Echocardiography is an effective means of assessing cardiac valve function. It is useful for a rapid qualitative assessment or a more comprehensive assessment for all forms of valve function using transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE). Doppler assessment allows an accurate quantitative measurement of the severity of stenotic and regurgitant lesions. The extent to which the critical care echocardiographer applies the sophisticated tools of the cardiologist to assess valvular heart disease is highly variable. By training, background, and interest, cardiologists often take the lead in this aspect of echocardiography. However, the intensivist who performs echocardiography should have some fundamental competence in assessing valve function, as many patients in the intensive care unit (ICU) may have valve dysfunction that adversely impacts their cardiopulmonary status.

In general, the intensivist will be interested primarily in the identification of catastrophic valve failure or valve dysfunction that is sufficiently severe to impact the hemodynamic functioning of the patient. Conversely, the identification of lesser degrees of valve disease or normal valve function are also of interest, as the intensivist may then determine that valve failure is not a contributing factor to the patient’s critical illness. This chapter will review the echocardiographic assessment of valve function from the perspective of the bedside intensivist.

Intensivists who perform critical care echocardiography (CCE) will typically demonstrate competence in basic CCE (several standard two-dimensional [2-D] views without comprehensive training in Doppler), but may also have competence in advanced CCE (see also Chapter 4). The latter is equivalent to level 2 training by standard cardiology criteria.¹ Intensivists who have basic training in echocardiography have a limited ability to assess valve function. Without training in quantitative spectral Doppler measurements, the basic-level examiner can identify obvious mechanical failure of the mitral valve (MV; e.g., a flail leaflet, ruptured chordae, or ruptured papillary muscle) or obvious aortic valve (AV) disruption. Severe stenosis of these valves may also be apparent. By definition, intensivists with training in basic echocardiography do not have comprehensive Doppler training and lack the ability to perform quantitative measurements of valve function.

The qualitative assessment of valve function is, however, in the domain of the basic critical care echocardiographer and may be carried out using color Doppler. This is not to suggest that the use of color Doppler is straightforward and without nuance. The pitfalls of color Doppler include gain settings, wall jet effects,² angle effects, and shadowing by surrounding structures, such as prosthetic valve apparatus or a calcified annulus, and are not intuitively obvious. Of particular concern with these pitfalls is that the echocardiographer may miss a severe valvular lesion due to misinterpretation of the color Doppler image. Thus, a key cognitive skill for the basic critical care echocardiographer is to recognize when to call for a consultation from a more experienced echocardiographer. If there is the possibility of significant valve dysfunction, a comprehensive study should be performed by an echocardiographer with advanced training.

Intensivists with proficiency in advanced CCE have, by definition, the capability to assess valve function that is similar to that of a fully trained cardiology echocardiographer. This proficiency may be particularly useful when immediate cardiology echocardiography services are not available. The advanced intensivist echocardiographer who is directly involved at the patient’s bedside is also able to immediately perform the study. Patients with severe valve failure may have life-threatening hemodynamic failure requiring prompt intervention, such as vasoactive medication, mechanical assist devices, or valve replacement. This cannot wait for the convenience of a delayed echocardiogram.

A common indication for bedside echocardiography in the ICU is to identify a cause for cardiopulmonary failure. The assessment of valve function is a key part of the bedside examination for several reasons. First, severe valve failure may be the primary cause of the shock state or respiratory failure. Early recognition of severe valve failure may allow for lifesaving interventions. Second, significant valve dysfunction may combine with another disease process to worsen cardiopulmonary failure. It is essential that the coexisting valve lesion be identified, as this may have a major influence on management. Finally, the absence of significant valvular dysfunction is useful information in a patient with hemodynamic failure.

The focus here is on the identification and quantification of major valve failure, as this is the most immediate concern of the bedside critical care clinician. Comprehensive assessment of valve function requires training in Doppler analysis, so some of the following discussion assumes interest or prior knowledge in advanced CCE.

The evaluation of the TV focuses on the assessment of tricuspid regurgitation (TR), as tricuspid stenosis is an uncommon lesion. The echocardiographic examination of the TV starts with 2-D analysis of the valve and support structures. A flail leaflet, lack of coaptation, vegetation or mass, right ventricular or right atrial (RA) dilation, tricuspid annular calcification, or the presence of hardware (pacer wire, valve repair/replacement), all suggest the possibility of significant TR. The 2-D study includes examination of the valve from multiple sites: parasternal long- and short-axis, apical four-chamber, and subcostal. The severity of TR by color Doppler is classed as mild, moderate, and severe. It is important to properly set the color gain and to interrogate the jet at multiple angles. The severity of TR may be measured semiquantitatively by measuring the color jet area.³ Minimal TR may often be detected in normal individuals.⁴ A simple “eyeball” method of judging severity is to consider that TR is severe when the jet hits the back wall of the RA or occupies the entire RA (Figure 15-1 and Video 15-1). Severe TR is often associated with volume overload of the right ventricle; although this finding is not specific to TR. Spectral Doppler of the TR jet may provide additional information of severity. If the intensity of the continuous-wave (CW) Doppler TR signal is greater than that of the inflow signal, or if the CW TR jet has a truncated downslope, the TR is likely to be severe. Measurement of the CW jet velocity permits estimation of pulmonary arterial systolic pressure (PASP). However, PASP does not necessarily correlate with the severity of TR. In theory, the severity of TR is amenable to quantitative measurements using the continuity principle or proximal isovelocity surface area (PISA) method. In practice, this is seldom performed or required in the ICU setting.

The evaluation of the PV generally focuses on assessment for pulmonic valve regurgitation (PR), as PV stenosis is uncommon. Trace PR is often detected in normal individuals. More severe PR may be seen with endocarditis or pulmonary hypertension. The echocardiographic examination of the PV starts with 2-D imaging of the valve. Rarely, a vegetation may involve the valve, or a leaflet prolapse may be identified. The PV is difficult to image with 2-D technique and is usually limited to the parasternal short-axis view and a short-axis view from the subcostal region. Color Doppler is the primary means of detecting PR (Figure 15-2 and Video 15-2). The subcostal approach is frequently a superior angle for Doppler analysis because the interrogation line may be placed parallel with the blood flow through the PV and proximal pulmonary artery. Regurgitation is detected by color Doppler and is classed as trace, mild, moderate, or severe.³ Because PR usually has minimal hemodynamic consequence, clinical echocardiographers often use an “eyeball” approach to grading the severity of PR. Spectral Doppler analysis of valve function is not generally used to assess the severity of PR. However, spectral Doppler of the PV area is important for other reasons, such as the measurement of cardiac shunts, pulmonary artery diastolic pressure, and indirect evidence for pulmonary arterial hypertension.

Aortic stenosis is a common valvular lesion in the critical care unit. When it is severe, it has major hemodynamic consequences. When it coexists with other causes of shock, such as distributive shock, it complicates hemodynamic management. Many patients come to the ICU with the diagnosis already established. However, in others, it is unknown at the time of presentation. The intensivist with basic-level echocardiography training may suspect the diagnosis by 2-D scanning. The stenotic valve is often hyperechoic or heavily calcified with obviously reduced movement (Figure 15-3 and Video 15-3).

Advanced level training is required for a complete assessment of the AV. This begins with 2-D study to rule out sub- or supravalular stenosis or a stenotic bicuspid valve, which lack the characteristic 2-D features of typical AS. However, these entities have the same physiological consequence. Included in the 2-D examination is planimetry of the valve area in short axis both by TTE or TEE.⁵

Three methods for identifying severe AS exist. Spectral Doppler analysis is the most reliable method of identifying severe AS. As the AV area narrows, the velocity of blood flow through it rises. The peak velocity across the valve is measured with CW Doppler and reliably reflects the pressure gradient across the valve according to the modified Bernoulli equation.⁶ A second method for quantification of AS is the continuity equation.⁷ This is based on the principle that the stroke volume measured at one point in the heart should equal the stroke volume at another point in the heart (barring shunt or valvular regurgitation). A final method compares the velocity (or velocity time integral [VTI]) of the left ventricular outflow tract (LVOT) to that of the AV.⁸

Commonly accepted values indicating severe AS include⁹:

1. 
   

   Peak AV velocity >4.5 m/s.

   
   
2. 
   

   Mean pressure gradient across the AV >50 mm Hg.

   
   
3. 
   

   AV area <0.75 cm²

   
   
4. 
   

   LVOT VTI/aortic VTI <0.25.

Accurate assessment of AS requires skill in advanced echocardiography. Common pitfalls include underestimation of the peak velocity and mean pressure gradient due to poor CW Doppler interrogation angle. The AS jet may also be eccentric; therefore, the examiner must use multiple points of measurement, including the suprasternal and right parasternal sites. This may require the use of a small, nonimaging CW transducer. Further, assessing AS is frequently more difficult using TEE, compared to TTE which may provide more parallel alignment with blood flow through the valve. Accurate measurement of the LVOT diameter is required, as any error is squared in the calculation of the LVOT area. The LVOT VTI may be overestimated if the pulsed wave (PW) sample volume is placed too close to the AV with resulting measurement of flow acceleration near the valve orifice. Patients with poor LV function and AS may have pseudosevere AS that improves when the measurements are made during dobutamine infusion.¹⁰

Trace or mild clinically inconsequential AR by color Doppler analysis is a common finding of CCE. On the other hand, acute severe AR may be immediately life threatening because the LV has no time to adapt to the sudden volume overload, resulting in fulminant pulmonary edema compounded by a low-flow state. The aortic balloon pump is specifically contraindicated with severe AR, and urgent valve replacement may be life saving. Chronic severe AR is often well tolerated because the LV has had time to dilate; and, with the maintenance of good LV function, forward flow is maintained without elevation of hydrostatic pressure in the lung. However, chronic severe AR may eventually lead to hemodynamic failure. When it coexists with other causes of shock, it may complicate hemodynamic management. The degree of regurgitation is afterload sensitive, so that the identification of significant AR has an important influence on acute hemodynamic management.

The evaluation for AR begins with the 2-D examination. Dilation of the aortic root, proximal aortic dissection (Figure 15-4 and Video 15-4), abnormal valve architecture, noncoaptation or prolapse of valve leaflets (Figure 15-5 and Video 15-5), or vegetation (Figure 15-6 and Video 15-6), all suggest the possibility of significant AR. M-mode findings of severe AR include anterior MV diastolic fluttering, early closure of the MV, and the presence of a B-wave on M-mode of the MV. AR may occur due to dilation of the aortic ring with valvular incompetence from nonapposition of the leaflets. Valve anatomy may be normal in this situation. Alternatively, AR may occur due to structural failure of the valve itself from such factors as endocarditis, rheumatic heart disease, Marfan’s syndrome, congenitally abnormal valves, degenerative calcific changes, or aortic dissection. None of these anatomic abnormalities allow determination of the severity of AR.