R
ecent research shows that a significant portion of doctors and nurses who work with pulmonary artery catheters have a knowledge deficit about them. Nurses are the first line users of pulmonary artery catheters. In intensive care units all over the world, nurses titrate vasoactive drips, give or hold medications, and use in other ways, the information gleaned from the pulmonary artery catheter every day. A knowledge deficit, even a modest one, can have significant consequences to many patients.
In addition, though PACs were very popular throughout the 1980s, their use has waned in recent years for a variety of reasons that will be discussed in the text. This makes the PAC, a high risk, low use device. As with all such technology, frequency of use plays a major role in proper use. A frequently used device, such as an arterial line, is associated with a lower risk of negative events, then an infrequently used device such as a PAC. Frequent refresher classes serve to improve familiarity with the device, but should not substitute for hands on practice.
Hands on practice should be facilitated every time a patient with a PAC is on the unit. Nurses with significant PAC experience, should be on hand, and as many nurses on the unit as possible, should be given the opportunity to be observed performing typical PAC interventions. These would include: leveling, zeroing and calibrating the transducer, troubleshooting the waveform, and obtaining various readings from the catheter. The readings are perhaps the most difficult as familiarity to various waveforms and the influence of respirations on them, both spontaneous and mechanical, can be confusing. Measuring pulmonary artery occlusive pressure (PAOP) can be fraught with danger for those unfamiliar with the technique, and as such, the ability to perform this task should be routinely assessed. Cardiac output measurements and SvO2 measurements can be dangerous too if done incorrectly, however the major issue with both of these is the introduction of user error, skewing the results and dictating improper treatment of the patient.
1) Discuss the history of the Swan-Ganz pulmonary artery catheter
2) List three potential complications of Swan-Ganz catheter insertion
3) Explain the steps necessary to confirm the accuracy of the Swan-Ganz readings
4) List three waveform problems and at least one method to correct the problem
5) List the characteristics of the RAP, RVP, PAOP, and PAOP waveforms
6) Discuss the expected changes in Swan-Ganz readings associated with various
conditions.
7) List at least one intervention for various abnormal Swan-Ganz readings.
8) List at least three interventions for proper Swan-Ganz catheter maintenance.
This course has been approved for two contact hours by the Florida Board of Nursing provider number NCE3510.
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lthough it was first demonstrated that a catheter could be passed into the heart, without dire consequences, in 1929, it was not until the 1970's that development of the pulmonary artery catheter took hold. There were two major developments that made the pulmonary artery catheter the tool it is today.
The first development was due to a simple, non-medical observation - that sailboats follow the wind direction. One problem associated with pulmonary artery catheters was; how can the catheter get one into the pulmonary artery? Getting into the right atrium, and even the right ventricle, is relatively easy. Many methods were proposed, but none were developed. Then, more than a decade after the concept was first proposed, Dr. Swan was on a family outing and noticed how briskly sail boats moved, even in very light breezes. Developmentally, it was easier to create a balloon tipped catheter, rather than a sail based design, so to expedite research, the balloon tip was tried first, to test the theory. The balloon tip was so successful that all attempts at creating a sail based design were abandoned.
Around the same time, Dr. William Ganz was working on apparatus for determining cardiac output using the thermodilution method. This research was incorporated into the pulmonary catheter developed by Dr. Swan, and the Swan-Ganz, pulmonary artery catheter, was born.
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he pulmonary artery catheter is not complicated to insert. It is a well orchestrated dance between the patient's heart and the catheter. The nurse assembles the instruments and the physician plays them. Since you may not assist with a PAC insertion very often, it is important to know what you need and what to expect. We will cover what position the patient should be in, what equipment we need to have ready, and what we need to watch out for on the monitor to assist the physician as his or her concentration will be focused on maintaining sterility and manipulating the catheter.
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ost nurses believe that the reason for the head down position is to engorge the blood vessels that the doctor is attempting to access. While this is indeed one of the reasons, it is not the primary reason. Vein engorgement increases the size and pressure in the blood vessel, and makes it less compressible. That means that the blood vessel is less likely to collapse when pushed on with the needle. The other reason we use the head down position, is because when the patient is flat (or in the head up position) there may be times during the respiratory cycle when the pressure in the central venous system is actually slightly below atmospheric pressure. This normally does not pose a problem, but when a central vein is punctured, as it is when inserting a PAC, this can be dangerous.
If the pressure in the vein is lower than atmospheric pressure then, when the vessel is punctured, there is a small risk that air may be "sucked" into the blood vessel causing an air embolism in the pulmonary vasculature. If we put the head lower than the heart, then the pressure in the upper central veins such as the internal jugular and the subclavian, is markedly increased, causing the engorgement. This increase in pressure, all but assures that the pressure in these large veins will be greater than atmospheric pressure. This is the main reason for placing the patient in Trendelenburg position; vein engorgement is a secondary benefit!
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t is difficult enough assisting with a PAC insertion without having to run all over the place getting supplies. Therefore, we will briefly discuss the various pieces of equipment you will need to insert a pulmonary artery catheter.
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irst, you need a way to get the PAC into the patient. This is usually accomplished using an introducer sheath. This is just a larger than normal diameter central line. It is also much shorter and stiffer. It does not need to go into the patient very far, just into the entry vessel (subclavian, internal jugular or femoral vein). Once there, it allows us access to the central venous system. If a patient already has a central line, the physician may opt to use that to expedite accessing the central venous system, and then remove that catheter and replace it with the introducer sheath apparatus.
Figure 1 - The introducer sheath has an infusion to act like a central line, and a self-sealing membrane to allow passage of the PAC.
Outside the patient, the introducer sheath has two parts. One is referred to as a side port, or infusion port. It connects to the stiff introducer sheath by familiar, flexible IV tubing. It allows us to use the introducer sheath as a central venous line in the absence of a PAC. You should also have a resealable cap to place on this end after it is inserted. The other is the end of the stiff portion of the sheath. It has a self-sealing rubberized membrane. It allows passage of the PAC, or traditional central venous catheter, or simply a transvenous pacing wire. When the PAC is inserted it passes through this membrane and it hugs it just like a diver's wet suit. When the PAC is pulled out, the membrane seals shut, but can be used again for a new catheter insertion. This membrane area can not be used to infuse IV fluids as there is no connection device present.
O
f course, you need a pulmonary artery catheter kit. There are several types, usually one type is used almost exclusively in a particular unit. If there are more than one type of kit available, be sure to find out the physicians preference. The most common types are the normal four port catheter (Thermistor, balloon, proximal injectate port and PA distal port), pacing catheter (same as four port with additional port for pacing wire usually labeled RV port, or pacing port; Figure 1), and the continuous cardiac output catheter (additional connector for heating element).
For each infusion port you will need to have a end cap if you use a needleless system; most kits only come with caps that need a needle. You will also need syringes and some flush. The flush can be saline, or heparinized saline, typically 100 units per ml. Follow your institutional policies regarding which to use. If the patient has a heparin allergy or a history of heparin induced thrombocytopenia, then saline will have to do.
Extra sterile gauze pads and a bottle of betadine wash are good to have in case the physician needs to clean a larger area or switch locations. A central line dressing, preferably transparent, as well as any biostatic materials are also not in the packages and should be available as institutional policy dictates.
A hand towel should be available to serve as a positioning device. Frequently, physicians will place a rolled towel behind the shoulder blades to accentuate the patient's anatomy, permitting easier access. Also, a pad should be placed under the area where insertion is attempted. If not, be prepared to change the patient s linens as occasionally blood will get on the bed. You can also wrap a towel around the patient's head to keep their hair clean. You may want to offer the physician, and all those close to the field a face mask with shield. This is just in case an artery, which runs right next to the vein, is hit. If this occurs, blood may squirt out with significant force.
You will also want a pressure tubing setup for each port you will be monitoring. This will include at least one pressure bag, one bag of flush fluid (0.9% saline with or without heparin), and the cables necessary to connect the transducers to your monitor. Additionally, you will need a set of cardiac output tubing with the injection syringe and a 250 ml bag of normal saline to draw up for the cardiac output measurements.
Since the pulmonary artery catheter is going into the blood stream and through the heart, sterility is vital. Therefore, sterile gloves should be used and a sterile gown should be worn. Sometimes the physician will put on a regular, impervious gown that is not sterile. This can be eliminated most times by having the appropriate gown ready and offering it. If they refuse, you should advise them that the gown they have chosen is not sterile - many cases of catheter site infection and endocarditis secondary to catheters can be traced back to poor sterile technique during insertion.
Although not necessary to be in the room, you should know where a second introducer kit and PAC kit is, just in case contamination occurs. Guidewires, which are easily dropped and/or contaminated, are another item you should have on your unit and have easy access to. Search these duplicate items out before the procedure. You may even show a couple of aides, or other nurses where these items are in case they are needed quickly.
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he nurse is, for the majority of the insertion procedure, a bystander. That is not to diminish the role they play. While the doctor is focused on the insertion site, the guide wire, the catheter itself and maintaining sterility, the nurse is an extra set of eyes.
The nurse should ensure that all the ports of the catheter are flushed with a pressure bag of saline (heparinized or not is based on physician preference and/or hospital policy). Accidental infusion of an air bubble could be problematic, even in the small amounts that are present in the PAC tubing.
After the ports are flushed, the nurse should ensure that the pressure tubing that will be connecting to the pulmonary artery port of the catheter is zeroed to atmospheric pressure (see zeroing the transducer). This ensures an accurate reading of pressures in the central venous system. Your next job is to connect the transducer tubing to the pulmonary artery port of the PAC. The physician will be wearing sterile gloves so care must be taken.
Figure 2 - A tracing of the CVP waveform.
After connecting the tubing to the connector, the nurse should monitor the connection location in reference to the sterile field. Also, now that the catheter is connected to the monitor, the central venous pressure can be monitored (see figure 2). This will help confirm that the catheter is indeed in the venous system. Once the waveform is confirmed, the PAC is advanced, slowly. During advancement the nurse has the primary duty of monitoring the patient s vital signs and rhythm. Of particular importance are the oxygen saturation, SpO2, and the heart rhythm.
As the catheter passes into the right atrium, there is little change in the waveform. However, there is a risk of triggering atrial fibrillation as the catheter tip, in the whirlwind of swirling blood flow, is flung against the atrial walls. This impact can cause ectopic foci to be stimulated and may induce PACs or other atrial dysrhythmias. If such rhythm changes occur, the nurse should inform the doctor. Many patients, in whom PAC insertion is deemed necessary, are particularly intolerant of atrial fibrillation. Pulling the catheter back a bit, and into the superior vena cava, is usually all that is needed to terminate the dysrhythmias.
Figure 3 - A tracing showing conversion of the CVP to the RVP waveform during PA cath insertion.
The next thing the monitoring nurse should observe is the PAC waveform should change as in figure 3. This new, taller waveform, represents the right ventricular waveform and occurs as the catheter tip travels through the tricuspid valve. It may come and go at first as the catheter tip passes by the influence of the tricuspid valve.
Although this change in waveform, from right atrial to right ventricular, is a good and expected occurrence, it is also a sign that the nurse should be extra vigilant. Now that the PAC tip has passed the tricuspid valve, the turbulent blood flow can cause the tip to impact the tissue of the right ventricle and potentially cause dysrhythmias including ventrcular fibrillation! It is not uncommon to see PVCs and even short, non-sustained runs of ventricular tachycardia. The nurse should advise the physician that the ectopy is occurring.
Once the PAC tip is in the right ventricle, the balloon is inflated. This is where Dr. Swan's visionary development comes into play. The balloon acts as a sail and, hopefully, follows the flow of blood from the right ventricle to the pulmonary artery taking the catheter tip with it.
The other benefit of the balloon inflation at this time is that it acts as a buffer between the small, hard PAC tip, and the right ventricular tissue. Instead of a few cells getting intermittently hit with a hard, small pointed object, now there are a much larger number of cells getting hit by a softer, larger surface area balloon. Imagine the difference being hit with a real baseball bat and a blow up toy baseball bat. This decreases the irritability of the right ventricle and reduces the potential for ventricular ectopy.
Figure 4 - A tracing showing the conversion from RVP to PAP waveform during PA cath insertion.
Now we are in the home stretch.
As the PAC passes through the pulmonic valve, the waveform changes again as shown in figure 4. The PAC is now in the pulmonary artery and we are getting a pulmonary artery pressure waveform. We could just simply deflate the balloon and secure the catheter, but in order to perform cardiac output readings, we need to be able to obtain the PAOP.
In order to do this we advance the PAC, with the balloon still inflated, until the pulmonary artery pressure waveform suddenly drops off. This indicates that the flow of blood from the right ventricle is no longer getting to the PAC tip - we have the PAOP waveform (Figure 5).
Figure 5 - A tracing showing the conversion from the PAP to PAOP waveform with ballon inflation during PA cath insertion.
The PAOP waveform appears similar to the CVP waveform shown earlier in figure 2 and it is easy to confuse the two. There are differences however. The PAOP pressures are normally higher than the CVP pressures. In addition, we can presume which waveform we are observing from where it the heart we are monitoring.
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ow that the catheter is in, the physician goes off to dictate the procedure note, but the nurse's job is just starting. There are a number of important things to do to assess the catheter, the waveform and the patient. Let's get to it.
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isplaying a waveform is not difficult, but it is not automatic. A chest X-ray should be ordered to confirm that the catheter is in the correct location. It is also very important to secure the PAC to prevent accidental removal. Note the markings on the catheter (see figure 6) and calculate the depth of insertion before securing the catheter. Thick black marks are 50 centimeters, and thin black marks are 10 centimeters. It is uncommon for the catheter to be inserted exact multiples of ten centimeters, so you may have to estimate the distance from the closest marks that are visible. Document this measurement in the chart; it is also helpful if you document the measurement on the dressing itself.
Figure 6 - A drawing of a Swan-Ganz catheter showing the various ports and measuring units.
Now you can dress the insertion site. Cleanse the blood from the site and allow to dry. Many facilities are using a disk under the dressing that inhibits bacterial growth. There are studies that suggest that this reduces infection rates, however the best way to do this is to use aseptic technique on insertion and with each dressing change. Clear dressings are preferred to allow observation of the site for signs of infection; drainage, edema and erythema.
Before securing the dressing it is recommended to put a tension reducing coil in the external tubing. Then, when the tubing gets tugged on the coiled tubing will unwrap before the catheter it pulled out. This extra safety measure has saved me more times than I can to admit. It is very easy to be so caught up in patient care such as turning an uncooperative patient, or sliding a backboard for chest compressions under a coding patient, that you put tension on the PAC.
Once the depth of insertion is noted, the dressing applied and the tubing secured, now you can order the chest X-ray. This may be considered an extra step to some people; after all there was a pulmonary artery waveform during insertion. But, the chest X-ray accomplishes two additional things. First, it documents where the PAC is, see figure 6, in case there is a question of migration or other complication later. Second, it allows assessment for complications of insertion such as pneumothorax, or punctured blood vessels in the thoracic cavity. The catheter should not be used, except in life-threatening emergency situations, until the chest X-ray is read and confirms placement as in figure 7. Even though there is a good blood return, there are rare complications that can still be present. The catheter could have punctured through the pulmonary artery. Therefore, any IV fluids that are infused, would be going into the space around the pulmonary artery and lung tissue. This could cause a pericardial effusion or worse yet pericardial tamponade.
Figure 7 - A chest X-ray showing proper placement of the Swan-Ganz PA catheter in the right pulmonary artery.
The catheter could also have punctured a hole through the right ventricle into the left ventricle. This would cause a ventricular shunt to occur allowing mixing of venous and arterial blood. The drop in arterial oxygen saturation may be blamed on the patient s serious condition. It also could have went through the tissue surrounding the tricuspid valve, or the catheter could have tied itself in a knot. Granted all these complications are very uncommon, but waiting for the chest X-ray could be a lifesaver.
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hether or not you realize it, you are constantly under pressure. No, I don t mean from your boss, spouse, family or traffic, but from the atmosphere. You do not realize it, because it is always there - ever since you were born. It exerts constant pressure on your entire body, inside and out. Your right atrium, and the PAC passing through it, both feel this pressure. So, even though your heart can function as well in Denver, Colorado as it does in Philadelphia, Pennsylvania, there is a measurable difference in atmospheric pressures between the two cities, and therefore the pressure exerted on the right atrium and PAC. Is there a way to account for heart function, despite the varying effects of atmospheric pressure? Of course!
We must make some accommodation, or the normal pressure values for a patient will need to be adjusted depending on the altitude of the patient. The way we do this is called leveling and zeroing.
Figure 8 - The proper location of the phlebostatic axis.
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e are trying to compare the pressures inside the heart-lung system. Therefore, we want to eliminate the atmospheric pressure at the level of the heart. To accomplish this, we level the transducer to the level of the right atrium. (This is not technically correct, but using this point is close enough and easier to locate than the actual point.)
When the patient is supine, the point of the junction of the vena cava and the right atrium, is at the point where the nipple line and the mid-axillary line meet (see figure 8). This point is called the phlebostatic ("phlebo" = blood, and "static" = still) axis. This is the point where the blood will have the lowest pressure. If we set this point's pressure to represent our "zero" level, then we are saying that this is the point where the blood has no pressure, and therefore is not moving or is stationary - thus the tongue twisting name.
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ou have already seen all the waveforms: CVP, right ventricular, pulmonary artery and PAOP. The good thing about these waveforms, is that you can monitor more than one at a time. It is most common to monitor CVP and PAP as these two are needed to calculate cardiac output. Now you should connect a pressurized IV fluid bag with a transducer system, to the proximal injectate port of the PAC. This is the port where you will monitor the CVP from. You will need to make sure there are no air bubbles in the line before connecting the tubing and then you should flush the line, level and zero the transducer the same way you did for the initial PA distal port. Once that is accomplished, you should adjust your monitor to allow simultaneous display of both of these waveforms.
Right ventricular pressure monitoring is not routinely performed, however, if you do need to monitor it, the setup is the same as for the PAP and the CVP, except you connect the pressure line to the infusion port (also referred to as the RV port or the pacer port).
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ow you have two waveforms on your monitor. If you zeroed the lines then they are giving you numbers: systolic, diastolic and mean pressures. If you have no numbers associated with the pressure waveforms, then you probably forgot to zero the transducers. Zeroing the transducers are necessary anytime the monitoring equipment loses contact with the transducer. This can occur with power failure or if the cable becomes disconnected from the monitor or the tubing end. The transducer should also be re-zeroed anytime the patient position changes significantly.
Research shows that accurate pressure readings may be obtained in patients in a variety of positions including: side-lying (up to 30 degrees to the left or right), as well as with the head elevated up to 30 degrees. Ideally, the measurements should be taken in a flat-lying, supine position at least initially. Then, when the patient is repositioned, new readings can immediately be compared to the readings before repositioning to assess for their accuracy.
When you have pressure waveforms, and the appropriate readings, you must ensure that these readings accurately reflect the pressures in the heart. There are a number of points to assessing pressure waveforms and most are easy to identify and fix.
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hen monitoring pressure waveforms, it is all dependent on what the transducer sees. After all, the transducer is the actual pressure sensing device in the system. When pressure hits the transducer s membrane, it causes the membrane to vibrate. This vibration is converted into electrical signals and sent to the monitoring equipment which converts it into the pressure readings we see on the monitor, If something interferes with the waveforms that reach the transducer, the result will be erroneous pressure waveforms and readings.
Any device, violin string, hollow pipe, human or dog eardrum, also have a natural frequency that they prefer to vibrate at. The violin string can reproduce certain frequencies, but if you try to make the string vibrate much faster than its natural range, you will be disappointed with the results. If you try to vibrate the human eardrum at high frequencies, such as 40 kilohertz, the person will not hear it as its natural frequency range from 20 hertz to 20 kilohertz, but a dog will hear it because they can hear frequencies over 50 kilohertz! (1 hertz is one vibration per second; 1 kilohertz is 1,000 vibrations per second),
The higher the natural frequency of the whole transducer system, the better the accuracy of the waveforms and the subsequent readings. With a properly "tuned" transducer, it's time we discussed what can happen to the pressure wave as it travels from the blood vessel to the transducer.
Figure 9 - A graphic representation of the frequency response range. Note the amplitude change around 30 Hz where the frequency range of this material ends.
If the pressure waveform that the transducer receives is outside its frequency range the pressure waveform will be distorted. In figure 9, you will notice the amplitude of the waveform is about the same as the frequency increases - until the frequency reaches about 30 Hz. At that point the amplitude begins to vary wildly and the amplitude does not accurately reproduce the waveform. The measuring device's natural frequency range ends at that point.
L
iquids have certain properties that are important for the purpose of pressure monitoring, they are incompressible. The molecules of a liquid are able to move easily, but can not get any closer together without turning into a solid. When one molecule of a liquid receives any energy, sound waves or light waves for instance, it transmits it directly to the surrounding molecules with great efficiency. This is great if you want to transmit the energy (in the form of pressure waves) - which is exactly what we want to do! The goal is to take the energy generated in the bloodstream from the cardiac pulsations and transmit it (without as little loss as possible) to the transducer in the tubing so that it can be converted into a waveform on the monitor.
One important concept to understand is refraction. Refraction occurs when energy travels from one medium to another medium with different properties, for instance density. The direction and/or the intensity of the energy changes by bending as the density changes. You already understand refraction from routine, non-medical situations. Think about what happens to a straw that you partially submerge in a glass of juice. The part of the straw that is not submerged seems to be disconnected from the part outside of the juice. The reason is that the light waves traveling through the air are not refracted (bent) as they travel through the air because the density does not change. The light waves that start under water are only refracted, or bent, when they leave the dense juice and enter the less dense air.
Refraction is also at work when you swim underwater. When you are above water all the sounds around - children screaming, dogs barking, and horns honking - are clearly heard. When you go underwater, there is a sudden silence. All the sounds you heard above the water are gone or greatly muffled. The reason is refraction; sound waves travel through air well enough, but are scattered when they come in contact with the water because of the different density.
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he same thing can happen with the PAC pressure tubing. If the tubing is filled with nothing but normal saline solution, whatever energy enters the PA distal tip will be faithfully transmitted to the transducer. This is the ideal situation and the result is an accurate pressure waveform. However, two different kinds of interference can frequently occur that throw a wrench into the PAC tracings.
If there is a substance of a different density, or viscosity, in a part of the tubing, even a small part, then refraction will occur. The energy transmitted from the PA distal tip will be refracted as it encounters the different density material. The two materials that are common culprits in the refraction issue are air bubbles and blood. If the energy encounters an air bubble the energy will be scattered. Air is also highly compressible and will actually absorb some of the energy before dispersing it. Blood clots, on the other hand, is not compressible, and the energy will be refracted significantly, just as your voice refracts off a distant wall causing an echo.
The end result of all this refraction is a waveform that is not a true representation of the pressures in the blood stream, The energy reaching the transducer is always going to be lower than the actual pressure. This type of waveform interference is known as overdampened, or over damped waveform. Frequently, this will be most evident on the PAP waveform as a missing dicrotic notch. The lower pressure readings, if not identified as due to interference can frequently cause inappropriate interventions such as increasing the rate of vasoactive drips or administering fluid boluses. So, it is important to make sure the tubing is completely free of air bubbles and blood.
T
he tubing is another potential problem in the fidelity of the waveform reaching the transducer. Here, there are two major issues, length and extensibility. The longer the tubing, the more problems can occur. A necessary concept to understand is frequency response. You have met frequency response in real life many times. When you use a dog whistle to call your pet, you are relying on frequency response. Your dog s ear are able to vibrate in response to the high frequency, but your ears are not. The result is that Fido can hear the whistle but humans can't.
An example of frequency response can be demonstrated with a crystal glass and a soprano singer. A glass will vibrate if exposed to any loud sound. But, if given a moderately loud singer, hitting just the right note, the glass will shatter. The glass behaves differently given different frequency input.
The compliance of the tubing also effects the frequency response of the PAC monitoring system. When monitoring PAC pressures, stiffer is better. Stiff tubing has a higher natural frequency and therefore can respond better to the higher frequencies of the PAP waveform. Never connect common intravenous tubing between the catheter and the transducer because it is less compliant which lowers the natural frequency of the system.
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hip artifact can occur because of excessive tubing length. All pressure waveforms; arterial, intracranial and pulmonary artery, are able to respond appropriately to a variety of frequencies. In arterial and intracranial waveforms, the high frequency parts contribute little to the total waveform and thus contribute little to the tracings seen on the monitor. The high frequency components of the PAC waveforms, because of the turbulence of the blood in the pulmonary artery as well as other factors, contribute a significant amount to the PA waveforms. Longer tubing can interfere with the transducer receiving these higher frequency pieces of the pressure waveform. When this occurs, whip artifact is seen.
Whip artifact can also occur due to the movement of the catheter tip inside the pulmonary artery. As the turbulent blood flow flies past the catheter tip, the tip is thrashed about. This also occurs with a boat tied to a dock in a severe storm; it is rocked and whipped against the dock with significant force. When this occurs to the PAC tip, the force of impact on the blood vessel wall transmits energy to the transducer, which interprets it as part of the pressure waveform.
Whip artifact, regardless of the source, causes a falsely elevated systolic and falsely lowered diastolic pressure in the tracing. Thankfully the mean pressure remains accurate and should be used in decision making when whip artifact is present and unable to be resolved.
Whip artifact can test the pressure monitoring system before insertion occurs. Once the pressure line is ready to connect to the PA distal port, the nurse should flick the end of the tubing. The tracing on the monitor should exhibit a whip artifact.
T
he transducer system must be assessed for frequency response , which is commonly referred to as dampening. There must be some dampening of the pressure waveform or, like a bell that has been struck, the transducer system will ring indefinitely. That means when a pressure wave is received by the transducer, the transducer will continue to vibrate from that wave even as the next pressure wave signal arrives. This will cause chaos within our pressure monitoring system and give us incorrect readings.
Think of a drum. When you hit the drum it will vibrate for several seconds. So, the next drum beat will be affected by the first. If you do not want this to occur, you can dampen the drum after the first beat by placing you hand on the drum to stop the vibrations. Then remove your hand just before you are ready to strike it again and the first drum beat has no effect.
Figure 10 - A tracing showing a properly dampened fast flush waveform.
I
n order to test the system for overdamping or underdampening, the fast flush test should be performed at regular intervals. The fast flush exposes the transducer to the full force of the high pressure bag of normal saline. This causes the waveform to increase to the maximum the monitor can display and remain at that level, as a flat line, until the fast flush is terminated. After the flush is terminated, the waveform tracing should rapidly fall below the baseline and then rebound just as briskly as it does in figure 10. It may dip a second time and rebound again before the monitored waveform returns. The distance between the peaks of the fast flush tracing should be less than one millimeter or so apart.
Figure 11 - A tracing of an overdampened fast flush waveform. Note that the tracing after the test looks flattened due to the overdampening
If the system is overdamped then, when the fast flush is terminated, the waveform just slowly returns to baseline as in figure 11. This is an indication that something is absorbing some of the energy. The waveforms will look very smooth and the dicrotic notch of the PA waveform will disappear. Aspirating blood through the overdamped port and then flushing the line should correct the problem if it is in the system. If not, the problem may be with the patient. Hypotension is one possible cause for overdamping. If there is little blood in the vascular system, then there will be no back pressure on the valves when they close and there will be no dicrotic notch.
Figure 12 - An underdampened fast flush tracing. Notice the multiple oscillations.
As you can see in figure 12, if the system is underdamped, the fast flush test shows many oscillations before returning to baseline. More than two oscillations is considered underdamped. Underdampening is usually due to excessive tubing length. Removing any unnecessary tubing between the patient and the transducer may correct the problem. Otherwise, it may be whip artifact that can not be fixed as discussed earlier.
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any healthcare professionals, probably due to lack of proper training, do not know how to obtain proper pressure readings from the PAC. Many simply look at the monitor and write down the numbers the computer generates. This may be the right pressures, but they are just as likely to be wrong. There are many variables in measuring PAC pressures including: artifact, "running averages", respiratory artifact and patient positioning. We will cover measuring the pressures correctly when we discuss each pressure waveform.
The waveforms that are typically monitored are the CVP (RAP) and the PAP. The values these waveforms provide are necessary to compute the cardiac output and most of the calculated indices such as pulmonary artery resistance. Now that we are sure that the numbers are accurate, it is time to learn what they really tell us.
T
he pressure in the right atrium, commonly referred to as the central venous pressure, measures how much pressure the blood returning to the heart is under. The venous system has a high capacitance, That means it can adapt to various volume states. Veins, by virtue of thinner walls that lack muscles, stretch when the pressure increases. This stretch allows the veins to hold more, but increases the venous pressure. This can lead to swollen ankles and increased jugular venous distention. When more blood tries to enter the right atrium than the right atrium can hold, the result is an increase in the CVP. Thus CVP can be an indicator of fluid status. More blood volume causes the veins to stretch and increases the intravenous pressure; less blood volume causes the veins to constrict and decreases the intravenous pressure.
Though the CVP pressure can inform about fluid balance, it is a late indicator. Excessive fluid takes awhile to increase the CVP and frequently there are other indicators such as rales or pulmonary edema first. The CVP also represent the preload of the right ventricle. Preload is the amount of stretch in a chamber just before contraction. The more the stretch, the better the next contraction (up to a point of course). Thus, if the CVP is elevated then the pressure in the right ventricle, just before contraction is elevated. Conversely, if the CVP is low, then the preload of the right ventricle is low and the next contraction will be less efficient.
Remember what is going on inside the heart just before the right ventricle contracts. The tricuspid valve is open allowing blood to move freely between the right atrium and right ventricle. Therefore, the pressure in the right atrium and right ventricle should be identical, since they are openly connected. If you do not believe me, just look back to figure 3, you will notice that the CVP tracing and the RVP tracing share a common baseline.
The CVP is reported as a mean pressure measurement, not a systolic and diastolic as other pressures we discuss. Most times the number the monitor reports is fairly accurate and can be used. However, this fact should be verified by actually measuring the CVP using the correct technique at least once a shift. Normal range for the CVP varies from textbook to textbook, but a good range is 2 to 6 mmHg.
There are many potential causes of CVP elevation; fluid overload, right heart failure, (late) left heart failure have already been covered. Others include:
1) Tricuspid stenosis. which reduces the output of the right ventricle leaving it too full to receive all the blood from the right atrium resulting in increased CVP.
2) Pulmonary embolism, which also reduces the output of the right ventricle as above causing increased CVP.
3) Pericardial tamponade - the entire heart is under increased pressure due to the constriction of the pericardium. This allows less blood to be pumped forward, not because of the cardiac dysfunction, but simply because of the constriction.
Differentiating between each of these causes relies on interpreting all the hemodynamic information at our disposal and a careful assessment of the patient.
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o measure the CVP, we have to understand what is going on inside the chest cavity. First of all we must deal with respiratory artifact. Since, when we breathe, the pressure inside our chest cavity changes, we must eliminate the pressures changes related to breathing, from our pressure monitoring. Unfortunately, there is no way to eliminate the effect from the waveform, but there is a way to measure the pressure readings to minimize the effect of breathing on the numbers we record.
When we breathe naturally, the diaphragm contracts and drops. This causes the pressure in the semirigid chest cavity to decrease. The lungs expand and the pressure in the lungs decreases. The epiglottis opens and the outside air (where the pressure is higher) rushes in to raise the pressure again. Then the diaphragm relaxes and returns to its natural state and the pressure increases and pushes the air out.
So, the pressure on the heart, from the chest cavity, decreases during inspiration and increases with expiration. The natural, relaxed state of the diaphragm is at the end of expiration and so that is where we want to measure the CVP (and any PAC pressure reading) from.
Figure 13 - A tracing showing respiratory artifact commonly found in CVP waveforms.
In figure 13, you see a roller-coaster looking CVP waveform, This is due to the pressure changes associated with respirations. The waveform goes up with expiration and down with inspiration.
In a patient on mechanical ventilation, the relationship is reversed. The ventilator pushes air into the lungs causing the pressure in the chest cavity to rise, and then, when the ventilator stops pushing, then the air is allowed to escape, causing the pressure to fall.
Therefore, when looking at a waveform with respiratory artifact, such as figure 13, the waveform associated with end expiration will be different for spontaneously breathing patients and mechanically ventilated patients.
This is the case for all PAC pressure waveforms. The CVP, RVP, PA, and PAOP readings all use the wave that occurs at the end of expiration, just before the waveform begins to stray.
More specific for the CVP measurement is the exact timing in the waveform. This factor is related to what is going on inside the heart. We want to measure the pressure as the atria are relaxing. This occurs when the ventricles begin to contract. There are many ways to determine this, but the easiest way is to print out a strip with the ECG tracing and the CVP waveform. Then, the CVP measurement can be obtained by drawing a straight line from the end of the QRS complex to the CVP tracings as shown in figure 14
Figure 14 - A tracing showing one way to obtain a CVP measurement by drawing a vertical line from the end of the QRS complex through the CVP.
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he pulmonary artery pressure is reported as a systolic and a diastolic number. The normal range for the systolic PAP is 12 - 25 mmHg. There is variation in the normal range in various textbooks and institutions so check with your policies and ask several physicians what they believe a normal systolic PAP is. The diastolic PAP normal range is 7 to 15 mmHg. Again, the same caution is encouraged with this normal range. The mean PAP pressure has a normal range of 10 to 15 mmHg. A typical reading for the PA pressure is 20/12 with a mean of 13.
The pulmonary artery pressures measure the resistance of blood flow through the lungs. Again fluid overload, left heart failure, constrictive pericarditis, and pulmonary embolism can all cause the PAP to increase, but tricuspid and pulmonic valve stenosis will decrease the PAP because less blood can be ejected from the right ventricle. The same effect occurs with right ventricular failure, the lack of blood being pushed into the pulmonary artery will decrease the PAP readings.
Anything the increases the PA pressures will also lead to elevated CVP pressures, because the pressure will be transmitted back to the right ventricle when the pulmonic valve is open. And, once the right ventricular pressures are increased the pressure will be transmitted back to the right atrium when the tricuspid valve is open. But, anything that increases the right atrial or right ventricular pressures will not necessarily increase the PA pressures. This is helpful in diagnosing the cause of the pressure problems.
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he PAOP, colloquially referred to as "the wedge", gives valuable information about fluid status with respect to the left side of the heart. There is a special syringe that should ALWAYS be used when performing a PAOP reading. It has a stopping device at 1.5 milliliters. You should NEVER inflate the balloon with more than this amount and always with air, not fluid.
To perform a "wedge" measurement, connect the syringe, line up the arrow on the tubing (this opens the port) and slowly inject the air. This should take two or three seconds. Rapid inflation may cause a pulmonary artery rupture by not allowing it to accommodate the increasing pressure on the vessel. It could also have migrated into a smaller vessel that needs less than full balloon inflation to be occluded - again causing a pulmonary artery rupture. This is not something you ever want to happen.
Pulmonary rupture is such a feared consequence of PAOP measurement, that many institutions and physicians only permit PAOP measurements with a specifically written order. When the PAC is initially inserted, the physician should perform a PAOP reading. When this is documented, compare it to the pulmonary artery diastolic (PAD) pressure. They should differ by only a few points, with the PAD being about 2 to 4 mmHg higher than the PAD. Note the difference in the PAD and the PAOP and then you need not do any further PAOP measurements until there is a significant change in the patient's condition.
Another possible problem with measuring PAOP is that the balloon may rupture. When this occurs there will be no resistance to balloon inflation, because the air you are injecting is going directly into the bloodstream! Also, with balloon rupture, you may notice blood in the balloon port's tubing. If there is blood in the balloon tubing, IMMEDIATELY clamp off the port and do not perform PAOP anymore. Tape over the port, and "break the arrow" to lock the port and notify the physician. Injecting air or fluids to clear the blood could dislodge a clot or cause an air emboli - both potentially life-threatening interventions.
When the PAC balloon is inflated, the pressures from the right side of the heart can no longer reach the tip of the catheter. The tip of the catheter now measures the pressures in front of the catheter in the pulmonary artery. But, the pressure in the pulmonary artery in front of the catheter is really the pressure from the pulmonary veins pushing back on the blood in the pulmonary artery. This can be more easily seen with the distorted heart-lung graphic in figure 15.
Figure 15 - A figure of the heart-lung relationship and the PA catheter proper location
The PAOP is measured the same way as the CVP, by obtaining an ECG and PAOP tracing at the same time. This time however, the line is drawn from a point 0.08 to 0.12 sec (2 to 3 small boxes) after the QRS ends. This is just before the ventricle begins to contract and gives us the best reading of the left ventricular end diastolic pressure.
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he pressure pushing back into the pulmonary veins, comes from the left atrium. Therefore, a catheter in the right side of the heart, can measure pressures in the left side of the heart. There are some caveats however. If the patient has pulmonary hypertension or pulmonary embolism, conditions that specifically alter blood flow from the right side of the heart to the left side, then the PAOP does not accurately reflect left sided pressures.
That said, if the PAOP accurately reflects the left atrial pressure, then we can actually measure the pressure in the left ventricle - if the mitral valve is open. Remember, if two areas of the heart are openly connected, the pressure will quickly equalize in the two chambers. If the pressure in the left atrium was higher then the pressure in the left ventricle when the mitral valve is open, then blood would move from the higher pressure area into the lower pressure area and vice versa.
Therefore, we can measure the pressure in the left ventricle as long as the mitral valve is open. And, when is the mitral valve open? - during diastole, as the left ventricle is filling with blood. Therefore, the pressure the PAOP is measuring is actually the left ventricular pressure during diastole, or Left Ventricular End Diastolic Pressure (LVEDP). This pressure actually gives us preload for the left ventricle, which is directly related to the amount of stretch the left ventricle has just before it contracts (when we lose the connection with the left ventricle due to closure of the mitral valve).
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his is the first indicator of fluid imbalances. If the PAOP is too high, then the pressure in the left ventricle during diastole is too high. This means that the heart is having difficulty pumping the blood it receives forward. In general, this occurs due to fluid overload, or congestive heart failure of the left ventricle. This change occurs as soon as the fluid level starts to rise and, therefore, is a better indicator than the CVP.
If the PAOP is too low, this usually means that dehydration or volume loss is present. The fluid loss can be relative or actual. In sepsis fluid leaks from the blood vessels and enters the interstitial spaces. This will cause the PAOP to decrease as less blood returns to the heart, specifically the left ventricle, causing left ventricular preload to decrease. If the fluid loss is actual, as in dehydration or significant bleeding, then the result to the PAOP is the same - a decrease.
As a matter of fact, the ability to measure the PAOP is a primary reason for inserting the PAC in the first place. In patients with wet lungs there are two primary diagnoses that come to mind, CHF/pulmonary edema and ARDS. In congestive heart failure, the left ventricle receives more blood than it can handle and so the blood starts to back up causing an increase in the pressure in the pulmonary vasculature. This pressure increase can be handled to a certain point; after that magical point is reached, the pulmonary vessels begin to leak the excess fluid into the interstitial spaces around the blood vessels and eventually into the alveoli - causing rales (or occasionally wheezes). In this scenario, the wet lungs are associated with an elevated PAOP due to the back up of blood into the lungs.
Figure 16 - Chest X-ray showing congestive heart failure
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n acute respiratory distress syndrome (ARDS), there is fluid in the alveoli (and they initially look similar on chest x-ray see figure 16 and 17, but the mechanism is different. In ARDS, the fluid leaks because of inflammatory chemicals in the blood stream do their job, just in the wrong place. If you twist your ankle, you have damaged tissue. This damaged tissue releases chemicals, locally, that cause a cascade of events. The end result is that the pores of the capillaries to open to allow fluid and white blood cells to enter the damaged area. The result is a swollen ankle. In the lungs, the capillaries respond to the same chemicals and also allow fluid to leak through the capillary pores; this time into the interstitial tissue and the alveoli. The difference is that the PAOP is normal or low. This is because the left ventricle is not the problem; it is able to pump all the blood forward.
Figure 17 - Chest X-ray showing late ARDS
As you might imagine, the treatments for ARDS and CHF are different. In ARDS, the goal is to maximize oxygenation and tissue perfusion. To accomplish this, treatments include intravenous fluids and vasopressors, such as dopamine and norepinephrine, to maintain blood pressure. The delicate balance is to maximize cardiac output and tissue perfusion while allowing as little fluid to leak into the lungs as possible.
In CHF, the goal is to reduce total body fluid. If blood pressure is sufficient, then nitroglycerin drip can help by dilating the venous and arterial systems to allow more blood (and consequently fluid) to be stored in them. This keeps more blood from returning to the heart and decreases preload and can lower the PAOP. Another choice is diuretics, such as furosemide. This eliminates the fluid completely from the body, also decreasing left ventricular preload and consequently the fluid accumulation in the lungs.
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ardiac output can be measured with the pulmonary artery catheter using a method known as thermodilution. Thermodilution refers to injecting fluid, of a known temperature, and measuring the effect on the blood as it travels past the pulmonary artery catheter tip. All PACs have a thermistor, which is basically a temperature measuring device. If you inject room temperature normal saline into the injectate port of the pulmonary artery catheter, then the temperature of the blood will decrease by an amount related to the relative volumes of the injected fluid to the amount of blood in the heart.
The amount of time for the temperature of the blood to return to normal is directly related tot he cardiac output. When the cool normal saline is injected in the heart, the temperature of the blood is decreased. Then the heart contracts and ejects a certain percentage of the cooler blood, say 50%. Now an equal amount of new, body temperature blood, mixes with the cooled blood that is left. Then the heart contracts again and ejects 50% of this slightly warmer blood. This cycle happens over and over again, contraction ejects cooled blood and then adds warmer blood to the mix. How long the process takes to increase the blood temperature back to pre-injection levels tells us how fast the heart is pumping blood out of the heart - the cardiac output.
Figure 18 - An example of cardiac output waveforms and readings.
This temperature change can be represented as a graph of the temperature difference between the pre-injection blood and the post-injection blood. In figure 18, you will see three examples of this graph. The height of the curve represents the change in temperature and the length of the curve represents how much time has passed. The curves first grow taller as the injected blood gets ejected and passes the thermistor. Then the curves begin to grow smaller slowly as progressively warmer blood begins to pass by the temperature sensor. Eventually some time out in the future, the curves will return to the baseline. The computer does not need to wait for this to occur, it can predict the cardiac output based on the rate of return to baseline.
It is customary to obtain three separate readings, that differ by less than 10%, and average them to arrive at an average cardiac output. Successive injections can actually alter the readings - cool saline can stun the myocardium, especially in patients in shock. If there seems to be a wide variation in the readings then allow more time to pass between injections to allow the heart to recover more completely.
Also on figure 18, you will notice the temperature readings in the lower right hand corner. TB represents the pre-injection temperature of the blood. TI represents the temperature of the injectate, normal saline. The computer needs to know these numbers, and thankfully measures them itself. Finally, the large number in the lower right corner is the calculated average of the three readings.
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here is one final piece of information that the Swan-Ganz catheter can give us - the SvO2. Also known as the mixed venous blood gas, the SvO2 is an important indicator of how well the tissues are utilizing oxygen. Measuring this value, along with a simultaneous arterial blood gas, allows calculation of the oxygen content of the blood and a more complete assessment of the patient s oxygenation status.
Normal, healthy individuals usually use about 25% of the oxygen that is breathed in. If that person has an arterial oxygen saturation of 95% and uses 25% of that oxygen (that means that 75% of the oxygen returns to the heart), then that leaves the oxygen saturation of the returning blood as about 71% (95% x 0.25). The range of normal values for SvO2 is about 65 - 75%.
So, when should we become concerned? Let's think about that. If you have a patient who has respiratory failure from a gram negative rod pneumonia and the SvO2 is low, say 50%, with an SpO2 of 95% by pulse oximeter, should we be concerned about their oxygen level? What if the same patient's SvO2 suddenly increased to 82%? Which is more worrisome? The counter-intuitive answer is that higher SvO2 readings are more concerning.
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he SvO2 tells us how much blood is returning to the heart. From that we can tell how much oxygen the tissues are using. In our patient, we are concerned about development of septic shock because of the pneumonia. Remember the definition of shock, "inadequate tissue perfusion that results in organs receiving less oxygen than they need to do their job correctly." How do we know the blood the heart is pumping is getting the oxygen to the organs? One way is by determining how much blood they used.
By measuring SvO2, we know how much blood the body is using. If the SvO2 is high, that means tissues are not taking the oxygen out of the blood. Either the blood is not reaching the organs (DIC, arterial occlusion), or the tissues are not able to extract the oxygen reaching them. Either way, if the SvO2 is high, then organ failure, from tissue hypoxia may be on the horizon.
Conversely, a low SvO2 means that the organs are extracting oxygen at a high rate. The increased oxygen utilization could be due to fever, anxiety, pain, or anything else that increases the patient's metabolism. The lower SvO2 can also occur due to anemia. Less red blood cells can carry less oxygen. The arterial oxygenation would not be affected because the RBCs are all saturated with oxygen, but more of the cells would have to give up their oxygen to satisfy the tissues - resulting in a lower SvO2. So, a decrease in SvO2 could be due to fever, or anemia of critical illness, in our theoretical patient. Low (but not terribly low) SvO2 values indicate that tissues are extracting oxygen - a good sign.
SvO2 readings are much less commonly performed than the other readings we obtain from the PAC. A more thorough explanation of the topic is forthcoming in a future article.
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e are done with the values we can obtain by direct measurement. Now we are on to the computed values. There are a number of important values that we can obtain from the measured PAC values alone and with a few other numbers such as: heart rate, mean arterial blood pressure, height and weight. Actually reviewing the formulae for these computations is beyond the scope of this article, but look for another article in the next couple of months on this topic. For now, we will discuss the meaning and relevance of these other numbers.
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he normal cardiac output is 5.0 to 8.0 liters per minute. So, if two patients have a cardiac output of 6.0 liters per minute then, at least cardiac wise, the two are doing about the same - right? Not necessarily! What if one patient is five foot 2 inches tall and weighs 110 pounds, and the other is six foot four and weighs three hundred pounds? Since the major role of the heart is to perfuse body tissues, clearly the smaller patient is in better shape - her individual cells are receiving more blood per minute than the larger patient. How do we take that into account?
We can adjust the cardiac output value for the difference in size. The way we do that is to divide the cardiac output by the body surface area. Body surface area (BSA) is dependent on height and weight - the taller or heavier patients have a larger BSA. Let's say the smaller patient's BSA was 1, then her cardiac index would be 6.0 liters per minute (6.0 / 1). If the larger patient had a body surface area of 1.5 then the cardiac index would be 4.0 (6.0 / 1.5) - significantly lower.
Most times the computer in the monitoring equipment will automatically do the computation if the height and weight are entered.
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ardiac output is defined as heart rate times stroke volume (CO = HR x SV), This simple equation allows us to determine stroke volume if we know heart rate (off the monitor) and cardiac output (measured value). The computer will usually capture the heart rate for these purposes. Stroke volume is the amount of blood the heart ejects with one contraction. If stroke volume is low then the heart may be failing or there is insufficient blood volume (dehydration or blood loss); to differentiate we can look to the PAOP as discussed earlier.
There are many others such as left and right ventricular stroke work index which measures the amount of work the respective ventricle is doing, but they will be covered in a future article.
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ystemic vascular resistance, SVR for short, measures the resistance to ejecting blood from the left ventricle. It is a calculated value that is given by the formula
We can calculate cardiac output and can measure CVP and MAP (mean arterial pressure). This value is effected by total blood volume and artery size. Dilated arteries decrease the resistance to ejecting blood and therefore lower SVR. Conversely, constricted arteries cause the SVR to rise. This is one way the body regulates cardiac output and blood pressure. Small changes in the diameter of a blood vessel has dramatic effects on the pressure needed to push blood through that artery. If you double the size of the artery, you need 1/16th of the pressure to push blood through it. If you cut the artery size in half, then you need 16 times as much pressure to get the blood through that artery.
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ell, we have covered a great deal of information, but how does this help us? Granted, knowing the cardiac output/ index, PAOP and CVP have some benefit, but is that all you are going to get out of this lengthy article? No, there is a bit more - application. The Swan-Ganz catheter is indicated for many reasons (see table 1), but one major one is differentiating the four basic types of shock: Cardiogenic; Distributive, Obstructive, and Hypovolemic. Now, we are going to find out what the PAC shows with each type and why.
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hink about a car engine; in order to run efficiently and do the job of moving the car, it must have air and gasoline reach the spark plugs. If either air (oxygen) or gasoline (glucose) do not get to the spark plugs in sufficient quantity, then the engine runs inefficiently. It will sputter and gasp and, if the deficit is severe enough, the engine (organ) will stall (fail).
Shock is simply a sputtering engine driving the body. Simply defined, shock is insufficient delivery of the blood (and by association oxygen and glucose) to the tissues of the body to meet their demands. The tissues initially will try to compensate before they begin to dysfunction and finally start to fail. Organ failure, such as respiratory failure, renal failure, and altered mental status can all be signs of shock. Knowing which of the four types of shock a patient is in is vital to determine treatment. Something that works in one type of shock may not work in another and may even by dangerous.
Table 1 - A comparison of readings obtained from a Swan-Ganz catheter in the three major categories of shock .
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n cardiogenic shock, the problem is with the heart itself. For some reason the heart is not able to pump sufficient blood, Reasons for cardiogenic shock include: myocardial infarction, cardiomyopathy, drug toxicity (such as cocaine), inflammatory process (such as myocarditis), valve dysfunction (such as aortic or mitral valve regurgitation). Medications to support the heart are administered. These include: nitrates (nitroglycerin) to improve oxygen delivery and reduce SVR; inotropes (digoxin, dopamine) to improve contractility; beta-blockers (metoprolol, esmolol) to decrease myocardial oxygen demand, if the blood pressure tolerates it; diuretics (furosemide) to decrease preload (both CVP and PAOP); and possibly an intra-aortic balloon pump to decrease oxygen demand and improve cardiac output.
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n this form of shock, the heart is able to contract well enough to meet the body's needs, but the blood is being obstructed from its normal flow. Causes include: Massive pulmonary embolism (the right ventricle can't pump enough blood to the left ventricle), severe valve disease (such as aortic stenosis that blocks blood leaving the left ventricle), pericardial tamponade (where the increase in fluid around the heart squeezes the low pressure right side of the heart inhibiting return of blood to the heart and therefore the stroke volume) and severe ascites (increased abdominal pressure acts as a tourniquet stopping the blood in the low pressure venous system from returning to the heart, but allowing the higher pressure arterial blood to leave the heart.
Obstructive shock is usually classified under the heading of cardiogenic because, in both types of shock, the heart is unable to do its pumping job. There is a difference though. In cardiogenic shock you give drugs to support the heart's function, but in obstructive shock they will not work. Instead, you must remove the cause. There are some clues that the heart's dysfunction is from an obstruction though.
Muffled heart sounds, or a significant pericardial friction rub, can indicate pericardial tamponade. In the case of pericardial tamponade, all the diastolic pressures will be equalized. That means the CVP, RVP diastolic, PAP diastolic and PAOP will be roughly equal. That is because all the chambers of the heart are under high pressure, even during relaxation. All the diastolic pressures will be high and will share the same baseline (be essentially the same).
If pneumothorax is the cause, shortness of breath should be observed, and lung sounds should be absent or markedly diminished on one side of the chest.
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robably the most difficult type of shock to deal with, here there is sufficient blood volume in the vessels and the heart is able to pump reasonably well, however, the blood volume is not where it is supposed to be. Therefore, there is less blood returning to the heart (low CVP), and less blood going to the lungs (low PAOP and PAP). But, because the heart is working well, and the blood vessels are incorrectly dilated (lowering SVR), the heart can pump hugh amounts of blood in a minute (elevated CO/CI).
Causes for this type of shock are: sepsis (third spacing decreases blood volume returning to the heart), acute pancreatitis (same as sepsis), anaphylaxis (same as sepsis), and neurogenic (due to head or spinal cord injury and loss of vascular tone the blood leaves the heart and enters a lower than normal arterial system and decreased return to the heart occurs)
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his type of shock is frequently confused with distributive shock. They do share some characteristics as both have too little blood returning to the heart, but the reasons for this are different. In hypovolemic shock, there is an actual body deficit of fluid either from dehydration or bleeding. Because, the blood vessels are working correctly, they will constrict to try to raise blood pressure (raise SVR), decreasing the CO/CI, by lowering how much blood can be ejected with each heart beat. The Laboratory data, such as the hematocrit level and BUN-creatinine ratio, can help differentiate between these two causes, so we just need to be able to differentiate this shock from types of distributive shock.
A patient is admitted with pneumonia and is placed on a ventilator. His WBC count is markedly elevated and he is hypotensive, 82/36 by NIBP cuff and his rhythm is sinus tachycardia, rate 128 bpm. He is also showing signs of hypoperfusion such as confusion, oliguria (decreased urine output), and respiratory failure. This patient could be dehydrated, or could be in septic shock. Treatment is different, vasopressors such as dopamine could be catastrophic to a dehydrated patient, but are a valid treatment choice in septic shock. This is a common reason pulmonary artery catheters are inserted in the first place is to differentiate between these two types of shock in patients who do not respond to normal interventions.
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he PAC gives use valuable information about the patient's cardiovascular status and helps guide treatment. The prevalence of the PAC in the critical care units has declined significantly since the peak in the mid 1980's. This is partially due to the significant risks to the patient with PAC insertion, such as: pulmonary artery rupture, catheter related sepsis, and ventricular dysrhythmias. Other reasons include the fact that other less invasive tests such as echocardiogram, cardiac markers (CPK, troponin and B-type natriuretic peptide, for example) and others have replaced the PAC in many instances.
Because the PAC is a high risk, low use intervention, every opportunity to have hands-on practice should be utilized and at least yearly refreshers should be required. These refresher courses should include discussions of insertion techniques, connection to monitoring equipment, typical waveforms for each of those monitored as well as troubleshooting waveform for correctable and uncorrectable problems.
The Swan-Ganz pulmonary artery catheter is an important device to use and understand in the proper clinical context.
Stay tuned for the next article where we will delve into the shock syndromes, their causes and treatments. Coming soon.