POCUS for Aortic Stenosis

Authors: Monica Lopez, MD (EM PGY-2, McGovern Medical School at The University of Texas Health Science Center at Houston), Cody Dornhecker, MD, MPH (Emergency Medicine Attending Physician, Mercy Hospital South, St. Louis, MO), Kimberly A. Chambers, MD (Clinical Assistant Professor of EM, McGovern Medical School at The University of Texas Health Science Center at Houston), Richard Gordon Jr., MD (Associate Professor of EM and Ultrasound Fellowship Director, McGovern Medical School at The University of Texas Health Science Center at Houston) // Reviewed by: Stephen Alerhand, MD (@SAlerhand); Manny Singh, MD (@MPrizzleER); Brit Long, MD (@long_brit)

Case

An 83-year-old Caucasian male with a past medical history of hypertension, diabetes, atrial fibrillation, and prior pacemaker placement presents with a complaint of near syncope. He has had 3 episodes, 1 daily for the last 3 days. Each event occurred after walking 50 to 100 feet, which he was able to do previously. The symptoms resolve when he stops to rest. The first episode was associated with a left-sided chest pain and shortness of breath.

His vital signs are within normal limits, and his exam reveals a 4/6 systolic murmur and trace bilateral lower extremity edema. Initial workup that included CBC, BMP, troponin, EKG, and CXR were unremarkable. Bedside cardiac ultrasound was performed and revealed the following (Figure 1):

Figure 1 – Parasternal Long axis

Epidemiology and Pathophysiology

Amongst the noise and chaos of a busy Emergency Department (ED), it is easy to overlook cardiac valve disorders. Aortic stenosis (AS), in particular, is the most common valvulopathy in developed countries and has the potential to cause significant morbidity and mortality. Some estimates report that AS may occur in 2-3% of individuals over 65 years and can be present in > 10% of those ≥ 80 years old.¹ In the United States and other developed countries, conventional cardiac risk factors such as hypertension, hyperlipidemia, and diabetes predispose the valve to degenerative calcifications. Though rare in developed nations, rheumatic heart disease is a common risk factor for aortic stenosis in developing nations. While AS is an uncommon disease among the young, it may be present in those with congenital heart disease or a bicuspid aortic valve.^2,3,4

Regardless of the primary cause, the result is a reduction in aortic valve orifice area, limiting blood’s entry into the systemic circulation. A reduction in the aortic valve area is often progressive, which causes a higher aortic transvalvular gradient and increasing left ventricular (LV) afterload. Initially, the pressure overload is accommodated through concentric LV hypertrophy, but at the cost of further increased LV filling pressure and eventual compromised diastolic function. The natural history of aortic stenosis is a vicious cycle of LV dilation, resulting in a further reduction in LV function, cardiac output, increased filling pressure and myocardial demand, with a final pathway of heart failure and death of the patient.^2,3,5

Clinical Features

Aortic stenosis may exist for years, even in a severe state, with no symptoms or subtle symptoms such as decreased exercise tolerance or dizziness.  As the disease advances, the patient will experience more alarming symptoms such as chest pain and syncope. The classic triad of aortic stenosis – syncope, angina, dyspnea, “SAD symptoms” –  is associated with late stage disease.⁶ It is at this point where the diagnosis is critical because, if left untreated, decline can be steep. Alternatively, if the valve is replaced before there is irreversible damage to the myocardium, the patient may return to baseline function and typical life expectancy. Late stage symptoms are consistent with other forms of heart failure and can include sudden death.^2,3

Physical exam findings may vary greatly and be difficult to detect. The murmur associated with AS is a crescendo-decrescendo systolic ejection murmur heard best at the right upper sternal border and radiating to the carotids. This classic murmur is often heard in the mild to moderate disease state. Advanced AS may be associated with a less audible murmur secondary to a reduced ejection fraction. A patient may also exhibit a displaced point of maximal impulse, pulsus parvus et tardus (diminished carotid pulse with delayed upstroke), and a narrowed pulse pressure.^2,3,7

Diagnosis and Management

For patients presenting to the ED with symptoms concerning for AS, a workup including labs (CBC, BMP, PT/PTT/INR, Troponin), EKG, and CXR is indicated. Though these tests are often non-diagnostic, you may detect subtle abnormalities such as mild anemia (caused by hemolysis from shearing across the stenotic valve), LVH criteria on EKG, or an enlarged heart suggestive of heart failure on CXR. The gold standard for diagnosis is transthoracic echocardiogram, which will be discussed in more detail later.^2,3,7

Treatment is based on the severity of symptoms. Patients with AS rely on preload to maintain adequate cardiac output. If they present with hypotension, volume repletion is often necessary. If the patient remains hypotensive despite adequate fluid resuscitation, vasopressors may be required. The ideal vasopressor agent for critical AS would not stimulate tachycardia since the goals of therapy are to 1) maximize diastolic filling time and 2) minimize myocardial oxygen demand. As such, alpha-agonists are preferred to beta-agonists, and serious consideration should be given to the use of phenylephrine as a first-line agent. Norepinephrine would also be a reasonable option, however epinephrine should be avoided as a first-line agent.

Particularly important is the preservation of sinus rhythm for utilization of the atrial kick for preload. For rhythms such as atrial fibrillation or supraventricular tachycardia, cardioversion should be considered early in the management of the unstable critical AS patient. If the patient has signs and symptoms of pulmonary edema, non-invasive positive-pressure ventilation and oxygen are the mainstays of treatment. The use of other typical heart failure medications such as nitrates and diuretics is controversial. While there is the potential for these drugs to lead to worsening of the patient’s condition secondary to decreased preload, there is some recent evidence that shows nitrates may have some benefit by reducing afterload and leading to an overall increase in cardiac output.

If the patient requires intubation, care should be taken to avoid post-intubation hypotension secondary to induction and addition of positive pressure ventilation. If possible, make sure the patient is adequately volume resuscitated prior to intubation and consider more hemodynamically neutral induction agents such as etomidate, which could also be used in a reduced dose to avoid removal of basal catecholamines. Lastly, consider starting vasopressors prior to intubation, particularly if there is little time for pre-optimization. Ultimately, medical therapies are all temporizing measures, and patients will require admission for definitive management, that being aortic valve replacement.^2,3,7

Point of Care Ultrasound (POCUS) for AS

The assessment for AS begins with traditional 2D echo images to look for secondary signs of long-standing aortic stenosis. These findings include aortic root dilation, concentric LVH, left atrial dilation, and dilated right ventricle. A gross visual “eyeball” assessment of LV ejection fraction (EF) should also be performed. Reduced EF is not only a secondary sign of aortic stenosis, but also increases the complexity of AS assessment; low flow across the aortic valve due to a weak LV can lead to underestimation of AS severity. Color Doppler of the aortic and mitral valves should also be performed to look for evidence of aortic regurgitation or mitral regurgitation/stenosis. The presence of co-existing valvulopathies will alter the loading conditions of the LV and possibly lead one to over- or underestimate AS severity.⁸

Four Methods to assess AS severity

Qualitative Assessment

1. “Eyeball” method^8,9

a. Obtain a parasternal long, short, and apical 5-chamber view.

b. In each view, assess the appearance and mobility of the aortic valve.

c. A degenerative aortic valve will often manifest with thickened and echogenic valve cusps with very limited mobility (versus retained mobility with aortic sclerosis). In the case of bicuspid aorta, the leaflets may appear normal in echogenicity and mobility.

In this parasternal long axis view, the aortic valve leaflets are thin and highly mobile (Figure 2).

Contrasted with Figure 2, this parasternal long axis image shows thickened aortic valve leaflets with restricted movement (Figure 3).

Figure 3 – Thickened aortic valve leaflets with restricted movement

Quantitative Assessment

2. Peak Aortic Velocity (Jet Velocity)⁸

a. Obtain apical 5-chamber or 3-chamber view with the beam oriented as parallel to the direction of blood flow as possible.

b. Place continuous wave Doppler through the left ventricular outflow tract (LVOT) with the area of interest (hash mark) at the level of the aortic valve. (Note – continuous wave Doppler differs from pulsed wave Doppler in its ability to detect very high velocity flow – which is necessary for assessment of valve pathology)

c. Measure the peak velocity of the tallest curve

d. > 4 m/s = severe AS

Figure 4

Mean Transaortic Gradient (PG Mean) = 21.6 mmHg
Peak Aortic Velocity (Vmax) = 336.5 cm/s = 3.3 m/s

3. Mean Transaortic Gradient (mean pressure difference between LV and Aorta)⁸

a. Obtain a continuous wave Doppler spectrum using the same technique as above.

b. This time, trace the envelope of the curve to obtain an AV velocity time integral (VTI).

c. The calculations package of the machine will provide the mean gradient based on the aortic VTI using the Bernoulli equation. Recall that the Bernoulli equation describes the preservation of energy in fluid kinetics, wherein the velocity and pressure of a liquid maintain an inversely proportional relationship in an enclosed system: DP = 4(V₁²– V₂²). This means that once the velocity is calculated as VTI then the equation can be used to solve for the pressure.

d. > 40 mmHg = severe AS

Figure 5

Peak Aortic Velocity (AV Vmax) = 4.04 m/s
Aortic Valve Area (AVA VTI) = 0.7 cm²

4. Aortic Valve Area (AVA)⁸

a. From the parasternal long axis position, measure the LVOT diameter in mid systole.

Figure 6

In this parasternal long axis image the left ventricular outflow tract diameter (LVOTD) is measured just proximal to the aortic valve with the image frozen at mid systole.

b. From the apical 5- or apical 3-chamber view, with the beam oriented parallel to direction of flow, place the pulsed wave Doppler gate in the LVOT, ideally at the level where LVOT diameter was measured. Obtain a pulsed wave Doppler spectrum and trace the envelope of the spectrum. This will yield the LVOT VTI.

Figure 7

c. Next, from the apical 5 or apical 3 chamber window, obtain a continuous wave Doppler spectrum of the aortic valve (using the same technique for obtaining peak jet velocity or AV mean gradient).

d. Trace the aortic valve continuous wave Doppler spectrum to obtain the aortic valve VTI.

e. The machine calculations package will use the LVOT diameter, LVOT VTI, and aortic valve VTI to calculate the aortic valve area using the continuity equation: A₁V₁ = A₂V_{2 (}Figure 8)

f. AVA < 1cm² = severe aortic stenosis

Evidence

Potential Pitfalls

• Failure to maintain minimal Doppler angles (less than 20 degrees) relative to the direction of blood flow will significantly underestimate the velocity of blood flow, which subsequently introduces error into all downstream AS severity calculations.
• Eccentric AS jets can make jet velocity difficult to accurately assess, leading to underestimation of AS severity.
• Significant LV systolic dysfunction or LVH may lead to underestimation of peak velocity and mean gradient.
• Concurrent aortic regurgitation may lead to higher than expected peak velocity and mean gradient.
• Severe mitral regurgitation or mitral stenosis may lead to lower than expected mean gradient.

Case Resolution

Given the findings of severe AS on his ED point-of-care echocardiogram, the patient was admitted to the hospital for further evaluation. His transthoracic echocardiogram demonstrated an aortic valve peak velocity of 4.2 m/s, consistent with severe aortic stenosis. He was transferred to a facility with interventional cardiology capabilities for definitive management, where he underwent transcatheter aortic valve replacement and was later discharged in stable condition.

References

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