NIGEL R. WEBSTER
Academic Unit of Anaesthesia and Intensive Care, University of Aberdeen, Aberdeen,
U.K.
1
Introduction Renal system
The physiological responses to stress and trauma
Central nervous system
Haematological
Measurement of adequacy of tissue oxygenation
Summary
Cardiovascular system monitoring
Further reading
Respiratory system
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 misdirected therapy. 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 and consisted 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 patient’s status before the acute illness. APACHE II was introduced in

2
1985 and incorporated major changes in the 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 estimates provided 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 this review -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 - core
2.
Mean arterial pressure
3.
Heart rate
4.
Respiratory rate - ventilated or non-ventilated
5.
Oxygenation
FIO2 > 0.5 record A-aDO
2
FIO2 < 0.5 record PaO
2
6.
Arterial pH
7.
Serum sodium
8.
Serum potassium
9.
Serum creatinine
10.
Haematocrit
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 of the 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 also important. 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 to critical 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 nerve signals 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 activated by painful

3 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 of shock; 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 an important 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 of local 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. These responses to injury and ischaemia coordinate 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 supply of 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.
Oxygen delivery (DO
2
) (ml/min) = cardiac output (CO) x blood oxygen content
DO
2
= 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 PaO
2
, 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 close observation 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 the same as, nor a substitute for treatment.
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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 being aware of their environment and become incommunicative; and antagonism, when patients may resist interaction and display hostility to those around them. Altered cerebral blood flow may also be a reason for altered mental state.
The simple vital signs are not normal following trauma or major operation; patients are typically febrile, 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, blood pressure 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 compensatory hyperdynamic physiological response that is necessary for recovery. Increased minute ventilation, due to both tachypnoea and an increase in tidal volume is an expected response following 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.
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 commonly used 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 mimics that 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 degree of 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

5 critically ill patients . These three factors 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 available which can measure PO
2
and pH as well as some electrolytes (including potassium which is released 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 to monitor 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 oxygen delivery - 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 pH is 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
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-specific monitor. 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

6 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 now used 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 a wavelength 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 (SpO
2
), so allowing estimates of arterial saturation (SaO
2
) 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 the measurement 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 and oxyhaemoglobin due to a similar absorption spectrum.
In most ICU patients measurement of SpO
2
by pulse oximetry reflects arterial saturation and because of the relationship between SO
2
and PO
2
described by the haemoglobin dissociation curve, this is further extended to include an indication of PaO
2
. However, it should be remembered 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
PaO
2
is probably in excess of 9kPa
Haematocrit and Haemoglobin Concentration
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 rather than 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 sample gives 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 of changes 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 and kidney may become impaired and perfusion to these organs will be pressure dependent.
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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 the mean 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 cardiac output.
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 system or 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 subject to erroneous readings of both systolic and diastolic pressure depending on the damping of the system
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

8 therapy in a patient with 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 low approach), 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 ICU patient 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 6 and 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 or subclavian 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 <1.5ml) of air and the catheter is further advanced whilst monitoring the pressure waveforms. The catheter enters the pulmonary artery after having passed through the right ventricle. Transition from a right ventricular trace to a
PA trace is confirmed by an increased diastolic pressure. Eventually, the catheter tip wedges in a small branch of the pulmonary artery causing the waveform to flatten as there is no flow across the catheter. The stationary column of blood extending from the tip of the catheter to the left atrium approximates the left atrial pressure 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 flowdirected balloon tipped pulmonary artery catheter. Pressure is given as millimetres of mercury. RA, right atrium; RV, right ventricle; PA, pulmonary artery; PAOP, pulmonary artery occlusion pressure; PAWP, pulmonary artery wedge pressure

9
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 and pulmonary 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 of information 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 further increase 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 those with 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) = VO
2
/CaO
2
-CvO
2
Where CaO
2
is the arterial oxygen content, CvO
2
is the mixed venous oxygen content and
VO
2
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 also sensed 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 every few minutes without the need for an injection of cold solution.
Based on Ohm’s 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 to cardiac output itself as well as resistances and ventricular stroke work.
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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 a plateau of oxygen consumption is achieved.
Oxygen delivery (DO
2
) = 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
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 oxygen saturation 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 tissue extraction (oxygen utilisation).
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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 a normal 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 do not 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 CO
2
and, hence, the PCO
2
of fluid within the lumen of the gut is equilibrated with that of the cells 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 PCO
2
to guide therapy. The measurement of intraluminal PCO
2
is made using a silicone balloon of approximately 3ml capacity which is permeable to CO
2
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 of equilibration.
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 of a 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 the cardiovascular 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, 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 (SpO
2
) 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.
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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 PaO
2
, PaCO
2 and pH. A PaO
2
value of less than 8.0kPa and a PaCO
2
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 PaO
2
should always be interpreted in relation to the inspired oxygen tension (FIO
2
). 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. Online intravascular monitoring of PaO
2
, PaCO
2
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 of renal 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 be estimated by comparing the blood and urine sodium, potassium and urea.
Urine / plasma osmolality ratio of <1.2, urea ratio of <10 and a urinary sodium of
>40mmol/l indicates acute renal failure. The use of mannitol and loop diuretics should be taken into account as they can cause electrolyte abnormalities.
HEPATIC SYSTEM
The liver performs the important functions of synthesis, storage, metabolism and excretion of toxic products. Damage to the liver may not obviously affect its activity because of a considerable functional reserve. Consequently, tests of liver function alone are insensitive indicators of the degree of liver disease and indicators of cell damage are frequently used instead , for example measurement of hepatic enzymes.

13
The liver synthesises albumin, clotting factors, anti-thrombin III and protein C - all of which can be 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 prothrombin time 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 fresh frozen 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 transaminase activities 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 the central 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 CNS function 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 the supine position. The normal ICP is less than 10mmHg. Continuous measurement of ICP can be made 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 are fluid 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 frequently seen following head injury, subarachnoid haemorrhage, hepatic encephalopathy, brain tumours and encephalitis (Figure 5). ICP above 20-25mmHg is often amenable to therapeutic intervention including control of hypercapnia (using mechanical ventilation to maintain a PaCO
2
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

14
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 waves represent 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 of 4 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 uses only 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
Hemostatic 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) or D-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 be appreciated. 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.

15
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 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 of monitors 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. Chest 1991; 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 Eng 1988; 70: 128-34
Fiddian-Green RG, Haglund U, Gutierrez G, Shoemaker W. Goals for the resuscitation of shock. Crit Care Med 1993; 21: S25-31
 Knaus WA, Draper EA, Wagner DP et al. APACHE II: a severity of disease classification system for acutely ill patients. Crit Care Med 1985; 13: 818-29
 Knaus WA, Wagner DP, Draper EA et al. The APACHE III prognostic system.


Chest 1991; 100: 1619-36
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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: n.r.webster@abdn.ac.uk
©1999 The Royal College of Surgeons of Edinburgh,
J.R.Coll.Surg.Edinb.,44; 6: 386-93 http://www.rcsed.ac.uk/journal/vol44_6/4460010.htm#MEASUREMENT