Mitral stenosis and pregnancy: Current concepts in anaesthetic practice : Indian Journal of Anaesthesia

Secondary Logo

Journal Logo

Review Article

Mitral stenosis and pregnancy

Current concepts in anaesthetic practice

Kannan, M; Vijayanand, G

Author Information
doi: 10.4103/0019-5049.71043
  • Open



Rheumatic heart disease is still a major heart problem associated with pregnancy in India, despite its declining trend. The incidence of rheumatic mitral stenosis was 5.4 per 1,000 school children in 1995,[1] and it has been reduced to 0.5–0.64 per 1,000.[23] Rheumatic mitral stenosis forms 88% of the heart diseases complicating pregnancy in the tertiary referral centre in India.[4] The mortality and morbidity are considerably reduced[5] by better perinatal care, where the anaesthesiologist plays a major role in the multidisciplinary approach. Nevertheless, in the developed world, rheumatic disease has become uncommon and complex congenital heart disease is increasing in the recent decades. With the advent of intensive obstetric and anaesthetic care, the death rate of pregnant women with heart disease is lower in mitral stenosis compared with other congenital heart diseases like Eisenmenger’s syndrome, pulmonary vascular obstructive disease and Marfan’s syndrome with aortopathy.[6] Although mitral stenosis is often associated with mitral regurgitation, morbidity is usually related to mitral stenosis[7]


Cardiovascular changes during pregnancy

Although the physiologic changes in the cardiovascular system appear to begin in the first trimester, these changes continue into the second and third trimesters, when the cardiac output increases by approximately 40% of the pre-pregnant values. The cardiac output increases from the fifth week of pregnancy and reaches its maximum levels by 32 weeks. Cardiovascular changes during pregnancy are summarized in Table 1. The cardiovascular changes of pregnancy resolve by 3–6 months after delivery. It may even take a year for the residual effects of cardiovascular remodeling to subside.

Table 1:
Cardiovascular changes during pregnancy

When the normal mitral valve orifice area of 4–6 cm2 is progressively reduced to 2 cm2, the classical symptoms of mitral heart disease start appearing. Mitral stenosis prevents emptying of the left atrium and subsequent filling of the left ventricle, resulting in decreased stroke volume and decreased cardiac output. Consequent to the fixed cardiac output state, the heart cannot cope up with situations warranting increased metabolic demand or increased blood volume. When the stenosis progresses, the left atrium dilates and the left atrial pressure increases. A pressure gradient develops during diastole between the left atrium and the left ventricle. This pressure gradient is the haemodynamic hallmark of mitral stenosis. Hence, the back pressure on the pulmonary vessels leads to pulmonary congestion and, in severe cases, pulmonary oedema. Longstanding pulmonary venous congestion causes irreversible changes in the vessel wall, leading to chronic pulmonary hypertension.

Women with severe mitral stenosis often do not tolerate the cardiovascular demands of pregnancy. This increased volume load and tachycardia together cause the patients to deteriorate and advance from one New York Heart association (NYHA) class to another. The increased heart rate of pregnancy limits the time available for left ventricular filling, resulting in increased left atrial and pulmonary pressures and an increased likelihood of pulmonary oedema. When the pulmonary capillary pressure exceeds the blood oncotic pressure, pulmonary oedema develops. Atrial fibrillation worsens this scenario and about 80% of the cases of systemic emboli occur in patients with atrial fibrillation.

Cardiac decompensation and pulmonary oedema may occur in pregnant women with overt or silent mitral valve stenosis during the second or third trimester. The risk of maternal death is greatest during labour and during the immediate post-partum period. The sudden increase in the pre-load immediately after delivery, due to autotransfusion from the uterus, may flood the central circulation, resulting in severe pulmonary oedema. In addition, there continues to be autotransfusion of blood for 24–72 h after delivery. Thus, the risk of pulmonary oedema extends for several days after delivery.[8] The greatest risk occurs in the peripartum period, and most deaths occur between the second and ninth days post-partum. The haemodynamics during labour and puerperium are summarized in Tables 2 and 3.

Table 2:
Haemodynamics during labour
Table 3:
Haemodynamics during puerperium


Although clinical examination, electrocardiogram and X-ray chest reveal many relevant findings, echocardiography is the standard imaging tool used to assess patients with mitral stenosis. Echocardiography provides information regarding the area of the mitral valve, size of the left atrium, presence of thrombus and the size and function of the left ventricle and right-sided chambers. Doppler examination provides information about the severity of the stenosis, the presence of other associated valve lesions and the degree of pulmonary hypertension [Table 4]. Diagnostic cardiac catheterization is necessary only when echocardiography is non-diagnostic or results are discordant with clinical findings.

Table 4:
Severity grading of mitral stenosis

Prediction of mortality and morbidity

The maternal outcome seems to correlate well with the New York Heart Association (NYHA) functional classification.[910] Maternal cardiac complications, such as pulmonary oedema and arrhythmias, occurred in 35% of the pregnancies. The incidence of maternal cardiac complications correlates with the severity of the mitral stenosis (67% for severe, 38% for moderate and 26% for mild disease).[11] Mortality rates for class I and II amount to <1%, whereas they range between 5 and 15% for class III and IV. The peri-natal mortality rate for class III and IV is as high as 20–30%. Siu and others,[12] expanded on the NYHA classification and developed a system for predicting complications during pregnancy.

  1. Prior heart failure, arrhythmia, transient ischaemic attack or stroke.
  2. A baseline NYHA III class or more or cyanosis.
  3. Systemic ventricular dysfunction (ejection fraction, 40%).
  4. Pulmonary hypertension (pulmonary arterial systolic pressure 50% of systemic pressure).
  5. Left heart obstruction.
    • · Severe aortic stenosis (valve area, 1/cm2, Doppler jet velocity 4 m/s).
    • · Symptomatic or severe mitral stenosis.
  6. Severe aortic or mitral regurgitation with NYHA class III or IV symptoms.


Management of the pregnant woman requires a multidisciplinary team for optimal maternal and foetal outcomes. Antenatal management is directed towards avoiding cardiac decompensation, with regular assessment for volume overload and pulmonary oedema.


In symptomatic patients, medical treatment should be the first line of management. Treatment involves bed rest, oxygen therapy and diuretics. Beta-adrenergic receptor blockade is useful to prevent tachycardia during pregnancy. Propranolol or atenolol decreases the incidence of maternal pulmonary oedema without adverse effects on the foetus or neonate.[13] Recent trials conclude that digoxin has no role in prevention and in the treatment of cardiac failure.[14]

Atrial fibrillation requires aggressive treatment with digoxin and beta blockers to revert it to sinus rhythm and anticoagulation to prevent systemic embolization. Cardioversion should be performed if pharmacologic therapy fails to control the ventricular response. Anticoagulation, even in the absence of atrial fibrillation, is beneficial.[1516] Because of the paucity of data regarding the efficacy of anticoagulants during pregnancy, recommendations concerning their use during pregnancy are based largely on extrapolations from the data from non-pregnant patients, from case reports and from case series of pregnant patients.[17] Due to the high incidence of embryopathy during the first trimester and bleeding during parturition, warfarin should be used during 12–36 weeks of pregnancy only. Standard therapy during pregnancy would be

Therapy with low-molecular weight heparin (LMWH) instead of unfractionated heparin is gaining popularity. Although an “anti Xa” activity is used to monitor LMWH, no anti-Xa activity-based guidelines have been issued till date.[1820] Antibiotic prophylaxis for endocarditis is reserved only for patients with a previous history of endocarditis or presence of established infection.[21]

  • SC/IV heparin for up to 12 weeks antepartum (aPTT 1.5–2.5-times of normal)
  • Warfarin from 12 to 36 weeks (maintain INR 2.5–3.0)
  • SC/IV heparin after 36 weeks


If mitral stenosis is diagnosed before pregnancy, mitral commissurotomy is preferred. During pregnancy, the second trimester is the preferred period for any invasive procedure. Percutaneous valvuloplasty using the Inoue balloon technique has become the accepted treatment for patients with severe symptomatic mitral stenosis. Percutaneous balloon mitral valvuloplasty provides palliation for pregnant women with mitral stenosis, and the reported success rate is nearly 100%. Successful balloon valvuloplasty increases the valve area to >1.5 cm2without a substantial increase in mitral regurgitation.[22] Although the maternal outcome in percutaneous balloon mitral valvuloplasty and open commissurotomy are the same, the foetal loss is high in open commissurotomy, at a ratio of 1:8.[23] Valve replacement is reserved for severe cases with calcified valve and in mural thrombus where the maternal mortality is 1.5–5% and the foetal loss is 16–33%.[24]


The role of the anaesthesiologist begins by providing good labour analgesia. Most reports have recommended vaginal delivery under epidural anaesthesia, unless obstetrically contraindicated. Caesarean section is indicated for obstetric reasons only. In a study by Goldszmidt and others,[25] only 29–31% of the 522 women with heart disease required caesarean section and nearly 70% of them underwent vaginal delivery under epidural analgesia. Tachycardia, secondary to labour pain, increases flow across the mitral valve, producing sudden rises in left atrial pressure, leading to acute pulmonary oedema. This tachycardia is averted by epidural analgesia without significantly altering the patient haemodynamics.[26] 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.[2728] Sudden drops in systemic vascular resistance (SVR) in the presence of a fixed cardiac output can be prevented by small bolus doses of phenylephrine, with volume expansion when necessary.

Combined spinal–epidural analgesia during labour using intrathecal fentanyl 25 μg produces good analgesia without major haemodynamic changes during the first stage of labour. During the second stage of labour, only the uterine contractile force should be allowed rather than the maternal expulsive effort that is always associated with the valsalva maneuver. Therefore, the second stage of delivery should be cut short by instrumentation. Supplementary analgesia for instrumentation with slow epidural boluses of fentanyl and a low concentration of bupivacaine reduces SVR and the cardiac pre-load.[29] Low spinal anaesthesia for vaginal instrumental delivery has also been used with good results in these patients.[30]

Labour pain can affect multiple systems that determine the uteroplacental perfusion. Hence, foetal heart rate monitoring should be carried out during all stages of labour. Supplemental oxygen administration with pulse oximetry monitoring to minimize increases in pulmonary vascular resistance and maintenance of left uterine displacement for good venous return are mandatory. Supplementary epidural anaesthesia can be maintained throughout the immediate post-partum period and the catheter left in situ could provide anaesthesia for immediate or post-partum tubal sterilization.

Anaesthetic management of abdominal delivery

The goals for the anaesthetic management of patients with mitral stenosis are: (1) maintenance of an acceptable slow heart rate, (2) immediate treatment of acute atrial fibrillation and reversion to sinus rhythm, (3) avoidance of aortocaval compression, (4) maintenance of adequate venous return, (5) maintenance of adequate SVR and (6) prevention of pain, hypoxaemia, hypercarbia and acidosis, which may increase pulmonary vascular resistance.

There are no controlled studies examining the best type of anaesthetic technique in these patients and guidelines and standards are lacking. Therefore, individualizing the anaesthetic management according to the parturient’s cardiovascular status and the practitioners’ knowledge and experience of the existing treatment options is the key to success in these patients.[29] For the past two decades, regional anaesthesia has proved to be a safe technique in cardiac patients presenting for caesarean section. Epidural and continuous spinal anaesthetic techniques are attractive options.

One of the major advantages of epidural analgesia is that it can be administered in incremental doses and that the total dose could be titrated to the desired sensory level. This, coupled with the slower onset of anaesthesia, allows the maternal cardiovascular system to compensate for the occurrence of sympathetic blockade, resulting in a lower risk of hypotension and decreased uteroplacental perfusion. Moreover, the segmental blockade spares the lower extremity “muscle pump,” aiding in venous return, and also decreases the incidence of thromboembolic events. Invasive haemodynamic monitoring, judicious intravenous administration of crystalloid and administration of small bolus doses of phenylephrine maintain maternal haemodynamic stability.[30]

Continuous spinal anaesthesia, although infrequently practiced, could be a better option in some rare situations like accidental dural puncture. Dresner conducted 34 caesarean sections with cardiac disease under continuous spinal anaesthesia with a success rate of 99%.[31] Neuraxial block in an anticoagulated patient has the risk of epidural haematoma. The Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation (2003) has laid down valuable guidelines for such clinical situations.[32]

General anaesthesia has the disadvantage of increased pulmonary arterial pressure and tachycardia during laryngoscopy and tracheal intubation. Moreover, the adverse effects of positive-pressure ventilation on the venous return may ultimately lead to cardiac failure.[33]

Despite these disadvantages, if general anaesthesia is contemplated, tachycardia, inducing drugs like atropine, ketamine, pancuronium and meperidine, should be totally avoided. A beta-adrenergic receptor antagonist and an adequate dose of opioid like fentanyl should be administered before or during the induction of general anaesthesia. Because esmolol has a rapid onset and short duration of action, it is a better choice in controlling tachycardia. Since foetal bradycardia has been reported after esmolol, foetal heart rate should be monitored. Modified rapid sequence induction using etomidate, remifentanyl and succinylcholine is an ideal choice in tight stenosis with pulmonary hypertension.[3435] Maintenance of anaesthesia can be carried out with oxygen and nitrous oxide 50:50, isoflurane, opioids and vecuronium. With associated severe pulmonary hypertension, nitrous oxide can be omitted. At this juncture, invasive haemodynamic monitoring is an inevitable guide.

After delivery of the foetus, oxytocin 10–20 u in 1,000 ml of crystalloid should be administered at a rate of 40–80 mu/min. An infusion of oxytocin can lower the SVR as well as elevate the pulmonary vascular resistance, resulting in a drop in cardiac output. Care must be taken during its administration. Methylergonovine, or 15-methylprostaglandin F, produces severe hypertension, tachycardia and increased pulmonary vascular resistance.[3637]

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 on to pulmonary hypertension, pulmonary oedema and cardiac failure. Therefore, intensive monitoring and therapy should be continued till the haemodynamic parameters return to normal.


Rheumatic mitral stenosis complicating pregnancy is still a frequent cause of maternal death. A better understanding of the physiological changes in pregnancy and the pathological impact of mitral stenosis over pregnancy and a multidisciplinary approach in diagnosis and management reduce the mortality and morbidity.


1. Padmavati S. Present status of rheumatic fever and rheumatic heart disease in India Indian Heart J. 1995;47:395–8
2. Jose VJ, Gomathi M. Declining prevalence of rheumatic heart disease in rural schoolchildren in India: 2001-2002 Indian Heart J. 2003;55:158–60
3. Misra M, Mittal M, Singh R, Verma A, Rai R, Chandra G, et al Prevalence of rheumatic heart disease in school-going children of Eastern Uttar Pradesh Indian Heart J. 2007;59:42–3
4. Bhatla N, Lal S, Behera G, Kriplani A, Mittal S, Agarwal N, et al Cardiac disease in pregnancy Int J Gynaecol Obstet. 2003;82:153–9
5. Malhotra M, Sharma JB, Tripathii R, Arora P, Arora R. Maternal and fetal outcome in valvular heart disease Int J Gynaecol Obstet. 2004;84:11–6
6. Sawhney H, Aggarwal N, Suri V, Vasishta K, Sharma Y, Grover A. Maternal and perinatal outcome in rheumatic heart disease Int J Gynaecol Obstet. 2003;80:9–14
7. Elkayam U, Bitar F. Valvular heart disease and pregnancy J Am Coll Cardiol. 2005;46:223–30
8. Warnes CALibby P, Bonow RO, Mann DL, Zipes DP. Pregnancy and heart disease Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 20078th ed Philadelphia PA WB Saunders:1967–82
9. Madazli R, Sal V, Cift T, Guralp O, Goymen A. Pregnancy outcomes in women with heart disease Arch Gynecol Obstet. 2009 [In Press]
10. Sawhney H, Aggarwal N, Suri V, Vasishta K, Sharma Y, Grover A. Pregnancy outcomes in women with heart disease Int J Gynaecol Obstet. 2003;80:9–14
11. Silversides CK, Colman JM, Sermer M, Siu SC. Cardiac risk in pregnant women with rheumatic mitral stenosis Am J Cardiol. 2003;91:1382–5
12. Siu SC, Sermer M, Harrison DA, Grigoriadis E, Liu G, Sorensen S, et al Risk and predictors for pregnancy-related complications in women with heart disease Circulation. 1997;96:2789–94
13. Al Kasab SM, Sabag T, al Zaibag M, Awaad M, al Bitar I, Halim MA, et al Beta-adrenergic blockade in the management of pregnant women with mitral stenosis Am J Obstet Gynecol. 1990;165:37–40
14. . The effect of digoxin on the mortality and morbidity in patients with heart failure. The Digitalis Investigation Group N Engl J Med. 1997;336:525–33
15. Reimold SC, Rutherford JD. Valvular heart disease in pregnancy N Engl J Med. 2003;349:52–9
16. Hameed A, Akhter MW, Bitar F, Khan SA, Sarma R, Goodwin TM, et al Left atrial thrombosis in pregnant women with mitral stenosis and sinus rhythm Am J Obstet Gynecol. 2005;193:501–4
17. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, et al 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease J Am Coll Cardiol. 2008;52:e1–142
18. Favaloro EJ, Bonar R, Aboud M, Low J, Sioufi J, Wheeler M, et al How useful is the monitoring of (low molecular weight) heparin therapy by anti-Xa assay. A laboratory perspective? Lab Hematol. 2005;11:157–62
19. Hammerstingl C. Monitoring therapeutic anticoagulation with low molecular weight heparins: Is it useful or misleading.? Cardiovasc Hematol Agents Med Chem. 2008;6:282–6
20. Barbour LA. Thromboembolism in pregnancy. ACOG Committee on Practice Bulletins--Obstetrics Int J Gynaecol Obstet. 2001;75:203–12
21. . American College of Obstetricians and Gynecologists Committee on Obstetric Practice. Antibiotic prophylaxis for infective endocarditis. ACOG Committee Opinion No. 421. Washington DC, November 2008 Obstet Gynecol. 2008;112:1193–4
22. Fawzy ME, Kinsara AJ, Stefadouros M, Hegazy H, Kattan H, Chaudhary A, et al Long-term outcome of mitral balloon valvotomy in pregnant women J Heart Valve Dis. 2001;10:153–7
23. De Souza JA, Martinez EE Jr, Ambrose JA, Alves CM, Born D, Buffolo E, et al Percutaneous balloon mitral valvuloplasty in comparison with open mitral valve commissurotomy for mitral stenosis during pregnancy J Am Coll Cardiol. 2001;37:900–3
24. Sutton SW, Duncan MA, Chase VA, Marce RJ, Meyers TP, Wood RE. Cardiopulmonary bypass and mitral valve replacement during pregnancy Perfusion. 2005;20:359–68
25. Gomar C, Errando CL. Neuroaxial anaesthesia in obstetrical patients with cardiac disease Curr Opin Anaesthesiol. 2005;18:507–12
26. Sharma SK, Gambling DR, Gajraj NM, Truong C, Sidawi EJ. Anesthetic management of a parturient with mixed mitral valve disease and uncontrolled atrial fibrillation Int J Obstet Anesth. 1994;3:157–62
27. Stout KK, Otto CM. Pregnancy in women with valvular heart disease Heart. 2007;93:552–8
28. Hermmings GT, Whalley DG, O’Connor PH. Invasive monitoring and anesthesia management of patients with mitral stenosis Can J Anaesth. 1987;34:182–5
29. Ngan Kee WD, Shen J, Chiu AT, Lok I, Khaw KS. Combined spinal-epidural analgesia in the management of labouring parturients with mitral stenosis Anaesth Intensive Care. 1999;27:523–6
30. Langesaeter E, Dragsund M, Rosseland LA. Regional anaesthesia for a Caesarean section in women with cardiac disease: A prospective study Acta Anaesthesiol Scand. 2010;54:46–54
31. Dresner M, Pinder A. Anaesthesia for caesarean section in women with complex cardiac disease: 34 cases using the Braun Spinocath spinal catheter Int J Obstet Anesth. 2009;18:131–6
32. Horlocker TT, Wedel DJ, Benzon H, Brown DL, Enneking FK, Heit JA, et al Regional anesthesia in the anticoagulated Patient Defining the risks.(The Second ASRA Consensus Conference on Neuraxial Anesthesia Anticoagulation) Rerg Anesth Pain Med. 2003;28:172–97
33. Blaise G, Langleben D, Hubert B. Pulmonary arterial hypertension: Pathophysiology and anesthetic approach Anesthesiology. 2003;99:1415–32
34. Orme RM, Grange CS, Ainsworth QP, Grebenik CR. General anaesthesia using remifentanil for caesarean section in parturients with critical aortic stenosis: A series of four cases Int J Obstet Anesth. 2004;13:183–7
35. Chestnut DH. Obstetric anesthesia: Principles and practice 20094th ed Philadelphia Mosby Elsevier:892–5
36. Secher NJ, Arnsbo P, Wallin L. Haemodynamic effects of oxytocin (syntocinon) and methyl ergometrine (methergin) on the systemic and pulmonary circulations of pregnant anaesthetized women Acta Obstet Gynecol Scand. 1978;57:97–103
37. Secher NJ, Thayssen P, Arnsbo P, Olsen J. Effect of prostaglandin E2 and F2alpha on the systemic and pulmonary circulation in pregnant anesthetized women Acta Obstet Gynecol Scand. 1982;61:213–8

Source of Support: Nil

Conflict of Interest: None declared.


Labour analgesia and caesarean section; mitral stenosis; pregnancy

© 2010 Indian Journal of Anaesthesia | Published by Wolters Kluwer – Medknow