CCRN Review: Hemodynamic Monitoring Waveforms, Trouble Shooting and Complications

Hey everybody, before we get into today's podcast, I want to tell you a little bit about the membership community that I've created with you in mind. It's kind of a central hub, if you will, a place to go for continuing education hours that are accredited. I also do case study breakdowns. I offer up best practice guidelines and also recent article reviews. And if you're interested, you know, the price is really right. $25 a month, you really can't go wrong. Come and check it out. The website is khpmembershipcommunity.com. I will also put a link in the description. Enjoy today's podcast. Hello and welcome to episode eight of the CCRN review where today we're going to be looking at hemodynamic monitoring troubleshooting and complications. For those of you that are joining for the first time, this walk through the core curriculum is really kind of a tailor-made type series of podcasts where you can choose the podcasts that will best help you prepare for the CCRN. So for those of you that are new, welcome to my podcast series. And for those of you that have joined me in previous podcasts, thank you so much for coming back for another episode. Now before we get into today's content, I just want to mention a few things. The first being a reminder to be sure and subscribe and also to head on over to my website, which is called khppresence.com. If you head over to the website, you'll be able to subscribe at that point. You'll be able to see what is scheduled for upcoming podcasts throughout this month and upcoming months. You'll be able to access brain teasers, which are little, let's just call them study guides that I've put together to help you prepare to take the CCRN exam. On my website, feel free to download a brain teaser. The answers are there for you as well. So without further ado, let's get into today's content. If you'll remember from episode seven, we started talking about hemodynamic terms. We defined a lot of hemodynamic terms and talked a bit about some clinical and diagnostic applications of hemodynamic monitoring. We also started talking about ensuring accuracy in our hemodynamic monitoring by doing things like zeroing and calibrating and leveling to the phlegmestatic axis. And we also talked about performing the square wave test. We're going to continue onward today then talking about a little bit more about the waves. And then we're going to get into troubleshooting. In episode nine, we're going to get into clinical application of everything we've talked about. So we're going to be looking at some patient cases along with some numbers and applying the things that we learn to those clinical case studies. Because quite honestly, on the exam, you will have a fair amount of cases, I like to call some story problems where you have to look at the hemodynamics and determine the intervention that you would most likely see employed. So in the last episode, when we kind of walked the tip of the catheter through the different heart chambers and out into the pulmonary artery, we first started out talking about right atrial pressure, which very commonly we refer to as CVP. We also said that that right atrial pressure is a small little unilating waveform. Well, it's, yes, it's made up of little undulations, but there is some clinical application to why you're seeing what you're seeing. So when you have a waveform that you're looking at on the monitor, you always want to correlate electrical events with mechanical activity. And what I mean here is that you want to look at the EKG, which is the electrical event, and you want to correlate that with the mechanical event that we're seeing in terms of the right atrial pressure waveform. Because really what that little undulating waveform reflects for you is it reflects atrial contraction and then filling contraction filling contraction filling. Sometimes we actually see a wave associated with closure of the tricuspid valve. We don't always see that. That's known as a C wave. So let's just kind of bring the electricity together with the mechanics. So when we see a P wave, no big news flash to anyone that the P wave represents the spread of electricity through the atria. Now that spread will kind of culminate in kind of like a pause at the level of the AV node. Now that pause allows time for the atria to contract. So if you were to take an EKG waveform and draw a line down from the end of the P wave to intersect with your central venous pressure or right atrial pressure tracing, what you would identify then is what is called an A wave. An A wave represents atrial contraction. So when you look at electricity and then you look at your hemodynamic waveforms, which actually are mechanical, you think about mechanics, we have the P wave representing the spread of electricity through the atria and then we have the mechanics of it and that is the atria contracting and response to that. And that will produce for us what is known as an A wave. Now I want you to think about this physiologically. When the right atrium contracts, it completes right ventricular filling. So the last part of ventricular filling is when the atria contract. Now that isn't a new slash I'm sure to you because you know that that atrial contraction produces what we like to call atrial kick. We also know that when there's a clinical situation where we lose atrial contraction, let's say for example an atrial fibrillation, well now we lose up to 30% of ventricular filling or we lose our atrial kick and that can have a pretty big impact on our patients blood pressure. So again to summarize, at the end of the P wave you draw a line down, you find the A wave there. The A wave represents atrial contraction that also represents the time in which the right ventricle is at its fullest point. So really guys, we should be taking the mean value of the A wave to determine our pressure measurement. Just think about it now, we know that when the right atrium contracts and fills up that RV and it's at its very fullest point right after contraction, we know that to be right ventricular preload. So then why not take the mean value of the A wave to really determine what right ventricular preload is. So and that is best practice by the way, the use of the mean value of the A wave in order to determine right ventricular filling. Now sometimes guys, you can actually see a little bump the A wave that correlates with the end of the P wave if you draw a line down. But then there's another little bump that follows that which is called the C wave and the C wave really is tricuspid valve closure. Well, now you know for sure that that right ventricle is at its fullest point. So even looking for the bump right after the A wave, you'll find that C wave that really correlates with the maximum amount of filling in the right ventricle and it gives us the best pressure measurement. And so when you look at an A wave, when you take the highest and lowest point of the A wave, and you take a mean value of that to determine your right-sided filling, right in between the highest and lowest point of that A wave, if you see another bump, that's a C wave. And so it really reflects the importance of taking the mean value of the A wave which is right at that C wave where the tricuspid valve closes in order to determine the maximal amount of right ventricle. particular filling right before ejection. Now let's move on electrically from there. The P wave we said represents spread of electrical impulses throughout the atrium, the right atrium, and then we took a pause at the level of the AV node. Now we're headed downward, right? We're headed down the bundle of his to the right and left bundle branches and out to the perkinji fibers. And we know that electrically what that is going to give us is what is called a QRS complex. Okay, no big news flash to anybody. Now what you will also see is from a mechanics standpoint. You will see a V wave. A V wave represents the time in which the atrium are filling. Now think about this physiologically guys. The atria are filling while the ventricles are contracting. So as the right atrium is filling, the right ventricle is contracting. And so we would see the V wave for the right atrial pressure waveform immediately after the T wave. Okay, so electrical events preceding mechanical events. Now let's think about this for a second because after a while, you know, these waves kind of can get jumbled up in your head and if you're listening to this in your car, you're out running or walking, you really have to visualize this because you don't have an illustration in front of you. So let's think about it for a second. The a wave represents contraction of the right atrium in the central venous pressure tracing. Okay. Now if that person has tricuspid stenosis, let's say, that would cause a pretty elevated a wave. Now normally the a wave should be very small and undulating. If that right atrium is having to work extra hard against a stenotic tricuspid valve, we would see an elevated a wave as a result of that. Let me also ask you this. Here's a good brain teaser for you. In upcoming episodes, we are going to be also incorporating a lot of physical assessment. Okay. And in fact, I do have a podcast that I'm going to be dedicated just specifically to cardiovascular assessment. And there we are going to be talking about an S4. An S4 occurs immediately prior to systole, and an S4 occurs as a result of filling into a non-compliant ventricle. Maybe it's somebody with diastolic dysfunction related to hypertension. You know, we'll discuss those ideologies a bit later, because right now we're trying to understand this concept of a and V waves. So if you have a person that has, let's say, for example, atrial fibrillation, can a person with atrial fibrillation ever have an S4? Let me think about it. An S4 occurs during the end of diastole. We call it precystallic sound. Now, I want you to think physiologically now about what happens at the end of diastole. At the end of diastole, the atria, squeezed. Do they not? Normally, normally. And so, as the atrium, the right atrium squeezes, that gives us an A wave. Well, now I'm asking you a question about somebody with atrial fib. And when a patient goes into atrial fibrillation, we know that we lose that atrial contraction. So, can anybody with atrial fibrillation have an S4? The answer to that is no. And the reason for that is, is because you do not have atrial contraction. And you know that an S4 is produced when the atria try and kick that last bit of, of that 30% of ventricular filling down from the atria into the ventricles at the end of diastole. And that's why it's called an end diastolic or a pre-systolic sound. So, that's some clinical application of this knowledge. Now, over on the left side, the left atrium, if you were doing a pulmonary capillary wedge pressure or a pulmonary artery occlusive pressure as it's known now, or let's just plain all, you know, call it a wedge and be done with it. If you're doing a wedge pressure, you get the same kind of waves that you would over on the right side because it's an atrium. It's a venous pressure waveform. And it's occurring over on the left side. So, indeed, you would get an a wave as the left atrium contracts. The difference, though, is the fact that the a wave for the wedge is going to be in alignment with the end of the QRS complex, whereas we said the a wave with the right atrial pressure tracing was in alignment with the end of the p wave. And the reason for that should make sense to you. And that is, I want you to think about how the PA catheter is configured. Which port is closest to the transducer? Well, certainly the right atrial port or the proximal port is the closest to the transducer. And that's why you see the waves in alignment with the a wave in alignment with the end of the p wave, for example. Whereas when you're talking about the wedge pressure tracing, that comes from the distal port. That distal port is farther away from the transducer. And so, coming from the distal port, the a wave is going to wind up being in alignment a little bit later, like with the end of the QRS. It still means the same, only it's talking about left-sided events. So when you take a wedge pressure measurement, it should be a mean value of the a wave. Because that represents the time in which the left ventricle is at its fullest point and ready to eject. Oftentimes, we don't see a C wave. That kind of gets lost in the shuffle, being transmitted all the way from the distal tip of the catheter to the transducer. Now, what I want to bring up is the V wave. The V wave for the wedge pressure tracing is located in the T to P interval. In other words, right in between the end of the T wave from one complex and the beginning of the P wave for the next complex in the T to P interval. Now, who cares and why do we need to know this? Well, I want you to think about a patient post-MI. And I want you to think about a patient that has perhaps papillary muscle dysfunction. Maybe some of the cord A tendin A have torn off the papillary muscle. We know that the papillary muscle and the cord A tendin A really serve as anchors for the AV valves, both the mitral and tricuspid valves. So, again, the papillary muscle being a muscle, you have an anterior papillary muscle, you have a posterior papillary muscle. Being a muscle, they can be affected by myocardial infarction and necrosis. And all of a sudden, you have separation of the cord A tendin A from the papillary muscle. Now, how is that going to manifest? It's going to manifest in a big, huge V wave in the wedge pressure tracing. And this is almost invariably a question on the exam. And it's considered a high-scaled score question as well, because it causes you to really have to think more than just a rote memorization sort of a thing. So, what happens here? Now, think about it. A V wave just normally now is produced as an atrial, either right or left, fills. Okay? Now, when do the atrial? They fill when the AV valves are closed. That makes good sense. And so if we have a ruptured papillary muscle or torn cord A-10-A, what's going to happen is that mitre valve is not going to be able to close. Therefore, every time that ventricle contracts, instead of blood taking the pathway of highest resistance, which would be going out into the aorta, the blood will take the pathway of least resistance. And it will go from left ventricle into left atrium across that valve, that insufficient valve, and back into the pulmonary vascular bed via the pulmonary veins. Now this is a patient that will go into fluorid pulmonary edema very rapidly. You've got yourself, if you're not coding right now, you will be soon. So this is a patient that is in cardiogenic shock related to papillary muscle dysfunction or ruptured cord A-10-A, and the mortality rate on that is very high. So what you would see then is that big old V-wave in the wedge pressure tracing that is between the T and P of the upcoming complex, so in the T to P interval. Not only that, but you'll have a patient that, as I said, goes into cardiogenic shock, and they have a systolic murmur that's going to reach up and just grab you by the throat. So again, this is blending electrical with mechanical, with etiology, with physical assessment. The test really calls upon you to be able to do these kinds of things. Now a big old V-wave doesn't have to do with only papillary muscle rupture or torn cord A-10-A. That's not the only cause. You can have somebody that has this big old ventricle that's engorged with fluid, and the fluid in the pressure actually pull the anulus or the ring around the mitral valve, causing the leaflets to not be able to approximate. So the mitral valve is not closing properly. No matter how you look at it, if the mitral valve is not closing properly, you're going to have regurgio flow from the left ventricle to the left atrium, and you're going to have a patient that goes into pulmonary edema. So again, that big old murmur that comes at you too starts out softer and gets louder, louder, louder as the patient's mitral valve becomes less and less competent. So again, prepare your head for this on the exam, and that is the manifestation of a large V-wave and the fact that it has to do with mitral regurg. Let me also mention there are times in which, clinical situations in which we can have both an elevated A-wave and an elevated V-wave, and those would be in circumstances like cardiac tamponod or perhaps the person with constrictive paracarditis or hypervolemia. Those are some examples where we have overfilling hypervolemia heart failure, so we can see elevated A and V-waves. So one last thing about these A and V-waves that I want to mention, and that is that there are situations, one of them we named already, like atrial fibrillation, where we don't have an A-wave. And you may be saying yourself, well, wait a minute, K, just a little while ago, you told me that the way that I'm most accurate in measuring my hemodynamic wave is to look for the mean value or average value of the A-wave. Well, what do I do in patients with atrial fib? Well, it's actually quite easy, guys, and that is just to draw a line down from the end of the QRS complex and where it intersects the right atrial pressure waveform or wedge waveform for that matter at the end of exhalation. Oh, that's your value. That's your value when you don't have an A-wave. So think about the circumstances in which you wouldn't have an A-wave. So we don't have that uniform spread of impulses throughout the atrial. It could be somebody in a paste rhythm. It could be what we talked about atrial fib. It could also be somebody with a junctional type of rhythm. Another thing that we need to talk about is catheter fling or catheter whip. So this is where, literally, the tip of the catheter, the tip of the pulmonary artery catheter is like flinging around, if you will. And so when we talk about catheter fling or whip, it happens most often when the tip is going along with arterial flow versus against it. Let me explain this to you. We are much more likely to have a catheter whip effect in the pulmonary artery catheter when compared to a arterial line that's out in the radial artery. See, in the radial artery, the catheter is facing against arterial flow, whereas a PA catheter is kind of going with arterial flow out in the pulmonary artery. So we're much more likely to see kind of a flinging effect when it's out in the PA. And there are certain patient populations that are just set up for this. So we think about patients with pulmonary hypertension. So immediately, you know, it comes to mind, our COPD patients or perhaps our patients with mitral valve disease that have pulmonary hypertension as a result. That's where we can see an increased fling effect. So if you have a pulmonary artery catheter that's giving you a lot of fling or a lot of catheter whip, you can try not you yourself, but you know, your provider can try repositioning the tip a little bit and seeing if that is going to take care of the fling. Sometimes there's nothing we can do about it except to use a mean pressure, a mean PA pressure for targeting our interventions and our assessments. So if you have real bad whip or fling using the mean PA and just using it as a trending measure is probably your best bet. Next, we're going to take a look at some of the complications associated with hemodynamic monitoring, whether you're talking about a pulmonary artery catheter or some of the things we're going to cover apply to an arterial line as well. So the first one is an air embolus. That's why we put the patient in Trindellinburg in order to float a pulmonary artery catheter. That's also why we make special efforts to ensure that the monitoring tubing is free from air bubbles. There are no air bubbles in the transducer and also that all the lumens of the catheter are flushed prior to insertion. If an air embolism is suspected then the patient needs to be turned to the left side with head down and just so you know that is called Durant's maneuver. And then of course administering oxygen. Arterial puncture during venous cannulation that certainly is a possibility in patients that we are inserting a pulmonary artery catheter into because when you think about anatomy you think about the fact that the carotid artery and the jugular vein they kind of share the same sheath, the same covering. They're side by side and so indeed you could inadvertently puncture the carotid rather than the internal jugular. Now again we look at the type of flow that's coming out. Is it bright red and pulsatile then we think about carotid versus you know kind of more of a venous flow which is non-pulsatile. However, what if you have somebody which is your typical critical care patient that's crashing and that is you know somebody who is trying to get the right to get the right that has like not much of a blood pressure and their oxygen level is really low. So their saturation is real low. Well now the blood doesn't look bright red and it's not very pulsatile because the patient doesn't have much of a pressure. Well when in doubt pull it out and start again or you know think about other ways that you can assess. For example if we hook it up to our pressure lines are we getting an arterial or a venous waveform? If we're getting an arterial waveform we know we're in an artery. So again that arterial waveform is what? Sistally and then as it comes down we have a dichotic notch and then diastole versus a small little undulating waveform which would be venous. Now remember if this person is profoundly hypotensive in order to pick up on an arterial waveform if it's chosen that you're going to hook this up to the pressure tubing to see what kind of waveform it is you may have to change your scale if somebody has a real low blood pressure in order to be able to discern whether the waveform looks more arterial versus venous. Also balloon rupture balloon rupture is definitely a possible complication in using a pulmonary artery catheter. Yes the balloon is tested prior to insertion that's just common in best practice to do but at any point the balloon can be ruptured. Now typically I mean according to manufacturer recommendations the time that the catheter should be in at most is 72 hours and it's very commonplace for the manufacturer to say that the balloon is going to last for about 72 inflations. So you know just keep that in mind keep in mind also that it's plastic. We don't want to over inflate the balloon stop injecting the air as soon as you see a change from a pulmonary artery waveform to a wedge waveform and I need to mention here that you are going to wedge the catheter based on what your facility policy is. It's very commonplace for facilities to say we do not inflate the catheter tip. We do not do wedges. It is the resident or it might be the doctor or we don't wedge the catheter tip unless we have a doctor's order and that's fine too. Know what your policy says as to whether or not you inflate that catheter tip. Now going back to the CCRN keep in mind that on the exam they will expect you to know things about wedging the catheter tip even if in your specific facility it's not policy to do so. So we're only if we're allowed to we're only inflating until we have a change in waveform from pulmonary artery to the small little undulating waveform of a wedge. So if we're finding for example that we require very little volume in the balloon in order to go into the wedge waveform say we only put a half a CC in this balloon that actually can take up to 1.5 CCs. Now we only put in a half a CC and we're already in wedge position. What that suggests to you is that the catheter is starting to migrate and on the exam they're going to expect you to be able to recognize when a catheter migrates into a wedge position spontaneously because keep in mind as I said before the catheter's plastic. So we're putting something plastic into a human that is 98 plus degrees. Well when you put plastic into something 98 degrees it's going to warm up real nice and warm and it's going to soften and as this catheter softens you run the risk of the catheter tip migrating into a wedge position spontaneously and you get a wedge waveform without even wedging the catheter tip. Now if that is the case do not inflate the balloon. If that catheter tip has migrated into a small vessel and you see a PA all of a sudden go into a wedge do not inflate the catheter tip. I've had more than one nurse over the years say well I would just kind of put a little air in it see if I could pop it out. Well you're not going to pop it out the only thing you're going to pop is the patient's pulmonary artery. So it needs to be pulled back it needs to be repositioned because otherwise the patient is going to wind up with pulmonary infarct and we're going to be talking about pulmonary infarct in just a few moments. If your balloon does rupture and you would know that because you know you're trying to put some air in the balloon and to change it from a PA to a wedge waveform and you meet up with no resistance whatsoever the plunger goes in without any resistance that you feel on the other end and also you don't see a change in waveform then you need to think about that balloon as being ruptured. It should be labeled as such and it should not be used again and so then you know you're going to use the PAD as your trending measure the pulmonary artery diastolic which for many facilities who by policy don't allow wedging of the catheter tip they trim the PAD anyhow so it's a good trending measure when either you don't have a wedge or are unable to wedge the catheter tip. Clotting that can happen in the catheter so that's why we maintain our monitor tubing our tubing that we pressure tubing is the word that I was looking for that we hook up to our lines and whether you plan on it or not that transducer is typically going to deliver three to five CCs of flush fluid every hour and that's aside from any point at which you actually flush the tubing so if you have three transducers you're going to be giving 15 CCs of fluid per hour without you even doing any extra flushing so there's a strain gauge inside the transducer that allows for this little intermittent flushing to take place to keep the pressure line patent so if you do feel you have a clot and you've got a very dampened wave form again referring to your facility policy first to see what the the policy is around that you can pull back on and aspirate from the catheter in order to try and remove the clot and then see if you're able to flush using the manual flush device you are not using a a syringe to push into flush you're only using the flush device on the transducer in order to try and flush the line how about disrhythmia is disrhythmia is can certainly occur disrhythmia is can occur upon catheter insertion when you're moving from through that right ventricle and out into the PA and you know there's a couple of different reasons why you're provider once they get in the right atrium will inflate the catheter tip during insertion and one is it is a flow directed catheter so flow along with an inflated balloon will help kind of propel it forward but also the other thing is is that when you inflate that balloon it prevents the catheter tip from kind of stabbing at the right ventricular endocardium which could precipitate PVC's V-TAC irritable rhythms so it's also a nice touch to know when you're putting in a PAC you need to know kind of what your patient's K is right so do we have an irritable mild cardium from the get go maybe we need to bump up the K before we float in the pulmonary artery catheter your eyes need to be on the monitor during catheter insertion so that you can monitor for arrhythmias you can record opening pressures always nice to print a waveform while the catheter's going in so you can not only have documentation of opening pressures but also the waveforms that correlate with that and then keep in mind I just have to say one more time the accuracy of your pressures is only as good as whether you have prepared them to be so in other words your transducers at the phlegmestatic axis there's no bubbles in the system you've performed the the square wave test and you have only a couple of oscillations at the end of the squared wave test and you have all of your connections tight, no air bubbles and so on. Now another thing that we have to keep in mind during insertion is that and this is particularly kind of scary if you have somebody that has a left bundle branch block and that is when you enter in over on the right side of the heart over in the right ventricle you can close an intermittent right bundle branch block. So feature this for a second. Here you've got a patient that has a chronic left bundle branch block and now during pulmonary artery catheter insertion you've caused a transient right bundle branch block. So what does the patient have left guys? What they have left is perkingee fiber conduction at a rate of 20 to 40 per minute. So again having you know code card available, having precautions in place in case that that occurs and you know the nurses that know this best are the nurses in the cath lab that prepare for the possibility of this happening. Now sometimes we can have a catheter that has been placed in life is good and it's kind of business as usual and all of a sudden you start seeing what looks like a waveform that looks like V-tack and the catheter tip has slipped back into the right ventricle and you know that because you kind of lost your dichotic notch which was visible before in your PA and also the diastolic component of your waveform has dropped way down. So let's say for example you've just gone from a PA of 35 over 15 to now this wide bizarre V-tack looking waveform that is 35 over 2. So it looks like your catheter tip most likely has slipped back into the right ventricle. Your first intervention around that is going to be inflating the catheter tip. Now what we're doing by inflating the catheter tip is we're hoping that all the planets are aligned and that flow will grab on and just kind of guide that catheter tip back out into the PA. That's like if all the planets are aligned it doesn't always work out that way but we sure hope that it that it will. We can turn the patient over on their left side and and hope that it floats back out into the PA and that our waveform goes back to the 35 over 15 that it was before. So that's our hope but in addition to that we are inflating the catheter tip so that we don't have this catheter tip stabbing at the endocardium which could precipitate PVC's, V-tack, V-fib, all kinds of ugly looking dysrhythmias. So if we can float it back out there you know again we are not pushing in on the catheter. We are not repositioning it manually that is a provider that does that. Our nurse practice act does not cover us for advancing the catheter tip. We're just hoping that by inflating the catheter tip blood flow will drag it back out into the PA and if it does not guys we've got to get somebody to the bedside to reposition the catheter tip and if we don't have that available to us and the patients having PVC's we will need to deflate the catheter tip so deflate the balloon and pull the tip back into the right atrium if the patient is having arrhythmias as a result of it slipping back into the right ventricle. So again we inflate the balloon hoping it will float out into the PA if we can't get anybody to reposition the catheter tip and we've turned them on their left side we've tried the coughing we have tried everything that we know and we can't get it back out into the PA then we're going to have to deflate the balloon and then pull the tip back into the right atrium especially if that patient is having ventricular actipy as a result. This is very commonly by the way guys a CCRN question. Okay, embalye if you you know feel as though there's a clot again we're going to aspirate we're not going to push excegnination. Well this is why we're going to make sure that we have our transducers and waveforms visible to us. This is particularly true you know when you're thinking about somebody that has an arterial line in place that waveform and that pressure should always be displayed because if it's not and you have a disconnection excegnination is certainly a possibility. We could also have hematoma at the site that's definitely a possibility. Infection after all we're putting in a central line. If we're not using an internal jugular approach for the insertion of the pulmonary artery catheter and we're using a subclavian approach we have potential for pneumothorax so following the line insertion with the chest x-ray is extremely important as well. Pulmonary artery rupture there are lots of patients that are just like sitting duck set up for this to happen and that would include the elderly patients that have pre-existing pulmonary hypertension so you know the COPD is definitely come to mind. Patients receiving anti-coagulation, fibrinolidic or platelet inhibition therapy, patients that are hypothermic or postcardiac surgical patients. Now some ways that we can prevent that is we're only going to inflate the balloon to the maximum amount that it can no more than that right and that's only if we are allowed to buy our facilities policy so we're not going to inject any more than the maximum amount and we're not going to hold that amount in for any more than 15 seconds because we could cause as a result of this we could cause pulmonary artery rupture we also could cause a pulmonary infarction. Now how is it that we would recognize that somebody has a PA rupture? Well what we would see is sudden onset of hemoptosis along with dysmia and hypotension. Also we could see pulmonary infarction as a result of the catheter migrating into a spontaneous wedge position and what we would see associated with this is chest pain, dysmia and decrease in O2-SAT. Cyrombosis is the last one I just want to mention and I want you to think about an arterial line at this point. I want you to think about the person that develops thrombosis and all of a sudden starts developing cool fingers and also develops a modeled appearance to the hand and the nail beds think thrombosis at that point try to aspirate if you can't get anything out chances are I mean your waveform is going to be dampened. The catheter needs to be removed the arterial line catheter needs to be removed the provider notified and we need to follow up with some very close observation thereafter checking pulses seeing if we have reestablishment of warmth and color worst case scenario phybrinolytic therapy or embelectomy could be required. Well everybody this is the end of episode eight. Thank you so much for joining me. Please head over to my website and subscribe and in the meantime be thinking about episode number nine. Episode number nine will be putting together the waveforms with the numbers with all of the information we've talked about in the last couple of episodes. We'll be putting it all together in episode nine so I look forward to working with you then take care. Bye bye.