Echocardiography is the first investigation for suspicion of valvular disease; it brings important information both about the cause of valve dysfunction and about its severity.
In emergency, cardiac ultrasound has many advantages: it can be performed at the bedside, being widely available, it can be performed standing (orthopnea), is non-invasive. Can be performed by anesthesiologists intraoperatively. If transthoracic echocardiography (TTE) did not confirm a high clinical suspicion of severe valvular damage, especially dysfunction of the prosthesis, it is necessary transesophageal echocardiography (TEE).
Valvular emergencies are generally described as hemodynamic instability. It refers to the acute pathology of native valve and also prosthetic valve, either organic or metallic. Chronic valvular lesions rarely presents as acute hemodynamic deterioration, only in the final stages; Generally, this is caused by acute mitral and aortic regurgitation. Always, if unexplained acute pulmonary edema, ultrasound should be performed urgently!
The following signs (readily apparent on ultrasound) are common in acute regurgitations (which lead to left ventricle overload): severe regurgitated jet (the eccentric one may be understated), hyperdynamic left ventricle (in the absence of previous affection), pulmonary hypertension and possibly increased and hypokinetic right ventricle; is observed the pathology which caused the regurgitation, not always obvious to TTE, TEE is required.
Acute mitral regurgitation mechanisms: the spontaneous rupture of chordae (in particular in mitral valve prolapse), endocarditis (chordae rupture or perforation of the cusps, always in the case of endocarditis all valves need to be examined because the infection can spread from one to another, we can detect a vegetation, but not always, often is necessary TEE), complications of myocardial infarction (rupture of chordae or papillary muscles or in inferior myocardial infarction mitral regurgitation may occur due to kinetic disorder), trauma (ruptured chordae or cusps).
Mechanisms of acute aortic regurgitation are: endocarditis, aortic dissection type A and traumatic (fracture of cusps). In type A of aortic dissection, aortic regurgitation occurs by pulling the cusps by dilated aortic root, changing the geometry of valve or prolapse through the valve of dissection fold ,possibly involving the insertion of the cusps; usually,TTE detects severe aortic regurgitation , but it requires TEE to clarify its mechanism.
Prosthetic dysfunction occurs due to warping (for metallic prostheses: by thrombus, pannus, vegetation, that may cause only obstruction or association with regurgitation, and for the biological prostheses: vegetation, increased risk of warping appears especially when there is low cardiac output, atrial fibrillation and mitral position) or valvular regurgitation by the appearance of para-valvular leaks; it generally occur due to infectious endocarditis or suture failure, when the valve ring is very calcified; when there is a large leak, endocarditis should necessarily be sougth.
Echocardiography possible signs: de novo hiper-contractility, viewing of a jet with high velocity, “rocking valve” if it emerged from a large circumferential area, vegetation or degeneration. The prosthetic mitral regurgitant jets can be unnoticed at TTE and TEE is required; in patients with aortic and mitral metal prostheses, the aortic is better viewed in TTE because acoustic shadow given by mitral prosthesis at TEE.
Echocardiography is the investigation of choice in these pathologies. With higher accuracy, but with much lower availability it can be performed transthoracic 3D ultrasound and and the gold standard is 3D transesophageal echocardiography.