Download Ultrasonographic examination of the venae cavae

François Jardin
Antoine Vieillard-Baron
Ultrasonographic examination
of the venae cavae
There are two venae cavae in humans. The superior vena
cava (SVC) comprises the connection of the left and
right brachiocephalic veins and ends on the top of the
right atrium, after entering the pericardium. The inferior
vena cava (IVC) comprises the connection of the left and
right iliac veins and ends on the floor of right atrium,
after crossing the diaphragm. Whereas the SVC is an
intrathoracic vessel, the IVC is an intraabdominal one, its
short intrathoracic part being purely virtual. Both venae
cavae provide venous return to the right heart, approx.
25% via the SVC and 75% via IVC [1, 2].
Ultrasonographic examination of the SVC can be
performed by a transesophageal approach [3]. To remain
open this collapsible vessel requires a distending pressure
greater than the critical pressure producing collapse, i.e. its
closing pressure. Because lung inflation increases pleural
pressure more than right atrial pressure, the distending
pressure of the SVC, i.e. right atrial pressure minus pleural
pressure, is reduced by lung inflation, and may become
insufficient to maintain the vessel open in a hypovolemic
patient (Fig. 1). This collapsible vessel can be compared
to a “Starling resistor.” The influence of SVC zone conditions on respiratory changes in SVC diameter is illustrated
with clinical examples in Fig. 2.
We have thus proposed to use the SVC collapsibility
index, calculated as maximal expiratory diameter minus
minimal inspiratory diameter, divided by maximal expiratory diameter, as an index of fluid responsiveness in mechanically ventilated patients exhibiting circulatory failure [4]. This requires recording of a long-axis view of the
vessel using a multiplane transesophageal probe, by coupling motion mode with two-dimensional mode. Our measurements in a group of 66 patients with septic shock as
reported in a previous issue, demonstrated that a SVC collapsibility index higher than 36% predicts a positive response to volume expansion, marked by a significant increase in Doppler cardiac output, with 90% sensitivity and
100% specificity [4]. We also found a bimodal distribution for the SVC collapsibility index: most patients exhibited either a partial or complete collapse of the vessel or
the absence of significant change in its diameter during inflation. This confirms our hypothesis that the SVC can be
compared to a “Starling resistor” which obeys the all-ornothing law.
Ultrasonographic examination of the IVC can be performed by a transthoracic, subcostal approach [5, 6]. Mea-
Fig. 1 Simultaneous recordings of tracheal pressure (T ), pulmonary
capillary wedge pressure (PCWP), right atrial pressure (RA), and
esophageal pressure (E, as a surrogate for pleural pressure). During
lung inflation (inspiration) pleural pressure increases more than right
atrial (or central venous) pressure, leading to an inspiratory decrease
in venous distending pressure (arrows)
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Fig. 2 Left Schematic representation of
the superior vena cava (SVC) as a Starling
resistor, with an inflow pressure (the upper
body mean systemic pressure, MSP),
an outflow pressure (the central venous
pressure, itCVP), and an external pressure
(the pleural pressure, Ppl). Right panel
Cli nical examples illustrating the three
zone conditions. Top panel (condition 1)
Inflow pressure becomes lower than the
pleural pressure during lung inflation,
which produces a complete collapse of the
whole vessel. This setting is illustrated by
ultrasonographic examination of the venae
cavae in a hypovolemic patient exhibiting
low MSP. Middle panel (condition 2) the
outflow pressure is reduced, and lung
inflation produces a localized collapse at
entry into the right atrium. This setting
is illustrated (right) by ultrasonographic
examination after clamping of the inferior
vena cava during a surgical procedure,
a maneuver which suddenly decreases CVP
but does not change MSP. Bottom panel
(condition 3) Outflow pressure is much
greater than the external pressure, and
the SVC remains fully open during lung
inflation. This setting is illustrated (right)
by ultrasonographic examination of the
venae cavae after volume expansion
surement of IVC diameter in different positions has proven
useful in separating normal subjects from patients with elevated right atrial pressure [7]. In their famous study of
venous return Guyton et al. [8] observed in dogs that negative right atrial pressure from 0 down to –4 mm Hg increases venous return, but then beyond –4mm Hg, further
increase in the negative pressure causes no more increase
in the venous return. Guyton et al. explained this failure by
the collapse of the IVC when entering the thoracic cavity,
illustrating the inability of a collapsible vessel to transmit
a negative pressure. To our knowledge, the first demonstration of the reality of this phenomenon in humans was
provided by our group in asthmatic patients [9] (Fig. 3).
Fig. 4 M mode echocardiography of the inferior vena cava (IVC)
in a spontaneously breathing healthy volunteer (above) and in a mechanically ventilated patient (below). Cyclic changes in IVC diameters are opposite, the largest value being observed during expiration
Fig. 3 An example of M mode echocardiography of the inferior vena in spontaneous breathing, and during inspiration in positive pressure
cava (IVC) in spontaneously breathing asthmatic patients. Note the breathing
short duration of inspiration, accompanied by a collapse of the vessel, and the increased duration of the expiration (compare Fig. 4,
above)
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2
30
IVC Diam mm
25
20
1
15
r = .79
p = .0000
10
5
0
0
5
10
15
20
25
30
CVP mmHg
Fig. 5 Simultaneous measurement of central venous pressure
(CVP) and inferior vena cava diameter (IVC diam) recorded at
end-expiration in 108 mechanically ventilated patients. The pressure/diameter relationship for the vessel is characterized by an initial
ascending part (arrow 1), where the index of compliance (slope of
diameter/pressure curve) does not change, and a final horizontal part
(arrow 2), where the index of compliance progressively decreases,
reflecting distension
In a healthy subject breathing spontaneously, cyclic
changes in pleural pressure, which are transmitted to the
right atrial pressure, produce cyclic changes in venous
return, with an inspiratory acceleration, inducing an
inspiratory decrease in IVC diameter of approx. 50%
(Fig. 4, above) [5]. This cyclic change in vena cava
diameter is abolished, however, when the vessel is dilated
because, although some inspiratory increase in venous
return persists, the vessel actually stays on the horizontal
part of its pressure-diameter relationship (Fig. 5). This
is the case when cardiac tamponade [10] or severe right
ventricular failure is present [6].
In a mechanically ventilated patient, the inspiratory
phase produces an increase in pleural pressure, which is
transmitted to the right atrial pressure, thus reducing the
venous return. As a result respiratory changes in IVC diameter are reversed, compared with those observed during
spontaneous breathing, with an inspiratory increase, and
an expiratory decrease (Fig. 4, below). However, regarding
Fig. 6a,b Ultrasonographic examination
of the superior (a) and inferior (b) venae cavae in the same mechanically
ventilated patient, who exhibited hypotension. Transesophageal echocardiography
demonstrated a partial collapse of the SVC
at each inflation, whereas echocardiography by a subcostal approach demonstrated
a marked increase in IVC diameter.
After blood volume expansion cardiac
index significantly increased, hypotension
was corrected, and variations in vena
cava diameter disappeared. TP: tracheal
pressure
spontaneous breathing these changes are abolished by
vena cava dilatation produced by a high volume status,
and/or a high right atrial pressure, the inferior vena cava
staying on the horizontal part of its pressure-diameter
relationship (Fig. 5). Cyclic respiratory changes in IVC
diameter can thus be observed only with a normal or low
volume status in a mechanically ventilated patient. In
the past, these changes were poorly correlated with atrial
pressure during mechanical ventilation [11]. Lack of IVC
diameter variation in a mechanically ventilated patient
exhibiting circulatory failure rules out the patient’s ability
to respond fluid in more than 90% of cases [12].
Feissel et al. [12] first proposed the use of cyclic
respiratory changes in IVC diameter to detect fluid
responsiveness in a mechanically ventilated patient, and
their original findings are reported in a recent issue.
Expressing respiratory variability in IVC diameter as
maximal inspiratory diameter minus minimal expiratory
diameter, divided by the average value of the two diameters, they found that a 12% increase in inferior vena cava
diameter during lung inflation allowed discrimination between responders and non-responders to volume loading,
with a positive predictive value of 93% and a negative
predictive value of 92% [12]. The great merit of this work
is to propose a noninvasive parameter to evaluate volume
loading. Moreover, this echocardiographic measurement
is very easy at the bedside, and requires only minimal
experience in echocardiography (Fig. 6). The findings of
Feissel et al. are confirmed in an identical study by Barbier
et al. [13], which appears in the same issue. It remains to
be seen whether this index is still reliable in patients with
a significant increase in intra-abdominal pressure, which
could limit IVC diameter variations.
Another phenomenon occasionally observed in the
IVC during mechanical ventilation is backward flow,
which is not caused by tricuspid regurgitation but by
cyclic compression of the right atrium by lung inflation.
Such a sudden compression boosts blood backward from
the right atrium to the IVC and does not concern tricuspid
valve competency [14]. This backward flow might explain
in part the inaccuracy of the thermodilution method in
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measuring cardiac output in mechanically ventilated
patients [14].
In conclusion, ultrasonographic examination of the venae cavae provides new and accurate indices of fluid re-
sponsiveness in mechanically ventilated patients exhibiting circulatory failure. In our opinion, a complete evaluation of volume status in these patients should include both
IVC and SVC examination.
References
1. Mellander S, Johanson B (1968)
Control of resistance, exchange and
capacitance functions in the peripheral
circulation. Pharmacol Rev 20:117–196
2. Rushmer R (1970) Peripheral vascular
control. In Rushmer R (ed) Cardiovascular dynamics. WB Saunders,
Philadelphia, pp 113–147
3. Vieillard-Baron A, Augarde R, Prin S,
Page B, Beauchet A, Jardin F (2001)
Influence of superior vena caval zone
conditions on cyclic changes in right
ventricular outflow during respiratory
support. Anesthesiology 95:1083–1088
4. Vieillard-Baron A, Chergui K, Rabiller
A, Peyrouset O, Page B, Beauchet A,
Jardin F (2004) Superior vena caval
collapsibility as a gauge of volume
status in ventilated septic patients.
Intensive Care Med 30:1734–1739
5. Mintz G, Kotler M, Parry W, Iskandrian
A, Kane S (1981) Real-time inferior
vena caval ultrasonography: normal and
abnormal findings and its use in assessing right heart function. Circulation
64:1018–1025
6. Moreno F, Hagan A, Holmen J, Pryor
A, Strickland R, Castle H (1984)
Evaluation of size and dynamics of
the inferior vena cava as an index of
right-sided cardiac function. Am J
Cardiol 52:579–585
7. Nakao S, Come P, McKay R, Ransil B
(1987) Effects of positional changes on
inferior vena caval size and dynamics
and correlations with right-sided cardiac
pressures. Am J Cardiol 59:125–132
8. Guyton A, Lindsey A, Abernathy A,
Richardson T (1957) Venous return
at various right atrial pressures and
the normal venous return curve. Am J
Physiol 189:609–615
9. Jardin F, Farcot JC, Boisante L, Prost JF,
Guéret P, Bourdarias JP (1982) Mechanism of paradoxal pulse in bronchial
asthma. Circulation 66:887–894
10. Himelman R, Kircher B, Rockey D,
Schiller N (1988) Inferior vena cava
plethora with blunted respiratory response: a sensitive echocardiographic
sign of cardiac tamponade. J Am Coll
Cardiol 12:1470–1477
11. Jue J, Chung W, Schiller N (1992) Does
inferior vena cava size predict right
atrial pressure in patients receiving
mechanical ventilation. J Am Soc
Echocardiogr 5:613–619
12. Feissel M, Michard F, Faller JP, Teboul
JL (2004) The respiratory variation in
inferior vena cava diameter as a guide
to fluid therapy. Intensive Care Med
30:1834–1837
13. Barbier C, Loubières Y, Schmit
C, Hayon J, Ricôme JL, Jardin F,
Vieillard-Baron A (2004) Respiratory
changes in inferior vena cava diameter
are helpful in predicting fluid responsiveness in ventilated septic patients.
Intensive Care Med 30:1740–1746
14. Jullien T, Valtier B, Hongnat JM,
Dubourg O, Bourdarias JP, Jardin F
(1995) Incidence of tricuspid regurgitation and vena caval backward flow
in mechanically ventilated patients.
A color Doppler and contrast echocardiographic study. Chest 107:488–493