Mitral stenosis (MS) is one of the most unforgiving cardiovascular lesions encountered by anesthesiologists. Unlike many cardiac conditions where the heart dynamically adjusts output to surgical stress, MS traps the circulation within a fixed cardiac output state.
This “fixed-output” physiology is what makes anesthesia dangerous — and fascinating. A heart with MS cannot increase flow when systemic vascular resistance falls, nor can it tolerate rapid shifts in venous return. Every heartbeat, every breath, and every milliliter of fluid must be managed with intention.
1. High-Risk Condition:
Mitral stenosis transforms a compliant left atrium into a high-pressure chamber. This setup produces pulmonary venous congestion and reduces systemic perfusion. Even mild surgical stress or tachycardia may precipitate pulmonary edema or hypotensive collapse.
2. Risk of Complications:
Elevated left atrial pressure (LAP) chronically transmits backward into the pulmonary circuit, increasing pulmonary vascular resistance (PVR) and straining the right ventricle (RV). When the RV fails, the circulation spirals downward.
3. The Anesthesiologist’s Role:
Anesthesia in MS is not merely about keeping the patient asleep; it’s about synchronizing physiology. Every anesthetic choice alters HR, preload, or vascular tone — and in MS, even small deviations ripple through the system.
4. Consequences of Mismanagement:
Tachycardia shortens diastole, raising LAP. Hypoxia and hypercarbia constrict pulmonary vessels, worsening RV strain. Overzealous fluids flood the lungs; underhydration starves preload. Missteps can escalate to acute pulmonary edema, right heart failure, or death.
Mitral stenosis limits flow across the mitral valve, thereby restricting cardiac output (CO = HR × SV). Because stroke volume (SV) is fixed by the mechanical obstruction, CO becomes rate-dependent only within narrow limits.
According to Fick’s principle:
Oxygen delivery (DO₂) = CO × CaO₂
Any limitation in CO directly reduces systemic oxygen delivery. This is why hypotension in MS translates rapidly into tissue hypoxia, despite normal arterial oxygen content.
At the same time, sympathetic activation (triggered by anxiety, pain, or hypoxia) increases heart rate and contractility — but in MS, this response worsens congestion. The condition inverts normal compensatory physiology: what usually helps (tachycardia, high flow) here becomes harmful.
In effect, mitral stenosis converts the heart-lung system into a closed hydraulic circuit with little tolerance for flow variation — the anesthesiologist becomes the physiologic engineer maintaining that circuit.
References
Carabello BA. Modern management of mitral stenosis. Circulation. 2005;112(3):432–437.
Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update on the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2008;52(13):e1–e142.
Guyton AC, Hall JE. Textbook of Medical Physiology. 14th ed. Philadelphia: Elsevier; 2021.
West JB. Respiratory Physiology: The Essentials. 10th ed. Lippincott; 2016.
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