Hemodynamics is a 12-Letter Word! An intro to the basics. Part III: Stenosis and regurgitation

Jon E. Jenkins, RN, RCIS, Skaggs Community Health Center, Branson, Missouri
Jon E. Jenkins, RN, RCIS, Skaggs Community Health Center, Branson, Missouri
Certainly with the continued improvements in ultrasound technology, we often know prior to cardiac catheterization if a patient has valvular dysfunction. We often know the degree of severity as well, since ultrasound can measure velocities, areas and pressures. Some of you may have wondered why there is a need to even perform right heart catheterizations or pullbacks anymore with the advances in ultrasound technology. There are many reasons, but let's consider a couple of common scenarios. Often a patient is diagnosed via ultrasound with severe enough regurgitation or stenosis to warrant surgical repair or replacement. In this situation, the reason for performing a catheterization is two-fold. We need to do angiography in order to ensure the patient does not have coronary artery disease that would put them at risk for anesthesia, and the right heart catheterization to support/confirm the finding of the ultrasound. Another important scenario arises as a result of patient symptoms. Ultrasound can be very technique-dependent. If a patient has had an ultrasound showing no valvular pathologies or mild pathologies, yet is still experiencing symptoms of regurgitation or stenosis, then it may be the decision of the physician to proceed with a right heart catheterization. Sometimes a small area of the valve, perhaps just one leaflet, is incompetent or stenotic. This creates a small jet of blood either being regurgitated or impeded, which might have been missed by the ultrasound. Measuring pressures and waveforms in the cath lab allows us to get another look at what is occurring. Stenosis What is happening when a valve becomes stenotic or incompetent? We will discuss the results, as the causes are many for either situation. A stenotic valve can be thought of as a narrowing of the opening, similar to what we see in coronary arteries, i.e., a stenosis. Try this experiment. Get a garden hose and a drinking straw of the same length. Now, take a deep breath and exhale all the air in your lungs as forcefully and quickly as you can through the garden hose. Notice that it doesn't provide much resistance and the air can be expelled quickly. Now do the same thing, only through a drinking straw. Take note of how significantly more pressure is required to try and force the air through the straw. Plus, it takes more time. In addition, if you put your hand at the end of the straw and hose for each of these experiments, you will notice that from the straw, the air is more directed and of higher velocity. With a garden hose of the same length, the air is clearly more dissipated. The straw is an example of a stenotic valve. The garden hose represents a normal valve. There are a few things we need to understand from this experiment. What will be the effects of a stenotic valve on the heart? The stenotic valve (straw) requires more pressure to expel the blood. If you blew through both the hose and the straw for the exact same amount of time, you would not empty your lungs as completely through the straw as you would through the hose. A stenotic aortic valve, for instance, will require the left ventricle to generate more pressure in an attempt to empty the chamber. At first, the left ventricle will try and compensate to meet the demands of the increasing pressure. The ventricular muscle will hypertrophy (thicken) under the increased workload, just as when we lift weights our muscles will get larger and stronger. At the end of systole, the ventricle is unable to get all the blood out of the chamber through the stenotic valve, therefore leaving a higher volume and higher pressure in the ventricle at rest. Compensation occurs for a time, but eventually the ventricle will become dilated due to the increased pressure and workload. A dilated ventricle will not be as efficient. The physiology behind this is detailed and goes to the cellular level, so we will not discuss the reasoning here, but essentially, the ventricle will lose elasticity. Think of a worn-out rubber band that doesn't snap back as well as it used to. (This also is related to Starling's Law.) One additional long-term effect of aortic stenosis is a dilated aortic root, caused by the long-term jet (think of a wand at a car wash) of high pressure going into the aorta. The aorta has an elastic property to it which softens the sudden ejection of blood from the ventricle. If a high-pressure jet resulting from aortic stenosis is present, the aorta will stretch and dilate. Take a balloon and work on one area of it, stretching and stretching, back and forth. After a while, the elasticity of that area is decreased. When you try blow up the balloon, a herniation will occur because that area is weaker. How do we identify these conditions in the cath lab? To be honest, we may be approaching this question in a backwards fashion, as typically we would learn all the components of each waveform before attempting to identify pathologies from waveforms. However, it is not necessary to know the individual components of a waveform to identify stenosis. All that is required is to have two pressures to compare against one another. For regurgitation, you need one waveform and only need to identify two components. (Note: There are other ways of identifying these pathologies. You can certainly identify stenosis with a single waveform, but the intent of this article is to keep it simple. There are advanced techniques one can perform, but we will not discuss them here.) In order to identify stenosis, you need two waveforms: the one preceding the valve in question and the one following the valve in question. In order to identify aortic stenosis, you need a left ventricular waveform (preceding) and an aortic waveform (following). When we look for stenosis, we are looking for a gradient. A gradient is commonly identified as a graded change in the magnitude of some physical quantity or dimension. Simply put, it is the difference between the two pressures. In evaluating the aortic valve, we will look at the difference between the systolic pressures of the left ventricle and the aorta. Why the systolic pressures? It is when the aortic valve is opened. Stenosis is a narrowing, impeding the blood flow out of one structure into the other. Blood flows from one structure to the other when the valve is open. If we go back to Part I and look at the Wigger's diagram, the aortic valve is open during the systolic ejection period. If you put a kink in a garden hose, you don't know if the kink is impeding flow unless the water is turned on. Likewise, we look for stenosis (the kink in the hose) when the blood is flowing from one structure to the other (water turned on). There are two common ways aortic stenosis is identified in the cath lab. One way is doing simultaneous pressures. The other is doing a pullback measurement from the left ventricle to the aorta. Figure 1 demonstrates an example of aortic stenosis utilizing a pullback method. The catheter is placed into the left ventricle, recording started and then pulled back into the aorta. For stenosis we will compare the systolic, or peaks, pressure. In Figure 1, you can see the first tall peaked waveform is the left ventricular (LV) pressure and the systolic pressure is about 120mmHg. As the catheter is pulled back into the aorta, the systolic (peak of the triangular waveform) pressure drops to about 95mmHg. The gradient is the difference between the two pressures, so in this example, the gradient is approximately 25mmHg. We want to reiterate that the systolic pressures should be the same in a normal situation, as it is a time when the valve is open. We learned in Part I (March 2007) that when the valve is open, the pressures should be equalized. Figure 2 shows the other common method of diagnosing aortic stenosis. This is a two-transducer setup. The catheter in the left ventricle setup is on one channel and the second channel is connected to the side-port of the arterial sheath so you will see simultaneous tracings of the left ventricle and the aorta. (A side note on measuring pressures through the sheath with a catheter in place: it is recommended that you oversize the sheath by one French size to obtain an accurate pressure measurement. If you have a 6Fr catheter in the left ventricle, you would have a 7Fr arterial sheath. The premise is that if you have a 6Fr catheter in a 6Fr sheath, dampening of the pressure may occur as the catheter plugs the sheath, so to speak.) Figure 2 shows simultaneous pressures (meaning they overlap on the screen and are being recorded at the same time). Notice the peak of the arterial waveform is lower than the peak of the ventricular waveform. The difference is the gradient. If this were a 200mmHg scale, the gradient would be approximately 40mmHg. The next question is, what is a significant gradient? Unfortunately, the answer to that question cannot be satisfied by what we are studying here. Significance of a gradient is based on symptoms, other findings and the measurement of the valve area. The valve area is calculated by your hemodynamics system and is as based on cardiac output and body surface area. It is important to learn how to calculate valve areas and we may include this in detail in future installments. The standard method of calculating an aortic valve are is called the Gorlin formula or equation. It involves quite a few elements and is beyond the scope of this article. There is, however, a simplified version called the Hakki equation or formula. This equation states that the valve area is approximately equal to the cardiac output in litres per minute, divided by the square root of the peak gradient. Let's say we have a patient with an aortic pressure of 120/60, LV pressure of 170/15, cardiac output of 3.5 liters/minute. What is the aortic valve area? You would take 3.5 divided by the square root of 50 (peak gradient is 170 minus 120). This would give you a valve area of approximately 0.5cm2. The normal adult aortic valve opening is 3.0-4.0cm2. Aortic stenosis becomes hemodynamically significant when the area is about 1cm2 to 0.8cm2.1 What we have just learned can be applied to the right side of the heart as well. Just a re-labeling of chamber and waveforms is needed. To measure the pulmonic valve gradient, we would need a right ventricular waveform and pulmonary artery waveform. Look to see if there is a gradient or difference between the systolic pressures just as you do for the aortic valve. Normal pulmonic valve area is 2.5-3.8 cm2.2 Let's look at the mitral valve. Any time we talk about stenosis, we are looking for a gradient. In order to have a gradient, we need two waveforms to compare. For the mitral valve, we need the left atrial waveform (preceding the mitral valve) and the left ventricular waveform (following the mitral valve). Remember, we do not enter the left atrium, so the pulmonary capillary wedge pressure (PCWP) reflects the left atrial pressure. The stenosis is going to impact the blood flow when the valve should be opening fully. From our study of the cardiac cycle and Wigger's diagram (Part I), we know this is a comparison of the PCWP and the left ventricular end-diastolic pressure (LVEDP). We compare the mean PCWP with the LVEDP. You can measure these pressures either simultaneously or individually. For demonstration purposes, we will look at simultaneous analysis. If you were measuring them individually, you would find the difference between the LVEDP and the mean PCWP. If the LVEDP was 5mmHg and the mean PCWP was 15mmHg, the gradient is 10mmHg. Keep in mind that at the LVEDP point on the cardiac cycle, the mitral valve is open, with blood emptying into the LV, so the pressures should be equal (refer to Part I if you need to review). Figure 3 shows simultaneous LV and PCWP (Figure 4 is a similar example, only on 50mmHg scale). The PCWP is consistently above the LVEPD pressure; there is a difference, a gradient. Normally, you would see the bottom line of the LV tracing and the PCWP tracing following similar paths and being equal. Mitral valve measurements are: Normal mitral valve area: 4.0-5.0 cm2; Symptomatic mitral stenosis: 1.4-2.5 cm2; Critical mitral stenosis: 2.3 For tricuspid stenosis, you simply change the chambers and tracing to RA and RV. Normal tricuspid valve area is 8-10 cm2.4 For tricuspid stenosis, you simply change the chambers and tracing to right atrial (RA) and right ventricular (RV). Normal tricuspid valve area is 8-10 cm2.4 Regurgitation Let's discuss how to identify regurgitation. The causes and variations of valve disease are numerous, but the great thing about regurgitation is that the effects are similar to stenosis. When you think of regurgitation, think of a leaky valve. Think of a soda lid you get at a gas station. If you fill a cup and put a new lid on it without piercing the slots for the straw (leaflets) you can turn it upside down and not spill the fluid. Now if you pierce the cutout with a straw, remove the straw and turn it upside down, it will leak. The pierced, leaking lid is like a regurgitant valve. Let's look at the mitral valve, between the left atrium and left ventricle. Normally, the valve opens to allow blood from the atria into the ventricle. As the ventricular pressure rises, it slams the mitral valve shut and opens the aortic valve, forcing the blood out into the systemic circulation. If the mitral valve is regurgitant, then as the ventricular pressure rises, it still shuts, but not completely. As a result, a portion of the blood that is supposed to go to the systemic circulation is allowed back into the left atrium. We learned earlier that higher than normal volume and pressure have negative effects on the chambers of the heart. Over time, the left atrium will hypertrophy in order to compensate, and then eventually dilate and become less efficient and less elastic. Two components on the atrial waveform need to be identified. These are known as the a wave and v wave. The a wave is formed by the increase in pressure during atrial contraction. It correlates to the P wave on ECG. The v wave is formed during late atrial filling as blood continues to fill the atrium. It occurs just after the T wave on ECG. Two things to keep in mind are: 1) Are the waves in correlation to the ECG?; 2) Know that if you have simultaneous pressures, the V wave will be on or near the downslope of the ventricular waveform (the big wave you see on Figure 5). It's also important to note that when we evaluate the mitral valve, PCWP will be considered as a reflection of the LA pressure. The waveform will be delayed slightly from the ECG. Electricity moves faster than fluid, so the ECG will show atrial contraction just before the hemodynamic waveform will reflect the same. Especially from the wedge position, as now distance from the LA has to be taken into account. As one Cath Lab Digest editorial board member explains to his staff (and was kind enough to share with me), it is like throwing a rock into the middle of a pond. The rock hits the water in the center and creates waves, but it takes the wave a few moments to reach shore. By the time we can see the waves near shore, it is delayed from the actual event. Likewise, when the atrium contracts, there is a delay in transmitting that rise in pressure to your screen. The wave has to travel to the PCW position, through the catheter to your transducer. When looking at an atrial waveform (RA or PCWP), there will be two primary positive or upward waveforms (there is another positive wave called a c wave, but it is of no consequence to our discussion here). First, identify which wave is which. Correlate with ECG or LV waveform if provided. How does regurgitation influence a waveform? If regurgitation is present, it will be identified during the time the valve should be closed. In the instance of the atrial valves, it is when the ventricles are contracting. The valve closed to prevent the ventricle from forcing blood back into the atria. If the valve does not close, what happens to the volume and pressure of the blood in the atria during ventricular contraction? It should rise dramatically! To identify regurgitation, we should see a dramatic rise in pressure where there should be none. Remember where your catheter tip is. It is in the atrium, so if the valve doesn't close completely, you will get a sudden rush of volume and pressure from the ventricle. Figure 5 demonstrates mitral regurgitation on a 50mmHg scale with simultaneous LV pressure. Notice the large peaked waveform overlapping the downslope of the LV pressure. That is a very large v wave. Normally, the v wave represents the filling of the atrium from the lungs, but introduce a bad valve and now the volume and pressure are affected by the LV. Figure 6 shows the same scenario of mitral regurgitation, but without the simultaneous LV pressure. Notice the very small a wave just before the large v wave (labeled). For comparison, see Figure 4 for a normal atrial waveform. Typically the a wave and v wave are of similar magnitudes, similar peak pressures. In the case of a regurgitant valve, the v wave is larger. The best thing we can recommend is to start looking at all your waveforms when working in the cath lab. Consider printing them off from every case and start identifying the a waves and v waves. Ask experienced staff to help or even the physicians to aid in the identification. What you will find is a high variability among patients, resulting from the influence of inspiration/expiration, contrast in the pressure tubing, atrial fibrillation, etc. Once you can confidently identify the a wave and v wave, you can then assess if the v wave is large or elevated. In Part IV, we will be unpacking all the waveforms and learning to identify each component of the waveforms and what they represent. Looking at waveforms in the cath lab will be good practice until then and may help in your understanding regurgitation. Once again, if you want to look at the tricuspid valve, simply change the chambers and waveforms. Finally, let's review regurgitation involving the aortic or pulmonic valve. Our figures focus on aortic regurgitation, which is a little different. We are not looking at an increase in pressure anywhere; rather, a decrease or continuing fall of pressure. Let's start with a leaking aortic valve. In the cardiac cycle, the left ventricle begins to squeeze, increasing in pressure until the aortic valve opens. The blood is forcefully ejected into the aorta and continues until the volume and pressure of the ventricle decrease to below the pressure of the aorta and the aortic valve shuts. Normally when looking at the aortic pressure, we see a triangular waveform begin to rise. As the aortic valve is opened, the ventricular and aortic waveforms are the same until the blood stops coming from the ventricle and pressure falls. At this point, the aortic valve shuts, aiding in maintaining enough pressure in the aorta and systemic circulation to perfuse the body. The ventricle continues to fall in pressure until the atria begin to fill it again. The closing of the aortic valve is what keeps the aortic pressure from going all the way to the bottom of the pressure scale as the ventricular waveform does (i.e., aortic pressure is 120/80 versus ventricular pressure is 120/5). If we had no aortic valve, the aortic pressure would look just like the ventricular pressure. So if the aortic valve keeps the aortic pressure from falling too low or all the way to the baseline, what does a leaky valve do? It will allow the aortic pressure to fall further during diastole (the bottom number or the trough on the waveforms) below what is normal. Once the aortic valve closes normally, think of the aorta as a pressurized system, like a water line in your house. If you have a leak in the water line, the pressure will fall below what is normal. When trying to identify aortic regurgitation by waveform analysis, we look for a wide pulse pressure width (a large difference between systolic pressure and diastolic pressure; officially, Corrigan's wide pulse pressure). Instead of a normal pressure of 120/80, we might see a pressure of 120/40. Figure 7 shows a wide aortic (AO) waveform from top to bottom. It goes down further than what you would expect. A unique aspect of this condition is that this wide pulse pressure becomes amplified the further into the periphery you go. When assessing a femoral pulse, you may be able to identify what is called a water hammer pulse. Instead of feeling a nice normal pulse, you may feel a very hard, throbbing, bounding pulse. It's caused by the hard/nothing, hard/nothing biphasic pressure rather than the normal hard/medium, hard/medium biphasic pressure. Aortic regurgitation is easy to identify by its wide span of systolic over diastolic pressure. Please note that another condition that can cause a wide pressure width is calcification of the aorta, so every time you see a wider than normal pressure width, it may not always be aortic regurgitation. A calcified aorta loses compliance, not softening the forceful ejection ventricle, and therefore transmitting that all-then-nothing ejection by the ventricle. To identify pulmonic regurgitation, simply change the chamber and waveform to pulmonary artery. A Final Note We hope this has helped the reader gain some basic understanding and knowledge of the identification of common valvular dysfunctions. It is difficult, and we urge you to persevere your efforts to understand this material and in soliciting other knowledgeable staff to help you. There are many variables that can affect waveforms. Adding rhythm disturbances makes things even more difficult. Just be aware that in order appropriately diagnose and treat patients that physical findings on assessment of the patient (i.e., systolic/diastolic murmurs, ECG, symptoms, etc.) will need to be correlated with the hemodynamic findings. Stay tuned. Part IV is going to be good. We will return to normal waveforms and start unpacking what each component represents. We will address a waves, c waves, v waves, x and y descents, dicrotic notches and much more. Acknowledgments. We want to say thank you to Wes Todd for the use of his resources in compiling these articles. Wes has been a friend to the cardiovascular world for years and if any of our readers are seeking good study materials and wanting to prepare for the RCIS examination, Wes has excellent resources available at www.westodd.com. We also want to thank the review board for Cath Lab Digest. Their input has helped shape the content of these articles. Thanks to editor Rebecca Kapur for turning our Ozarkian language and grammar into something publishable. Finally, we appreciate all the emails and input we have gotten from you, the readers. This input is valuable to future installments and allows us to attempt to address the needs of cath labs and their staff. Part II Correction: We need to issue a clarification to the previous installment (Part II, May 2007). In the last section of Part II, we discussed dampening. The statement was made that true dampening can be differentiated from when the catheter tip is simply up against the wall of the artery. What needs to be clarified is that if the catheter tip is completely occluded when up against the arterial wall, then the pressure will be essentially zero, as is the case with dampening. So in fact it is not possible to differentiate this scenario. The intent of the statement was referring to what is typically seen in everyday practice. Generally, when the catheter is against the wall, it will not be completely occluded and this instance results in that squared-off waveform to which we were referring. We appreciate the attentive readers who pointed this out. Jon Jenkins can be contacted at jejenkins @ skaggs.net
References1. Matthews RJ. Cardiology Definitions. Accessed June 26, 2007. Available at: http://www.rjmatthewsmd.com/Definitions/aortic_stenosis.htm2. Caminos OW. Congenital Heart Diseases, Their Study and Treatment. 1999: MCI Publications. Accessed June 26, 2007. Available at: http://www.redtail.net/owc/3.html3. CTSNet: The Cardiothoracic Surgery Network. Mitral Valve Disease. Accessed June 26, 2007. Available at: http://www.ctsnet.org/doc/44704. Healthworks, Inc. Online Courses. Pathophysiology: Cardiovascular diseases and their clinical significance. Accessed June 26, 2007. Available at: http://www.healthworksonline.cc/ education/courses/PAT01/1.cfmSuggested Reading1. Todd JW. Todd’s Cardiovascular Review Book Volume I: CV Science, Patient Care, Anatomy, Physiology, and Pathology. 4th Ed. Spokane, WA; Cardiac Self-Assessment. Available on www.westodd.com2. Kern MJ. The Cardiac Catheterization Handbook. St Louis: Mosby, 2003.