Mitral stenosis
Anesthetic relevance


Anesthetic management

Preserve preload, maintain NRS, rate control to optimize diastole, avoid elevations in PVR. Preinduction arterial line. consider TEE.



Signs and symptoms

DOE, orthopnea, fatigue, peripheral edema, JVD




Diuresis, B-blocker or CCB for rate control, anticoagulation in Afib and/or LAA thrombus commisurotomy, valve replacement

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Mitral Stenosis is the narrowing of the outflow tract of the left atrium due to thickening/calcification of the mitral valve.

Anesthetic implications

Preoperative optimization

Examination highly suspicious for mitral stenosis should be further evaluated with Transthoracic echocardiography even if the patient is asymptomatic. TTE studies can confirm diagnosis and determine disease severity. In severe disease, commisurotomy or valve replacement should be considered prior to proceeding with elective surgery.

Intraoperative management


• Pre-induction A-line should be placed for close hemodynamic monitoring

• If severe, TEE can be used to guide fluid resuscitation and maintain euvolemia

• May consider central line placement for monitoring CVP and/or PA catheter


Maintain NSR since atrial systole contributes about 30% of LV filling, the onset of Afib can greatly reduce CO

Maintain Euvolemia since hypovolemia reduces preload and hypervolemia worsens mitral outflow leading to back flow failure

Avoid Tachycardia using b-blockers, or CCB to optimize diastole and preserve LV preload

Avoid elevated PAP as these patients are prone to exaggerated pulmonary hypoxic vasoconstriction. Therefore ensure adequate depth of anesthesia, avoid acidotic states, and avoid hypoxia/hypercapnia

Postoperative management

Depending on the severity of the lesion and the intraoperative course, patients may benefit from close hemodynamic monitoring in the acute post-operative phase.

Related surgical procedures

Mitral valve repair or replacement

Transcatheter mitral valve replacement

Cutaneous mitral ballon commissarotomy


The most common cause of MS is rheumatic heart disease. Despite decreases in the incidence of rheumatic heart diseases, MS remains prevalent in industrialized cases.

Decreased Left ventricular filling reduces preload, which decreases CO. Due to reduced LV filling, patients are susceptible to loss of atrial "kick", drastic changes in volume status, and tachycardia.

Elevated Left Atrial pressures leads to increased pulmonary artery pressure and development of pulmonary edema. Continual elevation in PVR leads to RV failure associated with TR and leftward shift of the inter ventricular septum, which subsequently decreases CO. Further elevation of LA pressure increases LA volume, which places patient at higher risk for developing Atrial fibrillation and LA thrombus.

Signs and symptoms


• Loud S1

• Early opening snap

• Rumbling diastolic murmur best auscultated at the PMI

• If severe, features of Cor Pulmonale

• Malar flush

• Prominent JVD

• Hepatosplenomegaly (±painful)

• Peripheral edema


• Many patients remain asymptomatic until they become pregnant or develop Atrial fibrillation

• Symptomatic patients Initially present similarly to Heart failure

• Dyspnea on exertion

• Orthopnea

• Paroxysmal nocturnal dyspnea

• Fatigue


Suspicion for mitral stenosis can be appreciated on physical examination. Diagnosis and disease severity can be determined using Echocardiography

Severity of Mitral Stenosis by Echocardiography
Degree Mitral Valve area (cm2) Mean gradient (mmHg) Pulmonary Artery pressure (mmHg)
Mild > 1.5 <5 <30
Moderate 1.0-1.5 5-10 30-50
Severe < 1.0 > 10 > 50


Asymptomatic patients with mitral stenosis do not require treatment. Intervention is required in patients with symptoms who have MS with valve area < 1.5 cm.


Those with mild symptoms can usually be controlled with diuresis. In the presence of Sinus tachycardia or Atrial fibrillation consider b-blockers or CCB for rate control to optimize diastolic function. For patients with Atrial fibrillations, LAA clot, and/or History of embolism consider anticoagulation with Vitamin K antagonist (not DOAC).


Percutaneous Balloon Commisurotomy is indicated young patients and/or those without heavy calcification, subvalvular distortion, LA thrombi, and/or severe MR. Outcomes are equivalent to those of more invasive procedures. This procedure requires catheter to pass transseptally from RA to LA, creating an ASD. ~75% of ASD close spontaneously, majority of remaining only produce clinically trivial left to right shunts, but percutaneous closure is sometimes necessary. NOTE: when Mitral stenosis 2/2 annular calcification there is NO benefit from percutaneous commisurotomy because there is no commissural fusion.

Surgical Commisurotomy is indicated in patients with severe subvalvular disease, valvular calcification, and/or LA thrombi. The procedure is performed ultimately via a dilator being passed through the commisure. Can either be approached directly via sternotomy (open commisurotomy) or indirectly through the LV via thoracotomy (closed commisurotomy). NOTE: when Mitral stenosis 2/2 annular calcification there is increased risk, making optimal medical therapy and Transcutaneous mitral valve replacement preferred treatment option.

Valve replacement indicated for patients with severe morphologic valve changes that makes balloon or surgical commisurotomy contraindicated. Chan et al. suggested better echocardiographic outcomes but no difference in mortality at 2.5 years but unable to uncover incidence of complications associated with valve replacement due to short follow up interval[1]. Those that receive a mechanical valve will require lifelong warfarin therapy. Whereas those that receive Bioprosthetic valve require warfarin for 3-6 months postoperatively.


Without treatment, the progression from mild symptoms to severe disability is approximately 7-9 years. Poor prognosis for those with anatomical impairments (Wilkison score ≥8), and peak mean gradient of ≥10mmHg[2],with a 10-year survival rates ranging from 34% to 61% and 20-year rates between 14% and 21%[3][4]. Outcomes are dependent upon pre procedural age, pre procedural functional status, history of pulmonary HTN, and degree of concomitant MR. Some data exists that statin therapy may slow progression[5].


• <50% pts have isolated MS; remaining have concomitant Mitral regurgitation (See: Mitral regurgitation)

• Up to 25% of pts have involvement of Aortic valve (See: Aortic stenosis,Aortic regurgitation)


  1. Chan, Vincent; Ruel, Marc; Mesana, Thierry G. (2011-10). "Mitral Valve Replacement Is a Viable Alternative to Mitral Valve Repair for Ischemic Mitral Regurgitation: A Case-Matched Study". The Annals of Thoracic Surgery. 92 (4): 1358–1366. doi:10.1016/j.athoracsur.2011.05.056. ISSN 0003-4975. Check date values in: |date= (help)
  2. Gordon, Stephen P.F.; Douglas, Pamela S.; Come, Patricia C.; Manning, Warren J. (1992-04). "Two-dimensional and Doppler echocardiographic determinants of the natural history of mitral valve narrowing in patients with rheumatic mitral stenosis: Implications for follow-up". Journal of the American College of Cardiology. 19 (5): 968–973. doi:10.1016/0735-1097(92)90280-z. ISSN 0735-1097. Check date values in: |date= (help)
  3. "THE COURSE OF MITRAL STENOSIS WITHOUT SURGERY: TEN- AND TWENTY-YEAR PERSPECTIVES". Annals of Internal Medicine. 52 (4): 741. 1960-04-01. doi:10.7326/0003-4819-52-4-741. ISSN 0003-4819.
  4. Olesen, K. H. (1962-05-01). "THE NATURAL HISTORY OF 271 PATIENTS WITH MITRAL STENOSIS UNDER MEDICAL TREATMENT". Heart. 24 (3): 349–357. doi:10.1136/hrt.24.3.349. ISSN 1355-6037.
  5. Antonini-Canterin, Francesco; Moura, Luis M.; Enache, Roxana; Leiballi, Elisa; Pavan, Daniela; Piazza, Rita; Popescu, Bogdan A.; Ginghină, Carmen; Nicolosi, Gian Luigi; Rajamannan, Nalini M. (2010-05-18). "Effect of Hydroxymethylglutaryl Coenzyme-A Reductase Inhibitors on the Long-Term Progression of Rheumatic Mitral Valve Disease". Circulation. 121 (19): 2130–2136. doi:10.1161/circulationaha.109.891598. ISSN 0009-7322.