THE

SWAN-GANZ

CATHETER

The following excerpts originally appeared as four articles1-4 from a five-part series by Devendra K. Amin, Prediman K. Shah, and HJC. Swan that was published in the April and May 1986 issues of Journal of Critical Illness. Disease-a-Month would like to express its gratitude to Jonathan Bigelow, Ellen Rosen, and the Editorial Staff at Cliggott Publishing Company for allowing us to reprint these contributions, which so well complement Dr. Swans preceding monograph. CHOOSING AND USING THE EQUIPMENT

To perform Swan-Ganz catheterization successfully, a basic understanding of the equipment used (both the cardiac catheter itself and the electronic hardware1 is as important as a thorough knowledge of the principles of hemodynamic monitoring. Meticulous attention to detail is essential to avoid errors, to minimize complications, and to achieve optimum results. In the first excerpt from their series, Dr. Swan and his colleagues provide practical, relevant information regarding the equipment used for Swan-Ganz catheterization. They discuss the types of catheters currently available and the electronic monitors to which the catheters are connected. In addition, they review the various factors that must be considered to ensure the quality of the electronic signals, and outline how the equipment must be referenced and calibrated so that the signals obtained through hemodynamic monitoring can be properly interpreted. THE CATHETER WE USE

The development of the original Swan-Ganz catheter was outlined in the preceding section. Although the basic concepts and design remain the same, the balloon flotation catheter has since undergone a variety of modifications to accommodate additional functions. A number of different catheters are now available. The catheter most often used at our institution is a quadriluminal, No. 7.5 French thermodilution catheter that includes an additional
OM, August1991 509

venous infusion port. (French units indicate the outside diameter of the catheter; one French unit equals 0.33 mm.) The typical catheter for hemodynamic monitoring is radiopaque, 110 cm long, made of polyvinyl chloride, and marked with black rings at lo-cm intervals from the tip. These markings allow one, in the absence of fluoroscopy, to determine when to inflate the balloon, when to suspect catheter looping, and, once the catheter is positioned, when to check for displacement. A black ring thicker than the rest identifies the 50-cm mark from the tip. The distal lumen terminates at the tip, whereas the right atrial lumen opens about 30 cm proximal to the tip. The venous infusion port opens about 1 cm above the right atrial lumen. A wire connects a thermistor bead, located 3 to 5 cm from the tip, to an external thermistor connector, which, in turn, is linked to a cardiac output computer. A latex balloon, the desired and maximal inflating capacity of which is between 1.0 and 1.5 mL (usually indicated on the catheter), is positioned near the tip in such a way that, when inflated for passage through the right heart chambers, it engulfs the tip. The larger surface of the balloon minimizes the risk of endocardial irritation and arrhythmias that would otherwise result from impingement of an unprotected catheter tip on the endocardium. The inflated balloon also facilitates advancement of the catheter tip across the right heart and into the pulmonary artery. Furthermore, balloon inflation causes slight distal migration of the catheter tip in a proximal pulmonary arterial branch; as a result, the inflated balloon occludes the branch, allowing measurement of pulmonary capillary wedge pressure. Other modifications to the standard Swan-Ganz catheter include incorporation of heparin in the outer wall of the catheter (heparin bonding) to reduce thrombogenicity, addition of electrodes for intracavitary electrocardiographic recording and pacing, and inclusion of fiberoptics to measure oxygen saturation in the pulmonary artery. A single catheter today can thus serve several functions:
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l l l l l

Measurement of cardiac output through thermodilution. Measurement of pulmonary artery and, hence, core body temperature. Monitoring of intracardiac pressures (right atrial and ventricular, pulmonary arterial, and capillary wedge pressures). Sampling of blood from central circulation for blood gas analysis. Infusion of medications, fluids, etc. Recording of intracavitary potentials. Pacing from atrial and ventricular sites. Continuous online measurement of oxygen saturation in the pulmonary artery.
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ELECTRONIC

MONITORING

EQUIPMENT

The fluid-filled Swan-Ganz catheter is connected via semirigid, noncompliant pressure tubing to pressure transducers. These transducers are, in essence, electromechanical devices consisting of a fluid-filled dome, a diaphragm, and a strain-gauge-Wheatstone bridge arrangement. Because fluid is incompressible, any motion of the fluid column in the catheter and pressure tubing is directly imparted to the diaphragm, unbalancing the bridge and generating an electric current directly proportional to the fluid motion. This current is then amplified and transmitted to oscilloscope equipment for display. To faithfully reproduce biologic signals, four other factors, in addition to properly functioning electronic equipment, must be considered: A system with a frequency response flat to adequate for most studies on human beings. However, reliability and recognition of pressure waveforms may be decidedly poor in patients who have very rapid heart rates (for example, those with heart beats in excess of 180 beats per minute).
Frequency Respome.15 to 20 Hz is generally Natural Frequency.Fluid-filled systems possess a natural frequency that is governed mainly by the length of pressure tubing used. When natural frequency decreases to within physiologic range (as occurs when excessively long pressure tubing is used), an overamplification of signals results, falsely elevating pressure readings. Consequently, we recommend that the length of the pressure tubing not exceed 3 to 4 ft. Damp&.-The opposite effect (loss of physiologic signal, or damping) most frequently results from air entrapped in the circuit. Air, unlike fluid, is compressible; thus, less to-and-fro motion is imparted to the transducer diaphragm per unit of pressure change if airisinthecircuit. Damping of the pulmonary artery pressure signal may make it difficult to differentiate that signaJ from the pulmonary capilkiry wedge pressure tracing. Damping w-ill also occur if the pressure tubing used is too pliable, because signal energv is lost in distending the tubing.

tTafh%?r Whip &.tif&-A problem more prwalent to the pulmonary circuit, catheter whip art&u3 results from motion imparted to the catheter with each cardiac contraction. It can lead to misinhrmation unless eliminated by use of appropriate higldiq~q filtern.

To quantify pressure signals accurately and reproducibly, the monitoring and recording system must be properly balanced and calibrated. When the patient is supine, the pressure transducer (or any convenient fluid-filled connection open to atmospheric pressure) is aligned with a point in the fourth intercostal space midway between the front and back of the chest (phlebostatic axis). This site serves as the standard zero reference point (Figure 1). The calibration of the monitor involves the introduction of a known pressure signal. Most hemodynamic monitoring systems that are currently available can be calibrated internally or externally. Internal calibration of either alone should be avoided, however, because transducer accuracy may vary by as much as
27%.

At our institution, all monitors are externally calibrated. This is done by attaching a mercury manometer to the pressure transducer and then raising the mercury column to the desired level (for example, 40 mm Hg for pulmonary pressures and 200 mm Hg for arterial pressures). The calibration control on the monitor is then adjusted to display the applied signal. Zero reference and calibration should be rechecked at appropriate

I---

--llll_-~

-____--_____-

-_I_-.---_

FIG 1.
To zero reference a pressure transducer, have the patient lie supine. Align the transducer (or any convenient fluid-filled connection open to atmospheric pressure) with a point in the fourth intercostal space, midway between the front and back of the patients chest (phlebostatic axis). Mark this point on the patients skin with indelible ink for easy and accurate realignment.

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intervals during each day of hemodynamic monitoring. tution, this is usually done every 8 to 12 hours1 INSERTION TECHNIQUE

At our insti-

Understanding the equipment is only the first step in cardiac catheterization. Obviously, even the best catheters and the finest electronic monitors are worthless unless they are properly used. In the second excerpt from their series, the authors outline their method of Swan-Ganz catheterization. They describe the special fluoroscopic suite they use most often for this procedure and present a minimum checklist of equipment that should be available whenever catheterization is performed. They then detail their preferred method of catheter insertion and advancement. Finally, they present practical pointers for minimizing the risks and maximizing the results from cardiac catheterization. FACILITIES AND EQUIPMENT

The flow-guided nature of the Swan-Ganz catheter permits us to perform catheterization at the bedside, using pressure and electrocardiographic monitoring for guidance. However, ready access to fluoroscopic equipment is desirable, particularly if catheterization is likely to be difficult (for example, in patients with dilated right heart chambers, severe tricuspid regurgitation, or pulmonary arterial hypertension) or whenever the catheter does not pass smoothly or advance properly. For this reason, most catheterizations in our coronary care unit are performed in a special procedures room that contains image-intensifying fluoroscopic equipment. Use of this room enables us to perform multiple procedures (at times, simultaneously) on critically ill patients, and provides us with maximum flexibility for space, safety, equipment, and asepsis. A minimum checklist of equipment required for catheter insertions is provided in Table 1. Many prepackaged kits are available today, and operators should become familiar with equipment available at their institutions. All equipment should be checked carefully before the procedure is begun. The pressure transducer should be zeroed and calibrated, using the methods outlined above. As precautionary measures, an intravenous line, lidocaine, atropine, and a defibrillator unit should be readily available. To minimize the small yet significant incidence of infections that are associated with catheter insertion, strict adherence to aseptic

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TABLE 1.
Checklist of Equipment for Swan-Ganz Catheter Minimally Insertion Required

Appropriate Swan-Ganz catheter Dilator-sheath-side arm assembly Three-way stopcocks Pressure tubing Transducers IS-gauge, thin-walled Cook needle Sterile gowns, drapes, gloves, etc. I% lidocaine Heparinized saline J-tipped guidewire Towel clips, syringes, suture material Electrocardiography and pressure monitoring equipment Intravenous line Atropine Defibrillator unit

techniques is crucial. At our institution, both the operator and the assistant perform a surgical scrub and wear sterile gloves, gowns, face masks and caps. All other personnel in the room are required to wear face masks and caps. As a practical point, the operator and assistant should also put on lead aprons before scrubbing. This avoids the need to break scrub later if fluoroscopy is required. The site chosen for catheter insertion should be considered a surgical site, and thus should receive meticulous preparation, including shaving and scrubbing with antiseptic solution, Sterile towels should be used to isolate the site and to provide as large a sterile area as possible. SITE OF INSERTION Access to the venous circulation may be gained by percutaneous cannulation (using a modified Seldinger technique) of the subclavian, internal jugular, external jugular, antecubital, or femoral vein. Alternatively, access can be established through a cutdown over a peripheral vein, such as the median basilic vein in the antecubital fossa. Percutaneous insertion is generally the quicker and thus the preferred method. However, cutdown of an antecubital vein is better for patients receiving anticoagulant medications or thrombolytic therapy, because the incision site is easily compressible should bleeding occur. A detailed comparison of the different routes of catheter insertion
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TABLE 2.
A Comparison Route Peripheral External jugular of Venous Access Routes Advantages Easy to learn Safe Does not interfere with cardiopulmonary resuscitation (CPRI Easy to learn Safe Preferred mute with anticoagulant or thmmbolytic therapy, because the site is easily compressible should bleeding occur Rapidly accessible Does not interfere with CPR Provides a straight mute to the heart Less restrictive to patient movement Disadvantages Valves may hinder catheter or guidewire insertion Stasis, thrombosis, and phlebitis are more common Stasis, thrombosis, infection, and venospasm are more common Catheter displacement is frequent Method of Cannulation

Percutaneous

Antecubital

Percutaneous/ cutdown

Central Internal jugular

Percutaneous

Subclavian

Percutaneous

Rapidly accessible Allows free neck and arm movement Easier to keep sterile

Femoral

Percutaneous

Rapidly accessible Does not interfere with CPR

Air embolism, carotid artery puncture, tracheal injury may occur Pneumothorax (more common in the left than the right internal jugular vein) Thoracic duct injury (left internal jugular vein only) Air emboiism, more frequent pneumothorax and hemothorax; subclavian artery puncture; Injury to newe bundle may occur Sepsis, in situ thrombosis, pulmonary embolism may occur

is given in Table 2. The exact site and method of insertion will depend on the experience and training of the operator and on the urgency of the situation. At our institution, the preferred route for catheter insertion is via the right internal jugular vein. We find that in skilled hands, it can be cannulated rapidly with a high degree of success and minimal rate of complications.
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METHOD

OF INTERNAL

JUGULAH

VEIN CANNULATION

A working knowledge of the anatomy of the neck, and in particular, the internal jugular vein is essential for low-risk, successful cannulation. Cannulation of the right internal jugular vein is preferable to the left, because it presents a straighter path to the heart and avoids the risk of damage to the large thoracic duct. In addition, pneumothorax is less likely to develop because the dome of the pleura is lower on the right. We use the posterior approach to enter the internal jugular vein. The patient is usually in the Trendelenberg position, unless he or she is severely orthopneic or has obvious jugular venous distention develop following assumption of a supine or semirecumbent position. Local anesthesia (2 to 4 mL of 1% lidocaine) is given. A 3-in-long, Id-gauge, thin-walled Cook needle, mounted on a syringe, is inserted bevel upward underneath the lateral border of the sternocleidomastoid muscle, about 5 cm above the clavicle (or just above the point where the external jugular vein crosses the muscle). The Cook needle is directed anteriorly toward the suprasternal notch at a steady 30- to 45degree angulation to the sagittal and horizontal planes. The vein is usually entered within 5 to 7 cm. At times, it may be helpful to use a Z-gauge exploring needle to locate the internal jugular vein before using the Cook needle for cannulation. Once free-flowing venous blood is obtained, the syringe is disconnected from the needle. It is important that the needle be occluded with a finger to prevent air embolism. (A water pressure difference of only 5 cm across a 14-gauge needle can result in the entry of about 100 mWs of air). A 40-cm-long, J-tipped flexible guidewire (diameter, 0.035 in.) is next inserted through the Cook needle into the vein. The guidewire should pass smoothly; forcible advancement should never be attempted. If difficulty is encountered, the guidewire should be withdrawn into the needle and twisted to change the direction of the J tip; the guidewire should then be readvanced into the vein. The guidewire should not be twisted while the J tip is still inside the vein. Further difficulty in advancement often indicates needle displacement. Should this occur, the guidewire should be removed and a syringe attached to the Cook needle. The needle should then be repositioned in the vein under continuous negative pressure. Gently rotating the needle also sometimes helps by directing the bevel away from the vessel wall. Once the guidewire is well within the vein, the Cook needle is removed and the skin puncture enlarged with a No. 11 scalpel blade.
516 DM, August 1991

This facilitates the passage of the dilator-sheath system that will be advanced over the guidewire into the vein. Care should be taken to ensure that the guidewire protrudes beyond the outer end of the dilator-sheath assembly at all times before and during advancement of the dilator-sheath. The operatorassistant (or a hemostat attached to the distal end of the guidewire) can help prevent inadvertent advancement of the guidewire. The dilator-sheath assembly should be advanced as a whole into the vein with a gentle rotating movement. Forcible insertion often results in damage to the sheath and thus should be avoided. Once in the vein, the dilator and guidewire are removed and the sheath is sutured in place. A variety of different dilator-sheath assemblies are available. We use a No. 8 French sheath with a one-way valve at the outer end and a side arm for blood sampling and infusion of fluids or drugs.

CATHETER

PREPARATION

AND INSERTION

Every catheter should be tested before insertion. The catheter shaft should be inspected for bends or kinks, particularly at the hub (breaks most commonly occur there). Next, the integrity of the balloon should be tested by inflating the balloon under water using air. Air bubbles indicate a leak, and the catheter should be replaced. Fluid should never be used to inflate the balloon because it often proves impossible to withdraw once instilled. Additionally, its noncompressible nature causes extremely high forces to be transmitted to vessel walls, which can lead to injury and rupture. Once inflated, the balloon should also be inspected for symmetry and for the completeness with which it protects the catheter tip. Some cardiac output computers allow one to pretest thermistor integrity. The thermistor connector is attached, via cable, to the computer, which will then test the thermistor and flash a warning, catheter fault, if a problem is found. Once the catheter passes muster, it is connected by means of three-way stopcocks and pressure tubing to appropriately balanced and calibrated pressure transducers. All lumens of the catheter are then flushed and filled with heparinized sterile saline. Finally, all air bubbles are carefully eliminated from the entire system by flushing it with heparinized saline. A tightly fitting plastic sleeve is often placed over the catheter, before insertion, to preserve a sterile length of the catheter outside the insertion site for subsequent catheter manipulation. The catheter is now ready for insertion.
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The balloon should remain deflated until the catheter tip is in an intrathoracic location; the correct location will be indicated by increased respiration-related pressure variation. In the average patient, the catheter tip will approach the right atrium when it is advanced between 10 and 15 cm from an internal jugular or subclavian vein. From the right or left antecubital fossa, it must be advanced about 40 to 50 cm. Once in the right atrium, the balloon is inflated to its recommended volume (1 to 1.5 mL). The catheter is then smoothly and rapidly advanced under continuous electrocardiographic and pressure monitoring (or fluoroscopy) across the tricuspid valve, through the right ventricle and pulmonary artery, and into pulmonary wedge position. Characteristic pressure changes should accompany its passage across each chamber and should be recorded, if possible (Figure 2).

In general, a catheter should reach the pulmonary artery within 50 to 55 cm if advanced from the internal jugular vein, and within 65 to 70 cm if inserted via a femoral or arm vein. If substantially greater

3almon deflate0 A. Balloon inflated

Swan-Ganz cathetel

Right atrial pressure (O-8 mm Hg)

. I

Pulmonary artery pressure (Systolic: 20-25 mm Hg, diastolic: 4-8 mm Hg)

Right vent&Jar pressure (Systolic: 2025 mm Hg, diastolic: 6-12 mm Hg)

FIG 2.
Normal hemodynamic pressures.

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lengths are required to reach the pulmonary artery, one should suspect catheter coiling. Occasionally, the catheter tip reverses direction after crossing the pulmonary valve and comes to lie in the papillary muscles of the right ventricle. This positioning results in a damped pressure that simulates a wedge tracing. Proper wedge position is most easily confirmed by fluoroscopy. In its absence, wedge position may be assumed if:
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l l l

Balloon inflation and deflation are consistently accompanied by disappearance and reappearance of pulmonary artery pressure. Catheter obstruction and damping artifact are excluded. Wedge tracing shows an appropriate waveform. Withdrawn blood has an oxygen saturation greater than or equal to that of systemic arterial blood with the balloon inflated.

When the balloon is deflated, the catheter shaft usually recoils into a more proximal position (optimally, within the right or left main pulmonary artery). From this proximal position, it should consistently float to wedge position with each subsequent balloon inflation. If fluoroscopy is available, a final check should be made to correct any catheter looping or redundancy, which might otherwise lead to distal migration and permanent wedging. Once correct positioning has been ensured, the catheter is carefully secured at the insertion site, using tape or sutures. An antibacterial ointment and dressing are then applied to the insertion site.

PRACTICAL

POINTERS

There are several specific situations to be alert for when inserting the Swan-Ganz catheter, to maximize the value of bedside hemodynamic monitoring and to minimize the risk of complications:
l

In most patients, once the catheter is in the right atrium, advancement to wedge position is completed within 20 to 30 seconds, even if the procedure is performed without fluoroscopy. Occasionally, however, it may be difficult to advance the catheter even as far as the right atrium. When a central vein has been used, this generally indicates that the tip of the sheath is lying against a vessel wall or in another central vein. Slight withdrawal and repositioning of the sheath will usually solve the problem. When a peripheral vein is used, venospasm may preclude cath-

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519

eter advancement. Venospasm may sometimes be overcome by gently moving the catheter back and forth inside the vein. Intravenous injection of small amounts of nitroglycerin or contrast dye may also be helpful. Catheter advancement may be especially difficult in patients with low cardiac output states, tricuspid regurgitation, pulmonary hypertension, or markedly dilated right heart chambers and right ventricular failure. The passage of the catheter may be facilitated by having the patient take deep breaths. We recommend that insertion be performed under fluoroscopy in these patients to avoid catheter entanglement and displacement. For this same reason, we suggest fluoroscopic guidance be used whenever cardiac catheterization is performed on patients who have had or will be undergoing additional procedures, such as placement of a temporary pacemaker. At times, successful catheter placement may be possible only if a guidewire (length, 120 cm; outer diameter, 0.021 in.) is placed inside the distal lumen. This improves catheter stiffness and torque control, and is particularly helpful in patients with severe pulmonary hypertension. In the absence of fluoroscopy, proper catheter placement may present problems in patients in whom pressure waveforms are difficult to interpret. Very noisy tracings are associated with both severe tachycardias and catheter whip artifact; however, typical waveform changes may not be discernible if the patient is tachypneic or has severe hypovolemic shock, or when there is signal damping. Severe mitral regurgitation (especially if acute) results in substantially elevated left atrial and pulmonary capillary wedge pressures, and markedly accentuated v waves that mimic pulmonary artery systolic pressures. These findings can lead to erroneous interpretation of pressure waveforms. The chances of an incorrect reading can be reduced if the pressure tracings are examined together with simultaneously obtained electrocardiographic tracings. The v wave occurs later in the cardiac cycle than does the pulmonary arterial systolic waveform and corresponds to the T wave on the electrocardiogram. This temporal separation in the two pressures thus serves as an easy way to confirm proper catheter positioning. Another commonly encountered problem is the correct interpretation of wedge tracings in patients with severe bronchospasm or on mechanical ventilators. Intrathoracic pressure varies markedly from expiration to inspiration in these patients; these wide pressure swings are transmitted to the catheter, making accurate interpretation of wedge pressure difficult. A variety of techniques have been suggested to overcome this
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problem. These include having the patient hold his or her breath, using electronically integrated mean pressure readings, and disconnecting the patient from the ventilator. However, none of these methods is as suitable as measuring all pressures at end-expiration because intrathoracic pressure is least variable at this stage of the respiratory cycle. Accordingly, we recommend that all pressures be recorded over at least two respiratory cycles and that they be measured at end-expiration, regardless of whether the patient is breathing spontaneously or with artificial support. Special care must be exercised any time the catheter traverses the right ventricle. The balloon must be kept inflated to protect the catheter tip, thereby reducing the risk of endocardial injury and cardiac dysrhythmias. Occasionally, the balloon may get entrapped in trabeculae, impeding further passage. In this situation, the balloon should be deflated before the catheter is withdrawn into the right atrium; the catheter can then be readvanced with the balloon inflated. Forcible withdrawal while the balloon is still inflated should never be attempted because it is likely to injure trabeculae or the tricuspid valve? RESULTS

TIPS ON INTERPRETING

Bedside hemodynamic monitoring is now an integral part of the care of critically ill patients. It has contributed significantly to our knowledge of the pathophysiology of a multitude of diseases and has allowed us to refine our therapeutic approaches to those diseases. Unfortunately, the simplicity and widespread applicability of hemodynamic monitoring (as well as its potential financial rewards) invite abuse and, consequently, an increased incidence of complications . In this excerpt, the authors explain how to get the best measurements of pulmonary capillary wedge pressure (PCWP), cardiac output, and arterial pressure. They review how such variables as catheter location and respiratory phases can affect pressure measurements, and they outline the technique they prefer for arterial cannulation. The authors also discuss the complications that are frequently associated with cardiac catheterization and what can be done to minimize their incidence. OBTAINING
PULMONARY

THE BEST MEASUREMENTS

CAPKLARY WEDGE PRESSURE

For best results, the catheter should be positioned in a large pulmonary artery, from which it can consistently float into wedge posiDM,Au@1st1991 521

tion. The goal is to obstruct a distal vessel passively, but not to occlude it distensively. If the catheter is positioned optimally under fluoroscopy, repeat wedge measurements may be obtained by full balloon inflation. If fluomscopy is not used, the balloon should be slowly inflated (in increments of 02 to 0.5 mL of air), while pulmonary artery pressure is continuously monitored. Wedge tracings obtained at substantially less than full inflation volumes suggest distal migration of the catheter tip, Such migration may result from a combination of forward thrusting of the catheter with each heart beat and loop shortening caused by catheter softening. The catheter should be repositioned-ideally, under fluoroscopy, but if such guidance is not available, by withdrawing 1 to 2 cm of the catheter at a time. Poor wedging may also result from patient movement (with resultant catheter displacement), positive end-expiratory pressure (PEEP) administration, or other forms of mechanical ventilation. Poor wedging may also be caused by eccentric balloon inflation, which permits the catheter tip to impinge on the vessel wall and thereby possibly rupture the vessel. Catheter position should be checked each time wedging occurs, and preferably daily, by overpenetrated chest roentgenograms. In most circumstances, PCWP reflects left atrial and left ventricular end-diastolic pressure. Its continuous monitoring, although desirable, is impractical, because chronic obstruction of a pulmonary artery is likely to lead to endothelial damage, pulmonary artery rupture, or pulmonary infarction. To reduce the risk of these complications, we recommend keeping wedge time to a minimum (8 to 15 seconds) and recording pressures over no more than two to four respiratory cycles. We also recommend substituting carefully measured end-expiratory pulmonary diastolic pressures for mean PCWPs whenever possible. In the absence of elevated pulmonary arteriolar resistance, these pressures usual@ approximate each other closely (less than 2 to 4 mm Hg dBemnce1.

It is generally assumed that, under most circumstances, PCWP accmte@ refbcts mean left atrial possum. However, this assumption iscorrocton.lyifthepu.lmonsryvascmar system distal to the catheter tip (that is, the puhnonary capIIIar%s and veins) is fmely patent andpmvidesadimct,l&m&Ued vafmdar connection between the ~~tipgnd~leftatrium-~,inesse~,~sPextension of the catheter. If any interruption, whether anatomic or f ** al occursinthissystem,vve4$epressu3ewillnolongerrefleet &left atrial pmsm. 5tz ml% Altgus! l!sl

In the upper lung (zone 11, where alveolar pressure commonly exceeds both pulmonary arterial and venous pressures, pulmonary capillaries are usually closed and no blood flow occurs. This effectively precludes reflection of left atrial pressures. In the central areas of the lung (zone 21, flow is primarily determined by the balance between pulmonary arterial and alveolar pressures only, because in these zones, alveolar pressure commonly exceeds pulmonary venous pressure. Balloon inflation and catheter wedging will, in fact, convert a zone 2 situation into a zone 1 situation by preventing blood flow. Thus, if the catheter is lodged in either zone 1 or zone 2, PCWP will not reflect mean left atrial pressure, but rather alveolar pressure. In the lower lung (zone 31, on the other hand, capillaries remain open, because both pulmonary artery and venous pressures exceed alveolar pressures. As a result, there is free communication between the left atrium and pulmonary arteries. Only if the catheter tip is located in zone 3 will wedge pressure truly reflect left atrial pressure. Thus, for greatest accuracy in measuring mean left atrial pressures, the catheter tip should be located in zone 3. Lateral chest roentgenograms may be necessary to ascertain that the catheter is positioned correctly below the left atrium. Fortunately, most of the lung is in zone 3 when a patient is supine; flow-directed catheters will usually enter zone 3 because most blood is flowing to this area. The incidence of non-zone 3 catheter placement is greater in patients with low vascular pressure resulting from hypovolemia, or in those with elevated intra-alveolar pressures (for example, as might develop following use of PEEP). However, as long as the catheter tip remains below the left atrium, zone 3 conditions will exist, despite even high levels of PEEP. Thus, wedge pressures can still provide reasonably accurate estimates of mean left atrial pressure; concomitant intrapleural or intraesophageal pressure measurements are unnecessary.

Respiration

and PCWP

The positive and negative swings in intrathoracic pressures associated with all forms of respiration directionally influence intraluminal pulmonary vascular pressures. During spontaneous breathing, intraluminal pressure is lower in inspiration than in expiration. However, the opposite occurs during mechanical ventilation: pressures in inspiration exceed those in expiration. Because intrathoracic pressure is closest to zero during end-expiration, regardless of whether the patient is breathing spontaneously or with the help of mechanical ventilation, all pressures should be measured during this phase to minimize the influence of intrathoracic pressure swings. Measuring wedge pressure accurately in patients receiving PEEP
DM, August 1991 623

can be problematic. These patients may have raised intraluminal pressures, yet the effective or transmural filling pressure (intraluminal pressure minus intrapleural pressure) may actually be normal or even low. In any given patient, the effect of PEEP on intrapleural pressure depends on that patients lung compliance. Thus, in a patient with decreased lung compliance in whom the effect on intrapleural pressure is minimal, intraluminal pressure reflects transmural pressure and actual filling pressure. However, in a patient with increased lung compliance, intrapleural pressure rises with PEEP and intraluminal pressure will no longer reflect true filling pressure. In general, there appears to be no need to discontinue PEEP to record PCWPs. However, in patients who have significant disparities in pressures on and off PEEP, it is probably best to measure intrapleural or intraesophageal pressures (and, thus, transmural filling pressures1 to guide therapy.

CARDIAC OUTPUT
A major advantage of the Swan-Ganz catheter is that it allows frequent, rapid, easy, and highly reproducible measurement of cardiac output by thermodilution. The techniques accuracy is comparable with other more laborious and technically demanding methods, such as the Fick procedure or indicator-dye dilution analysis using indocyanine green. Thermodilution uses heat as the indicator and, like dye dilution, requires complete mixing so that the blood sample detected by the pulmonary artery thermistor represents all the blood entering that artery. Complete mixing is believed to occur when the indicator and blood pass through two valves and a contracting chamber; this criterion is satisfied by injecting cold solution into the right atrium and then measuring the temperatufe change in the pulmonary artery. Cardiac output is automatically computed from these measurements by small microprocessor devices. The validity of results depends on the precision with which the technique is performed. In our experience, essentially comparable measurements of cardiac output can be obtained with either 10 mL of room temperature injectate or 5 or 10 mL of cold injectate. The injection technique itself should be smooth and rapid (preferably less than 5 seconds) to avoid dispersion of the injectate. When thermodilution is correctly performed, the average variability of results is approximately 4%. Thus, an observed change of +lO% almost certainly indicates a true directional change, and allows us to assess, easily and rapidly, alterations in the patients health status and to monitor the impact of treatment.
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The presence of significant tricuspid regurgitation may introduce errors in the measurement of cardiac output by thermodilution. Similarly, in a patient with an intracardiac shunt, measurement of right ventricular cardiac output by thermodilution will not reflect the left ventricular forward cardiac output. Thermodilution is not contraindicated in patients with either tricuspid regurgitation or intracardiac shunt, but the limitations of the technique should always be kept in mind.
SYSTEMIC ARTERlAL BLOOD PRESSURE

Measurement of systemic arterial blood pressure is a crucial element in the clinical and hemodynamic assessment of severely ill patients. In most patients, this important variable can be adequately monitored by a variety of indirect techniques, including auscultatory or microphone sphygmomanometry and Doppler measurements. Even semicontinuous monitoring can be obtained noninvasively with any of the 24hour ambulatory blood pressure recorders currently available. Despite these technologic advances, arterial pressure in the critically ill patient is still best evaluated by direct arterial cannulation. This technique allows more precise and continuous monitoring, and enables us to obtain repeated blood samples without causing additional discomfort to the patient or trauma to the vessel. Direct Versus Indirect Measurements A detailed comparison of direct and indirect arterial pressure monitoring is given in Table 3. Although the results of these two methods generally correlate well, indirect measurements are often quite inaccurate in patients with severe vasoconstriction. Noninvasive auscultatory methods depend on detection of Korotkoff sounds; in all probability, these sounds result from a combination of turbulent intermittent flow through the compressed vessel and vibrations of the arterial wall. In a patient with increased vascular resistance, both factors are attenuated. Distal flow is decreased as the pressure gradient across the compressed segment at the onset of flow (when cuff pressure is released) is reduced. Also, a stiffer vessel wall is less likely to vibrate. Thus, erroneously low pressure measurements may be obtained. It should also be remembered that blood pressure is a dynamic variable, deterined at any moment by the prevailing conditions in the arterial tree. Furthermore, peripherally measured blood pressure may differ significantly from that obtained in the ascending aorta. The pulse contour changes as it travels peripherally; the pulse wave is steeper and systolic pressure is higher because of arterial amplifiCM, August1991 625

TABLE
Method Noninvasive

3.
Between Noninvasive Advantages Atraumatic Easily learned and applied with minimal training and experience No side effects or complications and Invasive Methods of Blood Pressum Measurement Disadvantages At present, does not allow pressure waveform display Allows only semicontinuous measurement Does not allow blood sampling for arterial gas analysis or other tests Less accurate and often very difficult to obtain in critically Ill patients who are in shock or have hypotension or vasoconstrlction Accuracy of blood pressure measurements is affected by various mechanical factors, including cuff size, muscle contractions, and hearing acuity Requires skilled nursing assistance and intensive care facilities Requires more operator skill and learning Definitely higher risk of complications, including thrombosis, embolism, ischemia, and necrosis

A Comparison

Invasive

Allows continuous pressure waveform display and immediate recognition of changes in blood pressure Allows repeated blood sampling without added discomfort or trauma Gives reliable and accurate pressure measurement, even in critically ill patients who are in shock, have hypotension or vasoconstriction, or are receiving vasodllator therapy

cation from reflected waves and changes in the elastic nature and caliber of the arteries. However, peripheral diastolic pressure is lower and mean arterial pressure is essentially unchanged from that measured centrally. These differences may be substantially amplified with alterations
626 DM, August
1991

in arterial vasomotion (for example, severe vasoconstriction or vasodilation). Normally, systolic pressures measured in pedal or radial arteries tend to be 10% to 20% higher than simultaneously measured central systolic pressures. This difference is enhanced (20% to 30%) in patients with vasodilation and is seriously damped (0% to 5%) in patients with vasoconstriction. Thus, it is not uncommon for a peripherally hypotensive patient with high systemic vascular resistance to have a higher central blood pressure. This finding has obvious therapeutic implications.

The Technique

of Arterial

Cannulation

A number of different sites may be used for arterial cannulation; their respective merits and demerits are detailed in Table 4. As a general rule, the site should be easily accessible and have adequate collateral circulation. The vessel should be large enough to allow accurate pressure measurements. For most critically ill patients, the radial artery is preferred for cannulation because it is superficial, easy to cannulate, and easily compressible. In addition, its territory (the hand) receives a generous collateral flow through the ulnar artery and palmar arches. A modified Allens test, with or without Doppler plethysmography, may be performed to check the adequacy of the collateral circulation before radial artery cannulation is undertaken. The arterial site is cleansed with antiseptic solution and isolated with sterile covers. The patients hand is supported by a short arm board and the wrist is kept dorsiflexed with a roll of gauze tucked behind it. The operator should scrub and wear sterile gloves. After local skin infiltration with 1% lidocaine (without epinephrinel, the radial artery is percutaneously cannulated with a 20-gauge, &in. catheter-needle assembly. The needle is inserted at a 30- to 40-degree angle to the skin surface. When performing arterial cannulation, keep in mind that the needle bevel extends beyond the end of the plastic sheath; thus, blood will appear in the needle hub before the plastic sheath is actually in the artery. If the needle is removed before the plastic sheath is advanced into the artery, neither blood return nor pressure waveforms will be obtainable. When this occurs, the sheath should be withdrawn entirely before recannulation is attempted. The needle should never be reinserted blindly through the sheath, because this increases the risk of the plastic sheath tip being cut off. We find it practical to advance the catheter-needle assembly far enough to puncture the far side of the artery. We then remove the needle and gently withdraw the plastic sheath until a pulsatile backflow of blood is seen. We have not noted an increased incidence of hematoma with this approach. However, such a through-andDM, August 1991 527

TABLE 4.
Pressure Disadvantages Comparatively small DifIicult to cannulate and vasoconstrlcted Necrosis of overlying vessel in hypotensive patients skin may occur Comment Monitoring

A Comparison

Among

Arterial

Sites for Blood

Site

Advantages

Radial

artery

Superficial, easily accessible Good collateral flow Easy to keep sterile

Axillar-y

artery

Large vessel, accessible even in patients in shock or with vasoconstricted states Good collateral flow Low risk of thrombosis

Most common site for intra-arterial monitoring Use Allens test for adequacy of the collateral circulation Insert cannula as distally as possible Avoid using in patients receiving anticoagulants or with bleeding disorders

Femoral

artery

Large vessel, accessible even in patients in shock or with vasoconstricted states

Avoid puncturing the artery inguinal ligament

above

the

Brachial

artery

Easily

palpable

Injury to brachial plexus nerve bundles, axillary sheath hematoma, and secondary compression syndromes may occur Potential for central nervous system embollzation from proximity to central and carotid circulations Difficult to keep sterile and to compress Higher incidence of hematoma and retroperitoneal hemorrhage Less good collateral flow May lead to ischemic loss of hand and forearm Subfascial hematoma may lead to compression syndromes, including median nerve neuropathy and Volkmanns ischemic contractme

Avoid routine use Avoid using in patients receiving anticoagulants or with bleeding disorders

through insertion technique should obviously be avoided in anticoagulated patients or those being treated with thrombolytic drugs. After the intra-arterial location of the sheath has been confirmed, the cannula should be connected to a properly calibrated and zeroreferenced pressure transducer. The patency of the catheter can then be maintained by either intermittent or continuous flush devices, using heparinized saline. AVOIDING COMPLICATIONS

In general, the incidence of complications from Swan-Ganz catheterization is low. However, among those that have been reported are arrhythmias, thrombosis, infection, pulmonary artery rupture, and pulmonary infarction. Table 5 lists the more frequently encountered complications of Swan-Ganz catheterization, the causative factors that have been associated with those complications, and strategies you can use to prevent or manage those complications. Unfortunately, the inherent simplicity of Swan-Ganz catheterization and its widespread applicability in critically ill patients invites abuse of the technique. As a result, the past decade has seen a defiTABLE 5.
Complications Complication More common Arrhythmia Associated With Hemodynamic or Causative Monitoring Factors Preventioflreatment Associated

Endocardial catheter Prolonged Underlying

irritation from tip catheterization cardiac disease

Fully

inflate

balloon

Thrombosis

Infection

Inadequate Frequent Prolonged

aseptic technique catheter manipulation catheterization

Pulmonary infarction

Distal migration with persistent wedging Prolonged wedge time Thrombosis Forced flushing

Continuous flushing with heparinized solution Heparin bonding of catheter shaft Strict sterile technique should be used for insertion ?Plastic sleeve Remove catheter at first sign of infection; replace with a new catheter inserted at a new site if continued hemodynamic monitoring is indicated Vigilant monitoring for persistent wedging Withdraw catheter and reposition Obtain x-ray films daily to check catheter position iConrinued.1 529

DA4, August

1991

TABLE 5 (cont.).
Complication Balloon rupture Associated Repeated Excessive Prolonged Prolonged absorption resulting structural balloon or Causative Factors PreventionTreatment Do not inflate the balloon if a rupture is suspected Use pulmonary artery diastolic pressure whenever possible, because diastolic pressure measurements do not require balloon inflation inflations inflation volumes catheterization shelf life or of lipoproteins in weakened integrity of the

Less common Pulmonary artery rupture

Distensive occlusion of the pulmonary artery Balloon inflation with fluid Excess catheter looping Pulmonary hypertension

Complete block

heart

Cardiac injury Catheter knotting

tissue

Preexisting left bundle-branch block Loop tightening (exerts direct pressure on the conduction system) Forcible catheter withdrawal without deflated balloon Inadequate balloon inflation Repeated catheter manipulation Catheter insertion with deflated balloon Large, dilated fight ventricle

Inflate the balloon slowly under continuous pulmonaty arterial monitoring Discontinue inflation once pulmonary capillary wedge pressure is obtained Keep wedge time to a minimum (< 8 to 15 s) ? Prophylactic pacemaker

Always deflate withdrawing

the balloon the catheter

when

Avoid catheter redundancy Use estimates of average insertion lengths when catheterizing a patient fluomscopic guidance

without

nite, albeit small, rise in the incidence of complications associated with bedside hemodynamic monitoring. Most of these complications can be attributed to operator error or poor follow-up care. To minimize the rate of complications, physicians who are going to perform Swan-Ganz catheterization should be rigorously trained in this technique. In addition, the house staif and nursing personnel who care for catheterized patients should receive thorough in-service courses on a frequent basis. As we have stated before, close and meticulous attention to detail is essential to prevent complications and to achieve best results (Table 6). Arterial cannulation has been associated with such complications as thrombosis and embolism leading to ischemia and necrosis, hematoma and aneurysm formation, infection, hemorrhage, arteriovenous fistulas, and vasospasm. Some of these complications have been linked to specific sites of cannulation (Table 4). 530
DM,

August

1991

TABLE 6.
Guidelines for Best Results in Hemodynamic Monitoring Acquisition of Fressure Data Completely eliminate any air or blood clots from the system. Discard catheters or tubes with kinks or bends, Do not depend on internal calibration alone; use a mercury manometer for external calibration. Check calibration routinely (three or four times a day) or any time that unexpected pressures are recorded. Always recheck the zem reference and calibration before measuring pressures. Measure pressures at end-expiration, regardless of whether the patient is breathing spontaneously or is on mechanical ventilation. Derive pressures manually off hard copy when tracing artifact is present. Cardiac Output Measurements Ensure proper positioning of distal thermistor and right atrial lumen. Use 5 or 10 mL of cold injectate or 10 mL of mom temperature injectate. Injection should be rapid and smooth, with minimal time wasted between picking up the injectate syringe, turning on the computer switch, and actually injecting the fluid. Adjust the computer constant according to the type, volume, and temperature of the injectate and the type of catheter used (predetermined constants are available).

A variety of factors, not the least of which is the disorder for which direct arterial pressure monitoring was instituted, markedly influence the incidence of complications. Arterial puncture may be particularly difficult in patients with tortuous rigid arteries or in those with hypotension and associated vasoconstriction; cannulation may require multiple attempts, resulting in trauma to the vessel and an increased incidence of thrombosis. Thrombosis is also likely to develop in patients with severe peripheral vascular disease, diabetes mellitus, or Raynauds phenomenon. The incidence of thrombosis can also be increased by such mechanical factors as prolonged monitoring, intermittent (rather than continuous) flushing, and the use of non-Teflon catheters of a large caliber relative to the arterial lumen. In our opinion, direct arterial pressure monitoring should be used when indicated without undue reservation. However, because of the potentially serious complications associated with it, we recommend monitoring for the shortest duration possible. The risk of complications can further be reduced by using only a&gauge, nontapered, Teflon catheters for cannulation.3

INDICATIONS

FOR INSERTION bedside hemodynamic monitoring provides can or exclude clinically suspected cardiopulmonary
531

The information be used to confirm

DM,

August

1991

TABLE
When

7.
Hemodynamic Monitoring Should Be Used

1. In patients with acute myocardial infarction complicated by: Severe heart failure, low-output syndrome, or shock Mechanical lesions (for example, mitral regurgitation, ventricular septal rupture, or subacute cardiac rupture with tamponade) Recurrent severe, postinfarction ischemia 2. In critically ill patients with multiorgan or major organ dysfunction (for example, severe respiratory or renal failure, extensive trauma, extensive burns, severe sepsis, massive pulmonary embolism, suspected cardiac tamponade, persistent low-output syndrome, or shock) 3. Before, during, and after cardiac or noncardiac surgery in high-risk patients 4. In patients with chronic heart failure to: Assess ventricular function at rest, during exercise, and in response to therapeutic interventions Distinguish specific causes of the congestive heart failure (for example, constrictive pericarditis, restrictive cardiomyopathy, or precapillary pulmonary hypertension) 5. As a research tool for clinical investigation

disorders, help select appropriate therapeutic interventions, and follow a patients response to treatment in a precise and quantitative fashion. In at least some patient groups, hemodynamic monitoring can help establish a diagnosis. In the final excerpt from the series, Drs. Amin, Shah, and Swan discuss the clinical applications for hemodynamic monitoring (Table 7). Because this procedure should never be performed without a careful assessment of its risks, as well as its benefits, the authors also review the contraindications to this procedure. DIAGNOSTIC APPLICATIONS

The measurements provided by hemodynamic monitoring can be used to differentiate among a variety of cardiopulmonary disorders and thereby establish a diagnosis (Table 81. The disorders for which hemodynamic profiles have been established include the following: Acute Zschemic Right Ventricular Dysfunction.-Although this syndrome occurs in as many as 40% of patients with inferior infarctions, clinical recognition of acute ischemic right ventricular dysfunction is often inadequate. Ischemic right ventricular dysfunction may produce a state of low output and shock, the prognosis and treatment of which are different from that for shock due to severe left ventricular dysfunction. The characteristic hemodynamic profile of acute right ventricular dysfunction includes elevated right atrial pressure that equals or exceeds PCWP, a steep y descent, and a right ventricular pressure trac532 DA4 August

1991

ing that may show a diastolic dip and plateau (square root sign). These findings, however, can be detected in only about 50% of patients with acute ischemic right ventricular dysfunction (Figure 3); in other patients with this disorder, volume loading may be necessary to unmask these hemodynamic abnormalities.

Acute Mitral Regurgitation.-When severe, this syndrome often leads to profound hemodynamic alterations and shock. Findings in patients with acute mitral regurgitation include elevated left atrial pressure (LAP) and PCWP, large v waves in PCWP tracings and, at times, inflated v waves in pulmonary arterial pressure tracings (Figure 4).

Acute Ventricular Septal Rupture.Clinical differentiation of acute ventricular septal rupture from acute mitral regurgitation is sometimes difficult; even prominent v waves in PCWP tracings do not preclude ventricular septal rupture. However, the diagnosis of ventricular septal rupture can be confirmed by detection of an oxygen step-up in the right ventricular outflow tract and pulmonary artery. (Figure 5).

PCWP

FIG 3.
Equalization of right atrial (RA) and pulmonary arterial (PA) diastolic pressures, and pulmonary capillary wedge pressure (PCWP) suggests that the patient suffered an acute right ventricular infarction (A). Note the elevated right atrial pressure. Also characteristic of this disorder is a right atrial pressure tracing showing a steep y descent, followed by a diastolic plateau (B). (ECG = electrocardiogram.) DM,Au@x+tl991 533

TABLE 8.
Cardiopulmonary Profile Comments Disorders

How

Hemodynamic

Profiles

Differentiate

Disorder

Hemodvnamic

Ischemic

RV dysfunction

Increased RA, decreased SV, decreased CO, decreased AP, RA greater than or equal to PCWP

Acute

mitral

regurgitation

Acute

ventricular

septal

rupture

Increased PCWP, prominent v waves, sometimes reflecting onto the PA tracing as well Oxygen step-up from RA to RV and PA

Steep y descent RV diastolic dip and plateau (square mot sign) Volume loading may unmask hemodynamic changes v waves may not always differentiate mitral regurgitation from ventricular septal rupture RV forward output exceeds LV forward output Early recirculation on the thermodilution curve

Shock Ventriculopenic

Orthostatic tachycardia

Hypovolemic

Early

septic

2 2 3

Noncardiac pulmonary edema Massive pulmonary embolism

Increased PCWP, decreased SV, decreased CO, decreased AP, increased SVR Decreased or low-normal PCWP, decreased SV, decreased CO, decreased AP, increased SVR Increased PA, increased PVR, increased CO, decreased AP, decreased SVR Normal PCWP Decreased SV, decreased CO, decreased AP, increased PA, increased PVR, normal PCWP

SVR is elevated in and cardiac output is lowered in later stages Normal heart size PCWP is normal despite elevated pulmonary artery systolic and diastolic pressures

Increased RA, increased increased PA, increased to PCWP AP in

RV systolic pressure, PVR, normal PCWP

Increased RA, increased PCWP, RA equal decreased SV, decreased CO, decreased

Constrictive

pericarditis

Increased RA, increased PCWP, dip and plateau RV pressure, M- or W-shaped jugular venous pressure with preserved ,x and steep y descent

Restrictive

cardiomyopathy

Findings are similar to those described for constrictive pericarditis, but PCWP may be higher than RA; difference between PCWP and RA may be exaggerated by exercise

Tricuspid

regurgitation

Increased

RA, increased

RV end-diastolic

pressme

Left-sided pressures are often normal Pulmonary arterial and RV systolic pressures may reach systemic levels Paradoxical pulse Blunted y descent Prominent ,x descent on RA tracing Paradoxical pulse is rare Positive Kussmauls sign is common May simulate ischemic RV dysfunction or restrictive cardiomyopathy Simulates constrictive pericarditis; however, PA systolic pressure is usually greater than 50 mm Hg and diastolic plateau is less than one third peak RV systolic pressure. Thus, other tests are often needed for differentiation from constrictive pericarditis Blunted ,x descent, prominent v wave, steep y descent Ventrlcularization of RA pressure
vascular resistance; PA = mean

PCWP = pulmonary capillary wedge piass~re; SV = stroke volume; CO = cardiac output; AP = mean arterial pressure; SVR = systemic pulmonary artery pressure; PVR = pulmonary vascular resistance; RA = mean right atrial pressure; RV = right ventricular pressure.

60 I 40

E 20 0 PA PCWP

FIG 4.
Tall v waves in a pulmonary capillary regurgitation. (ECG = electrocardiogram; monary capillary wedge pressure.) wedge tracing indicate the presence PA = pulmonary artery pressure; of acute mitral PCWP = pul-

11!11111111111!111111111111111111111111 1!!!!!!!!!!!!!!!!!!!!!!1!!!1!!!!!!!!!!!

FIG 5.
Right atrial to pulmonary ventricular septal rupture tion of acute ventricular PA = pulmonary arterial;
536

arterial step-up in oxygen saturation is characteristic of acute following myocardial infarction. This finding permits differentiaseptal rupture from acute mitral regurgitation. (RA = right atrial; ART = radial artery pressure.)
D&4, August 1991

Septic S/m&.-The early (or warm) phase is generally characterized by elevated cardiac output and low systemic vascular resistance. In the later stages of septic shock, however, systemic vascular resistance usually increases and cardiac output generally decreases. Noncardiac Pulmonary Edema.-A variety of noncardiac clinical syndromes may be accompanied by increased pulmonary capillary permeability and pulmonary edema. Clinical differentiation of noncardiac pulmonary edema from edema secondary to cardiac disorders is difficult, because in both instances, patients are critically ill, have severe arterial blood gas abnormalities, and have roentgenographic evidence of generalized interstitial and alveolar infiltrates. However, distinguishing between the two types of edema is crucial, because therapeutic strategies and overall prognosis diifer markedly. Patients with noncardiac pulmonary edema have normal or near-normal PCWPs. In contrast, patients with heartfailure typically have elevated PCWPs and require diuretic therapy. Acute Massive Pulmonary Embolism.Massive pulmonary embolism can produce a clinical picture simulating that of cardiogenic shock. However, whereas ventriculopenic shock is associated with elevated PCWP, the patient with a massive pulmonary embolism will have elevated systolic and diastolic pulmonary artery pressures but no elevation in PCWP (Figure 6). Chronic Precapillary Pulmonary Hypertension.-Patients with this disorder often present with exertional dyspnea, chest pain, and symptoms of reduced cardiac output. Right heart catheterization in these patients usually reveals elevated right-sided pressures, with pulmonary arterial and right ventricular systolic pressures often reaching systemic arterial levels. In addition, pulmonary vascular resistance is markedly increased; however, left ventricular end-diastolic pressure, LAP, and PCWP are usually low or normal in these patients. Chronic precapillary pulmonary hypertension may result from obstructive airway disease, interstitial or parenchymal lung disease, recurrent pulmonary embolism, vasculitis, schistosomiasis, or idiopathic pulmonary vascular obliterative disease. Acute Cardiac Tamponade.-This disorder produces diastolic compression which, in turn, impairs ventricular filling. The result is low stroke volume and a fall in cardiac output, despite normal systolic function. Acute cardiac tamponade has a characteristic hemodynamic profile: equalization of right- and left-sided filling pressures, and a prominent systolic x descent and blunted y descent on right atrial pressure tracing. (Occasionally, the y descent is absent or even reversed.)
DM, August 1991 537

100 I E 0

60

FIG 6.
When shock developed following a massive ing revealed an acutely elevated pulmonary nary capillary wedge pressure (PCWP). chronic precapillary pulmonary hypertension. tery pressure.) pulmonary embolism, hemodynamic monitorarterial pressure (PA) with a normal pulmoSimilar findings often occur in patients with (ECG = electrocardiogram; ART = radial ar-

Unlike constrictive pericarditis, acute cardiac tamponade is usually associated with a prominent paradoxical pulse (Figure 7). However, patients with acute cardiac tamponade generally do not have Kussmauls sign or a dip and plateau in the right ventricular pressure tracing. Constrictive PericarditkLike cardiac tamponade, constrictive pericarditis produces diastolic equalization and elevation of rightand left-sided filling pressures (Figure 8A). Unlike cardiac tamponade, however, constrictive pericarditis is usually accompanied by a positive Kussmauls sign and an early diastolic dip followed by a pressure plateau in both right and left ventricular pressures. In patients with constrictive pericarditis, a characteristic M- or W-shaped jugular venous pressure tracing can be detected, with a preserved systolic )( descent and a prominent early diastolic y descent that coincides with the pericardial knock (Figure 8B).
53.9

DM,

August

1991

ECG

200 160 120 80 40 Before pericardiocentesis FIG 7.

A prominent arterial paradoxical pulse is a hallmark of cardiac tamponade; however, it generally disappears following pericardiocentesis. Note the sharp decrease in systolic and pulse pressures during respiration before pericardiocentesis. (ECG = electrocardiogram; INSP = normal inspiration.)

mm Hg

After pericardiocentesis

Restrictive Cardiomyopathy.-The hemodynamic profile of restrictive cardiomyopathy simulates that of constrictive pericarditisan M- or W-shaped jugular venous pressure tracing and a diastolic dip and plateau in right ventricular pressure tracing (Figure 8). Standard hemodynamic measurements may sometimes permit differentiation of restrictive cardiomyopathy from constrictive pericarditis. Left-sided filling pressures tend to be higher than rightsided filling pressures in patients with restrictive cardiomyopathy; this difference can be exaggerated with exercise. In addition, in patients with restrictive cardiomyopathy, the diastolic pressure plateau is usually less than one third the right ventricular systolic pressure and the right ventricular systolic pressure tends to exceed 50 mm Hg. However, considerable overlap in the hemodynamic findings of these two disorders frequently necessitates additional investigation. Tricuspid Regurgitation.-This disorder is associated with elevated right atrial and right ventricular end-diastolic pressures. Characteristically, the mean right atrial pressure demonstrates a rise or no fall with inspiration, an absent or diminished x descent, and a prominent early v wave (Figure 9). As the tricuspid regurgitation becomes more severe, however, the right atrial pressure tracing will increasingly resemble the right ventricular pressure tracing (ventricularization).
DM,Au@1st1991 539

0
RA

Inspiration

FIG 8.
Simultaneous right ventricular (RV) and left ventricular end-diastolic pressures, an early diastolic dip, and a sign) in patients with constrictive pericarditis (A). The reveals steep x and y descents (M or W pattern) and (positive Kussmauls sign) (B). A similar pattern may cardiomyopathy. (ECG = electrocardiogram) (LV) tracings show equalization of late diastolic plateau (square root right atrial (RA) pressure waveform an inspiratory increase in pressure be seen in patients with restrictive

540

DM, August

1991

60. 040 I E E 20

FIG 9.
A blunted x descent, prominent sures can be seen in this right tation. (ECG = electrocardiogram.) cv waves, and steep y descent, as well as elevated presatrial (RA) tracing, taken in a patient with tricuspid regurgi-

THERAPEUTIC

APPLICATIONS

The information provided by hemodynamic monitoring is quite precise and, thus, can help one to select the best treatment and to monitor closely the patients response to therapy in the critical care setting (Table 9). For example, rapidly acting, potent, intravenous drugs with short half-lives, which are the preferred therapeutic agents for many critically ill patients, require very careful titration; repeated assessment of hemodynamic variables makes such titration possible. Thus, vasodilators and inotropic agents can now be safely used in unstable patients. PROGNOSTIC APPLICATIONS

The concept that acute myocardial infarctions could be classified prognostically was introduced by Killip and Kimball; their classification system was based on clinical manifestations of different degrees of left ventricular dysfunction. Unfortunately, clinical assessment of left ventricular failure is not always accurate or precise; furthermore, as has been amply demonstrated, changes in clinical findings tend to lag significantly behind hemodynamic changes. Forrester, Chatterjee, and colleagues from our institution have used hemodynamic measurements to group patients with acute myocardial infarction into different subsets. The results of their investiDM, August1991
541

TABLE 9.
How Clinical Acute to Use Hemodynamic Diagnosis pulmonary edema Data to Choose Hemodynamic Increased PCWP, decreased CO Therapy Data Suggested Therapy

Diuretics, vasodilators Hemofiltrationdialysis if edema is associated with oliguria or anuria: Intra-aortic balloon counterpulsation support in special circumstances

Low output or shock syndromes Absolute or relative hypovolemia lschemic right ventricular dysfunction Early sepsis

Decreased Increased PCWP,

PCWP RA, normal normal PA

Volume

expansion

Incmased CO, decreased SVR, decreased AP

Ventriculopenic

Increased PCWP, increased PA, decreased CO, decreased AP

Pulmonary

embolism

Increased RA, decreased CO, decreased AP, increased PA, normal PCWP Increased PCWP, pulse RA, RA equals paradoxical

Cardiac

tamponade

Volume expansion with or without inotropic agents Volume loading VasopressorsAnotmpic drugs Specific treatment for causative organism Reduce preload with diuretics and/or vasodllatom Inotmpic agents and intra-aortic balloon counterpulsation in special circumstances Thmmbolytic or anticoagulant therapy after scintlgraphic or anglographic confirmation Echocardiographic confirmation, if time permits Pericardiocentesis
RA = mean right atrial pressure; resistance; AP = mean arterial

PCWP = pulmonary capillary wedge pressure; CO = cardiac output; PA = mean pulmonary artery pressure; SVR = systemic vascular pressure.

542

DM,

August

1991

TABLE
Predicting MvocardiaI

10.
Short-Term Infarctions Mortality by the Hemodynamic Profile in Patients With Acute

Pulmonary Capillary Wedge Pressure, mm 518 >18 518 >18

Hg

Cardiac

Index, >2.2 >2.2 52.2 52.2

L/min/m

Mortality, 3 9 23 51

gations have clearly demonstrated that these subsets have strong, short-term prognostic value (Table 10).
CONTRAINDICATIONS

Although there are no absolute contraindications to hemodynamic monitoring, this technique should never be performed in the absence of a proper indication or potential benefit to the patient. The newer heparin-bonded catheters may be contraindicated in patients with known heparin sensitivity. Furthermore, the indications for hemodynamic monitoring should be carefully reviewed in patients who are septic, have hypercoagulable conditions, or have received anticoagulants or recent thrombolytic therapy, because complications are more likely to develop in these patients.4
REFERENCES
1. Amin DK, Shah PK, Swan HJC: The Swan-Ganz the equipment. J Crit Ill 1986; 1:34-37. 2. Amin DK, Shah PK, Swan HJC: The Swan-Ganz
J Grit 3. Amin 4. 111 1986; 1~38-45. DK, Shah PK, Swan HJC: results. J Crit Ill 1986; 1:40-48.

catheter: catheter:
catheter:

Choosing Insertion
Tips

and using technique.

The Swan-Ganz

on interpreting

Amin DK, Shah PK, Swan HJC: The Swan-Ganz tion. J Grit ill 1986; 1:54-61.

catheter:

Indications

for inser-

DM, August

1991