Evaluation and Management of Shock

Olivier Axler, M.D., Ph.D., F.C.C.P.1

ABSTRACT

Shock is one of the most frequent situations encountered in the intensive care unit
(ICU). Important new concepts have emerged for shock management in recent years. The
concept of early goal-directed therapy has evolved from the basic management concepts for
septic shock delivered in a structured fashion. Numerous cardiovascular techniques,
methods, and strategies have been developed as novel alternatives to the use of the
pulmonary artery catheter. Among these techniques, echocardiography, esophageal Dop-
pler, and arterial pulse contour analysis show great promise. Prediction of responsiveness to
fluid administration is a key component of the management of shock, as is assessing
cardiovascular performance. The intensivist has several options to evaluate and treat shock.
Further research should yield additional important advances.

KEYWORDS: Shock, cardiovascular protocols, cardiovascular techniques; central

venous pressure; pulmonary arterial catheter

S hock is a common cause of admission in any OVERVIEW, DEFINITIONS, AND

intensive care unit (ICU) and also occurs frequently
during the course of critical illness. Shock is associated
with significant morbidity and mortality and represents a
medical emergency. Early, targeted therapy is crucial; the
first hour of care may be key to a successful outcome.1,2
Therefore, it is important that physicians are aware of
updated concepts and management guidelines for treat-
ing patients with shock. Although the principles of
shock management are well established, there is consid-
erable heterogeneity of bedside management.
This heterogeneity is apparent not only with
accurate clinical identification of a shock state3 but also
in regard to evaluation and therapy. Critical care soci-
eties and other experts have published evidence-based
guidelines for diagnostic criteria and therapeutic strat-
egies4–8; however, these recommendations generally fo-
cus on severe sepsis and septic shock. This article reviews
the traditional criteria and current guidelines for man-
agement of shock, the traditional and newer diagnostic
and monitoring techniques, and therapeutic strategies.
DIAGNOSIS OF SHOCK
Shock is traditionally defined by multisystem organ
hypoperfusion, whatever its specific cause, leading to
common physical signs. It can also be defined as an
inability to assure adequate cellular and tissue oxygen
supply and removal of waste products of cellular metab-
olism, thus overwhelming the compensatory mecha-
nisms of the organism.
The presentation of shock may be obvious but can
also be latent and incomplete, leading to a delayed
diagnosis, potentially worsening the prognosis and de-
creasing chances of reversal. The clinician must be
familiar with different clinical patterns of shock and
the pathophysiological aspects of shock, including car-
diovascular (ventricular pressure–volume curves, cardiac
function curves), biochemical (oxygenation cascades),
and immunological (mediators and cytokine cascades)
features.
The clinical signs and symptoms of shock have
been known for years9 and have been presented in

1
Cardiology Department, Centre Hospitalier Territorial Gaston
Bourret, Noumea, New Caledonia, France.
Address for correspondence and reprint requests: Olivier Axler,
M.D., Ph.D., F.C.C.P., Cardiology Department, CHT Gaston
Bourret, 98800 Noumea, New Caledonia, France. E-mail: olivier.
axler@canl.nc.
230
Non-pulmonary Critical Care: Managing Multisystem Critical Illness;
Guest Editor, Curtis N. Sessler, M.D.
Semin Respir Crit Care Med 2006;27:230–240. Copyright # 2006
by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York,
NY 10001, USA. Tel: +1(212) 584-4662.
DOI 10.1055/s-2006-945526. ISSN 1069-3424.

comprehensive reviews.1,10 Several points are worthy of
emphasis. First, the diagnosis must be made quickly,
followed by classification of type of shock. Second, the
sensitivity and specificity of each sign are highly variable.
Third, the quantitative aspects of these signs are useful
but vary depending upon the clinical circumstances. The
first step is to begin the correct resuscitation measures,
not only to achieve therapeutic goals but also to confirm
the diagnosis. Depending on the response to the ther-
apeutic intervention, the diagnosis can be confirmed or
corrected, allowing adjustment of treatment.
In its complete clinical presentation, shock clas-
sically includes: tachypnea; tachycardia; low systolic,
diastolic, and mean blood pressures (BPs); diaphoresis;
poorly perfused skin and extremities; cyanosis; mottling
of cool and moist extremities; altered mental status
(ranging from decreased state of consciousness to agi-
tation); and decreased urine output. Joly and Weil
emphasized the role of the ‘‘cold great toe,’’11 whereas
we have noted that cold knees have an excellent diag-
nostic specificity and sensitivity for shock (unpublished
data).
However, these signs are not always present con-
comitantly, and some of these features may be absent or
borderline. For instance, in classical shock, BP is de-
creased, and a commonly accepted threshold for a
resuscitation goal in septic shock is 65 mm Hg for
mean arterial pressure (MAP).6 However, not all hypo-
tensive states are associated with shock, and not all
shocks present with hypotension. In fact, some shock
states present with high BP at the onset because of the
adaptive adrenergic response. Early septic shock is clas-
sically ‘‘hyperdynamic,’’ with increased pulse pressure
and warm extremities. In addition, low BP is relative
to the baseline BP for a given patient. Invasively meas-
ured BP using an intra-arterial catheter is more accurate
than cuff measurements.12 Chronotropic medications, or
sinus or atrioventricular dysfunction, can blunt the
tachycardic response. Oliguria is often defined as urine
output less than 0.5 mL/kg/hr.6 From a laboratory
standpoint, blood lactate is a robust clue of shock arising
from cellular and tissue hypoxia,3 and precedes acidemia.
This was recently confirmed,2 with a threshold of
4 mmol/L consistent with shock. However, the specific-
ity of blood lactate is imperfect because any condition
exceeding the aerobic threshold leads to increased lactate
levels, and some metabolic conditions increase lactate
levels without shock (i.e., any sympathetic activation).13
Tissue hypercapnia is known to correlate well
with decreased blood flow.14 The first organ to be
studied was the gastric mucosa, but this technique has
largely been abandoned. Sublingual PCO2 has emerged
as a good predictor of shock (irrespective of cause), and
in some studies was superior to blood lactate levels and
mixed venous oxygen saturation (SVO2) or central
venous oxygen saturation (SCVO2).15,16
EVALUATION AND MANAGEMENT OF SHOCK/AXLER 231
TRADITIONAL AND NEWER METHODS
AND TECHNIQUES TO ASSESS
MECHANISMS OF SHOCK
Several simple tools used in the initial management of
shock (e.g., electrocardiogram; chest radiographs; routine
hospital chemistries; blood gases) are well known and will
not be further discussed here. In this section, invasive and
noninvasive techniques to assess hemodynamics are dis-
cussed. Measurement of central venous pressure (CVP)
or pulmonary artery pressure (PAP) may be useful to
classify the mechanism of shock. Further, measurement
of SCVO2 [via a catheter in the superior vena cava
(SVC)] or mixed SVO2 (via a pulmonary arterial cathe-
ter) may be useful to diagnose and monitor the impact of
therapeutic interventions in patients with shock.17
Arterial pulse contour techniques are used to
measure cardiac output (CO), and requires arterial
access.18,19 This technique is incorporated in more
sophisticated devices, measuring other parameters as
preload with an estimation of fluid responsiveness for
the LiDCO plus System (LiDCO Ltd., Cambridge,
UK) via a pulse power analysis.18–20 Another system,
PiCCO (Pulsion Medical Systems AG, Munich,
Germany) also measures intrathoracic volumes and
extravascular lung water from transpulmonary indica-
tor dilution.21,22 This latter technique mandates fem-
oral arterial and central venous access, whereas the
former requires only a radial artery and a peripheral
vein. Analysis of the systemic systolic pressure, pulse
pressure and stroke volume (SV), and their respiratory
variations, provides an excellent assessment of preload
and estimation of fluid responsiveness.19
Ultrasound techniques that are useful to assess
fluid status and cardiac function include esophageal
Doppler23 and echocardiography (transthoracic and
transesophageal).24 Methods such as monitoring splanch-
nic blood flow or monitoring the microcirculation with
videomicroscopy have been utilized in research investiga-
tions but have no or limited clinical utility.
Traditional Methods
CENTRAL VENOUS PRESSURE MONITORING
Although CVP was recently shown to be somewhat
inaccurate to assess preload,25,26 CVP, when integrated
into an algorithm, was a useful parameter to guide volume
administration in a cohort of septic patients.2 However,
CVP measurements should be interpreted with caution,
even at low or high values, when the value is used in
isolation.10,25–28 Some authors emphasize the need to
incorporate the cardiac and venous return curves for a
correct interpretation of CVP.29,30 Indeed, the basic con-
cept espoused is to use CVP with simultaneous measure-
ment of cardiac output. In a study of 33 ICU patients, the
right atrial pressure (RAP) decreased at least 1 mm Hg
232 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3
with inspiration [with a decreased pulmonary artery oc-
clusion pressure (PAOP) of at least 2 mm Hg with
inspiration] and increases in CO of ! 250 mL/min.30
This analysis can differentiate ‘‘relative hypovolemia’’ (or
more accurately a fluid responsive state) from euvolemia.
This concept was discussed in a recent excellent review.31
Despite the low reliability of CVP to assess preload, this
parameter continued to be widely measured by 93% of a
cohort of European intensivists in 1998.32
CENTRAL VENOUS OXYGEN SATURATION (SCVO2)
The O2 saturation in a central vein (most often the SVC)
was recently shown to be a key component of early goal-
directed therapy in the emergency department (ED)2;
values < 70% are consistent with incomplete resuscita-
tion. This parameter is less useful after several days of
severe critical illness and severe tissue oxygenation defi-
cit.17,33,34 A low SVO2 generally reflects low CO because
oxygen extraction by the tissues is greater in cardiac
failure.34,35 Low SCVO2 is also associated with a poor
prognosis34 and often appears earlier than any other
clinical sign of shock.2 In a cohort of patients with septic
shock, Rivers and colleagues demonstrated mortality
reduction of 15% by maintaining a therapeutic algorithm
that maintained the following parameters: SCVO2
> 70%; CVP > 8 to 12 mm Hg; MAP > 65 mm Hg;
urine output > 0.5 mL/kg/h.2 SCVO2 and SVO2 are
usually similar but can diverge in some cases, particularly
in severe sepsis, due to greater O2 extraction in the
hepatosplanchnic circulation. However, SCVO2 is pre-
ferred to SVO2 because it can be measured more simply
from a central venous catheter rather than a pulmonary
artery catheter (PAC).36–38 SCVO2 can be continuously
monitored using a special catheter or intermittently by
direct repeated samples. SCVO2 correlates with outcome
in all kinds of shock, even during cardiopulmonary
resuscitation.17,33,34 The research by Rivers and col-
leagues addressed very early shock,2 and studies have
not demonstrated benefit for patients later in the course
of shock when oxygen extraction may be impaired and
SCVO2 exceeds 80%.17,33,34
PULMONARY ARTERY CATHETERS
The PAC has been used to differentiate various mecha-
nisms of shock since the early 1970s, but utilization of data
from PACs has many pitfalls. First, hemodynamic values
are frequently misinterpreted, leading to incorrect treat-
ment.37,38 Second, recent studies found that the use of
PAC did not confer any benefit compared with no PAC
use36,39,39a,39b; further, some studies suggested deleterious
effects of PACs, particularly in patients presenting
with acute respiratory distress syndrome (ARDS) or
shock.35,36,39 However, PAC-directed therapy was shown
to be cost effective in the preoperative period.40–43 In
North America, there continues to be relatively wide-
spread use of PACs,6 whereas newer techniques such as
2006
ICU echocardiography24,44 and pulse contour analysis
techniques (PiCCO and LiDCO)18,19,21,22 have sup-
planted PACs in most European ICUs. Despite the
limitations of PACs, recent guidelines (e.g., the Survival
Sepsis Campaign) continue to recommend PACs for
the assessment of severe sepsis and septic shock.6 More-
over, a recent paper focusing on ‘‘practice parameters
for hemodynamic support of sepsis in adult patients’’
favors the use of PACs, and states that ‘‘echocardiography
may also be useful to assess ventricular volumes and
cardiac performance.’’7
Several measured and derived values are available
from a PAC to determine the mechanism of shock:
PAP, PAOP, right ventricular pressure (RVP) and
RAP, CO by thermodilution, and its modified deriva-
tives: (1) semicontinuous cardiac output (using a thermal
coil in the right ventricular portion of the PAC;
(2) calculation of right ventricular end-diastolic volume
(RVEDV) from measurement of right ventricular ejec-
tion fraction (RVEF); SVO2 and related oygenation
variables; oxygen consumption (VO2); oxygen delivery
(DO2); and O2 extraction ratio (O2ER).
Measurement of PAP is a very important param-
eter to diagnose pulmonary arterial hypertension (PAH)
as may be seen in ARDS, pulmonary embolism, right
ventricular infarction, obstructive lung disease, left heart
diseases, and primary PAH. Its measurement is generally
easy and its interpretation is the least problematic of all
PAC-derived data.
Using the PAOP is one of the most controversial
issues related to PAC. Classically, hypovolemic shock has
low right and left heart filling pressures, whereas left
ventricular cardiogenic shock is associated with elevated
PAOP and RAP. Historically, PAOP has been consid-
ered to provide information regarding preload and the
presence or absence of pulmonary edema. However,
measurement and interpretation of PAOP may be diffi-
cult.37,38,45 The utility of PAOP to assess volume status
has recently been challenged 25,26,46; this is also true for
RAP.25,26,46 This can be explained by a frequent absence
of linearity between left ventricular end-diastolic volume
(LVEDV) and left ventricular end-diastolic pressure
(LVEDP); second, disparity between LVEDP and
PAOP may exist. The LVEDV/LVEDP relationship
can be profoundly modified by LV compliance factors
such as left ventricular hypertrophy (LVH), myocardial
ischemia, positive end-expiratory pressure (PEEP), and
active exhalation. Further, PAOP can overestimate
LVEDP if mitral stenosis or mitral regurgitation are
present, and conversely underestimates LVEDP when
diastolic dysfunction or hypervolemia exist. These con-
ditions are frequent in patients presenting with shock but
are often not appreciated. Thus PAOP should be inter-
preted cautiously.45 Notwithstanding these pitfalls, 58%
of European intensivists continued to measure PAOP as
part of monitoring critically ill ICU patients in 1998.32

Measurement of CO is one of the most important
issues in the management of shock.1,47–49 Thermodilu-
tion is the gold standard method for measuring CO for
clinical use because measurement is relatively straight-
forward and does not present the same technical diffi-
culties as PAOP. Additionally, the thermodilution
technique was validated against electromagnetic flow,
Fick, and dye dilutions techniques. However, thermo-
dilution has important limitations. Specifically, thermo-
dilution can overestimate CO in low output states,
whereas significant tricuspid regurgitation leads to
underestimation of CO. Other confounding issues in-
clude intracardiac shunts and temperature issues.47 In
this context, echocardiography is helpful. Recently, the
left ventricular outflow tract (LVOT) pulsed Doppler
method has been employed as an alternative method to
measure CO.49,50 Some authors believe that this should
become the new gold standard49,50 unless significant
aortic valve disease exists.
Cardiac output can be monitored with a modified
PAC. This PAC incorporates a thermal coil in the right
ventricular portion of the catheter, and continuous CO
measurement is based on the delivery of electrically
generated heat to the blood near the right atrium and
ventricle and the resulting temperature change in the
PA. This technique avoids performing an intermittent
injection and yields a continuous CO display. The
accuracy is good compared with thermodilution, pro-
vided regular calibration is performed.51
Recent refinements of the PAC allow calculation
of RVEF. This catheter has a rapid-response thermo
‘‘slur’’ and intracardiac electrocardiogram electrode, al-
lowing the calculation of RVEF. Combined with SV,
the RVEF allows the calculation of right ventricular end
diastolic volume (RVEDV). This parameter has been
extensively studied in circulatory shock,52,53 but in the
most important studies comparing RVEDV before and
after a fluid challenge, significant difference was found in
only one of 15 studies.53 Intraindividual changes in
RDEDV with various treatments are more useful than
absolute values.25,52,54 Continuous fiberoptic measure-
ment of SVO2, coupled with traditional PAC parame-
ters, is available with some catheters.
Finally, the relationship of oxygen delivery/con-
sumption ratio (DO2/VO2) has been used for both
research and clinical indications among critically ill
patients for more than 3 decades.55 However, awareness
and incorporation of these variables into clinical proto-
cols have not been shown to influence outcome.55
Newer Methods
ECHOCARDIOGRAPHY-DOPPLER
Cardiac ultrasound (echocardiography) has increasingly
been utilized in ICUs within the past few years. Trans-
EVALUATION AND MANAGEMENT OF SHOCK/AXLER 233
thoracic echocardiography (TTE) is noninvasive and
relatively easy to perform after an adequate training.
Transesophageal echocardiography (TEE) is modestly
invasive and requires some degree of sedation for patient
comfort but is safe and highly accurate. Echocardiog-
raphy provides an excellent assessment of cardiac func-
tion and estimates left and right heart filling pressures
and can be useful to determine the cause of shock.56
Echocardiography provides acceptable estimates of most
parameters gleaned from pulmonary artery catheters
(PACs) (i.e., CO; right arterial pressure (RAP) from
inferior vena cava (IVC) size and ventilatory variations,
systolic pulmonary artery pressure (SPAP); left and right
ventricular filling pressures; ejection fraction; ventricular
interdependence; right heart function; diastolic dysfunc-
tion; left ventricular hypertrophy (LVH); ischemic heart
disease, valvular diseases, and so on). Recent publications
emphasized the value of echocardiography to predict
fluid responsiveness using heart–lung interactions ba-
sics.57–65 Many studies have shown that echocardiogra-
phy (either TTE or TEE) may be invaluable to monitor
therapeutic interventions or hemodynamic changes in
critically ill patients.62–80 TEE is more useful than TTE
for this purpose.66–79 In most of the studies, TEE
provided clinically useful information in 60 to 90% of
cases. More importantly, TEE had a direct favorable
impact on the acute care management.79
Our recent experience with TTE has been favor-
able (unpublished data). The value of TTE was recently
underscored in a study by Joseph et al, who noted
clinically useful and reliable information in 70 to 80%
of critically ill ICU patients who had TTE.80 Recent
improvement in imaging, software, and electronic sys-
tems have improved the quality and utility of images
gleaned from TTE. Transthoracic echocardiography is
useful as a diagnostic tool for critically ill patients in
shock (or impending shock) but in some cases, TEE is
necessary for a more accurate assessment.79 Specific
indications for TEE include: aortic dissection (when
computed tomographic angiography is inconclusive, or
to complete it if necessary); endocarditis (especially when
a valvular prosthesis is present); complicated cardiac
surgery; marked obesity; poor echogenicity with TTE;
intracavitary thrombi; and cardiac sources of emboli.
TEE is the preferred method to assess the SVC size
and its ventilatory variations, a new powerful parameter
to predict fluid volume responsiveness.64
In a patient with shock, echocardiography (usu-
ally TTE) can provide prompt (within 15 minutes)
assessment of critical variables, including size of cardiac
chambers; left and right systolic function; cardiac output
(49); wall motion abnormalities; valvular pathology; LV
filling pressures from a combination of parameters ob-
tained from mitral flow, Doppler tissue imaging (DTI),
pulmonary venous flow (PVF), early diastolic mitral flow
propagation velocity (Vp), PA pressures; RV filling
234 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3
pressures; and pericardial imaging. Echocardiography
can estimate fluid volume responsiveness using heart–
lung interactions. This concept assumes that the meas-
urement of some parameters before fluid loading can
predict a significant increase of cardiac ouput in hemo-
dynamically unstable patients.54 This estimation uses
inferior vena cava (IVC)62,63 or SVC,64 size and ven-
tilatory variations, as well as the respiratory variations of
the LVOT.57–59 These parameters correlated strongly in
these 5 studies with the concept of ‘‘fluid responsive-
ness.’’ The measurement of left heart filling pressures
requires more sophisticated echo devices. These two new
steps represent one of the major advances in the manage-
ment of shock.
Some echocardiographists prefer to use TTE first,
and then TEE if necessary, and some always use directly
TEE. This is an ongoing discussion, and this choice
depends upon the ability of each echocardiographist.
Published data regarding the assessment of pre-
load using echocardiography are disappointing. Preload
was initially assessed by measuring left ventricular end-
diastolic diameters, areas, or volumes; close correlations
were found with blood loss or expansion in normal
subjects81 or perioperative conditions.82 However, in
ICU settings, recent studies found that the left ventricle
end-diastolic area (LVEDA) failed to accurately predict
fluid requirement or fluid overload status, particularly
when compared with newer methods to assess fluid
responsiveness.57,83–85 Therefore, echocardiographic
measurements of LV and RV size are no longer used
to assess volume status. However, diameter of the IVC
and its ventilatory variations are invaluable to predict
fluid responsiveness. This measurement is simple to
assess, with a short learning curve (1 hour). The IVC
diameter and its ventilatory variations are measured with
TTE, on a subcostal view, in M mode. Measurement
parameters include IVC diameter (D) at end-expiration
(Dmin) and at end-inspiration (Dmax); distensibility
index of the IVC (dIVC) calculated as the ratio of
Dmax-Dmin:Dmin and expressed as a percentage, or
((Dmax-Dmin:Dmax þ Dmin):2 ).62,63,86 Measurement
of IVC size and respiratory variation is useful to predict
response to a fluid challenge.62,63,65 The useful threshold
was 12% of variability, with a positive and negative
predictive value of 93% and 92% in one study of septic
patients requiring mechanical ventilation (MV).62 An-
other group studied 23 patients in septic shock requiring
MV.63 The size and ventilatory variation of the IVC
(IVCVV) predicted a positive response to a fluid chal-
lenge [! 15% increase of the cardiac index (CI) follow-
ing a 7 mL/kg fluid challenge]. IVCVV was defined in
this study by Dmax-Dmin:Dmin. There was an excellent
correlation (r ¼ 0.9) between an 18% IVCVV at baseline
and ! 15% increase in CI after a fluid loading, with 90%
specificity and 90% sensitivity.63 Importantly, baseline
CVP did not accurately predict fluid responsiveness.
2006
Additionally, in a cohort of septic patients on MV,
measurement of the SVC by TEE, and ventilatory
collapsibility of the SVC predicted the cardiac response
to fluid challenge.64 The 36% threshold of variability
(Dmax-Dmin:Dmax) could define responders and non-
responders in CO, with 90% sensitivity and 87% specif-
icity.64 Although measurement of IVC diameter
ventilatory variations was studied only in septic patients
on MV, we use it in every patient in acute circulatory or
acute respiratory failure, even among patients not requir-
ing MV. However, outcomes data in these other patient
populations are lacking.
The second important new parameter in assessing
shock is the ventilatory variation of left ventricular out-
flow tract (LVOT) (called also aortic) Doppler veloc-
ities. Two studies found that this parameter was a strong
predictor of preload responsiveness: one in septic pa-
tients on MV (using TEE),57 and one with a rabbit
model.58 The first study defined the respiratory variation
as the ratio of the difference between maximal velocities
to the mean of these two velocities. A ventilatory
variation of LVOT blood flow velocity > 12% was
associated with a 15% increase of CI with a 91% positive
predictive value. A ventilatory variation < 12% had a
100% negative predictive value. This could imply that no
volume expansion was necessary with a high degree of
confidence. There was a high degree of correlation
between baseline ventilatory variation and degree of CI
increase after volume expansion.57 This important study
can be extended to TTE. We regularly use this method
in all patients in shock to assess potential fluid respon-
siveness. Patients must be on MV and well adapted to
their ventilator, and must be free of arrhythmias. Slama
et al found similar results in a rabbit model, using TTE,
with progressive blood withdrawal.58 In these two stud-
ies, this parameter was more powerful than all other
parameters (CVP, PAOP, left ventricular end-diastolic
area) that had been used for the past several years. The
most recent studies showed that ‘‘static’’ echocardio-
graphic parameters failed to consistently predict re-
sponse to fluid loading.57–59,83–85
The second important advance is the ability of
echocardiography to estimate LV and RV filling pres-
sures (LVFP and RVFP). These measurements were
extensively studied over the past 10 years in the cardio-
logical arena86–90 but were only recently applied to the
critically ill (noncardiac) patients in ICUs.91–93 These
measurements do not accurately measure preload, but
may predict fluid responsiveness. An algorithm is now
available to determine if LVFP are predictive of PAOP
as ‘‘high’’ (> 15 mm Hg) or ‘‘not high’’ ($ 15 mm Hg).
This analysis is usually applied when the LVEF is
decreased (< 45%). This algorithm is determined by
the analysis of the combination of pulsed Doppler of
mitral flow, tissue Doppler imaging, color M-mode of
mitral flow, pulmonary venous flow (PVF), left atrial

size, interatrial septum shape and movement, diastolic
PA pressure from pulmonary regurgitation. Mitral flow
pulsed Doppler shows an early wave (E wave) and a later
wave (A wave) if the rhythm is sinus. The peak velocities
are measured (Em and Am). A small E wave, with
an E:A ratio < 1, and an E deceleration time (DTE)
> 150 msec are usually associated with diastolic
LVFP < 15 mm Hg; when some discrepancies appear,
other parameters help to determine LVFP. These pa-
rameters are (1) the maximal early diastolic velocity (Ea)
of the mitral annulus at the lateral- or septal most basal
point, measured from DTI; (2) early flow (LV flow
propagation velocity) Vp using M-mode color Doppler;
(3) PVF, where the systolic fraction is measured: this
fraction is the ratio between the velocity time integral
(VTI) of the systolic component of PVF, to the sum of
the VTI of the diastolic and systolic waves (S:S þ D);
this ratio is nevertheless less and less used and replaced
by the difference between duration of pulmonary A wave
and mitral A wave (Apd–Amd) duration; if this ratio is
greater than 20 ms, this is in keeping with a high LVFP;
(4) left atrial (LA) diameter and area, an indirect
indicator of LVFP; (5) diastolic PAP (PAPd) obtained
from the end-diastolic velocity of the pulmonary regur-
gitant flow because this parameter approximates PAOP;
(6) interatrial septal motion and curvature; (7) mitral
regurgitant flow from continuous Doppler allows to
assess left ventricle diastolic pressure (LVDP) from the
difference between systolic blood pressure SBP and
pressure gradient from mitral regurgitation maximal
velocity; (8) aortic regurgitation flow from continuous
Doppler allows to assess LVFP (difference between
diastolic blood pressure (DBP) and diastolic left ven-
tricle-aorta ( LV–AO gradient). Systemic blood pres-
sures (BP) must be measured simultaneously. The
quantitative combination of mitral flow (Em, Am, E
wave deceleration time, DTEm), with DTI (Ea), early
flow Vp using M-mode color Doppler data, PVF, LA
size, and the other parameters just defined has led to an
algorithm to assess if LVFP are ‘‘high’’ (left atrial pressure
(LAP or PAOP > 15 mm Hg) or ‘‘not high’’ (normal or
low). These values can be estimated for ‘‘not high’’ LVFP:
Em:Ea < 1, DTE > 150 to 200 ms, Em:Vp < 1.5, Em/
Ea < 8, S/S þ D > 55%, LA size normal, Apd–Amd
< 20 ms (Amd ¼ duration of atrial mitral wave, Apd ¼
duration of atrial pulmonary wave), LVFP < 15 mmHg
from aortic and mitral regurgitation, atrial septum shifted
to the left.
LVFP can be estimated ‘‘high’’ (PAOP > 15 mm
Hg), if Em/Am > 2, DTE < 150 ms, Em/Vp > 2.5,
Em/Ea > 15, S/S þ D < 55%, LA size increased, Apd–
Amd > 20 ms, LVFP > 15 mmHg form aortic and
mitral regurgitation, atrial septum shifted to the right.
However, because areas of uncertainty exist, multiple
parameters must be examined. The order of importance
of measurements is as follows: LVEF, Em, Am, DTE,
EVALUATION AND MANAGEMENT OF SHOCK/AXLER 235
Ea, Em/E/a, Vp, Em/Vp, LA size. When LVEF is
normal (except in cases of LVH), LVFP is rarely high.
This algorithm has been used for several years in cardiac
patients89,90 but has only recently been tested among
critically ill noncardiac ICU patients.91–93
Right ventricular filling pressures can also be
assessed from systolic and mean PA pressures derived
from the tricuspid regurgitation jet and from the early
diastolic pulmonary regurgitant jet, respectively. IVC
size and its collapsibility index, as were discussed earlier,
are markers of RAP. Hepatic vein pulsed Doppler also
provides information on right heart filling pressures.
Despite these intriguing data, no study has exam-
ined the impact of echocardiography in critically ill
noncardiac ICU patients on mortality. Because echocar-
diography is commonly employed in many ICUs, a
randomized trial to assess the clinical impact of this
technique may be difficult to accomplish.61
ESOPHAGEAL DOPPLER MONITORING
Esophageal Doppler monitoring is an exciting method
to manage shock because it couples ultrasonography with
continuous monitoring capabilities.23 This is a simple
and quick technique, with a short period of training.
Analysis of the size and shapes of the waveform allows
therapeutic modifications regarding fluid therapy and
the use of inotropic, vasodilator, and vasopressor agents.
Outcome and hospital stay have improved with this
technique in high-risk surgical patients.23
VENOUS AND TISSUE PCO2
Venous and tissue PCO2 have been used for more than 3
decades to manage shock, but sublingual PCO2 has
emerged as the simplest and most reliable technique to
assess venous and tissue PCO2. In patients in the ED
and in the ICU, sublingual PCO2 indicates the presence
of shock but does not allow any classification of
shock.3,15,16
ARTERIAL PRESSURE VARIATION
Arterial pressure variation yields important information
for volume status in hemodynamically unstable patients
mechanically ventilated and perfectly sedated and may
predict fluid responsiveness in these patients. Measure-
ment of SV and pulse pressure respiratory variations
provides ancillary information.94–96 Values above 10 to
13% indicate with a high sensitivity and specificity that
a volume expansion will increase CO.94–96 Perel and
colleagues developed a respiratory systolic variation test
(RSVT) that uses three consecutive incremental pres-
sure-controlled (10, 20, and 30 cm H2O) breaths to test
the response of venous return, left ventricular stroke
volume (LVSV), and systolic arterial pressure. A slope is
then determined, and a prediction of an increased CO
can be tested with volume expansion.94,95 In interpreting
these tests, it is important to note that a positive fluid
236 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3
responsiveness test does not imply that there is an
indication for giving fluids, because a normal heart will
increase CO with any volume expansion. By contrast,
even in a real hypovolemic status, CO may not increase if
one or both ventricles is not on its ascending limb of the
Starling curve. Thus RSVT is not 100% sensitive and
specific. Performing and interpreting these tests require
a knowledge of heart–lung interactions.54,61
ARTERIAL PULSE CONTOUR ANALYSIS METHODS
Arterial pulse contour analysis permits continuous mon-
itoring of SV and CO.18,19,21,22 These methods calculate
the area under the systolic portion of the arterial pressure
waveform, which, divided by aortic impedance, allows
estimation of LVSV. Generally, the CO obtained by
these techniques is calibrated with an absolute CO value,
as an indicator dilution technique. Preload and fluid
responsiveness can be estimated, in continuously meas-
uring respiratory variations of systolic arterial pressure,
pulse pressure, pulse pressure variation (PPV), and
stroke volume (SV). Two systems are commercially
available using arterial pulse contour analysis: the
PiCCO system and the PulseCo or LiDCO system.
Although the basic principle to measure CO is the
same, the LiDCO system uses a very sophisticated algo-
rithm that appears very accurate. This algorithm is set up
on arterial pulse power analysis rather than morphology.94
This technology uses lithium (Li) as an indicator and has
been extensively tested in the United States and Europe
but is not available in some countries. We have used this
system extensively in our critically ill patients in New
Caledonia and have found it easy to use (unpublished
data). This technique generally uses a radial arterial
catheter and a peripheral or central venous catheter.
The PiCCO technology has been more
widely employed in ICUs, and enables measurement
of volumetric parameters and extravascular lung
water.18,19,21,22 The analysis of the wave form is simpler
than with with the LiDCO technology and is a calcu-
lation of the area under the systolic portion of the
arterial pressure waveform. Ideally, PiCCO requires a
femoral arterial catheter, but a peripheral vein may be
usable. This technology allows measurement of volu-
metric parameters such as the global end-diastolic
volume index (GEDVI) and the intrathoracic blood
volume index (ITBVI) by transcardiopulmonary ther-
modilution. These parameters are more accurate than
left and right cardiac filling pressures to estimate pre-
load in critically ill patients but do not reliably assess
fluid responsiveness.19,25
The noninvasive Modelflow-Finapress (Finapress
Medical Systems, Arnhem, The Netherlands) method
also uses similar arterial pulse contour analysis of finger
arterial pressure in critically ill patients.18 Expressed as
cardiac index (CI), the results are similar to studies using
more invasive methods.18
2006
THORACIC ELECTRICAL BIOIMPEDANCE
Thoracic electrical bioimpedance has been used by some
teams to assess CO continuously,3 but it has limited
application.
MANAGEMENT OF SHOCK
The classification of mechanisms of shock has been
elegantly analyzed elsewhere.1,3,10 The initial manage-
ment of shock requires an immediate clinical assessment,
basic vital signs, and clinical examination. Prompt as-
sessment and decision are imperative regarding fluid
resuscitation, MV, and use of inotropic, vasoconstrictor,
or vasodilator agents.1 Echocardiography can be per-
formed at the bedside and may be invaluable in planning
resuscitative efforts. A standardized ‘‘ABC’’ resuscitation
protocol [management that incorporates components of
airway (A), breathing (B), and circulation (C)] such as
advanced cardiac life support (ACLS) guidelines, can
improve outcomes in the first few minutes of severe
cardiorespiratory failure. Intubation and MV are corner-
stones of therapy in this setting.1
The circulation step has evolved recently because
such protocols have been shown to improve survival.1,2
Current guidelines for hemodynamic support of sepsis
advise following predetermined protocols in patients in
shock. The protocol espoused by Rivers and colleagues
advocates aggressive volume resuscitation in septic shock
and aims to achieve threshold values of multiple param-
eters (e.g., hemoglobin, MAP, CVP, SCVO2, urine
output, and lactate) within the first hour. Adoption of
this goal-directed protocol was associated with a clear
reduction of mortality. However, protocols must be dis-
cussed and accepted by whole ICU or ED teams. Further,
adoption of such protocols should not preclude careful
assessment of the causes of shock because therapeutic
interventions may differ depending upon the underlying
cause.1,6,7 Protocolized cardiovascular management based
on ventricular–arterial coupling has been proposed by
Pinsky.97,97a,97b The Pinsky protocol involves both im-
mediate and ‘‘second-step’’ procedures. The second step
relies on therapies based on specific mechanisms of shock.
Specific drugs and therapeutics are tailored to the under-
lying cause of shock (e.g., thrombolysis of a myocardial
infarction or pulmonary embolism; drainage for pericar-
dial tamponade; appropriate cardiovascular drugs, antiar-
rhythmic drugs, inotropic, vasoconstrictor, or vasodilator
agents; adequate fluid loading, etc.).1
COST-EFFECTIVENESS OF EACH METHOD
AND STRATEGY
Data comparing morbidity, mortality, and cost of ther-
apeutic interventions are critical.43
Regarding cost-effectiveness, only the PAC
has been extensively studied. Esophageal Doppler and

echocardiography are increasingly being used in many
ICUs, but outcomes data comparing these strategies to
conventional strategies are lacking. Randomized studies
to compare the clinical impact of echocardiography with
arterial pulse contour analysis would be of interest but to
our knowledge have not been done. The appropriate use
and optimal interpretation of data are at least as im-
portant as the choice of the technique itself.
DISCUSSION
Although the classification of shock has not changed,
several major changes have evolved within the past few
years. First, the major scientific critical care societies
have defined quantitative parameters (primarily for sep-
tic shock) to allow a faster and a more unified diagnosis
not only at the bedside but also for common inclusion
criteria in clinical studies.2,8,98,99 Second, early manage-
ment of patients in shock must be aggressive and
orchestrated. This critical time has been called ‘‘the
golden first hour,’’ and is to be compared with the delays
defined for thrombolysis of cerebral vascular accidents
(CVAs) and ST elevation myocardial infarction
(STEMI).
Within the past decade, novel techniques have
supplanted the use of PACs [e.g., echocardiography,
esophageal Doppler monitoring, arterial pulse contour
analysis (PiCCO and LiDCO technologies), sublin-
gual PCO2 monitoring, etc.]. Regarding echocardio-
graphy, we believe that a multilevel training can be
defined: a basic level with five to 20 diagnoses that can
be learned in a few hours,100and a second level that
would require traditional echocardiography training
(over 1 or more years). These two levels of training
are being set up in France.20 We think that every ICU
should have within its team an intensivist, also board
certified in cardiovascular diseases, and in echocardiog-
raphy. The choice of equipment is important. Within
the ICU, optimal equipment and technology are essen-
tial. In this setting, handheld machines are not ad-
equate for the sickest patients.101We believe that
echocardiography is the most important tool to
promptly diagnosis and treat shock. A careful echocar-
diographic examination can establish an accurate initial
diagnosis; serial studies 12 or 24 hours later may assist
in follow-up. For unstable patients, continuous mon-
itoring is required. The arterial pulse contour techni-
ques are useful in this context and can replace the
PAC. Importantly, CO, prediction of preload respon-
siveness with respiratory variations of systolic arterial
pressure, pulse pressure, SV, and other hemodynami-
cally derived variables can be obtained with these
techniques.18,19,21,22 Esophageal Doppler may also be
useful in such circumstances.23,59,96 Esophageal Dop-
pler was beneficial in patients requiring MV but less
in spontaneous breathing activity or with arrythmias,
EVALUATION AND MANAGEMENT OF SHOCK/AXLER 237
using passive leg raising.96,102 This is an important step
because previous studies assessing prediction of preload
responsiveness were validated in patients requiring
continuous MV and sedation. In patients with cardio-
vascular or respiratory instability, we use in our ICU,
echocardiography to predict fluid responsiveness using
IVC and aortic Doppler respiratory variations, even in
patients not requiring MV (unpublished data).
CONCLUSION
Within the last few years, protocol-driven management
of patients with shock has been associated with improved
outcomes. These sentinel studies focused on septic and
hypovolemic shock, but lessons learned may apply to
other types of shock states. Monitoring techniques that
couple measurement of CO with ventilatory variations
of systolic arterial pressure, pulse pressure, and SV
enhance the ability to predict fluid responsiveness in
circulatory failure. With this strategy, inappropriate
volume expansion can be avoided in some patients,
whereas patients who may benefit from fluid expansion
are more easily and readily identified.
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