In areas where rheumatic heart disease (RHD) is still prevalent, valvular heart disease affects about 2% by age 16, of which 65% have mitral regurgitation, 21% have aortic regurgitation, and 15% have mitral stenosis.1 PoCUS can help detect RHD,2 for which starting antibiotic prophylaxis with monthly penicillin G benzathine injections can dramatically reduce progression.3 In non-endemic areas, where RHD is rare, mitral regurgitation and aortic stenosis are the most prevalent valvular defects, both increasing with age, affecting about 9% and 3% of those over age 75, respectively.4
Surgery or other invasive procedures are the definitive treatment for significant valve disease and require referral to a capable specialty center. PoCUS enhances the clinical exam and helps generalists initiate optimal medical treatments sooner and identify patients to refer to specialty services. Conversely, if the pretest probability is low, PoCUS that includes color Doppler imaging (CDI), can identify those who do not need additional imaging to look for value disease.5,6 Judging when the pretest and posttest probability is low enough will depend on the operator's skill level and local standards of practice. When in doubt, refer for consultative imaging.
Plain B-Mode may reveal subtle or obvious signs of valve disease. These include leaflets or cusps that appear thickened, flailing backward, immobile, or not completely coming together. Color-Doppler imaging (CDI) mode reveals where high-speed blood flow occurs, significantly improving the ability to detect and confirm value disease. PoCUS should incorporate color Doppler whenever assessing the mitral and aortic valves. First, put the machine in the cardiac preset/mode, then obtain an optimal B-mode view, either PLAX or A4C, with the valve in question near the center of the image. After noting any clues of valve disease, change the mode to CDI and place the color box over the valve. The box should also include the preceding chamber when evaluating regurgitation. Look for a color jet that represents high-speed flow. Pay attention to the color hue, which signifies the direction of the flow. By convention, blues is flow away and reds towards (BART). If a jet is a mix of hues, it’s termed aliasing and represents high-velocity turbulent flow. Freezing a clip and scrolling through each frame can help visualize the abnormal jet.
Image 6.1 Parasternal long-axis view with subtle B-mode finding of a flailing posterior mitral valve leaflet in an elderly patient with hypertension and respiratory failure (A). Color-Doppler (CDI) mode identifies significant back-flow across the mitral valve, confirming mitral valve regurgitation (B).
Image 6.2 Parasternal long-axis view with subtle B-mode finding of incomplete closure of the aortic valve in a patient with acute respiratory failure and a to-fro murmur heard across the chest (A). Color-Doppler (CDI) mode identifies significant back-flow across the aortic valve, confirming aortic valve regurgitation (B).
PoCUS should identify obvious valve abnormalities. However, the CDI appearance of abnormal flow is influenced by multiple factors, such as whether the jet projects (eccentrically) along a chamber wall, the color scale and gain settings, and cardiac afterload, preload, and chamber compliance during the examination. Therefore, without advanced training and additional techniques, one should avoid assigning an exact severity. Instead, consider stating “but not fully defined” to signal the need for more imaging to define the defect. In this fashion, we would describe the valve disease in Image 6.1 as "flailing posterior MV leaflet with apparently large but not fully defined mitral valve insufficiency” and Image 6.2 as “apparently large but not fully defined aortic valve regurgitation.”
The mitral valve (MV) closes, generating the S1 sound to prevent retrograde flow into the left atrium during systole. The MV consists of two thin leaflets (anterior and posterior) arising from the surrounding mitral valve annulus. The chordae tendineae and papillary muscles (posterior-medial and antero-lateral) anchor these leaflets and prevent MV prolapse during systole. Mitral regurgitation (MR) or insufficiency is ‘functional’ or secondary when dilated left heart chambers and ventricular desynchrony (QRS prolongation) cause incomplete leaflet closure. MR is primary when it is due to leaflet perforation or cord rupture associated with degenerative changes, endocarditis, systemic inflammatory diseases, rheumatic heart disease, radiation, or congenital heart disease.
Chronic MR is the most common valve defect.1,4 It may be asymptomatic for 5-10 years due to compensatory cardiac changes, including LV and LA enlargement and increased LV ejection fraction. Decompensated chronic MR may mimic or coincide with progressive LV dysfunction. Acute MR presents with acute dyspnea and pulmonary edema, and a holosystolic murmur may be heard, loudest at the apex. PoCUS may reveal incomplete closure of the MV leaflets, a flailing leaflet associated with ruptured chordae, and an abnormal regurgitation jet in CDI mode.
Image 6.3 Parasternal long-axis view with B-mode shows abnormal movement of the mitral valve leaflets (A). CDI confirmed significant MR (B). An A4C view (C) also reveals abnormal mitral valve movements. Interpreting why there is MR is outside the scope of PoCUS, but endocarditis and RHD should be considered.
Treat pulmonary edema with oxygen, raising the head of the bed, and aggressive diuresis. Besides definitive valve replacement or repair, mitral regurgitation also benefits from LV afterload reduction, such as lowering blood pressure, using positive-pressure ventilation, or even an intra‐aortic balloon pump if available. It is also essential to consider and aggressively treat the underlying cause, such as heart failure causing chamber dilation with goal-directed medical therapy for HFrEF (note that MR will increase EF) or recurrent infections causing rheumatic heart disease with prophylactic penicillin injections.
Mitral stenosis is primarily associated with rheumatic heart disease (RHD) and has become rare in many high-resource settings.4 Stenosis or poor opening of the mitral valve usually progresses over years until it causes heart failure exacerbated by tachycardia or exercise with a high incidence of atrial fibrillation, thromboembolic disease, and pulmonary hypertension. A loud S1 and rolling, diastolic murmur, loudest at the apex, may be heard. Severe LA enlargement and elevated right-heart pressures displace the heart anteriorly against the chest wall, causing a palpable, even visible, parasternal heave and cardiomegaly with a straight left heart border on chest x-ray.
Image 6.4 Rheumatic heart disease with mitral stenosis where A4C (A) and PLAX (B) views reveal LA enlargement and thickened MV leaflets that do appear to separate.
PoCUS of significant mitral stenosis can reveal marked leaflet thickening, incomplete opening despite an anterior bulging motion of the MV leaflets, and color Doppler showing rapid forward flow across a relatively small part of the MV. However, do not confuse poor leaflet mobility with leaflets that barely open because of low overall forward flow.
Mitral stenosis slows LV filling, and patients with severe stenosis do worse when the relative time in diastole is shortened, which occurs when the heart rate increases. LV systolic function is usually intact, and pulmonary hypertension can be significant. As a result, LV afterload reduction can be harmful, especially when hypotension causes reflex tachycardia and impairs RV perfusion. Therefore, avoid vasodilators and positive-pressure ventilation in these patients. Pulmonary edema can improve with oxygen and diuretics. However, non-surgical treatment of mitral stenosis centers around heart rate and rhythm control to prevent tachycardia and give time for LV filling. Thromboembolic stroke associated with atrial fibrillation is also common and can be prevented with anticoagulation. It is also essential to provide monthly penicillin for those with mitral stenosis due to RHD.
The aortic valve (AV) closes (generating the S2 sound) to prevent retrograde flow back into the left ventricle during diastole. The AV normally consists of three cusps. However, some people have a bicuspid aortic valve with only two cusps, which increases the risk of aortic regurgitation (AR) or stenosis later in life.
It is easy to overlook clues of AR on B-mode imaging, especially when views are suboptimal. So, look for regurgitant flow with CDI over the aortic valve in optimized PLAX and A4C views.
Image 6.5 PLAX views of a patient with aortic regurgitation. With B-mode only (A), subtle findings are easily overlooked. The LV is spherical with reduced LVEF, and a dissection is visible in the ascending aorta (arrow). CDI (B) reveals apparent aortic regurgitation.
Chronic AR may be asymptomatic and well-tolerated until compensatory changes become inadequate. Patients with AR may exhibit signs of large stroke volume, wide pulse pressure, lower resting heart rate, and sometimes systolic hypertension. Regurgitant flow decreases as diastolic blood pressure drops, and tachycardia helps maintain forward flow by reducing the portion of time in diastole. Interestingly, a lower baseline diastolic blood pressure (≤60-65mmHg) and higher resting heart rate (≥70-80bpm) suggest more severe disease and are independent predictors of all-cause mortality. Still, patients with AR and systolic hypertension need antihypertensive treatments.7 Acute or decompensated AR causes pulmonary edema and hypotension, which requires urgent valve replacement. Consider positive pressure ventilation and aggressive efforts to maintain an adequate heart rate as a bridge to surgical treatment.
As populations age, aortic stenosis (AS) has become one of the most common forms of valvular heart disease. The following are all associated with developing AS.8,9
Image 6.6 PLAX view of a patient with LVH and aortic stenosis.
Aortic stenosis increases tension on the LV wall during systole. Over time, wall thickening helps relieve this stress. However, wall thickening impairs filling during diastole, which increases reliance on LA atrial pressure and sinus rhythm to fill the ventricle. The next chapter discusses this diastolic dysfunction in detail. In addition, greater wall tension and thickness increase oxygen demand, and eventually, demand ischemia limits LV function. Stenosis usually progresses without symptoms over years to decades. Symptoms eventually develop and progress rapidly with angina, lightheadedness with exertion, dyspnea, syncope, hypotension, and even sudden death. Aortic stenosis often causes a characteristic systolic murmur. PoCUS may reveal clues suggesting aortic valve disease, including thickened and calcified (hyperechoic) aortic valve cusps, reduced systolic opening of aortic valve cusps, and a bicuspid aortic valve.
Patients with suspected aortic stenosis should get consultative imaging. The only effective treatment for severe AS is surgical or percutaneous valve replacement. While awaiting valve replacement, patients with aortic stenosis benefit from treatment of hypertension and co-existing coronary artery disease, if present. However, only use diuretics to treat volume overload as patients with severe AS and LVH may be particularly vulnerable to hypovolemia-induced hypotension.10