Understanding cardiac failure in sepsis .pdf



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Intensive Care Med
DOI 10.1007/s00134-014-3367-8

Antoine Vieillard-Baron
M. Cecconi

Received: 14 March 2014
Accepted: 7 June 2014
Ó Springer-Verlag Berlin Heidelberg and
ESICM 2014

UNDERSTANDING THE DISEASE

Understanding cardiac failure in sepsis

A. Vieillard-Baron ())
Section Thorax-Vascular DiseaseAbdomen-Metabolism, Intensive Care Unit,
University Hospital Ambroise Pare´,
Assistance Publique-Hoˆpitaux de Paris,
92104 Boulogne-Billancourt, France
e-mail: antoine.vieillard-baron@apr.aphp.fr
Tel.: ?33149095605

A. Vieillard-Baron
Universite´ Versailles Saint Quentin en
Yvelines, 78000 Versailles, France
M. Cecconi
Anaesthesia and Adult Critical Care, St
George’s Hospital and St George’s
University of London, London, UK

Introduction

Definitions

Although dedicated to cardiac failure in sepsis, this short
review covers also other aspects of hemodynamic alterations in sepsis, such as cardiac preload, afterload, and
microcirculation. We believe that this is necessary as the
degree of cardiac dysfunction is determined not only by
cardiac contractility, but also by changes in afterload and
preload. In practice, left ventricular (LV) afterload may
exacerbate LV systolic dysfunction; on the other hand,
venous return may be impaired by right ventricular (RV)
systolic dysfunction. Fluid expansion and the consequent
changes in LV filling pressures have to be interpreted in
the context of the degree of LV diastolic function, which
is frequently impaired in sepsis. Finally, each of the above
has to be evaluated in the context of the adequacy of
tissue perfusion. Such inadequacy can be manifested by
markers of hypoperfusion such as elevated blood lactate
and decreased oxygen venous saturation (SvO2 and
ScvO2), although not without limitations.

Cardiac failure in sepsis could be defined as inadequacy
of cardiac output and oxygen delivery due to cardiac
dysfunction. Cardiac dysfunction may originate from
different mechanisms (Fig. 1). RV dysfunction can lead
to decreased venous return; LV diastolic dysfunction may
induce impairment of LV preload. LV systolic dysfunction, also usually called ‘‘septic cardiomyopathy,’’ is often
present. These have been described to occur in association
or alone. Cardiac dysfunction is reversible providing
patients recover.
In the literature, ‘‘septic cardiomyopathy’’ is a term
that usually focuses mainly on the left ventricle, whereas
it may concern impairment of both ventricles. In pressure–volume loop studies, it is characterized by depressed
LV intrinsic contractility, independent from changes in
afterload [1]. It is constant, although not automatically
associated with (LV) systolic dysfunction (see below for
more extensive discussion).

Sepsis-related LV systolic dysfunction
Traditionally, hemodynamic alterations in septic shock
are described as occurring as a continuum in several
consecutive phases. The first one is the so-called early
phase: Patients have a low-flow state related to hypovolemia. During this stage, volume expansion increases
cardiac output and improves patient’s perfusion [2]. After
the initial resuscitation phase, the hemodynamic profile of
the second phase is consistent with a hyperdynamic state,
with high cardiac output and low systemic vascular
resistance. According to this description, classical
knowledge says that there is no or minimal myocardial
depression during these two phases [2]. During the next
phase, the traditional understanding of the disease suggests that decreased cardiac output and increased systemic
vascular resistance are present; this is consistent with
cardiac failure [2]. According to traditional teaching,
during this process many patients are unable to maintain
adequate cardiac output. This leads to progressive metabolic acidosis, with finally multiorgan failure and death
[2].
Parker et al. [3] were the first to describe that the
above phases can overlap. With the development of
echocardiography in the intensive care unit (ICU), further
studies confirmed this finding. It is now known that cardiac dysfunction occurs ‘‘dynamically’’ and that it can be
present much earlier than just in the late stage of septic
Fig. 1 Main mechanisms of
cardiac dysfunction, their
consequences, and their
incidence (in brackets) in
severe sepsis and septic shock.
LV left ventricular, RV right
ventricular, ALI acute lung
injury, ARDS acute respiratory
distress syndrome

shock. In Parker’s study, LV systolic function was evaluated as early as possible after onset of shock (in practice
within the first 24 h). More than half of patients had LV
systolic dysfunction [3]. Cardiovascular alterations have
also been reported by the same group in healthy volunteers 3 h following injection of endotoxin. These subjects
had increased cardiac index, decreased systemic vascular
resistance, but also very early LV systolic dysfunction
unmasked by volume loading [4].
Understanding of how LV systolic dysfunction may
appear and evolve in sepsis is necessary to identify and
treat it early. LV systolic function depends on the coupling between left ventricle and the vascular tree
(afterload). Since intrinsic performance is always
impaired, occurrence of LV systolic dysfunction is
strongly associated with the level of LV afterload [5]. For
this reason, correction of LV afterload by norepinephrine
infusion may unmask septic cardiomyopathy. This is why
serial evaluations have to be done along the evolution and
treatment. The challenge is to use adequate parameters to
detect LV systolic dysfunction; For instance, many studies have reported that SvO2 is very often in the normal
range in severe sepsis or septic shock, independently of
cardiac function [6]. This was recently reemphasized by
Bouferrache et al. [7], who compared hemodynamic
diagnosis using transesophageal echocardiography (TEE)
and the recommendations of the Surviving Sepsis Campaign including central venous oxygen saturation. In that
DEPRESSED INTRINSIC MYOCARDIAL
PERFORMANCE (100%)






May induce cardiac dysfunction very early
May be unmasked according to preload
and afterload conditions
May lead to cardiac failure
Is reversible

LV DIASTOLIC DYSFUNCTION
(50%)




LV compliance impairment
with slight LV dilatation
LV relaxation impairment
May modify the tolerance
to fluids

LV SYSTOLIC DYSFUNCTION
(up to 60% at day 3)




Is afterload sensitive
Does not increase LV
filling pressure
Is usually corrected by
small dose of
dobutamine

RV SYSTOLIC DYSFUNCTION
(30-50%)





Can be isolated or
associated with
ALI/ARDS
Is dependent on
respiratory settings
Decreases venous return

right ventricle and its afterload. In the critically ill patient,
this is particularly relevant when mechanically ventilated;
this is even more important when acute lung injury is
present. Kimchi et al. [13] reported 52 % incidence of RV
systolic dysfunction occurring in patients without acute
respiratory failure. When acute lung injury is present,
acute cor pulmonale is not unusual. By increasing right
atrial pressure, RV systolic dysfunction leads to a
decrease in systemic venous return, protects the pulmonary circulation, and thus explains in part why LV
filling pressure remains in normal range despite LV systolic dysfunction when associated [3]. As a consequence,
this may explain the difficulty in detecting LV systolic
dysfunction by pulmonary artery catheter (PAC), which in
this situation usually records low cardiac output with
nonelevated pulmonary artery occlusion pressure
Sepsis-related LV diastolic dysfunction
(PAOP), not very suggestive of cardiac failure as usually
Parker et al. [3] reported dilatation of the left ventricle of expected. This was illustrated by Jardin et al. [14], who
more than 100 %. This finding was never confirmed; this found discrepancies between PAC and echocardiography
can be partially explained by technical limitations of the in half of patients.
device used. Most studies using echocardiography report
a slight increase in LV size in patients with decreased LV
ejection fraction when compared with patients with preserved ejection fraction. In a study by Suffredini et al. [4], Impact on management
injection of endotoxin in healthy volunteers induced a
significant decrease in the ratio between pulmonary cap- LV systolic dysfunction can be managed with the aid of
illary wedge pressure and LV end-diastolic volume index. inotropic agents. This should only be considered in
The authors also showed a moderate (?15 %) increase in patients with significant LV systolic dysfunction and tisLV end-diastolic volume after volume loading with a sue hypoperfusion. When evaluating cardiac function, one
pulmonary capillary wedge pressure that was lower than always has to take into consideration the adequacy of
in the control group [4]. These findings point to a slight tissue perfusion. While SvO2 and ScvO2 have some limimprovement in LV compliance. On the other hand, in a itations, ultimately the clinician has to rely on improving
large series of 262 patients with severe sepsis or septic the perfusion. Low ScvO2 probably diagnoses the need to
shock, Landesberg et al. [9] reported that half of patients improve tissue perfusion, whereas when it is high or
had a velocity of the mitral annulus in diastole (e’ wave) normal, other variables can be used. The pCO2 gap, i.e.,
of less than 8 cm/s. This is suggestive of impaired the central venous–arterial pCO2 difference, can be a
relaxation of the LV. This confirms previous results: valuable tool. In the future, real-time visualization and
Bouhemad et al. [10] found that the incidence of LV assessment of microcirculation may be possible too.
relaxation impairment was around 40 %, independent of Dobutamine infusion can increase LV ejection fraction
LV systolic dysfunction. Tachycardia may be involved in and cardiac output in case of LV systolic dysfunction
diastolic dysfunction and may also hamper diastolic [15]; this may lead to improvement of microcirculation
function evaluation.
too. Furthermore, septic patients who are able to increase
their cardiac output after dobutamine infusion have
improved survival [15]. Nevertheless, dobutamine may
also have deleterious effects, and its use should always be
considered with caution.
Sepsis-related RV systolic dysfunction
LV relaxation impairment can also be present in sepRV systolic dysfunction has been reported in sepsis and sis; it is important to bear this in mind, as its presence can
septic shock, using thermodilution technique [11]. Using lead to poor tolerance of fluid expansion [9]. Whether
echocardiography, it has been shown that it can be present evaluation of LV diastolic function may help physicians
either alone or in the presence of LV systolic dysfunction titrate fluid expansion remains to be resolved.
Finally, to obtain a complete picture of cardiac func[12], since a significant part of RV systolic function
depends on LV systolic function. Its incidence is difficult tion, the RV has to be evaluated too. Identification of RV
to determine since, as for the left ventricle, it may depend systolic dysfunction can help physicians to adapt respion the coupling between the intrinsic contraction of the ratory settings and norepinephrine infusion, a very useful
study, among the 14 patients with low cardiac output,
high lactate level, and decreased LV ejection fraction,
only 3 actually had decreased ScvO2 [7]. One of the
explanations is that microcirculation is impaired with
peripheral arteriovenous shunting. Using transthoracic
echocardiography (TTE) or TEE, 38 % incidence of LV
systolic dysfunction has been reported at day 1 following
admission for septic shock compared with 59 % incidence
at day 3 [8], the difference being explained by progressive correction of LV afterload. Then, persistence of
preserved LV systolic function could reflect persistent
vasoplegia leading to increased mortality [3].

drug to support the right ventricle in case of circulatory impaired together or in isolation. Echocardiography is
available in most units nowadays; it can provide a comimpairment.
plete assessment of cardiac function in a noninvasive
fashion. Echocardiographic evaluation has to be taken in
the context of a clinical evaluation. Treatment of ‘‘echocardiographic abnormalities’’ is not the final goal; the
Conclusions
final goal is to improve tissue perfusion.
Cardiac dysfunction is often present in sepsis. It has
several components, from systolic to diastolic dysfunc- Conflicts of interest The authors declare no conflict of interest
tion. The left ventricle and the right ventricle can be regarding this commentary.

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