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ABSTRACT
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 diagnosis and incomplete understanding of its intricate
in intensive care units worldwide. Its etiology is varied pathophysiology results in high mortality rates. Optimal
and complex and optimal resuscitation and intervention management requires a multidisciplinary team, ideally
1,2
varies with etiology. Aggressive diagnostic and thera- led by an intensivist, in a hospital setting with appro-
peutic interventions must occur simultaneously to avoid priate diagnostic and management capabilities.
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- HISTORICAL ASPECTS
nostic and therapeutic approach it is almost invariably Hippocrates described a posttraumatic syndrome
lethal. Despite significant technological advances in long before shock syndrome was used as a medical term.
critical care medicine, the combination of delay in 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 DEFINITION
by a French surgeon, Le Dran, to indicate a severe The definition of shock has continued to change con-
3
impact or jolt, but it was not until 1867 that the term siderably over the years. It can no longer be based on
became popularized when Edwin Morris published his blood pressure alone. Assessment of perfusion indepen-
4
Practical Treatise on Shock after Operations and Injuries. dent of arterial pressure has clearly demonstrated that
He defined it as a peculiar effect on the animal system, adequate blood pressure does not equal adequate
12,13
produced by violent injuries from any cause, or from cardiac output or tissue perfusion. Seemingly
violent mental emotions calling attention to a bodys adequate oxy- gen delivery (DO2) also does not
response to injury for the first time as opposed to guarantee oxygen or substrate utilization at a cellular
focusing on the immediate manifestations of trauma level. In sepsis, there is evidence suggesting that a
itself. By the late 1800s, Fisher suggested that a cellular disturbance may impair oxygen and substrate
general- ized vasomotor paralysis resulting in utilization.
14,15
Cyanide or carbon monoxide
5
splanchnic blood pooling was the cause of shock, and intoxication leads to cellular cytotoxic hypoxia, despite
a few years later Maphoter, suggested extravascular the presence of adequate DO2. Situa- tions as may
leakage of fluids was the cause of the clinical occur with sepsis and cyanide or carbon monoxide
6
findings seen in traumatic shock. poisoning have led to the concept of cyto- toxic or
In the 1900s Cannon, based on his battlefield cytopathic shock. In light of these new con- cepts,
experience during World War I, attributed the initiation regardless of the mechanism by which it occurs, when
of shock to more than mere blood loss with a cellular dysoxia occurs, a shock state is present, which
disturbance of the nervous system causing relaxation of ultimately leads to organ dysfunction and failure.
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 CLASSIFICATION
the intravascular space. In 1930, Alfred Blalock Shock has traditionally been classified into four cate-
challenged Cannons theory, arguing that blood loss gories: hypovolemic, distributive, cardiogenic, and ob-
8
would sufficiently explain the fall in cardiac output. In structive shock. More appropriate is to classify shock
the 1940s a cardiovascular physiologist, Carl Wiggers, into five categories to include cytotoxic shock (Table 1).
published a series of studies demonstrating that a
prolonged shock state could lead to irreversible
9
circulatory failure. Fluid resuscitation be- came the EPIDEMIOLOGY AND ETIOLOGY
standard of care in the management of these patients. The incidence and prevalence of shock are currently
Hypotension had become not only the hallmark of shock unknown. Several factors make it difficult to perform
but also the endpoint followed by most physi- cians epidemiological analysis of this entity. Regardless of its
while managing these patients. etiology, patients may die before getting to the hospital.
For a long time shock was considered to occur Furthermore, it is not a reportable diagnosis and there
only as a result of trauma. It was not until 1898, is still a lack of consensus regarding the definition of
during the Spanish American War, that sepsis was shock in general, and specific forms of shock. Not
10 surprisingly there is great variability in reported shock
described to cause shock. In 1906 Rosenau
published his obser- vations of a severe reaction incidence and mortality rates. Despite all these
occurring after a second injection of some foreign epidemiological diffi- culties, it is well known that all
proteins (i.e., anaphylactic shock). In 1935 Tennant types of shock carry a very high mortality.
and Wiggers demonstrated an immediate drop in Cardiogenic shock is the number one cause of
myocardial contraction when the heart was acutely mortality from coronary artery disease in the United
11
deprived of coronary perfusion.
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