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The Nomenclature, Definition and Distinction of Types of Shock
The Nomenclature, Definition and Distinction of Types of Shock
I
n the first descriptions of shock the focus was
Summary exclusively on traumatic hemorrhagic shock, but later
this changed and five different types of shock came to
Background: A severe mismatch between the supply and demand of oxygen is the
be distinguished (1). Although it is true that all types of
common feature of all types of shock. We present a newly developed, clinically
shock can lead to the same final stage of multiorgan
oriented classification of the various types of shock and their therapeutic impli-
failure as a result of the imbalance between oxygen de-
cations.
mand and supply, the differences in their pathogenesis
Methods: This review is based on pertinent publications (1990–2018) retrieved by a and pathophysiology make it desirable to change their
selective search in PubMed, and on the relevant guidelines and meta-analyses. classification, partly for teaching purposes, but also,
especially, because different therapeutic measures are
Results: There are only four major categories of shock, each of which is mainly needed for the different types of shock. The new classifi-
related to one of four organ systems. Hypovolemic shock relates to the blood and cation makes no claim to be binding, and the therapeutic
fluids compartment while distributive shock relates to the vascular system; cardio-
effects are as a rule limited primarily to restoration of
genic shock arises from primary cardiac dysfunction; and obstructive shock arises
vital functions, in particular cardiovascular function con-
from a blockage of the circulation. Hypovolemic shock is due to intravascular
sistent with survival.
volume loss and is treated by fluid replacement with balanced crystalloids.
For the reasons given above, the new classification
Distributive shock, on the other hand, is a state of relative hypovolemia resulting
comprises just four main categories:
from pathological redistribution of the absolute intravascular volume and is treated
● Hypovolemic shock
with a combination of vasoconstrictors and fluid replacement. Cardiogenic shock is
due to inadequate function of the heart, which shall be treated, depending on the
● Distributive shock
situation, with drugs, surgery, or other interventional procedures. In obstructive
● Cardiogenic shock
shock, hypoperfusion due to elevated resistance shall be treated with an immediate ● Obstructive shock.
life-saving intervention. Of these, hypovolemic shock is divided into four
subcategories and distributive shock into three. Ob-
Conclusion: The new classification is intended to facilitate the goal-driven treatment structive shock has been given a category of its own.
of shock in both the pre-hospital and the inpatient setting. A uniform treatment strat- Although this nomenclature and classification is
egy should be established for each of the four types of shock. schematic and there is some overlapping between the
main groups, these four main groups can be basically
Cite this as:
assigned to four organ systems (Figure 1) that, owing
Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W:
to differences in their pathogenesis and pathophysiol-
The nomenclature, definition and distinction of types of shock.
ogy, require group-specific—or, in other words,
Dtsch Arztebl Int 2018; 115: 757–68. DOI: 10.3238/arztebl.2018.0757
organ-specific—treatment (Figure 2):
● Blood and fluids compartment
● Vascular system
● Heart
● Circulatory system.
Because of the difficulty of carrying out prospec-
tive randomized studies in shock patients, the
Department of Anesthesiology, Intensive and Palliative Care Medicine, Städtisches Klinikum
Solingen gGmbH: Prof. Dr. med. Thomas Standl, MHBA recommendations for treatment are based largely on
Department of Anesthesiology and Intensive Care Medicine, University Hospital of Cologne:
guidelines and registry studies. If available, the
Prof. Dr. med. Thorsten Annecke, DESA
Institute of Clinical and Experimental Pharmacology at the University Medical Center Schleswig-
Holstein, Campus Kiel: Prof. Dr. med. Dr. rer. nat. Ingolf Cascorbi
Classification of types of shock
Surgical Center/Emergency Department, Department of Anesthesiology and Intensive Care, Univer-
sity Hospital Carl Gustav Carus, Technische Universität Dresden: Prof. Dr. med. Axel R. Heller, MBA, • Hypovolemic shock
DEAA • Distributive shock
Department of Cardiothoracic Surgery, Cardiac Center, University Hospital of Cologne: • Cardiogenic shock
PD Dr. med. Anton Sabashnikov • Obstructive shock
Department of Orthopedics and Trauma Surgery, Kath. Krankenhaus Hagen gGmbH:
PD Dr. med. Wolfram Teske
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recommendation grade (RG) from the guidelines is volume; massive loss of red blood cells intensifies the
given. Where no recommendation grade is available, tissue hypoxia.
the recommendation is that of the present authors Traumatic hemorrhagic shock is distinguished
(eTable 1). The effects of the interventions presented from hemorrhagic shock by the additional presence of
on survival and disability-free survival are in some major soft tissue injury which aggravates the shock. A
cases not strong. typical example of this type of shock is polytrauma,
most usually caused by road traffic accidents and falls
Learning goals from a great height. Diffuse bleeding, hypothermia
After reading this article, the reader should: (especially ≤ 34 °C), and acidosis lead to life-
● Be familiar with the new classification of types of threatening coagulopathy (3, 4). The soft tissue injury
shock leads to postacute inflammation, further reinforcing
● Understand the different pathogenesis and patho- this process. At the microcirculatory level, leuko-
physiology of the four main categories of shock cyte–endothelium interactions (5) and destruction of
● Know the different therapeutic approaches to the endothelial membrane-bound proteoglycans and gly-
various types of shock. cosaminoglycans cause microvascular dysfunction
with capillary leak syndrome. At the intracellular
Hypovolemic shock level a metabolic imbalance arises (6) with possible
Hypovolemic shock is a condition of inadequate organ mitochondrial damage (7) and a negative influence on
perfusion caused by loss of intravascular volume, the vasomotor system (8).
usually acute. The result is a drop in cardiac preload to Hypovolemic shock in the narrower sense and trau-
a critical level and reduced macro- and microcircu- matic hypovolemic shock show significant fluid loss
lation, with negative consequences for tissue without hemorrhage.
metabolism and the triggering of an inflammatory Hypovolemic shock in the narrower sense arises
reaction. from external or internal fluid loss coupled with
Hypovolemic shock is divided into four subtypes inadequate fluid intake. It can be caused by hyperther-
(2): mia, persistent vomiting and diarrhea (e.g., cholera),
● Hemorrhagic shock, resulting from acute hemor- or uncompensated renal losses (e.g., diabetes insipid-
rhage without major soft tissue injury us, hyperosmolar diabetic coma). Sequestration of
● Traumatic hemorrhagic shock, resulting from large quantities of fluid in the abdomen, e.g., in ileus
acute hemorrhage with soft tissue injury and, in or liver cirrhosis, also leads to a reduction of
addition, release of immune system activators circulating plasma volume. The pathologically raised
● Hypovolemic shock in the narrower sense, result- hematocrit as well as the increased leukocyte and
ing from a critical reduction in circulating plasma platelet interactions additionally impair the rheologic
volume without acute hemorrhage properties of the blood and can lead to persistent
● Traumatic hypovolemic shock, resulting from a organ damage even after the patient has been treated
critical reduction in circulating plasma volume for shock (“no-reflow phenomenon”).
without acute hemorrhage, due to soft tissue injury Typical causes of traumatic hypovolemic shock are
and the release of immune system mediators. large surface burns, chemical burns, and deep skin
lesions. The trauma also activates the coagulation
Pathogenesis and pathophysiology cascade and the immune system, potentiating the
The characteristic feature of both, hemorrhagic and impairment of the macro- and microcirculation. The
traumatic hemorrhagic shock is bleeding. However, inflammatory reaction results in damage to the en-
differences exist between the two subcategories in dothelium, increases capillary leak syndrome, and
terms of the extent of soft tissue damage. Clinically the causes severe coagulopathy (9, 10).
most significant cause of hemorrhagic shock is acute It may be possible to draw some cautious
bleeding from an isolated injury to a large blood vessel, conclusions about the incidence of traumatic hypo-
gastrointestinal bleeding, nontraumatic vascular volemic and traumatic hemorrhagic shock from the
rupture (e.g., aortic aneurysm), obstetric hemorrhage Trauma Registry of the German Trauma Society
(e.g., uterine atony), and hemorrhage in the region of (Deutsche Gesellschaft für Unfallchirurgie). In the
the ear, nose, and throat (vascular erosion). The shock 2017 annual report, out of 40 836 patients, 27 147
is triggered by the critical drop in circulating blood (66%) had a maximum severity of injury of AIS 3
758 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2018; 115: 757–68
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FIGURE 1
hypovo
Traum mic
s
id
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Sep
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B od
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(n a o v o
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Variou
Synoptic view of the four types of shock (inner, white field) with the organ systems primarily associated with them (outer corners), sites
and mechanisms of manifestation (outside the circle), and pathogenetic and pathophysiologic features (outer and middle sectors of the circle).
To maintain clarity, mixed types of shock are not depicted.
(Abbreviated Injury Score) or more, and 10 639 subtypes of hypovolemic shock, lead to a total of
(26%) had life-threatening injuries (ISS, Injury Se- about 50 000 patients per year (Table 1).
verity Score ≥ 11), on the basis of which the number
of patients can be calculated to be around 30 000 per Treatment
year. The incidence of gastrointestinal hemorrhage in The preclinical and clinical treatment of hypovolemic
Germany is around 100 000 patients per year, of shock consists of immediate intravascular volume
whom roughly 10 000 suffer hypovolemic shock. replacement (fluid resuscitation) with balanced crystal-
These figures, together with those for the remaining loids (recommendation grade: B) using wide-bore
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FIGURE 2
Pathophysiology strongly
The history strongly influences the suspected diagnosis
influences treatment
peripheral venous access and, in a patient who is hem- threshold values, red cell concentrate (RCC) trans-
orrhaging, rapid bleeding control (Table 2). To prevent fusions are given. Those with uncontrolled bleeding,
or alleviate hypoxia, endotracheal intubation with nor- irrespective of the current hemoglobin value, should
moventilation usually follows (recommendation grade: receive transfusions of RCC, fresh frozen plasma
A). The extent of blood loss can be roughly estimated (FFP), and platelet concentrates (PC). Patients with
using the ATLS (Advanced Trauma Life Support) score traumatic or peripartum bleeding should also be given
(11). Trauma patients with shock should be transferred 1 to 2 g tranexamic acid at an early stage (recommen-
directly to a trauma center (recommendation grade: B). dation grade: A) (14–16). Multidisciplinary treatment
Surgical management should be undertaken as includes early stabilization of coagulation by means
soon as possible using the damage control surgery of coagulation factors, either as individual factors or
(DCS) approach (12). Persisting hypotension, as FFP, together with surgical prevention of further
especially in patients with head trauma, should blood loss (17).
prompt administration of a vasconstrictor (e.g., In patients with gunshot or stab wounds to the
norepinephrine) to achieve a systolic arterial pressure body cavities or a ruptured aortic aneurysm, blood
(SAP) ≥ 90 mmHg (recommendation grade: B) (13). pressure shall be stabilized at a permissive hypo-
In patients with controllable bleeding up to tension (SAP = 70 to 80 mmHg) by norepinephrine
age-specific and comorbidity-specific hemoglobin infusion and moderate volume replacement until
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Septic shock
Sepsis is defined according to the current Sepsis-3 The core of the pathophysiology is the endothelial
criteria as a dysregulated response by the body to an in- dysfunction, which leads to dysregulation of vascular
fection resulting in life-threatening organ dysfunctions. tone resulting in vasodilation, impaired distribution,
These are characterized and quantified by an increase and volume shifting in the macro- and microcircu-
in SOFA (Sequential Organ Failure Assessment) score lation, and to a rise in vascular permeability (capillary
by ≥ 2 points (eTable 2) (19). In the emergency care leak syndrome) (22–25). Frequently, biventricular im-
setting, the “Quick SOFA” (qSOFA) score can be used paired myocardial function is also present in the form
for screening, requiring only a preliminary examination of septic cardiomyopathy (26), which contributes to
of state of consciousness, respiration rate, and blood patient mortality (26, 27). Septic shock is a mixed
pressure. If there are pathological alterations of these form of a variety of pathologies (hypovolemia,
parameters (obtunded consciousness, respiration rate vasodilation, impaired cardiac function, and
≥ 22/min, systolic blood pressure ≤ 90 mmHg), and if mitochondrial dysfunction) and is usually associated
infection is suspected, the presence of sepsis may be with complex coagulopathies (22–25).
assumed (20).
A lactate value above 2 mmol/L and persistent Treatment
hypotension requiring the administration of vaso- Apart from an increased level of alertness and rapid
pressors to keep mean arterial blood pressure (MAP) diagnosis, septic shock requires treatment to support
above 65 mmHg define septic shock (21). Hypo- the circulation by the infusion of balanced crystalloid
volemia as the sole cause of circulatory failure must solutions (recommendation grade: A), administration of
be ruled out, for example by echocardiography (19, vasopressors (norepinephrine, vasopressin if needed),
21). in some cases also inotropic drugs (e.g., dobutamine),
and organ replacement therapy (recommendation
Pathogenesis and pathophysiology grade: B) (Table 2). Advanced invasive monitoring is
Patients over the age of 65 years with immunosuppres- indicated to allow tailored therapy for the impaired
sion or underlying malignant disease are dispropor- hemodynamics. Echocardiography has a central part to
tionately affected. In some patients the inflammatory play here (22, 24, 28). In all sepsis patients, as soon as
response is small or nonexistent (19, 22, 23). In Ger- samples have been obtained for microbiological study,
many about 280 000 patients annually are affected by calculated broad-spectrum antibiotic therapy and (if
sepsis; the incidence is rising every year by about 5.7%, possible) source control (causal treatment) should be
and between 2007 and 2013 the mortality fell from started as soon as possible (recommendation grade: A)
27.0% to 24.3% (20). About 35% of these patients (29). Noninfectious disease involving extensive medi-
suffer from septic shock, representing a total of about ator activation (e.g., acute pancreatitis) may lead to a
100 000 patients per year (Table 1). clinical presentation similar to that of septic shock. This
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TABLE 2
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Glyceryl trinitrate*2 Cardiogenic shock Vasodilation to reduce preload Development of tolerance Continuously according to effect
in particular and need: 0.3–4 µg/kg per min
i. v.
Sodium Cardiogenic shock Vasodilation to reduce afterload Risk of cyanide toxicity Initially: 0.1 µg/kg per min i. v.,
nitroprusside*2 then: double the dose every 3–5
min up to 10 µg/kg per min i. v.
Hydrocortisone*5, *6 Septic shock with persistent Endogenous glucocorticoid, See Methylprednisolone Initially: 100 mg over 10 min
instability after fluid and substituted in patients with re- then: 200–500 mg/24 h i. v.
vasopressor therapy duced or no cortisol production
Adrenal insufficiency
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beta-blockers). Intensifying factors include physical ● Interruption of the descending connection from the
effort, stress, and acute infection. bulbar regulatory centers to the spinal cord,
Anaphylactoid shock is caused by physical, especially in patients who have sustained trauma
chemical, or osmotic hypersensitivity reactions that above the middle of the thoracic spine (paraple-
are IgE-independent. Mediators are released from gia).
mast cells and basophilic granulocytes independently At 15% to 20%, spinal cord injuries are the most
of any antigen–antibody reaction or presensitization. common cause of neurogenic shock (32), followed by
Typical triggers are X-ray contrast media. surgical intervention in the lumbar region (33). Neu-
The clinical presentation varies greatly from one rogenic shock can occur due to cerebral ischemia,
individual to another according to the dose and site of subarachnoid hemorrhage, meningitis, or, more
entry of the antigen and the degree of sensitization. rarely, during or after epileptic seizures, rapid onset of
Initially, skin manifestations, abdominal symptoms, Guillain–Barré syndrome, pandysautonomia, or
or respiratory symptoms may be prominent. Anaphy- cerebral herniation. Occasionally, neurogenic shock
lactic reactions may resolve spontaneously or may can be triggered by stress or severe pain, or even after
progress despite appropriate therapy. In anaphylaxis a karate kick.
with fatal outcome, thromboembolic events are seen Neurogenic shock is characterized by the sudden
as often as arrhythmias and ventricular dysfunction (30). drop of SAP to <100 mmHg and heart rate to <60/min
with obtunded consciousness (rapid onset in bulbar
Treatment injury) and, in patients with high spinal cord injury,
Patients with severe anaphylactic reactions require loss of spinal reflexes (34). The capacity of the
constant monitoring, as late reactions including splanchnic venous system and skeletal musculature
arrhythmias, myocardial ischemia, and respiratory fail- rises while systemic venous pressure drops markedly.
ure may manifest as late as 12 hours after the initial Mortality is around 20%.
event. In terms of drug treatment, for anaphylactic
shock especially the administration of epinephrine Treatment
(plus norepinephrine, if necessary) and forced fluid The critical element in treating neurogenic shock is the
replacement are required (31). In patients with treatment of the cause. In addition to rapid fluid
bronchospasm, β-sympathomimetics and, as second- replacement, norepinephrine is given at increasing
line treatment, glucocorticoids are indicated (as they dosages until peripheral vascular resistance rises (Table
are in patients with delayed progressive symptoms) 1). To restore vascular tone, direct- or indirect-acting
(31). Histamine antagonists suppress the histaminergic sympathomimetics can also be given (35). Miner-
effects (Table 2). Treatment for anaphylactoid shock is alocorticoids to increase plasma volume are also a
the same as for anaphylactic shock. therapeutic option.
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Corresponding author:
Prof. Dr. med. Thomas Standl, MHBA
Klinik für Anästhesie, Operative Intensiv- und Palliativmedizin
Städtisches Klinikum Solingen gGmbH
Gotenstr. 1,
42653 Solingen, Germany
standl@klinikumsolingen.de
►Supplementary material
eTables, eFigure:
www.aerzteblatt-international.de/18m0757
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CME credit for this unit can be obtained via cme.aerzteblatt.de until 3 February 2019
Only one answer is possible per question. Please select the answer that is most appropriate.
Question 1 Question 7
What is the cause of hypovolemic shock? What is the definition of sepsis according to the current
a) Increased vasoregulation with volume shift Sepsis-3 criteria?
b) Inadequate organ perfusion caused by loss of intravascular a) Dysregulated response by the body to an infection resulting
volume, usually acute in life-threatening organ dysfunctions
c) Cardiac output and myocardial pump failure b) Inadequate organ perfusion caused by loss of intravascular
d) Right heart–related circulatory failure due to obstruction volume
e) Decompensated valve stenosis c) Primarily a disorder of cardiac function in the form of a
critical reduction of the heart’s pumping capacity
Question 2 d) Obstruction of the great vessels or the heart
What is a typical feature of hemorrhagic shock? e) State of imbalance between sympathetic and parasympa-
a) Acute hemorrhage thetic regulation
b) Pallor of the lower extremities
c) Raised body temperature Question 8
d) Microvascular dysfunction Which of the following is a main symptom of toxic shock
e) Bradycardia syndrome?
a) Hypertension
Question 3 b) Tremor
Which of the following is often accompanied by traumatic c) Cardiac arrhythmias
hemorrhagic shock? d) Nonreactive pupils
a) Persistent diarrhea e) Skin rash
b) Acute cholera
c) Diabetic coma Question 9
d) Polytrauma sustained in a road traffic accident Which of the following patient groups has a dispropor-
e) Cirrhosis of the liver tionately high incidence of septic shock?
a) Patients over the age of 65 who are immunosuppressed or
Question 4 have underlying malignant disease
Which of the following is a typical cause of traumatic b) Children up to the age of 10 with neuroblastoma
hypovolemic shock? c) Adolescents up to the age of 20 who are dialysis-
a) Gastrointestinal bleeding dependent
b) Ruptured aneurysm d) Pregnant women with HELPP syndrome
c) Hypothermia due to cold exposure e) Men up to the age of 60 undergoing radiation therapy for
d) Myocardial infarction prostate cancer
e) Large surface burns
Question 10
Question 5 What is the most common trigger of anaphylactic shock
Roughly how many people (including subgroups) in adults?
develop hypovolemic shock every year in Germany? a) Food products
a) 5000 b) Medical drugs
b) 15 000 c) Insect venom
c) 25 000 d) Physical effort
d) 35 000 e) Acute infection
e) 50 000
Question 6
In patients with large surface burns, which of the follow-
ing can provide an indication of the fluid replacement
needed in the first 24 hours?
a) Fick’s law of diffusion
b) Beer–Lambert law
c) Modified Brooke formula
d) HOMA Index ►Participation is possible only via the Internet:
e) PROCAM Score cme.aerzteblatt.de
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eTABLE 1
Source: www.awmf.org/leitlinien/awmf-regelwerk/ll-entwicklung/awmf-regelwerk-03-leitlinienentwicklung/
ll-entwicklung-graduierung-der-empfehlungen.html
eTABLE 2
SOFA (Sequential Organ Failure Assessment) score as a basis for defining sepsis according to the ESCIM (European
Society for Intensive Care Medicine) consensus
Points
Organ Parameter 1 2 3 4
Lung PaO2/FiO2 mmHg <400 <300 <200 <100
with respir. support with respir. support
*Catecholamine dose low = dopamine ≤ 5 or dobutamine (each dose) for at least 1 hour
moderate = dopamine >5 or epinephrine/norepinephrine ≤ 0.1 µg/kg per min
high = dopamine >15 or epinephrine/norepinephrine >0.1 µg/kg per min
Deutsches Ärzteblatt International | Dtsch Arztebl Int 2018; 115: 757–68 | Supplementary material I
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eFIGURE
Hypothalamus
Afferent Efferent
NA
RVLM
Vagus nerve
NTS
Carotid sinus
Intermediolateral
column
Sympathetic
Aortic arch fibers
Thoracic baroreceptors
“low pressure” Sympathetic Greater and lesser
receptors trunk splanchnic nerves Splanchnic
vessels
Vasoconstrictor
fibers
II Deutsches Ärzteblatt International | Dtsch Arztebl Int 2018; 115: 757–68 | Supplementary material