Manual of Echocardiography Navin C Nanda, Gültekin Karakuş, Aleks Değirmencioğlu
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BasicsChapter 1

  1. How are ultrasound waves produced and how is the depth of a cardiac structure determined?
    An ultrasound transducer used for clinical examination consists of a piezoelectric crystal that when stimulated by electricity, vibrates emitting ultrasound waves generally at a frequency of 1–12 MHz (i.e. 1–12 million cycles per second). The frequency is much higher than what a human ear can hear (up to 20,000 cycles per second or 20 Hz). The speed of sound in a given tissue is the product of wavelength (distance between two consecutive peaks of the ultrasound wave) and the frequency. It is 1540 m/s in the heart and surrounding tissues. Because the same transducer also receives echoes returning from various tissues, the exact depth of any cardiac structure from the transducer can be determined. Currently used echo systems utilize phased array technology where the piezoelectric crystal is spliced into several strips and serial activation delay is used to alter the direction of the ultrasonic beam.
  2. What is resolution?
    Resolution is the ability to separate and differentiate two cardiac structures that are located close to each other.
  3. What is axial (spatial) resolution?
    Axial or spatial resolution is the ability to differentiate two structures that are located one below the other and therefore it depends on the wavelength. The two structures will appear as one structure unless they are at least one wavelength apart. Increasing the transducer frequency will improve axial resolution by shortening the wavelength; however, this will be at the expense of depth because of reduced penetration of the ultrasound beam (Figs. 1.1A to C).
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    Figs. 1.1A to C: Axial resolution: (A) Scatterers that are more than half of the wavelength apart will be displayed as two different echoes; (B) Scatterers that are closer together than half of the wavelength will be displayed as one echo; (C) Using a shorter wavelength (higher frequency), the two close scatterers will be displayed as two echoes.
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  1. What is lateral resolution?
    Lateral resolution is the ability to differentiate two structures that are located side by side and depends on the ultrasound beam width. Two cardiac structures situated at the same depth but closer together than the ultrasound beam width will appear as one structure. Narrowing the beam by focusing will differentiate them (Figs. 1.2A to C).
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    Figs. 1.2A to C: Lateral resolution: (A and B) Scatterers ≤ the ultrasound beam's width will be displayed as an echo of the beam's width; (C) Scatterers that are closer together than the beam's width will be displayed as one echo.
  2. What is temporal resolution?
    Temporal resolution is the ability to detect and differentiate two events that are occurring close together and depends on the frame rate. After emitting a pulse of ultrasound waves, the transducer has to wait for all the returning echoes to come back and produce a scan line before changing its position and sending the second pulse to generate a second scan line. Thus one two-dimensional (2D) image or frame consists of multiple scan lines, approximately 200 for a sector of 90° at a depth of 15 cm and taking about 40 ms to build. The higher the number of 2D images per second (frame rate), the higher will be the temporal resolution. It follows that reducing image depth, image line density (number of scan lines in one frame or 2D image), and sector angle will all increase the sweep time of the transducer and frame rate resulting in increased temporal resolution. A drawback of reducing line density is lowering of spatial resolution.
    A frame rate of at least 25 frames per second is needed for smooth viewing of cardiac motion (Figs. 1.3A and B).3
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    Figs. 1.3A and B: Transthoracic echocardiography, four-chamber view. By reducing the depth, the frame rate increases. (LA: Left atrium; LV: Left ventricle; RA: Right atrium; RV: Right ventricle; MV: Mitral valve; TV: Tricuspid valve).
  3. What is the difference between fundamental and harmonic imaging and what are their advantages and disadvantages?
    In fundamental imaging, the frequency of the returning echoes is same as the frequency of the transducer. However, in harmonic imaging, the transducer selects only the harmonic components of the returning ultrasonic signals whose frequency is twice, three times or more as compared to the transducer frequency. With harmonic imaging, the superior penetrating capability of lower frequency ultrasound waves can be combined with higher spatial resolution of higher frequency harmonic ultrasound waves, resulting in a higher resolution image with less noise and less artifactual echoes. Left ventricle (LV) endocardial border is better delineated with harmonic imaging than fundamental imaging. However, with harmonic imaging, cardiac valves may appear unduly thick and echogenic myocardium seen in some infiltrative diseases like amyloidosis may not be well visualized with harmonic imaging. Harmonic imaging has practically replaced fundamental imaging in routine echocardiographic examinations (Figs. 1.4A and B).
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    Figs. 1.4A and B: Apical four-chamber view: (A) Fundamental imaging; (B) Harmonic imaging (Abbreviations as in Figure 1.3).5
  4. What is meant by A-mode, B-mode, and M-mode echo?
    Ultrasound signals can be processed by tracing their contours and displaying them as energy amplitude or A-mode or converting this amplitude into brightness called B-mode. Displaying a B-mode scan line over time on a video screen results in M or motion mode.
  5. Which 2D echo setting gives the best image of a particular area of interest, for example, aortic valve (AV) morphology?
    Ideally, the sector depth and the sector width should be minimized to encompass only the AV viewed in short-axis (both will increase the frame rate) and the ultrasound beam focused at the AV level to improve both the temporal and lateral resolutions. The axial resolution can be improved by using a higher frequency transducer that will reduce the wavelength. The instrument gain should also be optimized as overly high gain will introduce noise and a very low gain will darken the image making it difficult to visualize the structures well. Zoom mode may be used to magnify the image but this does not improve image resolution.
 
ARTIFACTS
  1. What is acoustic shadowing and acoustic enhancement?
    Dense tissue such as calcification and metallic objects such as prosthetic valves will prevent penetration of the ultrasonic beam resulting in a dark echo-free area distally called acoustic shadowing. Conversely, an echo beam passing through fluid such as pericardial effusion will have no attenuation or energy loss and therefore the structure it encounters next will appear more echogenic than usual (acoustic enhancement) (Fig. 1.5).
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    Fig. 1.5: Transesophageal echocardiogram. Calcifications of the mitral ring cause an acoustic shadow (arrows) (Abbreviations as in Figure 1.3).6
  2. What are reverberation artifacts and how are they produced?
    These are produced by reflection of ultrasound waves between two or more highly reflective surfaces such that the resulting additional images are placed more distally. Artifacts are usually less echogenic than the real image but not always so. Artifacts may also extend to a neighboring structure or cardiac cavity and occasionally beyond the cardiac image revealing their true nature. Artifacts may aid in distinguishing an intracardiac catheter or pacemaker wire from a natural structure like a thickened muscle band. Contrast echo and three-dimensional (3D) echo are often useful in differentiating reverberation artifacts from a clot in the LV apex imaged in the apical four-chamber view. Reflections in the chest wall itself are responsible for reverberation artifacts in the LV apex. Asynchronous motion in relation to neighboring structures, lack of attachment to a structure, contradictory findings not keeping with the patient's clinical picture also help in the recognition of reverberation and other artifacts (Fig. 1.6).
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    Fig. 1.6: Apical four-chamber view: Reverberations (arrows) caused by mitral valve prosthesis (Abbreviations as in Figure 1.3).
  3. What are (a) mirror image, (b) double image, and (c) side lobe artifacts?
    a. Mirror image artifacts are a type of duplication artifacts. They occur when a structure is located above a more echogenic structure like the pleura such that the ultrasonic beam is deflected off this echogenic structure giving a second image below the first image produced in the usual manner. This is often seen during transesophageal echocardiography (TEE) when the descending thoracic AO image is duplicated below the pleural/lung interface. These artifacts may also occur with conventional and color Doppler where color flow signals in the left ventricle outflow (LVO) tract may be duplicated in the LA in the apical four-chamber view mimicking paravalvular metallic mitral valve (MV) prosthesis regurgitation.
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    b. Double image artifacts are also a type of duplication artifact but they result from refraction or bending of the ultrasonic beam as it encounters a structure and this may result in a duplicate image oriented side to side but not one below the other as occurs in a mirror image.
    c. Each ultrasound beam consists of a primary beam in the middle and two secondary side lobe beams on either side that are suppressed when they return to the transducer. However, if they encounter a strongly reflecting tissue, the image from the secondary beams is placed within the image of the primary structure and may extend beyond its limits. This is called a side lobe artifact. Adjusting the position of the transducer may help eliminate this artifact.
    Random artifacts may also occur from electrocautery during TEE but will disappear when the cautery is turned off. “Stitch artifacts” occur as discontinuous areas while performing live/real time 3D echo and result from transducer or patient motion during 3D data acquisition.
    Conversely, it is important not to misdiagnose common and uncommon cardiac structures like the Eustachian and Thebesian valves, Chiari network, crista terminalis, “coumadin ridge,” Lambl's excrescences, atrial septal aneurysm, intervertebral disk, and lipomatous atrial septal hypertrophy as ultrasound artifacts (Fig. 1.7).
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    Fig. 1.7: Apical four-chamber view: Side lobe artifact in the lateral wall of the left ventricle (arrow) (Abbreviations as in Figure 1.3).8
  4. Which of the following artifacts most likely cause a false image of LV apical thrombus?
    a. Side lobe artifact
    b. Reverberation/near field artifact
    c. Mirror artifact
    d. Acoustic shadowing
    The correct answer is b.
  5. Side lobe artifacts generated by a calcified aortic annulus may mimic ascending aortic dissection in the parasternal long-axis view. How can this be clarified?
    The side lobe artifact may present as a weak or inconstant signal, may extend beyond the wall of the aorta, and may disappear with transducer angulation. It would also not have the typical chaotic motion of an acute dissection flap (“a worm wiggling in the aorta”). In addition, it may not be seen in other views such as the suprasternal or right parasternal approaches. Also, clinically the patient may not have any signs or symptoms suspicious of dissection.
 
DOPPLER ECHOCARDIOGRAPHY
  1. What is the Doppler principle and the Doppler equation?
    When cardiac structures such as the blood particles (mainly RBCs) are moving within the ultrasonic beam toward or away from the transducer, there is a change in the frequency of the returning signals and this is called the Doppler frequency shift. The frequency is increased if the cells are moving toward the transducer and decreased if they are moving away. The Doppler equation states that the Doppler frequency shift (f) is directly proportional to the velocity of the blood cells (v), the transducer frequency and the cosine of the angle of incidence of the ultrasound beam to the direction of movement of the blood cells, and inversely proportional to the velocity of sound in tissue (c) that is assumed to be constant at 1540 m/s. If the transducer frequency is kept constant and the ultrasonic beam is kept parallel to the motion of blood cells (angle of incidence of the ultrasound beam 0°, cosine 0 = 1), then the velocity of blood flow can be calculated from the Doppler frequency shift that the machine can measure.
  2. What are the different types of Doppler used in clinical practice?
    These are (a) conventional Doppler [pulsed and continuous wave (CW)], (b) color Doppler, and (c) tissue Doppler imaging.
    a. Conventional Doppler: In pulsed Doppler, an ultrasound pulse is sent out and then the transducer waits till the returning signals come back before repeating a second pulse. This ensures measuring the Doppler frequency shift and the velocity of blood flow by placing a Doppler sample volume or “gate” at any point in the image.
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    However, there is an upper limit to the Doppler frequency shift or velocity that can be measured and if the blood flow velocity exceeds this limit (called the Nyquist limit that is defined as half the pulse repetition frequency (PRF) of the transducer), it wraps around on the opposite side of the Doppler baseline. This phenomenon is called aliasing and when significant the actual velocity cannot be measured. The PRF can be increased to some extent by reducing the sector depth.
    This problem of aliasing is obviated by CW Doppler where one crystal in the transducer continuously sends the Doppler beam and the other receives the returning signals continuously without waiting, so there is no delay. With this modality, very high velocities can be measured, but there is no range gating, i.e. it will detect the highest velocity in the path of the Doppler beam, but cannot identify the exact site of high velocity. This is generally not a problem in clinical practice. For example, one can identify a thickened and calcified AV by 2D echo and if in the apical five-chamber view a high velocity is noted by CW Doppler, it is obviously coming from the AV. A problem occurs when two adjacent stenotic areas are in tandem such as coexisting AV stenosis and sub or supravalvular stenosis, then CW Doppler would be unable to differentiate because of its inability to localize the individual sites of high gradients; 3D echo is useful in this regard.
    High PRF Doppler attempts to combine the advantages of both pulsed and CW Doppler by sending pulses at a very high frequency even before the returning signals from the previous pulse come back. This increases the Nyquist limit, and higher velocities can be measured, but it often results in depth ambiguity and, is therefore, generally not very reliable.
    b. Color Doppler: Color Doppler flow mapping is essentially an extension of pulsed Doppler technology. Multiple, adjacently located pulsed Doppler sample volumes are color coded so that flow toward the transducer is displayed as red and away as blue. When aliasing occurs, there will be an admixture of red and blue signals but in addition, for good measure, green is added resulting in an easily identifiable mosaic color pattern signifying high velocity and turbulent blood flow. This facilitates detection and assessment of stenotic and regurgitant valvular lesions. When performing color Doppler examination, a color coded bar is usually displayed on one side of the monitor screen with a bright yellow color on the top and a bright blue color at the bottom with lesser gradations of these colors displayed in between in a step-wise manner. The Nyquist limit for flow toward and away from the transducer is also noted at the top and bottom of the bar.
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    In reality, this bar should be displayed in the form of a circle and not as a rectangular bar since flow toward the transducer exceeding the Nyquist limit will turn from bright yellow to bright blue on first aliasing and as the velocity increases it will go through all the other gradations of color including very dark blue or practically black color. An important point to remember is any change in Nyquist limit also changes the color filter and thus will affect the size of color Doppler display. Similar changes will occur with alterations in color Doppler gain. Thus, these two settings need to be standardized when assessing semiquantitatively the severity of valvular regurgitation. These are further discussed in chapters pertaining to individual cardiac valves.
    c. Tissue Doppler imaging: In tissue Doppler imaging, the high velocity, low amplitude signals from blood cells are filtered out using a special filter and what remains are the low velocity, high amplitude signals from myocardial tissue. These are found useful in assessing LV and right ventricle (RV) systolic and diastolic functions and are described in the respective chapters (Figs. 1.8 to 1.10).
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    Fig. 1.8: Continuous wave Doppler: Here there are two separate crystals, one for transmitting and the other for receiving the signals (Abbreviations as in Figure 1.3).
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    Fig. 1.9: Pulsed wave Doppler: Here the transducer has just one crystal which does both the transmission and the reception (Abbreviations as in Figure 1.3).11
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    Fig. 1.10: Color flow Doppler: This is a variety of pulsed wave Doppler. Multiple points in the “region of interest” are analyzed and color-coded rapidly. (Abbreviations as in Figure 1.3).
  3. Which of the following statements is not true?
    a. If the Nyquist limit is low, color Doppler may overestimate the degree of valvular regurgitation.
    b. Decrease in 2D gain results in a better color Doppler study.
    c. An increase in color Doppler gain can result in overestimation of regurgitation severity.
    d. M-mode color Doppler has a higher frame rate than 2D color Doppler.
    e. With color Doppler, the lateral resolution is better than longitudinal (axial) resolution.
    The answer is e.
    Axial resolution is better than lateral resolution that is reduced in 2D color Doppler because of lower frame rates used. This is the reason for the recommendation to measure aortic regurgitation (AR) and mitral regurgitation (MR) vena contracts by 2D color Doppler not from the apical, but the parasternal long-axis view where the beam is perpendicular to the regurgitant flow.
    Color M-mode with its higher frame rate is useful in assessing valvular regurgitation in patients with tachycardia where it may not be diagnosed by 2D color Doppler with its lower frame rate and lower lateral resolution.
  4. Sometimes, LV apical hypertrophy may be undiagnosed by 2D echo. Which equipment settings can be helpful in its detection?
    Decreasing the Nyquist limit (and thus decreasing the color filter) and increasing color gain may show a narrow flow channel by color Doppler and delineate hypertrophied apical walls. Focusing the ultrasound beam in the apical region may also help.12
  5. What is Bernoulli equation and what are its limitations?
    Bernoulli equation states that in a fluid medium such as blood the pressure difference between any two selected points equals convective acceleration plus flow acceleration plus viscous friction. Convective acceleration represents the product of half the density of blood and the difference between the squares of the velocities at these points. This calculates to be approximately 4. If one assumes flow acceleration, viscous friction, and the velocity of blood proximal to obstruction to be negligible, the pressure gradient can be calculated as four times the square of the velocity (V) obtained by Doppler at the site of obstruction (4 × V2). This modified Bernoulli equation is commonly used in clinical practice not only to assess the severity of obstruction at various sites in the heart but also to measure the pulmonary artery (PA) systolic pressure in patients with tricuspid regurgitation (TR). Four times peak velocity of the TR jet gives the difference between the RV and right atrial (RA) pressures and if the RA pressure is known it can be added to obtain the RV systolic pressure that would be same as the PA pressure in the absence of any obstruction in the RV/PV. RA pressure can be estimated by examining the inferior vena cava using the 2D subcostal approach. If the IVC is not enlarged and collapses > 50% of its width during respiration, RA pressure is normal, (5 mm Hg or less), and if it is dilated and does not collapse at all or collapses < 50%, RA pressure is elevated at 10–15 mm Hg. For simplification and to improve the overall correlation with cardiac catheterization, some empirically add 10 mm Hg to the peak gradient derived from the TR jet to calculate the PA systolic pressure and assess the presence of pulmonary hypertension.
    There are some caveats to using the Bernoulli equation. The proximal velocity (V1) may be high in certain situations such as coarctation of the aorta, regurgitation coexisting with stenosis, and high output states caused by anemia, and needs to be taken into account when assessing pressure gradients. In such cases, one subtracts V1 from peak velocity (V2) and multiplies square of the difference by 4 to calculate the pressure gradient (4 × [V2 - V1]2). Pressure gradients are also affected by changes in stroke volume and cardiac output as well as flow rate and low pressure gradients can occur in conditions like low output severe AV stenosis. Low or negligible gradients are noted when a vessel is practically completely obstructed with hardly any flow passing through it. Doppler gradients are also underestimated in polycythemia because of increased viscous friction and blood density.
    Doppler measures the peak instantaneous velocity and gradient and this generally does not correlate with cardiac catheterization where nonsimultaneous peak-to-peak gradients are assessed. However, the mean gradients by both modalities correlate well.
  6. What is the principle of continuity equation and how can it be used to measure the area of a stenotic orifice?
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    The continuity equation is based on the premise that the volume of blood proximal and distal to stenosis is equal. The volume of blood proximal to stenosis can be calculated as the product of the velocity time integral (VTI) measured by pulsed Doppler (since the velocity would not be high) and the cross-sectional area (CSA) of the chamber or vessel assessed by 2D echo. Continuous wave Doppler can then be used to measure the high peak velocity and VTI at stenosis and from this the area of the stenosed orifice can be calculated as follows: proximal VTI × proximal CSA/VTI at stenosis. Since the ratio of proximal and distal VTIs is approximately same as the ratio of peak velocities, the equation can be simplified with some loss of accuracy by substituting peak velocities for VTI. The continuity equation is commonly used in clinical practice to measure AV area in patients with AV stenosis.
    Measurement of CSA by 2D echo and VTI by Doppler can be used to calculate the volume of flow anywhere in the cardiovascular system. For example, LV stroke volume can be assessed by placing a pulsed Doppler sample volume in the LVO tract and obtaining the VTI and multiplying this by the LVO CSA calculated by measuring the diameter (D) by 2D echo and assuming it to be circular: LVO VTI × (LVO D/2)2 × Π. RV stroke volume can be similarly calculated by measuring the VTI in the RV outflow tract by Doppler and the diameter by 2D echo. The difference between RV and LV stroke volumes can be used to calculate the volume of shunt in patients with congenital septal defects such as atrial septal defect (ASD) or ventricular septal defect (VSD).
 
M-MODE ECHOCARDIOGRAPHY
  1. What is the clinical usefulness of performing M-mode and color M-mode examinations?
    Two-dimensional echo-directed M-mode provides very high temporal resolution in the range of 1000 frames/s as compared to only 30–100 frames/s using 2D echo. Clinically, M-mode is most useful to time cardiac events and record and analyze high velocity movements. For example, early closure of the MV due to increased LV diastolic pressure from severe AR or increased PR interval due to first degree A:V block can be documented together with diastolic MR using color M-mode or Doppler.
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    High-frequency diastolic flutter of the MV points to AR jet striking the open MV leaflets, while systolic flutter is characteristic of vegetation and a flail MV. Coarse undulations of both MV and tricuspid valve (TV) are observed with atrial flutter and fibrillation. Reduced MV diastolic slopes with absence of A wave and posterior leaflet moving in the same direction as the anterior leaflet is characteristic of mitral stenosis that can be missed on 2D echo when it is mild in degree and not calcified. Mitral valve or TV prolapse especially when it is mid to late systolic is best detected by M-mode. MR and TR confined to mid/late systole in these patients is well delineated by color M-mode and this can prevent overestimation of severity by 2D color Doppler (see Chapter 3: Mitral Valve). Systolic anterior movements of the MV are also well visualized and timed by M-mode. In addition, mitral septal separation [increased distance between the mitral E point and the ventricular septum (VS)] may indicate LV systolic dysfunction and a prominent B point denotes increased LV end-diastolic pressure in the absence of atrioventricular (A:V) block. Intermittent or complete “sticking” of a mitral prosthesis is also well diagnosed by M-mode.
    High-frequency systolic flutter of the AV leaflets is a normal finding but coarse flutter is commonly seen in hypertrophic cardiomyopathy that may also show mid-systolic AV closure because of reduction in flow caused by the development of the systolic anterior movement of the MV. Prominent early systolic preclosure of the AV > 50% of initial excursion followed by fluttering is typical of discrete subaortic stenosis that may be missed by 2D echo as the membrane is often not well visualized. Prominent AV preclosure may also be noted in patients with dilated aneurysmal AO root and ascending AO and tetralogy of Fallot/truncus arteriosus. Mild AV preclosure is nonspecific and can be seen even in a normal patient. Gradual coasting of the AV toward closure may be noted when all of LV flow does not empty into the AO but is partially diverted as it may occur with a VSD or MR. This finding may also be noted with low cardiac output and premature ventricular contractions. Diastolic flutter, especially coarse, is noted with a flail AV due to endocarditis or trauma. A bicuspid AV may be indicated on M-mode by noting eccentric closure or changing eccentricity with a paint-brush appearance of the AV due to unequal cusp size or redundant folds, respectively. Any bicuspid AV will be significantly stenotic unless there is marked cusp redundancy that serves to increase the area of leaflet coaptation.
    Systolic flutter of the TV has been observed in patients with LV-RA shunts. Delayed TV closure as compared to MV closure is a hallmark of Ebstein's anomaly by M-mode. M-mode of the TV annulus in the apical four-chamber view (TAPSE) is currently routinely performed to assess RV longitudinal function. An excursion of < 16 mm is considered abnormal. Increased negative A wave (or A dip) or preclosure of the PV following atrial systole indicates increased RV diastolic pressure or low PA diastolic pressure or both and has been noted in patients with heart failure due to pulmonary hypertension, PV stenosis, and constrictive pericarditis. Mid-diastolic closure of the PV points to severe PV stenosis.
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    In these patients, the RV diastolic pressure exceeds the PA diastolic pressure leading to these M-mode findings. PV closure occurring in diastole prior to atrial systole is indicative of very severe PV stenosis.
    M-mode is also useful to time RA and RV wall collapse that may occur in pericardial effusion and provide useful information regarding impending tamponade. Respiratory variations in ventricular septal motion in patients with septal bounce and ventricular interdependence as well as respiratory changes in IVC size due to various pathologies are best assessed by M-mode. Because of high interface contrast, 2D-directed M-mode is also useful in making accurate measurements of cardiac chambers and great vessels, but care must be taken to ensure that the ultrasound beam is aligned exactly perpendicular to the walls imaged on 2D echo, otherwise errors will occur (Figs. 1.11 to 1.16).
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    Figs. 1.11A and B: (A) M-mode interrogation of the mitral valve in a patient with elevated left ventricular end-diastolic filling pressures demonstrates a “B” notch within the A-C slope, known as a “B-Bump” (arrow); (B) Another M-mode interrogation of the mitral valve demonstrating a “B-Bump” (arrows). There is also increased E-point to Septal Separation (EPSS; double-headed arrow). Normal EPSS is typically less than 1 cm (RV: Right ventricle; VS: Ventricular septum).
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    Fig. 1.12: Constrictive pericarditis: M-mode of the left ventricle from a parasternal short-axis window demonstrating abnormal relaxation of the ventricular walls in a patient with constrictive pericarditis. There is an early rapid diastolic deflection (first arrow) and a slow anterior septal motion later in diastole (second arrow) (LV: Left ventricle; ILW: Infero-lateral (posterior) wall; RV: Right ventricle; VS: Ventricular septum).
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    Fig. 1.13: Asymmetric aortic valve closure in a patient with a bicuspid aortic valve (AV). Closure line is anteriorly displaced (double-headed arrows).
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    Figs. 1.14 A and B: (A) Normal tricuspid annular plane systolic excursion measurement with M-mode through the right ventricular annulus from an apical four-chamber view. (B) Diminished tricuspid annular plane systolic excursion measurement (0.6 cm) in a patient with right ventricular systolic dysfunction (TA: Tricuspid valve annulus).
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    Fig. 1.15: Right ventricle (RV) diastolic collapse: M-mode of the right ventricle from the subcostal window in a patient with a pericardial effusion. The right ventricular free wall contracts with systole, briefly dilates during early diastole before collapsing during late diastole with increase in intrapericardial pressures (arrow). (PE: Pericardial effusion; RV: Right ventricular free wall; L: Liver).
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    Fig. 1.16: M-mode of the inferior vena cava (IVC) demonstrating dilatation. The IVC appears fixed in diameter and there is no significant respiratory variation (L: liver).19
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