INTENSIVE CARE
Shock: causes, initial
assessment and
investigations
Paul Teirney
Bilal Ahmed
Alistair Nichol
Abstract
Shock may result from a number of distinct disease processes and it is
commonly associated with trauma, infection and cardiovascular
dysfunction. Shock results in significant morbidity and mortality and
is a leading cause of death in hospital patients. In order to improve pa-
tient outcomes it is important to recognize shock early, then assess and
treat the shocked patient in a systematic way. While the cause of the
shocked state is sometimes obvious, in more difficult situations the
use of the clinical classification of shock into cardiogenic, obstructive,
hypovolaemic or distributive shock can help the clinician to discover
the underlying cause of the shock. However, it is important to note
that while this is a framework in practice there if often considerable
overlap between these different types of shock in clinical practice.
After identification of patients in shock, immediate life-saving resuscita-
tion with directed therapy to prevent further deterioration, worsening
organ failure and to improve outcome is vital. An ABCDE approach
can be a useful systematic way for initial assessment and resuscitation.
Basic monitoring should be instituted as soon as possible and in severe
or unresponsive shock this should be escalated to invasive monitoring.
Immediate generic laboratory, microbiological and radiological tests
should be carried out as soon as possible and should include a
blood lactate level. Further targeted tests should then be tailored to
the history, clinical findings and presumed aetiology of the shocked
state. These targeted investigations should help to pin point the spe-
cific cause of the shock and guide definitive management.
Keywords Assessment; critically ill; sepsis; shock; treatment
Royal College of Anaesthetists CPD Matrix: 2C03
Paul Teirney MB FCARCSI is an intensive care specialist registrar at the
St Vincent University Hospital, Dublin, Ireland. Conflicts of interest:
none declared.
Bilal Ahmed MBBS FCARCSI is an intensive care specialist registrar at
the St Vincent University Hospital, Ireland. Conflicts of interest: none
declared.
Alistair Nichol BA MB BCh BAO FCARCSI FCICM FJFICMI PhD is a
Consultant Intensivist at St Vincent’s University Hospital, Dublin,
Ireland and Honorary Intensivist at the Alfred Hospital, Melbourne,
Australia; Chair of Critical Care, University College Dublin and an
Associate Professor of the Australian and New Zealand Intensive
Care-Research Centre in the School of Public Health and Preventive
Medicine, Monash University, Australia. Conflicts of interest: none
declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 18:3
Learning objectives
After reading this article, you should understand that:
C Shock is associated with significant morbidity and mortality,
which may be reduced with early recognition and appropriate
treatment
C A generic approach to assessment and treatment of the
shocked patient is essential to facilitate rapid diagnosis of the
underlying cause while providing stabilizing interventions
C A classification of shock system can provide a rapid aid mem-
oire to the most likely underlying cause and most likely effec-
tive interventions
C Targeted investigations directed towards determining the sus-
pected cause of the shock
Introduction
Shock is one of the leading causes of death in hospital patients.
Shock is commonly associated with trauma, infection and car-
diovascular dysfunction. Traumatic injury is the leading cause of
death worldwide among persons between 5 and 44 years of age.1
The most common cause of death after traumatic injury is hae-
morrhagic shock. Shock associated with severe infection, which
is also known as septic shock, has received much attention
recently due to high profile campaigns.2 The mortality rates
associated with severe sepsis are 25e30%, but the development
of shock is associated with a mortality rate up to 70%. In the
United States the treatment of patients with severe sepsis costs an
average of $2200 per case, with an annual total cost of $16.7
billion nationally.3 Cardiogenic shock complicates 7e9% of pa-
tients presenting with myocardial infarction.4 The mortality of
cardiogenic shock is high, but has come down in recent years
from 60% in 1995 to 48% in 2004.4
It is clear that shock is common and associated with signifi-
cant morbidity and mortality. In an attempt to improve outcomes
it is vital that clinicians recognize shock early, rapidly assess and
treat patients in a systematic manner.
Recognition of shock
Definition
Shock is defined as acute circulatory failure with inadequate or
inappropriately distributed tissue perfusion resulting in general-
ized cellular hypoxia.
Clinical features of shock are usually those of tissue hypo-
perfusion (see Table 1). This is most easily detected in the skin
as central pallor, peripheral cyanosis, and increased capillary
refill time. It is important to note that the traditional vital signs
are less reliable indicators of shock and shock cannot be
excluded solely on the basis of normal blood pressure (systolic
blood pressure (SBP) <90 mmHg, mean arterial pressure (MAP)
<60 mmHg) or a reduction of >40 mmHg from baseline. The
complex interplay between the sympathetic and parasympathetic
autonomic nervous system can produce pulse rates and blood
pressures that are normal, high, or low. Furthermore, in shocked
patients with end-organ hypo-perfusion, oxygen delivery to the
tissues is not always reduced, and indeed may even be increased
in some classes of shock (i.e. severe sepsis).5
118 Ó 2016 Published by Elsevier Ltd.
 INTENSIVE CARE

e.g. mitral regurgitation due to papillary muscle rupture, can also

Signs of reduced end organ perfusion lead to cardiogenic shock.
Organ system Clinical features
Distributive
Neurological C Reduced level of consciousness Distributive shock can be due to sepsis, neurogenic (spinal) or
C Encephalopathy (confusion, agitation and/ anaphylactic shock. This type of shock can also occur with an
or drowsiness) adequate or increased cardiac output.
Cardiovascular C Reduced capillary refill (>3 seconds)
C Cold peripheries General approach to a shocked patient
C Central pallor Philosophy of approach
Respiratory C Tachypnoea >20 breaths/minute The goal is to identify patients that are in shock, provide immediate
C Central and peripheral cyanosis resuscitation with the aim to prevent further deterioration and
C Desaturation (SpO2 (peripheral oxygen restore the systemic circulation to a level that meets the body’s
saturation) <90%) tissue oxygen requirements (see Table 3).6 In tandem it is vital to
Renal C Urinary output <0.5 ml/kg per hour rapidly identify the cause of shock and to perform appropriate
tailored investigations and to institute definite management.
Table 1

Clinical classification Immediate management

Clinically, it is common to subdivide shock into cardiogenic, ABCDE approach

obstructive, hypovolaemic or distributive causes. These classes The A-B-C-D-E (Airway, Breathing, Circulation, Disability and
of shock can be separated based on the main mechanism of the Exposure) principle should be applied for initial assessment and
shock (i.e. cardiogenic-pump failure) and the resulting clinical resuscitation. It is important that this process be iterative with
presentation (see Table 2). However, in practice there can be frequent reassessments of the patient’s condition and response to
considerable overlap between the different types of shock. Shock initial therapies.
can arise through a variety of mechanisms simultaneously in a
Airway management
patient. For instance, in septic shock, there may be a combina-
Consider early intubation and ventilation for severe shock if there is
tion of reduced preload from increased vascular permeability and
respiratory distress, severe hypoxaemia, pronounced acidosis, or
vasodilatation (hypovolaemic), impaired myocardial contractility
coma. Intubation ensures protection from aspiration in the presence
(cardiogenic) caused by inflammatory mediators reducing pump
of a reduced conscious level. Where agitation is attributable to ce-
function, and inappropriate distribution of blood flow to tissue
rebral hypoxia, intubation and ventilation facilitates rapid treat-
beds (distributive).
ment without precipitating further respiratory compromise.
Hypovolaemic
Management of oxygenation and ventilation
Hypovolaemic shock is usually as a result of uncontrolled hae-
Once intubated, inspired oxygen can be maximized to 100% to
morrhage, but it can be due to excessive fluid loss from the
optimize oxygen delivery to the tissues. Mechanical ventilation
gastrointestinal and urinary tracts, and even from the skin in
will reduce oxygen consumption by the respiratory muscles at a
severe burns.
time when their oxygen supply is compromised.
Obstructive
Fluid resuscitation
Obstructive shock occurs when pump failure is due to extrinsic
Conditions that are associated with actual or relative hypo-
cardiac obstruction, rather than primary myocardial pathology.
volaemia respond well to restoration of intravascular volume.
The most common and potentially reversible causes being pul-
Titration of fluid administration to heart rate, blood pressure,
monary embolus, tension pneumothorax and cardiac tamponade.
urine output, lactate concentration is a good starting point prior
Cardiogenic to invasive monitoring. However, prediction of ongoing fluid
Cardiogenic shock is the result of intrinsic myocardial disease, responsiveness by objective measures is more difficult. For this
e.g. infarction, myocarditis. However, valvular abnormalities, purpose, passive leg raise test, pulse pressure and stroke volume

Classes of shock and resulting clinical presentation

Variable measured Hypovolaemic Obstructive Cardiogenic Distributive

Blood pressure
Central venous pressure [preload]
Capillary refill time
Skin temperature

Table 2

ANAESTHESIA AND INTENSIVE CARE MEDICINE 18:3 119 Ó 2016 Published by Elsevier Ltd.
 INTENSIVE CARE
Common clinical targets in shocked patients
Variable Goal
SpO2 (%) 93
Central venous pressure (CVP) 8
self-ventilating (mmHg)
CVP non-invasive/invasive mechanical 12
ventilation (mmHg)
MAP (mmHg) 65e90
Urine output 0.5 ml/kg/hour
Table 3
variation, IVC diameter, CVP and PAOP are among the most
commonly measured parameters. In the management of septic
shock, several recent RCTs of protocolized care (early goal
directed therapy) failed to demonstrate survival benefit over
standard care. However, these results should be interpreted in
the context of the already widespread adoption of international
guidelines on the initial management of sepsis.2
The patient with acute left ventricular failure complicated by
pulmonary oedema may conversely be intravascularly deplete,
and will benefit from careful fluid administration once afterload
reduction has been achieved. Fluid resuscitation in massive
haemorrhage secondary to trauma has moved from initial
resuscitation with crystalloid/colloid solutions to greater use of
blood products. Studies performed in the military setting
demonstrated improved survival with RBC:Plasma:PLT ratios
approaching 1:1:1. These findings have since been replicated in
the hospital setting and variations of these protocols have been
incorporated into transfusion guidelines worldwide.
The particular fluid used for resuscitation should prevent further
physiological derangement as far as possible, to this end compound
sodium lactate is our preferred solution. The use of HES solutions for
resuscitation increases renal complications.6 In other circumstances
fluid therapy can be harmful. A patient with acute myocardial
infarction or a compromising arrhythmia may progress to cardio-
genic shock with left ventricular failure and pulmonary oedema,
which may be aggravated by fluid therapy. Another scenario is se-
vere shock associated with ongoing non compressible haemor-
rhage, for example, penetrating trauma to the torso or a leaking
aortic aneurysm. There is evidence that large volume resuscitation
before surgical control of haemorrhage may not be helpful.7
Inotropes/vasopressor
The goals of inotrope/vasopressor therapy are to raise cardiac
output by increasing the heart rate and stroke volume for a given
preload and to regain adequate tone in the peripheral vascular
system. The initiation of inotropic/vasopressor support during
resuscitation is indicated when shock is unresponsive to initial
fluid management. This is seen in cardiogenic shock with pre-
dominant left ventricular failure or in severe septic shock after
fluid boluses are producing no further benefit or are giving rise to
significant increases in CVP. In septic and anaphylactic shock,
inappropriate vasodilatation and low systemic vascular resistance
are the principal problems after fluid resuscitation. Adrenaline is
the drug of choice for patients with anaphylactic shock.8 Various
vasopressor agents have been used in the treatment of septic
shock, including dopamine, adrenaline, noradrenaline, and
ANAESTHESIA AND INTENSIVE CARE MEDICINE 18:3
vasopressin. There is increasing evidence that noradrenaline may
be the agent of choice for patients with severe septic shock.9
Noradrenaline has been shown to increase cardiac output, renal
blood flow, and urine output when used in septic shock. As with all
vasopressors, noradrenaline infusions must be started cautiously
and titrated to achieve an adequate mean arterial blood pressure,
typically a minimum of 60e65 mmHg.
Monitoring
Basic monitoring should be instituted (non-invasive blood pres-
sure, pulse oximetry, and continuous ECG) as soon as possible.
Severe shock or unresponsive shock to initial management should
prompt a switch to invasive monitoring such as invasive arterial
blood pressure monitoring and central venous pressure monitoring
(CVP). CVP is often used as a surrogate for myocardial preload in
uncomplicated hypovolaemic shock. While the therapeutic efficacy
of the pulmonary artery catheter (PAC) remains controversial,10 the
measurements obtained from it are undoubtedly useful in differ-
entiating between the four major types of shock (see Table 2).
Intrathoracic blood volume, an alternative measure of cardiac
preload, offers theoretical advantages particularly in mechanically
ventilated patients, and is obtained using either double (COLD) or
single (PiCCO) indicator dilution.11,12 More recently, non-invasive
cardiac output monitoring using pulse contour analysis, thoracic
bioimpedance and bioreactance have been developed.
Immediate generic tests
 Laboratory tests such as full blood count, coagulation
profile, electrolytes, urea and creatinine, arterial blood gas,
lactate, and group and crossmatch should be sent imme-
diately. Blood lactate is elevated in all forms of shock and
indicates the presence of tissue hypoxia. The degree to
which it is elevated corresponds to the severity of the
shock and it is frequently used as a surrogate guide to the
effectiveness of therapeutic interventions.13
 Chest X ray e Allows for the assessment of acute pulmo-
nary (i.e. pneumonia etc) and extra-pulmonary (e.g.
pneumothorax or haemothorax) causes of shock. In the
context of trauma a C-spine and pelvic X-ray should also
be ordered immediately.
 ECG e Rapid assessment of dysrhythmias (i.e. tachy or
bradycardia), evidence of ischemia/infarct (ST elevation or
depression) or pulmonary embolism (rarely pathognomonic).
 ICU bedside sonography e Bedside ICU clinician performed
rapid assessment is become a more common tool in the
early rapid assessment of all potential types of shock.
Focused assessment using sonography in trauma (FAST) is
a rapid, non-invasive, bedside test with high sensitivity for
detecting haemoperitoneum. Extended FAST (eFAST) is
now being used to detect pneumothorax/haemothorax and
haemopericardium. It is a powerful tool when employed in
this setting and can be used to guide response to in-
terventions (i.e. fluid administration etc)
Targeted tests
These tests should be targeted to the specific cause of shock.
History, presenting symptoms and physical examination (Table
2) will point towards the probable cause. Investigations should
be tailored to the history and clinical findings.
120 Ó 2016 Published by Elsevier Ltd.
 INTENSIVE CARE
Hypovolaemic shock: hypovolaemic shock, due to concealed
haemorrhage, may require further invasive and radiological in-
vestigations such as diagnostic peritoneal lavage, FAST scan, or
CT scanning. When hypovolaemia is due to excessive gastroin-
testinal or renal losses, electrolyte disturbances can be severe,
and urea and creatinine are often markedly elevated. Haemo-
concentration may also be noted. Further investigations will
depend upon the likely pathology, but may include supine and
erect abdominal X-rays in bowel obstruction.
Obstructive shock: where the history and preliminary findings
raise the suspicion of pulmonary embolus, confirmatory tests
include spiral computed tomography (CT) and pulmonary angi-
ography. In obstructive shock echocardiography is important, as
it will give us useful information regarding cardiac tamponade or
massive pulmonary embolus.
Cardiogenic shock: in cardiogenic shock echocardiography is
invaluable, since it provides an objective measure of ventricular
function, can identify and quantify abnormalities of regional wall
motion and valvular function, and excludes cardiac tamponade
or massive pulmonary embolus.
Distributive shock: distributive shock in the critically ill is
frequently secondary to sepsis. Septic shock can lead to a rise or fall
in the white cell count. Best practice dictates that blood and other
relevant cultures are taken prior to initiating antibiotic therapy,
provided this does not result in a delay in the administration of
antibiotics. Computed tomography (CT) scans of brain, thorax,
abdomen and pelvis might be required to identify the source of
sepsis or any potential septic collection that is amenable to radio-
logical or surgical drainage (i.e. see Figure 1). CT is more often
performed to assist in the evaluation of a patient with suspected
infection in almost any location in the body. A CT scan with oral and
intravenous contrast can reliably identify an intra-abdominal
source of infection. The CT scan is the procedure of choice for the
identification of intra-abdominal conditions such as abscess,
Figure 1 CT thorax of acute respiratory distress syndrome with bilat-
eral pleural effusions and bibasal bilateral infiltrates.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 18:3
inflammatory bowel disease, pseudomembranous colitis, fistula
formation, perforation, mesenteric pathology, and sinus tracts If CT
scans are inconclusive then MRI scan might be required in some
cases such as osteomyelitis, prosthetic joint infection etc. Abdom-
inal ultrasound in acute cholecystitis and serum amylase/lipase and
abdominal CT scan in pancreatitis are useful.
Summary
Patients who are shocked are at high risk of death. It is imper-
ative that clinicians remain observant for the clinical signs of
shock and end organ dysfunction. Once identified, rapid assess-
ment, treatment and initial stabilization should occur while the
most likely source of shock identified and targeted investigations
and treatments then provided. A
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121 Ó 2016 Published by Elsevier Ltd.