternal expulsive
efforts, allowing fetal descent to be accomplished by uterine
contractions. This is to avoid the deleterious effects of the Valsalva
maneuver, which causes an undesirable increase in venous return.
Intrathecal opioid with low dose LA can be given for analgesia and
anaesthesia. The 2nd stage should be cut short by instrumentation.
LA to provides perineal anaesthesia
49. • CSE : intrathecal opioid +/- small dose of LA followed by slow epidural
infusion of a dilute solution of LA +/- opioid. (0.125% bupivacaine +
2µg/ml fentanyl).
• Epinephrine should be avoided as it may induce tachycardia.
• Phenylephrine- vesopressor of choice (no tachycardia)
• Invasive cardiac monitoring like radial artery cannulation and
pulmonary catheter are beneficial in assessing the cardiac
output, pulmonary artery pressure and for guiding fluid and drug
therapy, especially in NYHA III and IV patients.
• Foetal heart rate monitoring should be carried out during all stages of
labour.
• Pulse oximetry monitoring is mandatory.
• Supplementary epidural anaesthesia can be maintained throughout the
immediate post-partum period and the catheter left in situ could provide
anaesthesia for immediate or post-partum tubal sterilization.
50. CAESAREAN-SECTION
General anaesthesia NYHA class 3 and 4 patients .
Regional anaesthesia is preferred over general anaesthesia
in NYHA class 1 and2 patients
– Regional : Spinal & Epidural
Epidural anaesthesia - preferred over spinal anaesthesia :
More predictability and control over hemodynamic changes.
maintains systemic vascular resistance.
gradual onset of sympathetic block
Slower induction of anaesthesia and ensures maternal hemodynamic stability.
51.
Mitral stenosis:GA
General anaesthesia has the disadvantage of increased Pulmonary Arterial
pressure and tachycardia during laryngoscopy and tracheal intubation.
Premedication : sedative and anxiolytics are avoided.
Only counseling done to alleviate the anxiety.
Preoxygenation:done with 100% o2 for 5 min.
Induction :Inj. Thiopentone 3-4 mg/kg
Intubation: Inj.succinylcholine 1-1.5mg/kg
Maintained with opioids, neuromuscular blockers, nitrous oxide, and oxygen.
A beta-adrenergic receptor antagonist,
fentanyl, I.v xylocard should be administered before or during the induction of
anaesthesia to blunt intubation response.
The adverse effects of positive-pressure ventilation on the venous return may
ultimately leads to cardiac failure.
52. Continued……
Tachycardia inducing drugs like
atropine, ketamine, pancuronium and meperidine, should be
totally avoided.
Esmolol has a rapid onset and short duration of action, it is a better
choice in controlling tachycardia.
Modified rapid sequence induction using etomidate, remifentanyl and
succinylcholine is an ideal choice in tight stenosis with pulmonary
hypertension.
General anesthesia provides the advantages of definitive airway
control and the ability to use transesophageal echocardiographic
monitoring throughout the procedure.
Higher doses of inhalational agents should be avoided to prevent uterine
atony.
•Emergence must be carefully controlled to ensure avoidance of
tachycardia
53. Continued……
Diuretics should also be used cautiously because
hypovolemia can impair fetal blood supply
Reversal: Avoid tachycardia, extubation is done when
patient is fully awake.
After delivery oxytocin should be administered as
intravenous infusion preferably slowly. Stat i.v dosing
should be avoided
These Patients are at risk for haemodynamic
compromise and pulmonary oedema during
postpartum period,so require ICU care.
For postoperative analgesia :I.V opioid or NSAIDS
54. Conclusion
Irrespective of the mode of delivery and anaesthetic technique, these
patients are at a great risk of haemodynamic stress due to
autotransfusion of blood from the uterus. This may lead to pulmonary
hypertension, pulmonary oedema and cardiac failure.
Therefore, intensive monitoring and therapy should be continued till
the haemodynamic parameters return to normal.
As a rule, regurgitant valvular lesions are far better tolerated in
pregnancy than are stenotic lesions.
.
Patients with severe symptomatic valvular heart disease should ideally
be counselled against pregnancy.
In the event of pregnancy, early consultation between obstetrician and
anaesthesiologist allows for planning with regards to both the timing of
delivery and optimal analgesia/ anaesthesia.