Wall Motion Abnormalities Localization
Key Questions Addressed with Advanced CCEIs
- Is the heart preload sensitive?
- What is the efficacy and tolerance of a fluid challenge or fluid removal?
- What is LV systolic function?
- What is LV ejection performance?What is LV size?
- Are there segmental wall motion abnormalities?
- What is RV systolic function?
- Is acute cor pulmonale present?
- Is the RV cavity dilated?
- Is paradoxical septal motion present?
- Is RV systolic function impaired by ventilator settings?
- What are pulmonary arterial pressures?
- Is clinically relevant valvulopathy or a prosthetic valve dysfunction present?
- What is LV diastolic function?
- Are LV filling pressures elevated?
- Is the presence of an acute cor pulmonale related to a massive pulmonary embolism, to elevated intrathoracic pressures (from ventilator), or severe underlying lung disease?
- Is a thrombus in transit within the right atrium or ventricle?
- Is a thrombus entrapped into the proximal pulmonary artery/foramen ovale?
- Is circulatory failure related to pericardial tamponade?
- Is a clinically relevant pericardial effusion present?
- Is a localized mediastinal hematoma or a loculated pericardial effusion present (surgical/trauma settings)?
- Are intracardiac or intrapulmonary shunts present?
Cardiac Arrest-for effusion/PE as cause for PEA or lack of wall motion in Asystole
Trauma-to heart or great vessels
ChestPain-wall motion abnormalities
Unexplained Hypotension-pericardial Tamponade/hypovolemia/PE
Procedural Guidance-pacing and Pericardiocentesis
Long Axis of the heart if from the right shoulder to the left hip
Short axis is from the left shoulder to the right hip
15° angle to the chest wall
Marker towards the left hip
Aim towards the left midclavicle
If the pt is barrel chested, you may have to move off the Xiphoid to lower intercostals spaces.
Move off the Xiphoid to the right, not the left so the liver can be used as an acoustic window.
Ask patient to take a deep breath or increase the Vt on the ventilator
Rotate 90° clockwise from the four chamber and aim towards the left arm. Marker at the right hip
Subcostal Long Axis
Probe marker at the patients feet, scanning in sagittal plane
Along the line of right shoulder to left hip at 3rd or 4th ICS just lateral to the sternum
Probe marker is towards the right shoulder
Left shoulder to the right hip. Rotate 90° clockwise to the left shoulder
5th ICS under the breast at the PMI
pt should roll 30 to their left
Aim at the right shoulder with the marker towards the patients left
Sometimes, you must aim towards right elbow or head
Tricuspid is higher than mitral, should be on left of screen
Rotate 90° counterclockwise until the marker points towards the head
Evaluates the anterior and inferior wall
In the Apical 4 chamber, the transduce should then be rotated 75-90 degrees counterclockwise to image the apical 2 chamber view:
5) Apical 2-Chamber View: LV function should be assessed as well as any wall motion abnormalities. Descending aortic size should be assessed as well as flow quality by color imaging.
Continued rotation of the transducer will open up the LVOT and form the Apical 3-Chamber View:
6) Apical 3-Chamber View: global function and Wall motion abnormaliteis should be assessef. Pericardial effusions should be assessed. Color doppler should be placed in the LVOT and accrross the aortic valve. CW should be placed accross the aortic valve to assess for aortic stenosis.
Evaluates the aortic arch
Marker at the patients left
Always measure at right angles to the chamber
EF-clinicians estimate is as good as calculation
CVP-look at IVC and measure respiratory changes
M-Mode (Motion)-measure left ventricle in Parasternal long or short at mitral valve
<1 cm small, usually only behind the left ventricle
1-2 cm large, surrounds the whole heart
Usually hypoechoic, but can be echogenic if blood or pus are present.
5 center study of precordial US in 261 patients with penetrating truncal trauma: 225 (86.2%) TN, 29 (11.1%) TP 0 false negatives, 7 false positives Sensitivity = 100%, specificity = 96.9 (Ma OJ. Am J Emerg Med 2001; 19:284-6.)
Diastolic collapse of right ventricle, systolic collapse of atrium. Decreased Doppler flow through mitral valve during systole with inspiration (pulsus paradoxus)
If you freeze, mitral valve will be open during diastole
Hypokinesis-decreased wall thickness and motion
Akinesis-absent wall thickening and motion
Dyskinesis-paradoxical wall motion
Enlarged right ventricle.
Normal RV EDV is 21 mm ±1 mm, >25-30 is definitely abnormal
It is also normally less than ½ the size of the left ventricle in 4 chamber view
IVC Size Respiratory Change RA Pressure <1.5 total collapse 0-5 1.5-2.5 >50% collapse 5-10 1.5-2.5 <50% collapse 11-15 >2.5 <50% collapse 16-20 >2.5 No Change >20
Continued contraction of the valves is agonal
Adjust gain to allow posterior wall the highest time gain compensation
Decrease the dynamic range to decrease gray tones and emphasize blacks and whites
Can inject agitated saline as contrast to see exactly where you are. (Annals EM Supplement 44:4 OCTOBER 2004)
Crit Care Protocol
use a protocol, we do 4 standard views (long and short parasternal, apical 4, 5 and 2 chamber, and subcostal. We measure tricuspid regurgitant flow to give us fair good estimate with pulmonary artery systolic pressure, we use pulse wave Doppler of the pulmonary artery flow if we want both diastolic and systolic PAP, We use E/E’ parameter from tissue Doppler imaging plus left atrial size, plus left ventricular size to give us PCWP estimate. We use pulse wave transmitral flow to tell us about diastolic LV function (which other modalities won’t give you). We use size and respiratory variations of inferior vena cava for preload assessment. We use M-mode of the lateral tricuspid annulus to give us an index on RV contractility.
Best Article (Current Anaes & Crit Care 2006;17:237)
Echocardiography in the critically ill patient5.
Haemodynamic information Hypotension Assess volume status Left ventricular (LV) systolic function Regional wall motion abnormality Global dysfunction Transient dysfunction Left ventricular diastolic function Right ventricular function Outflow tract obstruction Valvular stenosis/regurgitation Pericardial effusion/tamponade Hypoxia Right ventricular function Right ventricular pressure Intracardiac shunts Pulmonary embolus Excluding infection Infective endocarditis
Assessment of left ventricular (LV) function
The assessment of LV function is the most common reason for performing bedside echocardiography in the ICU. LV systolic function can be assessed using echocardiography by measuring ejection fraction (EF−normal range 5575%), fractional shortening (FS−normal range 3042%) and cardiac output (CO). The relevant LV dimensions can be obtained from the parasternal long axis view and EF and FS can be calculated using the formula in Box 1. However, quantification of EF and FS has its limitations particularly, when accurate LV volumes and dimensions cannot be obtained due to suboptimal imaging.6 In this scenario, a visual estimate of global LV systolic function can be determined and graded normal LV systolic function or mild, moderate and severe impairment of LV systolic function.7
Box 1. Calculating ejection fraction and FS from LV dimensions obtained from echocardiography.
Estimation of stroke volume by the modified Simpson method (which requires accurate delineation of the endocardium in systole and diastole) is technically difficult in the critical care setting. It is far more practical and amenable to estimate stroke volume and CO, using Doppler-derived instantaneous blood flow velocity through a conduit with a known cross-sectional area (CSA). Using the LV outflow tract (LVOT) as the conduit is probably the most reliable and most commonly used application of this principle.8 The LV stroke volume is obtained by measuring the CSA of the LVOT multiplied by the transaortic flow velocity time integral (VTI) derived by spectral doppler tracing (see Box 2). The LVOT diameter is best measured in the parasternal long axis view 1 cm below the aortic valve and the transaortic VTI is obtained in the apical 5-chamber view.
Box 2. Estimating stroke volume and cardiac output by measuring the cross-sectional area of the LV outflow tract and the transaortic flow velocity time integral.
Cross-sectional area (CSA)=πr2=π(D/2)2 CSA=D2×0.785 (D is the measured LVOT diameter in cm) LV stroke volume=CSA×VTI Cardiac output (CO)=Stroke volume×Heart rate
The ability to assess the LV for regional wall motion abnormalities (RWMA) in the critically ill patient is essential particularly after a suspected myocardial ischemic event either in the perioperative patient, or in the patient who has acutely deteriorated haemodynamically. This involves dividing the left ventricle into 16 segments (see Fig. 1) each of which is then graded according to their movement, as follows:9
LV diastolic function
LV diastolic dysfunction is commonly seen in patients with hypertension, coronary artery disease, cardiomyopathy and many forms of valvular heart disease, and is a potential cause of pulmonary edema in patients with documented normal LV systolic function. Although there are number of ways for evaluating LV diastolic function, the commonly used methods in routine practice include Doppler assessment of mitral inflow, the pulmonary venous flow pattern and tissue Doppler imaging of the mitral annulus, using the apical 4-chamber view, with classical patterns portraying varying degree of LV diastolic dysfunction (see Fig. 2). Note that the pseudonormal mitral inflow trace can be distinguished from a normal mitral inflow trace, by examining the pulmonary venous flow, which should display atrial reversal.
Figure 2. Assessing for LV diastolic dysfunction using echocardiography by analyzing the mitral valve inflow pattern and pulmonary venous flow.
Assessment of right ventricular (RV) function
RV dysfunction is common in critically ill patients and its pathological role is underestimated in these patients. RV dysfunction can result from pressure or volume overload of RV. The two common causes for acute RV dysfunction are massive pulmonary embolus (PE) and acute respiratory distress syndrome (ARDS).10 Adequate assessment of RV function is needed in this condition, as the findings may alter therapy and is of prognostic value.11 Acute RV dysfunction may also be due to acute RV infarction, acute sickle cell crisis and sepsis.
Normal RV size is approximately two-thirds that of the left ventricle, and so RV dilatation should be easy to gauge. The qualitative assessment of RV systolic function can be done by visualizing the RV in multiple views (parasternal long axis, RV inflow tract view, apical 4-chamber view and subcostal). Abnormal RV wall motion occurs in inferior myocardial infarction and pulmonary hypertension. Interventricular septal movement can be used to assess RV dysfunction and differentiate volume overload from pressure overload of the RV. Septal flattening is common in RV dysfunction and if the septal distortion is only visualized during diastole, it is most likely due to volume overload, whereas in pressure overload, the septal flattening is usually present in both systole and diastole. Quantitative assessment of RV dysfunction such as RV wall thickness, RV fractional area change and long axis function by tissue Doppler imaging and myocardial performance index (MPI) are difficult in the critical care setting.
It is possible to estimate the RV systolic pressure (RVSP) from the addition of right atrial pressure (RAP) to pulmonary artery systolic pressure (PASP). PASP can be quantified from the peak velocity of the tricuspid regurgitation (TR) jet velocity, in the apical 4-chamber (using the Bernoulli equation). RAP can be estimated from the diameter of the inferior vena cava (IVC), visualized in the subcostal view, and the degree to which it collapses with inspiration (Box 3).
Box 3. Estimating the right ventricular systolic pressure from the pulmonary artery systolic pressure (PASP) and right atrial pressure (RAP). The PASP is estimated from the peak velocity of the tricuspid regurgitant (TR) jet. The RAP is estimated from the diameter of the inferior vena cava (IVC), and its collapse in inspiration.
RVSP=PASP+RAP PASP=4 (TR peak velocity)2 RAP (mmHg) IVC diameter (cm) Collapse on inspiration (%) <5 <2 100 510 <2 >50 1015 >2 2550 1520 >2 <25
Echocardiographic signs used in the diagnosis of acute pulmonary thromboembolism.13
1. Direct visualization of thrombus in the right sided chambers or the pulmonary artery 2. Right ventricular dilatation 3. Reduced right ventricular function 4. Reduced left ventricular cavity size 5. Dilated pulmonary arteries 6. Abnormal septal motion/systolic flattening of the septum 7. Significant (moderate to severe) TR 8. Increased velocity of TR jet 9. Dilatation of IVC
Saline Contrast for PFO
J Am Soc Echocard 2006;19:215
microbubbles already exist in saline
lung pressure breaks them down before the reach left heart
Apical 4 chamber or subcostal
once complete opacification of RA, observe when you see any in LA.
If <3 beats then it is a cardiac shunt
If >3 beats it is a pulmonary shunt
Valsalva or cough increases sens
false + can be ASD
Essential Echocardiography by Solomon
get these in LLR
measure LVOT diameter here
RV Inflow View
inferomedial tilt of the transducer gives long view of RA and RV
base-superior and rightward, mitral valve
midventricle-perpendicular to chest, papillary muscles, LV should be round in this view. if it is not you are getting oblique shot. assess contractility in this view
apex-move up torso or tilt more caudal. aortic valve
Angle towards pts right shoulder
Apex is at the top of the screen
Right ventricle has more trabeculae and doesnt reach LV apex
and tricuspid is closer to the apex
Tilt 10-20° anteriorly
Rotate 90° counterclockwise
Can see anterior and inferior walls
Look at septum with color Doppler
Move towards pts right angle to l shoulder
Assessment of systolic function
Perpendicular to PLAX
Just distal to mitral valve
At end diastole, beginning of QRS
PW post wave
Can calculate EF
Contraction-reduced, normal, hyperdynamic
EF 40-50%-mild reduction
< 30 severe
>75% in PLAX will have chamber gone during systole
Regional wall motion
Dysfunctional segments thicken less during systole
5 aneurysmal-remains deformed during diastole
Having pt sniff increases the sensitivity of the bubble study
Decreased LV size
apex still compresses in systole, but dyskinetic r free wall
However, in this study (Echocardiography. 2010 Jul;27(6):614-20) this might be an optical illusion from a hyperdynamic LV &
this study makes me doubt the specificity (Eur J Echocard (2005) 6, 11e14)
Other signs of PE or elevated Right Ventricular Pressures
Flat IV septum
Distension of IVC c loss of respiratory
Severe will have dilated hepatic veins
This window is probably the most familiar to EPs and surgeons and is most frequently included as the primary view of the heart in the FAST examination. The window is obtained by placing the probe under the xiphoid process and angling the plane of the US into the left chest. The view should include both atria and ventricles. The apex of the heart, a left-sided structure, should be seen on the right side of the screen as it is viewed, with the right-sided structures toward the left of the screen and adjacent to the liver. In a cardiology orientation, the probe indicator should be directed to the patients left, while in a general imaging orientation it should be directed to the patients right, resulting in the same image on the screen.
This window is obtained by placing the probe at the apex of the heart, typically slightly inferior and lateral to the nipple in males and under the breast in females. While probably the most difficult of the three primary windows to consistently visualize, it provides some of the best information when correctly obtained. The four-chamber view includes both ventricles and atria, with the apex at the top of the screen and the interventricular septum running vertically down the screen. In a cardiology orientation, the probe indicator is directed to the patients left (or down to the bed when patient is in a supine position), while in a general imaging orientation the probe indicator is directed to the patients right (or toward the ceiling in a supine patient). The net result is that in either convention, the same image is seen on the screen, with the left side of the heart on the right side of the screen as it is viewed and the right side of the heart on the left side of the screen as it is viewed.
The parasternal window is one of the most consistently available windows to the heart. The long axis view is obtained by placing the probe just to the left of the sternum in the second or third intercostal space with the US plane running from the base to the apex of the heart. The view should include the right ventricle anteriorly and the left atrium, ventricle, and aortic outflow tract posteriorly.
The parasternal view is obtained in cardiology by directing the probe to the patient’s right shoulder (opposite to the probe direction in other cardiology views) providing an image that is reversed from other windows, with the apex (a left-sided structure) on the left of the screen as it is viewed. This indicator direction makes sense when the examiner is on the patients left, as the view can be thought of as looking down through the long axis of the heart. However, this orientation is not intuitive when scanning from the patients right (where other US examinations are typically performed from) and essentially involves switching the probe indicator direction in order to obtain an image that is reversed from other cardiac images.
There are two potential solutions for the parasternal window when scanning from the patients right using a general imaging screen orientation. An attempt can be made to mimic the cardiology screen image by pointing the indicator to the patients left hip. This is sometimes called the “fourth-and-long” approach, as it involves directing the indicator to the 4 oclock position (or left hip) to obtain the long axis view. This is based on a partial but incomplete adoption of the cardiology approach and will result in an image that mimics what is seen in cardiology and many emergency medicine texts.
An alternate approach is to orient the indicator to the patients right in a general screen orientation, consistent with the indicator direction for the other windows to the heart. This provides an image that is flipped from that commonly seen in cardiology texts, but allows for a consistent probe orientation with consistent position of anatomic structures on the US screen, (i.e., the apex [patients left] on the right side of the screen as it is viewed). This approach has been previously described in the literature and is listed as an alternate approach in the Emergency Ultrasound Imaging Compendium.28,29
Pericardial Tamponade (Circulation 1984; 70 (6):966)
Right ventricular collapse is 92% sensitive and 100% specific
Right atrial collapse is 64% sensitive and 100% specific
atrial collapse occurs earlier
LVEF = 75.5 – (2.5 x EPSS)
Normal < 5 mm
EF < 50% > 7 mm
EF < 30% > 18 mm
M-mode measurement of ejection fraction
just beyond mitral leaflets
How to perform using doppler of LVOT (AJEM 2012; PMID 22795411)
Measure lvot in PLAX, when valve is wide open where leaflets attach
then in A5C, pulsed wave doppler just in front of valve
The 2 parameters required to calculate CI are the LVOT diameter and the VTI. The LVOT diameter is the diameter of the aortic outflow tract, which can be calculated by obtaining a parasternal long-axis view. The measurement is obtained by measuring the distance from the inner edge to inner edge, where the right aortic valve coronary cusp meets the interventricular septum to where the noncoronary cusp meets the anterior mitral valve leaflet, in a line parallel to the aortic annulus. Velocity time integral is an estimation of the distance that a column of blood travels in 1 systolic stroke, or stroke distance. Using ultrasound, the VTI can be measured by obtaining an apical 5-chamber view and then placing a pulsed-wave Doppler cursor near the aortic valve annulus. The Doppler signal is then traced using the cardiac software to calculate VTI.
After obtaining the LVOT diameter and VTI, CI can be calculated from the following equation: CI = stroke volume index (SVI) × HR, where SVI = stroke volume (SV)/body surface area, and SV = LVOT area × stroke distance, or SV = π × (LVOT diameter/2)2 × VTI. Heart rate is calculated by the ultrasound cardiac software during the VTI measurements, rather than from physical examination or bedside telemetry monitor.
Acute vs Chronic RV Dilation
A good way to determine acute vs chronic is to look at the free wall of the RV and measure from subxiphoid view (most perpendicular measurement). If less than 5mm likely an acute process and greater then chronic hypertrophy. Can also look for chronic dz clues by increasing RV trabecular hypertrophy and increase in size of the moderator band, also a sign of chronic RV hypertrophy. (HM) J Am Soc Echocardiogr. 2010;23:685-713