Shock Overview

Patrcia M. Veiga C. Mello, M.D.,1,2 Vinay K. Sharma,

M.D.,3
4
and R. Phillip Dellinger, M.D.

ABSTRACT

Despite improved understanding of the pathophysiology of shock and significant

advances in technology, it remains a serious problem associated with high morbidity and
mortality. Early treatment is essential but is hampered by the fact that signs and
symptoms of shock appear only after the shock state is well established and the bodys
compensatory mechanisms have started to fail. Although the causes of shock are
varied, the basic abnormality in all varieties is tissue and cellular dysoxia. In this
overview we discuss the definition, classification and pathogenesis of shock in light of
the recent advances in our understanding of its mechanisms. The epidemiology,
diagnosis, and management of the various types of shock are also briefly discussed.

KEYWORDS: Shock, hypoperfusion, septic shock, cardiogenic shock, hypovolemic

shock

Objectives: Upon completion of this article, the reader will: (1) appreciate divergent pathophysiology of different causes of shock; (2)
understand the importance of intervention on systemic manifestations of shock; and (3) be familiar with an algorithmic approach to
resuscitation of shock patients.
Accreditation: The University of Michigan is accredited by the Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credits: The University of Michigan designates this educational activity for a maximum of 1 category 1 credit toward the AMA
Physicians Recognition Award.

S hock is likely the most serious diagnosis made
in intensive care units worldwide. Its etiology is varied
and complex and optimal resuscitation and intervention
varies with etiology. Aggressive diagnostic and thera-
peutic interventions must occur simultaneously to avoid
irreversible cellular injury and microcirculatory failure.
Shock remains a major cause of mortality in any setting
in which it appears and without the appropriate diag-
nostic and therapeutic approach it is almost invariably
lethal. Despite significant technological advances in
critical care medicine, the combination of delay in
diagnosis and incomplete understanding of its intricate
pathophysiology results in high mortality rates. Optimal
management requires a multidisciplinary team, ideally
1,2
led by an intensivist, in a hospital setting with appro-
priate diagnostic and management capabilities.
HISTORICAL ASPECTS
Hippocrates described a posttraumatic syndrome
long before shock syndrome was used as a medical term.
The word shock is derived from the French word choquer,

Management of Shock; Editor in Chief, Joseph P. Lynch, III, M.D.; Guest Editors, Arthur P. Wheeler, M.D., Gordon R. Bernard, M.D. Seminars
in Respiratory and Critical Care Medicine, volume 25, number 6, 2004. Address for correspondence and reprint requests: R. Phillip Dellinger, M.D.,
Critical Care Section, Cooper University Hospital, One Cooper Plaza, 393 Dorrance, Camden, NJ 08103. E-mail: dellinger-phil@cooperhealth.
1 2
edu. Department of Critical Care Medicine, Hospital Sao Marcos, Teresina, Piau, Brazil; Hospital de Terapia Intensiva, Faculdade de
Ciencias Medicas, Universidade Estadual do Piau, Teresina, Piau, Brazil; 3Pulmonary and Critical Care Medicine Division, Graduate
4
Hospital, Drexel University, Philadelphia, Pennsylvania; Critical Care Section, Cooper University Hospital, Camden, New Jersey. Copyright #
2004 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. 1069-
3424,p;2004,25,06,619,628,ftx,en; srm00335x.
619
108 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 25, NUMBER 6 2004
 SHOCK OVERVIEW/VEIGA C. MELLO ET AL 109

meaning to collide with. The term choc was first used
by a French surgeon, Le Dran, to indicate a severe
3
impact or jolt, but it was not until 1867 that the term
became popularized when Edwin Morris published his
4
Practical Treatise on Shock after Operations and Injuries.
He defined it as a peculiar effect on the animal system,
produced by violent injuries from any cause, or from
violent mental emotions calling attention to a bodys
response to injury for the first time as opposed to
focusing on the immediate manifestations of trauma
itself. By the late 1800s, Fisher suggested that a
general- ized vasomotor paralysis resulting in
5
splanchnic blood pooling was the cause of shock, and
a few years later Maphoter, suggested extravascular
leakage of fluids was the cause of the clinical
6
findings seen in traumatic shock.
In the 1900s Cannon, based on his battlefield
experience during World War I, attributed the initiation
of shock to more than mere blood loss with a
disturbance of the nervous system causing relaxation of
7
blood vessels and hypotension. He proposed that a
toxic factor was released during shock leading to altered
capillary perme- ability and loss of blood volume from
the intravascular space. In 1930, Alfred Blalock
challenged Cannons theory, arguing that blood loss
8
would sufficiently explain the fall in cardiac output. In
the 1940s a cardiovascular physiologist, Carl Wiggers,
published a series of studies demonstrating that a
prolonged shock state could lead to irreversible
9
circulatory failure. Fluid resuscitation be- came the
standard of care in the management of these patients.
Hypotension had become not only the hallmark of shock
but also the endpoint followed by most physi- cians
while managing these patients.
For a long time shock was considered to occur
only as a result of trauma. It was not until 1898,
during the Spanish American War, that sepsis was
10
described to cause shock. In 1906 Rosenau
published his obser- vations of a severe reaction
occurring after a second injection of some foreign
proteins (i.e., anaphylactic shock). In 1935 Tennant
and Wiggers demonstrated an immediate drop in
myocardial contraction when the heart was acutely
11
deprived of coronary perfusion.
DEFINITION
The definition of shock has continued to change con-
siderably over the years. It can no longer be based on
blood pressure alone. Assessment of perfusion indepen-
dent of arterial pressure has clearly demonstrated that
adequate blood pressure does not equal adequate
12,13
cardiac output or tissue perfusion. Seemingly
adequate oxy- gen delivery (DO2) also does not
guarantee oxygen or substrate utilization at a cellular
level. In sepsis, there is evidence suggesting that a
cellular disturbance may impair oxygen and substrate
utilization.
14,15
Cyanide or carbon monoxide
intoxication leads to cellular cytotoxic hypoxia, despite
the presence of adequate DO2. Situa- tions as may
occur with sepsis and cyanide or carbon monoxide
poisoning have led to the concept of cyto- toxic or
cytopathic shock. In light of these new con- cepts,
regardless of the mechanism by which it occurs, when
cellular dysoxia occurs, a shock state is present, which
ultimately leads to organ dysfunction and failure.
CLASSIFICATION
Shock has traditionally been classified into four cate-
gories: hypovolemic, distributive, cardiogenic, and ob-
structive shock. More appropriate is to classify shock
into five categories to include cytotoxic shock (Table 1).
EPIDEMIOLOGY AND ETIOLOGY
The incidence and prevalence of shock are currently
unknown. Several factors make it difficult to perform
epidemiological analysis of this entity. Regardless of its
etiology, patients may die before getting to the hospital.
Furthermore, it is not a reportable diagnosis and there
is still a lack of consensus regarding the definition of
shock in general, and specific forms of shock. Not
surprisingly there is great variability in reported shock
incidence and mortality rates. Despite all these
epidemiological diffi- culties, it is well known that all
types of shock carry a very high mortality.
Cardiogenic shock is the number one cause of
mortality from coronary artery disease in the United

Table 1 Classification of Shock and Its Most Common Etiologies

Hypovolemic External and occult hemorrhages, skin losses (severe burns), third-spacing (pancreatitis, bowel obstruction, and
prolonged abdominal surgery), gastrointestinal tract losses (vomiting, diarrhea), urinary tract losses
Cardiogenic Acute myocardial infarction and its complications (e.g., acute mitral regurgitation, rupture of the interventricular
septum, rupture of the free wall), myocarditis, end-stage cardiomyopathy, myocardial contusion, myocardial
dysfunction after prolonged cardiopulmonary bypass, valvular heart disease, and hypertrophic obstructive
cardiomyopathy
Obstructive Cardiac tamponade, massive pulmonary embolism, tension pneumothorax, cor pulmonale, atrial myxoma,
coarctation of aorta
Distributive Septic shock, anaphylactic shock, neurogenic shock, adrenal crisis
Cytotoxic Cyanide intoxication, carbon monoxide intoxication, iron intoxication
 16
States. Estimated incidence ranges between 6 and obstructive or neurogenic shock. Regardless of comor-
8%,1720 and this rate has remained fairly stable from bidities or injuries, the shock state by itself will greatly
21
1975 to 1997. In the largest registry of patients with affect these patients prognosis and will be responsible
32,33
cardiogenic shock, 75% of patients had predominant left for significant increases in morbidity and mortality.
ventricular failure, 8% had acute mitral regurgitation,
5% had ventricular septal rupture, 3% had isolated
right PATHOPHYSIOLOGY
ventricular shock, 2% had tamponade or cardiac rupture, Cardiogenic shock occurs when myocardial damage
and 8% had shock resulting from other causes (such as (acute or acute on chronic) reaches a point where
myocarditis, end-stage cardiomyopathy, myocardial con- pump function is markedly impaired. As one enters
tusion, myocardial dysfunction after prolonged cardio- cardiogenic shock, stroke volume and cardiac output
pulmonary bypass, valvular heart disease, and decrease, reducing myocardial perfusion, which, in
22
hypertrophic obstructive cardiomyopathy). Early re- turn, exacerbates ischemia and creates a downward
perfusion strategies have improved survival rates in spiral. Compensatory mechanisms that are activated by
21
recent studies but mortality remains high. Several decreasing myocardial function eventually become ma-
studies have reported lower rates of shock (47%) with ladaptive. Increased heart rate and increased afterload
20,2325
the use of thrombolytics in myocardial infarction, resulting from catecholamine release increase
although no evidence has been found that this therapy is myocardial oxygen demand and worsen ischemia.
beneficial once shock has occurred.
17,25
Even lower Impaired diastolic filling due to tachycardia and
mortality rates are reported with revascularization stra- ischemia, combined with the kidneys attempt to
tegies.
26,27
Despite advanced supportive care in the increase preload by retaining fluid, result in pulmonary
management of heart failure and acute myocardial in- congestion and hypoxia.
farction, cardiogenic shock is still the most common Obstructive shock is characterized by inadequate
cause of in-hospital mortality in transmural myocardial ventricular filling due to cardiac compression or severe
infarction, with overall mortality rates remaining be- obstruction to ventricular inflow or outflow. In cardiac
tween 70 and 90%.
22,18 tamponade inadequate heart filling leads to decreased
Accurate assessment of the incidence of septic cardiac output, decreased blood pressure, reflex vasocon-
shock is also difficult to ascertain. In a study by the striction, and elevated intracardiac pressures despite
Centers for Disease Control and Prevention, the inci- inadequate filling. Massive pulmonary embolism leads
28 to obstruction of the pulmonary vessels by clot and
dence of sepsis in 1989 was 176 per 100,000. Septic
release of vasoconstrictive mediators. Elevation of
shock is reported as the thirteenth most frequent cause
29 right-sided pressures with a normal pulmonary artery
of mortality in the United States. A recent meta- occlusion pressure and low cardiac output reflects right
analysis found the mortality rate from septic shock to
30 ventricular failure due to increased pulmonary
be > 40% in most studies analyzed. The mortality resistance.
rate from septic shock observed in the placebo arms of Hypovolemic shock is characterized by loss of
randomized controlled trials have decreased over time circulating volume. Hypovolemia, tissue injury, and
most probably due to advances in supportive care pain result in an increase in sympathetic drive in an
(Table 2). Once the predominant cause of sepsis, gram- attempt to raise blood pressure by increasing heart rate,
negative bacteria now account for 38% of cases,
31 cardiac contractility, and peripheral vasomotor tone.
whereas 52% are due to gram-positive bacteria. Although initially beneficial, these adaptive measures
There has also been a dramatic (207%) increase in can eventually be harmful because the hypermetabolic
31
fungi as a cause of sepsis. state induced by the sympathetic drive can make tissues
Hypovolemic shock remains a major cause of more susceptible to local ischemia. Uneven peripheral
death in trauma patients but may also be seen as a vasoconstriction can result in maldistributive microcir-
complication of surgery and in patients with burns and culatory flow and tissue hypoxia. Compensatory
gastrointestinal bleeding. Trauma patients may also mechanisms fail when volume loss is > 25%. An
have impor- tant inflammatory component also occurs in
severe
34,35
Table 2 Change in Septic Shock Mortality Rates hypovolemic shock. Delays of just 2 hours in appro-
over Time priate resuscitation from volume losses exceeding 40%
No. of No. of Hospital Mortality
may result in inability to effectively correct tissue hypo-
Period Studies Patients Rate (%) 30
*Adapted from Friedman et al.
19581969* 13 668 61
19701979* 17 1378 53
19801989* 39 2594 55
19901997* 62 6256 45
19971992 30 7874 39
 36
perfusion. Despite adequate control of volume
loss, the patient may die as a consequence of
the systemic activa- tion of the inflammatory
cascade triggered by the initial insult that can
be further aggravated by reperfusion injury
37,38
phenomenon.
The characteristic feature of distributive
shock is a decline in peripheral vascular
resistance. Septic shock is
the classic example, but inflammatory y s
several other mediators (IL-1b, g h
conditions can lead to IL-6, IL-8, e i
a similar thrombox- anes, n p
hemodynamic profile. platelet-activating
factor, and M i
Trauma to the spinal
eicosanoids), s
cord may lead to e
neurogenic shock that which activate the t
u
is characterized by an coagulation and a
n
autonomic complement b l
dysfunction with loss systems, de- press o i
of peripheral vascular myocardial l k
tone with a relative contractility, and i e
hypovolemic state and lead to s l
severe hypotension. vasodilation m y
Bradycardia may also through inducible In general, .
be present and further nitric oxide constant oxygen 4

synthase 8
impair cardiac output. consumption
41,42
In anaphylactic activation. (VO2) is
5
shock, severe Nitric maintained over a 0
immunoglobulin E oxide is a key wide range of
player in DO2. At some In
(IgE)-mediated
distributive shock critical point, shock,
immediate
where it serves oxygen extraction decreased
hypersensitivity leads perfusion
to massive release of multiple cannot increase
physiological any further, and leads to
mediators from mast limited
cells and basophiles roles, including reductions in
neurotransmission DO2 will result oxidative
(especially histamine) metabolism
, regulation of in a reduction in
resulting in decreased resulting in
tissue perfusion VO2 (Fig. 1). This
vascular resistance, lactic acidosis
via vascular tone physiological
capillary leak, and from
and oxygen supply
impaired contractility. anaerobic
responsiveness, dependency is
Adrenal crisis is metabolism.
platelet primarily seen
another form of The degree
responsiveness, during low output
distributive shock, of lactate
renal volume circulatory shock. elevation
which, when volume
control, and It was initially correlates
resuscitated, evokes a antimicrobial thought that a with both the
hemodynamic profile 43,44
defense. pathological degree of
similar to septic shock.
Nitric oxide is the oxygen supply hypoperfusion
Tumor necrosis
major mediator of dependency was and the
factor alpha
vasodilation and present in mortality
(TNF-a) and
hypotension in patients with rate.
51
inter-
septic shock
45,46 septic shock (i.e., Regional
leukin-1 (IL-1) are the critical DO2
the dominant and may also be hypoperfusion
in- volved in the point is is indicated
cytokines in septic
39 development of increased and by decreased
shock. Increased VO2 is dependent
myocardial gastric
TNF-a levels are also on DO2 over a
40 depression.
47
It intramucosal
seen in heart failure wider range); 52,53
has also been pH and
and hemorrhagic however, this hepatic ve-
34 implicated in
shock. TNF-a is r nous oxygen
vascular
produced by e desaturation.
54
dysfunction seen
macrophages in l However, in
response to microbial in hemorrhagic a
shock.
35 most patients
antigens and other t
cytokines. It results in i
the release of o
additional O n
x
 assessment of patients in
shock; it is noninvasive,
can be performed at
bedside, and can
immediately reveal or
exclude several potential
etiologies of the shock
state. Recent studies have
suggested that
procalcitonin level is a
good marker of infection
and may help differentiate
septic from other shock
Figure 1 Relationship between 55,56
oxygen consumption (VO2) and
states.
oxygen delivery (DO2). Initial physical
examination should focus
with septic shock, there also on iden- tifying signs of
appears to be an inability of the tissue hypoperfusion and
tissues to extract oxygen from on differentiat- ing
15
the blood. Thus lactic cardiogenic shock from
acidosis may occur despite other types of shock
normal cardiac output and because initial volume
mixed venous oxygen resuscitation may be
saturation (SvO2). In cardio- different in the former. If
genic and hypovolemic shock, signs of fluid overload are
lactic acidosis occurs only after absent, a possible source
severe reduction in SvO2. of volume loss or infection
should be aggressively
sought. No sign, symptom,
D or laboratory test by itself
I is diagnostic of shock,
A perhaps with the
G exception of profound
N hypotension. Shock is easy
O to diagnose when a
S patient arrives in the
I emergency department
S with multiple stab wounds,
The first step for successful profuse bleeding, and
outcome with a shock state is immeasur- able blood
early recognition. It is pressure. The problem is
important to keep in mind recognizing it in more
that diabetic, cirrhotic, subtle presentations. It is
neutropenic, and elderly necessary to maintain a
patients may develop septic high index of suspicion
shock without a typical clinical and be alert to a group
picture or obvious source of of nonspecific signs and
infection. Basic evaluation symptoms that in the
should include metabolic panel, appropriate clinical context
hemogram, arterial blood gas, permits an early diagnosis
electrocardiogram, and chest of shock.
x-ray. It is important to
remember that a drop in
hemoglobin level occurs late in
hemorrhagic shock and volume
loss is best assessed by signs of
hypoperfusion. The
echocardiogram is increas-
ingly being used in the
Table 3 Hemodynamic Profiles and Main Therapeutic Intervention in the Various Shock States

Hemodynamic Profiles
of Shock Cardiac Output Preload Afterload Contractility Intervention
Hypovolemic # # " N Crystalloid or colloid, blood
Cardiogenic # " " # Inotropes, vasopressors
Septic Fluids, vasopressors
Prior to fluids # to N # # #
After fluids " N # #
Pulmonary Embolism # # " N Thrombolytic therapy
Pericardial tamponade # # " N Pericardiocentesis
Anaphylactic Fluids, inotropes, vasopressors
Prior to fluids to N # # #
After fluids " N # #
Adrenal Fluids, steroids, inotropes, vasopressors
Prior to fluids to N # # N
After fluids " N # N
 Hypotension is of lactic acid is a useful catheter is widely lactic acid levels.
present in most shock tool to assess severity and used, and much of Gastric tonometry has
states and will usually follow adequacy of its reported been shown to
catch the attention of therapeutic man- negative effect on predict mortality and
the physician, but euvers,
58,59
but lactic acid outcome may be may help determine
unfortunately only changes may not occur the result of poor splanchnic perfusion
occurs once the early enough to be a under- standing and guide
compensatory me- sentinel marker for shock. and improper resuscitation.
67,68

chanisms are At least in sepsis, elevated utilization of How- ever, the

64
overwhelmed. In lactic acid levels have data. In addition difficulty of technique
hypovolemic shock, been shown to occur with to ascertaining and interpretation of
ta- chycardia occurs normal intracellular filling pressures, the data, and the
after 15% of the oxygenation.
60
Further- flow, and oxygen increased cost
circulating volume is more, elevated lactic in- dices, specific associated with
lost. However, despite acid levels may occur pathological gastric tonometry,
being a sensitive sign due to comorbid diagnoses linked have limited its
of shock it is conditions, especially liver to shock may be clinical applicability.
nonspecific, and it is failure because it is made (Table 3). Cardiogenic
important to be aware cleared by the liver. Elevated right- shock may present
that this response may However, in a recent post sided and low PA with signs of
be blunted in patients hoc analysis of early, goal- occlusion pressure increased central
who are on b- directed therapy in septic in the setting of venous pressure,
blockers or calcium patients with lactic acute inferior pulmonary edema,
acidosis (> 4 mmol/L) myo- cardial third heart sound, and
channel blockers.
and mean arterial infarction should
Mottled skin and cold peripheral
pressure above 100 mm raise the
extremities, altered vasoconstriction;
Hg, patients in the suspicion of right
consciousness, thirst, although pulmonary
protocol group had ventricular
concen- trated urine, 65 edema may be absent
oliguria, and elevated significantly lower infarct. Central in right ventricular
creatinine may be mortality than those in the venous oxygen infarct. Arrhythmia
standard therapy group.
61 saturation (ScvO2) and mitral
present. In
hemorrhage almost Measurement of is easier to obtain regurgitation murmur
30% of volume will cardiac output and SvO2, than pulmonary may also be present.
as well as calculation of artery mixed Echocardiography
be
DO2, VO2, and oxygen venous saturation helps evaluate systolic
lost before the patient
57
extraction ratios can be and may function and can reveal
becomes hypotensive.
achieved with a potentially be a papillary muscle
An earlier
pulmonary artery (PA) good surro- gate rupture, mitral
sign is narrowing of
catheter. Despite the for SvO2 in septic
the pulse pressure due 66
regurgitation,
controversies regarding shock. ventricular septal
to catecho- lamine- 62,63
stimulated elevation of its use, the Hypoperfusion is the defects, and free-wall
diastolic blood hallmark of shock. 69
rupture.
Assess-
pressure in response Kussmauls
ment of oxygen
to the low circulating sign, pulsus
57 transport
volume. Further- paradoxus, distant
parameters is the
more, not only can heart sounds on
best way of
shock occur in the auscultation, and
determining the
absence of decreased voltage on
presence of global
hypotension, it may tissue elec- trocardiogram
persist even once hypoperfusion. may be present in
hypotension has been However, regional cardiac tamponade.
reversed. Blood tissue Equalization of
pressure may be hypoperfusion pressures is diagnostic
maintained with may be present of this condition with
vasopressors at the despite normal mean right atrial,
cost of worsening values of oxygen right ventricular end
oxygen debt. transport variables, diastolic, and PA
Measurement base deficit, and occlusion pressures
within 5 mm
Hg of one
another. The central venous pressure tracing may show a
rapid x descent and a blunted y descent, reflecting present with abdominal pain, nausea, vomiting, hy-
ventricular inflow obstruction. Echocardiogram reveals
pericardial effusion, and may show ventricular septal
deviation to the left and right ventricular collapse during
systole.
Distributive shock, frequently referred as warm
shock, is characterized by peripheral vasodilation and a
hyperdynamic cardiac status that prevails until later
stages when myocardial depression ultimately leads to
decreased cardiac output. Evidence of infection,
presence of spinal trauma or a trigger for anaphylaxis
will help
Figure 2 Diagnostic and management approach to shock.
differentiate the underlying etiology. Adrenal crisis may
pothermia, refractory hypotension, hyponatremia, and
hyperkalemia.
MANAGEMENT
The approach to the patient with shock must be
dynamic with diagnostic and therapeutic maneuvers
occurring simultaneously, striving to avoid further
injury, by improving tissue perfusion (Fig. 2). With the
exception of cardiogenic shock, aggressive fluid
resuscitation is
usually required. often mistakenly used as a strategies, emergency sur- though often
However, cardiogenic sign of intravascular gery, intraaortic balloon administered during
shock due to right volume overload. Studies pump, and artificial initial resuscitation.
ventricular infarction have shown that neither ventricular support devices Several studies
also requires volume physical examination
71,72 (LVAD [left ventricular performed in the
resusci- tation. Fluids nor central venous assist device] / BiVAD trauma population
should be given until pressure monitoring
73,74
is [biventricular assist have shown worse
signs of hypoperfu- accurate in determining device]). Revascularization outcome with
sion resolve or signs left ventricular volume strategies have proven to aggressive volume
of volume overload status. For that purpose a be most beneficial if resuscita- tion prior to
appear. Constant PA catheter placement under- taken within the bleeding control,
reassessment is key first few hours after the probably due to
offers a more accurate
and the effects of insult.
27,78,79 disruption of the
assessment of intravas- 8082
each therapeutic cular volume status and Obstructive shock hemostatic plug.
intervention on signs of tissue perfusion, better due to cardiac tamponade However, delayed
tissue hypoperfusion delinea- tion of the re- quires needle, catheter, resuscita- tion may
should guide therapy. hemodynamic profile, and or surgical drainage of the exacerbate the
There has been no dynamic observation of the pericardial fluid. Fluid inflammatory
conclusive evidence effect of each therapeutic and vasoactive drugs may component trig- gered
favoring the use of intervention (Table 3). It be required to support by hypovolemic shock
either crystalloid or can help guide both fluid circulation while awaiting leading to multiple
colloid solutions in resuscitation and decom- pression. In shock organ failure and
70 37,83
volume resuscitation. vasopressor or positive due to pulmonary death. Therefore,
Blood transfusion inotrope titration. embolism, cardiac it seems that judicious
should be instituted However, use of a PA arrhythmias should be fluid resuscitation to
to maintain an catheter is controversial corrected, a fluid challenge maintain
adequate DO2 given recent studies given, and thrombolytic hemodynamic stability
and/or SvO2 or when indicating no benefit or therapy considered. The with avoidance of
significant blood loss is perhaps even harm from role of va- soactive drugs overload prior to
57
apparent. place- ment. The PA is less clear. bleeding control is
Endotracheal catheter has some In hypovolemic prudent.
intubation and limitations; cardiac output shock, volume In septic shock,
mechanical ventilation measured by resuscitation is the initial treatment
are thermodilution may be indicated and vasopressors remains antibiotic
o falsely in- creased (e.g., should be avoided if therapy and source
f in severe tricuspid possible, control. Appropriate
t regurgitation or in anti- biotic therapy
84,85
e intracardiac shunt). In improves outcome.
n such instances, cardiac In addition, vo- lume
output calculation using resuscitation is
r Ficks method may be used paramount. The fluid
e in addition to the PA deficit in septic shock
q catheter to more is often 6 L or more in
u accurately estimate cardiac the first 24 hours and
i output and tissue vasopressor support
r perfusion. Noninvasive should not be utilized
e methods of estimating in place of adequate
d cardiac output include intravascular volume.
. thoracic electrical Traditionally,
Adequate 75 dopamine has been the
bioimpedance and pulse 86
assessment of 76 vasopressor of choice.
intravascular volume contour analysis. However, one study
sta- tus is a challenge. However, the accuracy of has suggested that
Occult hypovolemia these systems has been norepinephrine is
77
due to extravas- cular questioned. more easily titrated to
loss of fluid is In cardiogenic achieve hemodynamic
frequently shock, therapeutic goals and may be
underestimated and measures in- clude early associated with better
peripheral edema is revascularization outcome.
87
A recent
study has found that higher circulating
emphasized supranormal volume that may
the cardiac output and mask early signs
importance of DO2 did not of shock.
instituting lower mortality Athletes have a
aggressive when used to higher circulating
therapy early reverse tissue volume and
and targeting hypoxia (as in cardiac output,
normal septic and a lower
ScvO2 patients).
9196
resting heart rate.
88
saturation. However, when Thus signs of
Recombinant used in a shock may also be
human prophylactic delayed in these
activated approach (i.e., patients. Patients
protein C before organ with heart block
has been failure devel- and a pacemaker
clearly ops), there may not be able to
demon- appears to be a mount a
strated to survival tachycardic
improve advantage.
97101
response.
outcome in When
89
septic shock. shock occurs due
In septic to more than one
shock etiol- ogy, a
patients with mixture of signs
impaired may be present
adrenal and the hemo-
responsivenes dynamic profile
s, will not show the
hydrocortison classic pattern of
e plus one particular
fluorocortison type of shock, but
e may also a mixture of
improve
90 features. It is
survival. important to be
It has able to recognize
been such a patient
suggested that and adapt the
maintaining a management
supra- normal accordingly. The
cardiac physical signs and
output in
hemodynamic
patients with
profiles may also
shock should
be altered by pre-
increase DO2
existing
and VO2,
comorbidities.
decrease any Cirrhotic and
oxygen debt
pregnant patients
pre- sent, and
have a lower
potentially
systemic vascular
improve
resistance and a
survival.
hyperdy- namic
Randomized
controlled hemodynamic
trials have profile in the
been absence of a
performed to distri- butive
test this shock. Pregnant
strategy but patients have a
C of Critical low blood M.
O Care pressure Microcirc
Medicine. produced by ulatory
N
Recommendati muscle injury. oxygenati
C Arch Surg on and
ons for services
L and personnel 1930;20:959 shunting
U for delivery of 996 in sepsis
S care in a 9. Wiggers CJ. and
I critical care The Physiology of shock.
O setting. Crit Shock. Crit Care
Care Med Cambridge: Med
N Harvard
S 1988;16:809 1999;27:
811 University 1369
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101. Wilson J, Woods I, Fawcett J, known that all types of anaphylactic shock, although no
et al. Reducing the risk of shock carry a very high neurogenic shock, evidence has been
major elective surgery: mortality. Cardiogenic adrenal crisis Cytotoxic found that this
randomised controlled trial of
preoperative optimisation of shock is the number Cyanide intoxication, therapy is beneficial
oxygen delivery. BMJ 1999; one cause of mortality carbon monoxide once shock has
3 from coronary artery intoxication, iron occurred.17,25
1
8 disease in the United intoxication States.16 Even lower
: Table 1 Classification Estimated incidence mortality rates are
1
0 of Shock and Its Most ranges between 6 and reported with
9 Common Etiologies 8%,1720 and this rate revascularization
9

Hypovolemic External has remained fairly stra- tegies.26,27
1 and occult stable from 1975 to Despite advanced
1 hemorrhages, skin 1997.21 In the largest supportive care in
0
3 losses (severe burns), registry of patients with the management of
third-spacing cardiogenic shock, 75% heart failure and
(pancreatitis, bowel of patients had acute myocardial in-
obstruction, and predominant left farction, cardiogenic
prolonged abdominal ventricular failure, 8% shock is still the
surgery), had acute mitral most common cause
gastrointestinal tract regurgitation, 5% had of in-hospital
desy losses (vomiting, ventricular septal mortality in
TranslateTurn off instant diarrhea), urinary tract rupture, 3% had transmural
translation losses Cardiogenic isolated right myocardial
Acute myocardial ventricular shock, 2% infarction, with
infarction and its had tamponade or overall mortality
complications (e.g., cardiac rupture, and 8% rates remaining be-
acute mitral had shock resulting tween 70 and
Showing translation for regurgitation, rupture of from other causes (such 90%.22,18 Accurate
EPIDEMIOLOGY AND the interventricular as myocarditis, end- assessment of the
ETIOLOGY The incidence septum, rupture of the stage cardiomyopathy, incidence of septic
and prevalence of shock are free wall), myocarditis, myocardial con- tusion, shock is also
currently unknown. Several end-stage myocardial dysfunction difficult to ascertain.
factors make it difficult to cardiomyopathy, after prolonged cardio- In a study by the
perform epidemiological myocardial contusion, pulmonary bypass, Centers for Disease
analysis of this entity. myocardial dysfunction valvular heart disease, Control and
Regardless of its etiology, after prolonged and hypertrophic Prevention, the inci-
patients may die before cardiopulmonary obstructive dence of sepsis in
getting to the hospital. bypass, valvular heart cardiomyopathy).22 1989 was 176 per
Furthermore, it is not a disease, and Early re- perfusion 100,000.28 Septic
reportable diagnosis and hypertrophic strategies have shock is reported as
there is still a lack of obstructive improved survival rates the thirteenth most
consensus regarding the cardiomyopathy in recent studies but frequent cause of
definition of shock in Obstructive Cardiac mortality remains mortality in the
general, and specific forms tamponade, massive high.21 Several studies United States.29 A
of shock. Not surprisingly pulmonary embolism, have reported lower recent meta-analysis
there is great variability in tension pneumothorax, rates of shock (47%) found the mortality
reported shock incidence cor pulmonale, atrial with the use of rate from septic
and mortality rates. Despite myxoma, coarctation of thrombolytics in shock to be > 40%
all these epidemiological aorta Distributive myocardial in most studies
analyzed.30 The mortality
rate from septic shock
observed in the placebo
arms of randomized
controlled trials have
decreased over time most
probably due to advances in
supportive care (Table 2).
Once the predominant
cause of sepsis, gram-
negative bacteria now
account for 38% of cases,
whereas 52% are due to
gram-positive bacteria.31
There has also been a
dramatic (207%) increase
in fungi as a cause of
sepsis.31 Hypovolemic
shock remains a major
cause of death in trauma
patients but may also be
seen as a complication of
surgery and in patients with
burns and gastrointestinal
bleeding. Trauma patients
may also have Table 2
Change in Septic Shock
Mortality Rates over Time
obstructive or neurogenic
shock. Regardless of
comor- bidities or injuries,
the shock state by itself will
greatly affect these patients
prognosis and will be
responsible for significant
increases in morbidity and
mortality.32,33
PATHOPHYSIOLOGY
Cardiogenic shock occurs
when myocardial damage
(acute or acute on chronic)
reaches a point where pump
function is markedly
impaired. As one enters
cardiogenic shock, stroke
volume and cardiac output
decrease, reducing
myocardial perfusion,
which, in turn, exacerbates
ischemia and creates a
downward spiral. occlusion pressure and Period Studies
Compensatory low cardiac output Patients Rate (%)
mechanisms that are reflects right 19581969* 13 668
activated by decreasing ventricular failure due 61 19701979* 17
myocardial function to increased pulmonary 1378 53 1980
eventually become ma- resistance. 1989* 39 2594 55
ladaptive. Increased Hypovolemic shock is 19901997* 62
heart rate and increased characterized by loss of 6256 45 19971992
afterload resulting from circulating volume. 30 7874 39
catecholamine release Hypovolemia, tissue *Adapted from
increase myocardial injury, and pain result Friedman et al.30
oxygen demand and in an increase in perfusion.36
worsen ischemia. sympathetic drive in an Despite adequate
Impaired diastolic attempt to raise blood control of volume
filling due to pressure by increasing loss, the patient may
tachycardia and heart rate, cardiac die as a
ischemia, combined contractility, and consequence of the
with the kidneys peripheral vasomotor systemic activa- tion
attempt to increase tone. Although initially of the inflammatory
preload by retaining beneficial, these cascade triggered by
fluid, result in adaptive measures can the initial insult that
pulmonary congestion eventually be harmful can be further
and hypoxia. because the aggravated by
Obstructive shock is hypermetabolic state reperfusion injury
characterized by induced by the phenomenon.37,38
inadequate ventricular sympathetic drive can The characteristic
filling due to cardiac make tissues more feature of
compression or severe susceptible to local distributive shock is
obstruction to ischemia. Uneven a decline in
ventricular inflow or peripheral peripheral vascular
outflow. In cardiac vasoconstriction can resistance. Septic
tamponade inadequate result in maldistributive shock is the classic
heart filling leads to microcir- culatory flow example, but several
decreased cardiac and tissue hypoxia. other conditions can
output, decreased blood Compensatory lead to a similar
pressure, reflex mechanisms fail when hemodynamic
vasocon- striction, and volume loss is > 25%. profile. Trauma to
elevated intracardiac An impor- tant the spinal cord may
pressures despite inflammatory lead to neurogenic
inadequate filling. component also occurs shock that is
Massive pulmonary in severe hypovolemic characterized by an
embolism leads to shock.34,35 Delays of autonomic
obstruction of the just 2 hours in appro- dysfunction with
pulmonary vessels by priate resuscitation loss of peripheral
clot and release of from volume losses vascular tone with a
vasoconstrictive exceeding 40% No. of relative
mediators. Elevation of No. of Hospital hypovolemic state
right-sided pressures Mortality may result in and severe
with a normal inability to effectively hypotension.
pulmonary artery correct tissue hypo- Bradycardia may
also be present and further
impair cardiac output. In
anaphylactic shock, severe
immunoglobulin E (IgE)-
mediated immediate
hypersensitivity leads to
massive release of
mediators from mast cells
and basophiles (especially
histamine) resulting in
decreased vascular
resistance, capillary leak,
and impaired contractility.
Adrenal crisis is another
form of distributive shock,
which, when volume
resuscitated, evokes a
hemodynamic profile
similar to septic shock.
Tumor necrosis factor alpha
(TNF-a) and inter- leukin-1
(IL-1) are the dominant
cytokines in septic
shock.39 Increased TNF-a
levels are also seen in heart
failure40 and hemorrhagic
shock.34 TNF-a is
produced by macrophages
in response to microbial
antigens and other
cytokines. It results in the
release of additional
inflammatory mediators
(IL-1b, IL-6, IL-8,
thrombox- anes, platelet-
activating factor, and
eicosanoids), which
activate the coagulation and
complement systems, de-
press myocardial
contractility, and lead to
vasodilation through
inducible nitric oxide
synthase activation.41,42
Nitric oxide is a key player
in distributive shock where
it serves multiple
physiological roles,
including
neurotransmission,
regulation of tissue shock, decreased clinical picture or
perfusion via vascular perfusion leads to obvious source of
tone and limited oxidative infection. Basic
responsiveness, platelet metabolism resulting in evaluation should
responsiveness, renal lactic acidosis from include metabolic
volume control, and anaerobic metabolism. panel, hemogram,
antimicrobial The degree of lactate arterial blood gas,
defense.43,44 Nitric elevation correlates electrocardiogram,
oxide is the major with both the degree of and chest x-ray. It is
mediator of hypoperfusion and the important to
vasodilation and mortality rate.51 remember that a
hypotension in septic Regional drop in hemoglobin
shock45,46 and may hypoperfusion is level occurs late in
also be in- volved in the indicated by decreased hemorrhagic shock
development of gastric intramucosal and volume loss is
myocardial pH52,53 and hepatic best assessed by
depression.47 It has ve- nous oxygen signs of
also been implicated in desaturation.54 hypoperfusion. The
vascular dysfunction However, in most echocardiogram is
seen in hemorrhagic patients Figure 1 increas- ingly being
shock.35 Oxygen Relationship between used in the
Metabolism In general, oxygen consumption assessment of
constant oxygen (VO2) and oxygen patients in shock; it
consumption (VO2) is delivery (DO2). with is noninvasive, can
maintained over a wide septic shock, there also be performed at
range of DO2. At some appears to be an bedside, and can
critical point, oxygen inability of the tissues immediately reveal
extraction cannot to extract oxygen from or exclude several
increase any further, the blood.15 Thus potential etiologies
and reductions in DO2 lactic acidosis may of the shock state.
will result in a occur despite normal Recent studies have
reduction in VO2 (Fig. cardiac output and suggested that
1). This physiological mixed venous oxygen procalcitonin level
oxygen supply saturation (SvO2). In is a good marker of
dependency is primarily cardio- genic and infection and may
seen during low output hypovolemic shock, help differentiate
circulatory shock. It lactic acidosis occurs septic from other
was initially thought only after severe shock states.55,56
that a pathological reduction in SvO2. Initial physical
oxygen supply DIAGNOSIS The first examination should
dependency was step for successful focus on iden-
present in patients with outcome with a shock tifying signs of
septic shock (i.e., the state is early tissue
critical DO2 point is recognition. It is hypoperfusion and
increased and VO2 is important to keep in on differentiat- ing
dependent on DO2 over mind that diabetic, cardiogenic shock
a wider range); cirrhotic, neutropenic, from other types of
however, this and elderly patients shock because
relationship is may develop septic initial volume
unlikely.4850 In shock without a typical resuscitation may be
different in the former. If
signs of fluid overload are
absent, a possible source of
volume loss or infection
should be aggressively
sought. No sign, symptom,
or laboratory test by itself
is diagnostic of shock,
perhaps with the exception
of profound hypotension.
Shock is easy to diagnose
when a patient arrives in
the emergency department
with multiple stab wounds,
profuse bleeding, and
immeasur- able blood
pressure. The problem is
recognizing it in more
subtle presentations. It is
necessary to maintain a
high index of suspicion and
be alert to a group of
nonspecific signs and
symptoms that in the
appropriate clinical context
permits an early diagnosis
of shock. Table 3
Hemodynamic Profiles and
Main Therapeutic
Intervention in the Various
Shock States
Hemodynamic Profiles of
Shock Cardiac Output
Preload Afterload
Contractility Intervention
Hypovolemic # # " N
Crystalloid or colloid,
blood Cardiogenic Septic #
" " # Inotropes,
vasopressors Fluids,
vasopressors Prior to fluids
After fluids Pulmonary
Embolism # to N " # # N #
# # " # # N Thrombolytic
therapy Pericardial
tamponade Anaphylactic #
# " N Pericardiocentesis
Fluids, inotropes,
vasopressors Prior to fluids
After fluids Adrenal to N "
# N # # # # Fluids, it may persist even controversies
steroids, inotropes, once hypotension has regarding its
vasopressors Prior to been reversed. Blood use,62,63 the
fluids to N # # N After pressure may be catheter is widely
fluids " N # N maintained with used, and much of
Hypotension is present vasopressors at the cost its reported negative
in most shock states of worsening oxygen effect on outcome
and will usually catch debt. Measurement of may be the result of
the attention of the lactic acid is a useful poor under-
physician, but tool to assess severity standing and
unfortunately only and follow adequacy of improper utilization
occurs once the therapeutic man- of data.64 In
compensatory me- euvers,58,59 but lactic addition to
chanisms are acid changes may not ascertaining filling
overwhelmed. In occur early enough to pressures, flow, and
hypovolemic shock, ta- be a sentinel marker for oxygen in- dices,
chycardia occurs after shock. At least in specific
15% of the circulating sepsis, elevated lactic pathological
volume is lost. acid levels have been diagnoses linked to
However, despite being shown to occur with shock may be made
a sensitive sign of normal intracellular (Table 3). Elevated
shock it is nonspecific, oxygenation.60 right-sided and low
and it is important to be Further- more, elevated PA occlusion
aware that this response lactic acid levels may pressure in the
may be blunted in occur due to comorbid setting of acute
patients who are on b- conditions, especially inferior myo-
blockers or calcium liver failure because it cardial infarction
channel blockers. is cleared by the liver. should raise the
Mottled skin and cold However, in a recent suspicion of right
extremities, altered post hoc analysis of ventricular
consciousness, thirst, early, goal-directed infarct.65 Central
concen- trated urine, therapy in septic venous oxygen
oliguria, and elevated patients with lactic saturation (ScvO2)
creatinine may be acidosis (> 4 mmol/L) is easier to obtain
present. In hemorrhage and mean arterial than pulmonary
almost 30% of volume pressure above 100 mm artery mixed venous
will be lost before the Hg, patients in the saturation and may
patient becomes protocol group had potentially be a
hypotensive.57 An significantly lower good surro- gate for
earlier sign is mortality than those in SvO2 in septic
narrowing of the pulse the standard therapy shock.66
pressure due to group.61 Measurement Hypoperfusion is
catecho- lamine- of cardiac output and the hallmark of
stimulated elevation of SvO2, as well as shock. Assess- ment
diastolic blood pressure calculation of DO2, of oxygen transport
in response to the low VO2, and oxygen parameters is the
circulating volume.57 extraction ratios can be best way of
Further- more, not only achieved with a determining the
can shock occur in the pulmonary artery (PA) presence of global
absence of hypotension, catheter. Despite the tissue
hypoperfusion. However,
regional tissue
hypoperfusion may be
present despite normal
values of oxygen transport
variables, base deficit, and
lactic acid levels. Gastric
tonometry has been shown
to predict mortality and
may help determine
splanchnic perfusion and
guide resuscitation.67,68
How- ever, the difficulty of
technique and interpretation
of the data, and the
increased cost associated
with gastric tonometry,
have limited its clinical
applicability. Cardiogenic
shock may present with
signs of increased central
venous pressure,
pulmonary edema, third
heart sound, and peripheral
vasoconstriction; although
pulmonary edema may be
absent in right ventricular
infarct. Arrhythmia and
mitral regurgitation
murmur may also be
present. Echocardiography
helps evaluate systolic
function and can reveal
papillary muscle rupture,
mitral regurgitation,
ventricular septal defects,
and free-wall rupture.69
Kussmauls sign, pulsus
paradoxus, distant heart
sounds on auscultation, and
decreased voltage on elec-
trocardiogram may be
present in cardiac
tamponade. Equalization of
pressures is diagnostic of
this condition with mean
right atrial, right ventricular
end diastolic, and PA
occlusion pressures within
5 mm Hg of one another.
The central venous etiology, patients may myocardial
pressure tracing may die before getting to the dysfunction after
show a rapid x hospital. Furthermore, prolonged
descent and a blunted it is not a reportable cardiopulmonary
y descent, reflecting diagnosis and there is bypass, valvular
ventricular inflow still a lack of consensus heart disease, and
obstruction. regarding the definition hypertrophic
Echocardiogram of shock in general, and obstructive
reveals pericardial specific forms of shock. cardiomyopathy
effusion, and may show Not surprisingly there Obstructive Cardiac
ventricular septal is great variability in tamponade, massive
deviation to the left and reported shock pulmonary
right ventricular incidence and mortality embolism, tension
collapse during systole. rates. Despite all these pneumothorax, cor
Distributive shock, epidemiological diffi- pulmonale, atrial
frequently referred as culties, it is well known myxoma,
warm shock, is that all types of shock coarctation of aorta
characterized by carry a very high Distributive Septic
peripheral vasodilation mortality. Cardiogenic shock, anaphylactic
and a hyperdynamic shock is the number shock, neurogenic
cardiac status that one cause of mortality shock, adrenal crisis
prevails until later from coronary artery Cytotoxic Cyanide
stages when myocardial disease in the United intoxication, carbon
depression ultimately Table 1 Classification monoxide
leads to decreased of Shock and Its Most intoxication, iron
cardiac output. Common Etiologies intoxication
Evidence of infection, Hypovolemic External States.16 Estimated
presence of spinal and occult incidence ranges
trauma or a trigger for hemorrhages, skin between 6 and
anaphylaxis will help losses (severe burns), 8%,1720 and this
differentiate the third-spacing rate has remained
underlying etiology. (pancreatitis, bowel fairly stable from
Adrenal crisis may obstruction, and 1975 to 1997.21 In
present with abdominal prolonged abdominal the largest registry
pain, nausea, vomiting, surgery), of patients with
hy- pothermia, gastrointestinal tract cardiogenic shock,
refractory hypotension, losses (vomiting, 75% of patients had
hyponatremia, and diarrhea), urinary tract predominant left
hyperkalemia. losses Cardiogenic ventricular failure,
Translate instead Acute myocardial 8% had acute mitral
EPIDEMIOLOGY infarction and its regurgitation, 5%
AND ETIOLOGY The complications (e.g., had ventricular
incidence and acute mitral septal rupture, 3%
prevalence of shock are regurgitation, rupture of had isolated right
currently unknown. the interventricular ventricular shock,
Several factors make it septum, rupture of the 2% had tamponade
difficult to perform free wall), myocarditis, or cardiac rupture,
epidemiological end-stage and 8% had shock
analysis of this entity. cardiomyopathy, resulting from other
Regardless of its myocardial contusion, causes (such as
myocarditis, end-stage
cardiomyopathy,
myocardial con- tusion,
myocardial dysfunction
after prolonged cardio-
pulmonary bypass, valvular
heart disease, and
hypertrophic obstructive
cardiomyopathy).22 Early
re- perfusion strategies
have improved survival
rates in recent studies but
mortality remains high.21
Several studies have
reported lower rates of
shock (47%) with the use
of thrombolytics in
myocardial
infarction,20,2325
although no evidence has
been found that this therapy
is beneficial once shock has
occurred.17,25 Even lower
mortality rates are reported
with revascularization stra-
tegies.26,27 Despite
advanced supportive care in
the management of heart
failure and acute
myocardial in- farction,
cardiogenic shock is still
the most common cause of
in-hospital mortality in
transmural myocardial
infarction, with overall
mortality rates remaining
be- tween 70 and
90%.22,18 Accurate
assessment of the incidence
of septic shock is also
difficult to ascertain. In a
study by the Centers for
Disease Control and
Prevention, the inci- dence
of sepsis in 1989 was 176
per 100,000.28 Septic
shock is reported as the
thirteenth most frequent
cause of mortality in the
United States.29 A recent
meta-analysis found the Cardiogenic shock pressure, reflex
mortality rate from occurs when vasocon- striction,
septic shock to be > myocardial damage and elevated
40% in most studies (acute or acute on intracardiac
analyzed.30 The chronic) reaches a point pressures despite
mortality rate from where pump function is inadequate filling.
septic shock observed markedly impaired. As Massive pulmonary
in the placebo arms of one enters cardiogenic embolism leads to
randomized controlled shock, stroke volume obstruction of the
trials have decreased and cardiac output pulmonary vessels
over time most decrease, reducing by clot and release
probably due to myocardial perfusion, of vasoconstrictive
advances in supportive which, in turn, mediators. Elevation
care (Table 2). Once the exacerbates ischemia of right-sided
predominant cause of and creates a pressures with a
sepsis, gram-negative downward spiral. normal pulmonary
bacteria now account Compensatory artery occlusion
for 38% of cases, mechanisms that are pressure and low
whereas 52% are due to activated by decreasing cardiac output
gram-positive myocardial function reflects right
bacteria.31 There has eventually become ma- ventricular failure
also been a dramatic ladaptive. Increased due to increased
(207%) increase in heart rate and increased pulmonary
fungi as a cause of afterload resulting from resistance.
sepsis.31 Hypovolemic catecholamine release Hypovolemic shock
shock remains a major increase myocardial is characterized by
cause of death in oxygen demand and loss of circulating
trauma patients but may worsen ischemia. volume.
also be seen as a Impaired diastolic Hypovolemia, tissue
complication of surgery filling due to injury, and pain
and in patients with tachycardia and result in an increase
burns and ischemia, combined in sympathetic drive
gastrointestinal with the kidneys in an attempt to
bleeding. Trauma attempt to increase raise blood pressure
patients may also have preload by retaining by increasing heart
Table 2 Change in fluid, result in rate, cardiac
Septic Shock Mortality pulmonary congestion contractility, and
Rates over Time and hypoxia. peripheral
obstructive or Obstructive shock is vasomotor tone.
neurogenic shock. characterized by Although initially
Regardless of comor- inadequate ventricular beneficial, these
bidities or injuries, the filling due to cardiac adaptive measures
shock state by itself compression or severe can eventually be
will greatly affect these obstruction to harmful because the
patients prognosis and ventricular inflow or hypermetabolic
will be responsible for outflow. In cardiac state induced by the
significant increases in tamponade inadequate sympathetic drive
morbidity and heart filling leads to can make tissues
mortality.32,33 decreased cardiac more susceptible to
PATHOPHYSIOLOGY output, decreased blood local ischemia.
Uneven peripheral
vasoconstriction can result
in maldistributive microcir-
culatory flow and tissue
hypoxia. Compensatory
mechanisms fail when
volume loss is > 25%. An
impor- tant inflammatory
component also occurs in
severe hypovolemic
shock.34,35 Delays of just
2 hours in appro- priate
resuscitation from volume
losses exceeding 40% No.
of No. of Hospital
Mortality may result in
inability to effectively
correct tissue hypo- Period
Studies Patients Rate (%)
19581969* 13 668 61
19701979* 17 1378 53
19801989* 39 2594 55
19901997* 62 6256 45
19971992 30 7874 39
*Adapted from Friedman et
al.30 perfusion.36 Despite
adequate control of volume
loss, the patient may die as
a consequence of the
systemic activa- tion of the
inflammatory cascade
triggered by the initial
insult that can be further
aggravated by reperfusion
injury phenomenon.37,38
The characteristic feature
of distributive shock is a
decline in peripheral
vascular resistance. Septic
shock is the classic
example, but several other
conditions can lead to a
similar hemodynamic
profile. Trauma to the
spinal cord may lead to
neurogenic shock that is
characterized by an
autonomic dysfunction with
loss of peripheral vascular
tone with a relative
hypovolemic state and myocardial thought that a
severe hypotension. contractility, and lead pathological oxygen
Bradycardia may also to vasodilation through supply dependency
be present and further inducible nitric oxide was present in
impair cardiac output. synthase patients with septic
In anaphylactic shock, activation.41,42 Nitric shock (i.e., the
severe immunoglobulin oxide is a key player in critical DO2 point is
E (IgE)-mediated distributive shock increased and VO2
immediate where it serves multiple is dependent on
hypersensitivity leads physiological roles, DO2 over a wider
to massive release of including range); however,
mediators from mast neurotransmission, this relationship is
cells and basophiles regulation of tissue unlikely.4850 In
(especially histamine) perfusion via vascular shock, decreased
resulting in decreased tone and perfusion leads to
vascular resistance, responsiveness, platelet limited oxidative
capillary leak, and responsiveness, renal metabolism
impaired contractility. volume control, and resulting in lactic
Adrenal crisis is antimicrobial acidosis from
another form of defense.43,44 Nitric anaerobic
distributive shock, oxide is the major metabolism. The
which, when volume mediator of degree of lactate
resuscitated, evokes a vasodilation and elevation correlates
hemodynamic profile hypotension in septic with both the degree
similar to septic shock. shock45,46 and may of hypoperfusion
Tumor necrosis factor also be in- volved in and the mortality
alpha (TNF-a) and the development of rate.51 Regional
inter- leukin-1 (IL-1) myocardial hypoperfusion is
are the dominant depression.47 It has indicated by
cytokines in septic also been implicated in decreased gastric
shock.39 Increased vascular dysfunction intramucosal
TNF-a levels are also seen in hemorrhagic pH52,53 and
seen in heart failure40 shock.35 Oxygen hepatic ve- nous
and hemorrhagic Metabolism In general, oxygen
shock.34 TNF-a is constant oxygen desaturation.54
produced by consumption (VO2) is However, in most
macrophages in maintained over a wide patients Figure 1
response to microbial range of DO2. At some Relationship
antigens and other critical point, oxygen between oxygen
cytokines. It results in extraction cannot consumption (VO2)
the release of additional increase any further, and oxygen delivery
inflammatory mediators and reductions in DO2 (DO2). with septic
(IL-1b, IL-6, IL-8, will result in a shock, there also
thrombox- anes, reduction in VO2 (Fig. appears to be an
platelet-activating 1). This physiological inability of the
factor, and oxygen supply tissues to extract
eicosanoids), which dependency is oxygen from the
activate the coagulation primarily seen during blood.15 Thus lactic
and complement low output circulatory acidosis may occur
systems, de- press shock. It was initially despite normal
cardiac output and mixed
venous oxygen saturation
(SvO2). In cardio- genic
and hypovolemic shock,
lactic acidosis occurs only
after severe reduction in
SvO2. DIAGNOSIS The
first step for successful
outcome with a shock state
is early recognition. It is
important to keep in mind
that diabetic, cirrhotic,
neutropenic, and elderly
patients may develop septic
shock without a typical
clinical picture or obvious
source of infection. Basic
evaluation should include
metabolic panel,
hemogram, arterial blood
gas, electrocardiogram, and
chest x-ray. It is important
to remember that a drop in
hemoglobin level occurs
late in hemorrhagic shock
and volume loss is best
assessed by signs of
hypoperfusion. The
echocardiogram is increas-
ingly being used in the
assessment of patients in
shock; it is noninvasive,
can be performed at
bedside, and can
immediately reveal or
exclude several potential
etiologies of the shock
state. Recent studies have
suggested that procalcitonin
level is a good marker of
infection and may help
differentiate septic from
other shock states.55,56
Initial physical examination
should focus on iden-
tifying signs of tissue
hypoperfusion and on
differentiat- ing cardiogenic
shock from other types of
shock because initial
volume resuscitation Pulmonary Embolism # narrowing of the
may be different in the to N " # # N # # # " # # pulse pressure due
former. If signs of fluid N Thrombolytic to catecho- lamine-
overload are absent, a therapy Pericardial stimulated elevation
possible source of tamponade of diastolic blood
volume loss or Anaphylactic # # " N pressure in response
infection should be Pericardiocentesis to the low
aggressively sought. No Fluids, inotropes, circulating
sign, symptom, or vasopressors Prior to volume.57 Further-
laboratory test by itself fluids After fluids more, not only can
is diagnostic of shock, Adrenal to N " # N # # shock occur in the
perhaps with the # # Fluids, steroids, absence of
exception of profound inotropes, vasopressors hypotension, it may
hypotension. Shock is Prior to fluids to N # # persist even once
easy to diagnose when N After fluids " N # N hypotension has
a patient arrives in the Hypotension is present been reversed.
emergency department in most shock states Blood pressure may
with multiple stab and will usually catch be maintained with
wounds, profuse the attention of the vasopressors at the
bleeding, and physician, but cost of worsening
immeasur- able blood unfortunately only oxygen debt.
pressure. The problem occurs once the Measurement of
is recognizing it in compensatory me- lactic acid is a
more subtle chanisms are useful tool to assess
presentations. It is overwhelmed. In severity and follow
necessary to maintain a hypovolemic shock, ta- adequacy of
high index of suspicion chycardia occurs after therapeutic man-
and be alert to a group 15% of the circulating euvers,58,59 but
of nonspecific signs volume is lost. lactic acid changes
and symptoms that in However, despite being may not occur early
the appropriate clinical a sensitive sign of enough to be a
context permits an early shock it is nonspecific, sentinel marker for
diagnosis of shock. and it is important to be shock. At least in
Table 3 Hemodynamic aware that this response sepsis, elevated
Profiles and Main may be blunted in lactic acid levels
Therapeutic patients who are on b- have been shown to
Intervention in the blockers or calcium occur with normal
Various Shock States channel blockers. intracellular
Hemodynamic Profiles Mottled skin and cold oxygenation.60
of Shock Cardiac extremities, altered Further- more,
Output Preload consciousness, thirst, elevated lactic acid
Afterload Contractility concen- trated urine, levels may occur
Intervention oliguria, and elevated due to comorbid
Hypovolemic # # " N creatinine may be conditions,
Crystalloid or colloid, present. In hemorrhage especially liver
blood Cardiogenic almost 30% of volume failure because it is
Septic # " " # Inotropes, will be lost before the cleared by the liver.
vasopressors Fluids, patient becomes However, in a recent
vasopressors Prior to hypotensive.57 An post hoc analysis of
fluids After fluids earlier sign is early, goal-directed
therapy in septic patients
with lactic acidosis (> 4
mmol/L) and mean arterial
pressure above 100 mm
Hg, patients in the protocol
group had significantly
lower mortality than those
in the standard therapy
group.61 Measurement of
cardiac output and SvO2,
as well as calculation of
DO2, VO2, and oxygen
extraction ratios can be
achieved with a pulmonary
artery (PA) catheter.
Despite the controversies
regarding its use,62,63 the
catheter is widely used, and
much of its reported
negative effect on outcome
may be the result of poor
under- standing and
improper utilization of
data.64 In addition to
ascertaining filling
pressures, flow, and oxygen
in- dices, specific
pathological diagnoses
linked to shock may be
made (Table 3). Elevated
right-sided and low PA
occlusion pressure in the
setting of acute inferior
myo- cardial infarction
should raise the suspicion
of right ventricular
infarct.65 Central venous
oxygen saturation (ScvO2)
is easier to obtain than
pulmonary artery mixed
venous saturation and may
potentially be a good surro-
gate for SvO2 in septic
shock.66 Hypoperfusion is
the hallmark of shock.
Assess- ment of oxygen
transport parameters is the
best way of determining the
presence of global tissue
hypoperfusion. However,
regional tissue cardiac tamponade. Insiden dan
hypoperfusion may be Equalization of prevalensi syok saat
present despite normal pressures is diagnostic ini tidak diketahui.
values of oxygen of this condition with Beberapa faktor
transport variables, mean right atrial, right membuat sulit untuk
base deficit, and lactic ventricular end melakukan analisis
acid levels. Gastric diastolic, and PA epidemiologi dari
tonometry has been occlusion pressures entitas ini. Terlepas
shown to predict within 5 mm Hg of one dari etiologinya,
mortality and may help another. The central pasien mungkin
determine splanchnic venous pressure tracing meninggal sebelum
perfusion and guide may show a rapid x sampai ke rumah
resuscitation.67,68 descent and a blunted sakit. Selain itu,
How- ever, the y descent, reflecting bukan diagnosis
difficulty of technique ventricular inflow dilaporkan dan
and interpretation of the obstruction. masih ada
data, and the increased Echocardiogram kurangnya
cost associated with reveals pericardial konsensus mengenai
gastric tonometry, have effusion, and may show definisi syok pada
limited its clinical ventricular septal umumnya, dan
applicability. deviation to the left and bentuk-bentuk
Cardiogenic shock may right ventricular khusus dari shock.
present with signs of collapse during systole. Tidak
increased central Distributive shock, mengherankan ada
venous pressure, frequently referred as variabilitas yang
pulmonary edema, third warm shock, is besar dalam
heart sound, and characterized by melaporkan
peripheral peripheral vasodilation kejadian shock dan
vasoconstriction; and a hyperdynamic mortalitas.
although pulmonary cardiac status that Meskipun semua
edema may be absent in prevails until later kesulitan
right ventricular infarct. stages when myocardial epidemiologi ini,
Arrhythmia and mitral depression ultimately adalah juga
regurgitation murmur leads to decreased diketahui bahwa
may also be present. cardiac output. semua jenis shock
Echocardiography Evidence of infection, membawa kematian
helps evaluate systolic presence of spinal sangat tinggi.
function and can reveal trauma or a trigger for syok kardiogenik
papillary muscle anaphylaxis will help adalah nomor satu
rupture, mitral differentiate the penyebab kematian
regurgitation, underlying etiology. dari penyakit arteri
ventricular septal Adrenal crisis may koroner di Inggris
defects, and free-wall present with abdominal Tabel 1 Klasifikasi
rupture.69 Kussmauls pain, nausea, vomiting, Syok dan Its
sign, pulsus paradoxus, hy- pothermia, Etiologi Paling
distant heart sounds on refractory hypotension, Umum
auscultation, and hyponatremia, and Hipovolemik
decreased voltage on hyperkalemia. Eksternal dan
elec- trocardiogram EPIDEMIOLOGI DAN perdarahan
may be present in ETIOLOGI okultisme, kerugian
kulit (luka bakar), ketiga
spasi (pankreatitis,
obstruksi usus, dan
pembedahan perut
berkepanjangan), kerugian
saluran pencernaan
(muntah, diare), kerugian
saluran kemih
infark miokard akut
kardiogenik dan
komplikasinya (misalnya,
regurgitasi akut mitral,
pecahnya septum
interventrikular, pecahnya
dinding gratis), miokarditis,
stadium akhir
kardiomiopati, memar
miokard, disfungsi miokard
setelah memotong
berkepanjangan
cardiopulmonary, penyakit
jantung katup, dan
hipertrofi kardiomiopati
obstruktif
Obstruktif tamponade
jantung, emboli paru masif,
ketegangan pneumotoraks,
cor pulmonale, myxoma
atrium, koarktasio aorta
syok distributif Septic,
shock anafilaksis, shock
neurogenik, krisis adrenal
Sitotoksik Sianida
keracunan, keracunan
karbon monoksida,
keracunan besi
Insiden Perkiraan States.16
berkisar antara 6 dan
8%, 17-20 dan tingkat ini
tetap cukup stabil dari
1975-1997,21 Dalam
registry terbesar pasien
dengan syok kardiogenik,
75% pasien memiliki
kegagalan ventrikel kiri
yang dominan, 8%
memiliki regurgitasi mitral
akut, 5% memiliki ruptur
septum ventrikel, 3%
memiliki hak terisolasi
syok ventrikel, 2% kematian secara sebagai komplikasi
memiliki tamponade keseluruhan sisa tween dari operasi dan
atau ruptur jantung, dan 70 dan 90% .22,18 pada pasien dengan
8% memiliki kejutan penilaian yang akurat luka bakar dan
yang dihasilkan dari dari kejadian syok perdarahan
penyebab lain (seperti septik juga sulit gastrointestinal.
miokarditis, stadium dipastikan. Dalam pasien trauma
akhir kardiomiopati, sebuah studi oleh Pusat mungkin juga
tusion con- miokard, Pengendalian dan memiliki
disfungsi miokard Pencegahan Penyakit, Tabel 2 Perubahan
setelah memotong paru yang insidensi sepsis Septic shock Angka
cardio berkepanjangan, pada tahun 1989 adalah Kematian lebih
penyakit jantung katup, 176 per 100,000.28 Waktu
dan hipertrofi syok septik dilaporkan obstruktif atau
kardiomiopati sebagai penyebab neurogenic shock.
obstruktif) .22 strategi paling sering ketiga Terlepas dari
perfusi re- awal telah belas dari kematian di bidities comor- atau
meningkat tingkat States.29 Inggris A cedera, negara
ketahanan hidup di meta-analisis ini kejutan dengan
studi terbaru tapi ditemukan mortalitas sendirinya akan
kematian tetap tingkat dari syok septik sangat
Beberapa penelitian menjadi> 40% di mempengaruhi
high.21 telah kebanyakan studi prognosis pasien ini
melaporkan tingkat analyzed.30 tingkat 'dan akan
yang lebih rendah kematian dari syok bertanggung jawab
shock (4-7%) dengan septik diamati di lengan untuk peningkatan
menggunakan plasebo dari uji coba yang signifikan
trombolitik di infark terkontrol secara acak dalam morbiditas
miokard, 20,23- 25 telah menurun dari dan mortality.32,33
meskipun tidak ada waktu ke waktu yang PATOFISIOLOGI
bukti telah ditemukan paling mungkin karena syok kardiogenik
bahwa terapi ini sangat kemajuan dalam terjadi ketika
bermanfaat sekali perawatan suportif kerusakan miokard
kejutan memiliki (Tabel 2). Setelah (akut atau akut pada
occurred.17,25 Bahkan penyebab dominan dari kronis) mencapai
lebih rendah tingkat sepsis, bakteri gram titik di mana fungsi
kematian dilaporkan negatif sekarang pompa nyata
dengan tegies.26,27 account untuk 38% dari terganggu. Sebagai
revaskularisasi stra- kasus, sedangkan 52% salah satu memasuki
meskipun perawatan adalah karena gram- syok kardiogenik,
suportif maju dalam positif bacteria.31 Ada stroke volume dan
pengelolaan gagal juga dramatis (207%) penurunan curah
jantung dan di- miokard peningkatan jamur jantung, mengurangi
akut farction, syok sebagai penyebab perfusi miokard,
kardiogenik masih sepsis. 31 yang, pada
merupakan penyebab syok hipovolemik tetap gilirannya,
paling umum kematian menjadi penyebab memperburuk
di rumah sakit di infark utama kematian pada iskemia dan
miokard transmural, pasien trauma, tetapi menciptakan spiral.
dengan tingkat juga dapat dilihat mekanisme
kompensasi yang diaktifkan
oleh penurunan fungsi
miokard akhirnya menjadi
ladaptive ma-. Peningkatan
denyut jantung dan
peningkatan afterload
akibat katekolamin rilis
peningkatan kebutuhan
oksigen miokard dan
memperburuk iskemia.
pengisian diastolik
gangguan karena takikardia
dan iskemia,
dikombinasikan dengan
upaya ginjal untuk
meningkatkan preload
dengan mempertahankan
cairan, mengakibatkan
kemacetan paru dan
hipoksia.
syok obstruktif ditandai
dengan pengisian ventrikel
yang tidak memadai karena
kompresi jantung atau
obstruksi parah inflow
ventrikel atau keluar.
Dalam tamponade jantung
mengisi jantung yang tidak
memadai menyebabkan
penurunan curah jantung,
tekanan darah menurun,
vasokonstriksi refleks, dan
tekanan intrakardiak tinggi
meskipun mengisi
memadai. emboli paru
masif menyebabkan
obstruksi pembuluh paru
oleh bekuan dan pelepasan
mediator vasokonstriksi.
Peningkatan tekanan sisi
kanan dengan normal paru
tekanan oklusi arteri dan
curah jantung yang rendah
mencerminkan kegagalan
ventrikel kanan karena
peningkatan resistensi paru.
syok hipovolemik ditandai
dengan hilangnya volume
sirkulasi. Hipovolemia,
cedera jaringan, dan
hasilnya rasa sakit 1980-1989 * 39 2594 (terutama histamin)
peningkatan dalam 55 yang
drive simpatik dalam 1990-1997 * 62 6256 mengakibatkan
upaya untuk 45 1997-1992 30 7874 resistensi menurun
meningkatkan tekanan 39 vaskular, kebocoran
darah dengan * Diadaptasi dari kapiler, dan
meningkatkan denyut Friedman et al.30 gangguan
jantung, kontraktilitas perfusion.36 Meskipun kontraktilitas. Krisis
jantung, dan tonus kontrol yang memadai adrenal adalah
vasomotor perifer. dari hilangnya volume, bentuk lain dari
Meski awalnya pasien mungkin mati syok distributif,
menguntungkan, sebagai konsekuensi yang, ketika volume
langkah-langkah dari aktifasi sistemik diresusitasi,
adaptif akhirnya dapat dari kaskade inflamasi membangkitkan
berbahaya karena dipicu oleh penghinaan profil hemodinamik
keadaan hipermetabolik awal yang dapat lebih mirip dengan syok
yang disebabkan oleh diperburuk oleh cedera septik.
drive simpatik dapat reperfusi Tumor necrosis
membuat jaringan lebih phenomenon.37,38 factor alpha (TNF-
rentan terhadap iskemia Fitur karakteristik syok a) dan antar
lokal. Merata distributif adalah interleukin-1 (IL-1)
vasokonstriksi perifer penurunan resistensi adalah sitokin yang
dapat mengakibatkan pembuluh darah perifer. dominan di
maldistributive aliran syok septik adalah shock.39 septic
culatory microcir- dan contoh klasik, namun Peningkatan TNF-a
hipoksia jaringan. beberapa kondisi lain tingkat juga terlihat
mekanisme kompensasi dapat menyebabkan di failure40 jantung
gagal ketika kehilangan profil yang sama dan hemorrhagic
volume> 25%. hemodinamik. Trauma shock.34 TNF-a
Komponen inflamasi pada sumsum tulang diproduksi oleh
tant impor- juga terjadi belakang dapat makrofag dalam
di parah menyebabkan syok menanggapi antigen
Penundaan shock.34,35 neurogenik yang mikroba dan sitokin
hipovolemik hanya 2 ditandai dengan lainnya. Hasilnya
jam di tindakan- disfungsi otonom pelepasan mediator
resusitasi priate dari dengan hilangnya tonus tambahan inflamasi
kerugian volume yang pembuluh darah perifer (IL-1b, IL-6, IL-8,
melebihi 40% dengan keadaan dan anes thrombox-,
Jumlah berat hipovolemik platelet-activating
Jumlah hipotensi relatif. factor, dan
Kematian rumah sakit Bradikardia juga dapat eikosanoid), yang
dapat mengakibatkan hadir dan selanjutnya mengaktifkan
ketidakmampuan untuk merusak cardiac output. koagulasi dan
secara efektif benar Pada syok anafilaktik, melengkapi sistem,
jaringan hipo Studi berat imunoglobulin E de- tekan
Periode Pasien Rate (IgE) -dimediasi segera kontraktilitas
(%) hipersensitivitas miokard, dan
1958-1969 * 13 668 61 mengarah ke rilis besar menyebabkan
1970-1979 * 17 1378 mediator dari sel mast vasodilatasi melalui
53 dan basophiles diinduksi nitrat
oksida sintase
activation.41,42
Nitrat oksida adalah
pemain kunci dalam syok
distributif mana melayani
peran ganda fisiologis,
termasuk neurotransmisi,
regulasi perfusi jaringan
melalui tonus pembuluh
darah dan responsif,
tanggap platelet, kontrol
volume ginjal, dan
defense.43,44 antimikroba
Nitrat oksida adalah
mediator utama vasodilatasi
dan hipotensi di shock45,46
septik dan mungkin juga
dilibatkan dalam
pengembangan
depression.47 miokard Ini
juga telah terlibat dalam
disfungsi vaskular dilihat di
hemoragik shock.35
oksigen metabolisme
Secara umum, konsumsi
oksigen yang konstan
(VO2) dipertahankan
selama berbagai DO2. Di
beberapa titik kritis,
ekstraksi oksigen tidak
dapat meningkatkan lebih
jauh, dan pengurangan
DO2 akan menghasilkan
pengurangan VO2
(Gambar. 1). suplai oksigen
ketergantungan fisiologis
ini terutama terlihat selama
output yang rendah kejutan
peredaran. Pada awalnya
berpikir bahwa suplai
oksigen ketergantungan
patologis hadir pada pasien
dengan syok septik (yaitu,
titik DO2 kritis meningkat
dan VO2 tergantung pada
DO2 pada rentang yang
lebih luas); Namun, ini
hubungan adalah
unlikely.48-50
Pada syok, penurunan
perfusi menyebabkan tua dapat volume awal
metabolisme oksidatif mengembangkan syok mungkin berbeda di
terbatas mengakibatkan septik tanpa gambaran bekas. Jika tanda-
asidosis laktat dari klinis yang khas atau tanda kelebihan
metabolisme anaerobik. sumber infeksi yang cairan yang absen,
Tingkat elevasi laktat jelas. evaluasi dasar kemungkinan
berkorelasi dengan harus mencakup panel sumber kehilangan
kedua tingkat metabolik, hemogram, volume atau infeksi
hipoperfusi dan rate.51 gas darah arteri, harus agresif dicari
kematian hipoperfusi elektrokardiogram, dan akan. Tidak ada
Regional ditunjukkan x-ray dada. Penting tanda-tanda, gejala,
dengan penurunan untuk diingat bahwa atau uji
lambung pH52,53 penurunan kadar laboratorium
intramucosal dan hati hemoglobin terjadi di dengan sendirinya
ve- desaturation.54 akhir syok hemoragik merupakan
oksigen nous Namun, dan kehilangan volume diagnostik shock,
pada kebanyakan yang terbaik dinilai mungkin dengan
pasien oleh tanda-tanda pengecualian dari
Gambar 1 Hubungan hipoperfusi. hipotensi yang
antara konsumsi Echocardiogram mendalam. Shock
oksigen (VO2) dan NASIONAL mudah untuk
pengiriman oksigen bertambahnya ingly mendiagnosa ketika
(DO2). yang digunakan dalam pasien tiba di
dengan syok septik, ada penilaian pasien shock; departemen darurat
juga tampaknya itu adalah non-invasif, dengan beberapa
menjadi dapat dilakukan di luka tusukan,
ketidakmampuan samping tempat tidur, perdarahan hebat,
jaringan untuk dan dapat segera dan immeasur-
mengekstrak oksigen mengungkap atau tekanan darah
dari blood.15 asidosis mengecualikan mampu.
demikian laktat dapat beberapa etiologi Masalahnya adalah
terjadi meskipun curah potensial dari negara mengakui dalam
jantung normal dan shock. Penelitian presentasi lebih
saturasi oksigen vena terbaru menunjukkan halus. Hal ini
campuran (SvO2). bahwa tingkat diperlukan untuk
Dalam cardio syok procalcitonin mempertahankan
genic dan hipovolemik, merupakan penanda indeks kecurigaan
asidosis laktat terjadi yang baik dari infeksi yang tinggi dan
hanya setelah dan dapat membantu waspada terhadap
penurunan berat di membedakan septic sekelompok tanda
SvO2. dari states.55,56 syok spesifik dan gejala
DIAGNOSA lainnya yang dalam konteks
Langkah pertama untuk Pemeriksaan fisik awal klinis yang sesuai
hasil yang sukses harus fokus pada tanda- memungkinkan
dengan keadaan shock tanda mengidentifikai diagnosis awal
pengakuan awal. Hal hipoperfusi jaringan syok.
ini penting untuk dan pada differentiat- Tabel 3
diingat bahwa pasien ing syok kardiogenik hemodinamik Profil
diabetes, sirosis, dari jenis lain syok dan Main Terapi
neutropenia, dan orang karena resusitasi Intervensi di Syok
Serikat Berbagai
Profil hemodinamik Shock
Curah jantung
preload
afterload
kontraktilitas
Intervensi
Hipovolemik # # "N
kristaloid atau koloid, darah
kardiogenik
Septic # "" # inotropik,
vasopresor
Cairan, vasopressors
Sebelum cairan
setelah cairan
Pulmonary Embolism #
untuk N
" kreatinin dapat hadir.
##
N hampir 30% dari
##
# "#
# menjadi hypotensive.57
N An sebelumnya
terapi trombolitik
tamponade perikardial
Anafilaksis # # "N
Pericardiocentesis
Cairan, inotropik,
vasopresor
Sebelum cairan
setelah cairan
Adrenal untuk N
"#
N#
##
# bahkan sekali hipotensi
Cairan, steroid, inotropik,
vasopresor
Sebelum cairan untuk N # #
N Setelah cairan "N # N
Hipotensi hadir di sebagian
besar negara shock dan
biasanya akan menarik
perhatian dari dokter, tapi
sayangnya hanya terjadi
sekali chanisms saya-
kompensasi kewalahan.
Pada syok hipovolemik,
chycardia TA terjadi setelah
15% dari volume laktat mungkin tidak pemanfaatan yang
sirkulasi hilang. terjadi cukup awal tidak tepat data.64
Namun, meskipun untuk menjadi penanda Selain memastikan
tanda sensitif shock itu sentinel untuk shock. mengisi tekanan,
spesifik, dan penting Setidaknya dalam aliran, dan oksigen
untuk menyadari bahwa sepsis, kadar asam di- dadu, diagnosis
respon ini dapat tumpul laktat yang tinggi telah patologis tertentu
pada pasien yang terbukti terjadi dengan terkait dengan syok
berada di blockers b- oxygenation.60 dapat dilakukan
atau calcium channel intraseluler yang (Tabel 3).
blockers. kulit normal Selanjutnya, Peningkatan sisi
berbintik-bintik dan kadar asam laktat yang kanan dan rendah
ekstremitas dingin, tinggi dapat terjadi PA tekanan oklusi
perubahan kesadaran, karena kondisi dalam pengaturan
rasa haus, air seni komorbiditas, terutama infark miokard
terkonsentrasi, oliguria, kegagalan hati karena rendah akut harus
dan peningkatan dibersihkan oleh hati. meningkatkan
Namun, dalam analisis kecurigaan dari
Dalam perdarahan terbaru post hoc dari saturasi oksigen
awal, yang diarahkan vena sentral
volume akan pada tujuan terapi pada ventrikel kanan
hilang sebelum pasien pasien sepsis dengan infarct.65 (ScvO2)
asidosis laktat (> 4 lebih mudah untuk
mmol / L) dan tekanan mendapatkan dari
tanda penyempitan arteri rata di atas 100 arteri pulmonalis
tekanan nadi karena mm Hg, pasien dalam saturasi vena
catecho- elevasi kelompok protokol campuran dan
lamine-dirangsang memiliki angka berpotensi menjadi
tekanan darah diastolik kematian secara gerbang surro- baik
dalam menanggapi signifikan lebih rendah untuk SvO2 di
rendah beredar dibandingkan di shock.66 septic
volume.57 Selanjutnya, group.61 terapi standar Hipoperfusi adalah
tidak hanya bisa Pengukuran curah ciri khas dari shock.
mengejutkan terjadi jantung dan SvO2, serta Menilai-
tanpa adanya hipotensi, perhitungan DO2, ment parameter
mungkin bertahan VO2, dan rasio transportasi oksigen
ekstraksi oksigen dapat adalah cara terbaik
memiliki telah terbalik. dicapai dengan arteri untuk menentukan
Tekanan darah dapat pulmonalis (PA) adanya hipoperfusi
dipertahankan dengan kateter. Meskipun jaringan global.
vasopressor pada biaya kontroversi mengenai Namun, hipoperfusi
memburuknya utang penggunaannya, 62,63 jaringan regional
oksigen. yang dapat hadir
Pengukuran asam laktat kateter secara luas meskipun nilai
adalah alat yang digunakan, dan banyak normal variabel
berguna untuk menilai efek negatif yang transportasi oksigen,
tingkat keparahan dan dilaporkan pada hasil defisit basa, dan
ikuti kecukupan euvers mungkin hasil dari kadar asam laktat.
mandat terapi, 58,59 berdiri miskin tonometry lambung
tetapi perubahan asam pemahaman dan telah terbukti untuk
memprediksi kematian dan
dapat membantu
menentukan perfusi
splanknik dan membimbing
resuscitation.67,68 Akan
tetapi, kesulitan teknik dan
interpretasi data, dan biaya
meningkat terkait dengan
tonometry lambung, telah
membatasi penerapan
klinis.
syok kardiogenik mungkin
hadir dengan tanda-tanda
peningkatan tekanan vena
sentral, edema paru, bunyi
jantung ketiga, dan
vasokonstriksi perifer;
meskipun edema paru dapat
absen di infark ventrikel
kanan. Aritmia dan mitral
regurgitasi murmur juga
dapat hadir.
Echocardiography
membantu mengevaluasi
fungsi sistolik dan dapat
mengungkapkan pecah
papiler otot, regurgitasi
mitral, defek septum
ventrikel, dan bebas-
dinding rupture.69
tanda Kussmaul, pulsus
paradoksus, jantung jauh
terdengar pada auskultasi,
dan penurunan tegangan
pada trocardiogram pemilu
dapat hadir di tamponade
jantung. Pemerataan
tekanan adalah diagnostik
dari kondisi ini dengan
rata-rata kanan atrium,
ventrikel kanan akhir
diastolik, dan tekanan
oklusi PA dalam 5 mm Hg
dari satu
lain. Pusat tekanan tracing
vena mungkin
menunjukkan '' x ''
keturunan cepat dan '' y ''
keturunan tumpul,
mencerminkan obstruksi
aliran ventrikel.
Ekokardiogram
mengungkapkan efusi
perikardial, dan dapat
menunjukkan septum
deviasi ventrikel
runtuhnya ventrikel kiri
dan kanan selama
sistol.
syok distributif, sering
disebut sebagai '' hangat
shock, '' ditandai
dengan vasodilatasi
perifer dan status
jantung hiperdinamik
yang berlaku sampai
tahap-tahap selanjutnya
ketika depresi miokard
akhirnya mengarah ke
penurunan curah
jantung. Bukti infeksi,
kehadiran trauma
tulang belakang atau
pemicu untuk
anafilaksis akan
membantu
membedakan etiologi
yang mendasari. Krisis
adrenal mungkin hadir
dengan nyeri perut,
mual, muntah,
pothermia hidrokarbon,
hipotensi refrakter,
hiponatremia, dan
hiperkalemia.
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