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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5769_Библиотеки_им_академика_М_И_Перельмана
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370 oracic ultrasound
From a hemodynamic point of view, in aortic valvular stenosis one can measure the pressure
gradient across the valve using the transvalvular flow velocity peak of the continuous wave
spectrum. Normally the flow peak velocity is less than 2 m/sec, and the maximum pressure
gradient is therefore less than 16 mm/Hg (Fig. 7).
Table 7 illustrates a severity classification of aortic stenosis.
Figure 7 – Flow peak velocity through the aortic valve assessed by continuous Doppler sampling in a
normal subject.
Table 7 – Severity classification of aortic stenosis
Aortic stenosis Mild Moderate Severe
Jet velocity (m/sec)
Mean pressure gradient (mm/Hg)
Valve area (cm2)
Adapted from: Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.
2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of
patients with valvular heart disease: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. 2008;52:1-142
< 3
< 25
> 1.5
3-4
25-40
1-1.5
> 4
> 40
< 1
If a jet greater than 4 m/sec is identified, then severe aortic stenosis is highly probable. is
value corresponds to a peak pressure gradient greater than 64 mm/Hg. If the flow velocity is
within normal limits or mildly increased, a critical aortic stenosis can be excluded in subjects
with normal left ventricular systolic function.
e sonographer must remember that the gradient is dependent on both the valve area
and the transvalvular flow. An increase of transvalvular flow (as in aortic regurgitation or in
elevated cardiac output conditions) can determine a high gradient, whereas a low flow can
underestimate a stenosis.
When the peak pressure gradient is between 25 and 60 mm/Hg, cardiac output is relevant for
the punctual estimation of the stenosis severity. In these cases, for a more precise evaluation,
the valve area estimation by the continuity equation is useful.
➣ Mitral stenosis
By two dimensional assessment, the mitral leaflets show a mobility parallel to the septum
(anterior leaflet) and to the posterior wall (posterior leaflet). Normally, the distance between
Echodynamics 371
the valvular edges and the respective walls is less than 5 mm in the moment of maximum
excursion. e posterior mitral leaflet is shorter than the anterior and shows a minor excursion.
rough the values of the mitral flow velocity, Bernoulli equation calculates transvalvular
mean and maximum gradient values in mm/Hg. Mean gradient is the relevant haemodynamic
finding. A mean gradient <5 mm/Hg identifies a mild mitral stenosis, a value >10 mm/Hg a
severe stenosis. An intermediate stenosis shows values between 5 and 10 mm/Hg. However,
mitral gradient is not the best marker of the severity of mitral stenosis since it is dependent
on the mitral valve area (MVA) as well as a number of other factors that influence transmitral
flow rate, the most important being heart rate, cardiac output and associated mitral regurgitation. erefore a precise assessment of mitral stenosis should rely mostly on valve area.
Planimetry using 2D echocardiography of the mitral orifice in mid diastole has the advantage
of being a direct measurement of valvular area. A valvular area less than 1 cm2 is indicative
of a severe stenosis, whereas a normal area is between 4 and 6 cm2 (Table 8).
A more complex method employs the Pressure Half Time (PHT). PHT is defined as the
time interval in milliseconds between the maximum mitral gradient in early diastole and the
time point where the gradient is half the maximum initial value. e decline of the velocity
of diastolic transmitral blood flow is inversely proportional to valve area (cm2), and mitral
valve area (MVA) is derived using the empirical formula:
MVA = 220/PHT
Table 8 – Recommendations for classification of mitral stenosis
Mild Moderate Severe
Specific findings
Valve area (cm2)
Supportive findings
Mean gradient (mm/Hg)
Pulmonary artery pressure
Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP, Iung B, Otto
CM, Pellikka PA, Quinones M. Echocardiographic assessment of valve stenosis: EAE/ASE
recommendations for clinical practice. 2009;10:1-25
> 1.5
< 5
< 30
1-1.5
5-10
30-50
< 1
> 10
> 50
➣ Assessment of contractile function of the left ventricle
Although ejection fraction (EF) is a widely used index of contractile function (see Chapter 10),
it has major limitations, not only related to subjectivity and interobserver variability of the
estimation. EF is sensitive to changes in preload and afterload. Moreover, there is little correlation between EF and symptoms, exercise capacity, maximum oxygen consumption and
cardiac filling pressures in subjects with heart failure.
e rate of left ventricular pressure change during contraction (dP/dt) is an useful index of
contractility independent from load. From the Doppler mitral regurgitation spectral signal,
the time interval (∆t) between 1 m/sec (atrioventricular pressure gradient = 4 mm/Hg) and 3
m/sec (atrioventricular gradient = 36 mm/Hg) on the slope is calculated (Fig. 8). erefore:
dP/dt = 36 − 4/∆t or 32/∆t
372 oracic ultrasound
Doppler derived dP/dt correlates well with catheter measured dP/dt.
e main limitation of this method is that it assumes a negligible left atrial pressure. On the
contrary, it remains particularly interesting in patient with aortic or mitral regurgitation,
when EF is often misleading.
Normal dP/dt is >1200 mm/Hg/sec, a value <800 mm/Hg/sec is indicative of severe dysfunction, and values between 1200 and 800 mm/Hg/sec are seen in subjects with mild/moderate
dysfunction.
Figure 8 – Assessment of dP/dt by analyzing the mitralic regurgitant flow. The rate of ventricular
pressure change between 4 and 36 mm/Hg allows to estimate the left ventricular contractile function. In
this case the value is 1185 mm/Hg/sec.
➣ Assessment of segmental contractility of the left ventricle
Accurate interpretation of regional wall motion requires the evaluation of wall thickening and
systolic endocardial motion for each LV segment. e American Society of Echocardiography
recommends a 17-segment model of regional wall motion evaluation (Fig. 9). is semiquantitative estimate allows to classify the segments as hyperkinetic, normal, hypokinetic,
akinetic, or dyskinetic (Table 9).
Figure 9 – Segmental wall anatomy of the left ventricle in the parasternal short axis view at the basal,
mid and apical level.
Echodynamics 373
Table 9 – Scoring system for grading wall motion
Score Wall motion Systolic endocardial motion Systolic wall thickening
1
2
3
4
5
Normal
Hypokinesis
Akinesis
Diskinesis
Aneurysmal
Normal
Reduced (< 5 mm)
Absent
Outward
Diastolic deformity
30- 50%
< 30%
Absent
Thinning
Absent or thinning
➣ Dynamic left outflow tract obstruction
An important argument for the critical care physician is the evaluation of a dynamic left
outflow tract obstruction (DLOTO)15. DLOTO is classically associated with hypertrophic
obstructive cardiomyopathy. However this condition can occur after myocardial infarction,
acute myocardial ischemia, following mitral valvuloplasty, with atrial fibrillation and during
dobutamine stress test. More interestingly, reduced left ventricular end diastolic dimensions
due to hypertrophy, hypovolemia, vasodilation and enhanced myocardial contractility (during
inotropic therapy) are recognized precipitants of DLOTO.
erefore, in many critical settings DLOTO without hypertrophic cardiomyopathy is not an
uncommon cause of hypotension and shock resistant to cathecolamines. In this condition,
the clinical features of reduced cardiac output, relatively high pulmonary venous pressure and
low systemic blood pressure may easily be mistaken for cardiogenic shock due to other causes.
Because DLOTO is a dynamic obstruction due to systolic movement of the anterior mitral
leaflet (SAM) into the outflow tract, the diagnosis by echocardiography is primarily inspective. In parasternal long axis or apical five chambers view, the anterior mitral leaflet is seen
suctioned during systole in the left ventricular outflow tract. Moreover, in the apical five
chambers view continuous Doppler imaging allows the quantification of the obstruction
through the measurement of the gradient (by Bernoulli equation).
e diagnosis of DLOTO in the setting of a hypotensive patient is critical because it contraindicates every positive inotropic drug, and permits to estimate the indication and the
beneficial effect of administering volume, phenylephrine, norepinephrine and beta-blockers.
➣ Left atrial volume
Left atrial volume (LAV) is the best method of left atrial quantification and is computed from
the biplane area and length:
LAV = ( 0 .85) · A1 · A2/L
where A1 is the left atrium area from the four chamber view, A2 is the left atrium area from the
two chambers view, and L is the left atrium length from mitral plane to superior left atrium.
Left atrium enlarges when the left atrial pressure rises to maintain the left ventricle filling.
erefore left atrial enlargement is the hallmark of a chronic elevation in left ventricular
diastolic pressure.
An LAV of 32 ml/m2 or greater represents an independent predictor of atrial fibrillation,
stroke, heart failure, and cardiovascular death.
374 oracic ultrasound
➣ Left ventricular filling pressures (LVFP)
Numerous methods to estimate LVFP with echocardiography exist. However they are empirical techniques, because there is no physical relationship useful to extract absolute pressure
values. In Chapter 10, the role of E/E’ ratio as indicator of high or low LVFP was described,
but this estimate is not absolute and quantitative, and it shows a large range of uncertainty
for intermediate values. LVFP may be estimated by subtracting the peak left ventricular-left
atrial pressure difference (systolic left atrio-ventricular pressure gradient, from continuous wave
Doppler of mitral regurgitation) from systolic blood pressure. However, with this method we
must subtract two large numbers with high relative errors, to yield a small number.
Some studies have shown that E/E’ is linearly related to left atrial pressure. A strong relation
was observed16 between pulmonary capillary wedge pressure and E/E’ ratio in subjects with
sinus tachicardia, irrespective of the mitralic inflow pattern and ejection fraction (r = 0.86,
Wedge pressure = 1.55+ 1.47 (E/E’)).
A common question in critical care is whether the patient with bilateral pulmonary infiltrates
has cardiogenic edema or acute lung injury. Lung ultrasonography allows the intensivist to
distinguish between cardiogenic and pneumogenic interstitial syndrome (see Chapter 7). e
finding of A lines with sliding lung at chest sonography rules out a pulmonary edema and
indicates that pulmonary artery occlusion pressure (PAOP) and left atrial pressure is normal
or only mildly increased (<18 mm/Hg)
between pneumogenic, cardiogenic or mixed interstitial syndrome. A pneumogenic interstitial
syndrome does not exclude an overimposed wet lung from cardiac failure, whereas a pure
cardiogenic interstitial syndrome (pulmonary edema) confirms high PAOP. A focal area of
interstitial syndrome generally excludes high PAOP19.
Although chest sonography is useful for distinguishing between cardiogenic and pneumogenic lungs and as indirect estimator for high left ventricular filling pressure or high PAOP
(in the absence of mitral stenosis), a complementary non invasive hemodynamic evaluation
is often necessary. is assessment is particularly decisive when lung ultrasound detects a B
Lines pattern (Tab. 10).
17,18
. A profuse B Lines pattern requires to distinguish
Table 10 – Hemodynamic findings useful to distinguish between cardiogenic and pneumogenic B Lines
Findings Cardiogenic B Lines Pneumogenic B lines
Left ventricular function
E wave velocity
E/A ratio
E wave deceleration time
E/E’ ratio
Normal or depressed
> 50 cm/sec
1 or > 1
< 150 msec
>15
Normal or slightly depressed
< 50 cm/sec
< 1
> 150 msec
< 8
Fig. 10 shows an advanced algorithmic approach for detecting high PAOP by an integrated
cardiopulmonary ultrasound evaluation.
➣ Systemic vascular resistance (SVR)
SVR is an integral therapeutic component of patients with heart failure and shock. Doppler
echocardiography provides a reliable noninvasive assessment of this index when the ratio of
peak mitral regurgitant velocity (MRV,m/sec) to left ventricular outflow velocity-time integral
(VTILOVT) is calculated (Fig. 11). MRV/VTILOVT correlates well with systemic vascular
Echodynamics 375
Figure 10 - Advanced algorithmic approach for detecting high PAOP by an integrated cardiopulmonary
ultrasound evaluation.
Figure 11 – Systemic vascular resistance assessment (SVR) in a patient with heart failure. The mitral
regurgitant jet velocity is 4.9 m/sec, Velocity time integral (VTI) assessed placing the pulsed Doppler
gate inside the left ventricular outflow tract is 10.4. The ratio between systolic mitral regurgitant velocity
and VTI is 0.44. This value is significant for high SVR.
376 oracic ultrasound
resistance. A ratio >0.27 has a 70% sensitivity and a 77% specificity to identify SVR >14
Wood units*, a ratio <0.2 has a 92% sensitivity and a 88% specificity to identify SVR <10
Wood units20.
*Units for measuring vascular resistance are dyn∙sec∙cm-5 or Pa∙sec∙m-3. mm/Hg∙min∙L-1 is numerically
equivalent to Wood units. To convert from Wood units to MPa∙sec∙m-3 you must multiply by 8. To convert
from Wood units to dyn∙sec∙cm-5 you must multiply by 80.
➣ Systolic function of the right ventricle
A systolic excursion of the tricuspid annulus (TAPSE) greater than 17 mm is indicative of
right ventricular normal function (EF > 40%) (Fig. 12). Using tissue Doppler imaging, a
peak systolic velocity of the tricuspid annulus >12 cm/sec indicates a normal right ventricle
ejection fraction (normal values between 11.5 and 21 cm/sec).
Figure 12 – TAPSE measurement in M-mode.
➣ Right ventricular infarction (RVI)
RVI occurs in 30% of patients with inferior myocardial infarction who present with hypotension and it should be excluded in patients presenting with low cardiac output and maintained
left ventricular systolic function with dry lungs. Management of patients with RVI is critical,
since a considerable degree of raised right atrial pressure is required to secure an adequate
left cardiac output.
Depressed right ventricular free wall long axis amplitude, measured by TAPSE, represents
a sensitive finding for right ventricular infarction. A tricuspid valve annulus peak systolic
velocity less than 12 cm/s had a sensitivity, specificity, and negative predictive value of 81%,
82%, and 92%, respectively, for RV infarction21. Moreover, a short early diastolic deceleration
time (right E wave), particularly in the presence of raised systemic venous pressure (large cava
vein), suggests a restrictive right ventricular physiology and high right atrial pressure. Finally,
a degree of tricuspid regurgitation is usually present as a manifestation of right ventricle and
tricuspid ring enlargement.
➣ Pulmonary hypertension
Pulmonary hypertension (PH) occurs either as a primary pathology (PAH) or as secondary to other
cardiovascular disease. It is defined as mean pulmonary artery pressure (mPAP) >25 mmHg at rest.
A diagnosis of pulmonary arterial hypertension (PAH) requires pulmonary vascular resistances
(PVR) ≥3 mmHg/L, min (Wood units) and wedge, left atrial pressure or left ventricular end
diastolic pressure ≤15 mm/Hg.
Echodynamics 377
When a patient with pulmonary hypertension is encountered, echocardiography plays a
fundamental role in identifying cardiovascular
abnormalities that confirm a secondary pulmonary hypertension. Table 11 outlines the
primary and secondary causes of pulmonary
hypertension.
Generally, the diagnosis of primary pulmonary hypertension is a diagnosis of exclusion,
because echocardiography is less valuable
for detecting its etiology. Echocardiographic
examination should be tailored to any cardiac
entity able to have resulted in pulmonary hypertension. Pulmonary embolism is discussed
in Chapter 7. Common causes of pulmonary
venous hypertension are mitral valvular diseases and left ventricular systolic and diastolic
dysfunction.
e echocardiographic manifestations of right
heart hypertension result in dilation and eventual hypertrophy of the right ventricle. e
majority of patients with significant pulmo-
Table 11 – Pulmonary hypertension, etiologies
Shunt related
Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
Related to venous pulmonary hypertension
Mitral stenosis
Mitral regurgitation
Left ventricular systolic dysfunction
Left ventricular diastolic dysfunction
Restrictive cardiomyopathy
Pulmonary vein stenosis/thrombosis
Pulmonary embolism (acute or chronic)
Primary pulmonary hypertension
Pulmonary disease
Obstructive lung disease
Restrictive lung disease
High altitude
Hypoventilation and Obesity
Miscellaneous (Anorexigens, toxins)
nary hypertension will have evidence of right
atrial dilation with tricuspid regurgitation, ranging from mild to severe (Fig. 13). Moreover,
many patients with significant pulmonary hypertension will have evidence of abnormal left
ventricular filling caused by septal hypertrophy and right ventricular pressure overload. is
is expressed by a reduced mitral valve E/A ratio.
Figure 13 – Above: Large regurgitant tricuspid jet. Below: continuous wave Doppler image of a high
speed velocity tricuspid jet in the same patient. According to Bernouilli equation the peak pressure
gradient between right atrium and right ventricle is high (near 40 mm/Hg).
378 oracic ultrasound
Right ventricular pressure is routinely estimated by analyzing the tricuspid regurgitation
velocity (see Chapter 10). However, the tricuspid regurgitant jet is often not easily detected.
In many cases, measurement of the pulmonary flow acceleration time (AT) could be used
for the estimation of right ventricular pressure and systolic pulmonary pressure. e AT is
defined as the time from the onset to the maximal velocity of the pulmonary forward flow
obtained by pulsed Doppler in the right ventricular outflow tract (VTIRVOT) close to the
pulmonary valve. An AT of less than 100 msec indicates a high probability of pulmonary
hypertension (above 38 mm/Hg)22.
Contrast echocardiography is employed to detect the presence of significant right to left shunt.
If pulmonary hypertension is present and is secondary to an atrial septal defect (and not related
to the stretching of the forame ovale), the magnitude of the shunt will be substantial and
the contrast will appear nearly instantaneous and continuous throughout the cardiac cycle.
Ultrasound study of the lung allows to capture many important diagnostic data. In case of
pulmonary embolism, the acoustic pattern of the lung is generally normal. Mitral valvular
diseases and left ventricular dysfunction with high telediastolic ventricular pressure cause a
cardiogenic interstitial syndrome. e pure chronic obstructive pulmonary disease leaves
lung acoustic unchanged. Diffuse interstitial lung diseases show a pneumogenic interstitial
syndrome. Finally, the ARDS presents a characteristic lung ultrasound picture characterized
by patched pulmonary interstitial syndrome and gravitational consolidations
23,24,25,26
.
➣ Pulmonary vascular resistance (PVR)
e evaluation of PVR is of paramount importance in many settings, being one of the
parameters used to define pulmonary arterial hypertension and its prognostic evaluation.
Moreover, the assessment of PVR contributes to the management of patients with advanced
cardiovascular and pulmonary pathology, and it is used to evaluate the response to pharmacologic therapy in patients with congestive heart failure.
Some early studies attempted to compare hemodynamic variables with Doppler-derived
pulmonary flow velocity measurements, without a good correlation. More recently, however,
several indexes for this evaluation has been validated.
A simple method was proposed by Abbas et al.26 PVR is calculated by the ratio of peak
tricuspid regurgitant velocity (TRV in m/sec) to the right ventricular outflow tract velocitytime integral (VTI RVOT), obtained by Doppler ultrasound measurement. According to the
author, the proposed simplified equation is
PVR (Wood Units) ≈ 10 × TRV/ VTIRVOT
Patients with TRV/VTIRVOT ratio <0.2 are likely to have low PVR values. More precisely,
a TRV/VTIRVOT cutoff value of 0.175 shows a sensitivity of 77% and a specificity of 81%
to determine PVR >2 Wood units. A cutoff value of 7.6 WU has 85% sensitivity and 92%
specificity for identifying patients with poor prognoses
27,28
.
When pulmonary pressures are increased, a complete noninvasive description of pulmonary
hemodynamics should be performed
15.
ese data may integrate lung ultrasonography in an
advanced, sonographically directed, diagnostic approach. For example, pulmonary arterial
hypertension (PAH) is characterized by highly increased pulmonary pressures and PVR,
whereas the lungs show a normal ultrasound pattern, confirmed by the assessment of a normal
Echodynamics 379
pulmonary wedge pressure. In PH due to lung diseases, pulmonary pressure is generally modest and PVR may be mildly or moderately increased. Lungs may be abnormal at ultrasound
(interstitial syndrome), whereas the pulmonary wedge pressure, in the absence of concomitant
left heart disease, is normal. Table 12 outlines the changes in some hemodynamic parameters
in pulmonary hypertension.
Table 12 – Hemodynamic parameters in pulmonary hypertension
Condition Pulmonary
pressure
Pulmonary arterial hypertension
Left heart diseases
Lung diseases
Acute pulmonary embolism
Chronic pulmonary tromboembolism
+++
+/++
+
+/++
+++
Wedge
pressure
=/+
+++
=/+
=/+
=/+
Pulmonary vascular
resistance
+++
=
+/++
+
+++
➣ Left ventricular performance and dynamic changes in afterload
Left ventricular performance is influenced by afterload. In a hypotensive or vasodilated
patient, left ventricular ejection fraction may appear normal, because of the reduced cardiac
workload. us, the physician may judge “adequate” the cardiac function and dismiss the
option of inotropic support. In this case, a preexisting cardiac dysfunction may be unmasked
later, after the normalization of the blood pressure. erefore, a precise evaluation of the
true left ventricular function, and the need of inotropic support, is only possible through a
continuous reassessment of cardiac function by echocardiography.
➤ Recommended readings
Feigembaum H, Armstrong WF, Ryan T. Feigembaum’s Echocardiography. Lippincott Willims & Wilkins,
Philadelphia 2005.
Sarti A, Lorini FL (Eds). Echocardiography for intensivists. Springer Verlag Italia, 2012.
De Backer et al. (eds) Hemodynamic monitoring using echocardiography in the critically ill. Springer-Verlag,
Berlin-Heidelberg, 2011.
Otto CM. Textbook of clinical echocardiography. Elsevier Saunders, 3° Ed.,Philadelphia, PA, 2007.
Griffee MJ, Merkel MJ, Wei KS. e role of echocardiography in hemodynamic assessment of septic shock.
Crit Care Clin 2010;26.365-382.
Abraham J, Abraham TP. e role of echocardiography in hemodynamic assessment in heart failure. Heart
Failure Clin 2009;5:191-208.
➤ Bibliography
1. Vignon P. Hemodynamic assessment of critically ill patients using echocardiography Doppler. Curr Opin
Crit Care 2005;11:227-34.
2. Boyd JH, Walley KR. e role of echocardiography in hemodynamic monitoring. Curr Opin Crit Care
2009;15:239-43.
3. Galderisi M. Diastolic dysfunction and diastolic heart failure: diagnostic, prognostic and therapeutics
aspects. Cardiovascular Ultrasound; 2005:3:9.
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