Echocardiography has become the anesthesiologist’s most powerful hemodynamic monitor. It transforms invisible physiology into visual data, revealing real-time interactions between preload, afterload, contractility, and valvular function. In perioperative medicine, where every fluctuation in pressure or rhythm may destabilize a fragile circulation, echocardiography provides not merely diagnosis but predictive insight.
The patient under discussion represents a common yet complex scenario in modern anesthesia:
A post-transcatheter aortic valve replacement (TAVR) heart with a 20 mm MYVAL prosthesis,
Moderate degenerative mitral stenosis (MVA 1.6–1.8 cm²),
Mild mitral regurgitation (Grade I),
Mitral annular calcification (MAC),
Mild pulmonary hypertension (RVSP ≈ 28 + RAP),
Preserved left ventricular ejection fraction (64%), and
Grade I LV diastolic dysfunction.
For the anesthesiologist, these findings translate to a fixed inflow (MS) and regulated outflow (TAVR) system with narrow margins for hemodynamic tolerance. The combination demands exquisite balance between heart rate control, rhythm preservation, and volume optimization.
This chapter integrates the basic science, echocardiographic interpretation, and anesthetic application of such valvular pathology across varying emergency surgical risks.
The mitral valve complex is not a passive orifice; it is a dynamic structural unit linking atrial contraction to ventricular compliance. Its components function as an integrated mechanism that regulates unidirectional diastolic flow and prevents systolic backflow.
During diastole, the pressure gradient between LA and LV determines the rate of flow through the mitral orifice:
where ΔP = LA–LV pressure difference and R = diastolic resistance of the valve.
In a healthy valve, resistance is minimal (MVA 4–6 cm²). In mitral stenosis, even a small reduction in valve area exponentially increases resistance because flow is proportional to the square root of the pressure gradient (Bernoulli principle). Consequently, small increments in HR or flow demand cause disproportionate rises in LA pressure.
The anesthesiologist’s goal is to maintain a steady, low-resistance gradient—achieved by controlling heart rate, rhythm, and venous return.
Mitral valve pathology disturbs both diastolic filling and systolic ejection. The present patient demonstrates a predominantly stenotic lesion with a minor regurgitant component, producing a paradoxical combination of underfilling and backflow. Understanding these mechanisms at a cellular, chamber, and circulatory level is fundamental for anesthetic planning.
3.1.1 Hemodynamic Mechanism
Mitral stenosis (MS) narrows the diastolic inflow orifice, creating resistance between the pulmonary venous circulation and LV cavity. To maintain output, the LA must generate higher pressures, resulting in:
↑ LA pressure → pulmonary venous hypertension,
↑ pulmonary vascular resistance (PVR) due to vascular remodeling,
↑ RV afterload → tricuspid...
