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com
17

REVIEW

Critical care in the emergency department: shock and

circulatory support
C A Graham, T R J Parke
...............................................................................................................................

Emerg Med J 2005;22:1721. doi: 10.1136/emj.2003.012450

Effective resuscitation includes the rapid identification and will produce organ failure and, in the context of
global hypoperfusion, multiple organ failure
correction of an inadequate circulation. Shock is said to be ensues. The aim of resuscitation is to prevent
present when systemic hypoperfusion results in severe shock worsening and to restore the circulation to
dysfunction of the vital organs. The finding of normal a level that meets the bodys tissue oxygen
requirements.
haemodynamic parameters, for example blood pressure, Shock can arise through a variety of mechan-
does not exclude shock in itself. This paper reviews the isms. Pump failure may be attributable to
pathophysiology, resuscitation, and continuing inadequate preload (for example, severe bleed-
ing), myocardial failure, or excessive afterload.
management of the patient presenting with shock to the Shock can also occur with an adequate or
emergency department. increased cardiac output as seen in distributive
........................................................................... shock (for example, septic or anaphylactic
shock). Vital tissues remain ischaemic as much
of the cardiac output is distributed inappropri-
ately through vascular beds.
The mechanisms producing shock may also be
CLINICAL SCENARIO very complex involving combinations of these
A 61 year old man is admitted to the resuscita- factors. For example, in septic shock, there may
tion room with shortness of breath. He has a be reduced preload from increased vascular
medical history of ischaemic heart disease permeability and venodilatation, impaired myo-
treated with quadruple coronary artery bypass cardial contractility caused by inflammatory
grafting five years ago. He has been unwell for mediators, and tissue hypoxia from inappropri-
the past 48 hours with a productive cough, ate distribution of blood flow.
lethargy, and fever. Compensatory mechanisms are activated in
Vital signs on arrival include temperature of response to tissue hypoperfusion. Acutely, the
35.2C, respiratory rate 40/min, pulse 130 beats/ adrenergic autonomic nervous system is acti-
min, non-invasive blood pressure 70/40 mm Hg, vated. Venoconstriction increases the preload to
and oxygen saturation of 90% on 15 l/min face the heart; vasoconstriction of all non-essential
mask oxygen using a non-rebreather bag. He is arterial beds sustains arterial blood pressure and
poorly perfused, cold, and shut down. Initial myocardial contractility is maximised. This
blood gas analysis shows a mixed respiratory and response attempts to optimise cardiac output
metabolic acidosis. and maintain an adequate perfusion pressure to
the coronary arteries and brain. Thus, the early
Questions stages of uncomplicated shock are characterised
N Is this patient suffering from shock? by tachycardia and a comparatively normal blood
N What is the pathophysiology of the shock
process?
pressure.
Further compensatory neuroendocrine mech-
N What should the initial management in the
first 15 minutes be for this patient?
anisms are activated in the kidney. This delayed
effect consists of rennin-angiotensin-aldosterone
mediated renal retention of salt and water to
further maximise preload and improve cardiac
PHYSIOLOGY output.
Shock is defined as acute circulatory failure with Hypotension occurs once the compensatory
inadequate or inappropriately distributed tissue mechanisms have been overwhelmed, or the
See end of article for perfusion resulting in generalised cellular autonomic nervous system is unable to respond
authors affiliations
....................... hypoxia. Circulating blood must meet the tissues effectively. Reasons for this include advanced
metabolic requirements rather than achieve set age, concurrent medication (for example b block),
Correspondence to: haemodynamic variables (for example, a normal autonomic neuropathy, or adrenal insufficiency.
Dr T R J Parke, Accident
and Emergency blood pressure). The presence of shock is best In profound shock other autonomic mechan-
Department, Southern detected by looking for evidence of compromised isms, primarily vagal, may come into play. In the
General Hospital, end organ perfusion. presence of low cardiac filling pressures in severe
Glasgow G51 4TF, UK; In early shock a switch from aerobic to hypovolaemia, the tachycardia response to shock
tim.parke@sgh.scot.nhs.uk
anaerobic metabolism compensates temporarily.
Accepted for publication Lactate accumulates as a result of this anaerobic Abbreviations: ED, emergency department; IV,
8 April 2004 metabolism. Hypoxia eventually causes cellular intravenous; ECG, electrocardiography; CVP, central
....................... and then tissue necrosis. Loss of sufficient tissue venous pressure

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18 Graham, Parke

may be replaced with a reflex bradycardia. As shock INITIAL MANAGEMENT OF THE CIRCULATION
progresses, cells in ischaemic tissues switch to anaerobic Is a fluid challenge indicated?
metabolism and lactic acidosis stimulates compensatory This can be a difficult decision to make on clinical grounds
hyperventilation. and often depends on the context in which the patient has
Identification and treatment of shock in the emergency presented. Conditions that are associated with actual or
department is based on sound knowledge of these physiolo- relative hypovolaemia respond well to restoration of vascular
gical principles. volume. Such conditions should be identified early. Blood
loss can be assumed to be the cause of shock after trauma, at
CLINICAL FEATURES OF SHOCK least initially, while a search is carried out for haemorrhage
Clinical features of acute circulatory failure are usually those into the chest, pelvis, abdomen, or externally.
of tissue hypoperfusion. This is most easily detected in the In conditions such as diabetic ketoacidosis, bowel obstruc-
skin as central pallor, peripheral cyanosis, and sluggish tion, or severe diarrhoea and vomiting, it is reasonable to
capillary return. Other clinical evidence could include a raised assume initially that salt and water depletion have caused
respiratory rate, confusion, or coma. Renal hypoperfusion is hypovolaemic shock.
indicated by a diminished urine output. Cardiac ischaemia If it is clear that shock has been caused by hypovolaemia,
may be manifest on electrocardiographic monitoring. Arterial IV fluids should be started. Patients should receive an initial
blood gas analysis may show a metabolic (lactic) acidosis. bolus of one to two litres of IV fluid rapidly and be reassessed.
The traditional vital signs are less reliable indicators of The choice of fluid remains controversial, but crystalloids,
shock. The interplay between the sympathetic and para- particularly Ringers lactate, have become widely supported.1
sympathetic autonomic nervous system can produce pulse There is no place for inotropes in the management of severe
rates and blood pressures that are normal, high, or low. hypovolaemia unless the patient is in established cardiac
Shock cannot be excluded solely on the basis of normal vital arrest, as they may precipitate severe arrhythmias that may in
signs. turn worsen the shock state.
Blood sugar measurement can identify patients with shock In other circumstances fluid therapy can be harmful. A
secondary to hyperglycaemia (diabetic ketoacidosis and patient with acute myocardial infarction or compromising
hyperosmolar states) and with hypoglycaemia, which may arrhythmia may progress to cardiogenic shock with left
resemble shock clinically. ventricular failure and pulmonary oedema. Such patients
may be identified by a previous cardiac history, recent chest
pain, or ECG changes together with the clinical and
INITIAL MANAGEMENT OF SHOCK IN THE radiological signs of acute pulmonary oedema. Additional
EMERGENCY DEPARTMENT fluid loading in these patients may increase an already
Ideally, patients suffering from shock are identified at triage increased left ventricular end diastolic pressure and worsen
and transferred to the resuscitation room. All patients should pulmonary oedema with no useful gain in terms of cardiac
be given high flow oxygen, have intravenous (IV) access output. This is attributable to the flat nature of the Starling
secured, and have basic monitoring instituted (non-invasive curve in the failing heart. Initial mangement in these
blood pressure, pulse oximetry, and continuous ECG). circumstances is targeted at immediate treatment of any
arrhythmia and early inotropic support, together with
MANAGEMENT OF AIRWAY AND BREATHING aggressive management of pulmonary oedema.
Does the patient require intubation and ventilation? A second scenario in which fluids may be harmful is
Consider early intubation and ventilation for severe shock if where there is severe shock associated with ongoing non-
there is respiratory distress, severe hypoxaemia, pronounced compressible haemorrhage, for example, penetrating trauma
acidosis, or coma. Intubation ensures protection from to the torso or a leaking aortic aneurysm. There is evidence
aspiration in the presence of a reduced conscious level. that large volume resuscitation before surgical control of
Where agitation is attributable to cerebral hypoxia, intuba- haemorrhage is harmful2 and these patients should be treated
tion and ventilation permits rapid treatment without using the principles of hypotensive resuscitation. This
precipitating further respiratory compromise. Inspired oxy- approach has been shown to lead to fewer complications
gen can be maximised to 100% to optimise oxygen delivery to such as dilutional coagulopathy, hypothermia, and post-
the tissues. Finally, the increased work of breathing with its operative adult respiratory distress syndrome.2
resultant oxygen requirements is removed. It entails giving minimal, ideally no, IV fluid to the patient
Profoundly shocked patients, particularly with severe until they are in the operating room and at the point of
acidosis or impaired conscious level, should be intubated surgical control of haemorrhage. Enough fluid is given to
and ventilated within 15 minutes of arrival in the resuscita- maintain consciousness (brain perfusion). Blood is the
tion room. Senior anaesthetic and intensive care input should colloid of choice if significant blood loss is suspected.
be sought at an early stage. Induction carries particular risks Hypotensive resuscitation is not recommended, however in
in the presence of severe shock, with a significant chance of the context of blunt multiple trauma and where there is
precipitating profound circulatory collapse through the evidence of serious head injury, a systolic pressure of at least
myocardial depressant effects and vasodilating properties of 90 mm Hg must be maintained.3 4
many induction agents.
A rapid sequence intubation technique is required using Should we give a fluid bolus in shock of uncertain
comparatively cardio-stable agents such as etomidate or aetiology?
ketamine. Modified doses will be needed, particularly in the If anaphylactic shock is suspected (rash, wheeze, allergen
presence of hypotension. Pre-loading the circulation with IV exposure), then fluid therapy is appropriate along with
fluids to correct hypovolaemia may be necessary, and the use intramuscular adrenaline (epinephrine).57 Similarly, if septic
of pressor agents may be urgently required. Low tidal shock is suspected (petechial rash, high fever, presence of
volumes and peak inspiratory pressures should be the aim infective source, rigid abdomen), then fluids should be
immediately after intubation to prevent the reduction in given.8 9 In addition to maldistribution, septic shock also
venous return that is associated with positive pressure has a large hypovolaemic component because of the extra-
ventilation. vasation of plasma through the leaking vasculature.8 9

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Shock in the emergency department 19

Occasionally a patient will present with shock with no show an increasing metabolic acidosis, then any earlier
immediate obvious precipitant. The usual causes are occult decision not to ventilate may need urgent review.
haemorrhage (such as upper gastrointestinal haemorrhage If the circulation is still inadequate and there is clinical
without haemetemesis or melaena or concealed obstetric/ evidence of shock, it is desirable at this stage to assess the
gynaecological blood loss), hidden sepsis (silent intraperito- degree of filling of the venous circulation by using a central
neal perforation, early meningococcaemia, or toxic shock venous pressure (CVP) monitored fluid challenge.
syndrome), or a silent cardiovascular event (pulmonary The response of the CVP to a fluid challenge, 250 ml of IV
embolus, myocardial infarction). crystalloid given over two minutes, gives an indication of the
Most of these conditions, including myocardial infarction compliance of the venous system. If the system remains
without left ventricular failure, will be improved by a fluid highly compliant (minimal rise in pressure with further
challenge. fluid), then further fluid boluses may continue to increase
A fluid challenge, usually 250 ml of crystalloid solution via the cardiac output depending on the Starling curve of the
a wide bore cannula over two minutes, should be given in the right ventricle at that time. If the right heart is becoming
first instance. The response to this fluid challenge should be non-compliant (that is, significant rise in pressure, greater
noted and if the patient seems to improve (blood pressure up, than 3 mm Hg) with further fluid, it suggests that the
heart rate down, peripheral perfusion improved), then fluid systemic venous system is full and that further fluid will
loss should be assumed and further fluid should be given. simply overload the right ventricle.
It must be remembered that the CVP does not measure the
CASE PROGRESSION filling pressures on the left side of the heart. This filling
The patient in the resuscitation room is struggling for breath pressure has a greater influence on cardiac output and the
and is obviously tired. He is given a 250 ml crystalloid fluid formation of pulmonary oedema in overload states. This
challenge over two minutes with a slight improvement in means that CVP monitoring can be misleading. For example,
blood pressure, to 90/50 mm Hg, but no change in heart rate in pulmonary embolism the CVP may be high and show a rise
or respiratory rate. His peripheral perfusion has improved a in response to fluid challenge because of outflow obstruction
little. of the right ventricle. Any attempts to treat fluid overload
A decision is made to proceed with intubation and (for example, diuretics) would be ineffective and possibly
ventilation, and he undergoes rapid sequence intubation dangerous.
using etomidate, fentanyl, and suxamethonium. He is Conversely, in a patient with an extensive anterior
sedated with low dose infusions of morphine and midazolam, myocardial infarction, comparatively normal right ventricular
paralysed, and ventilated with low tidal volumes. Haemo- function may occur with a severely impaired left ventricle.
dynamically he tolerates this reasonably well. Further IV The CVP may be low and show a minimal rise in response to a
fluids are given and a urinary catheter is inserted to assess fluid challenge. The left ventricular filling pressures may
ongoing urine output. however be high and further injudicious fluid administration
Invasive haemodynamic monitoring is started, consisting risks the formation of pulmonary oedema.
of a radial arterial line and a triple lumen right internal Despite this, CVP monitoring is simple and ideally used
jugular central venous catheter. Despite 2.5 litres of IV early in the ED setting. Transducer based continuous
crystalloid, his invasive arterial blood pressure remains at monitoring is mandatory; manometer systems are inaccurate
85/45 mm Hg and there is clinical evidence of peripheral shut and cannot be recommended. It is good practice to continue
down. His urine output is 10 ml in the first hour. using CVP guided fluid challenges for as long as a clinical
Chest radiography in the resuscitation room shows a right response is elicited or until the CVP begins to rise. At this
lower lobe pneumonia and no evidence of pulmonary stage, if the patient remains shocked then inotrope therapy
oedema. A 12 lead ECG shows a sinus tachycardia, Q waves should be considered.
in leads V2, V3, and V4, but no acute changes. In addition to monitoring the CVP, unresponsive shock
should prompt a switch to invasive arterial blood pressure
Questions monitoring.8 Non-invasive monitoring is inaccurate at low
N Would you give him further fluid? pressures and is not sufficiently responsive to guide the
N Is it time to start inotropes? If so, which inotropes? minute by minute changes of complex shock management.
N What other treatments might you consider? Furthermore, whether the patient is ventilated or not by this
stage, frequent repeated measurements of blood gas pres-
N Where does this man need to be transferred to? sures will be necessary. It is recommended that the invasive
pressures together with continuous ECG monitoring and
SECONDARY MANAGEMENT pulse oximetry are all displayed on one monitor screen
Many patients will respond to high flow oxygen and IV fluid simultaneously to permit the integration of all available
therapy and peripheral perfusion will improve. Signs of an information.
adequate response to treatment include an improving
conscious level, warm peripheries, and reasonable urine INOTROPES
output (.1 ml/kg/h). Under these circumstances a diagnosis The initiation of inotropic support in the resuscitation room is
should be sought and the patient should be referred indicated where shock with or without hypotension is
appropriately. There is evidence that patients presenting with unresponsive to fluid management. This is seen in cardio-
haemodynamic instability after trauma have a better out- genic shock with predominant left ventricular failure or in
come if managed in a critical care setting after discharge from severe septic shock after CVP guided fluid boluses are
the ED.10 The same criteria should apply to septic patients producing no further benefit or are giving rise to significant
who should be managed in a high dependency area. increases in CVP. Inotropes may also be required in the post-
cardiac arrest setting and in anaphylactic or neurogenic
POOR RESPONSE TO INITIAL TREATMENT shock that is resistant to fluid therapy.
In severe or ongoing hypovolaemic shock, and in advanced The goals of inotrope therapy are to raise cardiac output by
septic shock, initial management may make little or no increasing the heart rate and stroke volume for a given
difference. If the patients conscious level is deteriorating, preload and to exert an appropriate effect on the peripheral
haemodynamic parameters worsening, or blood pressures vascular system. In cardiogenic shock, where the adrenergic

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20 Graham, Parke

compensatory mechanisms are usually fully activated and flutter, may require cardioversion if there is haemodynamic
systemic vascular resistance is usually high, the use of compromise.
inotropes may increase the afterload on the failing left Pulmonary embolism and cardiac tamponade are often
ventricle. This must be weighed against the need to maintain suspected when shock is resistant to IV fluid therapy and a
an acceptable mean arterial pressure to permit adequate high CVP is found. Both conditions can be conveniently
perfusion of the brain, kidneys, and the heart itself. differentiated in the resuscitation room by emergency ECG
Furthermore, in an ischaemic failing myocardium, the cost and specific treatment can then be started.
of using inotropes is increased myocardial oxygen consump- Tension pneumothorax should be identified during the
tion and further ischaemia, particularly if the inotrope primary assessment of breathing in shock patients, but
produces a pronounced tachycardia.8 should be remembered as an important cause of severe
Dobutamine has positive inotropic and chronotropic circulatory collapse. It may occur immediately after the
effects, together with a useful degree of vasodilatation.8 initiation of mechanical ventilation or shortly after an
Consequently, in severe cardiogenic shock with pulmonary attempt at central venous cannulation.
oedema and an adequate systolic blood pressure (.90 mm Patients with septic shock should be given early and
Hg), it is the agent of choice. It must be introduced slowly to adequate antibiotics in the resuscitation room.15 Adequate
avoid tachycardia and arrhythmias. In the presence of an treatment of sepsis may require urgent surgical intervention
inadequate preload it also commonly causes hypotension. to drain abscesses or exteriorise perforated bowel. A brief
If hypotension is prominent, especially in the post-arrest period of active resuscitation before emergency surgery may
situation, adrenaline may be a more appropriate agent.8 be beneficial.1 16
Despite the hazards of increasing myocardial work, the In the absence of any obvious hypovolaemic, cardiac, septic
perfusion of critical organs must be maintained acutely. or anaphylactic cause for shock, more unusual causes should
In septic and anaphylactic shock, inappropriate vasodilata- be considered. Shock that is resistant to fluid and inotrope
tion and low systemic vascular resistance are the principal therapy may be attributable to an addisonian crisis. If this is a
problems after fluid resuscitation.8 Adrenaline is the drug of possibility a bolus of IV hydrocortisone should be given
choice for patients with anaphylactic shock.7 Various promptly after taking a venous blood sample for random
vasopressor agents have been used in the treatment of septic cortisol concentrations.
shock, including dopamine, adrenaline, noradrenaline, and Certain toxins may also provoke cardiovascular collapse
vasopressin.8 but in general the treatment is supportive and cardiovascular
There is increasing evidence that noradrenaline may be the management should proceed along similar lines as for sepsis.
agent of choice for patients with severe septic shock.11 Shock in otherwise fit young women should prompt
Noradrenaline has been shown to increase cardiac output, consideration of a diagnosis of toxic shock syndrome and
renal blood flow, and urine output when used in septic initial investigation should include a digital vaginal and
shock.8 As with all inotropes, noradrenaline infusions must speculum examination.
be started cautiously and titrated to achieve an adequate
mean arterial blood pressure, typically .65 mm Hg. SUMMARY
Inotropes should be given via a dedicated lumen through a Shock is defined by critical tissue hypoperfusion. It must be
central venous line.8 It is very difficult to titrate doses rapidly reversed before organ damage is sustained and
accurately unless continuous intra-arterial blood pressure irreversible. Treatment should therefore begin in the resusci-
monitoring has been established. Any patient requiring tation room of the ED and should consist of oxygen therapy
inotropes for circulatory support in the ED should be with or without ventilatory support and a rapid appraisal of
definitively managed in an intensive care setting.8 the likely causes. Patients with exsanguinating haemorrhage
Transfer to the intensive care unit should be carried out from penetrating torso trauma or ruptured abdominal aortic
with full portable monitoring. It may be more appropriate in aneurysms should be transferred to the operating room for
certain circumstances to transfer patients directly to the definitive management using hypotensive resuscitation.
operating room, endoscopy suite, or cardiac catheterisation In all other shock states, except cardiogenic shock with left
laboratory for definitive management before intensive care ventricular failure, intravenous fluids are indicated. Unless
unit admission. this normalises the patients condition, more invasive
There is some evidence from a single centre study in the US investigation and treatment should be started promptly.
that early goal directed therapy in the ED management of This should consist of invasive haemodynamic monitoring
severe sepsis may improve outcome, and this may influence and repeated IV fluid challenges with CVP guidance.
the way that patients with septic shock are treated in the ED In shock states unresponsive to intravascular fluid expan-
in the future.1 sion, or in cardiogenic shock where fluid challenges may be
hazardous, inotrope therapy is required. The choice of
SPECIFIC TREATMENT OF CAUSES OF SHOCK inotrope should be guided by the nature of the problem
Shock is clearly not a diagnosis in itself. The aetiology of and the haemodynamic parameters in individual cases. In all
shock should be sought aggressively while the primary and shock states reversible factors should be rapidly sought and
secondary management is carried out to protect and increase corrected.
tissue perfusion. Some treatable causes of shock are worthy Patients admitted to the ED with all but the most simply
of particular mention. Hypovolaemia attributable to haemor- managed forms of shock should be transferred to a critical
rhage that is continuing requires early definitive surgical care area once stabilised.
management, particularly in trauma.2 1214 Ongoing blood loss
is usually detected by the failure of fluid boluses to improve QUESTIONS
the clinical picture in the face of falling or static CVP [Answers in the text]
measurement.
Arrhythmias when present should be considered as N What is the definition and clinical features of shock?
potentially contributing to or causing low cardiac output.
Bradyarrhythmias may require treatment with atropine or
N What are the hazards of intubation and ventilation in
shocked patients and what steps can be taken to minimise
pacing. Tachyarrhythmias, typically atrial fibrillation or them?

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Shock in the emergency department 21

N Explain the utility of a fluid challenge in patients with

shock of unclear aetiology.
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We thank Mr Malcolm Gordon, Dr Phil Munro, and Dr Joan Barber 13 Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage
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..................... 14 Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring of hemorrhagic
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C A Graham, T R J Parke, Accident and Emergency Department, 15 Kollef MH, Sherman G, Ward S, et al. Inadequate antimicrobial treatment of
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Critical care in the emergency department:

shock and circulatory support
C A Graham and T R J Parke

Emerg Med J 2005 22: 17-21

doi: 10.1136/emj.2003.012450

Updated information and services can be found at:

http://emj.bmj.com/content/22/1/17

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