Download Chapter 1 Echocardiographic Assessment of Cardiac Output and

C HAPTER 1
Echocardiographic Assessment of
Cardiac Output and Ejection
Fraction
Jay Blankenship, MD
Mike Mallin, MD, RDCS, RDMS
S ECTION 1
Echocardiography has been shown to be an effective, noninvasive
Introduction
shown that non-cardiologists can safely and accurately use echocardi-
method of assessing cardiac function.
Furthermore, it has been
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:
H IGHLIGHTS
Echo is an effective, noninvasive method for measuring CO.
Non-cardiologists can measure CO.
CO=SV x HR
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
SV=LVOT area x VTI
2
S ECTION 2
The LVOT area is approximated by assuming that it is the shape of a
Measuring LVOT Area
LVOT. Once obtained, a person’s LVOT area does not change. You
circle. Thus, the area is determined by measuring the diameter of the
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).
F IGURE 1.1 - Parasternal Long Axis View
H IGHLIGHTS
LVOT is measured in the parasternal long axis view.
Zoom in on the LVOT to get good visualization of the aortic
root.
I MAGE 1.1 - Parasternal Long Axis View
Measure LVOT in mid-systole, with maximal separation of leaflets.
3
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 leaflets). Importantly, the diameter of the LVOT should be measured perpendicular to the direction of the LVOT and should be performed in
mid-systole, with maximal separation of leaflets (Image 1.2).
I MAGE 1.2 - LVOT Diameter
Measured in mid-systole at base of Ao leaflets.
LVOT area can then be calculated using the following formula:
LVOT area (cm2) =
4
S ECTION 3
To calculate VTI, pulsed wave Doppler is used to measure the veloc-
Measuring VTI
cal 5 chamber view of the heart (Figure 1.2, Image 1.3, Figure 1.3,
ity of flow across the LVOT. First, obtain an apical long axis or apiImage 1.4).
F IGURE 1.2 - Apical 5 Chamber
View
H IGHLIGHTS
Measure VTI in the apical long axis or 5 chamber view.
I MAGE 1.3 - Apical 5 Chamber VTI Measurement
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.
5
F IGURE 1.3 - Apical Long Axis
View
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 measurement package (often found under “CO” or “Ao” in the cardiac
measurements section) and trace the waveform of one ejection period (Image 1.5).
I MAGE 1.5 - VTI Tracing
I MAGE 1.4 - Apical Long Axis VTI Measurement
6
Doing this will calculate a value for VTI by taking area under the
curve. This measurement is essentially taking the integral of a velocity, so the VTI will be reported in cm. Stroke volume can then be calculated using the following formula:
SV (cm3) = Area LVOT (cm2) x VTI(cm)
SV =
P ITFALLS
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 therefore SV.
2. When measuring diameter of LVOT, ensure that the measurement
is taken in mid-systole. Failure to do this can result in underestimation 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
S ECTION 4
Patient care often requires an assessment of a patient’s volume status
Passive Leg Raise
many other pathologic states require rapid volume repletion. How-
to direct a course of treatment. Sepsis, hypotension, pancreatitis and
ever, overzealous administration of fluid can be detrimental, particularly in patients with known congestive heart failure. In such cases,
echocardiography can be used as a non-invasive method of determining the fluid status of a patient using the passive leg raise (PLR) maneuver. The PLR maneuver enables the physician to deliver a reversible, 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).
H IGHLIGHTS
F IGURE 1.4 - PLR Baseline Position
Passive leg raise is a noninvasive method of estimating volume
responsiveness.
Logistically, this can be difficult in the ED.
8
The patient should then be placed recumbent with legs elevated to
M OVIE 1.1 - One Minute Ultrasound Passive Leg Raise Demo
45°, and SV should be reassessed after approximately 30-90 seconds4 (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 appropriate elevation of legs during the second measurement of SV.
F IGURE 1.5 - PLR Legs Elevated Position
9
S ECTION 5
Assessing the Ejection
Fraction
Although most echocardiographers use the “eyeball” technique to
estimate the left ventricular ejection fraction (LVEF), there are additional methods for estimation. These include:
§
Fractional shortening (FS)
§
Simpson’s Method (Method of Discs)
§
E-point septal separation (EPSS)
F RACTIONAL S HORTENING
Fractional shortening uses an anterior-posterior measurement of the
left ventricular dimension to estimate ejection fraction. This measurement 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
H IGHLIGHTS
abnormalities. The measurement is made at end systole (LVESD - end
The “eyeball” technique for assessing ejection fraction when
This measurement should be made 1cm apically from the septal-
performed by experienced sonographers is as good as quantita-
aortic attachment and perpendicular to the long axis of the heart in
tive methods.
the parasternal long axis or parasternal short axis window and
A normal FS is 25-45%.
systolic diameter) and end diastole (LVEDD - end diastolic diameter).
should bisect the chordae tendineae (Image 1.6, 1.7). A normal fractional shortening is between 25-45%.
A normal EPSS is <7mm.
Pearl: The FS is typically ½ the total ejection fraction
10
I MAGE 1.7 - Normal FS
S IMPSON ’ S M ETHOD
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 diastole 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.
EPSS
I MAGE 1.6 - Reduced FS
E-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 cardiomyopathy. 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 visualized. If the MV is touching the septum on visual inspection, the patient’s EF can be described as normal, or greater than 55%.
11
If the MV is not touching the septum, the distance from the MV dur-
STEP 2: Obtain adequate view of MV (Movie 1.2).
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
M OVIE 1.2 - MV View
consistent with a reduced ejection fraction.
I MAGE 1.8 - Location of EPSS Measurement
STEP 3: Place M-mode ice pick through tip of MV (Image 1.9).
S TEPS TO E VALUATE EPSS
I MAGE 1.9 - Location of M-Mode for EPSS
STEP 1: Obtain parasternal long axis window (Figure 1.6).
F IGURE 1.6 - Probe Placement for
PSLA Window
12
STEP 4: Initiate M-mode tracing (Image 1.10).
I MAGE 1.12 - Normal EPSS and Thus LVEF
I MAGE 1.10 - M-Mode
Button
STEP 5: Identify the E and A waves of the MV (Images 1.11, 1.12).
I MAGE 1.11 - M-Mode Through Mitral Valve
STEP 6: Measure distance from tip of MV to septum (Image 1.13).
I MAGE 1.13 - E and A Waves of Mitral Valve
13
Example of normal EPSS in patient with normal LVEF (Image 1.14):
Examples of elevated EPSS in patient with severely reduced LVEF (Image 1.15, Movie 1.3):
I MAGE 1.14 - Location of EPSS Measurement
I MAGE 1.15 - Increased EPSS and Thus
Reduced LVEF
M OVIE 1.3 - Increased EPSS and Thus
Reduced LVEF
14
A recent MRI study created an equation that can be used to estimate
a LVEF based on the EPSS distance:
8
LVEF = 75.5 - 2.5 x EPSS
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
S UMMARY
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 estimate the LVEF.
the MV anterior leaflet in diastole causing the EPSS to be elevated despite a normal EF (Image 1.16).
I MAGE 1.16 - AI Jet Preventing Normal MV Opening
2)
Mitral Stenosis (MS): Although rare, moderate to severe MS
can cause decreased excursion of the MV anterior leaflet, and
thus elevate the EPSS.
15
6. Preau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive
REFERENCES
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 coronary 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 separation and comparison to magnetic resonance imaging.
1. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and poten-
Am J Car-
diol. 2006;97(1):137-40.
tial clinical utility of goal-directed transthoracic echocardiography
performed by noncardiologist intensivists using a small handcarried device (SonoHeart) in critically ill patients. Journal of Cardiothoracic and Vascular Anesthesia. Apr 2005;19(2):155-159.
2. Armstrong W, Ryan T. Echocardiography. Seventh ed. Philadelphia (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.
16
C HAPTER 2
Right Heart
Haney Mallemat, MD
S ECTION 1
Acute right ventricular (RV) dysfunction may occur in patients with
Introduction
cardiography can assist at the bedside to diagnose the etiology
critical illness and is often challenging to diagnose and treat.1 Echo(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 dysfunction 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, however, the right ventricle is sensitive to changes in pulmonary and systemic pressure and volume, which may affect a patient’s hemodynamic status and acute management.
H IGHLIGHTS
Echocardiography of the RV can be helpful in:
-
PE
-
Fluid resuscitation
-
Chronic RV failure
-
Hemodynamic status
18
S ECTION 2
The right ventricle is the most anterior chamber of the heart, lying di-
Normal Anatomy and Physiology
and is often described as a “U” shaped structure, as it wraps around
rectly behind the sternum. The RV has a complex geometric shape
the left ventricle.3 The RV can be visualized from the standard cardiac views; the inferior vena cava (IVC) should also be included in
the assessment of the RV because it helps determine right atrial pressures. The RV can be visualized from the following four views:
1. Parasternal long-axis (PLA) view (Movie 2.1).
M OVIE 2.1 - Parasternal Long-Axis View
H IGHLIGHTS
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.
19
4. Subcostal long-axis view (Movie 2.4).
2. Parasternal short-axis view (Movie 2.2).
M OVIE 2.4 - Subcostal Long-Axis View
M OVIE 2.2 - Parasternal Short-Axis View
3. Apical four-chamber (A4C) view (Movie 2.3).
M OVIE 2.3 - Apical Four-Chamber View
The RV is sometimes described as three distinct portions due to its
complex geometric shape:
1. Inflow (or body) portion
a. Begins at the tricuspid valve and extends to the apex.
b. This portion is smooth-walled with minimal trabeculations.
2. Apex
a. 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 portion
a. 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).
20
B ORDERS OF THE RV
The interventricular septum is the medial border of the RV and it is
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 hypertension) and increased afterload (e.g., left heart failure) may cause hy-
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 pathology and will be described later in this chapter (Movie 2.6).
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
M OVIE 2.6 - Interventricular Septum
The free wall should be measured from the subcostal
view during diastole; this is the view where the free wall is most perpendicular to the plane of the ultrasound beam and hence, the most
accurate measurement (Movie 2.5).
M OVIE 2.5 - Measuring RV Free Wall
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 typically 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).
21
P ATTERN OF C ONTRACTILITY
RV C ORONARY B LOOD F LOW
The RV and the LV differ in their pattern of contraction. The LV con-
The majority of RV coronary blood flow is from the right coronary
tracts in multiple planes; however, the majority of contraction occurs
artery (RCA).4 The RCA perfuses the RV free wall and the inferior
concentrically around the midpoint of the LV. The RV, on the other
wall of the LV. The posterior descending artery, which is a branch of
hand, contracts longitudinally; contracting from the tricuspid valve to-
the RCA, perfuses the inferior portion of the interventricular septum.
wards the apex and outflow tract.
The moderator band is perfused by the left anterior descending ar-
6
This longitudinal pattern of con-
traction is often described as “peristaltic” or like an “accordion”
tery (LAD); branches of the LAD may also perfuse the RV apex.
(Movie 2.7).
M OVIE 2.7 - Pattern of Contraction
The RV has approximately 25% of the muscle mass of the left ventricle, despite the fact that the RV must deliver the same amount of cardiac output as the LV. The RV is able to match the LV in cardiac output because the pulmonary vascular system is a high-flow and lowresistance 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.
22
S ECTION 3
A SSESSING RV S IZE
RV Size & Function Assessment
The thin-walled right ventricle is sensitive to acute changes in pressure and/or volume. The RV may acutely dilate in response, increasing its overall dimensions and volume in response to these changes.4
It is therefore important to determine the RV size during initial assessment with echocardiography, as it may help lead to the cause of the
presenting disease.7
Q UALITATIVE A SSESSMENT : T HE “E YEBALL ” M ETHOD
The simplest method of assessing RV size is an “eyeball” method using the apical 4-chamber view.8 The RV normally appears triangularshaped 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).
H IGHLIGHTS
The simplest method of assessing the RV size is the “eyeball”
M OVIE 2.8 - “Eyeball” Method
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.
23
As the RV becomes mild to moderately dilated, the RV:LV ratio increases 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” assessment, it has been found to be relatively accurate with good interobserver reliability.9
P EARLS FOR I DENTIFYING 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 distinguish the RV from the LV3 (Movie 2.10):
Qualitative Assessment of RV Size
Normal
RV:LV Ratio
0.6:1
Mild-Moderately Dilated
0.7-1:1
Severely Dilated
>1:1
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.
Q UANTITATIVE A SSESSMENT
A quantitative assessment of RV size can also be made from the apical four-chamber view.
Three measurements are taken during dias-
tole; two transverse diameters and one longitudinal (Movie 2.9).
3. Tilting the probe anteriorly will visualize the “fifth” chamber of
the apical view, also known as the aortic outflow track; this ventricle must therefore be the LV.
M OVIE 2.10 - RV Identity Pearls
M OVIE 2.9 - Quantitative Assessment
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
24
A SSESSING RV S YSTOLIC F UNCTION
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
Adding an M-mode to this assessment may improve accuracy. To use
M-mode, place the cursor to the lateral border of the tricuspid annulus and observe contractility over a few cardiac cycles and then
freeze the image; calipers are then used to measure the annular displacement (Movie 2.11).
M OVIE 2.11 - Measuring TAPSE
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 M ETHOD
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 indicates reduced RV systolic function.5
TAPSE<1.6cm
Abnormal
RVFAC M ETHOD
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 imaged 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 en25
docardium is traced completely around the chamber including trabeculations, 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 endocardium to obtain the end-systolic area (or ESA).
The RVFAC will automatically be derived or can be calculated by using the formula:
RV Fractional Area Change V ENTRICULAR O VERLOAD
The thin-walled RV pumps blood to the left heart with a similar cardiac output as the muscular LV. The RV achieves this under normal
filling and loading conditions because the pulmonary system is a lowpressure system. If the RV becomes overwhelmed by either pressure
or volume overload, however, ventricular function may become abnormal. There are two categories of RV dysfunction:
1)
Pressure overload leading to systolic dysfunction.
2)
Volume overload leading to diastolic dysfunction.
FAC = (EDA-ESA)/EDA × 100
FAC<35%
Abnormal
S YSTOLIC (P RESSURE ) O VERLOAD
Acute or chronic increases in RV afterload (e.g., pulmonary embolism, pulmonary hypertension, etc.) lead to systolic (or pressure)
An RVFAC less than 35% is considered to be abnormal systolic func-
overload.10 The RV accommodates increases in pressure by “balloon-
tion, while greater than 40% is considered normal.5 Although this
ing” out the RV free wall. As a result, the interventricular septum be-
quantitative method of RV systolic assessment is validated and widely
comes flattened or “D” shaped when observed from the parasternal
accepted, it is not uncommon for experienced cardiologists to offi-
short-axis view (Movie 2.12).
cially use the “eyeball” method assessment.
M OVIE 2.12 - Systolic Overload
26
Septal flattening (also known as paradoxical septal motion or septal
a manner similar to acute pressure overload; septal flattening (a “D”
dyskinesia) occurs during both systole and diastole, in contrast to the
shaped septum) visualized in the parasternal short-axis view.4
normal shape of the interventricular septum, which is concave with
though this “D” shaped septum looks similar to pressure overload,
respect to the LV in both systole and diastole. In extreme cases, LV
the difference is that septal flattening from volume overload occurs at
filling and cardiac output may be compromised when the septum flat-
the end of diastole, while the septum is normal in contour during sys-
tens and encroaches on the LV cavity.
tole (Movie 2.13).
The RV may accommodate chronic increases in afterload through hypertrophy of the free wall. Recall that measurement of the free wall
should be made during diastole from the subcostal view, as the ultrasound beam is most perpendicular to the free wall; RV free wall
Al-
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.
M OVIE 2.13 - Diastolic Overload
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 trabeculations, papillary muscles, and the moderator band.
A clinically challenging situation arises when attempting to determine
whether a patient with chronic RV afterload develops acute-onchronic pressure overload (i.e., patient with chronic pulmonary hypertension develops an acute pulmonary embolism). In these cases,
prior echocardiograms should be reviewed and compared to the current echocardiogram for any changes.
D IASTOLIC (V OLUME ) O VERLOAD
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
27
N ON -I NVASIVE M EASUREMENT OF PASP
hepatic vein. For how to measure the IVC, see the Fluid Responsive-
Invasive right heart catheters are typically used to measure pulmonary artery systolic pressures (PASP) for diagnosing or monitoring
certain conditions (e.g., pulmonary hypertension).
B-mode ultra-
ness chapter in Introduction to Bedside Ultrasound Volume 1.
M OVIE 2.14 - PASP Assessment
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
IVC (cm)
Collapse
CVP
Normal
<2.1
>50%
3 (0-5)
dle of the jet and the peak velocity is obtained. If the ultrasound ma-
In Between
</> 2.1
</>50%
8 (5-10)
chine has the appropriate calculation package, the peak RV systolic
High
>2.1
<50%
15 (10-20)
valve to look for tricuspid regurgitation (TR). If TR is observed, the
cursor for continuous wave (CW) Doppler is placed through the mid-
velocity of the jet is measured and the calculation package will automatically 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 absolute 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
The final step is to add the peak RV systolic pressure and RAP to derive the PASP.
elevated.
12,5
A PASP greater than 36mmHg is considered
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>36mmHG
Abnormal
28
S ECTION 4
A CUTE P ULMONARY E MBOLISM
RV Pathology
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 clinical 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 embolism 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).
H IGHLIGHTS
RV pressure overload and systolic dysfunction may suggest
M OVIE 2.15 - Pulmonary Embolism
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.
29
The presence of acute RV dysfunction with the acute onset of hypotension may also help with the decision to treat a pulmonary embolism
with thrombolytic therapy in the proper clinical context.17
A CUTE RV M YOCARDIAL I NFARCTION
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-
McConnell’s sign was a commonly cited echocardiographic finding
clusion, echocardiography may detect segmental wall motion abnor-
associated with acute pulmonary embolism. McConnell’s sign is de-
mality (i.e., hypokinesis, akinesis, or dyskinesis) and/or a reduction
fined by the presence of RV mid-wall hypokinesis with normal contrac-
in myocardial thickening.3 The presence of McConnell’s sign (hypoki-
tion of the apex (Movie 2.16). First described in 1996, McConnell’s
nesis of the mid RV free wall with normal apical contraction) may
sign was once believed to be a very specific echocardiographic find-
also suggest AMI, and other modalities should be used to distinguish
ing for an acute pulmonary embolism.18 Since its initial description,
the clinical picture from acute pulmonary embolism and other
however, McConnell’s sign has been found in several other clinical
diseases.19
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 McConnell’s sign actually had an acute RV myocardial infarction (AMI).
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
19
anterior, lateral and portions of the inferior wall.
M OVIE 2.16 - McConnell’s Sign
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 provides perfusion to these territories.
30
P ERICARDIAL T AMPONADE AND THE RV
Pericardial effusions may occur from a variety of disorders (e.g.,
Several signs of impending tamponade can be detected with bedside
ultrasound. These include:
HIV, uremia, trauma) and ultrasound can be used to diagnose the ef-
a. Right atrial systolic collapse
fusion, as well as assist with ultrasound-guided pericardiocentesis.20
b. Right ventricular diastolic collapse
Pericardial tamponade is the physiologic state in which increasing
c. Reciprocal respiratory changes in the RV and LV filling
pressure within the pericardial space may exceed the pressure within
d. Plethora of the inferior vena cava
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 Bedside Ultrasound Volume 1 for additional information.
T AMPONADE : A R EVIEW OF P HYSIOLOGY
Accumulation of fluid in the pericardial space progressively reduces
RA S YSTOLIC C OLL APSE
The right atrial (RA) free wall is thin and sensitive to increases in
intra-pericardial pressures. As a result, critical intra-pericardial pressures 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).
filling of the low-pressure right-sided heart chambers, regardless of
the initial insult or underlying pathology. If the pericardial fluid accu-
M OVIE 2.17 - Pericardial Tamponade
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 collapse. 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.
31
RV D IASTOLIC C OLL APSE
M OVIE 2.19 - M-Mode Pericardial Effusion
RV free wall collapse during diastole may also be seen with pericardial tamponade. RV collapse is best visualized in either the parasternal long-axis or subcostal long-axis view (Movie 2.18).
M OVIE 2.18 - Pericardial Tamponade
R ESPIROPHASIC D OPPLER I NFLOW V ELOCIT Y
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
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
motion
11
(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 infiltrative cardiomyopathies (e.g., amyloidosis); diastolic collapse may
be masked despite relatively elevated intra-pericardial pressures.23
RV inflow velocity through the tricuspid valve. When expiration begins, the left side of the heart fills, resulting in an increased LV inflow
velocity through the mitral valve; the right-heart simultaneously normalizes the RV inflow velocity.
Over a normal respiratory cycle
there should be no more than 25% and 15% variation of inflow velocity 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
32
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 1012mmHg during inspiration) observed in pericardial tamponade.
The apical four-chamber view is the best view to assess variation of
inflow velocities.
I NFERIOR V ENA C AVA (IVC) P LETHORA
Pericardial tamponade increases right heart pressures. This is reflected 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 echocardiographic signs are also present and may help rule it out if a pericardial effusion is present (effusion but no tamponade)28 (Movie 2.21).
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
M OVIE 2.21 - Plethoric IVC
probe) are then measured for the maximum and minimum velocities
and the percentage of variation recorded. This measurement is sometimes made with a respirometer to determine the phase of respiration, 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).
M OVIE 2.20 - Respirophasic Variation
C ONCLUSION
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.
33
S ECTION 5
REFERENCES
Echocardiography. J Am Soc Echocardiogr. 2010 Jul;23(7):685713.
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.
1. Etchecopar-Chevreuil C, Francois B, Clavel M, et al. Cardiac mor-
9. Vieillard-Baron A, Charron C, Cergui K, et al. Bedside echocardio-
phological and functional changes during early septic shock: a
graphic evaluation of hemodynamics in sepsis: is a qualitative
transesophageal study. Intensive Care Med. 2008;34:250-56.
evaluation sufficient? Intensive Care Medicine. 2006;32:1547-52.
2. Torbicki A, Perrier A, Kostantinides S, et al. Guidelines on the di-
10. Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index
agnosis and management of acute pulmonary embolism. Eur
for separation of right ventricular volume and pressure overload. J
Heart J. 2008;29:2276-315.
Am Coll Cardiol. 1985;5:918-27.
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. Philadelphia, PA: Saunders Elsevier; 2009.
5. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardio-
11. Oh JK, Seward JB, Tajik AJ. The Echo Manual. 3rd edition. Philadelphia, 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.
graphic assessment of the right heart in adults: a report from the
13. Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E.
American Society of Echocardiography endorsed by the Euro-
Quantitative assessment of pulmonary hypertension in patients
pean Association of Echocardiography, a registered branch of the
with tricuspid regurgitation using continuous wave Doppler ultra-
European Society of Cardiology, and the Canadian Society of
sound. J Am Coll Cardiol. 1985;6:359- 365.
34
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-
22. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic compression of the right atrium: A new echocardiographic sign if cardiac
tamponade. Circulation. 1983;68:294-301.
cardiography combined with clinical and electrocardiographic
23. Leimgruber PP, Klopfenstein HS, Wann LS, Brooks HL. The hemo-
data to predict acute pulmonary embolism. Eur Heart J.
dynamic derangement associated with right ventricular diastolic
1996;17:779-786.
collapse in cardiac tamponade: An experimental echocardio-
16. Roy PM, Colombet I, Durieux P, et al. Systematic review and
meta-analysis of strategies for the diagnosis of suspected pulmonary embolism. Br Med J. 2005;331:259.
17. Guyatt GH, Akl EA, Crowther M, et al. Executive Summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American 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 pulmonary embolism. Am J Cardiol. 1996 Aug 15;78(4):469-73.
19. Casazza F, Bongarzoni A, Capozi A, et al. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular 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 tamponade: an unseen danger? Am J Emerg Med. 2000;18:339-340.
graphic study. Circulation. 1983;68:612-620.
24. Gonzalez MS, Basnight MA, Appleton CP. Experimental Cardiac
Tamponade: A hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics 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 velocities during experimental cardiac tamponade. J Am Coll Cardiol. 1991;18:234-42.
27. Himelman RB, Kircher B, Rockey DC, Schiller NB. Inferior vena
cava plethora with blunted respiratory response: A sensitive echo-
35
cardiographic sign of cardiac tamponade. J Am Coll Cardiol.
1988;12:1470-77.
28. Eisenberg MJ, Schiller NB. Bayes’ theorem and the echocardiographic diagnosis of cardiac tamponade. Am J. Cardiol. 1991;
68:1242-44.
36
C HAPTER 3
Diastology
Mike Mallin, MD, RDCS, RDMS
S ECTION 1
Diastole is the period of the cardiac cycle between the closure of the
Introduction
diastole is to fill the left ventricle in preparation for systole.
aortic valve and closure of the mitral valve. The primary function of
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 echocardiography. 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 fraction (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-
H IGHLIGHTS
utes to the health care crisis in the U.S.
Diastology is the science of quantifying how well the LV relaxes
A thorough diastolic evaluation should be performed on patients
and complies.
whenever a complete echocardiogram is performed.
50% of heart failure is diastolic only.
The physical exam is not accurate in diagnosing heart failure.
The diastolic
evaluation itself takes only a few minutes and can help identify elevations in cardiac filling pressures and offer prognostic information.2,3
Diastolic dysfunction has been shown to more appropriately correlate with cardiac filling pressures than LV EF. For this reason, a more
focused diastolic exam can be performed when interested in the relation of diastolic dysfunction to symptomatic heart failure in patients
with dyspnea, weight gain, or other concerning findings for volume
overload.
38
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
39
S ECTION 2
The physiology of diastolic function is possibly the most complicated
Physiology
ply echocardiography for diastolic evaluation.
aspect of the topic, but it is paramount in understanding how to apThe diastolic filling
period of the cardiac cycle can be broken into two phases:
1) E Wave: The early filling phase, which is dominated by myocardial 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).
F IGURE 3.1 - The Push-Pull Relationship of LV Filling
H IGHLIGHTS
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 waiting to fill the left ventricle.
The early filling phase represents the LV pulling blood from the LA by
creating a relative negative intraventricular pressure by the post systolic relaxation of the LV chamber. This effect is secondary to the tor40
sional recoil of the left ventricle. In a normal heart, almost all of the
angiotensin II system, and eventually increased preload and filling
filling of the LV occurs during the “pull.” As diastolic function wors-
pressures. This is the body’s method of continuing to fill a thickened,
ens, the LV loses the ability to “pull” blood into the LV and the body
stiff LV: by increasing filling pressures through an elevation in pre-
has to retain fluid to increase the LA loading pressure.
load. This process causes the symptoms we all know as heart failure
This repre-
sents a change from “pull” to “push”, where LA pressure has to ele-
(Figure 3.2).
vate to overcome the poor relaxation and compliance of the left ventricle (Movie 3.1).
F IGURE 3.2 - Physiology
M OVIE 3.1 - Explanation of the Forces in Diastole
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 renin41
S ECTION 3
Evaluating Diastolic
Function
Q UALITATIVE E VALUATION
Diastolic dysfunction can be inferred from two key observational findings on bedside ultrasound. First, a patient with elevated filling pressures, 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 apical 4 chamber view (Image 3.1).
I MAGE 3.1 - Measurement of LA Area
H IGHLIGHTS
Qualitative: Large LA, poor descent of the base.
Quantitative: PW Doppler of MV inflow, TDI of septal MV annulus.
Key Values:
- Elevated PCWP > 12mmHg
- Elevated LVEDP > 16mmHg
- Normal E velocity < 100cm/s
o Normal e’ velocity > 8cm/s
o Normal E/e‘ < 15
This window can be difficult to obtain, but a normal atrial size in an
otherwise healthy patient is often the extent to which diastolic dysfunction need be evaluated. A typical LA volume is measured at end
42
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-
M OVIE 3.2 - Qualitative Evaluation of the LA and Descent
of the Base
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 relaxation during early diastole, and thus normal diastolic filling. Slow
or minimal descent of the base is consistent with diastolic dysfunction.
I MAGE 3.2 - Location of Mitral Annulus
43
Q UANTITATIVE E VALUATION
The waveform obtained includes the E and A waves, where “E” re-
Quantitative evaluation of diastolic function is obtained by performing 2 specific Doppler measurements: Mitral valve inflow and tissue
Doppler imaging.
fers to early filling and “A” refers to the atrial kick (Image 3.3).
I MAGE 3.3 - Mitral Valve Inflow Pattern
M ITRAL V ALVE I NFLOW
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 diastole. 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).
I LLUSTRATION 3.1 - Location of
Doppler Gate for MV Inflow
The variations of mitral valve inflow patterns are broken into 4 different types (Figure 3.3).
•
Normal: E>A
•
Impaired Relaxation: E<A
•
Pseudonormal: E>A
•
Restrictive: E>>>A
44
F IGURE 3.3 - The Different MV Inflow Patterns
Normal: Normal filling pressures, Left Ventricular End Diastolic Pressure (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 myocardium’s inability to relax, thus less blood flow occurs during the
The severity of diastolic dysfunction worsens from normal to restrictive (Figure 3.4).
F IGURE 3.4 - Doppler of MV Inflow and TDI Patterns
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 order 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.
45
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 approaching 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.
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 filter, 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).
MV inflow patterns are a spectrum and change with the patient’s volume 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
I LLUSTRATION 3.2 - TDI Gate Location for TDI
Waveform Analysis
significant diuresis. Once a patient’s MV inflow pattern is impaired,
they typically never go back to normal since the damage to the myocardium has already been done. However, patients can move between impaired, pseudonormal, and restrictive as their preload and
filling pressures change.
T ISSUE D OPPLER I MAGING
TDI measures the speed of the myocardium as it moves during diastole. 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 diastolic function worsens.
As the ventricle becomes stiffer, it moves
slower and the descent of the base is diminished.
46
The waveform produced displays an e’ wave and a’ wave, which signify the same aspect of diastole as in the MV inflow pattern: e’ represents 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 movement 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’ velocity is < 8cm/s, the patient has diastolic dysfunction. Thus, when
differentiating between normal and pseudonormal MV inflow patterns, the TDI measurement can be extremely helpful.
F IGURE 3.5 - Grading of Diastolic Failure
Estimating LVEDP: The LVEDP can be estimated by dividing the E velocity 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.
F IGURE 3.6- Estimating LVEDP
I MAGE 3.4 - Normal TDI Waveform
47
M OVIE 3.3 - Diastology How-To
M OVIE 3.4 - One Minute Ultrasound Diastolic Demo
48
S ECTION 4
A CUTE D YSPNEA
Clinical Application
Patients can present with symptoms of an acute heart failure exacerbation without systolic dysfunction. While the majority of these patients also have a reduced ejection fraction, diastolic dysfunction can
be the underlying cause rather than systolic dysfunction. Pseudonormal or restrictive patterns identify those patients with elevated LVEDP
and may help identify those patients that need diuresis.
V OLUME O VERLOAD
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-
H IGHLIGHTS
Diastolic dysfunction can be useful in the following clinical
scenarios:
-
Acute heart failure
-
Volume overload
-
Critical patients requiring massive volume resuscitation
tern. Therefore, it is not unusual for patients with heart failure to transition from restrictive to impaired relaxation over the course of their
diuresis.
M ASSIVE V OLUME R ESUSCITATION
Diastology can be used for directing fluid resuscitation or simply indicating those patients at higher risk for pulmonary edema with massive 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 elevated PCWP. Thus, one option would be to fluid bolus the patient until the E/e’ reached 15, although this has not been adequately studied. It is important to note that other methods of detecting fluid re49
sponsiveness have been more rigorously studied, such as passive lag
raise, Ao velocity variation, or even the IVC changes with respiration. (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.
50
S ECTION 5
L IMITATIONS
Limitations
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. Arrhythmias, such as atrial fibrillation, destroy the A waves and cause irregular 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.
H IGHLIGHTS
C ONSTRICTIVE P ERICARDITIS
Limitations of diastolic evaluation include operator error,
This also causes elevated filling pressures in the setting of a normal
change in Doppler measurements due to angle of insonation,
LV EF and can present as acute heart failure.
and irregularities in waveforms from certain clinical conditions.
have respiratory variation of MV inflow velocities >25% with expira-
Other causes of heart failure symptoms in patients with normal
EF also exist.
However, patients
tion, diastolic flow reversal in the hepatic veins, and typically have a
septal e’ velocity > the lateral annulus e’ velocity (Image 3.5).
51
I MAGE 3.5 - Location of Mitral Annulus
C ONCLUSION
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 population of patients. If one takes the time to learn it, patients will reap
the benefits.
The latter of these findings is unique to constrictive pericarditis and is
due to the retained vertical excursion, thus the septal e’ velocity being greater than the lateral e’ velocity.17
M ITRAL R EGURGITATION (MR)
Moderate to severe MR can lead to significant elevations in peak E
velocities of mitral valve inflow. While this increase in E wave velocity 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
52
S ECTION 6
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