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Clinical Update
Aortic Valve Stenosis — An Overview and Knowledge Assessment
Aortic valve stenosis (AS) affects approximately 1.5 million people in the United States. Around 500,000 patients suffer from severe AS and an estimated 250,000 patients have severe, symptomatic AS.1 Many of these patients are elderly and often they are high-risk surgical candidates. Without an aortic valve replacement (AVR), as many as 50 percent of patients with severe AS will not survive more than two years after the onset of symptoms.2
As the average life expectancy increases, more people are developing atherosclerotic AS, the most common form of AS. Small percentages of patients with complications of rheumatic disease and bicuspid valves make up most of the other AS patients. With the advent of transcatheter aortic valve replacement (TAVR), many patients who were too high risk for open surgery now have viable treatment options, including TAVR and revascularization using stents. Because treatment options for the highest risk subsets of patients have significantly increased, it is more important than ever to correctly diagnose AS and perform a comprehensive diagnostic workup. While echocardiography is the first choice for diagnosis of AS, the cath lab still has an important role in the diagnosis and treatment of AS.
Symptoms
Patients with AS are often asymptomatic for decades before presenting with symptoms and these symptoms tend to develop gradually. AS symptoms and clinical findings include exertional dyspnea or chest tightness, fatigue, syncope, shortness of breath, palpitations, heart murmur, and progressive inability to exercise.2,3,4 Exertional dyspnea is the most common initial complaint, even in patients with normal left ventricular (LV) systolic function, and it often relates to abnormal LV diastolic function. Once a patient becomes symptomatic, it is important to evaluate the patient for severe AS4.
Severe, symptomatic AS carries a poor prognosis if left untreated. The three major signs and symptoms of AS are syncope, hypertrophic heart failure, and angina. These are associated with mortality rates as high as 50% within two years.3 Syncope, hypertrophy, and angina are important to recognize and are a catalyst for AS replacement, either by TAVR or open surgery. Syncope, in the presence of severe AS, is associated with decreased cerebral perfusion, hypertrophy is indicative of the heart being overworked as a result of severe AS, and angina is associated with decreased perfusion and is often associated with obstructive coronary disease.4 Heart failure is a sign of advanced disease and patients may present with a variety of classic heart failure symptoms, including shortness of breath and fatigue. It is important to correctly diagnose the patient before hypertrophic heart failure occurs, as decreased ejection fraction is a predictor of poor outcomes for patients3,4 (Figure 1). Criteria for Evaluating Aortic Valve Stenosis
Highly trained and skilled operators are necessary to successfully diagnose and treat AS. The general cath lab criteria to diagnose severe AS is a valve area of <1.0 cm2, with a mean pressure gradient of >40 mmHg. Moderate AS is considered to be >1.0 to 1.5 cm2 and a normal aortic valve should be 2.5-4.0 cm2.3,4,5 Once a patient becomes symptomatic, it is essential for the patient to be successfully diagnosed and treated. However, in the case of low gradient/low output AS, there may be severe AS with a significantly lower gradient. AS may also be overestimated in low gradient/low output cases. Low gradient/low output AS may require additional studies, including a dobutamine challenge, to confirm the diagnosis of severe AS. Therefore, the data for severe AS must factor in other variables such as cardiac output, left ventricular function, and the severity of the gradient.
When making the diagnosis of AS, echocardiography is considered the gold standard. Echocardiography assesses the valve, how well it opens, and how calcified the valve is. It helps determine the etiology and assess aortic regurgitation, dilatation of the aorta, LV wall thickness, and contractility of the heart muscle. However, echocardiography, like any other imaging modality, has limitations. Echo uses the continuity equation to measure the severity of AS. This formula states that if there are no shunts between two areas, then flow in one area must equal the flow in the second area. It is calculated by taking the stroke volume and dividing it by the aortic valve velocity time integral (VTI), which determines the aortic valve area (AVA). The stroke volume can be calculated by measuring the left ventricular outflow tract (LVOT) diameter, squaring it and multiplying it by the constant .785, which will give you the cross-sectional area (CSA) of the LVOT. The CSA is then multiplied by the LVOT VTI, which gives you the stroke volume.6 The continuity equation formula is AVA= LVOT diam2 x 0.78540 x LVOT VTI/aortic valve VTI.5,6
There are several limitations with echo that can cause this formula to under or overestimate the aortic valve area. This includes the LVOT being measured incorrectly or not being parallel to flow, which would underestimate the aortic valve gradient. The major limitation of Doppler echocardiography in assessing the severity of aortic stenosis is underestimation of the gradient. Poor image quality can also make it impossible to accurately assess the severity of AS. Certain body habitus types, obesity, and other variables may affect the ability of the sound beam to be placed parallel to the aortic stenosis velocity jet. Thus, in a patient with clinical features of severe aortic stenosis but echo/Doppler findings of mild to moderate aortic stenosis, further evaluation with repeat Doppler or cardiac catheterization may be required.7,8
Rarely, Doppler may overestimate the severity of aortic stenosis in patients with severe anemia (hemoglobin <8 g/dL), a small aortic root, or sequential stenoses in parallel (coexistent LVOT and valvular obstruction).3 In these cases, the cath lab may provide critical information about the severity of AS and may be the more reliable diagnostic tool for confirming its severity. Along with supporting inconclusive echocardiography findings, the cath lab provides other critical information for the physicians.7,8
Low gradient/low cardiac output is a critical issue that makes it more complicated to assess AS. The major issue with low gradient/low flow AS is in trying to determine whether the aortic valve function is compromised because of the AS or if the low contractile function of the left ventricle is the causing the valve to appear more diseased than it actually is. This determination helps differentiate between true and pseudo AS.
Cath Lab Management
The cardiac cath lab generally evaluates AS in subsets where the echocardiography is inconclusive, or on cases of low gradient/low output AS. While echocardiography is considered the diagnostic tool of choice for AS, the cath lab may still be required to confirm the diagnosis of severe AS. The cath lab also has other important roles in the workup of AS patients. The workup in the cath lab includes coronary angiography, right heart catheterization with cardiac output assessment, two transducer gradient assessments, and ilio-femoral angiography to determine if a patient can have percutaneous valve repair via the femoral artery.
Coronary Angiography
Generally, the incidence of associated coronary artery disease has been reported to be 50% in patients with aortic stenosis who are older than 50 years.8,9 Because angina caused by AS symptoms are similar to those of coronary artery disease (CAD), and most AS patients are elderly, it is essential to evaluate coronary arteries prior to making a decision on surgery versus TAVR. In the lab, the aortic root is often dilated and a larger Judkins left catheter should be considered for left coronary angiography via the femoral approach. Coronary angiography should also be performed in patients younger than 35 years if they have LV systolic dysfunction, symptoms or signs suggestive of coronary artery disease, or two or more risk factors for premature coronary artery disease, excluding gender.8,9
Cardiac Hemodynamics/Cardiac Output
Right and left heart catheterization plays a significant role in the cath lab evaluation of patients with AS. Hemodynamics evaluate the left- and right-sided pressures of the heart, which can be affected by AS. Because dilated or hypertrophic cardiomyopathy may be associated with AS, it is important to evaluate cardiac hemodynamics to assess left heart function.
Advanced AS can also cause mitral valve regurgitation and significantly increase the risk of developing atrial fibrillation. It may increase right-sided heart pressures, and patients with advanced AS may develop pulmonary hypertension and right-sided heart failure. According to Kiefer and Bashore, pulmonary hypertension is underappreciated in AS patients and needs to be fully evaluated, as it impacts surgical morbidity and mortality rates.10 Since pulmonary hypertension and right-sided heart failure are associated with poorer patient outcomes, quality hemodynamics provide critical information about a patient’s overall cardiac health. Understanding the hemodynamics and fully assessing the patient’s cardiac health allows the cardiologists and surgeons determine the best treatments for AS patients.
Right heart catheterization is also necessary to perform thermodilution (TD) and Fick cardiac output options. The Fick cardiac output uses the patient’s body surface area or weight to calculate predicted oxygen consumption. This number is divided by the difference between aortic and pulmonary arterial saturation, multiplied by hemoglobin, the Fick constant 1.36, and a constant of 10 that converts the output into liters/minute (Figure 3). In patients with low output/low gradient AS, an accurate cardiac output is essential for an accurate diagnosis.
According to Kern, “Fick CO is calculated as oxygen consumption divided by the arteriovenous oxygen concentration difference (in milliliters of oxygen). Remember O2 saturation percentages are converted to amount (or content) of O2 using the following formula: content (1.36 x hemoglobin x O2 saturation x 10).”11 Cardiac output, measured in milliliters/minute is a critical value in diagnosing AS. It is expressed as the numerator in the Gorlin equation. The importance of measuring cardiac output for AS diagnosis cannot be underestimated. In order to accurately assess cardiac output, the patient should not be over sedated, and the patient should not be falsely dependent on supplemental O2. Artificially elevating the arterial O2 levels with supplemental O2 can alter cardiac output and sedation can depress respirations and aortic saturation, which can also corrupt cardiac output data. The Fick formula can be calculated with the following formulas (Ao=aortic; Pa=pulmonary artery; Sat=saturation; BSA=body surface area)11:
Fick CO = Weight (kg)x 3ml
(AoSat-PaSat) x 1.36 x Hemoglobin x 10
or
Fick CO = BSA x 125
(AoSat-PaSat) x 1.36 x Hemoglobin x 10
When measuring cardiac output, it is optimal to calculate outputs immediately before collecting the AS data. The heart rate and saturation levels may change during the procedure and this can also affect the reliability of data collection. For high cardiac output states, the TD method should be considered, especially for borderline cases, as a slight difference in aortic or venous saturations can radically alter Fick cardiac output when it is high. Limitations of the TD swan include regurgitant disease, arrhythmia, and low output states. When choosing a cardiac output method, it is important to consider the many variables that can influence the accuracy of the cardiac output for AS calculation.
Aortic Valve Disease Assessment With Two Transducers
Two transducers allow assessment of pressure gradients and also offer the ability to assess a mean gradient, which is the gold standard for determining gradients. It is more accurate than peak to peak, because peak to peak is not a real-time physiological assessment, and the mean gradient evaluates the AS across the entire systolic ejection period. The systolic ejection period begins with the opening of the aortic valve, and ends with the dicrotic notch, indicating closure of the aortic valve. Frequent zeroing and proper transducer setup insures the most accurate data.
When using two transducers, make sure both measurements are on the same scale, that both transducers have excellent signal fidelity, and that the correct cardiac output has been recorded. This allows the Gorlin formula to be calculated in real time by the computer. The aortic pressures should be measured before crossing the aortic valve into the left ventricle. If there is air in one of the ports, a defective transducer, or other issues affecting the accuracy of the measurements, they need to be addressed before crossing the aortic valve and assessing the gradient.
For measuring AS, the Langston style pigtail catheter is optimal for assessing gradients, because the pigtail is in the LV and the proximal port of the catheter sits in the descending aorta. The other alternative for measuring AS is to use the femoral artery and a pigtail catheter. This can create false gradients for several reasons:
- Because of flow dynamics, the femoral artery can actually have a pressure that is slightly higher than the central aorta.
- If there is peripheral vascular disease, the femoral artery pressures may be falsely decreased in relationship to the central aorta. In this case, a long sheath should be used to cross the area creating the false gradient.
- There are also phase shifting issues with femoral/LV measurements. There is a natural delay in flow dynamics from the LV/central aorta to the femoral artery. Therefore, improper phase shifting of an LV/femoral artery waveform can falsify the severity of AS.
Any of these scenarios can cause the collection of false data and corrupt the study. Therefore, when using this technique, simultaneous pressures must be evaluated in the ascending aorta and the femoral before and after the AS assessment. The systems should also be zeroed at this time to make sure both transducers are accurate.
Abdominal/Femoral Angiography to Assess TAVR Access Routes
The abdominal aorta and ilio-femoral arteries can be assessed for TAVR access using a markered pigtail catheter. Markered pigtail catheters have radiopaque marks at 1 cm intervals, which help determine the length and diameter of the vessels. A single digital subtraction angiography (DSA) run can survey the vessels with a total volume of 10-20 ccs of contrast. While computed tomography is often used to assess these vessels, a small contrast injection can provide important preliminary information as part of an AS workup.
Gorlin Formula
In the cath lab, the Gorlin formula is the primary tool for determining the severity of AS. It factors in the cardiac output (CO), systolic ejection period, heart rate and gradient to determine the severity of AS. The Gorlin formula is stated as
CO(milliliters)
SEP x HR x 44.3 x√Mean Gradient
The Gorlin formula was originally designed to assess mitral valve stenosis and according to Nishimura et al, there are no empirical constants for measuring the other heart valves.12 Therefore, other data such as gradient, pressure contours, and the health of the ventricle also need to be considered when assessing AS with the Gorlin method. In order to perform the Gorlin calculation properly, it is also necessary to have a reliable cardiac output. For most patients, the Fick is considered the gold standard output performed in the cath lab. The TD may be valuable in high output states, where slight differences in saturation levels can significantly alter the reliability of the Fick output. As the population ages, there are more cases of low output/low gradient AS being identified. Figures 2 and 3 demonstrate the correct alignment of hemodynamics to interpret the mean and peak gradients.
Correct phase shifting is essential when assessing the mean gradient. Improper shifting to the left or right may significantly alter the mean gradient. This is because the mean gradient is calculated using a calculus-based Simpson curve that studies the gradient throughout the systolic ejection period. The curve is only accurate when the upstroke (isovolumetric contraction) of the ventricle and the upstroke point of the aortic waverform bisect (Figure 3). Therefore, learning how to phase shift two transducer measurements is essential for an accurate AS diagnosis. This is even more important in cases of low gradient/low output cases, where a slight phase shifting misalignment can have a dramatic impact on cath lab data.
To accurately measure and hand calculate the systolic ejection period in the Gorlin equation, the preferred paper speed is 100 mm/sec paper speed. If the paper speed is 25 mm/sec, the systolic ejection period (SEP) must be multiplied by 4, and if the paper speed is 50 mm/sec, the SEP needs to be multiplied by 2. It is important to remember that the SEP is a time assessment and that the measurement recorded on paper is distance. In order to convert a measured SEP, the measured value needs to be divided by 10. Therefore, if a SEP is measured at 4 cm, it would become 0.4 seconds when calculating the Gorlin formula.
The Hakki and quick formulas allow operators to rapidly determine the severity of AS. The Hakki formula simply divides the square root of the mean gradient into the cardiac output (liters/sec). This method is generally accurate within 20% and helps cath lab staff make quick, real-time estimates of AS severity. For instance, a patient with a cardiac output of 5 and a gradient of 25 mmHg would have a valve area of 1.0 cm2 by the Hakki method. When performing a cardiac catheterization, the Hakki formula allows the physician to calculate a general range for AS and determine the accuracy of the workup.
Low Gradient/Low Output
One of the major challenges in diagnosing AS is a state known as low gradient/low output. The classic criterion for severe AS is a mean gradient of greater than 40 mmHg with valve area of <1.0 cm2. In the case of low gradient/low output AS, a patient with a low cardiac output may be diagnosed with severe AS, even when the mean valve gradient is low. In either the cath lab or the echo lab, a dobutamine challenge can be used to assess patients with low output/low gradient AS. In low gradient/low output patients, they may have gradients less than 40 mmHg, but still have significant gradients by Gorlin formula.
Low gradient/low flow AS may occur with depressed or preserved left ventricular ejection fraction (LVEF), and both situations are among the most challenging encountered in patients with valvular heart disease. Low LV function with a gradient responds more favorably than low gradients with normalized ejection fraction (EF), due to other underlying cardiac disease. In both cases, the decrease in gradient relative to AS severity is due to a reduction in transvalvular flow. The main challenge in patients with depressed LVEF is to distinguish between true severe vs pseudo-severe stenosis and to accurately assess the severity of myocardial impairment.13-17
Low LVEF, low gradient/low flow severe AS is generally characterized by the combination of an effective orifice area (EOA) ≤1.0 cm2 or ≤0.6 cm2/m2 when indexed for body surface area, a low mean transvalvular gradient (i.e., <40 mmHg) and a low LVEF (≤40%), causing a low flow state. Several criteria have been proposed in the literature to define the low flow state in AS, including a cardiac index <3.0 l/min/m2 and a stroke volume index <35 ml/m2.14-17
Dobutamine Stress
For patients with low gradient/low output AS, it is important to confirm true versus pseudo AS. Patients with true AS will benefit from surgery/TAVR, while those with pseudo will not. Echocardiography or the cath lab can perform a dobutamine stress test to confirm the presence of significant AS.14-17 It is important to assess the coronary arteries for disease, as this may determine if dobutamine can be safely administered. Dobutamine is a powerful inotropic agent, and when administered as part of stress echocardiography exam or as part of an AS workup, can help determine if a low output/low gradient is true or false. If a patient truly has severe AS, the gradient will increase as the inotropic effect of dobutamine increases the workload of the heart. If the gradient decreases or doesn’t change, it means that there is not true AS, and that the patient will not benefit from surgery or TAVR. The AS gradients in these cases is caused by depressed heart function rather than critical AS. Figure 4 demonstrates the diagnosis of true, severe AS for a patient whose diagnosis was unclear on initial echocardiogram and cath lab evaluation.In conclusion, AS treatment strategies have significantly improved over the past decade. It is a disease that carries a high mortality rate when it is symptomatic and untreated. AS generally occurs in older patients who used to have poor treatment options, with high morbidity and mortality rates. As treatment options have improved, it is essential to work up patients, especially the low output/low gradient subsets. It is important for cath lab staff to understand that AS workups are more than plugging in data. Many cath lab staff also participate in TAVR procedures or perform certain procedures for the surgeons and cardiologists. Therefore, cath lab staff needs to understand the clinical data that confirm or exclude the diagnosis of severe AS. This review was designed to reinforce clinical skills and readers can undertake the following knowledge assessment to assist in understanding key issues in diagnosing aortic valve stenosis.
References
- Bach DS, Radeva JI, Birnbaum HG, Fournier AA, Tuttle EG. Prevalence, referral patterns, testing, and surgery in aortic valve disease: leaving women and elderly patients behind? J Heart Valve Dis. 2007 Jul; 16(4): 362-369.
- Otto, CM. Timing of aortic valve surgery. Heart. 2000; 84(2): 211-218.
- Problem: Aortic Valve Stenosis. American Heart Association, September 7, 2017. Available online at https://www.heart.org/HEARTORG/Conditions/More/HeartValveProblemsandDisease/Problem-Aortic-Valve-Stenosis_UCM_450437_Article.jsp#.WbljyoprzyZ. Accessed September 13, 2017.
- Ren X. Aortic stenosis workup. Theheart.org/Medscape. March 4, 2017. Available online at https://emedicine.medscape.com/article/150638-workup#c8. Accessed September 13, 2017.
- Baumgartner H, Hung J, Bermejo J, et al; American Society of Echocardiography; European Association of Echocardiography. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009 Jan; 22(1): 1-23; quiz 101-2. doi: 10.1016/j.echo.2008.11.029.
- Dahou A, Pibarot P. Low-flow low-gradient aortic stenosis: when is it severe? Expert Analysis. American College of Cardiology. January 15, 2015. Available online at https://www.acc.org/latest-in-cardiology/articles/2015/12/08/09/53/low-flow-low-gradient-aortic-stenosis-when-is-it-severe. Accessed September 13, 2017.
- Everett RJ, Newby DE, Jabbour A, et al. The role of imaging in aortic valve disease. Curr Cardiovasc Imaging Rep. 2016; 9: 21.
- Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC); European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012 Oct.; 33(19): 2451-2496.
- Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia, PA: Elsevier Saunders; 2012.
- Kiefer TL, Bashore TM. Pulmonary hypertension related to left-sided cardiac pathology. Pulm Med. 2011; 2011: 381787. doi: 10.1155/2011/381787.
- Kern M. Measurement of cardiac output in the cath lab: how accurate is it? Cath Lab Digest. 2014; 22(7): 4-8.
- Nishimura RA, Otto CM, Bonow RO, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jun 10; 63(22): 2438-2488. doi: 10.1016/j.jacc.2014.02.537.
- Leeson P, Augustine D, Mitchell AR, Becher H. Echocardiography (Oxford Specialist Handbooks in Cardiology). 2nd ed. Oxford, United Kingdom: Oxford University Press; 2012.
- Czarny M, Resar JR. Diagnosis and management of valvular aortic stenosis. Clin Med Insights Cardiol. 2014 Oct 19; 8(Suppl 1): 15-24. doi: 10.4137/CMC.S15716. eCollection 2014.
- Pibarot P, Dumesnil JG. Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction. J Am Coll Cardiol. 2012 Nov 6; 60(19): 1845-1853. doi: 10.1016/j.jacc.2012.06.051.
- Mohty D. Clinical manifestations and diagnosis of low gradient severe aortic stenosis. UpToDate. May 18, 2017. Available online at https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-low-gradient-severe-aortic-stenosis. Accessed September 13, 2017.
- Baumgartner H, Hung J, Bermejo J, et al; American Society of Echocardiography; European Association of Echocardiography. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009 Jan; 22(1): 1-23; quiz 101-2. doi: 10.1016/j.echo.2008.11.029.
1Jefferson College of Health Professions, Philadelphia, Pennsylvania;
2Cardiac Cath Lab/ Electrophysiology, Pennsylvania Hospital, Philadelphia, Pennsylvania; Adjunct Assistant Professor, Jefferson College of Health Professions, Philadelphia, Pennsylvania
The authors can be contacted via Richard Merschen, EdS, RT(R)(CV), RCIS, at richardmerschen@verizon.net.
Disclosure: The authors report no conflicts of interest regarding the content herein.
Test Yourself: AS Knowledge Assessment Tool
Questions:
1. What is the Gorlin equation for aortic valve stenosis?
a. Cardiac output x heart rate x 44.3/square root of gradient.
b. Cardiac output/SEP x HR/44.3 x square root of gradient.
c. Cardiac output/DFP x 37.7/square root of gradient.
2. What is the systolic ejection period (SEP)?
a. Period of time that mitral valve empties into left ventricle.
b. It represents the time that the aortic valve is open.
c. It represents the time that the aortic valve is closed.
d. All of the above.
3. What is the difference between peak to peak and mean gradient?
a. The peak-to-peak gradient shows the systolic peak of each heartbeat. The mean gradient assesses the gradient throughout the SEP.
b. The peak to peak considers the entire SEP.
c. The peak to peak is more reliable in case with arrhythmia.
d. The mean gradient is only accurate with a TD swan.
4. How is the systolic ejection period (SEP) measured?
a. Measure from the a wave of the wedge to the v wave.
b. Measure from the upstroke of the aortic pressure to the dicrotic notch.
c. Measure the dicrotic notch to the a wave of the next beat.
5. Is peak to peak or mean gradient more reliable for measuring the severity of aortic stenosis?
a. Peak to peak.
b. They have equal value.
c. Mean gradient.
6. What is the normal size of an aortic valve?
a. A normal aortic valve is between 2.5-4cm2.
b. Between 6-8 cm2.
c. Between 1.5-4.5 cm2.
d. Between 3-6 cm2.
7. What is considered the classic definition of critical AS?
a. Valve area >1.0 cm2.
b. Valve area of <1.0 cm2 and mean gradient of 40 mmHg.
c. Valve area <5.0 cm and gradient >40 mmHg
8. Why is cardiac catheterization performed on AS patients who already have disease confirmed by echocardiography?
a. To assess hemodynamics, evaluate coronary artery disease, and assess the ilio-femoral arteries for TAVR access.
b. To confirm the accuracy of echocardiography and evaluate aortic regurgitation.
c. Cardiac catheterization is the gold standard for evaluating AS. The echocardiogram is only a screening tool.
9. What is the Hakki formula?
a. The formula to detect mitral regurgitation using flow dynamics.
b. The formula to detect AS using cardiac output (CO)/mitral valve gradient (MVG).
c. A formula to detect pulmonary hypertension using trans-pulmonary gradients.
10. What are the potential disadvantages of using the femoral artery sheath for AS gradient measurements?
a. Can falsely overestimate.
b. Can falsely underestimate.
c. Errors due to improper phase shifting.
d. All of the above.
11. Which catheter allows for simultaneous measurement in the ventricle and thoracic aorta?
a. A single lumen catheter with a pullback through the aortic valve.
b. A sheath in the femoral artery and a pigtail catheter in the LV.
c. A dual lumen pigtail catheter, with the pigtail in the LV and a proximal port in the central aorta.
12. How often does the wire need to be removed and flushed?
a. Every 5 minutes.
b. Every 10 minutes.
c. Every 2 minutes.
d. The patient is heparinized. It is unnecessary.
13. For high cardiac output states, is Fick or TD superior?
a. They are the same.
b. Fick is more accurate.
c. TD is more accurate.
14. What is the Fick cardiac output on this patient (Table A)?a. 3.0 liters/min.
b. 4.0 liters/min.
c. 5.0 liters/min.
d. 6.0 liters/min.
15. What is the valve area on this patient?
a. 0.84 cm2
b. 1.1 m2
c. 1.5 m2
16. What is the constant used to calculate the valve area?
a. 37.7
b. 40.6
c. 44.3
17. Which three symptoms are strong predictors of two-year mortality in AS patients and are associated with symptomatic AS?
a. Syncope, hypertrophy, angina.
b. Pulmonary hypertension, fatigue, and GERD.
c. Syncope, edema, lethargy.
18. What are the primary causes of AS in adults?
a. Rheumatic fever
b. Bicuspid valve
c. Aging/atherosclerotic disease
19. For most AS patients, what is the gold standard imaging modality?
a. Cardiac catheterization with two-transducer AS evaluation
b. Echocardiography
c. Dobutamine stress test
d. Computed tomography
20. What is low gradient/low output AS?
a. A rare situation where the low cardiac output is the cause of aortic regurgitation.
b. A diagnosis of AS made with a TD swan.
c. A gradient of AS and aortic insufficiency causing turbulent flow through the valve.
d. The diagnosis of AS in which the patient has a low cardiac output and a gradient of <40 mmHg.
Answers are below.
AS Knowledge Assessment Tool Answers
Answer Key:
1. B 6. A 11. C 16. C
2. B 7. B 12. C 17. A
3. A 8. A 13. C 18. C
4. B 9. B 14. B 19. B
5. C 10. D 15. A 20. D
- Answer: B. The Gorlin equation uses the cardiac output in milliliters and divides it by systolic ejection period x heart rate. This calculates the flow area, which is then divided by the constant 44.3 x square root of the gradient. To simplify the formula, the cardiac output can be divided by SEP x HR x 44.3 x mean gradient square.
- Answer: B. The systolic ejection period (SEP) is the time from the opening to the closing of the aortic valve. It is measured in distance, but needs to be converted to time. The distance is converted to time by dividing distance/10.
- Answer: A. The mean gradient uses a calculus-based Simpson curve to assess the gradient throughout the entire systolic ejection period, while the peak-to-peak gradient is not done in real time, due to the natural delay between the LV and aortic peaks. It is important to correctly phase shift when performing mean gradients, or the data may be skewed. On 100 mm/sec, a planimetry model can be hand drawn to measure the curve throughout the systolic ejection period.
- Answer: B. Take a ruler and measure from the time aortic systole begins until the dicrotic notch. The distance should be measured on 100 mm/sec paper speed. If paper speed is 50, multiply by 2 and if the paper speed is 25, multiply by 4 to accurately record the SEP. For optimal hand calculation, use a gradient that was calculated on 100 mm/sec and has proper phase shifting.
- Answer: C. The mean gradient is considered more accurate and may be altered by poor phase shifting of the hemodynamics. The mean gradient assesses AS throughout the SEP and is more comprehensive in determining the severity of the gradient. It uses planimetry and evaluates the entire curve of the systolic ejection period to calculate the aortic valve area.
- Answer: A. The normal, adult aortic valve is between 2.5 to 4.0 cm2.
- Answer: B. AS below 1cm2 with a mean gradient of >40 mmHg is considered severe and below 0.7 is critical. The standards for treatment are changing and symptoms are also a major consideration in determining the significance of aortic valve stenosis.
- Answer: A. Many of the patients are elderly and are at increased risk for CAD. A patient with AS and CAD requires treatment for both pathologies, and this becomes an important consideration on therapy. Cardiac catheterization may make the difference between TAVR and open surgery, and changes risk quantification for patients with AS.
- Answer: B. The Hakki formula/quick formula is designed to allow operators to quickly interpret AS during the procedure. It takes CO and divides it by the square root of the gradient. While this method may be 20% off on many patients, it still allows the operator to sense whether the accumulated data is accurate.
- Answer: D. There are several potential pitfalls from using the femoral artery and LV to assess gradients. First, the femoral artery may actually have a slightly higher pressure than the central aorta due to flow velocity as blood rushes through the descending aorta to the lower extremities. Second, any disease in the aorta-iliac system above the sheath tip may have a gradient associated with peripheral vascular disease and falsely calculate the gradient. In all cases using the LV/ femoral artery method, dual pressures need to be taken in the ascending aorta and femoral arteries pre and post gradient assessment. There is a delay in signal between the LV and femoral artery.
- Answer: C. A Langston style pigtail has the pigtail in the LV and a proximal port that sits in the descending aorta. This prevents gradients from the femoral sheath, and also minimizes the need to phase shift, as the flow assessed is from the central aorta.
- Answer: C. The wire should be removed and the catheter should be aspirated/flushed every 2 minutes when attempting to cross a diseased aortic valve. Heparin can also be administered if there is concern about debris on the valve that may shower and cause cerebrovascular accident (CVA).
- Answer: C. When patients have very high cardiac outputs, the TD method can be valuable for obtaining CO. Very slight difference in AO or PA sat can significantly alter CO levels on these patients. Fick cardiac output is generally considered to be superior in normal or low cardiac output states.
- Answer: B. The Fick cardiac output is 4.0 liters/min. The numerator takes body surface (1.36) x 125 = 170. The denominator takes the saturations (0.95-0.64) x hemoglobin (10) x the constants 10 x 1.36 = 42.16. 170/42.6 = 4.06 l/min.
- Answer: A. The valve area takes the cardiac output and converts it to milliliters. 4.06l/min = 4060mls/min. 4060/ HR (75) x SEP (.20) = 201 flow area. Next, divide 201/44.3 x square root of mean gradient 28.65 (5.3) = 0.84 cm2.
- Answer: C. 44.3 is the constant used to calculate aortic valve area with the Gorlin formula. 37.7 is used to calculate the mitral valve area.
- Answer: A. The symptoms of angina, hypertrophic heart failure, and syncope are associated with a 2-year mortality rate of up to 50%. This is higher than the mortality rates of many types of stage 4 cancer.
- Answer: C. Aging, along with calcification of the aortic valve, is the most common cause of AS. Rheumatic fever, once a major factor in valvular heart disease, is very uncommon and bicuspid valves are found in 2-3% of the population.
- Answer: B.
- Answer: D. Low gradient/low output AS is a complex diagnosis. It implies that a patient has severe AS, even when their gradient doesn’t reach the classical clinical criteria of a valve area <1.0 cm2. In this case, to confirm the diagnosis of severe AS, dobutamine may be used. Its inotropic effect can increase the gradient as the heart works harder. If the gradient doesn’t increase with the increased workload and output, it is indicative of a false finding.
