Pulmonic Stenosis

Created on Tue, 06/30/2015 - 17:11
Last updated on Wed, 05/16/2018 - 01:43

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Keep them well filled, maintain good contractility with milrinone and aim for a high diastolic pressure.

Physiological consequences of pulmonic stenosis

The pulmonic valve is not one usually prone to isolated stenosis, and when it is found it is usually a congenital thing. The normal gradient across it is about 5-10mmHg, with a systolic RV pressure under 30mmHg. It can get up to 60% stenosis before anybody notices symptoms. A gradient of 50mmHg is considered mild, between 50 and 100 mmHg is considered moderate, and over 100mmHg is considered severe pulmonic stenosis.

As with aortic stenosis, a concentric hypertrophy of the prevalve ventricle occurs. The RV becomes hypertrophic and diastolic RV failure develops. Subendocardial blood supply to the RV becomes compromised and it becomes more prone to ischaemia.

Strategies to compensate for the physiological consequences of pulmonic stenosis

Preload

Preload needs to be kept high. The diastolic failure of the right ventricle relies on higher filling pressures, in view of decreased RV compliance.

Rate

On one hand, the heart rate needs to be fast to maintain an adequate pulmonary forward flow; on the other hand it needs to be slow to allow diastolic filling of the RV, and to allow subendocardial perfusion during relaxation. Which is more important? This will be an individual thing. Experiment with the patient. There may be a magic number.

Rhythm

Yes, the noncompliant RV is dependent to some extent on the right atrium for its diastolic filling. However, many of these patients have AF, and you must work with what you have.

Contractility

Contractility of the right ventricle is all-important. It tends to already be in a hypertrophied hypercontractile state. Anything which diminishes this contractility is undesirable. Similarly, evidence of poor RV contractility should be interpreted as an acute milrinone deficiency.

Afterload

Systemic and pulmonary vascular resistance is meaningless, as the stenosis is at the level of the valve will not respond to pharmacologic intervention of vascular structures beyond that valve. Having said this, it is important to maintain a certain systemic diastolic pressure. If this is allowed to decrease, coronary filling will be impaired and the RV subendocardium will not be well perfused.

 

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)

Stiefel, Alexander, and Volker AW Kreye. "On the haemodynamic differences between sodium nitroprusside, nitroglycerin, and isosorbide nitrates." Naunyn-Schmiedeberg's archives of pharmacology 325.3 (1984): 270-274.