 \227 60 l \227 t C m \200 where I = amount of indicator injected, Cm = mean concentration of the indicator, an d t = curve duration. Traditionally, indocyanine green was injected into a central vein wit h arterial blood repeatedly sampled to construct a time-concentration curve with a rapid up stroke and an exponential decay. Plotting the dye decay curve semi-logarithmically and extr apolating values to the origin produces cardiac output. The LiDCO device is based on a similar principle, though using lithium as the \200\230dye \200\231. This can be injected into a peripheral vein and sampled from the radial artery. Advantages \200 Reasonably accurate and less invasive than pulmonary artery placement. Other information de rived. Disadvantages \200 \200 Accumulation of lithium with multiple repeated measurements. Measurement/calibration takes >10min. Ideally, 2 \200\2233 lithium time- concentration curves should be performed per cal ibration to improve the coef \201 cient of variation. Can underestimate low output values. Inaccurate with moderate/severe valvular regurgitation, major pulmonary embolism, intracar diac shunt. Paralyzing agents and severe hyponatraemia interfere with lithium measurement. Lithium should not be used in pregnant patients. \200 CARDIAC OUTPUT \200\224INDICATOR DILUTION 183 See also: Basic resuscitation, p338; Fluid challenge, p342; Hypotension, p380; Heart failur e \200\224 assessment, p398. 184 CHAPTER 9 Cardiovascular monitoring Cardiac output \200\224Doppler ultrasound Doppler ultrasound An ultrasound beam of known fr equency is re \202 ected by moving blood corpuscles with a shift in frequency proportional to blood \202 ow velocity. The actual velocity is calculated from the Doppler equation; this requires the cosine of the vector between the direction of the ultrasound beam and tha t of blood \202 ow. This has been applied to blood \202 ow in the ascending aorta and a ortic arch (via a suprasternal approach), descending thoracic aorta (oesophageal approach), and intracardiac \202 ow (e.g. transmitral from an apical approach). Spectral analysis o f the Doppler frequency shifts produces velocity-time waveforms, the area of which represen ts \200\230stroke distance \200\231, i.e. the distance traveled by a column of blood with each left ventricular systole. (See \201 gure 9.4). The product of stroke distance and ao rtic (or mitral valve) cross-sectional area is stroke volume. Cross- sectional area can be measured echocardiographically. However, as both operator expertise and equipment is requir ed, this additional measure- ment can be either ignored or assumed from nomograms to provid e a reasonable estimate of stroke volume. Advantages \200 \200 \200 Quick and minimally invasive. Reasonably accurate if performed properly. Measures left hear t output, unaffected by mitral (unless measured transmitrally) or tricuspid regurgitation, or by intracardiac shunts. Continuous (via oesophageal approach) \200\224but may need repos itioning. Other information on contractility, preload, and afterload from waveform shape (s ee \201 gure 9.5). Multiple studies showing outcome bene \201 t in high-risk surgical pa tients from guided \202 uid optimization intra-operatively or post-operatively. \200 Disadvantages \200 \200 Non-continuous (unless via esophagus). Learning curve to ensure correct signal is insonated (85 \200\22310 oesophageal, 815 \200\22320 with suprasternal and 30+ with intracardiac). N ot reliable with turbulent \202 ow conditions, e.g. intra-aortic balloon counterpulsation (oesophageal), aortic stenosis or regurgitation (suprasternal or intracardiac from aortic out \202 ow tract), mitral regurgitation (transmitral). Oesophageal approach assumes propo rtionality of \202 ow going to upper and lower body is maintained (approximately 30:70) \200\224this will change during aortic cross-clamping (vascular surgery) or use of epidural . Suprasternal measurements can be hampered by short neck or obesity (probe has to get behi nd sternum to insonate ascending aorta or arch correctly), mediastinal air (e.g. post-cardi ac surgery), and co-located vessels, e.g. innominate artery. CARDIAC OUTPUT \200\224DOPPLER ULTRASOUND 185 VELOCITY mean acceleration peak velocity stroke distance TIME flow time cycle time Fig. 9.4 Doppler velocity-time waveform. Corrected \202 ow time (FTc) = \202 ow time corrected to heart rate of 60bpm. Normal ra nge is 330 \200\223360ms. The FTc is inversely related to systemic vascular resistance. Thu s, FTc falls with decreased preload or increased afterload (e.g. hypovolaemia, vasoconstric tion, obstruction such as PE or tamponade) while FTc increases with vasodilatation. Peak ve locity (and acceleration) are markers of left ventricular contractility and are age-depende nt (see table below). Values increase with positive inotropy and fall with negative inotrop ic states (e.g. heart failure, beta-blockade). Age 20 50 70 Normal range of peak velocity (cm/s) 90 \200\223120 60 \200\22380 50 \200\22370 Preload increase Preload decrease Predominant change Afterload reduction Afterload increase Positive inotropy Negative inotropy Fig. 9.5 Effect of haemodynamic changes on Doppler velocity-time waveform shape. See also: Basic resuscitation, p338; Fluid challenge, p342; Hypotension, p380; Heart failur e \200\224assessment, p398. 186 CHAPTER 9 Cardiovascular monitoring Cardiac output \200\224pulse contour analysis Pulse contour analysis The concept of this te chnique is that the contour of the arterial pres- sure waveform is proportional to stroke v olume. This, in theory, allows continuous, minimally invasive monitoring of cardiac output. However, it is greatly in \202 uenced by arterial compliance (the relationship between pr essure and volume) and aortic impedance. Thus, the major challenges for technologies using this approach are to assess arterial compliance con- sistently and accurately in an individ ual patient and to be able to track changes in cardiac output closely when there are concur rent changes in compliance, e.g. during rapid blood loss, vasodilatation, or changes in tem perature. This is complicated further by the changing morphology of the blood pressure waveform as it travels down peripheral arteries, especially during alterations in blood \202 ow redistr ibution, e.g. with severe vasoconstriction. It is also essential to ensure a correctly damp ed pressure waveform and non-kinking of the arm (radial) or groin (femoral). There are several commercial devices which use their own proprietary algorithms to estimate stroke volume. The LiDCOplus and PiCCO systems use an alternative cardiac output measuring technique (lithium dye dilution and peripheral thermodilution, respectively) in tandem for initial calibra- tion and subsequent re-calibration. The Flotrac and LiDCOrapid systems de rive an estimate of cardiac output without a calibrating device using the patient \200\231s blood pressure, gender, age, and body surface area. There are sig- ni \201 cant concerns regarding the overall accuracy of these systems and their ability to follow trends, especia lly those devices not calibrated against a reference technique. Even in calibrated systems, the literature suggest the need for frequent routine recalibration (1 \200\2234 hourly) or earlier if circulatory status changes to any signi \201 cant extent. Advantages \200 \200 Continuous \202 ow monitoring. Uses data from an arterial cannula already in situ for pre ssure monitoring. Assessment of \202 uid responsiveness using pulse pressure, systolic pr essure, or stroke volume variation. Disadvantages \200 Changes in vascular compliance (e.g. with changes in blood pressure, cardiac output, vascul ar resistance, body temperature) affect accuracy, thus regular recalibration is needed. Ina bility to con \201 rm accuracy of non-calibrated devices (stroke volume estimation or tren d following) unless a reference technique is used. Requires a good quality, non-obstructed, non-damped waveform. Ongoing debate about relative signal quality from radial vs femoral. Unreliable with arrhythmias. Unreliable with aortic stenosis and severe peripheral vascular disease. Cannot be used with intra-aortic balloon counterpulsation. \200 \200 \200 \200 CARDIAC OUTPUT \200\224PULSE CONTOUR ANALYSIS 187 See also: Basic resuscitation, p338; Fluid challenge, p342; Hypotension, p380; Heart failur e \200\224assessment, p392. 188 CHAPTER 9 Cardiovascular monitoring Cardiac output \200\224other techniques Thoracic bio-impedance Impedance changes originate in the thoracic aorta when blood is ejected from the left ventricle. This effect is used to determine stroke volume from formulas utilizing the electrical \201 eld size of the thor ax, baseline thoracic impedance, and \202 uctuation related to systole and ventricular ej ection time. A correction factor for sex, height, and weight is also used. The technique si mply utilizes four pairs of electrodes placed in proscribed positions on the neck and thora x; these are connected to a dedicated monitor which measures thoracic impedance to a low am plitude, high (70kHz) frequency 2.5mA current applied across the electrodes. Advantages Quick, safe, totally non-invasive, reasonably accurate in normal, spontane- ousl y breathing subjects. Disadvantages Discrepancies in critically ill patients, (especially those with arrhythmias, tachycardias, intrathoracic \202 uid shifts, anatomical deformities, aortic regur- gitat ion, metal within the thorax, inability to verify signal). Thoracic bioreactance This novel technology increases the signal-to-noise ratio by 100-fol d over bio-impedance. Four pairs of double electrodes are sited on the thorax (just below t he sternum) and the mid-axial line just below the shoulders. The upper electrodes emit a lo w-level electrical current that is sensed by their lower pairs. The signal utilizes both bi oimpedance and the relationship between the amount of thoracic \202 uid at any given time -point, and frequency shifts occurring as the electric current crosses the thorax. This pro duces the haemodynamic reactance waveform. Clinical experience of its accuracy and reliabil ity, particularly in critically ill patients, is limited at present. Direct Fick The amount of substance passing into a \202 owing system equals the dif- fere nce in concentration of the substance on each side of the system multiplied by \202 ow wi thin the system. Cardiac output is usually calculated by dividing total body O2 consumption by the difference in O2 content between arterial and mixed venous blood. Alternatively, CO 2 production can be used as the indicator. Arterial CO2 can be derived non-invasively from end-tidal CO2 while mixed venous CO2 can be determined by rapid rebreathing into a bag unti l CO2 levels have equilibrated. Advantages \200\230Gold standard \200\231 for cardiac outp ut estimation. Disadvantages For VO2: Invasive (requires measurement of mixed venous blood), requires leak -free, open circuit or an unwieldy, closed circuit technique, oxygen consumption measuremen ts via metabolic cart unreliable if FIO2 is high, lung oxygen consumption not measured by p ulmonary artery catheter technique (may be high in ARDS, pneumonia ). For CO2: Non-invasive but requires normal lung function, and is thus not generally applicable in ICU patients. CARDIAC OUTPUT \200\224OTHER TECHNIQUES 189 See also: Basic resuscitation, p338; Fluid challenge, p342; Hypotension, p380; Heart failur e \200\224 assessment, p392. 190 CHAPTER 9 Cardiovascular monitoring Pressure and stroke volume variation These can be used, within strict limitations (see belo w), to assess the like- lihood of responsiveness of the circulation to a \202 uid challen ge. It is based on the variation in size and height of the arterial pressure waveform durin g the respiratory cycle (see \201 gure 9.6). In spontaneously breathing subjects, BP decr eases on inspiration due to decreased left heart output. The range in normal subjects is 5 \200\22310mmHg. The reverse is seen during positive pressure ventilation where BP decreases on expiration. Pulsus paradoxus is an exaggeration of this phenomenon seen with marked cha nges in intrathoracic pressure (e.g. severe asthma) or impaired left heart \201 lling (e. g. pericardial tamponade). Stroke volume variation (SVV) SVmax \200\223 SVmin 0.5 (SVmax + SVmin) Pulse pressure variation (PPV) PPmax \200\223 PPmin 0.5 (PPmax + PPmin) Variation >10 \200\22315% (the optimal positive and negative predictive values vary between studies) suggests a high likelihood of preload responsive- ness. It can also indicate dele terious effects of PEEP on the circulation. Systolic pressure variation (SPV) The difference between maximal and minimal values of syst olic pressure during one breath. As well as SPV, the delta down ( \224down) component (diff erence between systolic pressure during a short period of apnoea and the lowest value durin g a breath) >5mmHg also predicts volume responsiveness. Advocates for the different measurements all claim superiority of their favored techinque o ver the others. Pulse pressure depends on stroke volume and arterial compliance while systo lic pressure depends on stroke volume, arterial compliance, and diastolic pressure. Limitations of PPV, SPV, and SVV \200 Use only in mechanically ventilated, deeply sedated 9 paralyzed patients in full control mo de ventilation (i.e. no spontaneous triggered breaths) receiving \201 xed rate tidal volu mes (generally \211 10mL/kg). Not reliable with arrhythmias. Unreliable in spontaneously b reathing, non-intubated patients where tidal volumes are smaller and variable. Major risk o f volume overload in conditions which also result in LV under \201 lling, e.g. obstruction (e.g. pulmonary embolus, tamponade, atrial myxoma) or right heart failure (e.g. right vent ricular infarction). Vasodilatation may increase SVV. Recruitment of abdominal muscles and forced expiration is a common \201 nding in ICU patients, resulting in a large rise in BP during expiration 9 changes in SV, thus rendering unreliable results. \200 \200 PRESSURE AND STROKE VOLUME VARIATION 191 PPmax PPmin SPV SVmax SVmin PP Pulse pressure SV Stroke volume SPV Systolic pressure variation Fig. 9.6 Pulse pressure, systolic pressure, and stroke volume variation. See also: Fluid challenge, p342. 192 CHAPTER 9 Cardiovascular monitoring Echocardiography Combines structural as well as dynamic assessment of the heart using ultra sound re \202 ected off various interfaces. Transthoracic or transoesophageal probes provide information on valve integrity, global (di astolic and systolic) and regional ventricular function, wall thickness, pericardial \202 uid or thickening, aortic dissection, ventricular volumes, ejection fraction, and pulmonar y pressures. It can also diagnose intracardiac masses (e.g. myxoma, clot), endocarditis, an d pulmonary embolism. Different parts of the heart can be best imaged from different approaches, e.g. apical four -chamber (see \201 gure 9.7), left parasternal long axis (see \201 gure 9.8), subcostal . Echocardiography can be used in single (M-mode) or 2-dimensional modes. Echocardiography is often combined with integral Doppler ultrasound for cardiac output esti mation derived from combined measurement of aortic diameter plus \202 ow at various sites , e.g left ventricular out \202 ow tract, aorta, transmitral. Analytical software or formu las can also enable compu- tation of cardiac output from estimations of ventricular volumes . Advantages \200 \200 \200 Non-invasive, safe. Relatively quick. Provides other useful information on cardiac structur e and function. Disadvantages \200 \200 \200 Expensive equipment. Lengthy learning curve and inter-observer variability. Body habitus or pathology (e.g. emphysema) may impair image quality. ECHOCARDIOGRAPHY 193 Fig. 9.7 Apical four-chamber view. Fig. 9.8 Parasternal long axis view. RV right ventricle; LVOT left venricular out \202 ow tract; AV aortic valve; MV mitral valve; LA left atrium; RA right atrium. See also: Cardiac output \200\224Doppler ultrasound, p184. 194 CHAPTER 9 Cardiovascular monitoring Tissue perfusion monitoring Near-infrared spectroscopy (NIRS) This non-invasive technique u tilizes near-infrared light to quantitate tissue oxyhaemoglobin concentration (StO2) or, mo re accurately, microvas- cular oxygenation in arterioles, capillaries, and venules. It may measure oxymyoglobin, though to what extent this in \202 uences the measurement is uncerta in. It is usually measured in a peripheral muscle, such as the thenar eminence or deltoid. As resting values vary widely in normal subjects (70 \200\22395%), it is a poor indicator o f mild to moderate shock states. It can be useful in detecting peripheral compartment syndr ome. More utility can be gained from the rate of fall in StO2 during proximal arterial occl usion (and/ or rise in StO2 on release of occlusion). A reduced rate of fall on occlusion s uggests decreased tissue O2 utilization 9 microvascular perfusion. Specialized spectrophotometers have the ability to detect mitochondrial cytochrome oxidase redox states \200\224this has been studied predominantly in neonatal brains, though there i s potential for extrapolation to other organs. StO2 has been shown to relate to interstitia l tissue PO2. Cautions \200 Reliability poor if used in muscle groups with signi \201 cant overlying adipose tissue, e .g. pectoral muscle in females, deltoid in the obese. Dark skin pigmentation may affect the readings. Microvascular circulation visualization This non-invasive technique uses sidestream dark \201 eld imaging (SDF) to visualize the microcirculation. An earlier technique used orthogo nal polarization spectroscopy (OPS), but this is no longer commercially avail- able. Brie \202 y, OPS utilized polarized light scattered by the tissue and col- lected by the objecti ve lens. High quality images of the microcirculation were obtained by absorbing surface str uctures lit up by depolarised light returning from deeper structures. SDF uses the same pri nciple but, rather than polarized light, uses light-emitting diodes that are isolated from its inner image-conducting core. The technique is mainly used sublingually, but can be applied to other areas, e.g. rectum, bowel stoma, or directly to internal organs during surgery. The device software enables of \202 ine semi-quantitative analysis of microcirculatory alterations affecting capillary de nsity and heterogeneity of blood \202 ow. The proportion of perfused capillaries may vary as may \202 ow characteristics within separate capillaries, e.g. continuous or stop- go. Plasma and cellular factors, e.g. viscosity, red cell rheology, degree of platelet and neu trophil rolling, and endothelial swelling \200\224all affect microv- ascular \202 ow char acteristics. Microvascular thrombosis is rare. It is a research tool at present providing images of the microcirculation in different orga n beds in a variety of conditions. Persisting abnormalities are a good prognostic indicator in shock. Applicability of changes in the sublingual circulation to other beds is uncertai n at present; discrepancy was shown with the intestinal microcirculation in sepsis. Cautions \200 Excess probe pressure will affect the microcirculation. TISSUE PERFUSION MONITORING 195 See also: Other neurological monitoring, p206. 196 CHAPTER 9 Cardiovascular monitoring Gut tonometry A gas permeable silicone balloon attached to a sampling tube is passed into t he lumen of the gut nasogastrically. Devices exist for tonometry in the stomach or sigmoid colon although they are now rarely used. The tonometer allows indirect measurement of the P CO2 of the gut mucosa and calculation of the pH of the mucosa. Indications Gut mucosal hypoperfusion is an early consequence of hypovolaemia. Covert circu latory inadequacy due to hypovolaemia may be detected as gut mucosal acidosis and has been related to post-operative complications after major surgery. In critically ill patients, th ere is some evidence that prevention of gut mucosal acidosis improves outcome. The sigmoid colon tonometer is useful to detect ischaemic colitis early (e.g. after abdominal vascular surgery). Technique Saline tonometry In the original technique, the tonometer balloon was prepared by degas- sing and \201 lling with 2.5mL 0.9% saline. The saline was withdrawn into a syrin ge connected to the sampling tube prior to insertion. After insertion, the saline was passe d back into the balloon. The PCO2 of the saline in the balloon equilibrated with the PCO2 o f the gut lumen over a period of 30 \200\22390min. At steady state, it was assumed that the PCO2 of the gut lumen and gut mucosa were in equilibrium. Time correction factors were der ived for partial equilibration between the balloon saline and the gut lumen. The measuremen t was completed by sampling the saline from the balloon and an arterial blood sample for me asurement of [HCO3 Gas tonometry Using air in the tonometry balloon allows more rapid equil ibration between the tonometer and the luminal PCO2. A modi \201 ed capnom- eter automatic ally \201 lls the balloon with air and samples the PCO2 after 5 \200\22310min equilibrati on. Subsequent cycles of balloon \201 lling do not use fresh air so CO2 equilibration is quicker. Tonometric PCO2 may be compared with end-tidal PCO2 (measured with the same capnom eter) \216 \216 \227 KK \200\223]. \216 arterial HCO \216 3 + pHi 6.1 log \200\223 10 tonometer PCO 2 as an estimate of arterial PCO2. With a normal capnogram, a balloon PCO2 signi \201 cantly higher than end-tidal PCO2 implies gut mucosal hypo- perfusion. pH vs regional PCO2 The pH of the gut mucosa (pHi) may be calculated using a modi \201 ed Henderson \200\223Hasselba ch equation, where K is the time-dependent equili- bration constant. However, most of the v ariation in the measurement is due to variation in regional PCO2. Comparing regional PCO2 with PaCO2 gives as much information as making the calculation of p Hi, and overcomes the problematic assumption that arterial [HCO3 \200\223] is equivalent to mucosal capillary [HCO3 \200\223]. GUT TONOMETRY 197 See also: Blood gas machine, p152; Blood gas analysis, p154; Tissue perfusion monitoring, p 198. This page intentionally left blank 199 Chapter 10 Neurological monitoring Intracranial pressure monitoring 200 Jugular venous bulb saturation 202 EEG/CFM monitoring 204 Other neurological monitoring 206 200 CHAPTER 10 Neurological monitoring Intracranial pressure monitoring Indications To con \201 rm the diagnosis of raised intrac ranial pressure (ICP) and monitor treatment. May be used in cases of head injury, particula rly if ventilated, Glasgow coma score \211 8, or with an abnormal CT scan. Also used in en cephalopathy, post-neurosurgery, and in selected cases of intracranial hemorrhage. Although a raised ICP can be related to poor prognosis after head injury, the converse is not true. Sustained reduction of raised ICP (or maintenance of cerebral perfusion pressure) in head injury may improve outcome although large controlled trials are lacking. Methods of monitoring intracranial pressure Ventricular monitoring A catheter is inserted i nto the lateral ventricle via a burr hole. The catheter may be connected to a pressure tran sducer or may contain a \201 breoptic pressure monitoring device. Both catheters require regular cali- bration according to the manufacturers \200\231 instructions. Both systems sh ould be tested for patency and damping by temporarily raising intracranial pres- sure (e.g. with a cough or by occluding a jugular vein). CSF may be drained through the ventricular c atheter to reduce intracranial pressure. Subdural monitoring The dura is opened via a burr hole and a hollow bolt inserted into the skull. The bolt may be connected to a pressure transducer or admit a \201 breoptic or hig h- \201 delity pressure monitoring device. A subdural bolt is easier to insert than ventri cular monitors. The main disadvantages of subdural monitoring are a tendency to underestima te ICP and damping effects. Again calibration and patency testing should be done regularly. Complications \200 \200 Infection, particularly after \201 ve days. Hemorrhage, particularly with coagulopathy or dif \201 cult insertion. Using ICP monitoring Normal ICP is <10mmHg. A raised ICP is usually treated when >25mmHg in head injury. As ICP increases, there are often sustained rises in ICP to 50 \200\223100mmH g lasting for 5 \200\22320min, increasing with frequency as the baseline ICP rises. This is associated with 60% mortality. Cerebral per- fusion pressure (CPP) is the difference betwe en mean BP and mean ICP. Treatment aimed at reducing ICP may also reduce mean BP. It is imp ortant to maintain CPP at >50 \200\22360mmHg. INTRACRANIAL PRESSURE MONITORING 201 See also: Intracranial hemorrhage, p448; Subarachnoid hemorrhage, p450; Raised intracranial pressure, p454; Head injury (1), p586. 202 CHAPTER 10 Neurological monitoring Jugular venous bulb saturation Retrograde passage of a \201 breoptic catheter from the in ternal jugular vein into the jugular bulb enables continuous monitoring of jugular venous b ulb saturation (SjO2). This can be used in conjunction with other monitors of cerebral haem odynamics such as middle cerebral blood \202 ow, cerebral arterio-venous lactate differen ce, and intracranial pressure to direct man- agement. Principles of SjO2 management \200 \200 Normal values are approximately 65 \200\22370%. In absence of anemia and with normal SaO2, SjO2 >75% suggests luxury perfusion or global infarction. SjO2 <54% corresponds to cerebral hypoperfusion while values <40% suggest global ischaemia, and are usually associated with increased cerebral lactate production. Knowledge of SjO2 allows optimization of brain blood \202 ow to avoid: (i) excessive or inadequate perfusion, and (ii) iatrogenically-induced hypoperfusion through treating raised intracranial pressure aggressively with diuretics an d hyperventilation. Studies in trauma patients have found higher mortality with episodes of jugular venous desaturation and a signi \201 cant relationship between CPP and SjO2 when CPP is <70mmHg. A falling SjO2 may be an indication to increase CPP, though no prospective randomized trial has yet been performed to study the effect on outcome. Approximately 85% o f cerebral venous drainage passes down one of the internal jugular veins (usually right). S jO2 usually represents drainage from both hemispheres and is equal on both sides. However, after focal injury, this pattern of drainage may alter. Insertion technique 1. 2. 3. 4. 5. Insert introducer sheath rostrally in internal jugular vein. Calibrate \201 breoptic cath eter pre-insertion. Insert catheter via introducer sheath; advance to jugular bulb. Withdra w introducer sheath. Con \201 rm: (i) free aspiration of blood via catheter, (ii) satisfac tory light intensity reading, (iii) satisfactory positioning of catheter tip by lateral cer vical X-ray (high in jugular bulb, above level of 2nd cervical vertebra). Perform in vivo c alibration, repeat calibration 12-hourly. 6. Troubleshooting If the catheter is sited too low in the jugular bulb, erroneous SjO2 values may result from mixing of intracerebral and extracerebral venous blood. This could be part icularly pertinent when cerebral blood \202 ow is low. \200 Ensure light intensity read ing is satisfactory; if too high, the catheter may be abutting against a wall, and if low, the catheter may not be patent or have a small clot over the tip. Before treating the patie nt, always con \201 rm the veracity of low readings against a blood sample drawn from the catheter and measured in a co-oximeter.