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CHAPTER 1
Echocardiographic Assessment of Cardiac Output and Ejection Fraction
Jay Blankenship, MDMike Mallin, MD, RDCS, RDMS
HIGHLIGHTS
Echo is an effective, noninvasive method for measuring CO.
Non-cardiologists can measure CO.
CO=SV x HR
SV=LVOT area x VTI
SECTION 1
IntroductionEchocardiography has been shown to be an effective, noninvasive method of assessing cardiac function. Furthermore, it has been shown that non-cardiologists can safely and accurately use echocardi-ography to assess cardiac function.1
Cardiac output (CO) is the volume of blood pumped out of the heart per minute. Measured in liters/minute, CO can be calculated using heart rate (HR) and stroke volume (SV).
CO = SV x HR
Echocardiography can be used to measure SV using a method called pulsed waveform Doppler. This method allows approximation of the stroke volume by taking two measurements:
1) The left ventricular outflow tract (LVOT) area.
2) The range of velocities of blood flow across the LVOT, also known as velocity time integral (VTI).2,3
SV = LVOT area x VTI
2
HIGHLIGHTS
LVOT is measured in the parasternal long axis view.
Zoom in on the LVOT to get good visualization of the aortic root.
Measure LVOT in mid-systole, with maximal separation of leaf-lets.
SECTION 2
Measuring LVOT AreaThe LVOT area is approximated by assuming that it is the shape of a circle. Thus, the area is determined by measuring the diameter of the LVOT. Once obtained, a person’s LVOT area does not change. You only need to obtain the LVOT once, and future CO measurements can use old LVOT area measurements.
To determine the LVOT area, first obtain a parasternal long axis view of the heart (Figure 1.1, Image 1.1).
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FIGURE 1.1 - Parasternal Long Axis View
IMAGE 1.1 - Parasternal Long Axis View
Zoom in on the LVOT, ensuring good visualization of the aortic root. The diameter should be obtained by measuring from inner edge to inner edge at the level of the aortic annulus (attachment of valve leaf-lets). Importantly, the diameter of the LVOT should be measured per-pendicular to the direction of the LVOT and should be performed in mid-systole, with maximal separation of leaflets (Image 1.2).
LVOT area can then be calculated using the following formula:
LVOT area (cm2) =
4
Measured in mid-systole at base of Ao leaflets.
IMAGE 1.2 - LVOT Diameter
HIGHLIGHTS
Measure VTI in the apical long axis or 5 chamber view.
SV (cm3) = Area LVOT (cm2) x VTI(cm)
The Doppler wave should be in line with the flow of blood through the LVOT.
In patients with an irregular heart rate, the VTI measurement should be obtained 5-10 times and then averaged.
SECTION 3
Measuring VTITo calculate VTI, pulsed wave Doppler is used to measure the veloc-ity of flow across the LVOT. First, obtain an apical long axis or api-cal 5 chamber view of the heart (Figure 1.2, Image 1.3, Figure 1.3, Image 1.4).
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FIGURE 1.2 - Apical 5 Chamber View
IMAGE 1.3 - Apical 5 Chamber VTI Measurement
It is important that the pulsed wave Doppler gate is in line with the LVOT, thus the necessity that an apical window is obtained. Select the pulsed wave Doppler mode and place the Doppler gate parallel to and in the center of the LVOT at the level where the diameter was measured (Images 1.3, 1.4). This will produce a waveform tracing of the velocities of blood flowing out of the LVOT with each heartbeat. The waveform will be negative since the blood is flowing away from the transducer. Next, select “LVOT VTI” through the machine’s meas-urement package (often found under “CO” or “Ao” in the cardiac measurements section) and trace the waveform of one ejection pe-riod (Image 1.5).
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FIGURE 1.3 - Apical Long Axis View
IMAGE 1.4 - Apical Long Axis VTI Measurement
IMAGE 1.5 - VTI Tracing
Doing this will calculate a value for VTI by taking area under the curve. This measurement is essentially taking the integral of a veloc-ity, so the VTI will be reported in cm. Stroke volume can then be cal-culated using the following formula:
SV (cm3) = Area LVOT (cm2) x VTI(cm)
SV =
PITFALLS
1. When measuring VTI, the Doppler wave should be in line with the flow of blood through the LVOT. Any angle between the Doppler wave and LVOT can result in underestimation of VTI, and there-fore SV.
2. When measuring diameter of LVOT, ensure that the measurement is taken in mid-systole. Failure to do this can result in underestima-tion of LVOT area, and therefore SV.
3. In patients with an irregular heart rate, the VTI measurement should be obtained 5-10 times and then averaged.
7
HIGHLIGHTS
Passive leg raise is a noninvasive method of estimating volume responsiveness.
Logistically, this can be difficult in the ED.
SECTION 4
Passive Leg RaisePatient care often requires an assessment of a patient’s volume status to direct a course of treatment. Sepsis, hypotension, pancreatitis and many other pathologic states require rapid volume repletion. How-ever, overzealous administration of fluid can be detrimental, particu-larly in patients with known congestive heart failure. In such cases, echocardiography can be used as a non-invasive method of determin-ing the fluid status of a patient using the passive leg raise (PLR) ma-neuver. The PLR maneuver enables the physician to deliver a reversi-ble, endogenous fluid bolus of approximately 250cc immediately. To perform PLR, initial measurement of SV should be obtained with the patient in a semi-recumbent position with the head of the bed at 45° (Figure 1.4).
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FIGURE 1.4 - PLR Baseline Position
The patient should then be placed recumbent with legs elevated to 45°, and SV should be reassessed after approximately 30-90 sec-onds4 (Figure 1.5). A change in SV of >10% after PLR has been shown to be a sensitive predictor of volume responsiveness.5,6 If stroke volume does not increase, the patient likely will not benefit from fluid administration. To perform PLR consistently and accurately (Movie 1.1), it is helpful to have a foam wedge to ensure appropri-ate elevation of legs during the second measurement of SV.
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FIGURE 1.5 - PLR Legs Elevated Position
MOVIE 1.1 - One Minute Ultrasound Passive Leg Raise Demo
HIGHLIGHTS
The “eyeball” technique for assessing ejection fraction when performed by experienced sonographers is as good as quantita-tive methods.
A normal FS is 25-45%.
A normal EPSS is <7mm.
SECTION 5
Assessing the Ejection Fraction
Although most echocardiographers use the “eyeball” technique to estimate the left ventricular ejection fraction (LVEF), there are addi-tional methods for estimation. These include:
§ Fractional shortening (FS)§ Simpson’s Method (Method of Discs)§ E-point septal separation (EPSS)
FRACTIONAL SHORTENING
Fractional shortening uses an anterior-posterior measurement of the left ventricular dimension to estimate ejection fraction. This measure-ment does not take into account the 3D shape of the ventricle and is fraught with error in patients with prior CAD history and wall motion abnormalities. The measurement is made at end systole (LVESD - end systolic diameter) and end diastole (LVEDD - end diastolic diameter). This measurement should be made 1cm apically from the septal-aortic attachment and perpendicular to the long axis of the heart in the parasternal long axis or parasternal short axis window and should bisect the chordae tendineae (Image 1.6, 1.7). A normal frac-tional shortening is between 25-45%.
Pearl: The FS is typically ½ the total ejection fraction
10
SIMPSON’S METHOD
The Simpson’s Method of Discs uses a computer package and a bit of upper level algebra to estimate the end diastolic and end systolic volumes of the LV. It requires a cardiac package on your ultrasound machine and adequate views of the apical 4 chamber and apical 2 chamber with traced endocardial borders in both systole and dias-tole for each. This method is the most time consuming, but it gives the most accurate estimation of LVEF. Its specific description is be-yond the scope of this book, but more information can be found here.
EPSSE-Point septal separation or EPSS is a commonly taught and easy method for assessment of the left ventricular ejection. This method has been described and used since the late 1970s.7 EPSS is a quick and dirty estimation of the LVEF and depends on free movement of the mitral valve. Thus, it can be inaccurate in disease processes that affect the MV such as mitral stenosis, calcification, significant aortic insufficiency and dilation of the mitral annulus from dilated cardiomy-opathy. Nevertheless, in most instances the EPSS offers the novice sonographer a quick and easy method to estimate the LVEF.
To measure the EPSS, a parasternal long axis window is obtained and the image is maximized so that the mitral valve is well visual-ized. If the MV is touching the septum on visual inspection, the pa-tient’s EF can be described as normal, or greater than 55%.
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IMAGE 1.7 - Normal FS
IMAGE 1.6 - Reduced FS
If the MV is not touching the septum, the distance from the MV dur-ing the E-point and the septum should be measured (Image 1.8). A distance <0.7cm is consistent with a normal EF. A distance >1.0cm is consistent with a reduced ejection fraction.
STEPS TO EVALUATE EPSS
STEP 1: Obtain parasternal long axis window (Figure 1.6).
STEP 2: Obtain adequate view of MV (Movie 1.2).
STEP 3: Place M-mode ice pick through tip of MV (Image 1.9).
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IMAGE 1.8 - Location of EPSS Measurement
FIGURE 1.6 - Probe Placement for PSLA Window
IMAGE 1.9 - Location of M-Mode for EPSS
MOVIE 1.2 - MV View
STEP 4: Initiate M-mode tracing (Image 1.10).
STEP 5: Identify the E and A waves of the MV (Images 1.11, 1.12). STEP 6: Measure distance from tip of MV to septum (Image 1.13).
13
IMAGE 1.10 - M-Mode Button
IMAGE 1.11 - M-Mode Through Mitral Valve IMAGE 1.13 - E and A Waves of Mitral Valve
IMAGE 1.12 - Normal EPSS and Thus LVEF
Example of normal EPSS in patient with normal LVEF (Image 1.14): Examples of elevated EPSS in patient with severely reduced LVEF (Im-age 1.15, Movie 1.3):
MOVIE 1.3 - Increased EPSS and Thus Reduced LVEF
IMAGE 1.14 - Location of EPSS Measurement
14
IMAGE 1.15 - Increased EPSS and Thus Reduced LVEF
A recent MRI study created an equation that can be used to estimate a LVEF based on the EPSS distance:8
Although EPSS is usually an accurate measure of LVEF, there are a few occasions when the EPSS may falsely underestimate the LVEF:
1) Aortic insufficiency (AI): The AI regurgitant jet can push down the MV anterior leaflet in diastole causing the EPSS to be ele-vated despite a normal EF (Image 1.16).
2) Mitral Stenosis (MS): Although rare, moderate to severe MS can cause decreased excursion of the MV anterior leaflet, and thus elevate the EPSS.
SUMMARY
In conclusion, there are multiple ways to estimate a patient’s LVEF. Although these methods may be useful, none have been proven to be more accurate than a trained eye using visual estimation. Prac-tice is the best way to learn to estimate LVEF. In the meantime while you are learning, EPSS and FS may be acceptable methods to esti-mate the LVEF.
IMAGE 1.16 - AI Jet Preventing Normal MV Opening
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LVEF = 75.5 - 2.5 x EPSS
REFERENCES
1. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and poten-tial clinical utility of goal-directed transthoracic echocardiography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically ill patients. Journal of Car-diothoracic and Vascular Anesthesia. Apr 2005;19(2):155-159.
2. Armstrong W, Ryan T. Echocardiography. Seventh ed. Philadel-phia (PA): Lippincott, Williams, & Wilkins; 2010.
3. Oh J, Seward JB, Tajik AJ. The Echo Manual. 3rd ed. Lippincott, Williams, & Wilkins; 2006.
4. Monnet X, Teboul JL. Passive leg raising. Intensive Care Medicine. Apr 2008;34(4):659-663.
5. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Critical Care Medicine. May 2006;34(5):1402-1407.
6. Preau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis. Critical Care Medicine. Mar 2010;38(3):819-825.
7. Ahmadpour H, Shah AA, Allen JW, et al. Mitral E point septal separation: a reliable index of left ventricular performance in coro-nary artery disease. Am Heart J. 1983 Jul;106(1):21-8.
8. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point septal separa-tion and comparison to magnetic resonance imaging. Am J Car-diol. 2006;97(1):137-40.
16
CHAPTER 2
Right Heart
Haney Mallemat, MD
HIGHLIGHTS
Echocardiography of the RV can be helpful in:
- PE
- Fluid resuscitation
- Chronic RV failure
- Hemodynamic status
SECTION 1
IntroductionAcute right ventricular (RV) dysfunction may occur in patients with critical illness and is often challenging to diagnose and treat.1 Echo-cardiography can assist at the bedside to diagnose the etiology (e.g., pulmonary embolus) and monitor the response to therapy.2 Echocardiography can also identify patients with chronic RV failure if they present with other illnesses; knowledge of pre-existing RV dys-function may be important during their acute management (e.g., avoiding massive fluid resuscitation in patients with hypotension and severe RV dysfunction).
Hemodynamic assessment has classically focused on the left ventricle (LV), with little focus on the right. As this chapter will discuss, how-ever, the right ventricle is sensitive to changes in pulmonary and sys-temic pressure and volume, which may affect a patient’s hemody-namic status and acute management.
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HIGHLIGHTS
The RV has 3 distinct portions:
- Inflow Portion
- Apex
- Outflow Portion
The RCA perfuses the RV free wall.
The moderator band is perfused by the LAD.
SECTION 2
Normal Anatomy and PhysiologyThe right ventricle is the most anterior chamber of the heart, lying di-rectly behind the sternum. The RV has a complex geometric shape and is often described as a “U” shaped structure, as it wraps around the left ventricle.3 The RV can be visualized from the standard car-diac views; the inferior vena cava (IVC) should also be included in the assessment of the RV because it helps determine right atrial pres-sures. The RV can be visualized from the following four views:
1. Parasternal long-axis (PLA) view (Movie 2.1).
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MOVIE 2.1 - Parasternal Long-Axis View
2. Parasternal short-axis view (Movie 2.2).
3. Apical four-chamber (A4C) view (Movie 2.3).
4. Subcostal long-axis view (Movie 2.4).
The RV is sometimes described as three distinct portions due to its complex geometric shape:
1. Inflow (or body) portiona. Begins at the tricuspid valve and extends to the apex.b. This portion is smooth-walled with minimal trabeculations.
2. Apexa. Begins after the inflow portion.b. Is heavily trabeculated and contains the moderator band.c. When the apex is hypertrophied, thick trabeculations
may be mistaken for intra-cardiac tumors or thrombus.4
3. Outflow portiona. Begins distal to the apex, ends just proximal to the pulmo-
nary valve.b. Is the portion visualized in the PLA view (Movie 2.1).
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MOVIE 2.2 - Parasternal Short-Axis View
MOVIE 2.3 - Apical Four-Chamber View
MOVIE 2.4 - Subcostal Long-Axis View
BORDERS OF THE RV
The lateral border of the RV is the free wall; it is normally thin and should measure 5mm or less.5 Diseases or conditions causing in-creased pulmonary vascular resistance (e.g., pulmonary hyperten-sion) and increased afterload (e.g., left heart failure) may cause hy-pertrophy and increase the thickness of the free wall.1 Diseases such as hypertrophic cardiomyopathies and infiltrative cardiomyopathies may also result in increased free wall thickness without an increase in afterload.4 The free wall should be measured from the subcostal view during diastole; this is the view where the free wall is most per-pendicular to the plane of the ultrasound beam and hence, the most accurate measurement (Movie 2.5).
The interventricular septum is the medial border of the RV and it is shared with the left ventricle. The interventricular septum normally remains concave with respect to the LV throughout both systole and diastole; changes in this relationship, however, represent RV pathol-ogy and will be described later in this chapter (Movie 2.6).
The tri-leaflet tricuspid valve (TV) comprises the inferior border of the RV, and consists of the anterior, posterior, and septal leaflets. The superior border is poorly defined due to the complex geometric shape of the RV, but the apex of the apical 4-chamber view is typi-cally chosen. Of note, the tricuspid valve inflow view is usually the only view in which the posterior leaflet of the TV can be viewed (Movie 2.1).
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MOVIE 2.5 - Measuring RV Free Wall
MOVIE 2.6 - Interventricular Septum
PATTERN OF CONTRACTILITY
The RV and the LV differ in their pattern of contraction. The LV con-tracts in multiple planes; however, the majority of contraction occurs concentrically around the midpoint of the LV. The RV, on the other hand, contracts longitudinally; contracting from the tricuspid valve to-wards the apex and outflow tract.6 This longitudinal pattern of con-traction is often described as “peristaltic” or like an “accordion” (Movie 2.7).
The RV has approximately 25% of the muscle mass of the left ventri-cle, despite the fact that the RV must deliver the same amount of car-diac output as the LV. The RV is able to match the LV in cardiac out-put because the pulmonary vascular system is a high-flow and low-resistance circuit.6 The contractile force of the RV is mostly supplied by the free wall of the RV, but up to 33% of the force is contributed by the interventricular septum with contribution from the LV.
RV CORONARY BLOOD FLOW
The majority of RV coronary blood flow is from the right coronary artery (RCA).4 The RCA perfuses the RV free wall and the inferior wall of the LV. The posterior descending artery, which is a branch of the RCA, perfuses the inferior portion of the interventricular septum. The moderator band is perfused by the left anterior descending ar-tery (LAD); branches of the LAD may also perfuse the RV apex.
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MOVIE 2.7 - Pattern of Contraction
HIGHLIGHTS
The simplest method of assessing the RV size is the “eyeball” method using the apical 4-chamber view.
The normal RV/LV ratio is 0.6:1 in diastole.
Pressure and volume overload can be identified by a “D” shaped RV.
SECTION 3
RV Size & Function AssessmentASSESSING RV SIZE
The thin-walled right ventricle is sensitive to acute changes in pres-sure and/or volume. The RV may acutely dilate in response, increas-ing its overall dimensions and volume in response to these changes.4 It is therefore important to determine the RV size during initial assess-ment with echocardiography, as it may help lead to the cause of the presenting disease.7
QUALITATIVE ASSESSMENT: THE “EYEBALL” METHOD
The simplest method of assessing RV size is an “eyeball” method us-ing the apical 4-chamber view.8 The RV normally appears triangular-shaped and is two-thirds the size of the LV from this view, i.e., RV:LV is 0.6:1, as measured in diastole (Movie 2.8).
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MOVIE 2.8 - “Eyeball” Method
As the RV becomes mild to moderately dilated, the RV:LV ratio in-creases to 0.7-1:1. When the RV is severely dilated, the RV:LV ratio is >1:1. Although this method is qualitative and an “eyeball” assess-ment, it has been found to be relatively accurate with good inter-observer reliability.9
Qualitative Assessment of RV Size RV:LV RatioNormal 0.6:1
Mild-Moderately Dilated 0.7-1:1Severely Dilated >1:1
QUANTITATIVE ASSESSMENT
A quantitative assessment of RV size can also be made from the api-cal four-chamber view. Three measurements are taken during dias-tole; two transverse diameters and one longitudinal (Movie 2.9).
The RV is Enlarged When: 1) The base of the RV (or annulus of TV) measures > 35mm. 2) The mid-cavity of the RV is > 42mm. 3) The longitudinal diameter of the RV (base to apex) is > 86mm.5
PEARLS FOR IDENTIFYING THE RV
Severe RV dilation causes distortion of the ventricular anatomy to the extent that the novice sonographer may mistake the RV for the LV in the apical four-chamber view. Remember the following pearls to dis-tinguish the RV from the LV3 (Movie 2.10):
1. The tricuspid valve is more apically displaced within the RV, as compared to the mitral valve within the LV.
2. The RV always contains the moderator band, while the LV does not.
3. Tilting the probe anteriorly will visualize the “fifth” chamber of the apical view, also known as the aortic outflow track; this ven-tricle must therefore be the LV.
24
MOVIE 2.9 - Quantitative AssessmentMOVIE 2.10 - RV Identity Pearls
ASSESSING RV SYSTOLIC FUNCTION
Several diseases may lead to RV systolic dysfunction (e.g., RV acute myocardial infarction, sub-massive pulmonary embolism, etc.). Early detection may assist in the diagnosis, as well as monitoring response to therapy.7 Assessing systolic function, however, may be difficult due to the complex geometry of the RV and the longitudinal pattern of contraction. Two methods commonly used to assess RV systolic function are the:
1) Tricuspid annular plane of systolic excursion (or TAPSE) method
2) RV fractional area change (or RVFAC) method
Both methods assess RV systolic function from the apical four-chamber view.
TAPSE METHOD
The RV contracts longitudinally from the base to the apex (RV7). Therefore, the more the annulus of the TV is displaced during systole, the better the systolic function. Conversely, the less the TV annulus moves, the poorer the systolic function. TAPSE is a simple method in which the annular displacement of the TV is measured over a cardiac cycle and is performed from the apical four-chamber view. A normal TAPSE is 16-20mm, and a TAPSE less than 16mm is abnormal and in-dicates reduced RV systolic function.5
TAPSE<1.6cmAbnormal
Adding an M-mode to this assessment may improve accuracy. To use M-mode, place the cursor to the lateral border of the tricuspid annu-lus and observe contractility over a few cardiac cycles and then freeze the image; calipers are then used to measure the annular dis-placement (Movie 2.11).
RVFAC METHOD
RV systolic function can also be assessed by the RV fractional area change method. This method assesses the change in RV area from diastole to systole. To perform the method of RVFAC, the RV is im-aged from the apical four-chamber view and attempts to minimize RV foreshortening should be made. If available on your machine, the appropriate cardiac package should then be opened. The image should first be frozen and cine back to end-diastole, then the RV en-
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MOVIE 2.11 - Measuring TAPSE
docardium is traced completely around the chamber including trabe-culations, papillary muscles, and the moderator band. Once this area is completely traced, an area is calculated and will appear on the screen; this is the end-diastolic area (or EDA). Next, cine to the end of systole during the same cardiac cycle and trace the RV endo-cardium to obtain the end-systolic area (or ESA).
The RVFAC will automatically be derived or can be calculated by us-ing the formula:
RV Fractional Area Change FAC = (EDA-ESA)/EDA × 100
FAC<35%Abnormal
An RVFAC less than 35% is considered to be abnormal systolic func-tion, while greater than 40% is considered normal.5 Although this quantitative method of RV systolic assessment is validated and widely accepted, it is not uncommon for experienced cardiologists to offi-cially use the “eyeball” method assessment.
VENTRICULAR OVERLOAD
The thin-walled RV pumps blood to the left heart with a similar car-diac output as the muscular LV. The RV achieves this under normal filling and loading conditions because the pulmonary system is a low-pressure system. If the RV becomes overwhelmed by either pressure or volume overload, however, ventricular function may become ab-normal. There are two categories of RV dysfunction:
1) Pressure overload leading to systolic dysfunction. 2) Volume overload leading to diastolic dysfunction.
SYSTOLIC (PRESSURE) OVERLOAD
Acute or chronic increases in RV afterload (e.g., pulmonary embo-lism, pulmonary hypertension, etc.) lead to systolic (or pressure) overload.10 The RV accommodates increases in pressure by “balloon-ing” out the RV free wall. As a result, the interventricular septum be-comes flattened or “D” shaped when observed from the parasternal short-axis view (Movie 2.12).
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MOVIE 2.12 - Systolic Overload
Septal flattening (also known as paradoxical septal motion or septal dyskinesia) occurs during both systole and diastole, in contrast to the normal shape of the interventricular septum, which is concave with respect to the LV in both systole and diastole. In extreme cases, LV filling and cardiac output may be compromised when the septum flat-tens and encroaches on the LV cavity.
The RV may accommodate chronic increases in afterload through hy-pertrophy of the free wall. Recall that measurement of the free wall should be made during diastole from the subcostal view, as the ultra-sound beam is most perpendicular to the free wall; RV free wall measurements of greater than 5mm indicate hypertrophy from chronic overload (Movie 2.5).6 Other echocardiographic signs of chronic RV pressure overload include hypertrophy of apical trabecu-lations, papillary muscles, and the moderator band.
A clinically challenging situation arises when attempting to determine whether a patient with chronic RV afterload develops acute-on-chronic pressure overload (i.e., patient with chronic pulmonary hy-pertension develops an acute pulmonary embolism). In these cases, prior echocardiograms should be reviewed and compared to the cur-rent echocardiogram for any changes.
DIASTOLIC (VOLUME) OVERLOAD
Acute volume (or diastolic) overload may occur with massive volume resuscitation (e.g., massive transfusion in hemorrhagic shock) and may lead to RV diastolic dysfunction. If volume overload occurs, the RV can acutely adapt by dilating or “ballooning” out the free wall in
a manner similar to acute pressure overload; septal flattening (a “D” shaped septum) visualized in the parasternal short-axis view.4 Al-though this “D” shaped septum looks similar to pressure overload, the difference is that septal flattening from volume overload occurs at the end of diastole, while the septum is normal in contour during sys-tole (Movie 2.13). As was the case in pressure (or systolic) over-load, volume overload may compromise LV filling and cardiac output when the septum flattens and encroaches on the LV cavity.
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MOVIE 2.13 - Diastolic Overload
NON-INVASIVE MEASUREMENT OF PASPInvasive right heart catheters are typically used to measure pulmo-nary artery systolic pressures (PASP) for diagnosing or monitoring certain conditions (e.g., pulmonary hypertension). B-mode ultra-sound and Doppler, however, can be used to non-invasively estimate right heart pressures.11 Estimation of PASP requires deriving two measurements:
1) The peak RV systolic velocity (measured from tricuspid valve).2) The right atrial pressure (measured from IVC).
The first step is to obtain the peak RV systolic velocity, which is done by imaging the tricuspid valve (TV) in either the apical four-chamber view, RV inflow view (from the parasternal long-axis view), or parasternal short-axis view at the level of the aortic valve. Next, once the TV is visualized, a color Doppler box is placed over the valve to look for tricuspid regurgitation (TR). If TR is observed, the cursor for continuous wave (CW) Doppler is placed through the mid-dle of the jet and the peak velocity is obtained. If the ultrasound ma-chine has the appropriate calculation package, the peak RV systolic velocity of the jet is measured and the calculation package will auto-matically convert this value into a pressure (Movie 2.14).
The next step is to estimate the right atrial pressure (RAP). The RAP is obtained by visualizing the IVC from the subxiphoid view. The ab-solute size of the IVC and the change in diameter with respirations will estimate the RAP. IVC measurements should be made just distal to the junction of the IVC to the right atrium, just inferior to the first
hepatic vein. For how to measure the IVC, see the Fluid Responsive-ness chapter in Introduction to Bedside Ultrasound Volume 1.
IVC (cm) Collapse CVP
Normal <2.1 >50% 3 (0-5)
In Between </> 2.1 </>50% 8 (5-10)
High >2.1 <50% 15 (10-20)
The final step is to add the peak RV systolic pressure and RAP to de-rive the PASP. A PASP greater than 36mmHg is considered elevated.12,5 Limitations of this method include lack of an acoustic window to visualize the TV and the inability to define a TR jet (even with the coexistence of pulmonary hypertension).13
PASP>36mmHGAbnormal
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MOVIE 2.14 - PASP Assessment
HIGHLIGHTS
RV pressure overload and systolic dysfunction may suggest acute pulmonary embolism.
McConnell’s sign has a very poor specificity, possibly as low as 30%.
Signs of pericardial tamponade include: RA systolic collapse, RV diastolic collapse, reciprocal respiratory changes in the RV and LV filling, and plethora of the IVC.
SECTION 4
RV PathologyACUTE PULMONARY EMBOLISM
Acute pulmonary embolism causes significant morbidity and mortality worldwide,14 and bedside echocardiography can be used as a tool to help detect the presence of this disease when other suggestive clini-cal signs and symptoms are also present.15
Bedside echocardiography does not have adequate sensitivity to rule out pulmonary embolism alone, but may be suggested if found in conjunction with other findings.16 For example, RV pressure over-load and systolic dysfunction may suggest acute pulmonary embo-lism if a significant pulmonary clot burden is present. Acute pressure overload and RV dilation may also lead to dilation of the tricuspid valve annulus and tricuspid regurgitation, which can be detected with echocardiography (Movie 2.15).
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MOVIE 2.15 - Pulmonary Embolism
The presence of acute RV dysfunction with the acute onset of hypoten-sion may also help with the decision to treat a pulmonary embolism with thrombolytic therapy in the proper clinical context.17
McConnell’s sign was a commonly cited echocardiographic finding associated with acute pulmonary embolism. McConnell’s sign is de-fined by the presence of RV mid-wall hypokinesis with normal contrac-tion of the apex (Movie 2.16). First described in 1996, McConnell’s sign was once believed to be a very specific echocardiographic find-ing for an acute pulmonary embolism.18 Since its initial description, however, McConnell’s sign has been found in several other clinical conditions (e.g., pulmonary hypertension, acute respiratory distress syndrome, RV myocardial infarction, etc.). Casazza et al. demon-strated that McConnell’s sign has a very poor specificity (30%) for acute PE, and found that a significant number of patients with McCon-nell’s sign actually had an acute RV myocardial infarction (AMI).19
ACUTE RV MYOCARDIAL INFARCTION
Bedside ultrasound can assist in the diagnosis of an acute myocardial infarction of the RV.4,5 Depending on the size and duration of the oc-clusion, echocardiography may detect segmental wall motion abnor-mality (i.e., hypokinesis, akinesis, or dyskinesis) and/or a reduction in myocardial thickening.3 The presence of McConnell’s sign (hypoki-nesis of the mid RV free wall with normal apical contraction) may also suggest AMI, and other modalities should be used to distinguish the clinical picture from acute pulmonary embolism and other diseases.19
When an AMI of the RV is suspected, the RV should be inspected in multiple views to visualize the geometrically complex ventricle5:
1) Parasternal long-axis view examines the RV outflow tract.
2) Parasternal short-axis view (papillary muscle level) visualizes anterior, lateral and portions of the inferior wall.
3) Apical four-chamber view visualizes the lateral RV free wall and apex.
4) Subcostal long-axis view visualizes the inferior RV free wall.
5) Subcostal short-axis view visualizes the RV outflow tract and a portion of the RV inferior wall.
Particular attention should also be given when imaging the inferior wall of the LV and the inferior LV septum because the RCA also pro-vides perfusion to these territories.
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MOVIE 2.16 - McConnell’s Sign
PERICARDIAL TAMPONADE AND THE RV
Pericardial effusions may occur from a variety of disorders (e.g., HIV, uremia, trauma) and ultrasound can be used to diagnose the ef-fusion, as well as assist with ultrasound-guided pericardiocentesis.20 Pericardial tamponade is the physiologic state in which increasing pressure within the pericardial space may exceed the pressure within the heart (or the intra-cardiac pressure). Over time, this may result in reduced cardiac filling, cardiac output, and hemodynamic collapse. Tamponade is a clinical diagnosis, but ultrasound can demonstrate early signs of impending tamponade, even before hypotension develops.4,21 See the Basic Cardiac chapter in Introduction to Bed-side Ultrasound Volume 1 for additional information.
TAMPONADE: A REVIEW OF PHYSIOLOGY
Accumulation of fluid in the pericardial space progressively reduces filling of the low-pressure right-sided heart chambers, regardless of the initial insult or underlying pathology. If the pericardial fluid accu-mulates chronically, the pericardium can adapt by increasing in size to accommodate the rising intra-pericardial pressures. On the other hand, rapidly accumulating effusions are not well tolerated, and small but rapid effusions can acutely result in cardiovascular col-lapse. Whether an effusion develops acutely or chronically, there is a critical point where the rising intra-pericardial pressures exceed the pressures within the right side of the heart; this results in a reduction in cardiac filling and subsequently cardiac output.
Several signs of impending tamponade can be detected with bedside ultrasound. These include:
a. Right atrial systolic collapseb. Right ventricular diastolic collapsec. Reciprocal respiratory changes in the RV and LV fillingd. Plethora of the inferior vena cava
RA SYSTOLIC COLLAPSE
The right atrial (RA) free wall is thin and sensitive to increases in intra-pericardial pressures. As a result, critical intra-pericardial pres-sures result in systolic collapse of the RA free wall (best viewed from apical four-chamber view) and is a sign of tamponade physiology. Although brief RA systolic collapse may be normally seen, collapse persisting for greater than 1/3 of atrial systole is 94% sensitive and 100% specific for pericardial tamponade22 (Movie 2.17).
31
MOVIE 2.17 - Pericardial Tamponade
RV DIASTOLIC COLLAPSE
RV free wall collapse during diastole may also be seen with pericar-dial tamponade. RV collapse is best visualized in either the paraster-nal long-axis or subcostal long-axis view (Movie 2.18).
Once the appropriate window is obtained, an indentation of the RV can be visualized during diastole. An M-mode cursor may be placed through the RV free wall to better visualize the abnormal free wall motion11 (Movie 2.19).
Diastolic collapse of the RV free wall is less sensitive than RA systolic collapse (60% vs. 94%) but is a very specific sign of tamponade (100%).4 The sensitivity of RV diastolic collapse may be reduced, however, with conditions such as RV free wall hypertrophy and infil-trative cardiomyopathies (e.g., amyloidosis); diastolic collapse may be masked despite relatively elevated intra-pericardial pressures.23
RESPIROPHASIC DOPPLER INFLOW VELOCITY
Inspiration causes negative intra-thoracic pressures, which pulls open (i.e., away from the septum) the free wall of the right ventricle under normal conditions. This creates a negative pressure within the right side of the heart, leading to increased venous return and right-sided cardiac filling. Increases in right heart filling result in an increased RV inflow velocity through the tricuspid valve. When expiration be-gins, the left side of the heart fills, resulting in an increased LV inflow velocity through the mitral valve; the right-heart simultaneously nor-malizes the RV inflow velocity. Over a normal respiratory cycle there should be no more than 25% and 15% variation of inflow ve-locity for the tricuspid and mitral valves, respectively.11
An exaggeration in the variation of inflow velocities is observed when tamponade physiology is present. This occurs because the RV free wall cannot pull open against the dense pericardial effusion. Therefore, as the right heart fills during inspiration, the septum is pushed over into the LV to accommodate RV filling; the result is that
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MOVIE 2.18 - Pericardial Tamponade
MOVIE 2.19 - M-Mode Pericardial Effusion
the LV fills less effectively and the MV inflow velocity is reduced. With expiration, the LV inflow velocities increase and also become exaggerated as the septum shifts back towards the RV. Pericardial tamponade should be suspected when variations of more than 40% or 25% are observed for tricuspid and mitral inflow velocities, respectively.24-26 Of note, the previous description is the physiologic explanation of pulsus paradoxus (i.e., reduction in systolic BP by 10-12mmHg during inspiration) observed in pericardial tamponade.
The apical four-chamber view is the best view to assess variation of inflow velocities. To perform this exam, the sample volume for pulsed wave Doppler is placed at the tips of the leaflets of each valve. The velocities recorded above the baseline (i.e., toward the probe) are then measured for the maximum and minimum velocities and the percentage of variation recorded. This measurement is some-times made with a respirometer to determine the phase of respira-tion, although not mandatory.11 The Doppler sweep speed can be reduced to 12.5 meters per second to visualize more cardiac cycles, especially if the patient has tachycardia (Movie 2.20).
INFERIOR VENA CAVA (IVC) PLETHORA
Pericardial tamponade increases right heart pressures. This is re-flected by a dilated or plethoric IVC with less than 50% respiratory variation (recall that IVC size and respiratory variation reflect RA pressure). Although IVC plethora is not a specific sign of pericardial tamponade (40%), it has good sensitivity (97%).27 A plethoric IVC can be used to confirm pericardial tamponade when other echocar-diographic signs are also present and may help rule it out if a pericar-dial effusion is present (effusion but no tamponade)28 (Movie 2.21).
CONCLUSION
In summary, the geometrically complex RV is thin walled and has only 25% of the musculature of the LV, yet it produces the same amount of cardiac output. Several diseases can affect the RV, di-rectly or indirectly, leading to hemodynamic compromise. Familiarity with the various echocardiographic changes in RV morphology may lead to earlier identification of disease and potentially better patient outcomes by minimizing hemodynamic compromise.
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MOVIE 2.20 - Respirophasic Variation
MOVIE 2.21 - Plethoric IVC
SECTION 5
REFERENCES
1. Etchecopar-Chevreuil C, Francois B, Clavel M, et al. Cardiac mor-phological and functional changes during early septic shock: a transesophageal study. Intensive Care Med. 2008;34:250-56.
2. Torbicki A, Perrier A, Kostantinides S, et al. Guidelines on the di-agnosis and management of acute pulmonary embolism. Eur Heart J. 2008;29:2276-315.
3. Armstrong WF, Ryan T. Feigenbaum’s Echocardiography. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.
4. Otto CM. Textbook of Clinical Echocardiography. 4th ed. Philadel-phia, PA: Saunders Elsevier; 2009.
5. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardio-graphic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the Euro-pean Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of
Echocardiography. J Am Soc Echocardiogr. 2010 Jul;23(7):685- 713.
6. Levitov A, Mayo PH, Slonim AD. Critical Care Ultrasonography. McGraw Hill; 2009.
7. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically ill. Emerg Med Clin North America. 2010 Feb;28(1):29-56.
8. Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997;111:209-17.
9. Vieillard-Baron A, Charron C, Cergui K, et al. Bedside echocardio-graphic evaluation of hemodynamics in sepsis: is a qualitative evaluation sufficient? Intensive Care Medicine. 2006;32:1547-52.
10. Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol. 1985;5:918-27.
11. Oh JK, Seward JB, Tajik AJ. The Echo Manual. 3rd edition. Phila-delphia, PA: Lippincott Williams & Wilkins; 2006.
12. Badesch DB, Champion HC, Sanchez MA, et al. Diagnosis and assessment of pulmonary arterial hypertension. J Am Coll Cardiol. 2009;54:S55-66.
13. Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultra-sound. J Am Coll Cardiol. 1985;6:359- 365.
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14. Tapson VF. Acute pulmonary embolism. N Engl J Med. Mar 6 2008;358(10):1037-52.
15. Nazeyrollas P, Metz D, Jolly D, et al. Use of transthoracic echo- cardiography combined with clinical and electrocardiographic data to predict acute pulmonary embolism. Eur Heart J. 1996;17:779-786.
16. Roy PM, Colombet I, Durieux P, et al. Systematic review and meta-analysis of strategies for the diagnosis of suspected pulmo-nary embolism. Br Med J. 2005;331:259.
17. Guyatt GH, Akl EA, Crowther M, et al. Executive Summary: An-tithrombotic Therapy and Prevention of Thrombosis, 9th ed: Ameri-can College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(S2):7S-47S.
18. McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pul-monary embolism. Am J Cardiol. 1996 Aug 15;78(4):469-73.
19. Casazza F, Bongarzoni A, Capozi A, et al. Regional right ven-tricular dysfunction in acute pulmonary embolism and right ven-tricular infarction. Eur J. Echocardiography. 2005 Jan;6(1):11-4.
20. Blaivas M. Incidence of pericardial effusion in patients presenting to the emergency department with unexplained dyspnea. Acad Emerg Med. 2001;8:1143-1146.
21. Blaivas M, Graham S, Lambert MJ. Impending cardiac tampon-ade: an unseen danger? Am J Emerg Med. 2000;18:339-340.
22. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic compres-sion of the right atrium: A new echocardiographic sign if cardiac tamponade. Circulation. 1983;68:294-301.
23. Leimgruber PP, Klopfenstein HS, Wann LS, Brooks HL. The hemo-dynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade: An experimental echocardio-graphic study. Circulation. 1983;68:612-620.
24. Gonzalez MS, Basnight MA, Appleton CP. Experimental Cardiac Tamponade: A hemodynamic and Doppler echocardiographic re-examination of the relation of right and left heart ejection dynam-ics to the phase of respiration. J Am Coll Cardiol. 1991; 18:243-52.
25. Lang RM, Bierig M, Deveraux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, Developed in Conjunction with the European Association of Echocardiography, a Branch of the European Society of Cardiology. J Am Soc Echocardiography. 2005;18(12):1440-1463.
26. Picard MH, Sanfilippo AJ, Newell JB, et al. Quantitative relation between increased intrapericardial pressure and Doppler flow ve-locities during experimental cardiac tamponade. J Am Coll Car-diol. 1991;18:234-42.
27. Himelman RB, Kircher B, Rockey DC, Schiller NB. Inferior vena cava plethora with blunted respiratory response: A sensitive echo-
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cardiographic sign of cardiac tamponade. J Am Coll Cardiol. 1988;12:1470-77.
28. Eisenberg MJ, Schiller NB. Bayes’ theorem and the echocardio-graphic diagnosis of cardiac tamponade. Am J. Cardiol. 1991; 68:1242-44.
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CHAPTER 3
Diastology
Mike Mallin, MD, RDCS, RDMS
HIGHLIGHTS
Diastology is the science of quantifying how well the LV relaxes and complies.
50% of heart failure is diastolic only.
The physical exam is not accurate in diagnosing heart failure.
SECTION 1
IntroductionDiastole is the period of the cardiac cycle between the closure of the aortic valve and closure of the mitral valve. The primary function of diastole is to fill the left ventricle in preparation for systole.
For the purpose of this chapter diastology is the echocardiographic evaluation of the relaxation and compliance of the left ventricle (LV) and one of the most complicated and difficult aspects of echocardi-ography. This evaluation is considered an advanced skill, but it can be a valuable part of the echo evaluation in patients with dyspnea or signs of heart failure in the emergency department. According to the European Society of Cardiology, about 50% of patients with heart failure have “diastolic-only” failure, and thus a normal ejection frac-tion (EF).1 With 5 million Americans suffering from heart failure and an annual related heath care cost of 29.6 billion dollars, this disease represents a significant burden on the economy and greatly contrib-utes to the health care crisis in the U.S.
A thorough diastolic evaluation should be performed on patients whenever a complete echocardiogram is performed. The diastolic evaluation itself takes only a few minutes and can help identify eleva-tions in cardiac filling pressures and offer prognostic information.2,3 Diastolic dysfunction has been shown to more appropriately corre-late with cardiac filling pressures than LV EF. For this reason, a more focused diastolic exam can be performed when interested in the rela-tion of diastolic dysfunction to symptomatic heart failure in patients with dyspnea, weight gain, or other concerning findings for volume overload.
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Diastolic function in the evaluation of critically ill patients is an area of significant interest in critical care echocardiography. We know that diastolic and systolic dysfunction can help elicit those patients that are at risk of being fluid intolerant. 4,5 Some providers have even used changes in diastolic function to guide fluid therapy, although this has not been proven in the literature. While beyond the scope of this text, diastolic function can be used for multiple applications in critically ill patients, but it requires significant expertise to do so.6 An important application of diastolic dysfunction in sepsis is its use as a predictor of mortality. In one study, isolated diastolic dysfunction was found to have the highest hazard score of any predictor, even low urine output. 7
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HIGHLIGHTS
The diastolic filling period is controlled by left atrial pressure, myocardial relaxation, and compliance.
Intrinsic Functions:- Relaxation: Ability of the myocardium to relax in early
diastole and pull in blood.- Compliance: Ability of myocardium to accept a volume of
blood and continue to expand.
Filling Pressure:- Left atrial pressure: Pressure of the blood in the LA wait-
ing to fill the left ventricle.
SECTION 2
PhysiologyThe physiology of diastolic function is possibly the most complicated aspect of the topic, but it is paramount in understanding how to ap-ply echocardiography for diastolic evaluation. The diastolic filling period of the cardiac cycle can be broken into two phases:
1) E Wave: The early filling phase, which is dominated by myocar-dial relaxation and the left atrial (LA) filling pressure.
2) A Wave: The late filling phase, which is dominated by the LA contraction and left ventricular compliance.
This relationship is often described as a “push-pull” filling of the left ventricle (Figure 3.1).
The early filling phase represents the LV pulling blood from the LA by creating a relative negative intraventricular pressure by the post sys-tolic relaxation of the LV chamber. This effect is secondary to the tor-
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FIGURE 3.1 - The Push-Pull Relationship of LV Filling
sional recoil of the left ventricle. In a normal heart, almost all of the filling of the LV occurs during the “pull.” As diastolic function wors-ens, the LV loses the ability to “pull” blood into the LV and the body has to retain fluid to increase the LA loading pressure. This repre-sents a change from “pull” to “push”, where LA pressure has to ele-vate to overcome the poor relaxation and compliance of the left ven-tricle (Movie 3.1).
Most diastolic dysfunction is caused by longstanding hypertension. This disease leads to thickened LV walls from the constant increased afterload, which become stiff from hypertrophy.8 This stiffening causes worsening relaxation and compliance and impairs LV filling, which leads to decreased cardiac output, activation of the renin-
angiotensin II system, and eventually increased preload and filling pressures. This is the body’s method of continuing to fill a thickened, stiff LV: by increasing filling pressures through an elevation in pre-load. This process causes the symptoms we all know as heart failure (Figure 3.2).
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MOVIE 3.1 - Explanation of the Forces in Diastole
FIGURE 3.2 - Physiology
HIGHLIGHTS
Qualitative: Large LA, poor descent of the base.
Quantitative: PW Doppler of MV inflow, TDI of septal MV annu-lus. Key Values:
- Elevated PCWP > 12mmHg- Elevated LVEDP > 16mmHg- Normal E velocity < 100cm/so Normal e’ velocity > 8cm/so Normal E/e‘ < 15
SECTION 3
Evaluating Diastolic Function
QUALITATIVE EVALUATION
Diastolic dysfunction can be inferred from two key observational find-ings on bedside ultrasound. First, a patient with elevated filling pres-sures, and thus diastolic dysfunction, typically has a dilated, large left atrium. In fact, LA volume has been found to be very strongly associated with diastolic dysfunction and expresses the severity of diastolic dysfunction.9 The left atrial area is best measured in the api-cal 4 chamber view (Image 3.1).
This window can be difficult to obtain, but a normal atrial size in an otherwise healthy patient is often the extent to which diastolic dys-function need be evaluated. A typical LA volume is measured at end
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IMAGE 3.1 - Measurement of LA Area
systole and is less than 58ml, although a visual estimation is typically adequate for assessing the need for further diastolic assessment. An additional initial analysis of diastolic dysfunction is the visual assess-ment of descent of the base - the apical displacement of the septal mitral valve annulus during diastole (Image 3.2, Movie 3.2).
Adequate movement of the base is typically acceptable to rule out severe diastolic dysfunction, as greater movement suggests rapid re-laxation during early diastole, and thus normal diastolic filling. Slow or minimal descent of the base is consistent with diastolic dysfunction.
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IMAGE 3.2 - Location of Mitral Annulus
MOVIE 3.2 - Qualitative Evaluation of the LA and Descent of the Base
QUANTITATIVE EVALUATION
Quantitative evaluation of diastolic function is obtained by perform-ing 2 specific Doppler measurements: Mitral valve inflow and tissue Doppler imaging.
MITRAL VALVE INFLOW
Mitral valve (MV) inflow patterns are used to define the degree of diastolic dysfunction.10 This measurement tells us the velocity at which the blood is traveling as it passes through the MV during dias-tole. The ability of the LV to relax and comply to the changes in the pressure in the LA affects these velocity profiles. These measure-ments of the velocity profile can describe the severity of disease.11
This Doppler measurement is obtained by placing the pulsed wave (PW) Doppler gate at the very tips of the mitral valve leaflets in the apical 4 chamber window (Illustration 3.1).
The waveform obtained includes the E and A waves, where “E” re-fers to early filling and “A” refers to the atrial kick (Image 3.3).
The variations of mitral valve inflow patterns are broken into 4 differ-ent types (Figure 3.3).
• Normal: E>A
• Impaired Relaxation: E<A
• Pseudonormal: E>A
• Restrictive: E>>>A
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ILLUSTRATION 3.1 - Location of Doppler Gate for MV Inflow
IMAGE 3.3 - Mitral Valve Inflow Pattern
The severity of diastolic dysfunction worsens from normal to restric-tive (Figure 3.4).
Normal: Normal filling pressures, Left Ventricular End Diastolic Pres-sure (LVEDP) < 15mmHg
In normal MV filling, the majority of diastolic filling occurs during the early phase of the cardiac cycle, thus the E is greater than the A wave.
Impaired Relaxation: Normal filling pressures, LVEDP < 15mmHg
As the LV stiffens, the next chronologic phase in the progression of disease is Impaired Relaxation. This inflow pattern displays the myo-cardium’s inability to relax, thus less blood flow occurs during the early filling phase (low E velocity) and more occurs during the atrial kick (E<A). Although the myocardium is stiff at this point, the filling pressures are not elevated as the atrium makes up for the impaired relaxation without an increase in preload and filling pressure.
Pseudonormal: Increased filling pressure, LVEDP > 15mmHg
By this point in the disease process, the body has retained fluid in or-der to increase preload, and thus filling pressures, so that the LV can be appropriately filled during diastole. Appropriately, the increase in filling pressure and volume of the LA causes a significant pressure difference between the LV and the LA during early diastole, with the pressure in the LA being much higher than the LV. This leads to a higher E velocity and therefore E>A again.12 This pattern looks very similar to Normal, and thus requires tissue Doppler imaging (TDI) to differentiate. This patient is volume overloaded.
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FIGURE 3.3 - The Different MV Inflow Patterns
FIGURE 3.4 - Doppler of MV Inflow and TDI Patterns
Restrictive: increased filling pressure, LVEDP > 20mmHg
Restrictive is the most severe form of the disease and likely represents significant volume overload. On MV inflow, there is little to no A wave and the E wave is typically very large with E velocities ap-proaching 150-200cm/s. The pressure within the LV cavity during end diastole is now so high that the atrial kick is virtually ineffective at filling the LV, and thus there is little to no A wave on the MV inflow pattern.
MV inflow patterns are a spectrum and change with the patient’s vol-ume status. For example, a patient admitted in acute heart failure with an initial echo showing restrictive MV inflow pattern may have a repeat echo on hospital day 3 showing impaired relaxation due to significant diuresis. Once a patient’s MV inflow pattern is impaired, they typically never go back to normal since the damage to the myo-cardium has already been done. However, patients can move be-tween impaired, pseudonormal, and restrictive as their preload and filling pressures change.
TISSUE DOPPLER IMAGING
TDI measures the speed of the myocardium as it moves during dias-tole. As the LV fills, the ventricle elongates and the base of the heart (the portion including the MV, tricuspid valve, and atria) descends away from the probe. The speed at which the tissue moves while the ventricle is expanding changes as relaxation occurs, and thus dia-stolic function worsens. As the ventricle becomes stiffer, it moves slower and the descent of the base is diminished.
To obtain this measurement, the tissue Doppler imaging setting on the machine is used. TDI is simply a pulsed wave Doppler setting on some echo machines that automatically decreases the velocity scale to 0-20cm/s below the zero velocity baseline, decreases the wall fil-ter, and decreases the gain.13 (Note: You do not have to have a TDI setting on your machine to measure the velocity of the myocardium for this evaluation, although TDI is quicker.) The apical 4 chamber window is again used and the TDI gate is placed on the septum, just next to the MV septal leaflet11 (Illustration 3.2).
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ILLUSTRATION 3.2 - TDI Gate Location for TDI Waveform Analysis
The waveform produced displays an e’ wave and a’ wave, which sig-nify the same aspect of diastole as in the MV inflow pattern: e’ repre-sents early filling, and a’ represents the atrial kick. The e’ and a’ will be much slower than the E and A since they represent tissue move-ment rather than blood velocities13 (Figures 3.4, 3.5, Image 3.4).
A normal TDI displays an e’>a’ where the e’ velocity is > 8cm/s
As the diastolic dysfunction worsens, the e’ wave gets smaller and smaller as the myocardial velocity approaches zero. Once the e’ ve-locity is < 8cm/s, the patient has diastolic dysfunction. Thus, when differentiating between normal and pseudonormal MV inflow pat-terns, the TDI measurement can be extremely helpful.
Estimating LVEDP: The LVEDP can be estimated by dividing the E ve-locity by the e’ velocity (Figure 3.6). If this value is > 15mmHg, then the patient is believed to have an elevated LVEDP.15,16
Find out more about the topic of Tissue Doppler Imaging here.
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IMAGE 3.4 - Normal TDI Waveform
FIGURE 3.5 - Grading of Diastolic Failure
FIGURE 3.6- Estimating LVEDP
MOVIE 3.4 - One Minute Ultrasound Diastolic Demo
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MOVIE 3.3 - Diastology How-To
HIGHLIGHTS
Diastolic dysfunction can be useful in the following clinical scenarios:
- Acute heart failure- Volume overload - Critical patients requiring massive volume resuscitation
SECTION 4
Clinical ApplicationACUTE DYSPNEA
Patients can present with symptoms of an acute heart failure exacer-bation without systolic dysfunction. While the majority of these pa-tients also have a reduced ejection fraction, diastolic dysfunction can be the underlying cause rather than systolic dysfunction. Pseudonor-mal or restrictive patterns identify those patients with elevated LVEDP and may help identify those patients that need diuresis.
VOLUME OVERLOAD
In patients with acute heart failure exacerbations, diastolic function can be used to estimate the LVEDP, and thus the response to therapy. As mentioned previously, as LVEDP changes, so does the inflow pat-tern. Therefore, it is not unusual for patients with heart failure to tran-sition from restrictive to impaired relaxation over the course of their diuresis.
MASSIVE VOLUME RESUSCITATION
Diastology can be used for directing fluid resuscitation or simply indi-cating those patients at higher risk for pulmonary edema with mas-sive volume resuscitation. If used to direct fluid resuscitation, one would do so as if guiding volume resuscitation using the PCWP. We know that E/e’ > 15 indicates an elevated LVEDP and thus an ele-vated PCWP. Thus, one option would be to fluid bolus the patient un-til the E/e’ reached 15, although this has not been adequately stud-ied. It is important to note that other methods of detecting fluid re-
49
sponsiveness have been more rigorously studied, such as passive lag raise, Ao velocity variation, or even the IVC changes with respira-tion. (See the Fluid Responsiveness chapter in Introduction to Bedside Ultrasound Volume 1 for more information). If just being used to identify patients at risk, one would have concerns of fluid tolerance if the patient has impaired relaxation, pseudonormal or restrictive MV inflow patterns at the onset of volume resuscitation.
Also see: Ultrasound Podcast Diastology Part 1 and Part 2.
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HIGHLIGHTS
Limitations of diastolic evaluation include operator error, change in Doppler measurements due to angle of insonation, and irregularities in waveforms from certain clinical conditions.
Other causes of heart failure symptoms in patients with normal EF also exist.
SECTION 5
LimitationsLIMITATIONS
There are several limitations of diastolic evaluation of the heart using Doppler echocardiography. The first and most important is operator error. Doppler measurements change with the angle of insonation. Additionally, patients with tachycardia often have fused E and A waves, making mitral waveform patterns difficult to address. Arrhyth-mias, such as atrial fibrillation, destroy the A waves and cause irregu-lar heartbeats, which inevitably change the dP/dT from beat to beat. This makes diastolic evaluation virtually impossible.
There are also other causes of heart failure symptoms in patients with normal ejection fractions. These include constrictive pericarditis and mitral regurgitation.
CONSTRICTIVE PERICARDITIS
This also causes elevated filling pressures in the setting of a normal LV EF and can present as acute heart failure. However, patients have respiratory variation of MV inflow velocities >25% with expira-tion, diastolic flow reversal in the hepatic veins, and typically have a septal e’ velocity > the lateral annulus e’ velocity (Image 3.5).
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The latter of these findings is unique to constrictive pericarditis and is due to the retained vertical excursion, thus the septal e’ velocity be-ing greater than the lateral e’ velocity.17
MITRAL REGURGITATION (MR)
Moderate to severe MR can lead to significant elevations in peak E velocities of mitral valve inflow. While this increase in E wave veloc-ity does not necessarily mean diastolic dysfunction, the increased E/e’ ratio is predictive of the degree of MR disease and the need for hospitalization and mortality.18
CONCLUSION
In the end, diastology is a more advanced technique than identifying pericardial effusion and estimating global function. Nevertheless, it can be a very valuable tool that is applicable to a very large popula-tion of patients. If one takes the time to learn it, patients will reap the benefits.
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IMAGE 3.5 - Location of Mitral Annulus
SECTION 6
REFERENCES
1. Paulus WJ, Tschope C, Sanderson JE, et al. How to diagnose dia-stolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J. 2007. 28(20):2539-2550.
2. Nazerian P, Vanni S, Zanobetti M, et al. Diagnostic accuracy of emergency Doppler echocardiography for identification of acute left ventricular heart failure in patients with acute dyspnea: com-parison with Boston criteria and N-terminal prohormone brain na-triuretic peptide. Acad Emerg Med. 2010; 17(1):18-26.
3. Yu HC, Sanderson JE. Different prognostic significance of right and left ventricular diastolic dysfunction in heart failure. Clin Car-diol. 1999;22(8):504–512.
4. Sturgess DJ, Marwick TH, Joyce C, et al. Prediction of hospital outcome in septic shock: a prospective comparison of tissue Doppler and cardiac biomarkers. Crit Care. 2010;14(2):R44.
5. Payen D. Prediction of fluid challenge effect: filling pressure when left ventricular funciton is abnormal, diastolic volume when left ventricular function is normal. Crit Care. 2011;15(2):139.
6. Nagueh SF, Middleton KJ, Kopelen HA, et al. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;30:1527-1533.
7. Landesberg G, Gilon D, Meroz Y, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J. 2012;33(7):895-903.
8. Leite-Moreira AF. Current perspectives in diastolic dysfunction. Car-diovasc Res 1999;43:344-53.
9. Tsang TS, Barnes ME, Gersh BJ, et al. Left atrial volume as a mor-phophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol. 2002;90:1284-9.
10. Appleton CP, Jensen JL, Hatle LK, et al. Doppler Evaluation of left and right ventricular diastolic dysfunction: a technical guide for obtaining optimal flow velocity recordings. J Am Soc Echocar-diogr. 1997;10:271-291.
11. Naguech SF, Appleton CP, Thierry GC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardi-ography. J Am Soc Echocardiogr. 2009;22(2):130.
12. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow ve-locity patterns to the left ventricular diastolic function: new insights
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