ICN Victoria: Hilton on "Echo and Septic Cardiomyopathy"

Echo & Septic Cardiomyopathy
Andrew Hilton
ICU, Austin Hospital

Septic Cardiomyopathy...What is it?
Gram Positive Septic Shock

Gram Negative Septic Shock

Gram Positive Septic Shock Gram Negative Septic Shock

Septic Cardiomyopathy: Outline
A brief history…
Echophysiology of sepsis
Volume therapy and cardiac output
in sepsis
Other therapies and septic
cardiomyopathy

A Brief History Septic Cardiomyopathy...
COMPARI SON OF CARDIAC INDICES IN RECOVERY OR DEATH
ACUTE GENERAL PERITONITIS
Acute deaths (4)
Case Age CVP. Lact. CVP. Lact.
No. Diagnosis CI. BP. pH ABB Pyr. CI. BP. pH ABB Pyr.
(1) 53 WF
INITIAL AFTER 1 2-4 5-7
TREATMENT a DAYS I
'N
Kz
4L'-
3-
2-
I1 Delayed
deaths (3)
Circulatory and Metabolic Alterations Associated
Circulatory and Metabolic Alterations Associated
with Survival or Death in Peritonitis:
with Survival or Death in Peritonitis:
Clinical Analysis of 25 Cases
Clinical Analysis of 25 Cases
GEORGE H. A. CLOWES, JR.,* M.D., MIKAIO VUCINIC,** M.D.,
GEORGE H. A. CLOWES, JR.,* M.D., MIKAIO VUCINIC,** M.D.,
MICHAEL G. WEIDNER, M.D.
MICHAEL G. WEIDNER, M.D.
CLOWES, VUCINIC AND WEIDNER Annals of Surgery
June 1966
From the Department of Surgery, The Medical College of South Carolina,
From the Department of Surgery, The Medical College of South Carolina,
Charleston, S. C.
Charleston, S. C.
Initial Posttreatment
DIFFUSE purulent peritonitis remains a
life endangering situation 11, 13 despite ad-vances
in therapy based upon sound ob-servations
of the associated physiologic and
biochemical derangements.10' 42 Much is
known of the early fluid 11, 30 and electrolyte
derangements 7,14 in developing extensive
inflammation.6' 21 The frequently associated
respiratory failure 5, 24, 38 and the extensive
caloric energy expenditure accompanied
by nitrogen loss 25, 32 are understood as
cause for exhaustion. The pathogenesis and
lethal effects of renal shut-down have been
described.31' 35 42 Hemodynamic measure-ments
in septic or hypovolemic shock eluci-date
the initial metabolic disorders,7' 27, 39
yet little information is available concern-ing
the circulatory requirements for early
or late survival from the hazardous condi-tion
of widespread peritoneal infection.
It is the purpose of this paper to present
observations on the relationship of the car-
Presented before the Southern Surgical Associa-tion,
Dec. 7-9, 1965, Hot Springs, Va.
This investigation was supported by Research
Contract DA-49-193-MD-2312 of the U. S. Army,
Research and Development Command, and by
Grant HE-08373 from the National Institutes of
Health.
* Present address: Harvard Surgical Unit, Boston
City Hospital, Boston, Mass.
** Research Fellow and Trainee, N.I.H. Grad-uate
Training Grant 5T1-HE5337.
TABLE 1. Peritonitis-
diac output and the circulatory function metabolic state of patients suffering
spreading infectious peritonitis. From
these data it is possible to appreciate importance of the transport system in dangerous situation. The interdependence
of the various organ systems, including endocrines, becomes apparent in the main-tenance
of cellular metabolic activity
throughout the body.
When considering the effects of fulminat-ing
peritonitis, it is convenient to divide
its course into three phases: 1) inadequate
circulation and a metabolic state of shock
associated with hypovolemia, electrolyte
shifts 11, 28, 30 and bacteremia; 27, 40 2) of the septic process and the establish-ment
of an inflammatory barrier; this leads
to early recovery or 3) prolonged intra-sepsis, requiring drainage of multi-ple
abscesses or correction of intestinal 4° This third period is the time extreme wasting 25 and may lead ultimately
to exhaustion and death.10' 31 Whereas more than the resting basal cardiac output
is required for an uncomplicated recovery
from a major operation,7'9 survival in presence of sepsis and inflammation a considerable and sustained of circulation.' It appears that same is true in extensive peritonitis. When
this requirement is not satisfied for 866
DIFFUSE purulent peritonitis remains a
life endangering situation 11, 13 despite ad-vances
in therapy based upon sound ob-servations
of the associated physiologic and
biochemical derangements.10' 42 Much is
known of the early fluid 11, 30 and electrolyte
derangements 7,14 in developing extensive
inflammation.6' 21 The frequently associated
respiratory failure 5, 24, 38 and the extensive
caloric energy expenditure accompanied
by nitrogen loss 25, 32 are understood as
cause for exhaustion. The pathogenesis and
lethal effects of renal shut-down have been
described.31' 35 42 Hemodynamic measure-ments
in septic or hypovolemic shock eluci-date
the initial metabolic disorders,7' 27, 39
yet little information is available concern-ing
the circulatory requirements for early
or late survival from the hazardous condi-tion
of widespread peritoneal infection.
It is the purpose of this paper to present
observations on the relationship of the car-
Presented before the Southern Surgical Associa-tion,
Dec. 7-9, 1965, Hot Springs, Va.
This investigation was supported by Research
Contract DA-49-193-MD-2312 of the U. S. Army,
Research and Development Command, and by
Grant HE-08373 from the National Institutes of
Health.
* Present address: Harvard Surgical Unit, Boston
City Hospital, Boston, Mass.
** Research Fellow and Trainee, N.I.H. Grad-uate
Training Grant 5T1-HE5337.
diac output and the circulatory function the metabolic state of patients from spreading infectious peritonitis. data it is possible to appreciate of the transport system dangerous situation. The interdependence
of the various organ systems, including endocrines, becomes apparent in of cellular metabolic throughout the body.
When considering the effects of peritonitis, it is convenient its course into three phases: 1) inadequate
circulation and a metabolic state associated with hypovolemia, electrolyte
shifts 11, 28, 30 and bacteremia; 27, 40 of the septic process and the of an inflammatory barrier; to early recovery or 3) prolonged sepsis, requiring drainage abscesses or correction of intestinal 4° This third period is the extreme wasting 25 and may lead ultimately
to exhaustion and death.10' 31 Whereas more than the resting basal cardiac is required for an uncomplicated from a major operation,7'9 survival presence of sepsis and inflammation a considerable and sustained of circulation.' It appears same is true in extensive peritonitis. this requirement is not satisfied 866
Subhepatic
abscess spread
(2) 36 WM
Obstruction;
perforation
bowel
(3) 60 CM
Leak; duodenal
stump
(4) 39 CF
Perforation of
uterus;
hysterectomy
(5) 39 CM
Perforated
appendix
(6) 19 CM
Perforated ap-pendix;
diabetes
(7) 58 CM
Colon obstruc-tion;
perfor-ated
cecum
(8) 80 WM
Ca. colon;
4.4 13
146/80
2.7 3.0
68/50
3.5
110/80
7.44 +3 10/3 3.8
140/80
3.7 4
100/65
7.32 -6 28/5 4.6 5
96/72
1.5 0
102/60
7.37 - 7 23/4 4.0
99/60
3.5 5
146/72
2.3 5
110/78
7.59 +3 13/3 3.2 3.5
122/70
7.40 -2 20/5
7.36 +3 17/3
7.38 -4 20/4
7.50 -4 58/11
7.32 -8
7.35 -8
7.44 - 1 34/5
868
“If for any reason the sustained high
cardiac output was not maintained as
long as inflammation persisted, metabolic
acidosis and death supervened.”
1960 & 70’s

Is sepsis naturally hyperdynamic?
Variability in time and cause of
clinical presentation
Confounding effects of fluid
resuscitation prior to study
Confounding effects of other
cardio-respiratory support
therapies
Sepsis
“au naturel”...?
Is the septic
hyperdynamic state an artifact
of treatment?

1984

I 93 I 5 I MAY, 1988 substance A Brief History Septic Cardiomyopathy...
1988
clinical investigations
- Depressed Left Ventricular Performance*
Response to Volume Infusion in Patients with Sepsis
and Septic Shock
Frederick P Ognibene, M.D.; Margaret M. Parker, M.D.;
Charles Natanson, M.D. ; James H. Shelhamer, M.D.; and
Joseph E. Parrillo, M.D.
Volume infusion, to increase preload and to enhance
ventricular performance, is accepted as initial management
of septic shock. Recent evidence has demonstrated de-pressed
myocardial function in human septic shock. We
analyzed left ventricular performance during volume in-fusion
using serial data from simultaneously obtained
pulmonary artery catheter hemodynamic measurements
and radionuclide cineangiography. Critically ill control
subjects (n 14), patients with sepsis but without shock
(n 21), and patients with septic shock (n 21) had prevol-ume
infusion hemodynamic measurements determined and
S hock secondary to sepsis is a serious disorder with
significant morbidity and mortality despite its
early recognition and appropriate antibiotic therapy.
CHEST received statistically similar volumes of fluid similar increases in pulmonary capillary wedge There was a strong trend (p 0. 004) toward less in left ventricular stroke work index (LVSWI) infusion in patients with sepsis and septic shock with control subjects. The LVSWI response infusion was significantly less in patients with when compared with critically ill control subjects These data demonstrate significantly altered performance, as measured by LVSWI, in volume infusion in patients with septic shock.
sion is based on the Frank-Starling principle states that there is a relationship between end-volume (increased cardiac muscle stretch present in serum during the acute phases
ofseptic shock.3 In addition, the human cardiovascular
response to septic shock is generally characterized by
hypotension, a decreased systemic vascular resistance,
and an elevated cardiac index.
Volume infusion usually represents a first therapeu-tic
step in the management ofcritically ill, hypotensive
patients with a low ventricular preload during septic
shock.47 The therapeutic mechanism of volume infu-
*Froi the Critical Care Medicine Department, Clinical Center,
National Institutes of Health, Bethesda.
This paper was presented in part at the annual National Meeting
of the American Federation for Clinical Research, Washington,
May 3-6, 1985 and at the 15th Annual Educational and Scientific
Symposium ofthe Society ofCritical Care Medicine, Washington,
May 27-31, 1986.
Manuscript received August 21; revision accepted November 12.
Reprint requests: Dr Ognibene, National Institutes ofHealth, Bldg
10, Rm 10D48, Bethesthi 20892
preload. This is probably clue to abnormalities
and variations of left ventricular compliance which
occur in critically ill patients, including those with
sepsis.6’79 Recent data from a canine model of septic
shock that simulates human sepsis, as well as some
human data in septic shock patients, have also dem-onstrated
reversible alterations in ventricular contrac-tility
as measured by left ventricular stroke work. These changes in left ventricular stroke work persisted
despite volume infusion. Therefore, when all of these
studies are considered, left ventricular performance
in patients with septic shock can be altered by either
changes in ventricular compliance, changes in intrinsic
ventricular contractility, or changes in both aspects ventricular performance. There are no studies to date,
however, which have formally assessed both compli-ance
and contractility abnormalities of the left ventri-
I
I
/
/1 ; r
I /
60
50
(.4
E
E
40
3C
- ---Controls
---Sepsis without Shock
-Septic Shock
Downloaded From: http://journal.publications.chestnet.org/ by a Austin Health Library User on 11/01/2012
90 100 110 120
EDVI (ml/mP)
FIGURE 3. Frank-Starling relationships for each of the three patient
groups. EDVI is measured in mllm2 and is plotted along the
abscissa. LVSWI is measured in gm/m2 and is plotted along the
ordinate. Data points plotted represent the mean prevolume and
postvolume infusion values of EDVI and LVSWI for each patient
group.
from 2 j.g/min to 20 ig/min, and phenylephrine dosage
in one patient was 66 ig/min. The prevolume infusion
LVSWIs, postvolume infusion LVSWIs, and changes
in LVSWIs after volume infusion were statistically
identical in group 3 patients off and on vasopressor
agents. The postvolume infusion LVSWI in group 3
patients off vasopressors (n = 11) of 41.0 ± 3.5 gm/m2
and the post volume infusion LVSWI in group 3
patients on vasopressors (n = 10) of 41.2 ± 4.6 gm/m2
were both significantly less than the postvolume infu-sion
LVSWI of 54. 1 ± 3. 3 gm/m2 in group 1 (p<O. 05).
This demonstrates that group 3 patients with septic
shock had a significantly depressed ability to increase
ventricular performance, compared to group 1,
whether or not they were receiving vasopressor agents.
DISCUSSION
This study demonstrates that patients with sepsis
and septic shock have markedly abnormal ventricular
performance in response to volume infusion in the
acute stages of sepsis. In patients with sepsis and
septic shock, the volume infusion induced increases
in PCWP do not lead to substantial increases in
LVSWI. The data actually indicate that as a group, the
response of LVSWI in septic shock patients is nearly
flat. Ventricular contractility, as measured by LVSWI,
has been shown to be significantly depressed in
response to volume in septic dogs; however, the
ventricular contractility improves back to normal base-line

On presentation…

4 days later

On presentation… 4 days later

Left mid lateral thigh
(transverse)
Right mid lateral thigh
(transverse)

2000’s
Feature Articles
Actual incidence of global left ventricular hypokinesia in adult
septic shock
Antoine Vieillard-Baron, MD; Vincent Caille, MD; Cyril Charron, MD; Guillaume Belliard, MD;
Bernard Page, MD; François Jardin, MD
Rationale and Objective: To evaluate the actual incidence of
global left ventricular hypokinesia in septic shock.
Method: All mechanically ventilated patients treated for an
episode of septic shock in our unit were studied by transesoph-ageal
echocardiography, at least once a day, during the first 3
60% global LV
hypokinesis
days of hemodynamic support. In patients who recovered, echo-cardiography
was repeated after weaning from vasoactive agents.
Main measurements were obtained from the software of the
apparatus. Global left ventricular hypokinesia was defined as a
left ventricular ejection fraction of <45%.
Measurements and Main Results: During a 3-yr period (Janu-ary
2004 through December 2006), 67 patients free from previous
cardiac disease, and who survived for >48 hrs, were repeatedly
studied. Global left ventricular hypokinesia was observed in 26 of
Acute myocardial depression in
sepsis has been suspected for a
long time (1). Demonstrated
for the first time in a clinical
study using left ventricular (LV) radionu-clide
angiography by Parker et al. (2) in
1984, it was also illustrated the same year
using bedside echocardiography (3). This
depression may be severe enough to
mimic cardiogenic shock (4) but is usu-ally
reversible (2, 5). Despite these mul-tiple
demonstrations, occurrence of acute
EF < 45%
(Late)
myocardial depression in sepsis is proba-bly
underestimated. General guidelines
for septic shock management are usually
focused on volume (6 –9) and on the use
of vasoconstrictive agents, such as dopa-mine
or norepinephrine (6, 7, 9). The
need for an inotropic agent in septic
Crit Care Med 2008; 36:1701–1706
34% mortality
shock management is considered less fre-quent
(6, 7).
Bedside use of transesophageal echo-cardiography
to guide hemodynamic
support, which constituted our routine
strategy (10, 11), permitted accurate
evaluation of the incidence of acute LV
hypokinesia in sepsis. For this purpose,
we report here all the echocardio-graphic
records prospectively collected
in our unit during a 3-yr period during
the management of patients treated for
septic shock.
PATIENTS AND METHODS
Patients. Echocardiographic recordings
were obtained by a transesophageal approach
in all mechanically ventilated patients meet-ing
the same criteria for sepsis and circulatory
failure. Sepsis was defined as at least two of the
following conditions occurring within the
context of infection: temperature of !38°C or
"36°C, heart rate of !90 beats/min, and
white blood cell count of !12,000 or "4000
cells/mm3 (12). The causative bacterium was
subsequently identified based on positive cul-tures
(blood or a sample from a localized site
of infection) in 66% of cases. Circulatory fail-ure
was defined as a systolic radial artery pres-sure
of "90 mm Hg by invasive monitoring,
despite adequate fluid volume. Moribund pa-tients,
who did not survive for !48 hrs, and
thus who could not undergo three successive
studies, and patients with a documented his-tory
of cardiac failure were all excluded from
the analysis.
Transesophageal Echocardiographic
Study. Two-dimensional real-time echocar-diographic
studies were performed with a
wide-angle phased-array digital sector scanner
and a 5-MHz multiplane transesophageal
probe (Sequoia C 256, Siemens) by senior phy-sicians,
all having !2 yrs of experience in daily
practice of bedside transesophageal echocardi-ography.
The first study was performed at ad-mission
(day 1). Echocardiographic studies
were repeated after 12–24 hrs of vasoactive
support (second study, day 2), after 48 hrs of
vasoactive support (third study, day 3), and
after definitive weaning from vasoactive sup-port
(fourth study, day n). This protocol was
considered as part of routine clinical practice,
and no informed consent was required from
the patient’s next of kin, as confirmed by the
clinical research ethics committee of the
French Intensive Care Society.
During echocardiographic examination,
we first studied the superior vena cava in a
long-axis view, using the two-dimensional
view to direct the M-mode beam across the
maximum diameter. From this view, we mea-sured
changes in the diameter of the superior
vena cava during the respiratory cycle. As we
have previously described (13), these changes
permitted detection of fluid responsiveness.
Thus, if necessary, a rapid fluid expansion was
*See also pg. 1950.
From the Medical Intensive Care Unit, University
Hospital Ambroise Paré, Assistance Publique Hôpitaux
de Paris, Boulogne Cedex, France.
The authors have not disclosed any potential con-flicts
of interest.
For information regarding this article, E-mail:
francois.jardin@apr.ap-hop-paris.fr
Copyright © 2008 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
DOI: 10.1097/CCM.0b013e318174db05
these 67 patients at admission (primary hypokinesia) and in 14
after 24 or 48 hrs of hemodynamic support by norepinephrine
(secondary hypokinesia), leading to an overall hypokinesia rate of
60%. Left ventricular hypokinesia was partially corrected by do-butamine,
added to a reduced dosage of norepinephrine, or by
epinephrine. This reversible acute left ventricular dysfunction was
not associated with a worse prognosis.
Conclusion: Global left ventricular hypokinesia is very frequent
in adult septic shock and could be unmasked, in some patients,
by norepinephrine treatment. Left ventricular hypokinesia is usu-ally
corrected by addition of an inotropic agent to the hemody-namic
support. (Crit Care Med 2008; 36:1701–1706)
KEY WORDS: septic shock; echocardiography; cardiac function;
myocardial depression
EF > 45%
EF < 45%
(Early)
2. All individual measurements of left ventricular ejection fraction obtained at day 1 (LVEF1, admission), day 2 (LVEF2, after 12–24 hrs of vasoactive

tests were used to compare continuous
with normal distribution, and Mann-
test for variables with skewed distribution.
!2 test to compare categorical variables.
less than .05 was considered statistically
MAYO CLINIC PROCEEDINGS
Total patients, N=106
106 patients Normal were (%) enrolled. Myocardial Themeand ysfunction (%)
!SD
!15 years, and 53 patients (50%) were
38 (36) 68 (64)
Documented microbial infection with posi-tive
source cultures was present in 53 patients
36% of the study population had posi-tive
culture results.
6 (6)
frequency of any myocardial dysfunction
n"68). Left ventricular diastolic 4 (4)
dysfunc-tion
found in 39 patients (37%), 8 (8) LV 11 systolic (10)
dys-function
29 (27%), and RV dysfunction in 33 (31%)
LV diastolic dysfunction
A
LV
diastolic
21 (20)
LV
systolic
8 (8)
RV
10 (9)
Thirty-eight patients (36%) had normal
diastolic, LV systolic, and RV function and were
as patients with normal cardiac func-tion.
was overlap of myocardial dysfunction
with 4 patients (4%) demonstrating dia-stolic
dysfunction along with LV and RV systolic
B
C
LV diastolic dysfunction
50
40
30
20
10
0
% of total
Mild Moderate Severe Ind.
LV systolic dysfunction
100
80
60
40
20
0
% of total
RV dysfunction
50
Mild Moderate Severe
60
A
Clinical Spectrum, Frequency, and Significance of Myocardial
Dysfunction in Severe Sepsis and Septic Shock
Juan N. Pulido, MD; Bekele Afessa, MD; Mitsuru Masaki, MD, PhD; Toshinori Yuasa, MD, PhD; Shane Gillespie, DO;
Vitaly Herasevich, MD, PhD; Daniel R. Brown, MD, PhD; and Jae K. Oh, MD
MayoClinProc.2012;87(7):620-628
No increase in 30 day or
1 year mortality
2000’s

Pathophysiology of Septic Cardiomyopathy?
Mechanisms of sepsis-induced cardiac dysfunction
Crit Care Med 2007; 35:1599–1608
Myocardial edema vascular cardiac compliance (34, 50). In addition, is influenced by hypertension heart function (dilation will impair (52). Finally, intrinsic is affected, with performance (53).
Alain Rudiger, MD; Mervyn Singer, MD, FRCP
Objectives: To review mechanisms underlying sepsis-induced
cardiac dysfunction in general and intrinsic myocardial depres-sion
in particular.
Data Source: MEDLINE database.
Data Synthesis: Myocardial depression is a well-recognized
manifestation of organ dysfunction in sepsis. Due to the lack of a
generally accepted definition and the absence of large epidemi-ologic
studies, its frequency is uncertain. Echocardiographic
studies suggest that 40% to 50% of patients with prolonged septic
shock develop myocardial depression, as defined by a reduced
ejection fraction. Sepsis-related changes in circulating volume
and vessel tone inevitably affect cardiac performance. Although
the coronary circulation during sepsis is maintained or even
increased, alterations in the microcirculation are likely. Mitochon-drial
dysfunction, another feature of sepsis-induced organ dys-function,
will also place the cardiomyocytes at risk of adenosine
triphosphate depletion. However, clinical studies have demon-strated
that myocardial cell death is rare and that cardiac func-tion
is fully reversible in survivors. Hence, functional rather than
structural changes seem to be responsible for intrinsic myocar-dial
Sepsis, the systemic inflamma-tory
response syndrome to in-fection,
is the leading cause of
death in the critically ill (1, 2),
predominantly as a consequence of mul-tiple
organ failure. Myocardial dysfunc-tion
is a recognized manifestation of this
syndrome (3– 6). In light of a greater un-derstanding
of the underlying pathophys-iology,
a reappraisal of the literature is
warranted. We will review both clinical
and preclinical studies and integrate re-cent
overview on sepsis-induced cardiac dys-function
in general and on intrinsic myo-cardial
depression in particular. The wide
variety of possible pathophysiologic
mechanisms and space limitations do not
permit total coverage, but we hope that a
synthesis of current knowledge relating
to the major areas has been encapsulated
in this review (Fig. 1).
PATIENT STUDIES
Macrocirculatory insights into subcellular mecha-nisms.
Despite awareness of sepsis-induced
Our aim is to provide a detailed
myocardial dysfunction for several its frequency remains unknown.
is de-cades,
increased in Large epidemiologic studies are lacking,
and no consensus exists for a septic suitable
definition. A reduced ejection fraction
shock (54, (EF) was recorded in 25% of nonshocked
(7) and 50% of shocked septic patients (8)
as to the role as assessed by ventriculography and ther-modilution.
However, cardiac output was
normal or increased in all patients In de-spite
endotoxemic moderate to severe myocardial de-pression.
Notably, survivors had lower EF
1. Sepsis-induced cardiac dysfunction. Cardiac performance during sepsis is impaired and higher due end-diastolic to
volumes com-pared
cardiac microvascular with nonsurvivors, suggesting (56), a
swelling of with full recovery of cardiac seen in survivors at 7–10 days. heart dilation and decreased EF have also been described some studies (9, 10) although other studies (11).
More recent studies have used echocardiography. presenting hypotensive patients, left ventricular (LV) (EF !55%) during initial resuscitation
was an independent predictor (12). In a sequential study (13), unstable patients shock had normal LV end-diastolic but depressed LVEF and From the Bloomsbury Institute of Intensive Care
reduced stroke volumes. One severe hypokinesia with LVEF end-diastolic volume subsequently in survivors but tended in nonsurvivors. In other of septic shock lasting !48 hrs, 44% had systolic LV dysfunction Those with myocardial depression more fluids during the of intensive care unit stay and Medicine, Wolfson Institute for Biomedical Research
and Department of Medicine, University College Lon-don,
UK.
Supported, in part, by the Stiefel Zangger Founda-tion
and the Siegenthaler Foundation (AR), both in
Zurich, Switzerland.
The authors have not disclosed any potential con-flicts
of interest.
For information regarding this article, E-mail:
m.singer@ucl.ac.uk
Copyright © 2007 by the Society of Critical Care
depression during sepsis. The underlying mechanisms down-regulation of !-adrenergic receptors, depressed signaling pathways, impaired calcium liberation the sarcoplasmic reticulum, and impaired electromechanical at the myofibrillar level. Most, if not all, of these changes regulated by cytokines and nitric oxide.
Conclusions: Integrative studies are needed to distinguish hierarchy of the various mechanisms underlying septic dysfunction. As many of these changes are related inflammation and not to infection per se, a better understanding
of septic myocardial dysfunction may be usefully extended other systemic inflammatory conditions encountered ill. Myocardial depression may be arguably viewed adaptive event by reducing energy expenditure in when energy generation is limited, thereby preventing of cell death pathways and allowing the potential for recovery. (Crit Care Med 2007; 35:1599–1608)
KEY WORDS: sepsis; heart failure; !-adrenergic mitochondria; nitric oxide; calcium signaling

Echo-physiology of SCM: Systolic Function
TTE Parasternal SAX
Qualitative Assessment

TTE Apical 4C
Quantitative Assessment

LVOT VTI
14
LVOT
2 cm
SV = 44 ml

Echo-physiology of SCM: Diastolic Function

E 45 cm/s

TTE Apical 4C

e’ 4 cm/s
E:e’ = 11
Diastolic dysfunction and mortality
in severe sepsis and septic shock
Giora Landesberg et al
European Heart Journal (2012) 33, 895–903

Sepsis: Volume therapy & cardiac output
250 ml boluses until
PAWP 15 achieved
Fluid over 24 hr
to maintain PAWP 15
n = 26
Mean age 80
Expected CI 2.4 to 3.0

Effects of resuscitation with crystalloid fluids on
cardiac function in patients with severe sepsis
Zhi Xun Fang1, Yu Feng Li2, Xiao Qing Zhou3, Zhen Zhang4,
Jin Song Zhang5, Hai Ming Xia1, Guo Ping Xing3, Wei Ping
Shu1,
Ling Shen1 and GuoQing Yin*1
BMC Infectious Diseases 2008, 8:50 doi:10.1186/1471-2334-8-50
groups.
Cardiac output and blood pressure
On admission, all the patients had abnormal tempera-ture,
abnormal white blood cell count, hyperpnea, tachy-cardia,
decreased CO and hypotension.
Echocardiograms were recorded by the Teichholz method
from the left parasternal window, and the parameters of
cardiac function such as CO were read directly. At T0, the
CO was 3.17 ± 0.79 l/min in the Ns group, 3.37 ± 0.99 l/
min in the Hs group and 3.34 ± 0.65 l/min in the Sb
group. CO was compared at serial time points after fluid
In all three groups, MAP at T0 was lower than 70 mm Hg:
61.21 ± 9.69 mm Hg in the Ns group, 62.55 ± 10.95 mm
Hg in the Hs group and 59.38 ± 9.79 mm Hg in the Sb
group. Normal saline treatment resulted in a marked
increase of MAP at T60, 3.5% sodium chloride at T8h and
5% sodium bicarbonate at T30. MAP improved earlier in
the Sb group than in the Ns and Hs groups. However,
there were no differences in MAP among the three groups
at the same time points (Fig. 2).
On admission, the patients in all three groups suffered
from hyperpnea and tachycardia. Fluid resuscitation did
N= 94
NO pressors, inotropes, IPPV
Effects of fluid resuscitation on CO Figure 1 in the three groups
Effects of fluid resuscitation on CO in the three groups. The trial program and case grouping were carried out accord-ing
to the design indicated in Methods. CO was measured by Doppler echocardiography. There were no differences in CO
among the three groups at all the six time points. Comparing the CO variables in the same group, CO at T120 and T8h was sig-nificantly
higher than at T0 in the Ns group; the parameter at T8h was higher than at T0 in the Hs group; and CO at T60, T90, T120
and T8h were higher than that at T0 in the Sb group (*p < 0.05). CO improved earlier in the Sb group than in the Ns and Hs
groups.

Effects of resuscitation with crystalloid fluids on
cardiac function in patients with severe sepsis
Zhi Xun Fang1, Yu Feng Li2, Xiao Qing Zhou3, Zhen Zhang4,
Jin Song Zhang5, Hai Ming Xia1, Guo Ping Xing3, Wei Ping
Shu1,
Ling Shen1 and GuoQing Yin*1
BMC Infectious Diseases 2008, 8:50 doi:10.1186/1471-2334-8-50
groups.
Cardiac output and blood pressure
On admission, all the patients had abnormal tempera-ture,
abnormal white blood cell count, hyperpnea, tachy-cardia,
decreased CO and hypotension.
Echocardiograms were recorded by the Teichholz method
from the left parasternal window, and the parameters of
cardiac function such as CO were read directly. At T0, the
CO was 3.17 ± 0.79 l/min in the Ns group, 3.37 ± 0.99 l/
min in the Hs group and 3.34 ± 0.65 l/min in the Sb
group. CO was compared at serial time points after fluid
In all three groups, MAP at T0 was lower than 70 mm Hg:
61.21 ± 9.69 mm Hg in the Ns group, 62.55 ± 10.95 mm
Hg in the Hs group and 59.38 ± 9.79 mm Hg in the Sb
group. Normal saline treatment resulted in a marked
increase of MAP at T60, 3.5% sodium chloride at T8h and
5% sodium bicarbonate at T30. MAP improved earlier in
the Sb group than in the Ns and Hs groups. However,
there were no differences in MAP among the three groups
at the same time points (Fig. 2).
On admission, the patients in all three groups suffered
from hyperpnea and tachycardia. Fluid resuscitation did
Effects of fluid resuscitation on CO Figure 1 in the three groups
Effects of fluid resuscitation on CO in the three groups. The trial program and case grouping were carried out accord-ing
to the design indicated in Methods. CO was measured by Doppler echocardiography. There were no differences in CO
among the three groups at all the six time points. Comparing the CO variables in the same group, CO at T120 and T8h was sig-nificantly
higher than at T0 in the Ns group; the parameter at T8h was higher than at T0 in the Hs group; and CO at T60, T90, T120
and T8h were higher than that at T0 in the Sb group (*p < 0.05). CO improved earlier in the Sb group than in the Ns and Hs
groups.
5 ml/kg study fluid
at T0 min
20 ml/kg NS
at T100min
N= 94
NO pressors, inotropes, IPPV
Mean age 40

first quartile of age n Table # 59), r # .48 second quartile of yrs, n # 50), r # .54 third quartile of age n # 70), r # .68 fourth quartile of yrs, n # 49).
# .92). All these significantly lower In group 2, the cardiac output induced increase in dose were correlated with in PP (r # .21, p # .001, .29, p # .004), and .01) but not in DAP All these correlations lower than in group and .0007 for the changes and MAP, respectively). %) in stroke volume introduction/increase were correlated changes (in %) in PP SAP (r # .18, p # .17, p # .04) but not p 2. Hemodynamic variables in patients receiving volume expansion (n # 228)
Variable Category
Before Volume
Expansion
After Volume
Expansion
Heart rate (mean !SD, beats/min) Nonresponders 92 ! 23 90 ! 22a
Responders 98 ! 22 96 ! 21a,b
Systolic arterial pressure (mean ! SD, mm Hg) Nonresponders 107 ! 24 115 ! 26a
Responders 109 ! 21 129 ! 23a,b
Diastolic arterial pressure (mean ! SD, mm Hg) Nonresponders 52 ! 13 55 ! 13a
Mean arterial pressure (mean ! SD, mm Hg) Nonresponders 71 ! 16 75 ! 16a
Pulse arterial pressure (mean ! SD, mm Hg) Nonresponders 56 ! 19 60 ! 20a
Global end-diastolic volume (mean ! SD, mL/m2) Nonresponders 703 ! 185 808 ! 280a
Responders 649 ! 203b 766 ! 264a,b
Extravascular lung water (mean ! SD, mL/kg
predicted body weight)
Nonresponders
Responders
11 ! 5 11 ! 5
10 ! 6 10 ! 5
Cardiac index (mean ! SD, L/min/m2) Nonresponders 3.2 ! 1.0 3.4 ! 1.1a
Responders 2.7 ! 0.9b 3.5 ! 1.1b
“Responders” refers to patients in whom volume expansion increased cardiac index by !15% (n #
86). “Nonresponders” refers to the other patients (n # 142).
ap " .05 vs. before volume expansion (comparisons in rows); bp " .05 vs. nonresponders
(comparisons in columns).
500ml NS bolus
Arterial pressure allows monitoring the changes in cardiac output
induced by volume expansion but not by norepinephrine*
Xavier Monnet, et al.
Table 3. Hemodynamic variables in patients with an introduction/increase of norepinephrine
(n # 145)
Crit Care Med 2011; 39:1394–1399
Mean age 63

HR 127 MAP 60
45 yr male (IVDU)
Staph. bacteraemia...
Noradrenaline 30 μg/min

TTE Subsostal SAX
45 yr male (IVDU)
HR 138 MAP 60

45 yr male (IVDU)
HR 138 MAP 60

45 yr male (IVDU)
Staph. bacteraemia... 500 mls
HR 140 MAP 60
later...

Septic cardiomyopathy: Other therapies…
Day 1: 52 y male undifferentiated sepsis
multiple myeloma (remission)

Day 1: 52 y male undifferentiated sepsis
SV 40ml

Milrinone 0.2 μg/kg/min
Day4: 52 y male undifferentiated sepsis

Day4: 52 y male undifferentiated sepsis
SV 60ml

23 yr male septic shock for 24hr
Initial Rx: volume replacement & noradrenaline

Rx: volume replacement & noradrenaline

Metoprolol 12.5 mg bd
Next day...

Next day...
Metoprolol 12.5 mg bd
Effect of Heart Rate Control With Esmolol on Hemodynamic
and Clinical Outcomes in Patients With Septic Shock
A Randomized Clinical Trial
Andrea Morelli, et al.
JAMA. doi:10.1001/jama.2013.278477

Echo-physiology SCM: Summary
Systolic Function
Qualitative & quantitative assessment
Diastolic Function
Quantitative assessment
Volume State
Qualitative & quantitative assessment
Inotropes }
Volume therapy
Vasopressors
Role of beta-blockers &
non-adadrenergic agents?
Where does the flow go?

ICN Victoria: Hilton on "Echo and Septic Cardiomyopathy"

ICN Victoria: Hilton on "Echo and Septic Cardiomyopathy"

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ICN Victoria: Hilton on "Echo and Septic Cardiomyopathy"