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11
Echodynamics
➣ General considerations
Hemodynamics is the study of blood flow with its related forces. e evaluation of hemodynamic parameters is crucial for the diagnosis and the rational therapy of the critically ill
and the respiratory patients. Many instruments, with different complexity and methods, are
employed for assessing such parameters.
anks to the application of Doppler technology, both transthoracic and transesophageal
echography are useful bedside non invasive tools for providing hemodynamic information.
is non invasive, ultrasound-guided assessment can be called “Echodynamics”
Doppler sonography provides excellent assessment of hemodynamics that compares favorably
with more invasive and complex measurements. Monitoring using Pulmonary Artery Catheters
(PAC), for long time considered as the gold standard, has not yet to improve survival and
has many important limitations
Some information about the Doppler principle can be found in Chapter 1. Previous pages on
echocardiography (Chapter 10) have already discussed the applications of cardiac ultrasound
for a visual inspection and basic (focused) or intermediate hemodynamic interrogations (pressure determinations, stroke volume and diastolic function assessment).
is chapter briefly synthesizes the physical and methodological basis for the application of
the Doppler sonography in the hemodynamically instable and in the critically ill patient
For simplicity the discussion will cover only the use of transparietal ultrasound.
Finally, many important clinical considerations for an integrated approach to the
critical patient will appear in the next chapter
(Chapter 12, Integrated clinical ultrasound).
3,4,5
.
1,2
.
6,7,8
.
➣ Pathophysiologic targets
Echocardiography is currently the only method
that can provide real-time imaging of the heart
at bedside. It represents the first line modality
for estimating ventricular volumes, cardiac
performance and the pericardial space (Fig. 1).
ese arguments, that can be interpreted only
qualitatively, are covered in the chapter on
echocardiography in this book.
Preload assessment is important for the study
of the hypotensive patient. It can be evaluated
Figure 1 – A simple visual assessment of the
heart is determinant for detecting large deviation from normality. A: normal heart, B: enlargement of the right ventricle. C: enlargement and
remodeling of the left ventricle, and left atrial
enlargement. D: pericardial effusion.
361
362 oracic ultrasound
by measuring left ventricular end diastolic volume or area. ese measures generally reveal
small left ventricular cavities with a small hyperkinetic heart when the circulating volume is
low. Otherwise, a small, collapsed inferior cava vein is the hallmark of the hypovolemic patient (Fig. 2). e massively vasodilated patient without a severely impaired cardiac function,
shows a small inferior cava vein and small end systolic left ventricular area and volume. is
picture is characteristic of hyperdynamic septic and neurogenic shock (distributive shock).
Such observations can be suitably expanded to cover other important pathophysiologic
targets. In fact, a comprehensive Doppler analysis enables sufficiently accurate quantitative
assessment of stroke volume, cardiac output, ventricular filling pressure and systemic and
pulmonary vascular resistances (Fig. 3).
Figure 2 – A: small telediastolic left ventricular area (parasternal short axis view) and small left
telediastolic ventricular volume (four cambers view), with a small inferior cava vein (B), are hallmarks
of volume depletion.
Figure 3 – Patient with severe heart failure. Synthetic morpho-functional evaluation. Many concordant
information may be acquired by cardiac and hemodynamic ultrasound assessment. A: enlarged and remodeled
left ventricle. Large left atrium. B: very low ejection fraction. C: wide/tight early (E) mitralic inflow wave
(restrictive). D: small TDI E’ wave, and, as a result, high E/E’ ratio (high left ventricular filling pressure). E: high
velocity mitral regurgitant flow. F: low stroke distance (VTI). From these two parameters, a high mitral regurgitant
velocity/stroke distance ratio results (high systemic vascular resistances). Many other useful information may
be acquired during pleural and lung ultrasound. A concordance between different morpho-functional data
reinforces a clinical hypothesis and, above all, is basilar for monitoring and therapeutic purposes.
Echodynamics 363
A complete and quantitative sonographic assessment of the patient with heart failure, shock
and sepsis requires an advanced ultrasound skill. Although this book mainly describes basic
and intermediate ultrasound applications to the chest, a brief description of advanced applications of Doppler sonography to hemodynamics is useful for a better comprehension of
the previous and next pages.
Table 1 shows direct hemodynamic parameters and their echocardiographic correlates.
Table 2 shows calculated (indirect) hemodynamic parameters.
Table 3 summarizes the normal values of the most important cardiovascular measurements.
Table 1 – Echodynamic parameters
Hemodynamic parameter Echo correlate Comment
LVOT Velocity Time Integral (VTI) VTI Normally 18-22 cm
Stroke volume (ml) VTI ∙ LVOT area Accurate measure of LVOT
diameter is critical
Right atrial pressure (RAP) (mm/Hg) Inferior Caval vein
analysis
Left atrial pressure (LAP) (mm/Hg) SBP – 4(Vmr)
Ejection fraction (%) EDV-ESV / EDV Modified biplane Simpson’s rule
Pulmonary artery systolic pressure
(mm/Hg)
Pulmonary artery diastolic pressure
(mm/Hg)
Pulmonary capillary wedge pressure E/Em* Tissue Doppler analysis of
4(VTr)2 + RAP Continous Doppler of tricuspid
4(VPr)2 + RAP Continous Doppler of
2
Not valid in patients in positive
pressure ventilation
Exclude patients with acute
mitral regurgitation, prosthetic
mitral valve, and LVOT
obstruction
recommended
regurgitant jet velocity (VTr) is
necessary
pulmonary valve regurgitant jet
velocity (VPr) is necessary
mitral annulus is necessary.
E/Em represents the ratio
between the peak velocity of
early transmitral flow (pulsed
wave Doppler) and the speed of
early tissue relaxation velocity,
measured by Tissue Doppler
Imaging.
Abbreviations: VTI: Velocity Time Integral; LVOT: Left ventricular outflow tract; HR: Heart rate; SBP:
Systolic blood pressure; EDV: End diatolic volume; ESV: End systolic volume; Vmr: Mitral regurgitant
velocity; VTr: Tricuspid regurgitant velocity; VPr: Pulmonary valve regurgitant velocity; E/Em: ratio between
E and Em wave at Tissue Doppler Imaging
A normal E/Em is less than 10. A ratio greater than 15 predicts a left ventricular filling pressure greater
than 15 mm/Hg
364 oracic ultrasound
Table 2 – Indirect hemodynamic parameters
Hemodynamic parameter Equation
Body Surface Area (BSA) (m2) (Height in cm + Weight in Kg – 60)/100
Cardiac output (ml/min) HR X VTI X LVOT area
Cardiac index (ml/min ∙ m2) CO/BSA
Stroke volume index (ml/beat ∙ m2) SV/BSA
Systemic vascular resistence (SVR) (dyne ∙ sec/cm5) 80 (MAP – RAP) X1/CO
Pulmonary vascular resistence (PVR) (dyne ∙ sec/cm5) 80 (PAP – PCWP) X1/CO
Abbreviations: VTI: Velocity Time Integral; LVOT: Left ventricular outflow tract; HR: Heart rate; CO:
Cardiac output; SV: Stroke volume; BSA: Body surface area; MAP: Mean arterial pressure; RAP:
Right atrial pressure; PAP: Pulmonary artery pressure; PCWP: Pulmonary capillary wedge pressure
Table 3 – Normal values of the most important cardiovascular measurements
Cardiac output 4-7 L/min
Cardiac index 3.5-4 L/min
Stroke volume 42-52 ml
Stroke index 36-48 ml/m
2
Ejection fraction 55-75%
End diastolic LV area (4 ch) 33±8 cm
End systolic LV area (4 ch) 6±2 cm
End diastolic LV volume (4 ch) 60-95 ml/m
End systolic LV volume (4 ch) 18-32 ml/m
2
2
2
2
Right atrial pressure 1-8 mm/Hg
Pulmonary artery wedge pressure 5-15 mm/Hg
Right ventricular systolic pressure 15-25 mm/Hg
Right ventricular diastolic pressure 0-8 mm/Hg
Pulmonary artery systolic pressure 15-25 mm/Hg
Pulmonary artery diastolic pressure 8-15 mm/Hg
Systemic vascular resistance 1500-3000 dyn∙sec∙cm-5
or 18.7-37.5 WU
Pulmonary vascular resistance 100-250 dyn∙sec∙cm-5
or 1.25-3.12 WU
Echodynamics 365
➣ Shock
Shock is the clinical expression of circulatory failure that results in inadequate cellular oxygen
utilization9.
It results from four potential, and not necessarily exclusive, pathophysiological mechanisms:
hypovolemia, cardiogenic factors, obstruction (pulmonary embolism, cardiac tamponade,
tension pneumothorax), or distributive factors (sepsis, anaphylaxis, pancreatitis). In ICU,
septic shock is the most common form of shock (62%), whereas obstructive shock is relatively rare (2%). Cardiogenic shock occurs in 16% of cases, hypovolemic shock in 16% and
distributive shock in 2%.
e key for an etiologic diagnosis of shock is to identify the specific patterns in cardiocirculatory failure and shock (Tab 4)10.
Table 4 – Cardiocirculatory patterns in shock
Type of shock CVP and LVFP Cardiac output Systemic vascular
resistance
Hypovolemic low low high low
Cardiogenic high low high low
Septic
Hyperdynamic
Hypodynamic
Obstructive High and low low high low
Neurogenic low low low low
Hypoadrenal high or low low low or normal low
high or low
high or low
high
low
low
high
Venous O2
saturation
high
low or high
From a practical point of view, hypovolemic shock is characteristic, because volume depletion
is its main landmark. It is clearly expressed on heart and inferior cava vein (or internal jugular
vein). e diagnosis of cardiogenic shock is relatively easy if the clinician is able to evaluate the systolic function of the heart and the stroke volume. Neurogenic and Hypoadrenal
shock are relatively infrequent. Septic shock is usual in emergency and ICU and is the most
heterogeneous shock in its hemodynamic features. Tipically, the early phase of septic shock
is hyperdynamic, late phase is hypodynamic and it often shows an overlap with cardiogenic
shock (see later, sepsis related cardiomyopathy).
erefore, an atypical, mixed, imperfect, hypovolemic/cardiogenic shock is often a septic shock.
Finally, the diagnosis of obstructive shock in cardiac tamponade and in pulmonary embolism
is immediate. e first diagnosis is only inspective. e latter is clear if the clinician look at
the right heart and at the lung11.
➣ Physical considerations
ree main equations govern an echodynamic assessment:
• Flow equation
• Continuity equation
• Bernoulli equation
366 oracic ultrasound
According to the first equation, using the Doppler effect, the velocity of blood in an anatomic conduit (left ventricular outflow tract, just below the aortic valve) can be calculated.
By integrating the blood velocities over time (velocity time integral - VTI), a stroke distance
can be calculated. is is the distance (in cm) travelled by a column of blood during a fixed
time (a single cardiac cycle). By multiplying this by the cross-sectional area (measured in
B Mode) through which the column moves, a volume (SV) can be obtained according to
equation 12,13 (Fig. 4).
SV = VTI · πr2
where SV represents the Stroke Volume. Finally, Cardiac Output (CO) is the product of SV
and heart rate (HR):
CO=SV· HR
Figure 4 – Above: Assessment of the diameter of left ventricular outflow tract (LVOT) at the aortic
annulus during systole, using a parasternal long axis view. Below: Velocity time integral (VTI) assessment
using pulsed Doppler spectrum in four chambers view. The sample is placed 5 mm below the plane of the
aortic valve. Stroke volume is the product of VTI and LVOT area.
Based on the principle of conservation of mass, the Continuity Equation states that the flow
in one area must equal the flow in a second area, if there are no shunts between the two
areas. is principle is used for the determination of aortic valve area during the assessment
of aortic stenosis and for quantifying vascular stenosis. In aortic stenosis, the stroke volume
within the left ventricular outflow tract must equal the stroke volume through the stenotic
orifice. Because stroke volume is the product of cross sectional area and velocity time integral
(VTI), the continuity equation can be arranged to yield:
Aortic valve area = LVOT area · VTIOT/VTIAS
Echodynamics 367
Where LVOT represents the cross sectional area of the left ventricular outflow tract, and VTIOT/
VTIAS the ratio between VTI of the outflow tract and VTI of the aortic stenosis jet (Fig. 5).
Figure 5 – Above: Pulsed Doppler sampling of the ejected flow through the left ventricular outflow tract
in a normal subject, to calculate velocity-time integral (VTI). Below: Continuous wave Doppler envelope
directed through the aortic valve in the same subject. VTI is calculated. The aortic valve area may be
assessed according the continuity equation (in this normal case VTIOT/VTIAS is 0.88). Therefore aortic
the valve area is LVTO areaX0.88.
e Bernoulli equation is very important in hemodynamics:
P+1/2ρV2 + ρgh=constant
it is derived from the Navier-Stokes equation in the case of inviscid and steady flow conditions. When applied to two cross-sections of a vessel it gives rise to the following equation
P1 − P2 = 1/2ρ(V22 − V12) + ρg(h2 − h1)
where P1 and P2 are the upstream and downstream pressures, respectively; V1 and V2 are the
upstream and downstream velocities, respectively; ρ is blood density and can be supposed to
be 1.06 gr/cm3; g is the gravitational acceleration (9.8 m/sec2); h1 and h2 are the upstream
and downstream heights of the vessel, respectively. However, in practical clinical terms, the
difference between h1 and h2 is minimal, and therefore can be ignored (the addendum
ρg(h2-h1)= 0). Also, as the blood flows through a narrowed orifice, the proximal velocity V1
is much smaller compared to the velocity downstream V2. Because the equation involves the
square of both velocities, V1 has little impact in most cases. erefore, for routine clinical
applications, a pressure gradient is estimated only by measuring the downstream velocity V2.
P1 − P2 = 1/2V2
368 oracic ultrasound
Moreover, if the pressure gradient ∆P is converted from Pascal units to mmHg, the practical
and well known equation is obtained
∆P = 4V2
where V is the Doppler derived velocity in m/sec and ∆P represents the peak instantaneous
or maximal pressure gradient in mm Hg.
Bernoulli’s equation measures pressure difference (or gradient) between chambers and not
the absolute pressure within them. Calculation of the absolute pressure within a particular
chamber from the pressure gradient, obtained through Bernoulli’s equation, requires knowledge of a reference pressure and other assumptions.
A widespread use of Bernoulli’s equation is for the estimation of right ventricular and pulmonary artery systolic pressures. In this setting, the peak tricuspid regurgitant jet velocity,
obtained on continuous wave Doppler, is used to calculate peak pressure gradient between
the RV and RA during systole. Right ventricular systolic pressure (RVSP) is then calculated by
adding estimated right atrial pressure, calculated by the inferior cava volume and collapsibility,
to the measured gradient. Pulmonary artery systolic pressure (PASP) can be deduced from
this, because it would be equal to RVSP in the absence of pulmonary stenosis. In a similar
way pressure gradients can be calculated through aortic and mitral valves, and left atrial and
ventricular pressures consequently assessed.
A list of clinical applications of Bernoulli’s equation is provided in Table 5.
Table 5 – Clinical applications of Bernoulli’s equation
Clinical applications Utility
Peak velocity across a valve Valvular stenosis maximal gradient (mm/Hg)
Left ventricular outflow tract contour and
peak velocity
Mitral regurgitant velocity Left atrial pressure
Tricuspid regurgitant jet velocity Right ventricle systolic pressure, Pulmonary artery
Dynamic outflow tract obstruction, hypertrophic
obstructive cardiomyopathy
systolic pressure (in absence of pulmonary stenosis),
Pulmonary artery diastolic pressure
➣ Clinical implications
e most common use of the Bernoulli’s equation is to evaluate the severity of a valvular
stenosis and to assess transvalvular pressure gradients. For simplicity, we will discuss only the
mitral and aortic valves stenosis.
Aortic stenosis (AS) is the most frequent valvular heart disease. In a patient with chest pain,
syncope, pulmonary edema, arrhythmia, and unexplained hypotension or shock, a rapid
diagnosis of AS is crucial.
e development of AS-related symptoms marks a critical point of disease progression in
subjects with aortic stenosis for which there is no specific medical therapy.
Mitral stenosis is relatively less frequent and shows a relatively good prognosis, and surgery is
indicated only when symptoms appear, but this observation is being reconsidered based on
the risk of systemic embolization and the recurrences of pulmonary edema.
Echodynamics 369
On the other hand, valvular regurgitation14, which may be diagnosed only by visual and color
Doppler inspection (Fig. 6) (Tab. 6), is important in emergency and critical care medicine
if related to acute valvular or subvalvular disruption, infective endocarditis or to acute aortic
syndrome (in the case of acute aortic regurgitation).
Figure 6 – A: mitral regurgitation. B: tricuspid regurgitation. C: severe mitral regurgitation. D: aortic
regurgitation.
Table 6 – Inspective and color flow parameters for valvular regurgitation severity
Valve Modality Parameter Criteria for severe Comment
Aortic Color Doppler Jet area >60% LVOT area Instrument
Color Doppler Jet height >60% LVOT height
2D echocardiography LVED dimension > 7 cm Non specific,
2D echocardiography LVES dimension > 4.5 cm
Mitral 2D echocardiography LV size From large to very
2D echocardiography LA size
Color Doppler Jet area > 50% LA < 15% LA: mild
Abbreviations: LVOT: Left ventricular outflow tract; LVED: Left ventricular end diastolic; LVES: Left
ventricular end systolic; LV: Left ventricle; LA: Left atrium
large
dependent, eccentric
jet, temporal
variations
affected by multiple
factors
Normal size in mild
and grade II severity
15-30% LA: grade II
35-50% LA: grade III
➣ Valvular aortic stenosis
Normally, the aortic annulus is large between 1.4 and 2.6 cm. Aortic cusps show a systolic
excursion of 90°, arranging themselves parallel to the aortic wall. e normal, non-stenotic
aortic valve has an opening area of 3-4 cm2, which is equivalent to the area of the left ventricular outflow tract (LVOT) or aortic annulus.
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