Mitral Stenosis

Created on Tue, 06/30/2015 - 17:07
Last updated on Wed, 05/16/2018 - 00:54

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Keep a normal heart rate, be careful with fluids, use milrinone and avoid AF like the plague.

Physiological consequences of mitral stenosis

The diastolic filling of the left ventricle is impaired in mitral stenosis, with predictably negative effects on stroke volume and cardiac output. The diastolic removal of blood from the pulmonary circulation is similarly impaired. These people develop pulmonary oedema at the drop of a hat, particularly if they develop atrial fibrillation.

As for the aortic valve, the mitral valve area is measured as an index to body surface area, and is represented as cm2/m2.

Mild mitral stenosis is usually well compensated. At a valve index of around 1-2 cm2/m2 the patients tend to notice dyspnoea with exercise, because pressure begins to increase in the left atrium. Atrial dilatation results in a propensity towards AF, which is totally counterproductive.

Moderate mitral stenosis (a valve index below 1.5 cm2/m2) is usually associated with some degree of congestive heart failure. The left atrium is dilated, and pulmonary pressures rise, producing pulmonary arterial hypertension and right ventricular failure. The onset of AF can lead to hemodynamic instability due to loss of the "atrial kick".

Severe mitral stenosis (a valve index of less than 1.0 cm2/m2)is a major problem. Typically, symptoms are present even at rest. Cardiac output is reduced even in the absence of AF; there is simply not enough diastolic filling. The right ventricle dilates hideously, pushing the septum into the left chambers, decreasing LV compliance even further.

It is said that a mitral valve area of 0.3 to 0.4 cm2 is the smallest valve area compatible with life. 

Strategies to compensate for the physiological consequences of mitral stenosis

Preload

Forward flow relies on adequate preload. However, this is a delicate balance. Mitral stenosis patients already have increased pulmonary vascular pressures, and additional preload may be dangerous. Careful fluid boluses are required.

Rate

Diastolic filling of the left ventricle is fixed. One cannot alter the volume which fills the chamber. However, in order to fill it even with this small volume, time is required. Thus, tachycardia is to be avoided (because diastolic filling will be inadequate at rapid rates).

However, remember the fixed stroke volume. Without being able to manipulate stroke volume you are left with hear rate as the only determinant of cardiac output you can play with. Thus, sometimes you cannot run these people at a slow rate because their cardiac output will drop.

So, ideally, a rate of 70 would be a healthy compromise. There is no evidence for this - its an arbitrary number.

Rhythm

As one might expect, the atrium is all-important in this condition. Your whole body ends up run by your atrium. Sinus rhythm is vital. If AF develops, it is to be dealt with swiftly and harshly.

Contractility

With a stenotic mitral valve and fixed stroke volume, contractility becomes somewhat less important for the left ventricle. However, it is not unimportant. In the late stages of the disease the LV contractility becomes impaired, and some inotrope support becomes essential when the patient is critically ill.

The inotropes probably play a greater role in the management of right ventricular dysfunction. As pulmonary pressures rise, RV contractility becomes more important, as it will assist LV preload. In this context, inotropes (and particularly milrinone, with its pulmonary vasodilator properties) become important.

Afterload

In these people, the afterload is less important. In response to low cardiac output, the peripheries are already rather vasoconstricted. Adding more vasopressor to this situation will do little to help. The blood pressure is low not because of peripheral vasomotor tone, but because the forward flow though the mitral valve is fixed.

RV afterload is a special matter, and excesses in RV afterload are to be avoided. Any pulmonary vasoconstriction has an exaggerated effect on the cardiac output, particularly hypoxic vasoconstriction. Thus, avoid hypoxia, and make use of the pulmonary vasodilator properties of your inotropes.

 

References

Moore and Martin's chapter on valvular disease in "A Practical Approach to Cardiac Anaesthesia" is a must-read

(in general, that book is awesome)