C U I D A D O S C R I T I C O S Y E M E R G E N C I A
27
175 8 Critical care and emergency medicine D.F. TREACHER I.S. GRANT Clinical examination of the critically ill patient 176 Provision of critical care 178 Organisation of critical care 178 Critical care ‘outreach’ 178 Admission guidelines 178 Transport of the critically ill patient 179 Monitoring 179 General principles 179 Monitoring the circulation 179 Monitoring respiratory function 182 Physiology of the critically ill patient 182 Oxygen transport 182 Oxyhaemoglobin dissociation curve 184 Oxygen consumption 184 Relationship between oxygen consumption and delivery 184 Pathophysiology of the inflammatory response 185 Presenting problems in critical illness 186 Circulatory failure: ‘shock’ 186 Respiratory failure including ARDS 187 Renal failure 189 Neurological failure (coma) 189 Sepsis 189 Disseminated intravascular coagulation (DIC) 190 General principles of critical care management 190 Management of major organ failure 191 Circulatory support 191 Respiratory support 193 Renal support 197 Gastrointestinal and hepatic support 197 Neurological support 198 Management of sepsis 199 Discharge from intensive care 200 Withdrawal of care 200 Brain death 200 Scoring systems in critical care 200 Costs of intensive care 201 Outcome from critical care 201
C U I D A D O S C R I T I C O S Y E M E R G E N C I A
1. 8 D.F. TREACHER I.S. GRANT Critical care and emergency
medicine Clinical examination of the critically ill Presenting
problems in Discharge from intensive care 200 patient 176 critical
illness 186 Withdrawal of care 200 Circulatory failure: shock 186
Brain death 200 Provision of critical care 178 Respiratory failure
including Organisation of critical care 178 Scoring systems in
critical care 200 ARDS 187 Critical care outreach 178 Renal failure
189 Costs of intensive care 201 Admission guidelines 178
Neurological failure (coma) 189 Transport of the critically ill
Outcome from critical care 201 Sepsis 189 patient 179 Disseminated
intravascular Monitoring 179 coagulation (DIC) 190 General
principles 179 General principles of critical care Monitoring the
circulation 179 management 190 Monitoring respiratory function 182
Management of major organ Physiology of the critically ill failure
191 patient 182 Circulatory support 191 Oxygen transport 182
Respiratory support 193 Oxyhaemoglobin dissociation Renal support
197 curve 184 Gastrointestinal and hepatic Oxygen consumption 184
support 197 Relationship between oxygen Neurological support 198
consumption and delivery 184 Management of sepsis 199
Pathophysiology of the inflammatory response 185 175
2. CRITICAL CARE AND EMERGENCY MEDICINE CLINICAL EXAMINATION OF
THE CRITICALLY ILL PATIENT 1 Initial assessment 2 Immediate
management A irway Airway: ? Clear Support, ? Intubate Breathing:
Oxygen B reathing Continuous positive airway 8 Distress pressure
(CPAP), non-invasive Rate ventilation (NIV) Chest movement Intubate
and ventilate Auscultation Circulation: Venous access Fluids C
irculation Vasoactive drugs Pulse: Rate Rhythm 3 Monitoring Volume
Heart rate; ECG Blood pressure: Respiratory rate; Sp O2 Direct
arterial BP arterial line pressure Temperature GCS; pupil size,
reaction Peripheral perfusion: Urine output Peripheral pulses
Central venous pressure Temperature Colour Capillary refill 4
Initial investigations D isability Full blood count Conscious
level: Urea and electrolytes Glasgow Coma Scale Creatinine Pupil
responses Glucose Localising signs Arterial blood gas lactate
Coagulation Cultures: blood, urine, sputum Chest X-ray ECG
Recognising the critically ill patient Cardiovascular signs
Respiratory signs Neurological signs Cardiac arrest Threatened or
obstructed airway Threatened or obstructed airway Pulse rate <
40 or > 140 bpm Stridor, intercostal recession Absent gag or
cough reflex Systolic blood pressure Respiratory arrest Failure to
maintain normal PaO2 (BP) < 100 mmHg Respiratory rate < 8 or
> 35/min and PaCO2 Tissue hypoxia Respiratory distress: use of
Failure to obey commands Poor peripheral perfusion accessory
muscles; unable to Glasgow Coma Scale Metabolic acidosis speak in
complete sentences (GCS) < 10 Hyperlactataemia SpO2 < 90% on
high-flow O2 Sudden fall in level of consciousness Poor response to
volume Rising PaCO2 > 8 kPa (> 60 mmHg), (GCS fall > 2
points) resuscitation or > 2 kPa (> 15 mmHg) above Repeated
or prolonged seizures Oliguria: < 0.5 ml/kg/hr normal with
acidosis (check urea, creatinine, K+) 176
3. C L I N I C A L E X A M I N AT I O N O F T H E C R I T I C A
L LY I L L PAT I E N T Monitor displaying blood pressure/
Intravenous fluids right atrial pressure/heart rate/Sp O2 Infusion
Nitric pumps oxide cylinder 8 Intra-aortic Pacemaker Ventilator
Haemofiltration balloon pump (behind machine haemofiltration
machine) A patient with multi-organ failure supported by
haemodynamic monitoring, cardiac pacing, a counterpulsation aortic
balloon pump, haemofiltration and nitric oxide therapy. Shock
Multi-organ failure Central nervous system Sweating Confusion Coma
Reduced conscious level Intracerebral bleeding Confused,
unresponsive Acute respiratory distress syndrome Tachypnoea
Myocardial depression Liver failure with hyperbilirubinaemia
Hypotension Gastrointestinal tract Ileus Mucosal damage Tachycardia
with Haemorrhage low-volume pulse Endotoxin leak to portal vein
Disseminated intravascular coagulation Bleeding from vessel
puncture sites Cold cyanosed peripheries Skin Haemorrhages and
infarcts secondary to disseminated intravascular coagulation Poor
urine output Meningococcal sepsis: rash Ischaemia, gangrene
secondary to decreased flow and intravascular coagulation Some
features of shock. 177
4. CRITICAL CARE AND EMERGENCY MEDICINE A critically ill
patient is one at imminent risk of death; the teams (PARTs). In
some hospitals the medical emergency severity of illness must be
recognised early and appropriate team may be the cardiac arrest
team but with a wider measures taken promptly to assess, diagnose
and manage remit, while in others this service is provided by the
ICU or the illness. HDU team. The approach required in managing the
critically ill Criteria that identify deranged physiology (p. 176)
are patient differs from that required in less severely ill
patients used to alert the ward nursing and junior medical staff to
with immediate resuscitation and stabilisation of the impending
problems so that they can summon the outreach patients condition
taking precedence: team to assess the patient, institute initial
resuscitation and Priorities are: supervise transfer to ICU or HDU
as appropriate. prompt resuscitation, adhering to advanced life
support guidelines (p. 556) and the principles of ADMISSION
GUIDELINES cardiorespiratory management explained in this chapter 8
urgent treatment of life-threatening emergencies such as Rigid
rules to determine admission to ICU/HDU are hypotension,
hypoxaemia, hyperkalaemia, destined to fail because every case must
be evaluated on its hypoglycaemia and dysrhythmias own merits.
Nevertheless, broad guidelines are required analysis of the
deranged physiology to avoid unnecessary suffering and the waste of
valuable establishing the complete diagnosis in stages as further
resources caused by admitting patients who have nothing to history
and the results of investigations become available gain from
intensive care because they either are too well or careful
monitoring of the patients condition and have no realistic prospect
of recovery. The existence of an response to treatment. empty bed
does not justify admission. The guiding principle when considering
ICU/HDU admission should be the timely use of this resource in
patients who have a realistic PROVISION OF CRITICAL CARE prospect
of recovering to achieve a quality of life that they would value.
Patients who do warrant admission should ORGANISATION OF CRITICAL
CARE be identied early and admitted without delay since this
improves survival and reduces the length of stay on the ICU.
Critical care embraces both intensive care and high- The wishes of
the patient, if known, should be respected and dependency care.
Intensive care units (ICUs) are for the whatever decision is made
should be carefully explained to care of very ill patients with
potential or established organ the patients family. failure.
Initially established for the provision of mechanical If the
appropriateness of admission remains uncertain, ventilation for
patients with respiratory failure, ICUs now as may occur in the
A&E department when little history is monitor and support all
the major organ systems. High- available, the patient should be
given the benet of the doubt dependency care provides an
intermediate level of care at a and the indication for continued
active treatment reviewed point between intensive care and general
ward care; it is as further information becomes available (Box
8.1). appropriate both for patients who have had major surgery
There is now evidence that for patients undergoing and for those
with single-organ failure. Ideally the ICU high-risk elective or
emergency surgery the mortality, should be adjacent to the
high-dependency unit (HDU), morbidity and both ICU and hospital
length of stay are allowing the critical care medical team to
manage a reduced by pre-operative admission to ICU/HDU to combined
critical care department. improve cardiorespiratory status
(pre-optimisation). Such The intensive care specialist
(intensivist) should provide a patients are often elderly with
cardiorespiratory disease and holistic approach that coordinates
expert opinions from poor physiological reserve, and benet from a
protocol of other specialties (surgeons, physicians,
microbiologists) to intensive perioperative care. At present many
hospitals have produce an integrated plan of management that
recognises major problems in implementing this strategy due to a
the priorities in the treatment of multiple organ failure. shortage
of critical care beds. Specic indications for admission to ICU and
HDU are given in Box 8.2. CRITICAL CARE OUTREACH Critically ill
patients can be found throughout the hospital, in post-operative
recovery areas, coronary care units, the acute medical and surgical
wards and accident and 8.1 FACTORS IN THE ASSESSMENT OF A POSSIBLE
ICU ADMISSION emergency (A&E) departments. The purpose of
outreach is to achieve earlier identication of these patients so
that Primary diagnosis and other active medical problems assessment
and, if appropriate, transfer to ICU/HDU is Prognosis of underlying
condition Severity of physiological disturbanceis recovery still
possible? arranged before deterioration occurs to the point of Life
expectancy and anticipated quality of life post-discharge imminent
or actual cardiorespiratory arrest. Prompt Wishes of the patient
and/or relatives identication and treatment may even avert the need
for Availability of the required treatment/technology admission to
ICU/HDU. Many hospitals are now setting up N.B. Age alone should
not be a contraindication to admission. 178 medical emergency teams
or outreach/patient at risk
5. MONITORING 8.2 ADMISSION CRITERIA FOR ICU AND HDU attaching
each patient to a battery of alarming machines (p. 177). Much of
the bedside nurses time is spent observing, recording and reacting
to the information displayed by these Admission to ICU monitors,
particularly the electrocardiogram (ECG), CVP, Patients requiring
or likely to require endotracheal intubation and arterial blood
pressure (BP), temperature and ventilator invasive mechanical
ventilatory support data. The trends observed over time,
interpreted in relation Patients requiring support of two or more
organ systems (e.g. to changes in therapy, are an important guide
to the patients inotropes and haemoltration) Patients with chronic
impairment of one or more organ systems progress. (e.g. chronic
obstructive pulmonary disease (COPD) or severe The critically ill
patient should be monitored according to ischaemic heart disease
(IHD)) who also require support for acute the following principles:
reversible failure of another organ system Regular clinical
examination should never be neglected. Admission to HDU Simple
physical signs such as respiratory rate, the Patients who require
far more detailed observation or monitoring appearance of the
patient, restlessness, conscious level 8 than can be safely
provided on a general ward and indices of poor peripheral perfusion
(pale, cold Direct arterial blood pressure (BP) monitoring Central
venous pressure (CVP) monitoring skin, delayed capillary rell in
the nail bed) are just as Fluid balance important as a set of blood
gases or numbers Neurological observations, regular Glasgow Coma
Scale impressively displayed on expensive monitors. (GCS) recording
If there is conflict between clinical assessment and the Patients
requiring support for a single failing organ system but information
on a monitor, the monitor should be excluding invasive ventilatory
support Mask continuous positive airway pressure (CPAP) or presumed
to be wrong until all potential sources of error non-invasive
(mask) ventilation (NIPPV)Box 8.17, page 193 have been checked and
eliminated. For example, CVP Low- to medium-dose inotropic support
measurement may be erroneous because the line is Renal replacement
therapy in an otherwise stable patient blocked, the system has not
been reset to zero after a Patients no longer requiring intensive
care but who cannot be safely managed on a general ward change in
the patients position, the tip of the cannula is lying in the right
ventricle, or another infusion has been attached to the same
central line. Changes and trends are more important than any single
TRANSPORT OF THE CRITICALLY ILL measurement. PATIENT Many monitors
have alarms which will activate if certain maximum and minimum
values are breached. This is a Critically ill patients should be
transported to the most crucial safety feature and may, for
example, help to appropriate clinical area for their continuing
care. Before identify the fact that a patient has become
disconnected intra- or inter-hospital transfer is undertaken, the
patients from the ventilator. Despite the understandable desire to
condition must be stabilised. Appropriate monitoring should avoid
extra noise, the alarm limits should always be set be set up and if
there is clinical evidence of progressive to dene physiologically
safe limits for the variable respiratory failure or inability to
protect the airway, being monitored. endotracheal intubation and
ventilation are indicated. Sophisticated monitoring systems are
often invasive and Intubation, while often essential, may be
hazardous in the pose certain hazards, particularly infection (Box
8.3). patient with cardiorespiratory failure, and full monitoring
Always ask Is it necessary?, and cease monitoring as and
resuscitation facilities must be available. Hypovolaemia soon as
possible. and hypotension should be corrected and this will often
require monitoring of the central venous pressure (CVP). Transfer
to another hospital may be necessary for further investigations
(such as computed tomography, CT), or to MONITORING THE CIRCULATION
specialist liver failure, neurosurgical or cardiac surgical units.
The urgency of providing the specialist treatment has
Electrocardiogram (ECG) to be balanced against the stability of the
patients condition. Standard monitors display a single-lead ECG,
record heart It may be more appropriate to admit the patient to the
local rate and identify rhythm changes. More sophisticated ICU for
initial stabilisation before transfer. All critically ill machines
can print out rhythm strips and monitor ST patients should be
accompanied during transfer by an segment shift, which may be
useful in patients with appropriately trained medical escort.
ischaemic heart disease. Blood pressure MONITORING This may be
measured intermittently using an automated sphygmomanometer but in
critically ill patients continuous intra-arterial monitoring, using
a line placed in the radial GENERAL PRINCIPLES artery, is
preferable. It is important to appreciate that when there is
systemic vasoconstriction the mean arterial pressure On entering an
ICU, relatives, students and even clinicians may be normal or even
high although the cardiac output is may be intimidated by the
numerous tubes and cables low. Conversely, if there is peripheral
vasodilatation, as in 179
6. CRITICAL CARE AND EMERGENCY MEDICINE 8.3 COMPLICATIONS AND
PITFALLS OF CENTRAL Hypervolaemia VENOUS AND PULMONARY ARTERY (PA)
CANNULATION Normovolaemia At insertion Hypovolaemia
Pneumothoraxmore likely with subclavian than with internal jugular
approach Haematoma from accidental arterial puncture CVP Air
embolism Dysrhythmia Damage to thoracic duct with left internal
jugular or subclavian approach Knotting of catheter* Pulmonary
artery rupture* 8 In situ 0 15 30 Sepsis Time (min) Endocarditis
Thrombosis Fig. 8.1 The different responses observed in central
venous Pulmonary infarct* pressure (CVP) after a fluid challenge of
250 ml, depending on the Pulmonary artery rupture* intravascular
volume status of the patient. Erroneous information Inappropriate
response to information * Risk associated specically with PA
catheterisation. In severe hypovolaemia the RAP may be sustained by
peripheral venoconstriction, and transfusion may initially sepsis,
the mean arterial pressure may be low although the produce little
or no change in the CVP (Fig. 8.1). cardiac output is high.
Pulmonary artery wedge pressure (PAWP) Central venous pressure
(CVP) and PA catheterisation CVP or right atrial pressure (RAP) is
monitored using a In most situations the CVP is an adequate guide
to the lling catheter inserted via either the internal jugular or
the pressures of both sides of the heart; however, certain
subclavian vein with the distal end sited in the upper right
conditions such as pulmonary hypertension or right atrium. Although
on general wards and some HDUs ventricular dysfunction may lead to
raised CVP levels even measurements may be made using a saline-lled
manometer in the presence of hypovolaemia. If this is suspected, it
may tube, in ICU the line is transduced as for arterial pressure be
appropriate to insert a pulmonary artery flotation catheter
measurement. The zero reference point used is normally the (Fig.
8.2) so that pulmonary artery pressure and PAWP, mid-axillary line
(MAL), which approximates to the level of which approximates to
left atrial pressure, can be measured. the tricuspid valve or
mid-right atrium with the patient lying The mean PAWP normally lies
between 8 and 12 mmHg semi-supine. All intravascular pressures
quoted in this (measured from the mid-axillary line) but in left
heart failure chapter are referenced to that point. The classical
bedside it may be grossly elevated and even exceed 30 mmHg.
clinical examination uses the sternal angle as the zero Provided
the pulmonary capillary membranes are intact, the reference point
and this lies approximately 68 cm optimum PAWP when managing acute
circulatory failure in (depending on the antero-posterior chest
diameter) the critically ill patient is generally 1215 mmHg because
vertically above MAL. (Values of CVP measured from this this will
ensure good left ventricular lling without risking reference point
will therefore be 68 cm lower than values hydrostatic pulmonary
oedema. recorded from MAL.) These catheters may also be used to
measure cardiac The CVP is a useful means of assessing the need for
output, sample blood from the pulmonary artery (mixed intravascular
fluid replacement and the rate at which it venous samples) and, by
oximetry, provide continuous should be given. If the CVP is low in
the presence of a low monitoring of the mixed venous oxygen
saturation (SvO2). mean arterial pressure (MAP) or cardiac output,
fluid Measurement of SvO2 gives an indication of the adequacy of
resuscitation is necessary. However, a raised level does not
cardiac output in relation to the bodys metabolic require-
necessarily mean that the patient is adequately volume ments and is
especially useful in low cardiac output states. resuscitated. It
must be remembered that right heart function, pulmonary artery
pressure, intrathoracic pressure Cardiac output and venous tone
also influence CVP and may lead to a The most widely used method
for cardiac output measure- raised CVP even when the patient is
hypovolaemic. In ment is the thermodilution technique using a PA
catheter. A addition, positive pressure ventilation raises
intrathoracic bolus of cold 5% dextrose is rapidly injected into
the right pressure and causes marked swings in atrial pressures and
atrium via the CVP line and mixes with the total venous systemic
blood pressure in time with respiration. Pressure return in the
right ventricle, producing a drop in the measurements should be
recorded at end-expiration or, if pulmonary artery temperature that
is sensed by a thermistor safe, off the ventilator because these
values provide the most at the tip of the PA catheter. The cardiac
output is derived reliable measure of ventricular end-diastolic
transmural from the volume and temperature of the injectate and the
180 pressure. resulting change in temperature measured in the
pulmonary
7. MONITORING A Pulmonary artery Aorta LA B mmHg Balloon RA
Right Pulmonary ventricular pressure artery pressure 8 30 LV Wedge
20 (left atrial) RV pressure Right atrial 10 pressure Balloon
inflated 0 Fig. 8.2 A pulmonary artery catheter. A There is a small
balloon at the tip of the catheter and pressure can be measured
through the central lumen. The catheter is inserted via an internal
jugular, subclavian or femoral vein and advanced through the right
heart until its tip lies in the pulmonary artery. When the balloon
is deflated the pulmonary artery pressure can be recorded. B
Advancing the catheter while inflating the balloon will wedge the
catheter in the pulmonary artery. In this position blood cannot
flow past the balloon so the tip of the catheter will now record
the pressure transmitted from the pulmonary veins and left atrium.
This is known as the pulmonary artery wedge pressure and provides
an indirect measure of the left atrial pressure. artery; it is
inversely related to the area under the temperaturetime curve.
Although generally viewed as the gold standard for clinical
measurement of cardiac output, the error may be 1015%.
Thermodilution cardiac output measurement has been rened by the
development of PA catheters incorporating a heating element, which
raises blood temperature at frequent intervals, with the resultant
temperature change also Oesophageal detected by the thermistor.
These continuous cardiac Doppler probe output catheters dispense
with the need for injections of cold dextrose. Increasingly less
invasive methods for monitoring cardiac Stroke Peak output are
being used, such as oesophageal Doppler distance velocity
ultrasonography. This involves inserting a 6 mm probe into the
distal oesophagus to allow continuous monitoring of the aortic flow
signal from the descending aorta (Fig. 8.3). From the stroke
distance (area under velocity/time waveform), and using a
correction factor that incorporates the patients age, height and
weight, an estimate of left ventricular stroke volume and hence
cardiac output can be made. Peak velocity is an indicator of left
ventricular Flow performance while flow time is an indicator of
left time ventricular lling and peripheral resistance. Oesophageal
Doppler provides a rapid and clinically useful assessment of Fig.
8.3 Oesophageal Doppler ultrasonography. volume status and cardiac
performance to guide early fluid and vasoactive therapy. Urine
output Analysis of arterial pressure waveform is another means This
is a sensitive measure of renal perfusion, provided that of
continuously estimating cardiac output, and can be cali- the
kidneys are not damaged (e.g. acute tubular necrosis) or brated
either by transpulmonary thermodilution (PiCCO) or affected by
drugs (e.g. diuretics, dopamine), and can be lithium dilution
methods (LidCO). monitored accurately if a urinary catheter is in
place. It is 181
8. CRITICAL CARE AND EMERGENCY MEDICINE normally measured
hourly and the lower limit of normal Arterial blood gases is 0.5
ml/hr/kg body weight. These are usually measured several times a
day in a ventilated patient so that inspired oxygen (FIO2) and
minute Fluid balance volume can be adjusted to achieve the desired
PaO2 and Assessing fluid balance in critically ill patients is a
difcult PaCO2 respectively. Analysis of arterial blood gas results
is but important discipline. Weighing the patient daily can be also
a useful means of monitoring disturbances of acidbase helpful but
is extremely difcult, and assessment is usually balance (Ch. 16).
based on fluid balance charts which record: inputs: oral,
nasogastric and intravenous, classied as Lung function crystalloid
and colloid In ventilated patients lung function is monitored by:
outputs: urine, nasogastric, stulae, vomiting, diarrhoea
alveolararterial PO2 gradient and hypoxaemia index and surgical
drain losses. (PaO2/FIO2), both measures of gas exchange 8 arterial
and end-tidal CO2, reflecting alveolar The insensible loss from
skin, respiration etc. is normally 5001000 ml/day but can exceed 2
litres/day in a pyrexial ventilation patient with open wounds.
tidal volume (VT), respiratory rate (f), minute volume (VT f),
airway pressure and compliance, reflecting Peripheral/skin
temperature airways resistance, the stiffness of the lungs and the
This is conventionally measured over the dorsum of the ease with
which the patient can meet the required work foot and reflects
cutaneous blood flow and venous lling. of breathing. The gradient
between peripheral and central or core temperature (from rectal,
oesophageal or tympanic probes) Capnography may be used to assess
peripheral perfusion; a difference of The CO2 concentration in
inspired gas is zero, but during < 3C suggests that both
intravascular fluid replacement and expiration, after clearing the
physiological dead space, it tissue perfusion are adequate. rises
progressively to reach a plateau which represents the alveolar or
end-tidal CO2 concentration. This cyclical change Blood lactate,
hydrogen ion and base decit in CO2 concentration or capnogram is
measured using an A metabolic acidosis with base decit > 5
mmol/l requires infrared sensor inserted between the ventilator
tubing and explanation (p. 437). It often indicates increased
lactic acid the endotracheal tube. With normal lungs, the end-tidal
production in poorly perfused, hypoxic tissues and impaired CO2
closely mirrors PaCO2, and can be used to assess the lactate
metabolism due to poor hepatic perfusion. Serial adequacy of
alveolar ventilation. However, there may be lactate measurements
may therefore be helpful in moni- considerable discrepancies if
there is lung disease or impaired toring tissue perfusion and the
response to treatment. Other pulmonary perfusion (for example, due
to hypovolaemia). conditions such as acute renal failure,
ketoacidosis and Trends in end-tidal CO2 are useful in head injury
manage- poisoning may be the cause (p. 438). Large volume ment and
during the transport of ventilated patients. infusions of fluids
containing sodium chloride, e.g. in theatre In combination with the
gas flow and respiratory or during resuscitation, may lead to a
hyperchloraemic cycle data from the ventilator, CO2 production and
hence acidosis. metabolic rate may be calculated. MONITORING
RESPIRATORY FUNCTION PHYSIOLOGY OF THE CRITICALLY ILL Oxygen
saturation (SpO2) PATIENT This is measured by a probe, usually
attached to a nger or earlobe. Spectrophotometric analysis is used
to determine OXYGEN TRANSPORT the relative proportions of saturated
and desaturated haemoglobin. The technique is unreliable if
peripheral The major function of the heart, lungs and circulation
is perfusion is poor and may produce erroneous results in the
provision of oxygen and other nutrients to the various the presence
of nail polish, excessive movement or high organs and tissues of
the body. During this process carbon ambient light. In general,
arterial oxygenation is satisfactory dioxide and the other waste
products of metabolism are if SpO2 is greater than 90%. In the ICU,
sudden falls in SpO2 removed. The rate of supply and removal should
match the may be caused by: specic metabolic requirements of the
individual tissues. pneumothorax This requires adequate oxygen
uptake in the lungs, global displacement of the endotracheal tube
matching of delivery and consumption, and regional control
disconnection from the ventilator of the circulation. Failure to
supply sufcient oxygen to lung collapse due to thick secretions
blocking the meet the metabolic requirements of the tissues is the
proximal bronchial tree cardinal feature of circulatory failure or
shock. circulatory collapse causing a poor signal due to The
transport of oxygen from the atmosphere to the impaired peripheral
perfusion mitochondria within individual cells is illustrated in
Figure 182 error such as a detached probe. 8.4. The important
points to note are that:
9. PHYSIOLOGY OF THE C R I T I C A L LY ILL PAT I E N T PaO2
P50 SaO2 (97) CaO2 (200) (13) (3.5) DO2 Hb (150) QT (5) (1000) P
lO2 humidified (20) P lO2 dry (21) Diffusion of O2 in tissues
Capillary P O2 Heart and Arterial Venous lungs (13) (5.3)
Interstitial P O2 Expired dry Shunt (5.3 2.7) V i/e (5) P EO2
(15.9) (23%) VO2 P ECO2 (4.2) Intracellular PO2 (250) 8 (2.7 1.3)
VCO2 (200) Mitochondrial P O2 (1.3 0.7) PAO2 (14) P50 O2R Pv O2 Sv
O2 (75) CvO2 (150) (750) (5.3) Hb (150) QT (5) Calculations CaO2 =
(Hb x k x SaO2/100) + (PaO2 x 0.23) = 200 ml O2/l k = coefficient
of haemoglobin oxygen-binding capacity = 1.36 ml O2/gram of 100%
saturated Hb PaO2 x 0.23 = oxygen dissolved in plasma = 3 ml/l DO2
= QT x CaO2 = 1000 ml/min VO2 = QT (CaO2CV O2) = 250 ml/min OER =
VO2 /D O2 x 100 = 25% Fig. 8.4 Transport of oxygen from inspired
gas to the cell, demonstrating the oxygen cascade, with equations
for calculation of arterial oxygen content, global oxygen delivery,
consumption and extraction. Values in parentheses for a normal 70
kg individual (body surface area: 1.67 m2) breathing air (F IO2:
0.21) at standard atmospheric pressure (PB: 101 kPa). Partial
pressures of O2, CO2 in kPa; saturation in %; contents (CaO2, Cv
O2) in ml/litre; Hb in g/l; blood/gas flows (QT, Vi/e) in
litre/min; oxygen transport (DO2, O2R), VO2 and V CO2 in ml/min. To
convert kPa to mmHg, multiply by 7.5. CaO2 = arterial O2 content
O2R= oxygen return P I O2 = inspired PO2 SO2=oxygen saturation (%)
CvO2 = mixed venous O2 content PaO2= arterial PO2 PO2 = oxygen
partial pressure (kPa) SvO2 = mixed venous SO2 DO2 = oxygen
delivery PAO2 = alveolar PO2 PvO2 = venous PO2 V CO2 = CO2
production Hb = haemoglobin P ECO2= mixed expired PCO2 QT = cardiac
output Vi/e= minute volume: inspired/expired OER = oxygen
extraction ratio P EO2 = mixed expired PO2 SaO2 = arterial SO2 VO2
= oxygen consumption The movement of oxygen from pulmonary
capillary to patient who is both anaemic (Hb 60 g/l) and hypoxaemic
systemic tissue capillary, referred to as the global (SaO2 75%)
when breathing air (FIO2 0.21). oxygen delivery (DO2), relies on
convection or bulk flow Supplementary oxygen at FIO2 0.4 will
increase SaO2 to and is the product of cardiac output and arterial
oxygen 93%; CaO2 will increase by 24% but further increases in
content. FIO2 while increasing PaO2 cannot produce any further The
regional distribution of oxygen delivery is vital. If useful
increases in SaO2 or CaO2. However, increasing skin and muscle
receive high blood flows but the Hb to 90 g/l by blood transfusion
will result in a further splanchnic bed does not, the gut will
become hypoxic 50% increase in CaO2. even if overall oxygen
delivery is high. The movement of oxygen from tissue capillary to
cell The major determinants of the oxygen content of arterial
occurs by diffusion and depends on the gradient of blood (CaO2) are
the arterial oxygen saturation of oxygen partial pressures,
diffusion distance and the haemoglobin (SaO2) and the haemoglobin
concentration ability of the cell to take up and use oxygen.
Therefore (over 95% of oxygen carried in the blood is attached to
microcirculatory, tissue diffusion and cellular factors, as
haemoglobin). The shape of the oxyhaemoglobin well as DO2,
influence the oxygen status of the cell. dissociation curve
dictates that increases in PaO2 beyond Supranormal levels of oxygen
delivery cannot the level that ensures SaO2 is > 90% produce
relatively compensate for diffusion problems between capillary
small additional increases in CaO2 (Fig. 8.5). Consider a and cell,
nor for metabolic failure within the cell. 183
10. CRITICAL CARE AND EMERGENCY MEDICINE 100 approximately 250
ml/min for an adult of 70 kg undertaking normal daily activities.
VO2 may be calculated indirectly from the product of cardiac output
and the arterial mixed venous oxygen content difference (CaO2CvO2),
as shown Haemoglobin saturation SO2 (%) 80 in Figure 8.4, or
directly by sampling the inspired and Temperature mixed-expired
gases from the ventilator and measuring H+ inspired and expired
minute volume using either a mass 60 PaCO2 spectrometer or
metabolic cart. 2,3 DPG The oxygen saturation in the pulmonary
artery, otherwise known as the mixed venous oxygen saturation
(SvO2), 40 represents a measure of the oxygen not consumed by the
P50 tissues (DO2VO2). The saturation of venous blood from 8
different organs varies considerably; for example, the 20 hepatic
venous saturation usually does not exceed 60% but the renal venous
saturation may reach 90%, reflecting the great difference in both
the metabolic requirements 1 2 3 4 5 6 7 8 9 10 11 12 13 kPa of
these organs and the oxygen content of the blood 0 0 20 40 60 80
100 mmHg delivered to them. The SvO2 is influenced by changes PO2
(mmHg or kPa) both in oxygen delivery (DO2) and consumption (VO2)
and, Fig. 8.5 The relationship between oxygen tension (PO2) and
provided the microcirculation and the mechanisms for percentage
saturation of haemoglobin with oxygen (SO2). The cellular oxygen
uptake are intact, can be used to monitor dotted line illustrates
the rightward shift of the curve (i.e. P50 increases) whether
global oxygen delivery is adequate to meet overall caused by
increases in temperature, PaCO2, metabolic acidosis and demand. 2,3
diphosphoglycerate (DPG). The reoxygenation of the blood that
returns to the lungs and the resulting arterial saturation (SaO2)
will depend on how closely pulmonary ventilation and perfusion are
OXYHAEMOGLOBIN DISSOCIATION CURVE matched. If part of the pulmonary
blood flow perfuses non-ventilated parts of the lung, there will be
shunting, The oxyhaemoglobin dissociation curve (Fig. 8.5)
describes and the blood entering the left atrium will be
desaturated the relationship between the saturation of haemoglobin
in proportion to the size of this shunt and the level (SO2) and the
partial pressure (PO2) of oxygen in the blood. of SvO2. Due to the
shape of the curve, a small drop in PaO2 below 8 kPa (60 mmHg) will
cause a marked fall in SaO2. Its position and the effect of various
physico-chemical factors are dened by the PO2 at which 50% of the
haemoglobin is RELATIONSHIP BETWEEN OXYGEN saturated (P50), which
is normally 3.5 kPa (26 mmHg). CONSUMPTION AND DELIVERY A shift in
the curve will influence the uptake and release of oxygen by the Hb
molecule; for example, if the curve The tissue oxygen extraction
ratio (OER), which is 2025% moves to the right, the haemoglobin
saturation will be lower in a normal subject at rest, rises as
consumption increases for any given oxygen tension and therefore
less oxygen will or supply diminishes (Fig. 8.6). The maximum OER
is be taken up in the lungs but more will be released to the
approximately 60% for most tissues; at this point no further
tissues. As capillary PCO2 rises, the curve moves to the right,
increase in extraction can occur and any further increase
increasing unloading of oxygen in the tissuesa phenomenon in oxygen
consumption or decline in oxygen delivery will known as the Bohr
effect. cause tissue hypoxia, anaerobic metabolism and increased
Traditionally, the optimum haemoglobin concentration lactic acid
production. for critically ill patients had been considered to be
In sepsis the slope of maximum OER decreases, approximately 100
g/l, representing a balance between reflecting the reduced ability
of tissues to extract oxygen maximising the oxygen content of the
blood and avoiding (DE cf. AB on Fig. 8.6), but the curve does not
plateau regional microcirculatory problems due to increased and
oxygen consumption continues to increase even at viscosity.
However, recent evidence suggests an improved supranormal levels of
oxygen delivery. This concept outcome in critically ill patients if
the haemoglobin encouraged some physicians to treat septic shock
using concentration is maintained between 70 and 90 g/l, with the
vigorous intravenous fluid loading and inotropic support, exception
of the elderly and patients with coronary artery usually with
dobutamine, with the aim of achieving very disease, in whom a level
of 100 g/l remains appropriate. high oxygen deliveries (> 600
ml/min/m2) in the belief that this strategy would increase oxygen
consumption, relieve tissue hypoxia, prevent multiple organ failure
and OXYGEN CONSUMPTION improve prognosis. Trials have demonstrated
no benet in ICU patients with established organ failure but suggest
that The sum of the oxygen consumed by the various organs it may be
worthwhile if applied before organ failure 184 represents the
global oxygen consumption (VO2) and is supervenes (Box 8.4)
11. PHYSIOLOGY OF THE C R I T I C A L LY ILL PAT I E N T F 8.5
TERMINOLOGY USED TO DESCRIBE THE 300 INFLAMMATORY STATE E Infection
B C Invasion of normally sterile host tissue by microorganisms 200
Bacteraemia Oxygen consumption Viable bacteria in the blood (VO2)
ml/min Systemic inflammatory response syndrome (SIRS) 100
Encompasses inflammatory response to both infective and A
non-infective causes such as pancreatitis, trauma, D
cardiopulmonary bypass, vasculitis etc. Dened by presence of two or
more of: Temperature > 38.0C or < 36.0C 8 0 0 400 800 1200
Heart rate > 90/min Oxygen delivery (DO2) ml/min Respiratory
rate > 20/min PaCO2 < 4.3 kPa (< 32 mmHg) or ventilated
Fig. 8.6 The effects of changing oxygen delivery on consumption.
White blood count > 12 109/l or < 4 109/l The solid line
(ABC) represents the normal relationship and the dotted line (DEF)
the altered relationship believed to exist in sepsis. Sepsis
Systemic inflammatory response caused by documented infection EBM
8.4 EARLY GOAL-DIRECTED THERAPY IN Severe sepsis/SIRS SEVERE SEPSIS
Sepsis/SIRS with evidence of early organ dysfunction or In patients
with severe sepsis or septic shock managed initially in hypotension
A&E, early goal-directed therapy (EGT) reduced 60-day mortality
Septic/SIRS shock from 57% to 44%. Both groups were resuscitated
with similar targets for CVP, arterial blood pressure and urine
output, but in the Sepsis associated with organ failure and
hypotension (systolic EGT group additional goals were central
venous oxygen saturation BP < 90 mmHg or > 40 mmHg fall from
baseline) unresponsive > 70% and haematocrit > 30%, resulting
in more rapid fluid to fluid resuscitation resuscitation and higher
RBC transfusion rates in the rst 6 hours. Multiple organ
dysfunction syndrome (MODS) Rivers E, et al. N Engl J Med 2001;
345:13681377. Development of impaired organ function in critically
ill patients with SIRS If prompt treatment of underlying cause and
suitable organ support are not achieved, then multiple organ
failure (MOF) will ensue PATHOPHYSIOLOGY OF THE INFLAMMATORY
RESPONSE oxygen radicals and particularly pro-inflammatory
cytokines The mediators and clinical manifestations of the inflam-
(p. 66) are released into the circulation. matory response are
described on pages 7576. In critically The inflammatory and
coagulation cascades are ill patients these processes have
important consequences intimately related. The process of blood
clotting not only (Box 8.5). involves platelet activation and brin
deposition but also Fever, tachycardia with warm peripheries,
tachypnoea causes activation of leucocytes and endothelial cells.
and a raised white cell count traditionally prompt a diag-
Conversely, leucocyte activation induces tissue factor nosis of
sepsis with the implication that the clinical picture expression
and initiates coagulation. Control of the is caused by invading
microorganisms and their breakdown coagulation cascade is achieved
through the natural anti- products. However, other conditions such
as pancreatitis, coagulants antithrombin (AT) III, activated
protein C (APC) trauma, malignancy, tissue necrosis, aspiration
syndromes, and tissue factor pathway inhibitor (TFPI) which not
only liver failure, blood transfusion and drug reactions can all
regulate the initiation and amplication of the coagulation produce
the same clinical picture in the absence of infection. cascade but
also inhibit the pro-inflammatory cytokines. Deciency of ATIII and
APC (features of disseminated Local inflammation intravascular
coagulation (DIC), see below) facilitates The bodys initial
response to a noxious local insult is to thrombin generation and
promotes further endothelial cell produce a local inflammatory
response with sequestration dysfunction. and activation of white
blood cells and the release of a variety of mediators to deal with
the primary insult and Systemic inflammation prevent further damage
either locally or in distant organs. During a severe inflammatory
response systemic release Normally, a delicate balance is achieved
between pro- and of cytokines and other mediators triggers
widespread anti-inflammatory mediators. However, if the
inflammatory interaction between the coagulation pathways,
platelets, response is excessive, local control is lost and a large
array endothelial cells and white blood cells, particularly the of
mediators including prostaglandins, leukotrienes, free
polymorphonuclear cells (PMNs). These activated PMNs 185
12. CRITICAL CARE AND EMERGENCY MEDICINE express adhesion
factors (selectins) causing them initially to hypovolaemia due to
venodilatation and fluid loss through adhere to and roll along the
endothelium, then to adhere the leaky vascular endothelium) are
promptly controlled rmly and nally to migrate through the damaged
and before signicant organ failure occurs (early shock), the
disrupted endothelium into the extravascular, interstitial
prognosis is good. However, if the global and peripheral space
together with fluid and proteins, resulting in tissue circulatory
failure is not corrected promptly, and particularly oedema and
inflammation. A vicious circle of endothelial if the underlying
cause is not effectively treated, progressive injury, intravascular
coagulation, microvascular occlusion, deterioration in organ
function occurs and multiple organ tissue damage and further
release of inflammatory failure (MOF) ensues (late shock).
mediators ensues. The mortality of MOF is high and increases with
the All organs may become involved. This manifests in the number of
organs that have failed, the duration of organ lungs as the acute
respiratory distress syndrome (ARDS) failure and the patients age.
Failure of four or more organs and in the kidneys as acute tubular
necrosis (ATN), while is associated with a mortality > 80%. 8
widespread disruption of the coagulation system results in the
clinical picture of DIC. The endothelium itself produces mediators
that locally PRESENTING PROBLEMS IN control blood vessel tone:
endothelin 1, a potent vaso- CRITICAL ILLNESS constrictor, and
prostacyclin and nitric oxide (NO, p. 76) which are systemic
vasodilators. NO (which is also generated outside the endothelium)
is implicated in both the CIRCULATORY FAILURE: SHOCK myocardial
depression and the profoundly vasodilated circulation (both
arterioles and venules) that causes the Circulatory failure or
shock exists when the oxygen relative hypovolaemia and systemic
hypotension found in delivery (DO2) fails to meet the metabolic
requirements of septic/SIRS shock. the tissues. In the context of
critical illness, shock is often A major component of the tissue
damage in septic/SIRS considered to be synonymous with hypotension
and to shock is the inability to take up and use oxygen at dene the
state of circulatory failure. While hypotension is mitochondrial
level even if global oxygen delivery is a sinister development and
requires urgent attention, it is supranormal. This effective
bypassing of the tissues results most important to appreciate that
hypotension is often a late in a reduced arteriovenous oxygen
difference, a low oxygen manifestation of circulatory failure or
shock and that the extraction ratio, a raised plasma lactate and a
paradoxically cardiac output and oxygen delivery may be critically
low high mixed venous oxygen saturation (SvO2). even though the
blood pressure remains normal (Box 8.6); If both the precipitating
cause and accompanying the problem should be identied and treatment
instituted circulatory failure (hypotension and frequently severe
before the blood pressure falls. 8.6 TYPICAL CIRCULATORY
MEASUREMENTS IN A NORMAL ADULT AND IN VARIOUS CARDIORESPIRATORY
CONDITIONS THAT MAY CAUSE CIRCULATORY SHOCK RAP/CVP LAP/PAWP PAP
MAP Heart rate Cardiac CaO2 DO2 Clinical condition (mmHg) (mmHg)
(mmHg) (mmHg) (/min) output (l/min) SVR* PVR* (ml/l) (ml/min)
Normal 6 11 16 96 70 5 18 1 200 1000 Major haemorrhage 0 4 11 81
120 3 27 2.3 160 480 Left heart 8 20 24 96 100 3.7 24 1 180 670
failure Major pulmonary 12 6 36 81 110 2.5 28 12 160 400 embolism
Exacerbation of 11 10 42 82 100 6 12 5 150 900 COPD Septic shock
Pre-volume load 3 8 16 55 130 4.5 12 1.3 150 675 Post-volume load 9
15 23 60 120 7.5 7 1.1 140 1050 * Multiply by 80 to give SI units:
dyn.sec/cm5. To adjust for the size of the patient, the
measurements of flow and resistance are frequently indexed by
dividing by the patients body surface area. (RAP/LAP = right/left
atrial pressure; CVP = central venous pressure; PAWP = pulmonary
artery wedge pressure; PAP/MAP = pulmonary artery/mean arterial
pressure; SVR/PVR = systemic/pulmonary vascular resistance; Ca O2 =
arterial oxygen content; DO2 = global oxygen delivery; COPD =
chronic obstructive pulmonary disease) Note These values are merely
examples. The severity of the condition and pre-existing
cardiorespiratory disease will affect the precise gures obtained in
individual cases. Note that in contrast to other conditions the
oxygen delivery is high in septic shock after volume loading. When
the circulatory abnormalities have been dened in this way,
appropriate management may be planned. Pressures quoted referenced
to zero at mid-axilla as is usual practice in ICU. Subtract
vertical distance from mid-axilla to sternal angle (approx. 68
mmHg) if sternal angle used as reference point. 186
13. PRESENTING PROBLEMS IN CRITICAL ILLNESS The many causes of
circulatory failure or shock may 8.7 GENERAL FEATURES OF SHOCK
broadly be classied into: hypovolaemicany condition provoking a
major Hypotension (systolic BP < 100 mmHg) reduction in blood
volume, e.g. internal or external Tachycardia (> 100/min)
haemorrhage, severe burns, dehydration Cold, clammy skin Rapid,
shallow respiration cardiogenicany form of severe heart failure,
e.g. Drowsiness, confusion, irritability myocardial infarction,
acute mitral regurgitation Oliguria (urine output < 30 ml/hr)
obstructiveobstruction to blood flow around the Elevated or reduced
central venous pressure (see text) circulation, e.g. major
pulmonary embolism, cardiac Multi-organ failure tamponade, tension
pneumothorax neurogeniccaused by major brain or spinal injury
output. The central venous pressure (jugular venous producing
disruption of brain stem and neurogenic pressure, JVP) is typically
reduced in hypovolaemic and vasomotor control; may be associated
with neurogenic anaphylactic shock but elevated in cardiogenic and
8 pulmonary oedema obstructive shock, and may be low, normal or
high in anaphylacticinappropriate vasodilatation triggered by
neurogenic and septic shock. This is an important distinction an
allergen (e.g. bee sting) and direct measurement of the CVP or PAWP
(Fig. 8.2, septic/SIRSinfection or other causes of a systemic p.
181) may be very helpful if the physical signs are difcult
inflammatory response that produce widespread to interpret. Figure
8.7 indicates how the likely diagnosis endothelial damage with
vasodilatation, arteriovenous may be established by careful
analysis of the CVP, shunting, microvascular occlusion and tissue
oedema, peripheral perfusion, pulse volume and haematocrit. All
resulting in organ failure. forms of shock require early
identication and treatment because, if inadequate regional tissue
perfusion and cellular Clinical assessment and complications
dysoxia persist, multiple organ failure will develop. Although
dependent to some extent on the underlying cause, a range of
clinical features are common to most cases (Box 8.7 and p. 177).
RESPIRATORY FAILURE INCLUDING ARDS Hypovolaemic, cardiogenic and
obstructive causes of circulatory failure produce the classical
image of shock, The majority of patients admitted to ICU/HDU will
have with cold peripheries, weak central pulses and evidence of a
respiratory problems either as the primary cause of their low
cardiac output. In contrast, neurogenic, anaphylactic admission or
secondary to pathology elsewhere. Respiratory and septic shock are
usually associated with warm failure is formally classied on the
basis of blood gas peripheries, bounding pulses and features of a
high cardiac analysis into: Measure CVP (mmHg from mid-axillary
line) Raised Low Peripheral temperature Cold Warm Warm Cold Pulse
volume Reduced Increased Increased Reduced Haematocrit Normal
Normal Normal Normal Increased or reduced or increased or reduced
Diagnoses to consider Myocardial infarct Sepsis Sepsis Haemorrhage
Na/H2O loss Pulmonary embolus CO2 retention Anaphylaxis Tension
Over-transfusion Drugs/overdose GI tract GI tract pneumothorax CNS
lesions Trauma Ascites Cardiac tamponade Major vessel Renal Sepsis
Thorax Sepsis Abdomen Retroperitoneal Fig. 8.7 A guide to the
initial analysis and diagnosis of circulatory shock. 187
14. CRITICAL CARE AND EMERGENCY MEDICINE type 1hypoxaemia (PaO2
< 8 kPa (< 60 mmHg) when Adequate supplemental oxygen to
maintain SpO2 > 94% breathing air) without hypercapnia caused by
a failure of should be provided. If the inspired oxygen
concentration gas exchange due to mismatching of pulmonary required
exceeds 0.6, refer to the critical care team. ventilation and
perfusion Monitoring of SpO2 and arterial blood gases is helpful in
type 2hypoxaemia with hypercapnia (PaCO2 > 6.5 kPa documenting
progress. (> 49 mmHg)) due to alveolar hypoventilation which
Restless patients dependent on supplementary oxygen occurs when the
respiratory muscles cannot perform or with deteriorating conscious
level are at risk. If they sufcient effective work to clear the
carbon dioxide remove the mask or vomit, the resulting hypoxaemia
or produced by the body. aspiration may be catastrophic. An attempt
should be made to reduce the work of Although this distinction is
conceptually useful, it cannot breathing, e.g. by treating
bronchoconstriction or using be applied too rigidly in critically
ill patients since they CPAP (Box 8.17, p. 193). may change from
type 1 to 2 as their illness progresses. 8 For example, hypercapnia
may develop in pneumonia or pulmonary oedema as the patient tires
and can no longer ACUTE RESPIRATORY DISTRESS sustain the increased
work of breathing. SYNDROME (ARDS) Pulmonary problems in critically
ill patients can also be This describes the acute, diffuse
pulmonary inflammatory classied according to the functional
residual capacity response to either direct (via airway or chest
trauma) or (FRC, or the lung volume at the end of expiration).
indirect blood-borne insults that originate from extra- Examples of
low FRC include lung collapse, pneumonia and pulmonary pathology.
It is characterised by neutrophil pulmonary oedema; examples of a
high FRC (i.e. over- sequestration in pulmonary capillaries,
increased capillary distended lungs) include asthma, COPD and
bronchiolitis. permeability, protein-rich pulmonary oedema with
hyaline This allows logical management directed at improving lung
membrane formation, damage to type 2 pneumocytes compliance and
reducing the work of breathing. leading to surfactant depletion,
alveolar collapse and The more common causes of acute respiratory
failure reduction in lung compliance. If this early phase does
presenting to ICU/HDU for respiratory support are shown in not
resolve with treatment of the underlying cause, a Box 8.8.