Chapter 12 Monitoring of Surgical Patient

8/13/2019 Chapter 12 Monitoring of Surgical Patient

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CHAPTER 12 - Physiologic Monitoring of the Surgical Patient

Albert J. Varon Orlando C. Kirton Joseph M. Civetta

The primary reason for the surgeon's involvement in bedside critical care is theopportunity to understand and enhance the patient's physiologic response and torecognie and correct the pathophysiologic challenges. To do this effectively! thesurgeon must understand physiologic monitoring. "ithout a thorough #no$ledge ofthe physics and methods of monitoring! ensuring the %uality of numbers obtained!

perceiving their importance! and using measurements as a guide for therapy! selectionof proper therapy $ould be difficult! $ithout foundation! rote! or naive. Thus there aremany stimuli to obtain a fundamental #no$ledge of physiologic monitoring. Thischapter is designed to initiate a lifelong process! one that e&tends the capabilities ofthe surgeon! improves patient outcome! and advances surgical science.

(MO)*+AM,C MO+,TO-,+The traditional clinical evaluation! usually the initial assessment tool! is oftenunreliable in critically ill patients! since there may be ma/or changes in cardiovascularfunction that are not accompanied by obvious clinical findings. ,nvasivehemodynamic monitoring at the bedside provides information about cardiorespiratory

performance and guides therapy on a rational physiologic basis.

Arterial Catheteriation,ndicationsArterial catheteriation is indicated $henever there is a need for continuous

monitoring of blood pressure and0or fre%uent sampling of arterial blood. 1tates in$hich precise and continuous blood pressure data are necessary include shoc# of anyetiology! acute hypertensive crisis! use of potent vasoactive or inotropic drugs! highlevels of respiratory support 2high intrathoracic pressure3! high4ris# patientsundergoing e&tensive operations! controlled hypotensive anesthesia! and any situationin $hich any of the factors affecting cardiac function is rapidly changing. This is

particularly true in patients $ith shoc#! because indirect measurement of bloodpressure by a cuff has been proved inaccurate. 1e%uential analyses of blood gastensions and p are necessary in any acute illness involving cardiovascular orrespiratory dysfunction or $hen hyperventilation is instituted in patients $ith centralnervous system in/uries. An ind$elling arterial catheter also can provide ready access

for other blood samples necessary to chart the progression of multisystemic illness.

,nserting arterial lines is a relatively safe and ine&pensive procedure. There are noabsolute contraindications to arterial catheteriation per se! although bleedingdiathesis and anticoagulant therapy may increase the ris# of hemorrhagiccomplications. 1evere occlusive arterial disease $ith distal ischemia! the presence of avascular prosthesis! and local infection are contraindications to specific sites ofcatheteriation.

Clinical 5tility"ith an ind$elling arterial catheter and monitoring system! the systolic blood

pressure 21673! diastolic blood pressure 2)673! and mean arterial pressure 2MA73can be displayed continuously. The pulse rate can be calculated from the arterial


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tracing $hen the electrocardiogram 2(C3 is not available 2e.g.! during electrocauteryuse in surgery3.

)irect measurements of arterial pressure correlate rather poorly $ith indirectmeasurements. The disparities are due in part to physiologic considerations but are

largely conditioned by the fre%uency response of the monitoring systems. 6ecauseblood pressure trends are probably more important than absolute values! the mostimportant aspect of direct arterial pressure monitoring is that it constantly reminds theclinician to pay attention to the patient! to thin# about $hat is happening! and toreason $hy changes are occurring.

To obtain accurate data $hen measuring any pressure $ithin the vascular system! theclinician must understand the monitoring system and methods of calibration. Minordetails such as the use of long tubing and the presence of air bubbles or blood clots inthe system can ma#e the measurements unreliable.

Observation of the arterial pressure $aveform obtained $ith an arterial catheter andmonitoring system may permit a %ualitative assessment of the patient's cardiovascularstatus. The shape of the arterial pressure tracing represents a particular stro#e volumee/ected at a particular state of myocardial contractility. 8ualitative interpretation can

be made in a hypovolemic patient $ith a small stro#e volume that $ill create asmaller pressure $ave. As intravascular volume is replenished! the stro#e volumeincreases! and the arterial pressure tracing $ill increase in sie until it attains normalshape. ,f myocardial contractility is diminished! the rate of increase in aortic pressure$ill diminish! and the upslope of the arterial pressure tracing $ill become less verticaland assume a more tangential tra/ectory $ith the ape& moved to the right.

Although %uantitation of stro#e volume has been attempted using computers to solvethe e%uations necessary to relate the shape of the peripheral arterial pressure tracing toactual stro#e volume e/ected! critical illness introduces too many variables for thismeasurement to be reliable. The location of the dicrotic notch on the arterial$aveform also has been advocated as an indicator of the systemic vascular resistance9ho$ever! erber and associates $ere unable to demonstrate any statisticallysignificant correlation.

Analysis of the 167 variation during mechanical ventilation may offer importantinformation about the nature of lo$4flo$ states. The normal decrease in 167 after a

mechanical breath is more pronounced during hypovolemia but practicallynone&istent during congestive heart failure.

1ites of CatheteriationMany anatomic sites have been used to access the arterial circulation for continuousmonitoring. The superficial temporal! a&illary! brachial! radial! ulnar! femoral! anddorsalis pedis arteries have all been used. Although the selection of anatomic site forarterial catheteriation usually has an institutional bias! specific advantages anddisadvantages should be considered.

The dual blood supply to the hand and the superficial location of the vessel ma#e the

radial artery the most commonly used site for arterial catheteriation. Cannulation istechnically easy! as is securing the catheter in place! and there is a lo$ incidence of


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complications. The mean and end4 diastolic radial pressures are usually accurateestimates of the corresponding aortic pressures9 ho$ever! the systolic pressure at theradial artery is often much higher than that of the aorta due to overshoot caused by theresonant behavior of the radial artery. This e&aggeration is accentuated in stiff!arteriosclerotic radial arteries.

Most authors recommend assessing the ade%uacy of collateral circulation beforecannulation of the radial artery. The most commonly used test is the modified Allentest. The patient is instructed to elevate one hand! ma#e a fist! and clench it firmly!thus s%ueeing the blood from the vessels of the hand. After the e&aminer compressesat the same time both the radial and ulnar arteries! the patient lo$ers and opens thehand in a rela&ed fashion 2carefully so as not to overe&tend it3. The e&aminer thenreleases the pressure over the ulnar artery! and the time for return of color is noted. ,tis considered normal if the capillary blush of the hand is complete $ithin : s. Othermethods such as ultrasonic )oppler techni%ue! plethysmography! and pulse o&imetryalso have been used to assess the ade%uacy of the collateral arterial supply.

The a&illary artery has been recommended as suitable for long4term direct arterialpressure monitoring. ,ts use has been associated $ith relatively fe$ complications andno reported permanent se%uelae. The ma/or advantages include its larger sie!freedom for the patient's hand! and close pro&imity to the aorta so that there is betterrepresentation of the aortic pressure $aveform and minimal systolic pressureovershoot. 7ulsation and pressure are maintained even in the presence of shoc# $ithmar#ed peripheral vasoconstriction. Also! because of the e&tensive collateralcirculation that e&ists bet$een the thyrocervical trun# of the subclavian artery and thesubscapular artery 2$hich is a branch of the distal a&illary artery3! thrombosis of thea&illary artery $ill not lead to compromised flo$ in the distal arm. Ma/ordisadvantages are its rather deep location and mobility! $hich increase the technicaldifficulty for insertion! and its location $ithin the neurovascular sheath! $hich mayincrease the possibility of neurologic compromise if hematoma occurs.

The femoral artery also has been used for continuous blood pressure monitoring.Ma/or advantages are its superficial location and large sie! allo$ing easierlocaliation and cannulation $hen the pulses over more distal vessels are absent. Thema/or disadvantages are the presence of atherosclerotic occlusive disease in older

patients and the problems associated $ith maintaining a clean dressing in the presenceof draining abdominal $ounds and ostomies in surgical patients. ;urthermore!

bleeding at this site may be difficult to control or may occur in an occult manner intothe abdomen or thigh. )espite these potential disadvantages! studies have failed todemonstrate a higher complication rate in patients $ith femoral artery catheters.

The dorsalis pedis artery has no significant cannulation haards if collateral flo$ canbe demonstrated to the remainder of the foot through the posterior tibial artery. Thiscan be done by occluding the dorsalis pedis artery! blanching the great toe bycompressing the toenail for several seconds! and then releasing $hile observing returnof color. A )oppler techni%ue also can be used. Ma/or disadvantages are its relativelysmall sie 2$hich ma#es it more difficult to cannulate3 and overestimation of systolic

pressure at this level.


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The superficial temporal artery has been used e&tensively in infants and in someadults for continuous pressure monitoring. 6ecause of its small sie and tortuousity!ho$ever! surgical e&posure is re%uired for cannulation. ;urthermore! a very small but$orrisome incidence of neurologic complications due to cerebral emboliation has

been reported in infants.

The brachial artery is not used often because of the high complication rate associated$ith its use for cardiac catheteriation. Although this artery has been usedsuccessfully for short4term monitoring! there are little data to support the use of

prolonged brachial artery monitoring. ,f collateral circulation is inade%uate!obstruction of the brachial artery may be catastrophic! leading to loss of the forearmand hand. Other problems include the difficulty in maintaining the site in a$a#e!active patients and the possibility of hematoma formation in anticoagulated patients.The latter may lead to median nerve compression neuropathy and Vol#mann'scontracture.

ComplicationsCommon problems associated $ith arterial catheteriation are failure to cannulate!hematoma formation! and disconnection from the monitoring system $ith bleeding.The ma/ority of reports that describe the complications follo$ing radial arterycannulation have stressed the high incidence of early radial artery occlusion and therarity of late ischemic damage. -ecannulation of the occluded artery generally occurs

but may ta#e several $ee#s. The incidence of radial artery thrombosis has declinedprogressively as a result of the understanding of the effects of different catheter sies2smaller is better3 and materials 2Teflon is better3 and of the use of continuous heparinflo$ instead of intermittent flushing. ;actors associated $ith an increased ris# ofradial artery occlusion include female gender! lo$ cardiac output states! use ofvasoconstrictor drugs! severe peripheral vascular disease! small $rist circumference!insertion by surgical cut4do$n! multiple puncture attempts! hematoma formation! andincreased duration of cannulation.

,nfections related to arterial catheteriation also can occur. ;actors associated $ith anincreased ris# of infection include placement of the catheter for more than < days!insertion by surgical cut4do$n rather than percutaneously! and local inflammation.The rate of catheter4related infection varies from = to over > percent! but the ris# ofcatheter4related septicemia is very lo$.

Other possible complications include retrograde cerebral emboliation 2$hen flushingcatheters3! arteriovenous fistulas! and pseudoaneurysm formation. ;inally! inadvertentin/ection of vasoactive drugs or other agents into an artery can cause severe pain!distal ischemia! and tissue necrosis.

Central Venous Catheteriation,ndicationsThe most common indications for central venous catheteriation are to secure accessfor fluid therapy! drug infusions! or parenteral nutrition and for central venous

pressure 2CV73 monitoring. Central venous catheters also have been used to aspirateair in case of embolism during neurosurgical procedures in the sitting position! for

placement of cardiac pacema#ers or inferior vena cava filters! and for hemodialysisaccess.


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There are no absolute contraindications for CV7 catheter placement! althoughbleeding diatheses may increase the ris# of hemorrhagic complications. Vesselthrombosis! local infection or inflammation! and distortion by trauma or previoussurgery are considered contraindications to specific sites of catheteriation.

Clinical 5tility"hile central venous lines are placed primarily for venous access! useful informationoccasionally can be obtained by measuring the CV7. The CV7 may be useful in ahypotensive trauma patient to differentiate a pericardial tamponade fromhypovolemia. Analysis of the CV7 tracing also may be helpful in the differentialdiagnosis of certain cardiac arrhythmias 2a $aves are absent in atrial fibrillation3 andin the diagnosis of tricuspid insufficiency 2prominent v $aves3.

A properly placed catheter can be used to measure right atrial pressure! $hich! in theabsence of tricuspid valve disease! $ill reflect the right ventricular end4diastolic

pressure. CV7! therefore! can give information about the relationship bet$eenintravascular volume and right ventricular function but cannot be used to assess eitherof these factors independently. CV7 cannot be used to assess left ventricular functionin critically ill patients because ventricular disparity and independence of right andleft atrial pressures have been confirmed repeatedly in these patients. ;urthermore!CV7 is only a single parameter! in contradistinction to the more complete informationconcerning pressures! flo$! and venous gas measurements available $ith pulmonaryartery catheters.

"hen monitoring CV7! the catheter should be attached to a pressure transducer forelectronic measurement rather than to a $ater manometer. "ater manometry does not

permit visualiation of the pressure tracing and cannot provide reliable measurementsbecause of the fre%uency4response limitations of a fluid4filled column that cannotrespond to the full range of pressure variations.

1ites of CatheteriationThere are many anatomic routes to obtain access to the central venous circulation. Themost commonly chosen sites include the subclavian! internal /ugular! e&ternal /ugular!femoral! and brachiocephalic veins. The patient's anatomy and the operator'se&perience are the ma/or factors influencing site selection.

The subclavian vein can be cannulated $ith a high rate of success and may be theeasiest to cannulate in situations of profound volume depletion. Another advantage ofthis approach is the ease $ith $hich the catheter and the dressings can be secured.)isadvantages include the higher ris# of pneumothora& and the inability to compressthe vessel if bleeding occurs.

The internal /ugular vein has been cannulated $ith success rates similar to those of thesubclavian approach. The ma/or advantages of internal /ugular vein catheteriation arethe lo$er ris# of pneumothora& and the ability to compress the insertion site if

bleeding occurs. ,n addition! the right internal /ugular vein provides a straight path tothe superior vena cava! facilitating placement of catheters and pacema#ers. The

internal /ugular vein! ho$ever! may be more difficult to cannulate in patients $ithvolume depletion or shoc#. ;i&ation and dressing of catheters are also more difficult.


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Cannulation of the e&ternal /ugular vein has a lo$er incidence of complications but ahigher incidence of failure. 1ince catheters inserted through the nec# are moredifficult to fi& and dress than those in other sites! this approach is not suitable for

prolonged central venous access.

Although some authors have reported no higher incidence of complications fromfemoral cannulation than from subclavian or internal /ugular sites! concerns over theris# of infection and thrombosis continue to limit general acceptance of long4termfemoral cannulation in critically ill patients. Other peripheral veins! such as those inthe antecubital fossa! have been used for central venous access! but the high incidenceof thrombophlebitis and the fact that many catheters cannot be passed into the centralvenous circulation ma#e these routes undesirable in critically ill patients.

ComplicationsComplications can be divided into technical or mechanical complications! usually

occurring during catheter placement! and long4term complications related to thelength of time that the catheter remains in place. The list of technical and mechanicalcomplications is truly impressive? catheter malposition! dysrhythmias! emboliation2air or catheter fragments3! vascular in/ury 2hematoma! vessel laceration! falseaneurysm! or arteriovenous fistula3! cardiac in/ury 2atrial or ventricular perforation orcardiac tamponade3! pleural in/ury 2pneumothora&! hemothora&! or hydrothora&3!mediastinal in/ury 2hydromediastinum or hemomediastinum3! neurologic in/ury2phrenic nerve! brachial ple&us! or recurrent laryngeal nerve3! and in/ury to otherstructures 2trachea! thyroid! or thoracic duct3. 7neumothora& is the most fre%uentlyreported immediate complication of subclavian vein catheteriation! and arterial

puncture is the most common immediate complication of internal /ugular veincannulation. The literature suggests that serious mechanical complications of centralvenous catheteriation! although e&tremely rare! are associated $ith a high mortalityrate.

@ong4term complications related to the length of time the catheter is in place are dueto infection or thrombosis. +or$ood and associates studied triple4lumen catheterinfections in septic and nonseptic critically ill surgical patients. They found nocatheter4related infections or instances of septicemia in the nonseptic patients! but theincidence of catheter4related infection in the septic group $as :.B percent! $ith a >.:

percent incidence of septicemia. The catheter infection rate per == days! ho$ever!

$as only =.> for both septic and nonseptic patients combined! $hich is very similar torates previously published for single4lumen catheters. 1urface4modified centralvenous catheters have been developed to reduce catheter4related infection. Cathetersimpregnated $ith silver sulfadiaine and chlorhe&idine resist bacterial adherence and

biofilm formation. These catheters have been reported to have a significantly lo$erproportion of catheter4related infection compared $ith standard catheters.

At least three types of thrombi can develop in patients $ith central venous catheters?mural thrombus! catheter thrombus! and Dfibrin sleeveE or sleeve thrombus. Any ofthese thrombi may brea# loose spontaneously or may be set loose $hen the catheter isremoved. enerally! ho$ever! symptoms or clinical conse%uences do not occur.

1uperior vena cava syndrome does occur! especially in long4term patients $ho havehad many catheters placed.


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7ulmonary Artery Catheteriation,ndications1everal studies in critically ill patients have sho$n that the clinical assessment isinaccurate in predicting cardiac output! pulmonary artery occlusion pressure! and

systemic vascular resistance and that the information obtained from pulmonary arterycatheteriation prompts a change in therapy in


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not as reliable as the 7AO7! particularly if there is tachycardia or increasedpulmonary vascular resistance.

The 7AO7 represents the @A7 as long as the column of blood distal to the pulmonaryartery catheter tip is patent to the left atrium. This may not be so if the catheter is

positioned in an area of the lung $here the alveolar pressure e&ceeds pulmonaryvenous pressure 2one ! as described by "est3 2;ig. 43 or both pulmonary arteryand venous pressures 2"est's one 3! causing intermittent or continous collapse ofthe pulmonary capillaries. The 7AO7 may then reflect alveolar pressure and not @A7.This is particularly important if patients have lo$ pulmonary vascular pressures 2i.e.!hypovolemia3 and0or are treated $ith high levels of positive end4 e&piratory pressure27((73. ;ortunately! since the pulmonary artery catheter is flo$4directed! it is mostli#ely to pass into dependent areas of the lung $here blood flo$ is high and both

pulmonary artery and venous pressures e&ceed alveolar pressure 2"est's one B3. ,nthis location! the continuous column of blood bet$een the distal lumen of the catheterand the left atrium $ill remain patent! and the 7AO7 $ill reflect @A7. Another factor

favoring appropriate catheter position is that $hen the patient is supine! the volume oflung located above the heart and the hydrostatic gradient favoring the formation ofones and are decreased. ,f there is any doubt! a lateral chest &4ray can be used todetermine the location of the catheter tip in relation to the left atrium. ,f the tip of thecatheter is belo$ this chamber! one B conditions $ill e&ist even if high levels of7((7 are used.

,n the absence of mitral valve disease or premature mitral valve closure due to aorticregurgitation! the @A7 reflects the left ventricular end4diastolic pressure 2@V()73. ,fthere are no alterations in left ventricular compliance 2the relationship bet$een

pressure and volume3! @V()7 $ill reflect left ventricular end4diastolic volume2@V()V3. ,n the intact ventricle! @V()V reflects the end4diastolic stretch of themuscle fiber! $hich represents the true preload 2discussed later3.

-aising intrathoracic pressure introduces an artifact that affects all intrathoracicvascular pressures to an e&tent that depends on the state of pulmonary compliance. ,n

patients $ith acute respiratory insufficiency! compliance is often diminished! and theDstiffE lungs do not transmit alveolar pressure as readily to the pulmonary circulation.,n these patients! the 7((7 artifact on the 7AO7 measurement usually should note&ceed mmg for every F cmO of 7((7 applied. A greater discrepancy can beseen if the patient is hypovolemic or if the catheter is malpositioned as described

above. Another method of evaluating the effects of 7((7 on the 7AO7 measurementis to observe the decrement in 7AO7 $hen 7((7 is briefly removed. 7resumably! thisdecrement remains relatively constant and can be subtracted from subse%uent pressuremeasurements. Although removal of 7((7 may decrease arterial o&ygen tension andincrease physiologic shunt! these changes are rapidly reversible. ,f a physician

believes that the 7AO7 should be measured off 7((7! this probably should be done$hen 7((7 is discontinued for other reasons 2suctioning or changing breathingcircuits3! and increased concentrations of o&ygen should be given before and after7((7 is stopped. 7atients $ho are receiving very high levels of 7((7 or $hosecondition deteriorates $hen 7((7 is discontinued 2such as immediate bradycardia3should not have 7((7 removed for the e&clusive purpose of measuring 7AO7.


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1ince intravascular pressure measurements are affected by the intrathoracic pressurechanges during respiration! they should be performed at end4e&piration and obtainedfrom a calibrated strip4chart recorder or oscilloscope rather than from a digitaldisplay. Most digital displays are inaccurate because the unselective nature of time4

based electrical sampling and averaging includes positive and negative breathing

artifacts. The digital average then contains the very respiratory variations that can bee&cluded by visualiing the tracing and selecting the appropriate value.

The cardiac output is measured by the thermodilution techni%ue! $hich correlates $ell$ith both the ;ic# and the dye dilution methods. Thermodilution represents anapplication of the indicator dilution principle in $hich a change in the heat content ofthe blood is induced at one point in the circulation! and the resulting change intemperature is detected at a point do$nstream. This change is produced by a rapidin/ection of a #no$n volume of fluid at a #no$n temperature 2colder than the body3into the right atrium via the pro&imal port of the pulmonary artery catheter. Thechange in temperature is registered by a thermistor located < cm from the catheter tip.

This lo$ered temperature decreases the electrical resistance of the thermistor andresults in a thermodilution curve.

The measurement of CO is based on a modification of the 1te$art4 amiltone%uation?

C@,CK (-( ;O- (85AT,O+

The variables in the formula are essentially fi&ed before in/ection! e&cept for thedenominator. The denominator of the e%uation is the thermodilution curve produced

by in/ection of the indicator. A computer integrates the area under this curve! and theresulting calculation is displayed as the cardiac output in liters per minute. The areaunder the curve is inversely proportional to the CO9 that is! the larger the area underthe curve! the lo$er is the CO. ,n actuality! right ventricular output is being measured?,n the absence of intracardiac shunting! right and left ventricular cardiac outputs aree%uivalent.

The in/ectate solution can be either FG de&trose in $ater or normal saline. A volumeof = m@ of iced or room4temperature in/ectate is recommended. The in/ection should

be smooth! completed $ithin < s! and timed $ith a specific phase of the respiratorycycleHi.e.! in/ecting at pea# inspiration or end4e&halationHrather than randomly.

The measurement protocol should be consistent! and three measurements should beaveraged! since a single measurement is not reliable. ,f for any reason the fluid boluscannot be in/ected through the atrial port of the catheter 2e.g.! obstructed lumen3! itcan be administered through the venous infusion port! the right ventricular port! or theintroducer side port.

7itfalls in cardiac output measurement include in/ectate temperature different from thetemperature used to determine the computer constant or that of the fluid beingmonitored by the reference probe! delivered volume less than the one entered in thecomputation constant! incorrect computer constant! rapid infusion of intravenousfluids during measurements! electrical noise created by electrocautery! faulty catheter

lumens! improperly positioned catheter 2e.g.! if the catheter is in the $edge position or


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if the pro&imal lumen is above the atrium or $ithin the introducer sheath3! andpresence of intracardiac shunts or tricuspid regurgitation.

A continuous thermodilution techni%ue is no$ available for measuring CO.7ulmonary artery catheters are modified to locate a =4cm thermal filament in the

right ventricle during use. "ithout using any fluid in/ectate! the thermal filamentcontinually transfers a safe level of heat directly into the blood in a random on4offfashion. The resulting temperature changes are detected at the distal thermistorlocated in the pulmonary artery. These data are collected by a computer! $hich thenapplies a comple& formula to cross4correlate the temperature changes $ith the heat4input se%uence to produce the familiar thermodilution curve. CO is then computedfrom the area under the curve by using an e%uation similar to the one used forstandard bolus thermodilution. The continuous CO monitoring techni%ue has beenreported to be accurate and safe in critically ill patients.

7ulmonary artery catheters e%uipped $ith rapid4response thermistors and (C

electrodes have permitted the measurement of right ventricular e/ection fraction at thebedside9 ho$ever! the clinical utility of these systems remains unclear.

Catheter ,nsertionThe most commonly used pulmonary artery catheter is a I ;r =4cm catheter $ith adistal pulmonary artery lumen! a pro&imal lumen B= cm from the tip! a lumen forinflation of the balloon located at the catheter tip! and a thermistor for measurement ofcardiac output by the thermodilution method 2;ig. 4B3. +e$er catheters may containan additional lumen for fluid administration or for passing a pacing electrode!fiberoptic bundles for continuous measurement of the o&ygen saturation of mi&edvenous hemoglobin 21VO3! or a rapid4response thermistor to measure rightventricular e/ection fraction.

7reparation of the electronic monitoring e%uipment and testing of the cathetercomponents before insertion are essential because the displayed tracing is used tolocalie the position of the catheter tip during insertion. The pressure transducer must

be calibrated and eroed to the level of the left atrium. The catheter should be testedbefore insertion by 23 flushing the pro&imal and distal lumens to ensure that they arepatent! 23 inflating the balloon 2.F m@3 to detect asymmetry or lea#s! 2B3 testing thethermistor by connecting it to the cardiac output computer! and 2


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position! the $aveform needs to be inspected. The mean 7AO7 should be lo$er thanthe M7A7 and lo$er than or e%ual to the 7A)7. ,n the $edged position! arterialied

blood can be aspirated! or 1VO $ill increase to systemic arterial levels or above if ano&imetric pulmonary artery catheter is used. The latter is not an absolute criterion

because incomplete arterialiation of the sample can occur if the tip of the pulmonary

artery catheter lies $edged in a lo$ ventilation4 perfusion region.

ComplicationsThere are ris#s to pulmonary artery catheteriation! although they are typicallyinfre%uent and not usually life4threatening. ,n addition to the complications attributedto central venous cannulation! complications can occur during passage or after thecatheter is in place.

The most common complication during passage of the pulmonary artery catheter isthe development of dysrhythmias. They can occur in up to F= percent of patients! butless than percent of these are serious. The incidence of malignant dysrhythmias

during catheteriation seems to be lo$er $hen patients are in the head4up and rightlateral tilt position. Transient right bundle branch bloc# 2-6663 has been reported inB to : percent of catheteriations. 6ecause of the rare but grave conse%uences of-666 in patients $ith pree&isting left bundle branch bloc#! the use of standbye&ternal pacema#ers and e%uipment for transvenous pacema#er insertion has beenrecommended in these patients during catheteriation. Coiling! looping! or #notting inthe right ventricle can occur during catheter insertion. This can be avoided if no morethan = cm of catheter is inserted after a ventricular tracing is visualied and before a

pulmonary artery tracing appears. Aberrant catheter location! such as pleural!pericardial! peritoneal! aortic! vertebral artery! renal vein! and inferior vena cava! alsohave been reported.

Complications that can occur after the catheter is in place include infections!thromboembolism! and rupture of the pulmonary artery. ,nfections from pulmonaryartery catheters are directly related to the length and severity of illness. The incidenceof microbial coloniation of the catheter has been reported to be bet$een F.> and >.

percent! but only = to


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,n addition to the complications associated $ith catheter insertion and use!complications can result from delays in treatment due to time4consuming insertion

problems and from inappropriate treatment based on erroneous information orerroneous data interpretation. Complications of pulmonary artery catheteriation can

be minimied by meticulous attention to detail and by careful evaluation of the dataobtained.

)erived emodynamic 7arameters,n addition to the information directly provided by arterial and pulmonary arterycatheteriation! many parameters can be calculated. The derived hemodynamic

parameters 2Table 43 aid the clinician by %uantitating the relationships amongheart rate! filling pressures! resistance! contractility! and cardiac output.

Cardiac output 2CO3 is the sum of all stro#e volumes e/ected in a given time. ,t isusually represented as the product of average stro#e volume and heart rate 2beats per

minute3! $here stro#e volume is the amount of blood e/ected by the heart $ith eachcontraction. The primary determinants of stro#e volume are the ventricular preload!afterload! and contractility.

7reload is the passive load that establishes the initial muscle length of the cardiacfibers before contraction and therefore is not usually measured directly in critically ill

patients. On the basis of the $or# by Otto ;ran# and others! 1tarling described therelationship bet$een the resting fiber length of the myocardium and ventricular $or#.As resting fiber length increases! there is an increase in $or# performed onsubse%uent contraction. 6eyond a certain point! ho$ever! further increases in fiberlength $ill not increase e&ternal mechanical $or#! and $or# may decreaseHadescription of cardiac failure. The end4diastolic fiber length is proportional to the end4diastolic volume. ,f there is no change in ventricular compliance 2the relationship

bet$een pressure and volume3! @V()V is proportional to @V()7. 6ecause in mostclinical circumstances the 7AO7 provides a reliable measure of @V()7! changes in7AO7 fre%uently are used as an estimate of changes in left ventricular preload. ,ncritically ill patients! ho$ever! changes in ventricular compliance may affect therelationship bet$een @V()7 and @V()V. Therefore! caution should be ta#en ininterpretation of the 7AO7 as the sole measure of left ventricular preload. ,n clinical

practice! /udgments concerning preload ade%uacy are often best made empirically! byobserving the responses of 7AO7 and indices of cardiac performance to a rapid

alteration of intravascular volume.

The second determinant of stro#e volume is afterload. Afterload is the sum of all theloads against $hich the myocardial fibers must shorten during systole! including theaortic impedance! the arterial $all resistance! the peripheral vascular resistance! themass of blood in the aorta and great arteries! the viscosity of the blood! and the end4diastolic volume of the ventricle. ,n the clinical setting! the most commonly usedmeasure of ventricular afterload is the peripheral or systemic vascular resistance21V-3. Changes in 1V- usually reflect either altered blood viscosity or a change inthe radius of the vascular circuit. 1V-! ho$ever! does not necessarily reflect leftventricular loading conditions! since the true measure of ventricular afterload must

consider the interaction of factors internal and e&ternal to the myocardium. Althoughit is not physiologically correct to spea# of afterload in terms of 1V-! it is clinically


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useful to relate changes in 1V- to changes in ventricular afterload. 1ince sympatheticcontrol of the circulation mediated by peripheral baroreceptors is designed to maintain

blood pressure $ithin relatively narro$ limits! cardiac output is inversely proportionalto 1V- $henever this control is functioning. ,n the human circulatory system!ho$ever! additional factors are so often present that this relationship should not be

assumed to be a substitute for direct measurements and repeated calculations.

Contractility! the final determinant of stro#e volume! may be estimated in thelaboratory by the ma&imum velocity of contraction of the cardiac muscle fibers. Atthe bedside! $e only have inferences based on the stro#e $or# performed by theventricle as filling pressure 2DpreloadE3 changes. 7lotting the $or# done by theventricle for each beatHthe left ventircular stro#e $or# inde& 2@V1",3 or rightventricular stro#e $or# inde& 2-V1",3Hagainst an estimate of preload andcomparing that point $ith a normal range may be a useful means of assessing overallventricular function 2;ig. 4F3. An up$ard shift to the left has been interpreted as animprovement in ventricular performance. A shift do$n$ard and to the right has been

considered as a declining ventricular performance. The Dventricular function curvesEare influenced by changes in ventricular afterload and compliance and therefore donot reflect true contractility. At present! the method for assessing myocardialcontractility most $idely considered load4 independent is the end4systolic pressure4volume relationship 2(17V-3. The logistical difficulty of obtaining fre%uentventricular volume measurements in the intensive care unit 2,C53 limits the clinicalusefulness of this method. Thus plotting 7AO7 and stro#e $or# against normal curvesis an appropriate use of data currently available in the ,C5! but the underlying

physiology is often better understood if it is considered in terms of the ventricularpressure4volume relation.

An appreciation of the determinants of stro#e volume provides a rational approach inthe management of patients $ith lo$4perfusion states. The first and most commonintervention used to increase stro#e volume is to increase preload by augmentation ofintravascular volume. The level of 7AO7 that corresponds to optimal left ventricular

preload can be determined only by se%uentially assessing the effects of acutehemodynamic interventions on cardiac function and may vary over time in any

particular patient. ;luid can be administered rapidly in predetermined increments$hile changes in 7AO7 and in the indices of cardiac performance are monitored. Ama/or increase in 7AO7 during infusion suggests poor ventricular compliance!e&hausted preload reserve! and increased ris# of pulmonary edema $ith further

volume loading. ,f the 7AO7 rises modestly! if indices of cardiac performanceimprove! and if 7AO7 returns to $ithin several millimeters of mercury of the originalvalue $ithin = min of stopping the infusion! additional fluid can be given $ithouthigh ris# of e&acerbating pulmonary venous congestion. After a brief observation

period! this se%uence can be repeated until the hemodynamic parameters are ade%uateor the 7AO7 sho$s an unacceptable rise. ,f tissue perfusion remains inade%uate aftervolume optimiation! augmentation of stro#e volume may be accomplished byincreasing myocardial contractility $ith inotropic drugs and0or decreasing ventricularafterload $ith vasodilators. 1ome authors have reported reduced complications andimproved survival in perioperative patients $hen hemodynamic therapy $as aimed ataugmenting rather than simply normaliing hemodynamic and o&ygen4 transport

parameters. -ecent studies! ho$ever! found no advantage to the use of supranormaltarget values in a general population of critically ill patients.


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-(17,-ATO-* MO+,TO-,+Monitoring ventilation and gas e&change in critically ill surgical patients is of

particular importance in deciding if mechanical ventilation is indicated! assessingresponse to therapy! optimiing ventilator management! and deciding if a $eaning

trial is indicated. ,n addition! gas monitoring permits an assessment of the ade%uacyof o&ygen transport and calculation of derived parameters.

Ventilation Monitoring@ung Volumes1everal lung volume measurements are useful for monitoring ventilatory function inthe operating room and ,C5. These include tidal volume! vital capacity! minutevolume! and dead space.

Tidal volume 2VT3 is defined as the volume of air moved in or out of the lungs in anysingle breath. ,f the tidal volume is depressed! the patient may have difficulty in both

o&ygenation and ventilation. -apid! shallo$ breathing! as reflected by the respiratoryfre%uency 2f3 to tidal volume ratio 2f0VT ==3! is an accurate predictor of failure!and its absence 2f0VT L =3 is an accurate predictor of success! in $eaning patientsfrom mechanical ventilation. VT can be measured at the bedside using a hand4heldspirometer 2"right respirometer3. 6ecause moisture impairs its performance! theinstrument is most appropriate for intermittent monitoring. Continuous VT monitoringis facilitated by the presence of pneumotachometers in the breathing circuit of modernventilators. ,n order to obtain accurate VT measurements! the spirometer must belocated bet$een the ventilator * piece and the endotracheal tube. ,f the spirometer isinstead positioned on the e&piratory limb of the breathing circuit! the entire VTdelivered by a ventilator! not that actually received by the patient! is measured. 5nderconditions of decreased lung compliance or increased air$ay resistance! the higher

pea# inspiratory pressure 27,73 $ould result in an increase of gas volume compressedin the breathing circuit! $ith correspondingly less delivered to the patient. The

product of 7,7 2cmO3 N F 2m@0cmO3 provides an estimate of the compressionvolume of most circuits.

Vital capacity 2VC3 is defined as the ma&imal e&piration follo$ing a ma&imalinspiration. ,t can be readily measured at the bedside in a manner similar to the oneused for VT. The VC is reduced in diseases involving the respiratory muscles or theirneural path$ays! in obstructive and restrictive ventilatory impairment! and in patients

$ho fail to cooperate fully. VC is normally :F to IF m@0#g! and a value of = m@0#gor greater is commonly considered a favorable predictor of $eaning outcome. Thisvalue! ho$ever! is %uite dependent on patient cooperation! and its predictive po$er israther poor.

Minute volume 2or total ventilation3 2V2dot3 (3 is the total volume of air leaving thelung each minute 2product of VT and f3. Many ventilators display V2dot3 (! or it can

be measured $ith a "right spirometer. An increase in the minute volume re%uired tomaintain a normal arterial blood carbon dio&ide tension 27aCO3 suggests anincreased dead space relative to VT or an abnormally high carbon dio&ide 2CO3

production. A resting V2dot3 ( of less than = @ and the ability to double the resting

V2dot3 ( on command have been associated $ith successful $eaning frommechanical ventilation.


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The physiologic 2or effective! or total3 dead space 2V)3 is the portion of tidal volumethat does not participate in gas e&change. 7hysiologic dead space may be divided intot$o components? the volume of gas $ithin the conducting air$ays 2the anatomic deadspace3 and the volume of gas $ithin unperfused alveoli 2the alveolar dead space3. The

ratio of physiologic dead space to tidal volume 2V)0VT3 is calculated from the(nghoff e%uation 2modified from the 6ohr e%uation3 as follo$s?

V) 0 VT 7aCO 4 7(CO 0 7aCO$here 7(CO is the mean partial pressure of e&haled CO in the total e&haledvolume of gas after thorough mi&ing. +ormally! e&haled gas is collected in a bag overB min and the 7(CO CO is measured from the bag. The 7(CO CO should not beconfused $ith 7etCO! the partial pressure of end4tidal CO 2discussed later3. TheV)0VTratio provides a useful e&pression of the efficiency of ventilation. ,n healthysub/ects! the ratio is bet$een =.BB and =.


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7((7! this must be first subtracted from the plateau pressure before calculating staticthoracic compliance! that is!

1tatic compliance volume delivered 0 plateau pressure 4 7((7

The usual range for adult patients receiving mechanical ventilation is := to ==m@0cmO. )ecreased values are observed $ith disorders of the thoracic cage or areduction in the number of functioning lung units 2resection! bronchial intubation!

pneumothora&! pneumonia! atelectasis! or pulmonary edema3. "hen the staticcompliance is less than F m@0cmO! as in severe respiratory failure! difficulties in$eaning are common because of the increased $or# of breathing 2see belo$3.

The dynamic characteristic is calculated by dividing the volume delivered by the pea#2rather than the plateau3 air$ay pressure minus 7((7. ,t is not correct to call thisvalue dynamic compliance because it is actually an impedance measurement andincludes compliance and resistance components. The dynamic characteristic is

normally about F= to = m@0cmO. ,t may be decreased by disorders of the air$ays!lung parenchyma! or chest $all9 if it decreases to a greater e&tent than the staticcompliance! it suggests an increase in air$ay resistance 2e.g.! bronchospasm! mucous

plugging! #in#ing of the endotracheal tube3 or an e&cessive flo$ rate.

"or# of breathing! $hich relates to the product of the change in pressure and volume!is a measure of the process of overcoming the elastic and frictional forces of the lungand chest $all. The $or# of breathing in the critically ill patient $ho re%uiresventilatory support 2"O67t3 can be divided into three components? normal

physiologic $or# 2"O67hys3! $or# to overcome the pathophysiologic changes in thelung and chest $all 2"O6)is3! and $or# to overcome the imposed $or# of breathing2"O6,mp3 created by our methods of ventilatory support. The sum is total $or#.7hysiologic $or# of breathing consists of three elements? elastic $or#! flo$4resistive$or#! and inertial $or#. (lastic $or# is the $or# necessary to overcome the elasticforces of the lung and is inversely proportional to the compliance of the lung. ,fcompliance becomes diminished! the $or# of breathing increases dramatically. Thesecond element of physiologic $or# is flo$4resistive $or#! or the $or# that is neededto overcome the resistance of the air$ays and parenchymal tissues. This may increasethe pressure change necessary to inhale the same tidal volume but also adds anothercomponent of $or# during e&piration! that necessary to e&pel the gas from the lungsthrough the narro$ air$ays. The third component of physiologic $or# is the inertial

$or# to overcome the tendency of gas volume to remain at rest. This element isnegligible in comparison $ith the elastic and flo$4 resistive $or#. "hen a patientdevelops respiratory failure! in addition to the normal physiologic $or#! the patientmust overcome the increased $or# of breathing associated $ith the disease. This isclinically manifest as a change from a relatively large tidal volume at a slo$ rate to asmall tidal volume at a rapid rate. ;inally! the patient must do additional $or# to

breath spontaneously against a breathing apparatus that consists of the ventilatoritself! demand valve! tubing! e&halation valves! and most important! the endotrachealtube. 6anner and associates sho$ed that the endotracheal tube acts as a resistor inseries in the breathing apparatus! thereby causing an increase in $or# of breathing.,mposed $or# has been sho$n to e&ceed physiologic $or# of breathing by a factor of

: under conditions of spontaneous breathing through a narro$4internal4diameterendotracheal tube at a high inspiratory flo$ rate demand during continuous positive


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air$ay pressure. 7oor demand system sensitivity! ventilator dyssynchrony!malfunctioning demand valves! and inade%uate inspiratory flo$s are also contributingfactors.

The goal of ventilatory support is to carefully titrate the ventilator's contribution to

minute ventilation so that the patient's effort remains a nonfatiguing $or# load.;ailure to do so by supplying either too much or too little ventilatory support mayresult in unsuccessful $eaning trials and increase the duration of mechanicalventilation. +ormal range for "O67t is =.B to =.:J0@.

Microprocessor4based respiratory monitors such as the C74== 7ulmonary Monitor26iocore Monitoring 1ystems! ,rvine! CA3 measure many mechanical ventilation andrespiratory muscle parameters! including compliance! air$ay resistance! strength andendurance! and both patient and ventilator $or# of breathing. 7hysiologic data areaccrued from a miniature pneumotachograph and air$ay pressure sensor positioned

bet$een the * piece of the breathing circuit tubing and the endotracheal tube. A

catheter $ith a distally annealed balloon is positioned in the distal esophagus tomeasure changes in intraesophageal pressure as an estimate of changes inintrathoracic pressure. "e have employed this pulmonary monitor to evaluateune&plained tachypnea or respiratory distress! to guide endurance and strengthreconditioning! and to avoid iatrogenic ventilator dependency caused by inappropriateventilator settings in comple& long4term ventilated patients.

,ncorporation of $or#4of4breathing analysis into our pree&tubation trial allo$edsuccessful e&tubation in >I 2of F>3 patients $ho remained on mechanical ventilation

because of tachypnea 2respiratory rate bet$een B and F breaths per minute3secondary to e&cessive imposed $or# of breathing. (arlier e&tubation in this group of

patients resulted in a pro/ected net savings in e&cess of P>!===. ,ncorporating $or#4of4 breathing strategies also decreased the duration of ventilation in our trauma ,C5from . to


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hypoventilation! true intrapulmonary or intracardiac shunt! and decreased mi&edvenous o&ygen content. Although diffusion abnormalities may lead to hypo&emia if

pulmonary end4capillary blood fails to e%uilibrate fully $ith alveolar gas! suchconditions are uncommon. A decreased cardiac output in the presence of a constanto&ygen consumption! an increased o&ygen consumption in the presence of a constant

CO! and a decreased CO and an increased o&ygen consumption must all result in alo$er mi&ed venous o&ygen content and therefore also can produce arterialhypo&emia. ;ailure to recognie this nonpulmonary cause of hypo&emia may cause aclinician to falsely attribute a decreasing arterial blood o&ygen tension 27aO3 todeteriorating pulmonary function. Thus pulmonary and cardiac function must beassessed to evaluate any given set of arterial blood gases accurately. A decreasing7aO $ithout a change in 7aCOsuggests that blood o&ygenation is deterioratingdespite constant alveolar ventilation. ,n the acutely ill patient! this finding is usuallyattributable to ventilation4 perfusion imbalance or intrapulmonary shunting. Animportant feature of shunting is that as it increases! supplemental o&ygen has

progressively less effect on 7aO because shunted blood bypasses ventilated alveoli.

,ntrapulmonary shunting usually does not result in elevation of the 7aCO becausethe central chemoreceptors sense any rise in 7aCO and respond by increasingventilation.

The relation of 7O to 1O is described by the o&yhemoglobin dissociation curve2;ig. 4:3. The flat upper portion of the dissociation curve means that even if the7O in alveolar gas decreases some$hat! loading of o&ygen $ill be little affected.The steep lo$er part of the curve means that the peripheral tissues can $ithdra$ largeamounts of o&ygen for only a small decrease in capillary 7O. The curve shifts as theaffinity of hemoglobin for o&ygen changes. A shift to the right 2decreased affinity foro&ygen3 helps release o&ygen into the tissue. A shift to the left 2increased affinity foro&ygen3 causes less o&ygen to be available to tissue. The curve can be shifted to theright by increased erythrocyte !B4diphosphoglycerate concentration! temperature!7CO! and concentration of hydrogen ion 2decreased p3. Opposite changes shift it tothe left. Other conditions such as carbo&yhemoglobinemia and methemoglobinemiaalso can shift the o&yhemoglobin dissociation curve to the left and therefore interfere$ith peripheral o&ygen unloading. The position of the o&yhemoglobin dissociationcurve is defined by the 7F=! that is! the 7O at $hich hemoglobin is F= percentsaturated. +ormal hemoglobin has a 7F= of :.F mmg. "hen it is greater than thisvalue! the curve is shifted to the right9 $hen it is lo$er! the curve is shifted to the left.)espite a considerable amount of information! there is little evidence that shifts of the

o&yhemoglobin dissociation curve are clinically significant in the ma/ority of patients.,ndividuals $ith limited circulatory reserve! ho$ever! $ho cannot augment o&ygendelivery by the usual compensatory mechanisms of increased cardiac output andorgan blood flo$! may develop local tissue hypo&ia $hen an increased hemoglobin4o&ygen affinity state 2i.e.! al#alemia3 e&ists.

The 7aCO directly reflects the ade%uacy $ith $hich alveolar ventilation meetsmetabolic demands for CO e&cretion. The relationship bet$een 7aCO!COproduction 2V2dot3 CO3! and alveolar ventilation 2V2dot3 A3 in normal lungs isgiven by the e%uation

7aCO V2dot3 CO 0 V2dot3 A N K


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chemistry to develop miniaturied intravascular gas sensors that permit continuousmeasurement of p! 7O! and 7CO. The performance of fiberoptic continuousintraarterial blood gas monitors is comparable $ith that of modern blood gasanalyers. ;urther studies are needed! ho$ever! to determine the clinical utility of thisne$ methodology.

7arameters )erived from 6lood4as AnalysisJust as the derived hemodynamic parameters can be used to evaluate the choice andeffects of hemodynamic interventions! parameters derived from blood4gas analysis2Table 4B3 yield information about the ade%uacy of cardiopulmonary function inmeeting the tissue demands for o&ygen.

The o&ygen content of the blood is e%ual to the amount of o&ygen bound tohemoglobin plus the amount dissolved in plasma. The amount of bound o&ygen isdirectly related to the concentration of hemoglobin and to ho$ saturated thishemoglobin is $ith o&ygen 2i.e.! 1aO or 1VO3. The amount of o&ygen dissolved in

plasma depends on the o&ygen tension 2i.e.! 7aO or 7VO3. O&ygen delivery 2O3 isthe volume of o&ygen delivered from the heart each minute and is calculated as the

product of cardiac output and arterial o&ygen content 2CaO3. O&ygen consumption2V2dot3 O3 is the amount of o&ygen that diffuses from the capillaries into all tissuesand can be calculated according to the ;ic# principle as the product of CO andarteriovenous o&ygen content difference QC2a 4 7V3OR. ,f this e%uation is rearranged!the arteriovenous o&ygen content difference relates o&ygen consumption and CO2V2dot3 O0CO3. An increase in the arteriovenous o&ygen content difference indicatesthat either consumption is too high or flo$ is too lo$. ;inally! the o&ygen utiliationcoefficient or e&traction ratio 2O5C3! relates o&ygen consumption and o&ygendelivery 2V2dot3 O0O3. This parameter has been used in many ,C5s to evaluate theade%uacy of o&ygen transport.

The ade%uacy of o&ygen transport also must be assessed in relation to o&ygendemand! $hich is the amount of o&ygen re%uired by the body tissues to use aerobicmetabolism. Although o&ygen demand cannot be measured clinically! the relative

balance bet$een consumption and demand is best indicated by the presence of e&cesslactate in the blood. @actic acidosis means that demand e&ceeds consumption andanaerobic metabolism is present.

Although precise numerical end points cannot be defined! the parameters already

listed provide a frame$or# for testing a clinical hypothesis? ,f o&ygen delivery orconsumption is lo$! if utiliation is high! or if lactic acidosis is present! arterialo&ygen content might be augmented by increasing hemoglobin concentration oro&ygen saturation! or cardiac output might be increased by manipulation of preload!afterload! or contractility. A response might be considered beneficial if o&ygenconsumption increases! if utiliation returns to the normal range! or if lactic acidosisresolves.

7hysiologic right4to4left shunt or venous admi&ture 2sp0t3 estimates the fraction oftotal blood flo$ reaching the left side of the circulation $ithout participating in gase&change. 1hunt may occur 2uncommonly3 in adults via intracardiac shunts. More

commonly! increased venous admi&ture in critically ill patients is due to alterations inthe balance of pulmonary ventilation and perfusion 2lung areas that are perfused but


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not ventilated3. 6efore calculating venous admi&ture! it is necessary to calculatearterial! mi&ed venous! and pulmonary end4capillary o&ygen contents. The latter can

be calculated by using the alveolar o&ygen tension 27aO3 to estimate pulmonary end4capillary o&ygen tension and the o&yhemoglobin dissociation curve to estimate

pulmonary end4capillary hemoglobin saturation 2assume ==G if 7aO F= mmg3

2see Table 4B3.

Other indices! such as the alveolar4arterial o&ygen partial pressure difference 27aO 47aO3 and the arterial4to4alveolar o&ygen tension ratio 27aO07aO3! have beensuggested for evaluating the efficiency of gas e&change. These o&ygen tensionbasedindices! ho$ever! are inaccurate in predicting efficiency of gas e&change. Therelationship bet$een physiologic shunt and the o&ygen tensionbased indices isnonlinear and substantially influenced by changes in inspired o&ygen concentrationand arteriovenous o&ygen content difference.

The collection of the measured and derived cardiopulmonary parameters has been

called the cardiopulmonary profile. +ormal values can be seen in Tables 4 and 4B. The measured and derived data can be used to formulate a plan of interventionsdesigned to improve o&ygen delivery relative to myocardial and systemic needs. Thisanalysis is a dynamic process that evolves as ne$ data are obtained and response totherapy is incorporated. The process of generating a cardiopulmonary profile has beengreatly simplified by the use of programmable calculators and microcomputers.

CapnographyCapnography is the graphic display of COconcentration as a $aveform. ,t should not

be confused $ith capnometry! $hich refers to only the numerical presentation of theconcentration $ithout a $aveform. Capnography includes capnometry $hen thecapnographic display is calibrated.

Currently available systems for COanalysis include infrared spectroscopy! massspectrometry! and -aman scattering. ,n addition! a disposable! noninvasive! andine&pensive colorimetric device 2(asy Cap9 +ellcor 7uritan 6ennett! ,nc.! 7leasanton!CA3 is available. This device permits a semi%uantitative measurement of the end4tidalCO concentration $hen it is attached bet$een an endotracheal tube and aresuscitation bag.

,n the ma/ority of stand4alone capnographs! the COconcentration is measured by

infrared spectroscopy. A beam of infrared light is passed through the sampled gas.CO molecules in the light path absorb some of the infrared energy. The capnographcompares the amount of infrared light absorbed by the patient gas in the sample cell$ith the amount absorbed either by gas in a reference cell or by the sample cell duringa time of #no$n ero4gas concentration. The capnograph then displays theinstantaneous CO concentration.

as for analysis of CO may be aspirated from the air$ay 2sidestream capnography3or may be analyed as it flo$s through a sensor placed in the air$ay 2mainstreamcapnography3. 1idestream analyers offer advantages in that gas is sampled close tothe patient's mouth $ith the use of an ine&pensive! light$eight connector! and they

can be used in nonintubated patients. The ma/or disadvantage of these systems is thatanalysis is delayed because gas is routed through a capillary tube to the capnograph.


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Mainstream analyers generate a capnogram practically instantaneously because thegas is analyed as it passes through a sampling cuvette. The ma/or disadvantage ofthese systems is the $eight of the sensor and sampling cuvette. 6ecause the sensoritself is a sophisticated instrument! it needs to be treated carefully? ,t is fragile! and

replacements are e&pensive. The volume of the cuvette adds dead space to the system.

+ormally! there is a fairly predictable relationship bet$een the pea# e&haled or end4tidal CO 27etCO3 and the 7aCO. ,n healthy sub/ects $ith normal lungs! the7aCO is < to : mmg higher than the 7etCO. 7atients $ith chronic obstructivelung disease and other derangements associated $ith increased dead space 2seesection on @ung Volumes3 have an increased arterial to end4tidal CO gradient Q72a 4et3COR. This difference occurs because the e&haled gas from the alveolar dead space!$hich contains little or no CO! dilutes the CO4containing gas from the normallyventilated and perfused alveoli.

Measurement of 7etCO and 72a 4 et3COprovides insight into several normal andpathologic processes. 7etCOmeasurement is at present perhaps one of the mostreliable means of determining proper endotracheal tube placement. (sophagealintubation may produce one or a fe$ breaths containing CO during e&piration! but

because there is no CO in the stomach cavity! 7etCO rapidly decreases to ero.

7etCO has been found to correlate $ith cardiac output and coronary perfusionpressure during cardiopulmonary resuscitation 2C7-3 and $ith successfulresuscitation from and survival after cardiac arrest. 6ecause circulatory arrest createstotal dead space! if ventilation is continued! 7etCO disappears. An increase in7etCOprovides an immediate bedside validation of the efficacy of C7-! and if theincrease is abrupt! it provides the earliest evidence of successful resuscitation. The useof 7etCO to monitor resuscitation is predicated on maintaining a constant minuteventilation so that changes in 7etCOresult from changes in lung perfusion 2andtherefore cardiac output3 and not ventilation.

7etCO monitoring is e&tremely useful as a diagnostic tool in several situationsuni%ue to the operating room. These include the detection of air emboli duringneurosurgical procedures re%uiring the sitting position! the detection of increased CO

production in malignant hyperthermia! and the detection of disconnection ormalfunction of the anesthesia breathing circuit.

,n the ,C5 environment! 7etCO monitoring also can be used as a ventilatordisconnect alarm as $ell as a system to determine ventilator malfunction.Measurement of 7etCO has been proposed as a substitute for arterial blood gassampling during mechanical ventilation ad/ustment and $eaning in critically ill

patients. 7etCOtrends in these patients! ho$ever! are often misleading because the72a 4 et3COvaries greatly in a single individual.

The 72a 4 et3CO is primarily a reflection of dead4space ventilation! and its sie canserve as a gauge of physiologic aberration. ;actors related to the instrumentation andthe techni%ue used! ho$ever! also may contribute to the 72a 4 et3CO. ;or e&ample!

aspiration of room air through a loose connection or brea# in the circuit or sampling


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tube! a lea# around the cuff! or aspiration of fresh gases $ill dilute the e&haled COand result in an increased 72a 4 et3CO and an altered $aveform.

Analysis of the CO $aveform can provide valuable information. A detailed revie$of $aveform analysis is outside the scope of this chapter but can be found else$here

2ravenstein and associates3.

7ulse O&imetry7ulse o&imetry provides a reliable! real4time estimation of arterial hemoglobin o&ygensaturation. This noninvasive monitoring techni%ue has gained clinical acceptance inthe operating room! recovery room! and ,C5.

7ulse o&imeters estimate arterial hemoglobin saturation by measuring the absorbanceof light transmitted through $ell4perfused tissue! such as the finger or ear. The lightabsorbance is measured at t$o $avelengthsH::= 2red3 and >


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mmg. 1aOvalues in the range of perhaps I= to >F percent $ill reflect changes in7aO9 it is in this range that pulse o&imetry finds great value in monitoringcardiorespiratory disease and directing therapy. igh levels of saturation give noinformation about 7aO. 6ecause of the sigmoid shape of the o&yhemoglobindissociation curve 2see ;ig. 4:3! 1aO may not decrease despite a significant

deterioration in pulmonary gas e&change! i.e.! if 7aO fell from == to == mmg.1ince delivery of o&ygen to the tissues is proportional to 1aO! ho$ever! pulseo&imeters $ill detect changes before tissue o&ygenation is impaired.

Various physiologic and environmental factors interfere $ith the accuracy of pulseo&imetry. These include decreased amplitude of peripheral pulses 2hypovolemia!hypotension! hypothermia! vasoconstrictor infusions3! motion artifact! electrosurgicalinterference! bac#scatter from ambient light! and dyshemoglobinemias. 7redictors of

pulse o&imeter data failure in the operating room include A1A physical status B!

The pulse o&imeter can only distinguish o&yhemoglobin and deo&yhemoglobin. ,fother hemoglobin species are present! an error is introduced. @aboratory co4o&imeters!on the other hand! generally use more than t$o $avelengths and often can %uantifyother hemoglobin species directly. "hen dyshemoglobins such ascarbo&yhemoglobin and methemoglobin can be measured! it becomes meaningful todistinguish bet$een functional saturation Q== N o&yhemoglobin02o&yhemoglobin deo&yhemoglobin3R and fractional saturation Q== N o&yhemoglobin02o&yhemoglobin deo&yhemoglobin carbo&yhemoglobin methemoglobin3R. 6ar#er and colleagueshave sho$n that in the presence of elevated carbo&yhemoglobin or methemoglobinlevels! 1pO overestimates fractional saturation at all saturation values.Carbo&yhemoglobinemia may occur in heavy smo#ers or in patients $ho suffercarbon mono&ide inhalation. Methemoglobinemia may be induced by a large numberof drugs! including local anesthetics 2prilocaine! benocaine3! nitroglycerin!

phenacetin! phenytoin! 7yridium! and sulfonamides.

,ntravenously administered dyes! particularly methylene blue and indocyanine green!can temporarily induce artifactually lo$ saturation readings. )eeply pigmented s#inand opa%ue nail polish coatings may significantly decrease light transmission!rendering o&imeters inoperative. The presence of fetal hemoglobin!hyperbilirubinemia! or moderate anemia 2$ith hematocrits as lo$ as F percent3 does

not affect the accuracy of pulse o&imeters. )espite its limitations! pulse o&imetry isgenerally ac#no$ledged as one of the most significant advances in clinicalmonitoring.

Continuous Mi&ed Venous O&imetryMeasurement of the o&ygen saturation of mi&ed venous hemoglobin 21VO3 ishelpful in the assessment of the o&ygen supply4demand relationship in critically ill

patients. The use of improved fiberoptic o&imetry systems in conventional pulmonaryartery catheters has permitted continuous monitoring of 1VO and made bedsidemonitoring of this relationship practical.

1VO can be derived from the ;ic# e%uation 2see Table 4B3 that relates o&ygenconsumption! cardiac output! and arteriovenous o&ygen content difference. ,f the


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small %uantity of physically dissolved o&ygen in the blood is considered negligible!solving the ;ic# e%uation for 1VOyields

1VO 1aO 4 V2dot3 O 0 CO N b N .B> N =

Therefore! the determinants of 1VOinclude the principal components of o&ygendelivery QCO! hemoglobin 2b3! and 1aOR and o&ygen consumption. There is a poorcorrelation bet$een 1VO and any single component of the e%uation 2V2dot3 O! CO!1aO! b3! as $ould be e&pected! because there are four separate determinants. Thereis! ho$ever! a good correlation bet$een 1VO and all these components acting atonce.

"ith the preceding formula in mind! it is easy to understand that the 1VO $illdecrease $hen there is an imbalance bet$een o&ygen consumption and deliverycaused by an increase in V2dot3 O or a decrease in CO! b! or 1aO. 1VO $illincrease $hen the imbalance is due to changes in the opposite direction.

The normal range for 1VO in healthy sub/ects is =.:F to =.=! $ith an average valueof =.IF corresponding to a 7VO of


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illuminating light is absorbed! refracted! and reflected depending on the color and!therefore! o&yhemoglobin concentration of the blood. The reflected light is collected

by a second fiber and returned through the catheter to a photodetector in the opticalmodule 2;ig. 4>3. 5sing the relative intensities of the signals representing the lightlevels at the various $avelengths! a computer calculates the o&ygen saturation! and

the average for the preceding F s is displayed.

The saturation measured by catheter o&imetry correlates $ell $ith values obtainedfrom a laboratory co4o&imeter. The most common sources of error $hen measuring1vO are incorrect calibration and catheter malposition. Carbo&yhemoglobinemia!methemoglobinemia! and intravenous administration of methylene blue also can affectthe measurements.

Continuous 1VO monitoring serves three ma/or functions. ;irst! it serves as anindicator of the ade%uacy of the o&ygen supply4demand balance of perfused tissues.,n clinically stable patients! a normal and stable 1VO may be considered an

additional assurance of cardiopulmonary stability. ;urther assessments of cardiacoutput and arterial and mi&ed venous blood gas analyses are not necessary. 1econd!continuously measured 1VO may function as an early $arning signal of unto$ardevents. ,n this situation! although an alert has been given! the cause of the change in1VO is not necessarily clear because the change in 1VO is sensitive but notspecific. ,t may be necessary to measure cardiac output! 1aO! and b in this settingto identify the etiology of the 1VOchange. Third! continuously monitored 1VOmay improve the efficiency of the delivery of critical care by providing immediatefeedbac# as to the effectiveness of therapeutic interventions aimed at improvingo&ygen transport balance.

;inally! an important application of continuous venous o&imetry must be one of costcontainment in the ,C5. The potential of cost savings lies in the decreased use ofother modes for assessing o&ygen transport balance! e.g.! cardiac outputmeasurements and venous blood gas analyses. The savings in some institutions aregreater than the price of the catheter! and its use has been /udged cost4effective.

A1T-,C TO+OM(T-*eneral Considerations,schemia signifies failure to satisfy the metabolic needs of the cell secondary to eitherimpaired o&ygen delivery or impaired cellular o&ygen e&traction and utiliation.

Although hemodynamic and o&ygen4transport variables document the severity oftissue hypo&ia and o&ygen debt! they fail to accurately portray the comple&interactions bet$een energy re%uirements and supplies at the tissue level. astrictonometry has been proposed as a relatively noninvasive monitor of the ade%uacy ofaerobic metabolism in organs $hose superficial mucosal lining is e&tremelyvulnerable to lo$ flo$ and hypo&emia and in $hich blood flo$ is sacrificed first in

both shoc# and the systemic inflammatory response syndrome. The gastrointestinaltract therefore $ill display metabolic changes before other indices of o&ygenutiliation. ,n the ano&ic cell! uncompensated adenosine triphosphate 2AT73hydrolysis is associated $ith the intracellular accumulation of adenosine diphosphate2A)73! inorganic phosphate! and hydrogen ions $ith resulting intracellular acidosis.

These hydrogen ions lead to tissue acidosis! $ith unbound hydrogen ions combining


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$ith interstitial bicarbonate to form the $ea# acid carbonic acid that dissociates toproduce CO and $ater.

MeasurementsA tonometer is comprised of a semipermeable balloon connected to a sampling tube.

A dual4purpose productHa tonometer in combination $ith a standard vented gastricsumpHis commercially available 2T-,7 +1 Catheter9 Tonometrics )ivision!,nstrumentarium Corp.! Te$#sbury! MA3. The annealed balloon allo$s COgenerated in the superficial layers of the mucosa to e%uilibrate $ithin the salineinstilled into the balloon. The tonometer 7CO is multiplied by an e%uilibration factor2based on the e%uilibration period3 to derive the tissue 7COvalue. 5sing a modifiedversion of the enderson4asselbach e%uation! intramucosal p 2pi3 is thencalculated as follo$s?

pi :. log= CO4 B 0 =.=B N 7CO ss$here CO4 B represents the arterial bicarbonate concentration 2from a contemporary

sample of arterial blood3 in millie%uivalents per liter! 7CO ss represents thetonometrically measured steady4state carbon dio&ide tension! and =.=B represents aconstant that converts carbon dio&ide tension in plasma in millie%uivalents per liter

per millimeter of mercury to millie%uivalents per liter of carbonic acid. Themeasurement of intramucosal p depends also on the assumption that the bicarbonateconcentration in the $all of the organ is the same as that $hich is delivered to it byarterial blood and that the pK 2the dissociation constant3 is the same as that in the

plasma. The pK in plasma is not the same as that in the cytosol! but the value :. isthe best appro&imation of the pK $ithin the interstitial fluid of the superficial layersof the mucosa.

Clinical 5tility,ncomplete splanchnic cellular resuscitation has been associated $ith the developmentof multiple organ system failure! more fre%uent septic complications! and increasedmortality in the critically ill patient. Many studies have demonstrated the utility of guttonometry in various settings $here the perfusion status of the intestinal mucosa has

been of importance! such as in patients undergoing elective cardiac or abdominalaortic operations. ,n critically ill patients! gastric tonometry has been used as a

predictor of both organ dysfunction and mortality and has been sho$n to be a betterpredictor of mortality than base deficit! lactate! o&ygen delivery! and o&ygenconsumption.

;ailure of splanchnic resuscitation correlated $ith multiple organ system failure andincreased length of ,C5 stay in the hemodynamically unstable trauma patientadmitted to the ,C5 at the 5niversity of Miami0Jac#son Memorial ospital. Therelative ris# or li#elihood of death among incompletely resuscitated patients 2pi LI.B3 at < h as compared $ith completely resusciated patients 2pi U I.B3 $as


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in routine care areas $ere found to have a normal pi on transfer from theresuscitation area. The mean pi $as I.< S =.! I. in >F percent of patients andI.F in percent of patients. All patients survived9 none developed multiple organsystem failure.

Measurement of pi can provide clinicians $ith a metabolic end point ofresuscitation. pi therefore can be used to ensure the completion of resuscitation as

/udged by normaliation of gastric pi. Current methods reported in the literaturefocus only on increasing o&ygen delivery using fluid therapy and vasoactive agents$ith a4adrenergic action. 6ecause these induce splanchnic vasoconstriction! $hichleads to gastric intramucosal acidosis! our strategy employs splanchnic vasodilatoryagents to optimie systemic and mesenteric blood flo$ 2isoproterenol! dobutamine!nitroprusside! nitroglycerine! prostaglandin (3! reserving those agents $hich causesplanchnic vasoconstriction 2epinephrine! high4dose dopamine! phenylephrine!norepinephrine3 to treat severe hypotension 2MA7 L FF mmg3. ,f pi fallsune&pectedly! $e search for intraabdominal catastrophe! intraabdominal hypertension!

sepsis! tissue necrosis! line sepsis! nosocomial infection! unappreciated e&cess patientventilatory $or#! hypovolemia! and hypo&emia.

,nterventions to bloc# and modify the ischemia4reperfusion in/ury and restoresplanchnic perfusion can be incorporated into a resuscitation algorithm to reduce theincidence of bacterial translocation and systemic $hite cell priming before theensuing systemic inflammatory response.

-(+A@ MO+,TO-,+The primary reason for monitoring renal function is that the #idney serves as ane&cellent monitor of the ade%uacy of perfusion. The second ma/or indication formonitoring #idney function is to prevent acute parenchymal failure. ;inally! renalfunction monitoring is helpful in predicting drug clearance and proper dosemanagement.

5rine output fre%uently is monitored but may be misleading. Although very lo$ urineoutputs! less than =.F m@0#g0h! are consistently associated $ith lo$ glomerularfiltration rate 2;-3 values! levels greater than this also can be associated $ith lo$;- values. )iuresis created by an osmotic load 2radiographic contrast material orglucose3! administration of diuretics! or nonoliguric renal failure may give theclinician a false sense of security $hile the patient has deteriorating renal function.

Other methods of monitoring renal function are necessary. These include tests ofglomerular function and tests of tubular function.

lomerular ;unction Tests6lood urea nitrogen 265+3 often has been used to estimate renal function. 65+ isaffected by ;- and urea production. 7roduction may be increased if large amountsof nitrogen are administered during parenteral nutritional support! as a result ofgastrointestinal bleeding! or in catabolic states induced by trauma! sepsis! or steroids.5rea production may be lo$ered during starvation and in advanced liver disease.6ecause these factors are often interrelated in an unpredictable manner in critically ill

patients! 65+ is not a reliable monitor of renal function.


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The value of plasma creatinine as a measure of renal function far e&ceeds the value ofthe 65+. The serum creatinine level is directly proportional to the level of creatinine

production and inversely related to the ;-. ,n contrast to 65+ concentration!plasma creatinine levels are not influenced by protein metabolism or the rate of fluidflo$ through the renal tubules. "hen creatinine production is constant! the serum

creatinine level reflects ;-. The plasma creatinine level $ill double $ith a F=percent reduction in ;-! assuming that creatinine production remains constant.Acute reductions in the ;- rate are not immediately reflected! ho$ever! because itta#es < to I h for e%uilibration to occur.

Creatinine production is directly proportional to the muscle mass and its metabolism.,n rhabdomyolysis! creatinine formation e&ceeds its filtration rate! such that measuredserum creatinine levels increase. ,n conditions $here the s#eletal muscle mass isreduced 2e.g.! advanced age! immobiliation3! the endogenous creatinine pool isdiminished! and thus the serum creatinine concentration does not rise appropriately$ith impairment of renal function. Only $ith measurement of creatinine clearance can

the severity of such renal function loss be determined.

1erial determination of creatinine clearance is currently the most reliable method forclinically assessing ;- and the most sensitive test for predicting the onset of

perioperative renal dysfunction. Although measurements traditionally are performedusing a


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not begin to increase above normal until the ;- decreases to less than [email protected] m.

Tubular ;unction TestsTests that measure the concentrating ability of the renal tubules are used primarily in

the differential diagnosis of oliguria to differentiate a prerenal cause unresponsive to/udicious fluid therapy from intrinsic renal failure due to tubular dysfunction. Table4< summaries the differential diagnosis based on tubular function studies. Theutility of each depends on the ability of the renal tubular cells to physiologicallyrespond to a decreased e&tracellular fluid volume. Thus! $ith prerenal aotemia! thetubules can appropriately reabsorb sodium and $ater. ,n intrinsic renal failure! tubularfunction is mar#edly compromised! and the ability to reabsorb sodium and $ater isimpaired. Multifactorial renal dysfunction is most common9 rarely is an isolatedetiology discovered.

Tubular function tests are useful in oliguric patients 2urine output L F== m@0day3

because nonoliguric individuals typically have less severe tubular damage and theirlaboratory findings are li#ely to sho$ more overlap $ith the values of patients $ith

prerenal aotemia.

The fractional e&cretion of sodium 2;(+a3 appears to be the most reliable of thelaboratory tests for distinguishing prerenal aotemia from acute tubular necrosis. Thistest re%uires only simultaneously collected DspotE urine and blood samples. ;(+a can

be calculated as follo$s?

;(+a2G3 5+a07+a 0 5cr07cr N ==G

$here 5+a is the urinary sodium concentration 2in millie%uivalents per liter3! and7+a is the plasma sodium concentration 2in millie%uivalents per liter3.

The ;(+a value is normally less than to percent. ,n an oliguric patient! a value ofless than percent is usually due to a prerenal cause. A value greater than to B

percent in this setting suggests compromised tubular function. "hen the value rangesbet$een and B percent! the test is not discriminating.

Although the ;(+a is very useful! it is no$ apparent that a number of causes of acuterenal failure other than prerenal disease can! on occasion! be associated $ith a ;(+a

value of less than percent. These include nonoliguric acute tubular necrosis! acutetubular necrosis superimposed on chronic prerenal disease 2e.g.! advanced cardiac orliver disease3! administration of radiocontrast media or release of heme pigments2hemoglobin or myoglobin3! and renal allograft re/ection.

Thus the ;(+a test must be interpreted in light of the specific clinical setting andother laboratory data to be useful in patient management. Correct interpretation of;(+a or any of the other urinary indices is not possible if the patient had receiveddiuretics in the : to h preceding the test.

+(5-O@O,C MO+,TO-,+

Monitoring the function of the central nervous system may permit early recognition ofcerebral dysfunction and facilitate prompt intervention in situations in $hich


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aggressive early treatment favorably influences outcome. ,n the perioperative andtrauma settings! several methods have been used to evaluate brain function and theeffects of therapy. These include intracranial pressure monitoring! electrophysiologicmonitoring! transcranial )oppler ultrasonography! and /ugular venous o&imetry.

,ntracranial 7ressure Monitoring7hysical findings are often unreliable to ascertain the presence of increasedintracranial pressure 2,C73. Thus the only direct assessment of ,C7 is obtained bymeasurement.

Measuring ,C7 permits calculation of cerebral perfusion pressure 2C773! $hich isdefined as the difference bet$een the MA7 and ,C7. Thus isolated increases in ,C7 ordecreases in MA7 $ill result in a reduction in C77. The C77 may be insufficient if,C7 increases to more than = mmg. Although in the past one of the end points ofcentral nervous system monitoring $as felt to be the contol of ,C7 $ithin safe levels!emphasis has shifted to follo$ing C77 itself. Maintaining cerebral blood flo$ appears

to re%uire using an elevated minimal C77 threshold $hen treating the in/ured brain. AC77 level of at least I= mmg has been suggested.

The most common indication for ,C7 monitoring is severe head in/ury. 7atients $ith alasgo$ Coma 1cale 2C19 see Chap.


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associated ventricular catheter! ho$ever! catheter4tip strain4gauge or fiberopticdevices cannot be recalibrated after insertion. Conse%uently! if the devicemeasurement drifts! there is potential for inaccurate measurements! especially if the,C7 monitor is used for several days.

Complications of ,C7 devices include infection! hemorrhage! malfunction!obstruction! and malposition. 6acterial coloniation of ,C7 devices increasessignificantly after F days of implantation9 ho$ever! significant intracranial infectionsare uncommon.

(lectrophysiologic MonitoringThe electroencephalogram 2((3 reflects spontaneous and ongoing electrical activityrecorded on the surface of the scalp. ,ntraoperative (( recording has been used

primarily for monitoring the ade%uacy of cerebral perfusion during carotidendarterectomy. Other procedures in $hich (( recording has been used includecerebrovascular surgery! open heart surgery! epilepsy surgery! and induced

hypotension for a variety of surgical procedures. ,n the ,C5! (( recordings candetect the e&istence of subclinical epileptic seiures! $hich can cause a decreasedlevel of consciousness. 1tandard (( recording! ho$ever! is not used routinely in the,C5 because of insufficient technical personnel! the volume of data generated in ashort period! the difficulty of on4line (( interpretation! numerous electricallyinduced artifacts! and drug4induced suppression of electrical activity. To simplify(( recording and to ma#e it more useful for clinical application in the operatingroom and ,C5! some monitors process the ra$ data automatically. The compressedspectral array 2C1A3 is the most commonly used method of visually displaying such

processed (( information.

1ensory4evo#ed potentials 21(7s3 are minute electrophysiologic responses elicited bya stimulus and e&tracted from an ongoing (( by signal averaging. They reflect thefunctional integrity of specific sensory path$ays and serve to some e&tent as moregeneral indicators of function in ad/acent structures. 1omatosensory evo#ed potentials211(7s3 reflect the integrity of the dorsal spinal columns and the sensory corte& andmay be useful for monitoring during resection of spinal cord tumors! spineinstrumentation! carotid endarterectomy! and aortic surgery. 6rainstem auditory4evo#ed potentials 26A(7s3 reflect the integrity of the eighth cranial nerve and theauditory path$ays above the pons and are used for monitoring during surgery of the

posterior fossa. Visual evo#ed potentials 2V(7s3 may be used to monitor the optic

nerve and upper brainstem duri

Documents

Chapter 12 Monitoring of Surgical Patient