Valves 'n Stuff

Welcome back to Pulse Check. We're talking about valves today, as well as the ascending aorta, cardiac shunts and endocarditis. I'll try to keep it fresh, but I can't promise to keep you awake. If you're driving, I accept no responsibility if you fall asleep at the wheel. Let's get cracking. This is Pulse Check, episode three. Let's talk about valve reala heart disease, starting with aortic stenosis. The three main causes are degenerative calcific, bicuspid, and rheumatic. The symptoms of severe ASR, in order of disease progression, angina, syncopy, and dysnia, or ASD. If the AS has progressed to the point of syncopy, or if the patient is presenting the hospital with acute pulmonary edema, aka acute valve syndrome, generally this would merit inpatient valve replacement, rather than referral for outpatient intervention. There are numerous signs of severe AS, the most specific common signs that I look out for when examining a patient with AS for severity are one, absent or reduced A2. A2 being the second heart sound heard when the stethoscope is placed over the aortic valve, as opposed to P2, which is the second heart sound heard when the stethoscope is placed over the pulmonic region. Two, a late peaking or pancistolic murmur, noting that AS is usually harsh with onset in early systolic and peaking midcistly, i.e. ejection systolic. Whilst in severe AS, it takes more time for LV pressure to build up during systole, to the point that blood can be ejected from the stenozed aortic orophys. Hence, severe AS is later peaking, and three, a slow rising and delayed corded pulse, which is your pulsus parvis atardus, also reflecting that later systolic ejection. The other signs include an S4, which corresponds to the atrial wave of blood coming through in late diastole, and striking the non-compliant steth and thickened LV, an aortic thrill, which is quite rare and usually only present in very severe AS. LV failure signs like pulmonary edema, and also S2 paradoxical splitting. As a minor tangent, let me tell you about S2 splitting. S2 comprises the closure of the aortic and pulmonary valves, which happens at roughly the same time. You listen for S2 splitting at the pulmonic region i.e. the upper left sternal edge. It is normal to hear physiological S2 splitting, where during inspiration, the pulmonary valve closes slightly later than the aortic valve. Have a trial listening over your own upper left sternal edge during inspiration and expiration, and you might hear some subtle S2 splitting during inspiration. A wide split S2 is when you hear splitting during both inspiration and expiration, but the splitting is more pronounced during inspiration. A wide split S2 occurs in pulmonary hypertension and in right bundle branch block. A fixed split S2 is when you hear splitting during both inspiration and expiration, and the time difference between A2 and P2 is the same in both respiratory phases i.e. it's fixed. Fixed S2 splitting is heard in atroceptal defect. A paradoxical split S2 is when splitting is more pronounced during expiration, and this is classic for severe aortic stenosis, where the A2 occurs later than the P2. I would not expect the average doctor to be able to pick up on S2 splitting on a clinical exam. However, it does sound impressive if you can listen to an AS murmur and say, "I think this is severe AS, because there is an absent A2, it is late peaking, and there is a slow and delayed corroded upstroke." I remember the mnemonic ALS, absent A2, late peaking, slow and delayed corroded upstroke. On an echo, the standard criteria for severe ASR, a mean pressure gradient of 40 mmHG or more, an aortic valve peak velocity of 4 metres per second or more, and an aortic valve area of 1 centimetre squared or less. We also look at dimensionless index, which is the ratio between LV outflow track velocity and aortic valve velocity, where less than 0.25 is considered severe. Low flow, low gradient to severe aortic stenosis occurs when you have a mean pressure gradient of less than 40, but the LV ejection fraction is less than 50%. In this case, the mean pressure gradient could be low because the ejection fraction and stroke volume are too low to mount a high enough gradient for it to be severe by our criteria. The best test is a debutamine stress echo, where you run debutamine, while doing a trans thoracic echo to the point that LV ejection fraction improves to 50% and recheck the mean pressure gradient, and if it now reaches 40 mmHG, you have confirmed severe AS. Paradoxical, low flow, low gradient, severe aortic stenosis is where the mean pressure gradient is less than 40, the ejection fraction is 50% or more, but the stroke volume index is less than 35mm^2. This tends to occur in elderly patients with small hearts, usually from a long history of sedentary living. A debutamine stress echo isn't going to give us the answer. So in this case, we do a CT TAVI, which is a CT scan of the aortic valve, as well as the aorta and femoral arteries, which tells us the aortic valve calcium score and also delineates where the TAVI is anatomically feasible. If the aortic valve calcium score is 2000 or more in men, and 1200 or more in women, this indicates severe. Calcium scores, whether they be aortic valve or coronary artery calcium scores, are measured in a Gatson unit, but they are different scores. I.e. ordering a coronary artery calcium score will not tell you the aortic valve calcium score, trying up to confuse the two. Severe aortic stenosis of its own accord is not an indication for surgery. There are five main indications for intervention in severe aortic stenosis, which I remember with the mnemonic solve. S is symptomatic, i.e. a vagina, syncopate or disnia. O is other surgery required, such as coronary artery bypass graft surgery or aortic root surgery. L is LV ejection fraction less than 50%. V is very severe AS, which is a V max of 5 meters per second or more, and E is exercise stress test poor performance. In other words, many elderly patients with severe AS say they have no symptoms, but they don't actually exert themselves enough in day-to-day life for symptoms to manifest. So you put them on a treadmill, and if they perform poorly, then this is a class 2A recommendation for intervention. Intervention for severe aortic stenosis is a hot topic in cardiology. Two major randomized controlled trials were published in 2025, and these were early TAVA and evolved, and these tested early TAVA for severe asymptomatic aortic stenosis, versus monitoring and intervening, only if the patients met one of those other indications for intervention. Both studies had a mean follow-up of about three and a half years, and showed no difference in all cause mortality between the two groups. However, in both trials, within about two years, the majority of patients in the surveillance arm had met some criteria for intervention and received a TAVA. The main conclusion that I take away is that in severe asymptomatic AS, it is reasonable to have a surveillance approach, but these patients need good safety netting and at least six monthly echoes, because they are highly likely to need valve intervention within two years. Two other important trials were recovery, published in 2020, and avatar published in 2024, which looked at surgical aortic valve replacement in asymptomatic severe aortic stenosis. These studies showed that in younger patients with mean age in their 60s and very severe, that was recovery, or severe, that was avatar, asymptomatic aortic stenosis, early surgical aortic valve replacement had clear mortality benefit. I think that this is probably because younger patients with severe AS either have bicuspid aortic valves, or their aortic valve calcification progresses more rapidly than in elderly patients with severe AS. When you've established that a patient needs aortic valve intervention, we routinely perform a coronary angiogram, as well as a CT TAVA. The angiogram determines whether there is concomitant coronary disease, which would sway to performing a surgical aortic valve replacement over TAVA in those patients that could go either way. There are a number of different options for aortic valve intervention. Transcatheter aortic valve replacement, aka TAVA, or TAVA, is a percutaneous procedure where a bioprostatic or tissue aortic valve is inserted via the femoral artery, though uncommonly, can be inserted via an auxiliary or corroded approach, and is implanted on top of the pre-existing aortic valve. Surgical aortic valve replacement aka SAVA is an open heart procedure involving a stenotomy, cardiopulmonary bypass, excision of the native aortic valve, and replacement with either a mechanical or a bioprostatic aortic valve, aka tissue valve, aka poor sign or burval and valve. A mechanical aortic valve is going to last the rest of the patient's life, so is the preferred option in anyone less than about 60, with the downside being having to take warframe lifelong, with an INR target of 2.5 to 3.5. A bioprostatic valve replacement, whether that be a surgical or a transcaffit valve, lasts about 10 years, less for younger, more active patients, and longer for more sedentary patients, before it starts to degenerate and become severely stenotic and/or regurgitant, and need replacement again. As a general rule, TAVA is performed in age greater than 75, surgery in age less than 65, and in between is a gray zone that can go either way. Your pre-op CT TAVA and End Geogram may help with the decision, because those with low-lying coronary osteo, small aortic roots, calcified alvea outflow tracks, or concomitant coronary disease may be better off with a surgical aortic valve replacement. We also carefully consider the patients overall prognosis and expected lifespan. Consider a functionally excellent 70-year-old man, with severe symptomatic calcific aortic stenosis and no other comorbidities. You could do a surgical tissue valve, which would be expected to last 10 years, and then when that fails, do a TAVA, which will get him to his 90s. That would be acceptable. You wouldn't do a TAVA up front for him, because when that needs replacement, when he's about 80, you'd need to do a TAVA in TAVA, which is essentially three layers of valve superimposed, and as such, TAVA in TAVA has bad outcomes. Surgical removal of Tevi is also very hard. In contrast, a frail, 90-year-old, with severe symptomatic aortic stenosis and live expectancy of more than a year, should probably get a tabby. The other option here is balloon aortic valveular plastic, or Bav, which is simply ballooning open the aortic valve at high pressure, which might improve the mean pressure gradient from the 40s to say the 20s or 30s and buy the patient an extra six months or so of life. Bav is often reserved for critically unwell, severe AS patients with acute valve syndrome to get the amount of strife before definitive valve replacement is performed, or for palliative purposes in elderly patients with a short prognosis. Patients with bioproesthetic valves don't need warfarin, but should be on some kind of blood thinner as monotherapy long-term, whether that be aspirin or a doleach, if they have some other indication for doleach, to reduce the risk of valve thrombosis. The other option for aortic valve intervention in very young patients would be a rust procedure. There aren't a great deal of surges that can do this, but if you have access to a surgeon experience with this, you should consider it for the very young patient. In a rust procedure, you cut out the pulmonary and aortic valves, you put the pulmonary autographed, i.e. the pulmonary valve in the aortic valve position, and then you put either a homographed, so a human aortic valve in root, or a freestyle valve, so bovine root and valve, into the pulmonary position. This isn't going to last forever, they're going to need another valve intervention later down the track, let's say, in 20 or 30 years or so, but it's going to give them a good period of time where they don't have to be on warfarin. This might be a good option for a young, physically active patient who enjoys contact sports. The final scenario I'll give you is the young female of child-bearing age, with severe bicuspid aortic stenosis. Rather than putting in a mechanical valve and committing her to warfarin, which could prevent her from having children and breastfeeding, you could do a surgical tissue valve, give her 10 years or so to complete her family without needing to be on warfarin, and then do a mechanical valve. Moving on to the other valves. The echo criteria, for severe AR, MR and TR, are the domain of the imaging cardiologist and are not expected knowledge for any other physician. In essence, based on the coloured upless signals obtained during the echo, we can calculate quantitative parameters like the effective regurgent orophys area, regurgent fraction and a regurgent volume, and there are specific criteria for severity in each regurgent vebular disease, then a contractor width is also helpful. There are two other things that are highly suggestive that a regurgent valve is severe. The first is chamber dilation, AR and MR both volume-load the LV, so if there is LV dilation, that suggests the AR or MR is severe. TR volume-loads the RV, so RV dilation, particularly in the absence of pulmonary hypertension or other causes of RV dilation, suggests severe TR. The second is flora-versal, abdominal aortic flora-versal in AR, pulmonary vein flora-versal in MR, and a paddock vein flora-versal in TR, all suggests the valve regurgitation is severe. Let's talk about aortic regurgitation. I remember the most common causes with the mnemonic bread, B-R-E-D-D. These are by cuspid aortic valve, rheumatic heart disease, endocarditis, dilated aortic root or LV, and aortic dissection. On clinical examination, AR is a soft, early diastolic, decrescendo murmur, heard at either the left or right sternal edge around the third intercostal space. It is best heard when the patient is leaning forward on exploration, and with hand-grip maneuver. For the hand-grip maneuver, I get the patient to interlace their fingers and try to pull them apart, but there are other variations including just clenching the fists hard. Hand-grip maneuver increases the afterload, hence increasing the amount of regurgitation and the intensity of the murmur. There are also me features of severe AR. These include the water hammer pulse, which is where you gently palpate over where you'd expect to feel the radial and brachial arteries, and then you raise the patient's arm above their head, and you should feel the radial and brachial pulse intensity increase significantly. The water hammer pulse is one of the most over-cooled signs in medicine. Personally, I like to palpate over the patient's forearm when checking for water hammer pulse, as I find that to be more reliable. The other sign is a wide pulse pressure, i.e. the gap between the systolic and diastolic bud pressures being greater than 60 mmHG. There are numerous eponymous signs like Corrigan sign, which is the exaggerated coronate pulse, Quinky sign, which is nail-bed painling and flushing, and Demuset sign, which is head-bombing with each heartbeat. These all reflect a hyper-dynamic circulation with wide pulse pressure. The last I'll mention is the Austin Flint murmur, which is a diastolic rumble, caused by the AR regurgent jet striking and closing the interior mitral valve leaflet, essentially producing a functional mitral stenosis murmur. Like with AS, a symptomatic severe AR of its own accord doesn't mandate valve intervention. Indications for surgery in severe AR are symptoms i.e. NYHG class 2 short and sub-breath, LV ejection fraction of less than 55%, or a dilated left ventricle, and the guidelines use LV insustolic diameter of 50 mm or more. AR, both volume loads and pressure loads the LV, so you get LV dilation and hypertrophy, the combination of which we call eccentric hypertrophy. Whilst MR is only volume loading, so you get LV dilation without hypertrophy. Intervention for AR is generally surgical aortic valve replacement, but you can do tavi. While awaiting surgery, blood pressure management is important to reduce the arthload and hence reduce the amount of regurgitation. In acute severe AR, like in intercutitis or intersection, the LV hasn't adapted to this sudden increase in volume and afterload, so it can fail quickly, so aggressive arthload reduction is important, such as with IV nitroproside. Next is mitral regurgitation. If you liked bread for causes of AR, I'll give you bread for MR. Prolapse or flail of the leaflets, rheumatic heart disease, intercutitis, and dilated LV and/or LA. When I say dilated LV and LA, what happens here is the anulus of the valve stretches and causes functional or secondary MR or AR, or tier. Similar to AR, transthoracic echo is very good for determining if the lesion is severe. Though with that said, cardiac MRI is better, but sometimes it's hard to see the mechanism of MR with a TTE, for example, which leaflet is prolapsing or flailing, or is there some leaflet perforation for intercutitis? This when TO comes in, patients being referred to surgical repair or replacement often have a pre-op TO to assess mechanism of MR or AR. Prolapse is when you've got mixomanist degeneration of the valve, i.e. you've got a soft floppy valve. This can be familial, or associated with a connective tissue disease, such as marphans, L is danlos, or low is diat syndrome. Flail aortic valve is when you've got cord rupture. The way we see this on echo is that in a flail leaflet, the tip will actually point upward toward the left atrium, whereas with a prolapsed valve, the valve tip will still point toward the LV. I don't think you really need to know that. Mitral regurgitation is a soft pan systolic murmur, radiating to the axilla, louder in the left lateral position, and with expiration. Indications for surgery in severe MR are symptoms i.e., NYHA class 2 shotness of breath, LV ejection fraction of less than 60% or a dilated LV with LV and systolic diameter of 40mm or more. The guidelines quote LV and systolic diameter, but we more commonly refer to LV and diastolic diameter, where the other limit of normal is 5.6 cm, not that you need to know that. Mitral valve intervention is usually surgical repair or replacement. The other option is mitral valve transcatheter edge-to-edge repair, the first model being the mitral clip, where the mitral valve leaflets can be clipped together to reduce the amount of MR that still permit forward flow. The big trial for mitral valve TER was the co-apt trial published in 2018, which showed benefit for mitral clip in severe functional MR in patients with symptoms, despite optimized heiferif with LV ejection fraction of 20% to 50% LV and systolic diameter less than 70mm, so the LV hasn't dilated too much and a pulmonary pressure of less than 70 mmHG. Mitral valve TER can also be used in severe primary MR such as mitral valve prolapse in patients who are not surgical candidates if the anatomy is feasible. Another option is transcatheter mitral valve replacement, kind of like "tavvy" for the mitral valve, but this is still an evolving area. Next let's talk about tracuspid regurgitation. The main causes are pulmonary hypertension, pacing leads, carcinoid, rheumatic heart disease, endocarditis, and dilated right-sided chambers, including RV and RA, which in turn dilate the tracuspid annulus, causing functional or secondary TER, such as in longstanding permanent atrial fibrillation. As a side note, this is why we often opt for early rhythm control, strategy, and patients with AF, where feasible, because if you just rate control them and leave them in AF for decades, eventually they have increased risk of developing severe TER and RV failure. On clinical exam, tracuspid regurgitation is a soft, pancisolic murmur, ledges to the left lower sternal edge on inspiration. Patients with severe TER and features of right heart failure, i.e. peripheral edema, and acytes, should be commenced on phryzomide plus minus spironylactone. Tracuspid valve intervention isn't as clear cut as mitral or aortic valve intervention, with mortality benefits less decisive. The only ESC European Society of Cardiology class 1 recommendation for tracuspid valve intervention is in severe TER undergoing left-sided valve surgery. These patients might get either surgical tracuspid valve replacement or a tracuspid valve annular plasticity, which is a quicker and simpler procedure involving stitching a prosthetic ring around the tracuspid valve annulus to tighten it and reduce the amount of TR. Curgical tracuspid valve replacement is almost universally with a bioproesthetic valve, which lasts much longer than a bioproesthetic aortic or mitral valve, due to lower pressures and less mechanical stress in the right heart. And mechanical trick-spot valves have higher thrombotic risk due to relative stasis of blood in the right heart, so we're generally avoided. There is a class to A recommendation for tracuspid valve intervention in severe symptomatic TR despite diuretic therapy. These are the patients with recurrent hospital presentations with gross peripheral edema, societies and right heart failure. In these patients, the best time to intervene is early, before the patient develops significant RV dilation or cardiac cirrhosis. In addition to surgical tracuspid valve replacement, your other options are tracuspid valve, trance catheter, edged edged repair, with the most common devices being the triclip and pascal, where you clip two of the tracuspid valve leaflets together to reduce regurgitation, and trance catheter tracuspid valve replacement, which you can think of as like a tavvy for the tracuspid valve. Tracuspid valve interventions are another hot topic in cardiology. The tri-luminate study for tracuspid valve trance catheter edged edged repair, and the tri-send two study that trance catheter tracuspid valve replacement have both shown improvements in TR severity and in self-reported symptoms based on the KCCQ score, but no improvement in mortality and increased major bleeding in other period procedural complications. Still, the uptake is growing, largely because clinicians want to avoid their patients with severe TR having recurrent hospitalizations for right heart failure, where they can present 10 to 20 kilograms overloaded and require recurrent long hospital admissions for IV dioresis. The last valve healer problem I'll talk about is mitral stenosis. 99% of the time MS is due to rheumatic heart disease, with the remainder being due to severe mitral valve calcification. During about of rheumatic fever, from group A strep infection, molecular mimicry occurs with immune system misdirects its attack on valve tissue in addition to the bacteria, leading to comissural and leaflet edged fibrosis. This can also affect the aortic and tracuspid valves as well as the mitral. The valve then progressively degenerates over decades due to turbulent blood flow, later presenting as severe MS and or MR, and often with concomitant ASAR or TR. On clinical exam, patients with severe MS may have a prolonged mid-diastolic rumbling memory at the apex, pulmonary hypertension signs, an early opening snap, and an apical diastolic thrill. The severe MR memory is very soft and often missed, even when you're listening very closely for it. But remember the pulmonary hypertension signs by the six P's. Parastonal heave, loud P2, prominent JVP, pulmonary and tracuspid valve regurgitation, pulsatile liver, which is more a function of severe TR and peripheral edema. We manage mitral stenosis with beta blockers, which reduce the heart rate, thereby reducing the gradient across the valve. Severe symptomatic MS is generally managed with surgical mitral valve replacement, though percutaneous mitral bullion comissureotomy can be an option if the valve appears pliable on echo to buy some time. Now let's talk about some valve adjacent stuff, starting with the air-water. Regarding aneurysm or dilation of the ascending air-water or aerotic root, the standard cut-off for surgery is 5.5cm. If the patient has mouth ans or bicuspid aortic valve, the cut-off is 5cm. If they are having an aortic valve replacement for another reason, for example severe AS, the cut-off is 4.5cm, and if they have a low-is-diet syndrome, the cut-off is 4cm. Marfan syndrome is a connective tissue disease caused by fibral and 1 mutation. You can remember the features of it with the mnemonic "marfan" that's mitral valve prolapse, aortic root dilation, regurgitant aortic valve, fingers long, that's arachno-dactually, arms being greater than height, nasal voice, that's the high arched palate, and sternal excavation that's pectus excavatum. So his diet syndrome is another connective tissue disease caused by TGF-beder receptor 1 and 2 mutation. You can remember the tetrad with the mnemonic "ABCE" that's aortic aneurysm, bifidufular, cleft palate, and eyes widely spaced, which is hypertelerysm. Four centimeters is the threshold for surveillance, meriting one to yearly echoes as a general rule. But this is patient dependent, and obviously if the patient is not a surgical candidate, i.e. if they're 80s and beyond, it's probably not necessary to do the surveillance. We also need to have a bit of common sense. A four-centimeter aortic root, the patient who is 200 cm tall, is probably normal, and doesn't merit lifelong surveillance. A bental procedure is when you replace both the root and the aortic valve. For example, if you have severe AS with a dilated root, you do a bental procedure. If you meet the criteria for a root replacement, i.e. 5.5 cm or more in the standard patient, and you have a bicuspid aortic valve as well, the threshold to do a bental and replace the valve as well as the root is if the severity of the bicuspid AS is moderate or more, because you'd expect that it may progress, and you don't want to do two sternomies. The bental's prosthesis comes with a bioproesthetic aortic valve and a length of bioproesthetic aorta attached, which can be cut to the desired length and implanted. A David procedure is where you replace the root alone, which has greater technical difficulty than a bental, with a longer pump time and greater risk. Moving on to the cardiac shunts, a patent foramen ovale, or PFO, is present in 25% of adults. 5% of visible on echo, just by colour doppler, and most of the others will be visible by bubble study. A bubble study involves putting a three-way tap onto a standard IV cannula, aspirating one to two mils of blood into one syringe, placing a second syringe on the other port with around eight mils of saline and a tiny bit of air, mixing the blood and the saline, so it's in all in one syringe and then injecting the agitated saline while a cardiac tech images the intratural septum. We usually do a bubble study at rest, with cough and with falcelva. A positive bubble study is when you see bubbles cross from the right atrium into the left atrium. If these bubbles cross within about three cardiac cycles, it indicates an intratural shunt, either a PFO or an ASD. However, if the bubbles appear in the left atrium later, let's say after five to eight cycles, it suggests there is a pulmonary shunt, such as a pulmonary arteriovenous melformation. A PFO is a flap within the intratural septum, which is supposed to fuse after birth, whilst an ASD is when there is insufficient tissue, such that a physical gap exists with continuous left to right flow at rest. I remember that PFO has an F in it, so it's a flap whilst ASD is a gap. You percutaneously close a PFO if patients have cryptogenic stroke and they're less than 65, particularly if there's a large shunt or there's a higher rope score. The rope score is the risk of paradoxical embolism score. Patients with PFO and cryptogenic stroke score points if they have no history of diabetes, the non-smokers, the younger, they have no prior history of stroke or TAA, and there's a cortical infact on imaging. There are four types of ASD. A secundum ASD is most common or in 80%. A secundum ASD classically has a right bundle branch block pattern on ECG with inferior R-wave notching, called crocodile size. A premium ASD is next most common around 15%. The gap is closer to the mitral valve in a premium ASD, so essentially all patients have MR due to a mitral valve anterior leaflet cleft. Premium ASDs are closed surgically. Sinus venosus ASD is the next most common around 5%, and virtually all of these patients have partial anomalous pulmonary venous return with the right upper pulmonary vein draining into the right at room instead of the left at room. These are all managed surgically. The fourth type of ASD is an unruved coronary sinus, making up less than 1%. Secundum ASD merits closure if the patient has symptoms, or there is RV dilation with a QP to QS ratio of 1.5. QP is the stroke volume through the RV outflow tract, and QS is the stroke volume through the RV outflow tract, both mentioned on an echo. In a normal person, the right heart to suit RV outflow tract and the left heart RV outflow tract should have the same stroke volume, so ratio 1 to 1. If the QP to QS ratio is greater than 1.5, this indicates that significant left to right shunting is occurring because 50% more blood is being ejected from the RV than the RV. All patients with a PFO or ASD meeting indication for closure should have a toe to look for a partial anomalous pulmonary venous return, and also to assess the anatomy to see whether there's enough of a rim to permit percutaneous closure with an ASD closure device. If not, they need surgical closure. Patients with high pulmonary pressures on echo should have a right heart cath to check the pulmonary vascular resistance. PVR greater than 5 wood units essentially contradicts ASD closure because the patient would develop a immediate RV failure if you closed it. A ventricular septal defect can be muscular, membranous, outlet or inlet. VSD closure is indicated if the RV is dilated with QP to QS greater than 1.5. You get a dilated RV rather than RV in a VSD because the RV is the ventricle that is volume overloaded. Although it is a left to right shunt, blood is pumped from the RV straight into the RV outflow tract rather than loading the main RV chamber, so blood comes straight back through the pulmonary circulation and into the RV and loads the RV causing LV dilation. What about a patent ductus arteriosus or PDA? In a fetus, the ductus arteriosus is their to shunt blood from left pulmonary artery to the descending aorta in order to bypass the lungs. In adults with a patent ductus arteriosus, blood flows from descending aorta to left pulmonary artery, increasing the loading on the LV. We close a PDA if there's LV dilation and a net left to right shunt. Ticutaneous closure is preferred. Tetralogy of fellow is the tetrad of pulmonary stenosis, RV hypertrophy, overriding aorta and VSD, or PROV PROV. the most common surgical complication from fixing the pulmonary stenosis. pulmonary regurgitation. Eyes and mango syndrome occurs when you have an uncorrected shunt, usually a VSD, that develops right to left shunting over time due to progressive pulmonary hypertension. The two main clinical signs are cyanosis and clubbing. Often you don't actually hear a murmur. Care for patients with eyes and mango syndrome is centralized to adult congenital heart disease centers like Royal Melbourne Hospital and most cardiologists have very little experience in managing these patients. Management often starts with an endothaline receptor antagonist like embryosentin or placentin plus a PDE5 inhibitor like Tidalophil. We ensure these patients are in repeat to maintain a high hemoglobin, sometimes more than 200 to optimize oxygen delivery to the tissues. A heart lung transplant effectively cures the eyes and mangoes but should only be performed when the prognosis is measured closer to years. You don't want to do a heart lung transplantation too early because the median survival for eyes and mangoes is 53 whereas the median survival for a heart lung transplant is around 10 years or so. The last thing we'll talk about is infective endocarditis. Overall, the most common valves affected are the mitral, followed by the aortic, followed by the trachuspid valve. In IV drug users, the trachuspid valve is most commonly involved. The most common organism is staphorious, followed by viridan's group strep, interacook eye, corregulae's negative staph, strep bovis and the hasek organisms. In prosthetic valve endocarditis, staphorious is most common, whilst after tavi, interacook eye are most common. For IV drug use, it's staphorious. After dental procedures, it's a viridan's group strep, which colonise the mouth. If you have colorectal cancer, think about strep bovis, subtype galoliticus. For culture negative endocarditis, think about coxiella, bartonella and the hasek organisms. We use the modified jute criteria for diagnosing endocarditis. Definite endocarditis is when you've got two major, or one major and three minor, or five minor criteria features. I remember the numonic, B timer, B for the major criteria. That's bacteremia, meaning two positive blood cultures taken 12 hours apart, and E for endocardial involvement, as demonstrated on TTE or TO. Timer, T-I-M-E-R for the minor criteria. That's temperature, i.e. fever, immunological phenomena, i.e. osulos nodes and Roth spots, m for microbiological evidence, i.e. positive blood culture, but not meeting the bacteremia major criterion. For example, one positive blood culture, or two positive blood cultures, but taken less than 12 hours apart. E is for embolec phenomena, i.e. septic embolite, splitter hemorrhages, and janeway lesions, and r is for risk factors like IV drug use. Empyrico therapy is ben-pen flu clocks and gent. If you've got a prosthetic valve, Empyrico therapy is flu clocks, thank and gent. There's probably varies based on geographical area and antibiotic susceptibility profiles. Once the organism is identified, we adjust therapy based on organism and susceptibilities. TO is generally performed in all suspected endocarditis cases, even if there's a positive TTE. Unless, of course, they have isolated, right-sided, native valve infective endocarditis with really good quality trans-threatic images. TO is very good at imaging the left-sided valves, but not as good as imaging the right-sided valves. The other reason for not performing at TO is if they're not a surgical candidate. There's a strong reason for initial medical management, or if TO is felt to be too high risk, for example, the patient has a suffodial varicies or thrombocytopenia. We don't perform at TO routinely in staphoresbacteremia, only when there is a higher clinical suspicion of VIE. The verse to score, the IR-STA, can be helpful in deciding whether your staphoresbacteremia merits a toll. Points on the scoring system include cerebral or peripheral embelly, meningitis, intracurricular device, prior IE, or pre-existing native valve disease, IV drug use, persistent bacterimia, vertebral osteomyelitis, communia-quai bacterimia, severe septic shock, and CRP greater than 190. The indications for surgical intervention can be remembered with monomonic valver, V-A-L-V-E-R-R-R. That's valveric vegetation with heart failure, abscess, heart block or destructive lesion, left-sided staphoreus, or fungal endocarditis, vegetation that is mobile 10 millimeters or more, E for enduring bacterimia or fevers for five days or more, recurrent systemic embolitis by antibiotics, recurrent pulmonary embolitis by antibiotics with the right side of vegetation being more than 20 millimeters, or recurrent prosthetic valve endocarditis. Aortic root abscess is suspected in patients with an ECG showing lengthening PR intervals. Remember that the AV node lives near the aortic root and aortic valve, so lengthening PR intervals suggests that there might be bacteria and abscess around the aortic valve thus causing conduction defect and lengthening the PR interval. In suspected prosthetic valve endocarditis, if suspicion remains for IE, despite a negative TTD and TOE, another option is FDG PET CT. Finally, let's talk about antibiotic prophylaxis fandocarditis. Patients merit antibiotic prophylaxis if they have both a high-risk cardiac condition and they're having a high-risk procedure. High-risk cardiac conditions include a prosthetic valve cardiac transplant, so anotic congenital heart disease, not just uncorrected VSD or ASD, rheumatic heart disease or prior IE. Bicuspid aortic valve does not require antibiotic prophylaxis. High-risk procedures include invasive dental surgery, ENT surgery and gastrointestinal or genitoriurinary procedures in the presence of infection. If antibiotic prophylaxis is warranted, give amoxicillin 2 grams or clindermycin 600 milligrams pre-op. Well done again for outlasting another episode of Pulse Check. If you have a dilated aortic root or a severely regurgent aortic or martial valve, best check your blood pressure because it's probably high right now. Maybe take a top up of your end lot of pain or go get a massage. You deserve it. See you next time.