It Has Long Been Recognised That the Physiological Response of the Patient to a Stress or Disease Process Will Very Largely Determine the Outcome

8/6/2019 It Has Long Been Recognised That the Physiological Response of the Patient to a Stress or Disease Process Will Ver

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It has long been recognised that the physiological response of the patient to a stress or

disease process will very largely determine the outcome. It is important, therefore, to

monitor the physiological responses of patients since this not only allows the assessment of

physiological reserve but will also give a baseline against which the effectiveness of any

applied treatment can be judged. Basic knowledge of the principles of monitoring and

correct interpretation of data is important since a failure to do so can result in misdirectedtherapy. Much of what will be discussed in this review revolves around the maintenance of

normal aerobic metabolism and thus maintenance of viable cell function and measurement

of the degree of tissue oxygenation. Reduced supply of oxygen over demand for oxygen

results in cell injury and organ dysfunction. Only by assessing this dysfunction can

appropriate modifications of therapy be undertaken.

Keywords: monitors, critical care, tissue oxygenation

J.R.Coll.Surg.Edinb., 44, December 1999, 386-93

INTRODUCTION

The identification of the at risk patient or that patient who could benefit from intensive care

treatment is largely based on scoring systems which measure severity of illness. The scoring

system most frequently used is the APACHE system (Acute Physiological and Chronic Health

Evaluation) - usually APACHE II. The original APACHE system was introduced in 1981 andconsisted of two parts: 1) an APS (Acute Physiological Score) that reflected the degree of

physiological derangement; and 2) a chronic health evaluation that reflected the patients status

before the acute illness. APACHE II was introduced in 1985 and incorporated major changes inthe original APACHE system. The number of physiological variables was reduced from 34 to 12

and a higher score was assigned to acute renal failure and coma (the 12 variables are given in

Table 1). APACHE III was introduced in 1991 to expand and improve the prognostic estimatesprovided by APACHE II. The APACHE III system (which is only commercially available)

comprises an APACHE III score and a series of predictive equations linked to diagnosis and the

APACHE III database. It is the first part of the APACHE score which will be covered in thisreview -the physiological reserve and how to assess it.

Table 1: Twelve physiological variables measured in the acute physiological portion of the

APACHE II scoring system

1. Temperature - core2. Mean arterial pressure3. Heart rate

4. Respiratory rate - ventilated or non-ventilated

5. Oxygenation

FIO2 > 0.5 record A-aDO2FIO2 < 0.5 record PaO2

6. Arterial pH7. Serum sodium8. Serum potassium9. Serum creatinine10. Haematocrit


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11. White blood cell count

12. Glasgow coma score

It has long been recognised that the physiological response of the patient to a stress or disease

process will very largely determine the outcome. To an extent this will depend on the extent ofthe shock and injury; this tends to be minimal for minor surgery or injury and extensive for

major accidental or surgical trauma. However, the physiological reserve of the individual is alsoimportant. Signals that are initiated in injured or ischaemic tissues communicate the extent of the

injury systemically. These stress responses are necessary for the process of recovery from injury.

However, when trauma is severe, the resultant physiological responses are extensive and

sustained, such that the same responses may be detrimental and contribute to the progression tocritical illness and even death.

The stress response is initiated not only by injury but also by acute blood loss, shock, hypoxia,

acidosis, hypothermia, altered microcirculatory blood flow, and altered coagulation and immune

function. Another important stimulus which activates the stress response is pain. Afferent nervesignals from injured tissues converge on the hypothalamus and stimulate the hypothalamic-

pituitary axis, resulting in cortisol secretion. Pain is also a potent initiator of the sympathoadrenal

axis, so that sympathetic tone and adrenal secretion of catecholamines are immediately activatedby painful stimuli. Another initiator of the stress response is haemorrhage and intravascular

hypovolaemia. Haemorrhage results in the stimulation of volume and pressure receptors, which

activate the central nervous system. The response tends to be proportionate to the amount ofshock; both the degree and duration of blood volume deficit therefore, are important

determinants of the degree of physiological response to injury. Also, since haemorrhage and

hypovolaemia decrease cardiac output, tissue ischaemia may result. Tissue ischaemia is also animportant activator of physiological responses to injury, not only because it may potentiate

activation of the centrally mediated stress responses, but also because it leads to initiation oflocal responses, mediator release and cell activation. Other initiators of the stress response are

hypoxaemia, acidosis and hypercarbia, which all act at both local and central levels. Theseresponses to injury and ischaemia co-ordinate to act as signals, communicating systemically in a

quantitative manner, such that the physiological reaction is proportionate to the magnitude of

injury.

It is important to monitor the physiological responses. This not only allows the assessment of the

physiological reserve of the patient but will also give a baseline against which the effectiveness

of any applied treatment can be judged. Clearly, there are many physiological variables which

can be assessed and these range in complexity as well as degrees of invasiveness. However, it is

possible to considerably simplify the monitoring process.

The wellbeing of the patient is dependent upon the normal supply of oxygen and nutrients to the

tissues - and in particular to the vital organs. Monitoring of organ function therefore is essential -

for example urine output and mental status (measured as the Glasgow coma score). The supplyof oxygen to tissues and organs is crucial and this can be considered in the form of the equation

shown in Figure 1, which quantifies oxygen delivery.


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Oxygen delivery (DO2) (ml/min) = cardiac output (CO) x blood oxygen content

DO2 = CO x Hb (g/dl) x Saturation (%) x 1.34 x 10 / 100

Figure 1: The equation describing tissue oxygen delivery

The oxygen delivery equation addresses three important items in the delivery of oxygen to

tissues: a) cardiac output (which can be thought of as stroke volume x heart rate); b)haemoglobin; c) oxygen saturation (or PaO2, which is dependent on adequate ventilatory

function)

Distribution of blood flow within the microcirculation, and blood pressure itself are also

important and will be discussed in another review.

Monitoring helps in the early diagnosis of change in a physiological parameter and provides

guidelines towards institution of appropriate therapy. Basic knowledge of the principles of

monitoring equipment and correct interpretation of data is important since a failure to do so can

result in misdirected therapy. No amount of monitoring, however, can replace the closeobservation of clinical signs. Monitoring is not the same as treatment. The mere institution of

even the most invasive of monitoring techniques cannot alone alter outcome without

modification of treatment. It cannot, therefore, be emphasised enough that monitoring is not thesame as, nor a substitute for treatment.

THE PHYSIOLOGICAL RESPONSES TO STRESS AND TRAUMA

Following major trauma, patients exhibit characteristic behaviour. These include immobility,

when patients are fearful of moving or interacting; withdrawal, when patients may cease beingaware of their environment and become incommunicative; and antagonism, when patients may

resist interaction and display hostility to those around them. Altered cerebral blood flow mayalso be a reason for altered mental state.

The simple vital signs are not normal following trauma or major operation; patients are typicallyfebrile, hypertensive, with a tachycardia and tachypnoea. Fever is common in the hours and days

following resuscitation from moderate to severe trauma or major operations. It may be caused by

tissue inflammation and cytokine release. Following fluid resuscitation after trauma, bloodpressure may be low, normal, or high. Blood pressure correlates poorly with either blood volume

or flow. Sympathetic stimulation and high levels of circulating catecholamines cause

tachycardia. Following severe trauma, tachycardia typically persists even after hypovolaemia has

been corrected and pain controlled. In severe trauma or shock, however, tachycardia may not

occur, and heart rate may be normal or decreased; this may seriously impair the compensatoryhyperdynamic physiological response that is necessary for recovery. Increased minute

ventilation, due to both tachypnoea and an increase in tidal volume is an expected responsefollowing major operation or injury. It is driven by increased catecholamine levels and

sympathetic tone as well as by increased oxygen consumption and carbon dioxide production

following trauma.


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Urine output is often diminished early after trauma or operation because of hypovolaemia, a

decrease in renal blood flow, and a hormonal milieu that leads to sodium and water reab-

sorption. However, resuscitation with large volumes of crystalloid solutions as well as commonlyused osmotically active agents such as radiological contrast media and mannitol, increase urine

output. Thus, urine output may be decreased, normal, or increased following trauma, and may

not accurately reflect the intravascular volume.

Trauma is also usually followed by leucocytosis, especially granulocytosis. This pattern mimicsthat of sepsis, but it often occurs without infection.

MEASUREMENT OF ADEQUACY OF TISSUE OXYGENATION

Much of what will be discussed in this review revolves around the maintenance of normal

aerobic metabolism and thus maintenance of viable cell function and measurement of the degreeof tissue oxygenation. Reduced supply of oxygen over demand for oxygen results in cell injury.

Low blood flow states, microcirculatory failure and endotoxaemia are all important factors in the

pathogenesis of cell injury which may lead to organ failure in critically ill patients . These threefactors are all interlinked. Virtually all acute responses of cells to injury involve alterations of the

membrane systems and ischaemia and hypoxia cause cessation of normal mitochondrial activity

and thus interference with normal ATP synthesis.

The assessment of tissue oxygen supply is notoriously difficult although theoretically possible.Anaerobic tissues will produce lactate and not extract oxygen. Therefore, it is possible to

measure lactate and oxygen content in the venous blood draining individual tissues, which can be

compared with those of the arterial blood. In practice this approach can only be applied to a

limited number of organs where the relevant blood samples can be taken - these include the lung(systemic artery versus pulmonary artery), the liver (systemic artery versus hepatic vein) and the

brain (systemic artery versus jugular bulb). There are also microelectrode systems availablewhich can measure PO2 and pH as well as some electrolytes (including potassium which isreleased from ischaemic tissues) but again in practice these can only be placed in relatively few

sites (e.g. muscle). Laser Doppler flow monitoring can be used to assess local blood flow but this

does not look at oxygen uptake or utilisation. A further system, called NIRAS, has been used tomonitor cerebral blood flow and cerebral metabolic rate. This system uses infra-red light and,

therefore, has the problem of attenuation of the signal within tissues (a particular problem in the

adult skull).

Regional hypoperfusion occurs despite an apparently normal or even supranormal oxygendelivery - indeed this may be worsened by some drugs used routinely to maintain systemic blood

pressure and flow. Gastric tonometry (see below) is one indirect measurement which reflects

blood flow to the gastric mucosa. Some studies have demonstrated that gastric intramucosal pHis a better indicator of prognosis in the critically ill than any other single measurement of tissue

perfusion. Moreover, the direction of change in its value during resuscitation is highly predictive

of outcome.

CARDIOVASCULAR SYSTEM MONITORING


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Temperature

Peripheral temperature reflects tissue perfusion and is affected by vasoconstriction and low

cardiac output. Core temperature can be monitored at the tympanic membrane, oesophagus,bladder or rectum. There is an increased gradient between core and peripheral temperature in

shock states. Like arterial blood pressure, temperature gradients are a very useful non-specificmonitor. Thermistors are used commonly for monitoring core temperatures and are based on the

principle of changing resistance with temperature.

Electrocardiogram (ECG)

The ECG detects the voltage difference at the body surface and amplifies and displays the signal.

The ECG provides useful information about ischaemia, arrhythmias, electrolyte imbalance and

drug toxicity. Standard bipolar leads I, II and III have a limited role in detecting ischaemia.Modification of these leads (called lead CM5) can detect arrhythmias as well as ischaemia. CM5

lead has the negative electrode (right arm) at the manubrium and the positive electrode (left arm)

at V5 with the waveform selector switch turned to lead I. Many of the monitoring systems nowused in both the cardiac and general intensive care units are able to automatically recognise a

variety of arrythmias.

Pulse Oximetry

Oxygenated and reduced haemoglobin absorb light in the visible and near infra-red regions. By

comparing the ratio of light absorbed at a wavelength where absorption is very different with awavelength where absorption between the two forms is similar, the ratio of oxyhaemoglobin to

reduced haemoglobin - the haemoglobin saturation - can be measured. Advances in the design of

this technology has allowed just the absorption of light by the pulsatile component of

haemoglobin (i.e. arterial) in the finger or ear lobe to be measured (SpO2), so allowing estimatesof arterial saturation (SaO2) to be made.

In healthy patients the pulsatile component of the signal is only around 2% of the total absorption

making the signal to noise ratio of the measurement poor. At low haemoglobin levels themeasurement becomes unreliable. Furthermore, in critically ill patients peripheral perfusion is

often reduced, which further degrades the signal to a point at which reliable measurements of

saturation cannot be made. Pulse oximeters cannot distinguish between carboxyhaemoglobin andoxyhaemoglobin due to a similar absorption spectrum.

In most ICU patients measurement of SpO2 by pulse oximetry reflects arterial saturation and

because of the relationship between SO2

and PO2

described by the haemoglobin dissociationcurve, this is further extended to include an indication of PaO2. However, it should beremembered that most individuals will be at the flat portion of the dissociation curve and a

saturation of around 97% from the pulse oximeter will only suggest that the PaO2 is probably in

excess of 9kPa

Haematocrit and Haemoglobin Concentration


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Low haematocrit tends to be associated with improved peripheral perfusion because of decreased

viscosity -although the exact contribution of this fact to the perfusion in the patient is largely

unknown, since much of this hypothesis is based on what happens in glass capillary tubes ratherthan small blood vessels. However, there may be compromised tissue oxygen delivery due to

decreased oxygen carrying capacity.

Serial decline in haematocrit indicates continued bleeding, but haemodilution with crystalloids

can also result in a fall in the haematocrit. The percentage of red cells present in a blood samplegives an indication of adequacy of blood replacement following trauma and surgery. In the

critically ill patient an ideal haematocrit is probably 35%, with a haemoglobin concentration of

12-14 g/dl.

Arterial Blood Pressure

Arterial blood pressure is proportional to cardiac output when peripheral resistance is constant.

Arterial pressure is affected by changes in the volume status of the patient, vasomotor tone and

cardiac output. Blood pressure is maintained by physiological compensation in the face ofchanges in blood volume and cardiac output. Indeed blood pressure may be normal despite

grossly impaired cardiac function and, therefore, is only a crude indicator of the state of the

circulation. However, if blood pressure is inadequate then tissue perfusion will be inadequate.

Furthermore, in critical illness autoregulatory mechanisms in vascular beds such as the brain andkidney may become impaired and perfusion to these organs will be pressure dependent.

Flow to tissues is crucially dependent on mean blood pressure. This pressure is not simply an

average of the systolic and diastolic pressures but is weighted more towards the diastolic

pressure - one-third the sum of systolic plus twice the diastolic pressure. A knowledge of themean arterial pressure is also required for the calculation of systemic vascular resistance and is

often given automatically by many of the electrical monitors of blood pressure and cardiacoutput.

Indirect methods of measuring blood pressure include palpation, auscultation and

oscillotonometry. Direct arterial pressures can be recorded by inserting a cannula in the radial,

femoral or dorsalis paedis artery and connecting it to a zeroed and calibrated transducer which

converts pressure energy into electrical signals. The presence of air bubbles, leaks in the systemor blocked cannulae can produce an excessively damped trace. The system is said to be optimally

damped when the dicrotic notch of the waveform can be readily distinguished and the systolic

waveform is not too spiky (Figure 2).

Figure 2: Arterial blood pressure measured using a pressure transducer system is subjectto erroneous readings of both systolic and diastolic pressure depending on the damping of

the system


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Central Venous Pressure (CVP)

Central venous pressure is a useful, although not very accurate, tool for assessing the volume

status of the patient. CVP is the most common parameter used to guide fluid therapy in a patientwith hypovolaemia following trauma, shock, burns, or sepsis. CVP catheters can be inserted at

different sites but in each case the tip of the catheter should be intrathoracic. Sites used for the

insertion of cannulae include the external jugular vein, internal jugular vein (high or lowapproach), subclavian vein, femoral vein and the antecubital vein. The Seldinger technique is

used most commonly where the vein is punctured with a needle followed by insertion of a J-wire

through the needle. The needle is then removed and the catheter passed over the wire after prior

dilatation of the site if necessary. The subclavian site is probably the preferred site in the ICUpatient since it is associated with fewest infective complications - however it does have a higher

incidence of pneumothorax.

The value of the CVP can be obtained using a saline filled manometer, zeroed to the midaxillary

line as the reference point, or by using a pressure transducer. Normally CVP ranges between 6and 12 mmHg. There can be a discrepancy between CVP and left side heart filling pressures in

patient with chronic obstructive airways disease (COAD), pulmonary hypertension or mitral

valve disease.

Pulmonary Artery Occlusion Pressure (PAOP)

Pulmonary artery occlusion pressure is used to monitor the left ventricular end diastolic

pressures provided the mitral valve is normal. The balloon tipped pulmonary flotation catheter

(length 110cm) is introduced through an insertion sheath (placed in the internal jugular vein orsubclavian vein). The distal lumen is connected to a pressure transducer and pressure traces

displayed on the monitor assist in identification of the position of the catheter (Figure 3). Once

the catheter tip is in the right atrium the balloon is inflated with the recommended volume(usually


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and is termed pulmonary artery occlusion pressure. Normally the PAOP varies between 8 and

12mmHg. Patients with poor left ventricular function have a PAOP exceeding 18mmHg.

Figure 3: The pressure waveform changes observed during placement of a flow-directed

balloon tipped pulmonary artery catheter. Pressure is given as millimetres of mercury. RA,

right atrium; RV, right ventricle; PA, pulmonary artery; PAOP, pulmonary arteryocclusion pressure; PAWP, pulmonary artery wedge pressure

Pulmonary artery catheters are extremely useful in the critically ill patient since not only can

PAOP and cardiac output be measured but also the derived parameters, such as systemic andpulmonary vascular resistance and cardiac work, can be used to guide therapy. Clinical

applications of these catheters have widened to include oximetry (mixed venous oxygen

saturation), pacing and right ventricular ejection fraction. Modification of therapy as a result ofinformation derived from the pulmonary artery catheter data has been reported to improve the

outcome and shorten the hospital stay. By and large these modifications centre around changes in

cardiac filling pressure (PAOP) where fluid is given until PAOP rises without any furtherincrease in cardiac output; or by using inotropes to enhance cardiac output. The main indications

for the use of pulmonary artery catheters are poor left ventricular function (due to ischaemia,

valvular heart disease, cardiomyopathy and aneurysm), sepsis, burns, trauma, ARDS and thosewith major fluid shifts for other reasons. Recently there has been criticism of the over-use of

pulmonary artery catheters and in a large study (Connors et al) it was found that mortalitity was

higher in those patients in whom a PA catheter was used.

Cardiac Output and Haemodynamic Variables

Cardiac output can be measured using the Fick principle: Cardiac output (CO) = VO2 /CaO2-

CvO2

Where CaO2 is the arterial oxygen content, CvO2 is the mixed venous oxygen content and VO2 is

the oxygen consumption.

In practice a pulmonary artery catheter is used which has a temperature sensor at its end -thermistor tipped. Cold 5% dextrose or 0.9% saline (either 5 or 10ml) is rapidly injected into the

right atrium through the CVP lumen of the catheter and its temperature is automatically sensed at

the site of injection. The thermistor at the tip of the catheter within the pulmonary artery is alsosensed automatically and compared with that at the CVP injection port. A curve is obtained by

the cardiac output computer which plots temperature change with time. There are now catheters

available with heating wires built into them which automatically measure cardiac output everyfew minutes without the need for an injection of cold solution.


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Based on Ohms law, resistances (R) within the vascular system can be derived using the

pressure drop (potential difference or V) at a known flow rate or cardiac output (current or I).

R = V / I

Systemic vascular resistance (SVR) = mean arterial blood pressure - CVP / CO x 80

Pulmonary vascular resistance (PVR) = mean pulmonary artery pressure - PAOP / CO x 80

In each case the multiplication factor of 80 converts the resistance into commonly used units of

dyne.sec/cm-5 and normal values are 770-1500 and 20-120, respectively. The values from

individuals of varying sizes can be compared by indexing to body surface area and this applies tocardiac output itself as well as resistances and ventricular stroke work.

Left ventricular stroke work index (LVSWI) = Stroke volume index x mean arterial pressure x

0.0144

Again there is a correction factor of 0.0144 which converts the measurement to g.m/m2 and the

normal range is 44-68.

Despite normal cardiac output, poor tissue perfusion can cause the production of ischaemic

metabolites and lactic acidosis due to anaerobic metabolism. Shoemaker has proposed the

concept of delivery dependent oxygen consumption where the tissues extract oxygen in direct

proportion to blood flow (Figure 4). It is suggested that at a certain level of oxygen delivery aplateau of oxygen consumption is achieved.

Oxygen delivery (DO2) = Cardiac output (CO) x oxygen content of the blood ml/min

Oxygen content of the blood = haemoglobin(mg/dl) x % saturation x 1.34 x 10 ml/litre /100

Figure 4: Oxygen consumption and oxygen delivery curves showing a defined knee where

consumption of oxygen by the tissues becomes dependent upon delivery (supply

dependent). This point illustrates the importance of enhanced blood flow in sepsis where

the curve is said to be shifted, making supply dependency more likely


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Some idea of the adequacy of both supply and tissue uptake can be seen from monitoring the

mixed venous oxygen saturation (which can either be performed automatically by some

pulmonary artery catheters or by intermittent blood sampling and then measuring oxygensaturation using a co-oximeter). However, mixed venous saturation should be interpreted with

caution since there are many factors which may alter the value; including altered oxygen

delivery, altered arterial saturation, altered haemoglobin concentrations and altered tissueextraction (oxygen utilisation).

The aims of treatment on the ICU should not necessarily be to return the values of these

cardiovascular variables to normal, but to a level at which clinical improvement occurs. For

instance a patient with severe sepsis may already have a cardiac output that is twice that for anormal individual. However, in this patient even this figure is not high enough and the patient

may benefit from either fluid or inotropic agents to further increase cardiac output. Often these

particular patients respond to a given volume of fluid resuscitation in an abnormal way and donot generate the same increase in cardiac output that would be seen in a healthy person - thus

demonstrating the existence of myocardial depression.

Gastric Tonometry

Indirect measurement of mucosal pH may be performed since tissues are highly permeable to

CO2 and, hence, the PCO2 of fluid within the lumen of the gut is equilibrated with that of thecells in the superficial layers of the gut wall. The intramucosal pH (called pHi) can then be

determined using the Henderson-Hasselbalch equation although most workers now opt for

simply using the tissue PCO2 to guide therapy. The measurement of intraluminal PCO2 is madeusing a silicone balloon of approximately 3ml capacity which is permeable to CO2 and is

positioned at the distal end of a nasogastric tube (Tonometer TM, Tonometrics Inc., Bethesda,

MD). A sampling tube permits either the gas within the balloon to be directly sampled and

analysed directly or for saline to be added to the balloon and then withdrawn after a period ofequilibration.

It is suggested that acidosis within the gastric mucosa may be a major factor contributing to

stress ulceration (and consequent gastrointestinal haemorrhage) occurring in intensive care unit(ICU) patients. Furthermore, this localised acidosis is due to either: 1) demand for oxygen within

tissues which cannot be met by the available blood supply or 2) an impairment of oxygen

utilisation within these tissues. Hence, gastric mucosal ischaemia may be a local manifestation ofa more widespread process which affects the entire splanchnic circulation, and may be the easiest

index of impaired core tissue perfusion in critically ill patients, with oliguria and arterial

acidaemia occurring much later.

RESPIRATORY SYSTEM

Monitoring of the respiratory system on the ICU is often less sophisticated than that of thecardiovascular system. It consists largely of intermittent measurements of arterial blood gases

and manual recording of the ventilatory rate, pressures and volumes. Monitoring of the

respiratory system is extremely important. Increasing respiratory rate, shallow breathing patterns,


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paradoxical respiration, use of accessory muscles, tachycardia and excessive sweating all

indicate inadequate ventilation and impending respiratory failure.

Gas Exchange

Pulse oximetry (see above) is a simple and non-invasive method of monitoring oxygen saturation(SpO2) and is used to assess adequacy of gas exchange. Pulmonary artery catheters are now

available which use the same principle and can thus measure mixed venous oxygen saturation.

Arterial blood gases and pH are useful screening tests of pulmonary function and often the first

laboratory signs of impending lung problems are seen as changes in PaO2, PaCO2 and pH. APaO2 value of less than 8.0kPa and a PaCO2 greater than 6.0kPa, while breathing 50% oxygen in

the absence of COAD, indicates respiratory failure. Critically ill patients are usually receiving

supplemental oxygen and the PaO2 should always be interpreted in relation to the inspiredoxygen tension (FIO2). Patients with chronic pulmonary disease can tolerate abnormal blood gas

values, but the patient with normal lungs should always be given supplemental oxygen if at all

hypoxic followed by ventilatory support if the respiratory insufficiency does not improve.Intermittent analysis of blood gases gives useful information during mechanical ventilation and

weaning. On-line intravascular monitoring of PaO2, PaCO2 and pH is now available but its

usefulness over and above intermittent analysis has yet to be established.

RENAL SYSTEM

Urine Output

Hourly urine output is a very useful guide to the adequacy of cardiac output, splanchnic

perfusion and renal function. Measurement of the specific gravity and osmolality of the urine is

used to differentiate between pre-renal and renal failure.

Plasma and Urine Electrolytes, Urea and Creatinine

Trends of blood urea, creatinine and serum electrolytes are useful for evaluating the progress ofrenal function. Urea can rise in the absence of renal dysfunction in conditions such as

gastrointestinal bleeding, high protein intake and increased catabolism. Acute and chronic renal

failure result in rising urea and creatinine. The concentrating ability of the kidney can beestimated by comparing the blood and urine sodium, potassium and urea. Urine / plasma

osmolality ratio of


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indicators of the degree of liver disease and indicators of cell damage are frequently used

instead , for example measurement of hepatic enzymes.

The liver synthesises albumin, clotting factors, anti-thrombin III and protein C - all of which canbe used to assess liver function. Albumin, because of its long half-life, is not a sensitive measure

of acute liver dysfunction. Defects in clotting are reflected in the standard tests and prothrombintime is a useful guide for the monitoring of liver function. Factor VII has a half-life of 4-8 hours

and its measurement can be used to assess the severity of coagulopathy even in cases where freshfrozen plasma has been given.

A raised serum bilirubin concentration is frequently seen in liver disease. However, this is not

invariably so. Indeed, in acute hepatic failure patients are most often not jaundiced and have

normal or only slightly abnormal serum bilirubin levels. Greatly increased serum transaminaseactivities are characteristic of hepatocellular damage, while raised alkaline phosphatase activity

is seen in biliary obstruction.

CENTRAL NERVOUS SYSTEM

The requirement for sedatives, opioids and muscle relaxants make the clinical evaluation of thecentral nervous system extremely difficult. Intracranial pressure (ICP), electroencephalography

(EEG) and cerebral function monitoring (CFM) are used to monitor the function of the CNS in

those critically ill patients where such monitoring is required. However, monitoring CNSfunction by Glasgow coma score and other assessments of routine neurological status is an

essential part of the management of the critically ill patient

Intracranial Pressure (ICP)

ICP is assessed by measuring the ventricular pressure directly or indirectly with the patient in thesupine position. The normal ICP is less than 10mmHg. Continuous measurement of ICP can bemade by a variety of devices placed within the cranial vault via a small burr hole made in the

parietal or frontal areas of the non-dominant hemisphere. There are extradural devices; subdural

catheters or the LAD device; and intra-ventricular catheters. All except for the LAD device arefluid filled systems which are connected to conventional pressure transducer and recording

systems.

Cerebral oedema or haemorrhage within the cranial vault will rapidly increase the ICP because

the brain, unlike other organs, is rigidly confined with the skull. Increased ICP is most frequentlyseen following head injury, subarachnoid haemorrhage, hepatic encephalopathy, brain tumours

and encephalitis (Figure 5). ICP above 20-25mmHg is often amenable to therapeutic interventionincluding control of hypercapnia (using mechanical ventilation to maintain a PaCO2 of 4kPa),mannitol, slight head-up tilt and sedation with an intravenous anaesthetic agent such as propofol

or thiopental.

Figure 5: A compliance curve for ICP - pressure initially changes little with changes in

volume due to compensatory mechanisms. Beyond this range pressure suddenly increases

rapidly with even minor volume changes within the skull


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Three types of ICP wave have been described - A, B, and C waves. The A waves indicate a

dangerously low cerebral compliance when ICP can easily rise by up to 50mmHg and be

sustained for 5 to 20 minutes with only a very small increase in intracerebral volume. B wavesrepresent rhythmic oscillations once every 1-2 minutes and under these circumstances the ICP

can readily rise but will usually abruptly fall to normal levels. C waves occur with a frequency of4 to 8 per minute.

Cerebral Function Monitor (CFM)

The cerebral function monitor is a compact form of EEG where unwanted frequencies are

filtered and the result summated to give a more easily interpreted single trace. The CFM usesonly three electrodes and monitors electrical activity continuously. It is commonly used during

carotid artery surgery and in patients likely to convulse in the ITU.

HAEMATOLOGICAL

Haemostatic failure and acquired coagulopathies such as disseminated intravascular coagulation

are not uncommon in the ITU. Main causes of deficiencies in clotting factors are liver disease,vitamin K deficiency, anti-coagulant drugs, DIC and massive blood transfusion. Assessment of

clotting function is usually by measurement of prothrombin time, activated partial

thromboplastin time, fibrinogen concentration and either fibrin degradation products (FDPs) orD-dimer.

SUMMARY

Different patients respond to a similar insult in different ways and have different physiological

reserves. Assessment of physiological status is important in allowing these differences to beappreciated. In addition, many of the treatment options we use in the critically ill patient require

some form of physiological monitoring for us to gauge their effectiveness.

The response of the patient to surgical stress and trauma should be seen as an attempt to maintain

a normal supply of oxygen and nutrients to the tissues of the body. An equation which


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summarises the assessment of this response is the oxygen delivery equation. Monitoring is

focused to examine the components of this equation - cardiac output, haemoglobin concentration

and oxygenation of the blood. The most useful monitors are those which assess organ function.Whilst these modalities are few they are often easy to assess, for example Glasgow coma score,

urine output and core to periphery temperature gradient. No amount of monitoring can cure a

patient. However, the successful management of critically ill patients requires the use ofmonitors to allow formulation of appropriate management strategies.

FURTHER READING

Bakker J, Leon M, Coffernils M, Gris P, Kahn RJ, Vincent JL. Blood lactate levels are

superior to oxygen derived variables in predicting outcome in human septic

shock. Chest1991; 99: 956-62 Connors AF Jr, Speroff T, Dawson NV, Thomas C, Harrell FE Jr, Wagner D, Desbiens

N, Goldman L, Wu AW, Califf RM, Fulkerson WJ Jr, Vidaillet H, Broste S, Bellamy P,

Lynn J, Knaus WA. The effectiveness of right heart catheterization in the initial care of

critically ill patients.JAMA 1996; 276: 889-97 Eremin, OE, ed: The Scientific and Clinical Basis of Surgical Practice. Oxford: Oxford

University Press, in press

Fiddian-Green RG. Splanchnic ischaemia and multiple organ failure in the critically

ill.Ann R Coll Surg Eng1988; 70: 128-34

Fiddian-Green RG, Haglund U, Gutierrez G, Shoemaker W. Goals for the resuscitation ofshock. Crit Care Med1993; 21: S25-31

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Copyright date: 14th October 1999

Correspondence: Professor NR Webster, Anaesthesia and Intensive Care, Institute of Medical

Sciences, Foresterhill, Aberdeen AB25 2ZD, UK Email: [email protected]

1999 The Royal College of Surgeons of Edinburgh, J.R.Coll.Surg.Edinb.,44; 6: 386-93
mailto:[email protected]:[email protected]

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It Has Long Been Recognised That the Physiological Response of the Patient to a Stress or Disease Process Will Very Largely Determine the Outcome