Down and Dirty: Basic Heart 101

Gerard Lagasse, RCIS, Borgess Medical Center, Kalamazoo, Michigan

Gerard Lagasse, RCIS, Borgess Medical Center, Kalamazoo, Michigan

I recently had the good fortune to attend TCT 2005 in Washington, D.C. At the opening session of the nurse and tech conference, I could not help but notice that there were less than five hundred people present. Of those present, I talked to directors, managers, educators, sales representatives and educators, research staff and other conference attendees. I even spoke with two young ladies from Lewiston, Maine who had been in the field for about two years. (I’ll come back to the young ladies later, because they are, in a way, the reason for this article.) My experience at TCT helped me realize how few attendees actually represented working in-the-lab staff and how few of these staff had been given a chance at the fantastic learning opportunity offered by TCT. Today there are (at least) 1,500 cath labs in the United States. When I thought about the two young ladies coming from Lewiston, I also thought of the two staff coming from my hospital. I sensed that the sending of two staff per hospital was the norm. If you subtract attending directors, managers and other ancillary staff, then halve the remaining attendees by two, the resulting numbers are disappointing. The low numbers of hospitals actually sending staff to TCT is one example of how education has become a lower priority for working staff in this country. In 1992, there were 22 nurse educators employed full-time by my hospital. As of 2002, there is now one full-time educator left. In order to survive in this day and age of Medicare cuts, insurance discounts and companies dropping health benefits, hospitals have had to seriously cut corners just to survive. Unfortunately, one of the easiest corners to cut is education. It is not just my hospital, but I imagine, the fate of many hospitals in this country. Today, hospitals expect staff education to have been acquired while in school, from the dribble-down concept (an experienced staff person gets a new staff member and passes on his/her knowledge) and medical company inservices. The only problem is that nursing, EMT, pulmonary, exercise physiology and radiology schools do not teach cardiology at the level required for the cath lab. The dribble-down concept doesn’t work when the proctor himself has little basic cardiology knowledge from his own initial dribble-down training. As for company inservices, they are there to educate the staff on one thing the wonderful properties of the company’s product. New staff are quickly trained on balloons, wires, catheters, emergency procedures and how to create reports with the idea that they know the heart; after all, they are medical professionals and received the basics somewhere in their past (over thirty years ago for me, which really seems like a lifetime ago). I was a student of cardiopulmonary technology at Grossmont College. I learned the basics of heart operation in a cardiopulmonary setting. Today, there are too many cath labs and not enough trained (cath lab-trained) staff, so many hospitals hire medical professionals to work in the cardiac cath lab who lack essential knowledge to make the transition to the cath lab smooth and professional. Staff being hired are RTs (we have two), nurses, EMTs, pulmonary techs, exercise physiologists (we have three) and even transport personnel (we have one) who have shown an interest in cardiology. How do these personnel get the basics? At our facility, I usually wait until the preceptor feels the staff member is ready, then I give the staff member a quick down and dirty lesson, which involves taking the staff member to the break room and giving them an afternoon session on the heart. It is quick because a busy lab such as mine (over 6,000 patients in four labs last year) does not give us the opportunity of days or weeks to get a staff member up to speed. Down because we know we don’t have much time, so we better get to it. Dirty because I don’t refer to books, graphs, videos or computers, but instead use a couple of felt-tip markers and a pad of blank paper. The two ladies at TCT from Lewiston, Maine, that I mentioned earlier, are both RTs who had worked in the lab for two years. Talking to these two ladies reminded me of a recent class I had given to a new staff member. His name was Neb. Neb’s answers in the following exchange are not unique, but sadly, usual and expected: Gerry: Neb, when does the left ventricle start to contract? Neb: At the start of the Q-wave. Gerry: All right, then when does the heart stop contracting? Neb: At the onset of the S-wave. Gerry: Neb, what happens at the T-wave? Neb: Ventricular re-polarization. Gerry: All right, then what happens in the left ventricle between the S-wave and the T-wave? Poor Neb was left with his mouth hanging open. He didn’t know the answer. He just didn’t know or hadn’t thought about what happened in the left ventricle between the time of the S-wave and onset of the T-wave. I have had this happen to me too many times to think this is a Neb-alone problem. Neb is a new staff and is in his forties. He is a nurse with over 20 years experience, many spent in critical care, and with the last ten years in the ER. Neb fell into common and false assumptions on heart function that I have heard over and over for years from new staff. The misconceptions begin with a lack of understanding of the devices used to monitor heart performance during a procedure. We work in the computer age. We have computers at home attached to printers, routers, scanners and other peripherals. We walk into the cath lab and look at monitors, printers and peripherals. We observe EKGs, record pressures and type cath data in a procedural report. Staff are quickly trained to know catheters, wires, and stent sizes, and yet, the basics of cardiology are forgotten or overlooked. We look at pressure traces, oxygen levels and pressure changes, and most importantly, the video image of coronary arteries, meanwhile forgetting, not knowing, realizing, appreciating or thinking about how the heart works. The Heart 101 Let’s think about the heart not as a complicated organ, but rather as a circulating pump in a closed fluid system (Figure 1). The heart is basically made up of two pumps in a series. The first receives the blood from the body and sends it into the lungs for the process of respiration. The blood then returns to the heart pump, where the second pump sends it to the body to supply needed oxygen for the cellular process of aerobic respiration (called the Krebs cycle). For simplification, let’s look at the heart as a series of boxes with flow in a left-to-right direction. These boxes or chambers are separated by valves that only work in one direction. Flow is always from left to right, directed by virtue of the valves separating the chambers. The valves only work in one direction and work off pressure. When pressure on the left side of the valve is higher than the right side of the valve, the valve will open. When pressure on the right side of the valve is higher than the left side, then the valve will close. Let’s call this the rule of valves. The amazing thing is that the four chambers of the heart are always in motion. These chambers are all doing something simultaneously and we observing this action by way of monitors looking at pressures and the EKG. The Monitoring Process: Amplifiers In each chamber of the heart, you are looking at two things occurring simultaneously. One is an electrical event and the other a mechanical event, with the electrical event creating the mechanical response. Monitors, in this case what we call EKG monitors, show the electrical events of the heart. We measure the pressures generated by the heart using a different monitor, called a pressure monitor. To accomplish this monitoring process, we use two different kinds of amplifiers. To measure the mechanical compression going on within the heart, we use a transducer and a DC amplifier. The transducer at the side of the cath table is basically a variable resistor attached to a small diaphragm. When the heart contracts, a pressure wave is sent down the arteries, through the manifold and onto the diaphragm inside the transducer. As the diaphragm is moved by the pressure wave, the mechanical resistor (variable resistor) attached to the diaphragm changes its resistive value. This change on the resistor is seen as an electrical voltage change in the attached DC amplifier. The signal is sent to the monitor as a changing pressure waveform. Definition of a DC amplifier: An electrical circuit that increases the power, voltage or current of an applied signal. The amplifier takes the received signal and amplifies it to usable measurable parameter. Figure 2 shows examples of inputs and the resultant outputs of DC amplifiers. One problem new cath lab staff often encounter is the fact that the electrical activity of the heart is monitored by a totally different kind of amplifier than the DC amplifier. The EKG that we are familiar with is amplified by an AC amplifier, performing in a completely different manner than a DC amplifier. An AC amplifier only amplifies voltage variations (Figure 3). If a voltage stays constant for any length of time, the amplifier sees no changes and the signal goes back to baseline. Figure 4 is copied from Cardiovascular Dynamics (fourth edition) by Dr. Robert Rushner.1 It is an example of a cell depolarizing, superimposed with the resultant EKG. The action potential was amplified using an AC amplifier. When the amplifier sees no voltage changes, the monitor shows us a drop to baseline on the EKG. As the cells begin to repolarize, we see a drop toward baseline on the cellular action potential. As the change occurs on the action potential, we see a voltage change on the AC amplifier and recognize it as a T-wave. The upper record represents the ventricular, intracellular potential during a complete cardiac cycle, and the lower record represents a standard electrocardiography lead. The numbers on the upper tracing are used to designate phases in the cycle; the upstroke, the brief spike, the plateau, the rapid recovery and electrical diastole, respectively. Warren G. Guntheroth, Pediatric Electrocardiography2 This article is not about EKG interpretation, but about the EKG and heart contraction. Figure 4 does a good job at showing what happens to ventricular action potentials as seen through an AC amplifier. However, it misses the fact that the same thing is happening at the atrial level, except that the muscle mass is smaller, so that equates to a smaller action potential as seen in the diagram in Figure 5. The point, however, is the same. An AC amplifier only shows voltage changes. It is great for diagnosing tissue in the process of change such as ischemic tissue, bundle branch blocks, infarcted tissue and other electrical changes. Newer staff are often not exposed to the concept of amplifiers, so they have difficulties in relating changing action potentials to what is happening in the individual chambers of the heart. To summarize an important concept, when the EKG shows ventricular depolarization (onset of the Q-wave), the ventricular muscle cells begin to contract. The ventricular contraction goes on up to the T-wave. At the atrial level, the atrium begins to contract at the onset of the P-wave, and this contraction lasts until the Q-wave. The atrial’s own version of a T-wave is lost in the QRS. Now let’s look at the electrical constriction of heart muscle and give it a name. This muscular contraction is given the name of systole, whether it is an atrial or ventricular contraction. When the repolarization phase begins, the muscle relaxes and we call this diastole. In Figure 6, the phases of heart contraction and relaxation are added as a bar graph. Notice: 1. Atrial diastole occurs throughout the whole ventricular systolic period. 2. The atrium and ventricle both share a period of time when they are both in diastole. 3. Atrial systole always occurs during ventricular diastole. 4. These periods of systole and diastole are occurring in the atrium and ventricle at the same time and not as separate events. Heart Anatomy Now that we have covered amplifiers, and the effects of an AC amplifier on electrical depolarization, let’s look at the real subject of our interest: the heart. We will keep it simple. The heart is part of the circulatory system. We have the circulatory system (arteries and veins coursing through the body), the heart, and the lungs. That is the whole circulatory system in a nutshell. When a drop of blood leaves the left ventricle it will return to the right atrium within twenty seconds. This statement was told to me years ago and I never forgot it. It sounds hard to believe, doesn’t it? Remember that the circulatory system is a closed system. The total blood volume of an average man is approximately 8 percent of his total body weight. Accordingly, for a 70-kg man the total blood weight equals 0.08 x 70 kg, which means that the total blood volume is 5.6 kg. One kilogram of blood occupies 1 liter, therefore: Total blood volume = 5.6 liters3 The dominant feature of the cardiovascular system is the pumping of blood by the heart. In a resting normal man, the amount of blood pumped simultaneously by each half of the heart is approximately 5 liters/min. During heavy work or exercise, the volume may increase as much as fivefold to 25 liters/min.33 An exercising individual would be moving .417 liters per second. The total volume of blood in the body returns back to its starting point in 14 seconds. Amazing, isn’t it? The circulatory system is a closed system whose sole purpose is to circulate blood to one place to get oxygenated, pump the oxygenated blood through the body and then return the blood to its original starting point. Figure 7 is a simplified version of the circulatory system. Essentially, there are two pumps in a series, pushing blood through the body. The right side of the heart pushes the blood into the lungs, where respiration takes place. The oxygenated blood then goes into the left side of the heart, where it is pumped to the body. In the cells of the body, the oxygenated blood is used in the Krebs cycle for the production of adenosine triphosphate (ATP). The right-side pump and left-side pump are mirror images of one another. Each pump has the same basic anatomical structures and cardiac output, with the only difference being pressure levels. The right side pumps blood into the low resistance of the lungs where millions of capillaries bring blood into close contact with the alveoli. The left side of the heart pumps blood into a vascular system in the arms, legs, head and organs which are more resistive to flow. The always-left-to-right flow through the heart is controlled by valves located between the individual chambers of the heart. The atriums act as reservoirs. They receive and hold blood during ventricular systole and with the onset of diastole, empty themselves into the ventricles. The ventricles eject their supply of blood during ventricular systole and then, during diastole, receive blood from the atria. The pulmonary artery and aorta become engulfed with blood during ventricular systole. These arteries are both made of smooth muscle that expands with the onslaught of blood. During ventricular diastole, these arteries keep pressure on the received blood through their stretched configuration, constantly helping to push the received blood on its way through arteries, arterioles, capillaries, venules and veins. Heart Valves in Action Now that we have the idea of heart anatomy, let’s look at diastolic/systolic periods in regards to the heart pump and the operation of heart valves. When a chamber of the heart is in systole, it is creating constrictive pressure. When a chamber of the heart is in diastole, then its pressure is negligible. When pressure is greater on the left side of the valve than the other side, then that valve will open. When pressure is greater on the right side of the valve than the left side, then the valve will close. Figure 8 shows the effects of the P-wave and QRS on the heart. With atrial systole, the pressure will be greater in the atria than in the ventricles, and the tricuspid and mitral valves will be open. In ventricular systole, the pressure in the ventricles will be greater while the atria are in diastole, so the tricuspid and mitral valves will close. For the pulmonic and aortic valves, the rule of valves also applies. Ventricular systole lasts only until the T-wave. While ventricular systole is occurring, the pressure will be greater in the ventricles than in the pulmonary artery or aorta. The pulmonic and aortic valves will be open. The moment ventricular diastole occurs, the pressure drops to near nothing in the ventricles in regards to the arteries and these valves will close. The EKG and the Pump Now let’s take the EKG and the diastolic/systolic phases of the heart and relate it to the pressures developed in individual chambers of the heart. We need to start somewhere, and what better place than at the onset of the Q-wave and the right ventricular chamber? Let’s look at what is happening to the valves the moment before the Q-wave. The atrium is in systole and the ventricle is in diastole. The tricuspid valve is open and dumping blood into the ventricle. The pulmonary artery, which is made up of smooth muscle, is engorged with blood from the previous ventricular ejection. The pressure is high in the artery, while again the ventricle is in diastole. The rule of valves applies and the pulmonic valve is closed. At the Q-wave, when the ventricle starts to contract, we see the right ventricular pressure slightly above baseline (Figure 9). At the Q-wave, the Purkinje fibers fire off in the ventricle and the tissue begins to contract. The Purkinje fibers are embedded toward the apex of the heart. The apex begins the contracting motion, causing blood to be pushed upward and outward to the atrium and the outflow tract of the pulmonary artery. The pressure in the ventricle begins to build as the chamber gets smaller. The pressure increase from the ventricular contraction causes the pressure to be higher in the right ventricle than the pressure in the right atrium, which is now in diastole. The tricuspid valve follows the rule of valves, and closes at point A (Figure 9). At this time, the pulmonic valve is also closed, because the pressure in the pulmonary artery is higher than the lower pressure of the ventricle. With no place to go (as both the tricuspid and pulmonic valves are closed), the blood continues to become compressed into a smaller and smaller area, and the pressure increases even more. At some point during ventricular compression, the pressure in the right ventricle suddenly becomes higher than the decreasing pressure in the pulmonary artery (1mmhg is enough). The pulmonic valve opens and blood rushes into the pulmonary artery and onward into the lung field. Looking at Figure 10, we see something strange. The ventricle contracts from the Q-wave to the T-wave, but looking at the pressure, we can see a flattened pressure curve during systole. As the heart is contracting around the blood in the ventricular chamber, the blood is leaving the ventricle and going into the pulmonary artery. While the heart chamber is getting smaller, the volume is also getting smaller. The net effect is a constant, flattened pressure seen on the systolic pressure curve. The T-wave occurs (ventricular repolarization) and the heart becomes completely relaxed (diastole). The pressure within the heart chamber drops to zero. This sudden drop in ventricular pressure causes a few things to happen (Figure 11). The pressure is abruptly lower in the ventricle than in the pulmonary artery. The pulmonic valve, following the rule of valves, closes. Meanwhile, the atrium has been filling with blood from the superior vena cava (SVC), inferior vena cava (IVC) and coronary sinus during atrial diastole. The volume of blood in the atrium has weight, which equates to pressure. This atrial pressure, however small in magnitude, is still higher than the pressure in the ventricle. It causes the tricuspid valve to open, blood rushes into the ventricle and ventricular pressure begins to go up. The pressure in the right ventricle keeps going up as the volume in the chamber continues to increase. Basically, when you have ventricular and atrial diastole occurring at the same time, the tricuspid valve is wide open and you have one common chamber. The pressure will be the same in both chambers. Suddenly, the P-wave occurs. The atrium contracts and the blood that is already going down into the ventricle gets an extra push on its way. The atrial kick gives another ten percent increase of blood volume to the ventricle and is seen as a bump in the pressure curve. The Q-wave occurs and marks the end of diastolic pressure. EDP (end of diastolic pressure) is measured at the point of the Q-wave. Let's look at the right atrium at the Q point (Figure 12). The atrium is just finishing its contraction (A wave) and is still slightly up at the X point. The ventricle begins its contraction. The pressure is suddenly higher in the ventricle than in the atrium and the tricuspid valve closes. The tricuspid valve, upon closing, has blood on both sides of the valve. As the valve closes, the blood on the atrial side of the valve is pushed back into the atrium, causing a slight increase in pressure in the atrium. This is called the V-wave on the atrial curve. With the tricuspid valve closed, the atrium begins to fill with blood that is returning from the IVC, SVC and coronary sinus, and you see a gradual increase in atrial pressure (Figure 13). Remember that the whole circulatory system is a closed loop system. While the atrium is sitting passively (diastole) at the beginning of the right ventricular contraction, the blood is being ejected out of the left ventricle during this same time. The blood being ejected out is displacing blood in the aorta, which in turn is displacing blood somewhere else in the perivascular system. When one drop of blood is being pushed out of the heart by the left ventricle, a corresponding drop of blood is being pushed into the right atrium at the other end. The atrium continues to fill up to the T-wave. At the T-wave, the ventricle starts its period of diastole and becomes relaxed. The pressure in the ventricle is suddenly less than the pressure in the atrium and the rule of valves comes into play. The tricuspid opens and blood rushes to fill the empty cavity. The pressure momentarily drops in the atrium as the volume of blood drops into the ventricle. Again, remember that when the tricuspid valve opens, there is essentially no valve between the atrium and ventricle. There is no resistance between the chambers. Essentially, there is one chamber on the right side of the heart. The ventricular and atrial pressure are one and the same. At the P-wave, the atrium contracts and there is a bump in our atrial pressure curve. Now let’s look at what happens in the pulmonary artery at the onset of the Q-wave. At the Q-wave, the ventricle is contracting quickly and generating increasing pressure in the ventricle. Suddenly there is a one millimeter difference in pressure between the pressure in the ventricle and the pressure in the pulmonary artery, which has been going down. The pulmonic valve opens, allowing for the escape of blood into the pulmonary artery. The pressure seen in the pulmonary artery mimics the ventricular systolic pressure (Figure 14). At the onset of the T-wave, the ventricular pressure suddenly drops toward zero. The pulmonary pressure tries to follow, but the elasticity of the pulmonary artery is generating more pressure on the blood than the pressure seen in the ventricle. The rule of valves comes into play and the pulmonic valve closes. The stretched pulmonary artery wants to return back to its relaxed state. It attempts to do so by pushing blood into a place of less resistance. The only place available is the pulmonary tree. There is a gradual decrease in pressure in the pulmonary artery as this blood is gradually displaced into the lungs. The end result is the pressure curves we have seen many times. The important thing to remember is that all these things are happening at the same time. The process for right-sided pressures happens exactly the same on the left side of the heart (and also happens at the same time). (Figures 15-16) How the Brain Affects the Heart Figure 17 shows numbers associated with a normal 20-year-old heart. If you look at the pressure curve above the boxes, you can see the similarity in some of the numbers seen in the individual boxes. A 10 diastolic pressure in the LV is the same as a systolic pressure in the LA, which is the same as a pulmonic diastolic pressure. What keeps those pressures at these particular values? It has nothing to do with the heart. Remember that the heart is part of a closed system that takes oxygenated blood from the lungs and delivers it to the body. The oxygen can then be taken and used in the Krebs cycle to create ATP, which is then used to power up the cells of the body in order to keep the energy-consuming body alive and functioning. This closed system is controlled not by the heart, but by the brain, which determines the pressure and oxygen levels required to keep itself and the rest of the body alive and functioning. There are sensors located within the body which send important information to the brain, called baroreceptors and chemoreceptors. They are located in the carotid arteries (both baro and chemo) and in the kidneys (baro only). The sensors tell the brain, which then directs the heart, how fast or slow and how hard to contract in order to keep the appropriate oxygen and pressure levels necessary for proper body operation, especially in the brain and kidneys. When Good Valves Go Bad The block diagram in Figure 17 shows what happens to the heart when valves go bad. Stenotic aortic valve. If the aortic valve becomes stenotic, the brain doesn’t care; it just wants its oxygenated blood at a pressure for proper operation. If the brain is happy with its level of oxygenated blood, then that rate and force of contraction will be fixed. As the aortic (AO) pressure starts to drop due to the stenotic valve, the brain sees this decrease in pressure and tells the heart to pump more forcefully and/or faster. With the increase in ventricular contractile force, the AO pressure will remain normal or near normal, but in the left ventricle (LV), things will be different. The amount of blood leaving the heart is limited by the ventricles’ systolic period (Q-T interval) and the next heartbeat (the R-to-R) interval. If the ventricle can’t get all the blood out before the T-wave occurs because of the resistance of blood across the valve, what is still in the LV, stays in the LV, until the next R-wave. Ventricular diastolic pressure will be elevated because of residual blood being left behind at the T-wave. The mitral valve can’t open until the pressure in the atrium is greater than the pressure in the LV. This will cause increased pressure in the atrium to develop before it can overcome the ventricular pressure and open the mitral valve. This equates to increased atrial pressure. The pulmonary artery pressure will be elevated because of increased pressure in the left atrium (LA). This will cause the right ventricle (RV) to increase its pressure because the RV can’t get rid of its blood supply until it generates enough pressure to overcome the existing pressure in the pulmonary artery (PA). The same thing happens in the RA. In short, with aortic valve stenosis, the aortic pressures may be normal or near normal, but all pressures to the left of the aortic valve will increase. Stenotic mitral valve. If the mitral valve is stenotic, the AO pressure will be normal or near-normal (remember that the regulator is the brain and its baro/chemo receptors). LV systole will be normal. LV diastole will be below normal, because not all the blood in the atrium could get into the LV before the next Q-wave. In the LA, the pressure will be elevated, because the blood had to first get to a pressure level high enough to overcome the resistance of the mitral valve before emptying itself into the LV. PA pressures will be elevated, as well as RV and RA pressures. In short, pressures to the right of the mitral valve will be normal or near normal, and pressures to the left of the valve will be elevated. Pulmonic stenosis. With pulmonic stenosis, AO, LV, LA and pulmonary pressures will be normal or near normal. RV systole will be elevated to a level needed to overcome the resistance in the pulmonic valve. RA pressures will be elevated due to the blood left behind in the RV (remember, we are limited by the amount of time we have to contract the heart). As these examples show, for whichever valve is bad, pressures are elevated to the left of that valve, while to the right, pressures are usually normal or near-normal. Regurgitant valves: aortic and mitral. With a regurgitant valve, the process still plays out similarly to that of stenotic valves, but with some differences. In aortic valve regurgitation, the valve never closes completely. When the LV relaxes at the T-wave, the blood has two places to go: up the AO to the body and also back to a space of very low pressure, the LV. As a result, systolic pressure may be normal or near normal, while the diastolic pressure will be decreased. The LV will be receiving blood from the AO, so there will be increased pressure in the LV. This will cause a backup of pressure in the LA, where the mitral valve will be closed until there is enough pressure in the LA to overcome the existing LV diastolic pressure. This will cause a backup of pressure all the way through the heart. In mitral valve regurgitation, we will see normal AO pressures. There will be normal systolic LV pressures with an elevated diastolic pressure, because every time the LV contacts, a certain amount of blood is returned into the LA. This comes back into the LV during LV diastole, along with the blood that would normally be coming from the lung field. The returning regurgitant blood in the LA does cause a backup of blood in the lung field that has to overcome the pressure on the left atrium before blood can go back into the LA. It can be seen as increased pressure in the LA, PA, RV and RA. When valves go bad, by using the simple block diagram, it is fairly easy to see that pressures to the right of the bad valve change a little, while to the left of the valve, pressures will go up. Final Thoughts I am the proud owner of three sirolimus-coated stents. It has now been almost three pain-free years since I had my stents placed. Two stents were placed in the right coronary artery (RCA). One was placed at the bifurcation of the posterolateral artery (PLA) and posterior descending artery (PDA) branches, and the other was placed in the proximal RCA. What I went through is something that happens thousands of times every day in cath labs worldwide: the use of multiple stents in one vessel. It saves lives and returns many people to satisfying, productive lives, but at what cost? Reimbursement is still one stent per vessel. Hospitals pick up the difference and then cut corners wherever they can. Education of staff is often one of the first things to be cut. Our new, incoming staff are quickly trained to know the difference between a JR-4 and a WRDC, how to prepare bivalirudin and eptifibatide, and how to tell the RCA from LCA. Last year, my department diagnosed and helped over six thousand patients out of four cath labs. Since then, we have moved into a brand-new, all-Toshiba six cath lab wing. We have also acquired over six new staff. As a busy lab, we do not have a lot of free time available to teach cardiology essentials. I strongly believe this to be the case in a majority of cath labs. Down and Dirty was my answer to getting the essentials out quickly to new staff. You don’t need a computer, books, videos or a trained cardiologist. What you need is an hour or so of free time, a ruler and some colored pencils. It’s not fancy. The results may very well look like the pictures in this article (which was the intent). It’s not fancy. It doesn’t cover the difference between bi-cuspid and tricuspid, and the effect of papillary muscle and chordeae on the valves. It’s not intended to turn the new staff member into a cardiology fellow. What it does do is give new, incoming staff a sense of how the heart works, how all the chambers interact and how the pressures are created. Over the past few years, I can’t count the number of times I saw staff faces light up and heard, Wow! I remember seeing that in a book but I never understood what it meant until now. This information has helped many staff at my facility, and now I hope it will help you and your staff. Happy cathing! Gerard Lagasse can be contacted at glagasse@chartermi.net

1. Rushner R. Cardiovascular Dynamics, 4th ed. W.B. Saunders Co.: Philadelphia, 1976: 286.

2. Guntheroth WG. Pediatric Electrocardiography. W. B. Saunders Co.: Philadelphia, 1965.

3. Vander A, Sherman J, Luciano D. Human Physiology The mechanism of body function. McGraw-Hill, Inc.: New York, 1975: 229, 231.