Monitoring Hemodynamics in the Critically Ill

Symposium on Critical Care Medicine

Monitoring Hemodynamics in the Critically III DavidJ. MD.t David J. Pierson, M.D.* and Leonard D. Hudson, M.D.t

The clinician managing the critically ill patient must decide, for each individual patient and often several times during the course of illness, what physiologic variables to measure, how they should be measured, and how frequently these measurements should be made. Such decisions are made in order to obtain an appropriate amount of clinically uieful information for use in guiding therapy and preventing complications. In an era in which technological developments have brought increasingly sophisticated-and expensive-devices and techniques for hemodynamic monitoring to the bedside, the key concepts here are "physiologically appropriate" and "clinically useful." The clinician's responsibilities include not only providing the best available patient care, but also avoiding unnecessary increases in the hazards and costs of such care. Clinical data are helpful only if they are accurate. Too often in recent years devices and techniques have been put into wide clinical use before their accuracy and reliability have been proven or even tested. Too often, also, therapeutic decisions are made on the basis of "numbers" generated by apparatus and procedures the clinician does not fully understand. Such practices invite complications and virtually assure suboptimal patient care. Intelligent, safe patient management based on monitoring requires that the right measurements be made, that the data so generated be accurate, judgment and understanding in their use be and that the clinician's judglnent appropriate. The general areas to be discussed in this article are physical examination and catheterization of systemic and pulmonary arteries, with an emphasis on the purposes to be served by monitoring rather than on specific measurements, techniques, and devices. Five aspects of each general area are considered: (1) the physiologic basis for the measurement under consideration, including its inherent biological variability; (2) the main tech*Associate Professor of Medicine, University of Washington School of Medicine; Medical Director, Respiratory Therapy Department, Harborview Medical Center, Seattle, Washington tProfessor of Medicine, University of Washington School of Medicine; Medical Director, Intensive Care Units, and Chief, Respiratory Diseases Division, Harborview Medical Center, Seattle, Washington

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nical aspects of the measurement, including apparatus required, costs, insertion, and care of invasive devices, and the accuracy and reproducibility of the data generated; (3) the clinical interpretation of the data; (4) complications to be avoided; and (5) our recommendations for clinical use based on all of this information. The reader should understand that this review necessarily reflects the biases and opinions of the authors, particularly in areas in which scientific data are incomplete.

BEDSIDE OBSERVATION-AN INDISPENSABLE PART OF MONITORING Most of this article is concerned with the mechanical devices and invasive procedures used in hemodynamic monitoring. However, the clinician must keep in mind the central importance of bedside observation and physical examination in assessing and managing critically ill patients. There is no substitute for an alert, skilled observer at the bedside, regardless of other monitoring apparatus or procedures used. Several functions observable at the bedside cannot be replaced by numbers or machines. Mental status is a valuable indicator of the overall condition of a critically ill patient, and serial changes in this sign are of utmost importance. Repeated assessments of the patient's distress, agitation, and communicativeness arc valuable adjuncts to more objective physiologic data during the course and therapy of the illness. Although direct measurement of tissue perfusion is not routinely available, repeated assessments of skin color, temperature, moisture, and turgor provide a useful substitute that cannot be replaced by any currently available invasive measurement. Transcutaneous oxygen tension monitoring, while attractive theoretically as an index of arterial oxygenation, has not proven clinically acceptable in adult patients with hemodynamic instability for reasons that are obvious on bedside observation: the measurements obtained vary with skin perfusion and do not reflect core conditions. Hourly urine output is a good reflection of tissue perfusion. In the absence of intrinsic renal disease, a normal urine output indicates that cardiovascular function is adequate, even when systemic arterial blood pressure is in the hypotensive range; "low" systemic perfusion pressure does not necessarily demand immediate treatment or invasive hemodynamic monitoring, especially if normal renal function and mental status are preserved. Sphygmomanometric measurement of the brachial arterial blood pressure remains the mainstay of first-line hemodynamic monitoring. If a patient's blood pressure is normal and stable, other monitoring may be unnecessary. A primary problem with standard blood pressure measurements, however, is that they are intermittent, although recently available automated sphygmomanometers that measure systolic and diastolic blood pressure every two to three minutes may make invasive monitoring of arterial pressure unnecessary in many patients. Bedside observation is indispensable for the separation of artifact or equipment malfunction from physiologic catastrophe, and no technological

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development in the foreseeable future will permit patient monitoring withjudgment of a human interpreter. out clinical judgnlent Despite the value of bedside observation in critical care monitoring, several important physiologic functions cannot be reliably assessed by physical examination. Included among these are the adequacy of arterial oxygenation and of alveolar ventilation. Studies have shown that even the most experienced clinicians are unable to estimate effective ventilation 25 or l3 or respiratory acidosis with acceptable accuracy. In to detect hypoxemia I3 addition, cardiac filling pressures cannot be assessed reliably by physical examination in patients with pulmonary or cardiovascular dysfunction, so methods are required for the accurate monitoring of that more invasive lllethods these pressures in unstable patients with acute respiratory failure.

SYSTEMIC ARTERIAL CATHETERIZATION Purposes Cannulation of a peripheral or central systemic artery is performed so that blood pressure can be lllonitored monitored continuously and arterial blood specimens withdrawn repeatedly and painlessly. Arterial pressures displayed on a recorder may be expressed conventionally as systolic and diastolic or as lllean mean arterial pressure. Because of the high pressures involved in comparison with those measured with central venous or pulmonary arterial catheters, such noncardiovascular factors as body position and airway pressures do not alter their values substantially. Even in patients with hypotension, indicated values accurately reflect systemic arterial perfusion pressures so long as the catheter is patent and the apparatus is calibrated and functioning properly. Technical Considerations The apparatus required for systemic arterial pressure monitoring consists of a short, small-diallleter small-diameter Teflon catheter inserted percutaneously into an artery, connected via approp~iate small-bore tubing to a pressure transducer and monitor console, with ports for withdrawal of blood and infusion of irrigant solution. Although any artery can be used, the nondominant radial is preferred because in addition to its accessibility and easy manipulation it is not the sole blood supply to the hand, making ischemic complications less likely than with brachial or femoral sites. The ulnar artery supplies most of the hand's perfusion in nearly 90 per cent of individuals, 26 and the adequacy of AlIen's test. II The hand is collateral circulation can be tested easily using Alien's ischemic by finger compression of both radial and ulnar pulses; once made ischelllic it has blanched, the ulnar side is released, and the time required for color return is noted. If the hand is resuffused within 5 sec, a well-developed collateral circulation is present and the risk for distal ischemia is small, even if the radial artery becomes occluded. 44 Another site should be sought if more than 7 sec is needed to reperfuse the hand. 18 IS Doppler techniques may also be used to assess the adequacy of collateral arterial supply. A radial arterial monitoring catheter is inserted as follows. Only a

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small amount of local anesthetic is injected in order not to obliterate the sn1all palpable pulse. The wrist is stabilized and hyperextended, and using appropriate sterile technique a flexible cannula with stylette is introduced into the artery, pointed upstrealu upstream at an angle of approximately 30 degrees fi'om the horizontal. Once arterial blood is returned, the cannula is adfrom vanced into the artery, its intraluminal position confirmed, and the stylette removed. After the pressure monitoring apparatus has been connected, the system flushed, and correct positioning and patency reconfirmed on the monitor, the cannula is secured and all connections tightened. Adequate perfusion to the hand can then be reconfirmed. As with any pressure transducer and electronic monitoring system, systemic arterial catheters safe, appropriate management decisions using systeluic are only possible if all aspects of the system are functioning correctly and are properly calibrated. The details of equipment calibration and maintenance are beyond the scope of this article, but the technical requireluents requirements for stability, sensitivity, linearity, and adequate frequency response 44 must systems to be discussed. be met for these and the other systelus Complications systemic Insertion and subsequent physical presence of a catheter in a systeluic numerous cOluplications, complications, including vasospasm, thromboartery can cause nUluerous sis, embolization, compressive neuropathy, hemorrhage, aneurysm/pseudoaneurysm forluation, formation, arteriovenous fistula, infection, and inadvertent indoaneurysn1 IR When \Vhen specifically speCifically sought, thrombosis can be jection of drugs. I8 majority of patients; clinically detectable thrombosis demonstrated in the n1ajority with \vith arterial occlusion is, fortunately, much less frequent. Likewise, alemboli distal to the catheter are not rare, these are usually though minute eluboli of little clinical iluportance. importance. Ischemic cOluplications complications do occur, however, permanent disfigureluent disfigurement or eventual loss of digits. Antegrade often with perluanent embolization of throlubus thrombus or air during catheter flushing is a much luore more elubolization complication. Compressive neuropathy is more often seen after arserious cOlnplication. l , because it results froln· from' excessive terial puncture than with catheters 18 from the presence of the cathbleeding on entering the artery rather than froln much more con1luon, common, aleter once it is in place. Hematoma Helnatolna formation is lnuch importance. though usually of little clinical ilnportance. IB-gauge radial arterial catheter Disconnection of the tubing from an I8-gauge can cause exsanguination at the rate of one unit per min if cardiac output normal; bleeding is thus the lnost most potentially lethal cOlnplicacomplicais initially norlnal; importance of careful maintenance of the entire systion, underscoring the in1portance tem. Aneuryslns, Aneurysms, pseudoaneurysms, and arteriovenous fistulae may forln form teln. systemic arterial catheterization; the last occurs lnore more often as a result of systelnic femoral catheterization than with radial catheterization. with brachial and fen10ral 1& and although Bacterial infection of an arterial catheter has been reported, 18 complication is fortunately rare. Fithe resulting sepsis can be fatal, this cOlnplication nally, inadvertent injection of vasoactive drugs or other agents into an artery can cause severe pain, distal ischemia, and tissue necrosis. Although arterial catheters are convenient for repeated blood salnpling, sampling, they should not be used as an access site for drug adlninistration. administration. Several factors predispose to complications in patients with arterial

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catheters. 18 These relate to the patient's underlying condition, to the technique used in inserting and maintaining the catheter, and to properties of the catheter itself. Pre-existing arterial disease, as in patients with diabetes or severe atherosclerosis, makes ischemia and other complications more likely. Low cardiac output and peripheral vasoconstriction from pressor agents also predispose to complications, although unfortunately patients in whom these factors apply are those most likely to require insertion of an arterial catheter. Traumatic insertion or removal, and frequent or rough manipulation of the catheter when in place, increase the likelihood of vessel damage, bleeding, and other adverse occurrences. If the catheter and tubing are obscured from view, or if they are inspected and dressed infrequently, complications are less likely to be detected quickly and will be more serious. Catheter material relates directly to the likelihood of thrombosis. Polyvinyl chloride catheters are the most thrombogenic, while TFE Teflon and FEP Teflon catheters are the least so of currently available l7 , 18 1R The length of tinle time a catheter stays in place is generally cormaterials. 17, related with increasing incidence of complications of all kinds. Finally, thrombosis and ischeluia ischemia are closely related to catheter size and vessel diameter.66 These complications are less frequent with 20-gauge than with diameter. larger catheters. Prediction of adequate radial artery diameter for cathetmade by measuring wrist circumference. 77 erization can be lnade The incidence of all these complications can be substantially reduced if clinicians adhere to the general guidelines in Table 1. A certain frequency of adverse occurrences may be inevitable when invasive monitoring procedures are used in critically ill patients, but the steps listed should help to minimize these. Perhaps most important is the admonition not to use arterial catheters if they are not clearly necessary for physiologic assessment and lnanagelnent management decisions. Recommendations Arterial catheterization allows continuous monitoring of systemic arterial pressures. COlnpared Compared with repeated arterial puncture for blood gas analysis, arterial catheters cause less bleeding and less patient discomfort. These factors have led to a dramatic increase in the use of such catheters in intensive care in the past decade. To a certain extent this reflects appromonitoring in the unstable patient and results in priate concern for close lnonitoring better care. However, escalating costs cannot be ignored, and part of the comes frolu from increased numbers of blood gas analyses and more increase conles Table 1. 1. 2. 3. 4. .5. 6.

Prevention of Complications COlnplications from Arterial Catheters

Use radial (or dorsalis pedis) artery if possible Confirm adequate collateral circulation (Alien's Confirn1 (AlIen's test or Doppler) Use Teflon catheters, avoiding other materials Use 20-gauge catheters, avoiding larger ones Fix catheter securely in plain view infilsion of heparinized saline, avoiding Irrigate catheter continuously with slow infusion intermittent flushing I. Relllove Remove the catheter as soon as possible 7.

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continuous monitoring. It is easy to fall into a vicious cycle: arterial lines provide easier access to arterial blood; we measure arterial blood gases more often than in the past; since we therefore require more individual specimens, it follows that patients need arterial lines. This circular justification for an ever-increasing accumulation of physiologic information produces mushrooming hospital bills and greater risk for all the complications of systemic arterial catheterization, and emphasizes the importance of rational approaches to catheter insertion and data collection. Patients with unstable cardiovascular function or severe acute respiratory failure fitting the clinical definition of the adult respiratory distress syndrome (ARDS) require close monitoring and usually need arterial catheters. These patients are also most likely to receive intravenous pressor or vasodilating agents and positive end-respiratory pressure (PEEP), making further derangement of hemodynamics likely and providing further justification for monitoring with a systemic arterial catheter. Clear guidelines are harder to state for patients who are hemodynamically stable but who require arterial blood sampling during the course and therapy of acute respiratory failure. Early in the course of such illness, when rapid changes in therapy and physiologic response are most likely and frequent blood gas analysis will be needed (for example, more than four in 24 hours), it is reasonable to use an arterial line rather than repeated percutaneous arterial punctures. Depending on the clinical course, the catheter can be removed once the patient requires no more than three or four specimens daily. Although complications increase with the number of days an arterial catheter remains in place, it is reasonable to leave a functioning, properly maintained catheter in place rather than rotating between different anatomic sites, as long as it is still required for optimal patient care.

CENTRAL VENOUS PRESSURE MONITORING Measurement of central venous pressure (CVP) has been used to monitor fluid therapy as a measure of preload. The advantages are that CVP monitoring is safer and less expensive than pulmonary artery monitoring. Many of the risks of pulmonary artery catheterization can be avoided. The disadvantage is that CVP often may not reflect preload to the left heart. This is especially true in patients with pulmonary or cardiac disease. Abnormalities of right ventricular physiology will be strong determinants of the CVP. Therefore, CVP should not be used in patients with acute respiratory failure as a measure of left ventricular preload. PULMONARY ARTERY CATHETERIZATION Purposes

The physiologic functions that can be monitored with pulmonary artery catheterization include pressures, flows, and resistances. The most clinically useful pressures are the pulmonary artery pressures and pulmonary artery wedge pressure using the balloon occlusion technique. The

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flow measurelnent measurement is cardiac output. Vascular resistance is the pressure change across a vascular bed divided by flow. Thus, pulnl0nary pulmonary vascular = P PA - PPA "Cdgjcanliac from resistance (PVR == wedg/cardiac output) can be calculated fronl measurements made through the pulmonary artery catheter. Calculation of measureluents systemic vascular resistance (SVR) also requires the measureluent measurement of cardiac output. What do these measurements reflect? Cardiac output is a primary measure of the cardiac pump function. It is also an important determinant of oxygen transport to the tissue (arterial oxygen content X cardiac output). Cardiac output is the product of stroke volume times heart rate. Thus, stroke volume can be calculated from simultaneous measurements of cardiac output and heart rate. Stroke volume depends on several factors, including preload (diastolic filling volume, which determines the myocardial fiber stretch), afterload (the impedance or resistance against which the heart must pump), and contractility. Pulmonary artery pressures are also a result of several influences including the state of pulmonary vascular constriction or obstruction and/or obliteration. The pulmonary artery wedge or balloon occlusion pressure reflects the left atrial pressure if certain conditions are met. Balloon inflation of the pulmonary artery catheter occludes flow in the segment of the pulmonary arterial tree which is served by the branch of the pulmonary puhuonary artery in which the catheter is located. The pressure measured at the tip of the catheter with the balloon inflated will be the pressure at the first junction where veins from nonoccluded portions of the pulmonary circulation empty into the occluded areas. Because of the low resistance of these vessels, little difference exists between the pulmonary venous pressure (which is actually being measured) and the pressure in the left atrium. Therefore, as long as there is an open column of blood in the segrrlent segment without flow, "wedge" or balloon occlusion pressure will reflect the left atrial the "'wedge pressure. Since the left atrial pressure is similar to the left ventricular enddiastolic pressure, and since the end-diastolic pressure is an important determinant of the diastolic filling volume, the pulmonary artery wedge pressure is a reflection of left ventricular preload. However, there are several influences that may change the degree to which the left atrial pressure reflects diastolic filling or preload, and these must be taken into consideration. These influences include left ventricular compliance or stiffness, the pressure surrounding the heart Quxtacardiac Uuxtacardiac pressure), and the possibility of ventricular interdependence. In a ventricle that is made stiffer by hypertrophy, fibrosis, inflammation, or infarction, a higher filling pressure is necessary to result in the same end-diastolic filling volume compared with a normal ventricle. Conversely, a heart with a flabby ventricular wall, such as may occur in a patient with a chronic cardiomyopathy, may have a very large volume with a normal or low pressure compared with a heart with normal compliance. The compliance of the heart also depends on volume, with the compliance decreasing (the heart becoming stiffer) as the volume increases. In addition, changes in disease state or treatment may alter the compliance acutely. For example, inotropic agents result in a decreased compliance, whereas relief of ischemia increases compliance. The effect of pressures outside the heart on the wedge pressure or filling pressure will n

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be discussed below in the section on respiratory effects on intrathoracic Pulmonary vascular resistance and systemic vascular vascular pressures. Puhnonary resistance can be considered as representing the afterload to each of the ventricles, PVR reflecting the right ventricular afterload and SVR the left ventricular afterload. Clinical Indications The potential benefit of hemodynamic data from pulmonary artery catheterization in making diagnostic and/or therapeutic decisions must be weighed against the risk and expense of the monitoring itself. The clinician should always ask whether the data gathered would affect any therapeutic decisions made. In general, situations in which monitoring is useful have one or both of two goals: (1) maximizing cardiac output and tissue oxygen delivery, and (2) minimizing or avoiding pulmonary vascular congestion and pulmonary edema. Since these two goals often require conflicting therapeutic strategies, pulmonary artery catheterization is most often warranted in the patient in whom these goals are being balanced. Clinical situations in which these indications are present include (1) shock or hypotension (or a clinical situation in which the likelihood of hypotension is extremely high, such as major surgery with significant blood loss), and (2) pulmonary edema, either on a cardiogenic or increased permeability basis or both. In the case of hypotension or shock, hemodynamic data can be useful for both diagnosis and therapy. These data can help separate hypovolemia (decreased filling pressures), peripheral vasodilation (decreased SVR), and cardiogenic etiologies (decreased cardiac output). With pulmonary edema, hemodynamic monitoring can help separate a major cardiogenic element from increased permeability. Monitoring information is useful in fluid therapy with both types of pulmonary edema in order to reduce the pulmonary vascular congestion and leak. Often it is not required in patients with cardiogenic pulmonary edema, which usually responds readily to therapy, but may be most helpful to avoid adding a cardiogenic component to permeability edema (ARDS) or to monitor changes from therapy such as PEEP. Other general therapeutic indications are complicated patients in whom monitoring of vasoactive or fluid therapy would provide information which may be useful in changing therapeutic decisions. Technical Considerations The equipment involved in pulmonary artery catheter monitoring includes the catheter, appropriate tubing and connections, a pressure transducer, a flushing system, and a display system, including an oscilloscope and, if possible, a strip chart recorder. Details of insertion technique are beyond the scope of this article. However, the advantages and disadvantages of the various insertion sites and some general guidelines will be discussed. Placement of a pulmonary artery catheter can be done either percutaneously or via a cut-down. Possible sites include a peripheral antecubital site with catheterization of either the cephalic or basilic veins, the subclavian vein, the internal jugular vein, the external jugular vein, and the femoral vein. The antecubital site has a low infection rate and avoids central complications such as pneu-

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mothorax or hemothorax. Central placement of the line may be more difficult in some patients because of venous plexus formation at the shoulder or as the vein enters the thorax. The subclavian site provides easy accessibility and low infection rate, but carries the risk of pneumothorax and arterial puncture with hemorrhage. Line placement in the internal jugular vein has a lower incidence of arterial puncture and pneumothorax. A high incidence of thrombosis has been demonstrated at the internal jugular site, 12 In small children but comparable data are not available for other sites. 12 the external jugular vein is preferred because of its accessibility. The femoral vein has the disadvantage of increased infection risk and is usually avoided. Insertion of lines in any of these sites requires experience on the part of the person placing the catheter, or supervision by someone with experience. The physician placing the line should know the anatomy and possible anatomic variants, the possible complications, and the appropriate technique that will minimize these complications. If the line cannot be placed using proper and safe technique, then another site should be considered rather than violating the technical guidelines for placement during repeated further attempts, which markedly increases the risk of complications. Line placement should always be performed under sterile conditions. It is important to have the transducer, connective tubing, and flushing system prepared before the catheter is placed. Also, the transducers should be calibrated prior to the line placement attempt so that pressures can be monitored during catheter placement. Once the catheter, filled with the flush solution, is placed in the vessel, it should be advanced until the distal tip is in the thorax as confirmed by respiratory variation on the pressure tracing display on the oscilloscope. At this point, the balloon should be inflated and the catheter advanced slowly until a right ventricular configuration appears, then more rapidly until a pulmonary artery tracing is seen. Several criteria should be assessed in order to assure a proper "wedge" (actually balloon occlusion) po~ition.27 position.27 First, with the balloon deflated, a good pulmonary artery pulse contour should be seen on the oscilloscope. Then, inflation of the balloon with 0.8 to 1.2 ml should lead to prompt dampening of the amplitude and decrease of the pressure. If 0.6 ml or less is required to produce a wedge tracing, this implies that the catheter is too far distal. An atrial pressure wave form should be seen. The presence of a and v waves reflecting atrial pulsations assures a wedge position, although often good a and v waves may not be present. With balloon deflation prompt return of the pulmonary artery tracing should occur. One of the criteria for wedge position in the catheterization laboratory has been withdrawal of well-oxygenated (arterial) blood from the catheter. This is not as useful with the balloon occlusion technique and is usually not performed because the catheter is not truly wedged and, therefore, a larger arterial volume is required. If this technique is used, then 20 to 40 ml must be withdrawn before a fully oxygenated specimen can be obtained. Once it is determined that the catheter tip is correctly positioned, the catheter should be secured at the insertion site with sutures and a sterile dressing applied. A chest x-ray study should be obtained, both to verify verifY

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correct placement and to determine whether a pneulllothorax pneumothorax has developed. The course of the catheter through the right ventricle should be noted on chest roentgenogram. If there is any slack in the catheter, the tip may gradually progress distally in the lung, which could result in a permanent wedge position. The oscilloscope should allow the capability of displaying each pres- . monitored. Although it is not necessary to display sure wave form that is lllonitored. all of the pressure wave forms simultaneously, it is important to see each pressure wave form in order to ascertain the quality of the pressure measuring system. Digital displays are most commonly used and have practical advantages; however, they also have several limitations, some of which will be discussed below with respiratory effects on the vascular pressures. It is highly recommended that some type of strip chart recorder with a calionly.23 brated scale be available to avoid the limitations of digital display only. 23 Zeroing the transducer is an extremely important step.27 If the transducer is not zeroed correctly, then the clinician who looks at the recorder pressure values may come to inappropriate diagnostic and therapeutic decisions; this emphasizes the need not only for accuracy of the measurements, but also for correlation with other measurements and with the clinical situation. By convention, central hemodynamic pressure measurements are related to the level of the heart, specifically to the midllleasurements left atrium. Therefore, it is necessary to adjust the transducers so that the recorder reads zero when the transducer is exposed to a fluid column with its highest point being at the left atrial level. The stopcock on either port of the transducer should be opened to the atmosphere and zeroed to the point at which the fluid in the transducer assembly makes contact with the air. This should be moved up or down until this point is at the mid-chest level, which then becomes the reference point. This zeroing process can be done either by electronic methods or by physical adjustment of the zero point. It is assumed that the mid-chest level is the mid-atrial level or zero point if the patient is supine. Since the patient is often also nursed in a partly upright position, the so-called "phlebostatic axis or point" 'should be used, which is the mid-chest at the junction of the fourth intercostal space with the sternum. It has been demonstrated that if this reference point is used, the wedge pressure measurement with the patient in a partially upright position (up to 45 degrees) rarely differs from that in the supine position by more than 1 to 2 mm Hg.39 Since the pulmonary artery wedge pressure is only measured intermittently, it is important to verify verifY the zero before each measurement by opening the stopcock to air. Accurate measurements require a catheter-tubing-transducer system with an appropriate dynamic response. 16 A proper dynamic response to the measuring system can be best assured in two ways: (1) choosing the appropriate components to make up the system, and (2) checking the dynamic response with a fast-flush method. Important components include a short low-compliance tubing, a large diameter catheter, and transducers with small volume displacement. 16 The shortest tubing which practically can be set up should be used. In addition, the tubing should be transparent in order to allow easy detection and removal of air bubbles. The dynamic response can be checked by rapid flushing of the system. 16 If the fast-flush valve in the continuous flush device is opened and then allowed to rapidly

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close, a square wave is generated which can be detected uetected on the oscilloscope. Some overshoot of the baseline should occur with rapid return to the baseline. Calibration of the pressure tracing is usually accolnplished accomplished with an internal electronic system. However, periodically the system should be calibrated with a mercury manometer to ensure accurate pressure recordings. comDevelopment of the thermodilution cardiac output method with COlnmercially available thermodilution catheters has made the measurement of repeated cardiac outputs practical in the intensive care unit. Comparisons of the accuracy of the thermodilution, Fick, an dye-dilution methods of 35 Close cardiac output indicate that the three methods are of equal merit. merit.35 attention should be paid to details of the technique in order to obtain accurate and reproducible information. A good pulmonary artery tracing rapshould be present prior to the injection. The injection must be made rap-· idly and should be done at the same phase of inspiration for all measurements. At least three measurements should be performed, and they should Inents. measurements should be within ± 10 per cent, preferably ± 5 per cent. All measurelnents be recorded so that the clinician can inspect and rapidly ascertain if the time measurement at any given point in time is reproducible over a short tilne (rather than simply recording the mean value which could be the average of three relatively disparate measurements). When the mean of three measurements is used, reproducibility data suggest that a minimal difference of 12 to 15 per cent between determinations must be present to be of clinical significance. 35 The position of the pulmonary artery catheter tip is a factor in whether the measured wedge pressure accurately reflects the left atrial pressure. 37 As described above, there must be an open column of blood from the catheter tip through the pulmonary circulation to the left atrium. This, by definition, is a West zone 3 condition-that is, pulmonary artery pressure > pulmonary venous pressure> alveolar pressure. Therefore, the alveolar pressure does not result in total compression of the vasculature. If the alveolar pressure exceeds the pulmonary artery pressure, this by definition is a West zone 1 condition. Since alveolar pressure totally compresses the pulmonary capillaries, a column of blood is not open between the catheter pressure" in the zone 1 tip and the left atrium. Therefore, the "wedge pressure" condition no longer reflects left atrial pressure but will change as alveolar pressure changes. These zones are affected by the placement of the catheter tip, since the vascular pressures are influenced by gravity and thus are related to the distance up and down the lung. The alveolar pressure is not related to gravity but is related to atmospheric pressure. Therefore, a zone 1 condition can occur because the alveolar pressure is increased, such as may occur with high levels of PEEP, or because the catheter is above the mid-atrial n1id-atriallevel. level. Low vascular pressures also predispose to zone 1 conditions, especially with any positive alveolar pressure. The balloon flotation pulmonary artery catheters are flow-directed so they tend to go toward the dependent portion of the lung, usually at the mid-atrial level or below. 9g, 22 22 However, catheter tips can be positioned above the mid-atrium,33 predisposing to development of a zone 1 condition, particularly if PEEP is applied or air trapping from air flow obstruction is present.

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Respiratory Effects on Intrathoracic Vascular Pressures transmural The driving pressure at any point in the vascular tree is the transnlural pressure-that is, the pressure inside the vessel (or heart) Ininus minus the pressure outside. However, the pressure that is Ineasured measured by the catheter only reflects the intravascular or intracardiac pressure. For vascular pressures inside the thorax, the major factor determining the pressure surrounding the heart is the pleural pressure. Juxtacardiac Juxtacardiae pressure can be assumed to be the same as pleural pressure. Therefore, the the pleural pressure will affect the wedge pressure (or any intrathoracic pressure measurelnent). measurement). Normally, during spontaneous breathing, the intrapleural pressure is only a few cm H 220 below atmospheric pressure at end-expiration. Intrapleural pressure is somewhat lower (more negative) with each eaeh inspiration, but little change in the intrapleural pressure is required to produce inspiratory air flow if the lungs are normal (if there is no obstruction to airflow and cOInpliance compliance is normal). If air flow obstruction or decreased compliance is present, then much greater negative swings in the pleural pressure are present which result in marked ventilatory fluctuations in the intracardiac pressure with the intracardiac pressure being more negative than the transmural pressure. Since intracardiac pressure will be least affected at end-expiration, the pressure should be measured at this point in the ventilatory cycle. If the patient is receiving mechanical ventilation, pleural pressure at end-expiration should be similar to that in a norInal normal situation, but positive fluctuations in pleural pressure will occur with each positive pressure breath delivered by the ventilator. The more compliant the lungs, the more the alveolar pressure will be reflected in the pleural pressure. In patients receiving mechanical ventilation, the intracardiac pressure will be higher than the transmural pressure. Again, the least effect on intracardiac pressure will be seen at end-expiration. readmIt-a very If the mean wedge pressure is recorded from a digital readout-a common practice-these respiratory variations can result in a strikingly different wedge pressure than if it were determined at end-expiration. The practical approach to avoid clinically important inaccuracies is to screen for respiratory variation by watching the pressure tracing on a calibrated oscilloscope or on a strip chart recording. If respiratory variation is obvious (greater than 5 mm Hg difference with the ventilatory cycle), then the pressure tracing should be determined at end-expiration rather than using the mean pressure. IQ ID It is preferable to identify the point of end-expiration on a calibrated pressure tracing froIn from a strip chart recorder and Ineasure measure the actual pressure at that point. One can also calibrate the oscilloscope screen if a calibrated tracing is not available. If the equipment does not allow this possibility, then the diastolic digital reading should be used for wedge pressure if the patient is on mechanical ventilation, and the systolic wedge pressure should be used for patients spontaneously ventilating. However, this approach has limitations, especially in the patient on assisted ventilation who is making vigorous spontaneous respiratory efforts. Any new monitoring equipment which is purchased should allow a direct write-out of the pressure tracings. from the adnlinistration administration If the patient has a positive alveolar pressure froIn of PEEP or continuous positive airway pressure (CPAP), the intracardiac same extent as the intrapressure will be elevated by approximately the saIne

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pleural pressure. Methods to measure the intrapleural pressure are either difficult and cumbersome or carry risk. The juxtacardiac pressure can be estimated as being approximately one third to one half of the alveolar pres27 sure (1 to 2 mm Hg/5 cm H 22 0), depending on lung compliance. 27 The effect of PEEP on transmural pressure can also be judged by measuring the increment in wedge pressure with each increase in PEEP transmural pressure during the initial PEEP trial. We recommend that the transIuural be estimated by an estimate of the juxtacardiac pressure, rather than removing PEEP in order to measure the wedge pressure. In addition to the possible adverse effect on gas exchange from PEEP removal (usually transient if removal is brief), the hemodynamic situation will be changed since impedance to venous return to the heart will be reduced and a transient increase in venous return will result (so-called autotransfusion effect). These difficulties in measuring or calculating a true transIuural transmural pressure underscore the importance of evaluating relative changes in pressure measurements and correlation of the pressure measurements with flow measurements rather than relying on a single absolute pressure value. In addition to the effect on juxtacardiac pressure resulting froIu from PEEP, high levels of PEEP can produce a zone 1 condition as discussed above, particularly if the pulmonary artery pressure is relatively low. 37, 37. 40 PEEP in association with hypovolemia and/or catheter Thus, application of PEEPin mid-atrial level predisposes to a zone 1 condition. tip placement above the Iuid-atriallevel If a zone 1 condition develops, then the pressure measured with balloon occlusion no longer reflects the left atrial pressure but is a reflection of the alveolar pressure. Patients with severe chronic airflow obstruction, especially those requiring mechanical ventilation, may develop progressive air trapping. This air trapping leads to a positive alveolar pressure, including at the end of hemodynamic effects as the applicaexhalation. This will result in similar heIuodynamic more pronounced in that tion of PEEP. However, these effects are often Iuore the patient with chronic airflow obstruction usually has increased lung compliance and the alveolar pressure is transmitted to the pleural space to a greater extent than in the patient with ARDS and stiff lungs. Although it is widely known that patients with airflow obstruction on mechanical ventilation can have air trapping, the degree to which this can occur and the marked effect on hemodynamic measurements have not been widely recmeasuring the positive alveolar pressure ognized. Recently, a method of Ineasuring ("occult PEEP" or "auto-PEEP") in a patient receiving mechanical venti30 This is accomplished by transiently decreasing lation has been described. 30 the rate of the ventilator and momentarily occluding the exhalation port at the usual time of inspiration (the time at which the next breath would have been delivered if the rate was not decreased). This allows transient equilibration of pressure throughout the system, and the manometer on the ventilator or preferably a manometer attached to the proximal airway will then reflect the alveolar pressure. If this phenomenon is not recognized, may have systemic hypotension, low cardiac output, and yet a the patient Iuay high wedge pressure (due to the auto-PEEP effect on increasing juxtacardiac pressure). Thus, ~,! decision could be made to effect diuresis in the patient because of the high wedge pressure, which could result in hypovolemia and predispose to a further reduction in cardiac output. voleIuia

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Complications

Complications may occur both during catheter placement and while pulmonary artery. vs, IS. 31 Durthe catheter is being maintained in place in the puhnonary ing placelnent, placement, complications include hemorrhage, particularly froln from arterial puncture, and pneumothorax occurring during the insertion attelnpt. attempt. Arrhythmias, particularly premature ventricular contractions or short runs of ventricular tachycardia, may occur when the catheter passes through the thc right ventricle. 15, 15. 38 Usually these are transient and end when the catheter tip goes into the pulmonary artery, or they can be aborted by withdrawal of the catheter. However, fatal arrhythmias have been reported; serious arrhythmias are more common in patients with a recent Inyocardial myocardial infarcarrhythlnias tion or ischemia with hypoxemia or acidosis. Transient right bundle branch block can occur, but usually resolves within 24 hours. 15 IS Catheter coiling or looping, sOlnetimes sometimes with a knot developing in the catheter, Inay may occur. This usually occurs in the patient with low flow state. Once the catheter is in place, thrombi frequently form on the surface of the pulmonary artery catheter. Although consequences of throlnbus thrombus formation are infrequent, they can include pulmonary embolism, occlusive vascular thrombosis, and thrombotic endocardial vegetations. Heparin2! fonnation. 21 bonded catheters reportedly lower the incidence of thrombus forlnation. Pulmonary infarction can also occur with distal migration of the catheter to a permanent wedged position. Rupture of the pulmonary artery with fatal pulmonary hemorrhage has been reported. Any factors which predispose to distal migration of the catheter can predispose to pulmonary artery rupture since rupture usually occurs with inflation of the balloon when it is too far distal. It is important to inflate the balloon under constant pressure monitoring and stop instantly when 'Wedge or damped tracthe pulmonary artery pressure tracing changes to a wedge ing. The balloon inflation volume should be noted and if the wedge tracing is recorded with a balloon volume significantly less than that on the catheter shaft, the catheter should be pulled back to a position at which full or near-full balloon inflation volume produces a wedge tracing. . Colonization of the catheter is relatively common,2, 34 although the documented. true incidence of infection related to the catheter is not well docunlented. Factors which predispose to colonization of the catheter (positive blood cultures from blood drawn through the catheter while peripheral venous more than blood cultures are negative) include presence of the catheter for Inore more) repositionings 72 hours, a known site of infection, and repeated (3 or Inore) of the catheter. catheter.22 N Nonseptic onseptic cardiac vegetations have also been reported but are evidently rare. Clinical Interpretation of Data from the Swan-Ganz Catheter Pulmonary artery pressures have limitations in their interpretation because of the number of variables that can affect these pressures. Puhnonary Pulmonary artery diastolic pressures are occasionally used to reflect left atrial pressure when a wedge pressure can no longer be obtained. This has several limitations. It is of some help to know from previous pressure recordings that the pulmonary artery diastolic and the wedge pressure have a consistent relationship with one another. However, even in this circumstance, at may differ some later point in time the pulmonary artery diastolic pressure Inay

\10:-lITORINC HE~10DYNA~lICS HEI\IODYNA~lICS IN TIlE TilE CRITICALLY ILL \/10NITORING

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fi'om the wedge pressure.· pressure.:)3 Therefore, pulmonary artery diasubstantially frcnn stolic pressure as a nleasure measure of filling pressure should be interpreted with limitations of the pulmonary considerable caution. The lilnitations puhnonary artery wedge pressure are related to inaccurate measurelnents measurements or the artifacts discussed pulmonary artery wedge pressure to vary from the above which cause the puhnonary left atrial pressure. measurement of the Knowledge of the physiologic variables that affect lneasurelnent wedge pressure and the clinical situations in which the wedge pressure is likely to vary from either the transmural pressure or the left atrial pressure limitaallows more appropriate interpretation. However, because of these lilnitations it is important to relate the wedge pressure tracing to other measureimportant is its relation to cardiac output or preferably ments. Particularly ilnportant to stroke volume with the construction of a Starling curve. Administration of a fluid challenge to construct such a curve (or diuresis if volume overload is suspected) can be extremely helpful. Thus, the relative pressure in relation to the stroke volulne volume is more important than the absolute value of the wedge pressure. Cardiac Cardiae output also has limitations in its interpretati(m, both because inaccuracies can occur with the technical measurement tion, time. itself and also because the cardiac output can vary considerably with tilne. Therefore, comparison of the cardiac output from one day to the next has relatively little meaning. However, measurements of cardiac output over time periods with therapeutic changes take on lnore more meanrelatively short tilne ing, particularly if performed as described above with repeated measurements showing reproducible values. Thus, repeated measurements of carlnents diac output during fluid challenge or during a PEEP trial which are conducted over a relatively short time period can be helpful clinically. Tissue oxygen transport can be calculated from the arterial oxygen content times the cardiac output. Since arterial oxygen content depends primarily on hemoglobin saturation, this value can be lnarkedly markedly affected by prilnarily the FI0 22 on which the arterial blood gases are measured. Although a value of oxygen transport can be calculated, the regional distribution of the cardiac output is an extremely important factor in maintenance of normal vital organ function. Therefore, clinical observations of mental function, urine output, and assessment of peripheral blood flow, along with laboratory assessment of organ function, are critical and are not replaced by measuring seSSlnent oxygen transport. :VIixed pulmonary artery Mixed venous blood gases obtained through the puhnonary ~1ixed catheter are useful to the extent that they reflect tissue oxygenation. Mixed venous blood gases are particularly useful when a simultaneous arterial blood gas is measured and the arterial-venous oxygen difference is calculated. A falling mixed venous oxygen saturation or widening alveolar-arterial gradient for oxygen (A-aD0 22) suggests inadequate tissue perfusion. However, recent laboratory and clinical data suggest a limitation to the utility utilitv of this measurenlent. measurement. By the Fick principle: cardiac card iac output ou tpu t

=

oxygen consumption arterial-venous oxygen content difference

Therefore, in order for a \videning widening A-V0 A-VOz2 content difference to reflect a 'Therefore, fall in cardiac output and tissue oxygenation, it must be assumed that the

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oxygen consumption relnains remains unchanged. This assun1ption assumption lnay may be incorrect. First, there may be minute-to-minute changes in oxygen conSUlnpconsumption. Perhaps more important, it appears that once tissue oxygen delivery (cardiac output) is reduced beyond a certain point, then oxygen consumption may depend on tissue oxygen delivery. 11, 14, delivery.ll. 14. 29; 29, 32 In other words, once cardiac output falls to approximately 50 50 per cent of its resting value in studies with experimental animals, the oxygen consumption begins to decrease in a linear relationship to the decrease in cardiac output. 11, 29 Therefore, it is possible that extremely dangerous decreases in cardiac output (in terms of tissue function) may occur with no further change in the mixed venous oxygen saturation or A-V0 22 difference. Available data suggest that this probably only occurs in subjects with substantial impairment of cardiac output or other causes for reduced oxygen delivery. limitations of each of the hemodynamic values discussed From the lilnitations above, it is apparent that relative changes in hemodynamic measurements are more important than an absolute value. Also, relationships of one hemodynamic value with another and with the clinical situation must be emphasized. This emphasizes the importance of measuring multiple functions, including clinical information, with interpretation of each piece of information in the context of the entire clinical picture. Excessive reliance on any given single function in isolation from the others can lead to inappropriate clinical decisions.

REFERENCES 1. AlIen, Alien, E. V.: Thronlboangiitis Thromboangiitis obliterans: Methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am. J. Med. Sci., 178:237-244, 1929. 2. Applefeld, Apple£eJd, J. J., Caruthers, T. E., Reno, D. J., et al.: Assessment of the sterility of longterm cardiac catheterization using the thermodilution Swan-Ganz catheter. Chest, 74:377-380, 1978. . term pulmonary artery pressure monitoring in the 3. Archer, G., and Cobb, L. A.: Long ternl 180:747-752,1974. management of the critically ill. Ann. Surg., 180:747-752, 1974. 4, Armstrong, Armstrong. P. W., and Baigrie, R. S. (eds.): Hemodynalnic Hemodynamic Monitoring in the Critically 4. Ill. Hagerstown, Maryland, Harper and Row, 1980. H. F.: Long term radial artery cannulation: Effects on subsequent vessel vcssel func5. Bedford, R. tion. Crit. Care Med., 6:64--67, 1978. H.adial arterial function following percutaneous cannulation with 18- and 6. Bedford, R. F.: Radial 47:37--39, 1977. 20-gauge catheters. Anesthesiology, 47:37-39, circumference predicts the risk of radial arterial occlusion after 7. Bedford, R. F.: Wrist circunlference cannulation. Anesthesiology, 48:377-378, 1978. 8. Bedford, R. F., F" and Wolhnan, Wollman, H.: Complications of percutaneous percntaneous radial artery cannula38:228--236, 1973. tion. Anesthesiology, 38:228---236, . Benumof, J. L., Saidnlan, Saidman, L. J., Arkin, D. B., etal.: et al.: Where pulnlonary pulmonary arterial catheters 9. Benunlof, 46:33~338, 1977. go: Intrathoracic distribution. Anesthesiology, 46:33~338, Hauscher, L. A.: Pulnlonary Pulmonary vascular pressure 10. Berryhill, R. E., Benumof, J. L., and Rauscher, reading at the end of exhalation. Anesthesiology, 49:365-368, 1978. 11. Cain, S. M.: Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia. J. Appl. Physiol., 42:228---234, 42:228--234, 1977. pulmo12. Chastre, J., Cornud, F., Bouchama, A., et al.: Thrombosis as a complication of pulnloN, Engl. J. l\led., 306:278-Med., 306:278nary-artery catheterization via the internal jugular vein. N. 281, 1982.

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13. Comroe, Comroe. J. H., Jr., and Botelho, S.: The unreliability of cyanosis in the recognition of Am. J. Med. ScL, Sci., 214:1-6, 1947. arterial anoxemia. anoxenlia. Aln. J. P., Weg, vVeg, J. G., et al.: The dependence of oxygen uptake on 14. Danek, S. J., J., Lynch, J. oxygen delivery in the adult respiratory distress syndrome. Am. Rev. Respir. Dis., 122:387-396, 1980. 15. Elliott, C. G., Zimmerman, G. A., and Clemmer, T. P.: Complications of pulmonary artery catheterization in the care of critically ill patients. A prospective study. Chest, 76:647-652, 1979. preswre measurement-Dynamic response requirenlents. requirements. 16. Gardner, R. M.: Direct blood pressure Anesthesiology, 54:227-236, 1981. a!.: Percutaneous indwelling radial-artery radial-arter\ 17. Gardner, R. M., Schwartz, R., Wong, H. C., et al.: monitoring cardiovascular function. filllction. N. Engl. J. Med., 290:1227-1231, 290:1227-1231. catheters for Inonitoring 1974. Care. 18. Gauer, P. K., and Downs, J. B.: Complications of arterial catheterization. Respir. Care, 27:435--444, 27:435-444, 1982. J.: Comparison of intraesophageal balloon pressure measurements with a 19. Gillespie, D. J.: Hev. Respir. Dis., 126:583nasogastric-esophageal balloon system in volunteers. Am. Rev. 126:58~ 585, 1982. c., et al.: Retrograde dissection and rupture 20. Gomez-Arnau, J., Montero, C. G., Luengo, C., of pulmonary artery after catheter use in pulmonary hypertension. Crit. Care Med., 10:694-695, 1982. throm21. Hoar, P. F., Wilson, R. M., Mangano, D. T., et al.: Heparin bonding reduces thronlbogenicity of pulmonary-artery catheters. N. Engl. J. J. Med., 305:99~995, 305:993-995, 1981. 22. Kronberg, G. M., Quan, S. F., Schlobohm, R. H. M., et al.: a!.: A-natolnic Ailatomic locations of the tips pulmonary artery catheters in supine patients. Anesthesiology, Anesthesiologv, 51 :467-469, 1979. of pulnl0nary 23. Maran, A. G.: Variables in puhnonary pulmonary capillary wedge pressure: Variation with intrathoracic pressure, graphic and digital recorders. Crit. Care Med., 8:102-105, 8:102--105, 1980. 24. Marini, J., O'Quin, R., Culver, B., et al.: Estimation of transmural cardiac pressures during ventilation with PEEP. J. Appl. Physiol., 53:384-391, 1982. 25. 2.'5. Mithoefer, J. J. D., Bossman, O. G., Thiebeault, D. W., et al.: "The The clinical estimation of alveolar ventilation. Am. Rev. Respir. Dis., 98:868-871, 1968. 26. Mozersky, D. J., Buckley, C. J., Hagood, C. 0., et al.: Ultrasonic evaluation of the palmar circulation. Am. J. Surg., 126:810-812, 1973. 27. O'Quin, R., and Marini, J. J.: Pulmonary artery occlusion pressure: Clinical physiology, measurement, and interpretation. Am. Rev. Respir. Dis., in press. 28. Pape, L. A., Haffajee, M. B., Markis, J. E., et al.: a!.: Fatal pulmonary hemorrhage after use 90:344-347,1977. of the flow-directed balloon-tipped catheter. Ann. Intern. Med., 90:344-347, 1977. 29. Pepe, P. E., and Culver, B. H.: Dependence of oxygen consumption on oxygen delivery Hespir. during cardiac output reduction by positive end-expiratory pressure. Am. Rev. Respir. Dis., 125:84, 1982. ' 30. Pepe, Pe pe , P. E., and Marini, ~larini, J. J.: Occult positive end-expiratory pressure in mechanically mechanicall) 126:166--170, 1982. ventilated patients with airflow obstruction. Am. Rev. Respir. Dis., 126:166-170, 31. Puri, V. K., Carlson, R. W., Bander, J. J., J., et al.: a!.: Complications of vascular catheterization in the criticallv critically ill. Crit. Care Med., 8:495--499, 8:495-499, 1980. 1980 . . Hhodes, G. R., :'IIewell, J. C., c., Shah, D., et al.: Increased oxygen consumption acconlpaaccompa32. Rhodes, New~ll, J. nying increased oxygen delivery with hypertonic mannitol in adult respiratory distress syndrome. Surgery, 84:490--497, 84:49~97, 1978. Shashv, D. M., Dauber,!. Dauber, 1. M., P£ister, Pfister, S., et al.: a!.: Swan-Ganz catheter location and left 33. Shasby, atri~l pressure determine the accuracy of the wedge pressure when positive end-expiatrial 80:666--670, 1981. ratory pressure is used. Chest, 80:666-670, 34. Singh, S., Nelson, N., Acosta, 1., et al.: Catheter colonization and bacteremia with pulmonary and arterial catheters. Crit. Care Med., 10:736-739, 10:736--739, 1982. lnonary 35. Stetz, C. W., \V., Miller, R. G., Kelly, G. E., et al.: Reliability of the thermodilution method Am. Rev. Respir. Dis., in the determination of cardiac output in clinical practice. Aln. 126:1001-1004, 1982. 36. Suter, P. "I., M., Lindauer, J. M., Fairley, H. B., et al.: Errors in data derived from pulmonary artery blood gas values. Crit. Care Med., 3:175-181, 1974. 37. Tooker, J., Huseby, J., and Butler, J.: The effect of Swan-Ganz height on the wedge pressure-left atrial pressure relationship in edema during positive-pressure ventilation. Anl. Am. Rev. Respir. Dis., 117:721-725, 1978. J

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I.: Catheter-induced arrhythlnias. arrhythmias. Am. Heart J., 88:588:38. Voukydis, P. c., C., and Cohen, S. 1.: ,592, 1974. 592, :39. 39. Woods, \Voods, S. L., Grose, B. L., and Laurent-Bopp, D.: Effect of backrest position on pul~urs., 18:21, 1982. monary artery pressures in critically ill patients. Cardiovasc. Nurs., 40. Zarins, C. K., Virgilio, R. W., Smith, D. E., et al.: The effect of vascular volunle volume on positive end-expiratory pressure-induced cardiac depression and wedge-left atrial pres23:348-360, 1977. sure discrepancy. J. Surg. Res., 23::348-:360, Harborview Medical Center ZA-62 325 Ninth Avenue Seattle, Washington 98104