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Cardiac Surgery previously undiagnosed large trabecular ventricular septal of the Neonate and Infant cheap vasodilan online american express heart attack 3d. Intraoperative follow-up of patients with ventricular septal defect and elevated device closure of ventricular septal defects cheap vasodilan online amex blood pressure limits. Transcatheter device closure of muscular ventricular lar septal defects: follow-up concerning anatomic and surgical septal defect discount 20mg vasodilan visa blood pressure medication long term effects. Asian Cardiovasc Thorac supposedly multiple defects within the apical part of the mus- Ann 2002;10:228–30. Clinical and myocardial approach for intracardiac repair using video-assisted cardios- status after left ventriculotomy for ventricular septal defect copy. Techniques surgery for neonates and young children with congenital heart and results in the management of multiple ventricular septal disease: 5 years of experience. In the past, it was only ation through the true pulmonary arteries alone to remain slightly more common than transposition of the great arteries, alive preoperatively. Despite its advantages, be complex congenital heart disease, while those lesions less elective one-stage repair of the asymptomatic baby in early complex than tetralogy, such as atrial and ventricular septal infancy is not universally accepted. Some centers prefer a two-stage pulmonary stenosis, without complicating additional anoma- approach involving placement of an initial systemic to lies, such as absent pulmonary valve syndrome or complete pulmonary artery shunt. Some true from an embryological and morphological perspective, centers advocate placement of a monocusp valve at the time of initial repair,6 while others accept the pulmonary it is not useful when one considers surgical management. Percutaneous transcatheter that the true pulmonary arteries and the pulmonary vascular insertion of a stent-mounted, glutaraldehyde-treated bovine 347 348 Comprehensive Surgical Management of Congenital Heart Disease, Second Edition valve in the pulmonary position (Melody valve, Medtronic, points of stenosis. However, the most important associa- other three valves that are united by a single fbrous skeleton. Approximately The consequence of underdevelopment of the subpulmonary 40% of individuals with microdeletion of chromosome 22 infundibulum is that the aortic valve comes to lie more ante- have congenital heart disease. In addition, the underdevelopment of the sues, particularly affecting development of the third and subpulmonary infundibulum results in it having a narrower fourth branchial pouches. In addition to affecting conotrun- lumen resulting in less blood fow through the pulmonary cal development, it may affect development of the thymus valve and main pulmonary artery so that these structures are including differentiation and induction of tolerance in usually hypoplastic. T-cells and the parathyroid glands resulting in the immune dysfunction and hypocalcemia that are features of DiGeorge syndrome. This means that the defect is between the conal review the embryology of the development of the pulmonary septum and ventricular septum and therefore can also be arteries. The proximal main pulmonary artery is formed by than anterior malalignment and are also used to describe a division of the original conotruncus. There is a variable degree of anterior specifc cells in the embryo with green fuorescent protein malalignment of the conal septum relative to the ventricular have clarifed the role of neural crest cells in the development septum. It is the anteriorly protruding conal septum that is at of conotruncal anomalies such as tetralogy (see Chapter 16, least in part responsible for the right ventricular outfow tract Coarctation of the Aorta). It is almost always large The conotruncus (“bulbus” or “bulbus cordis”) is usually sub- enough to be unrestrictive from a pressure perspective so that divided by a process of spiral septation into relatively equally right ventricular pressure is equal to left ventricular pressure sized great vessels, namely the aorta and the main pulmonary and is therefore systemic. This may be because it is simply small, although monary artery may be hypoplastic relative to the aorta. The more likely it is in part obstructed by adjacent tricuspid valve conotruncus is in continuity with the dorsal aorta. If there is associated severe right ventricular outfow tion points between the main pulmonary artery and the branch tract obstruction, the pressure in the right ventricle can be pulmonary arteries (right and left pulmonary artery) can be suprasystemic which can result in severe right ventricular Tetralogy of Fallot with Pulmonary Stenosis 349 NormalNormal wall resulting in an hourglass-like narrowing at the sinotu- bular junction, that is, supravalvar pulmonary stenosis. The Septal bandSeptal band features described to this point are those that are likely to Right ventricularRight ventricular be encountered during repair in the neonatal period or early outﬂow tractoutﬂow tract infancy. In time, however, there will be progression of right ventricular hypertrophy including the moderator band and other muscle bundles toward the mid-body of the right ven- tricle. As the obstruction becomes increasingly muscular rather TricuspidTricuspid InfundibularInfundibular than fxed, that is secondary to valvar pulmonary stenosis pulmonary valvepulmonary valve septumseptum and pulmonary annular hypoplasia, there is an increasing (a)(a) risk of cyanotic spells during which the child temporarily can become profoundly hypoxic. Tetralogy of FallotTetralogy of Fallot Right ventricularRight ventricular other anatomical features of tof outﬂow tractoutﬂow tract with pulmonary stenosis Right Ventricular Hypertrophy It is normal for the right ventricle to be exposed to systemic pressure during in-utero development so that the right ventri- cle is similar in wall thickness to the left ventricle until birth, even in children who do not have congenital heart disease.
The specific origins of the coronary endothelial cells have been the rigorously debated purchase vasodilan 20 mg with mastercard blood pressure 8959; as a number of different approaches for determining their origins have resulted in conflicting conclusions (99 order vasodilan toronto blood pressure over 160,100 discount vasodilan 20mg with amex blood pressure vinegar,101). Regardless of the cellular origins, the signals that regulate coronary development are derived from both the epicardium and cardiac myocytes (99). Both metabolic (hypoxia) and mechanical factors stimulate growth factors that promote angiogenesis (102). The coronary vessels begin to coalesce from mesenchymal cells via vasculogenic processes in the extracellular matrix-rich, subepicardial space between the epicardium and the myocardium (105). The subepicardial space is not only the initial site of coronary vessel formation, but also the site of large-caliber coronary vessels in adults. Coronary vessels form as blood cell–filled cul-de-sacs until capillary projections from these vessels surround and become patent with the aorta (106,107). Once aortic perfusion has been established, these capillary beds quickly remodel into the left and right main coronary arteries and subsequent coronary vessels. In rodents this remodeling of capillary beds into muscular arteries happens over the course of hours. The signaling mechanisms that direct early coronary capillary beds to surround the aorta instead of the other great vessels such as the pulmonary artery are not clear. Nor is it unclear how the cusps are selected for coronary artery investiture and why one cusp is avoided. The noncoronary cusp is deeply embedded in the atrioventricular septum, specifically the annulus fibrosus, and thus the capillary beds have limited access to this sinus of the aortic valve. However, how atypical coronary vascular patterns affect cardiac performance or health are not always clear. It is generally thought that once formed, the coronary vessels sprout from their location in the subepicardial space and dive into the forming compact myocardium so that each cardiac myocyte is proximal to a capillary via angiogenic processes. Presumably, hemodynamics drive the rapid remodeling of the coronary capillary beds into the large-caliber main coronary arteries and the formation of the coronary system. Physiologic feedback between the myocardium and coronary vessel development is also affected by mechanical stimuli. As blood flows through the developing vessels, endothelial cells are exposed to shear stress, which is a function of fluid flow velocity and viscosity. Endothelial cells are equipped with a variety of “mechanosensors” that respond to shear stress and stimulate the expression of a variety of genes required for endothelial function and differentiation of arteries and veins (111). In humans, the number of arterioles and capillaries steadily increases during the first postnatal year (112). Myocardial Growth and Remodeling Cardiac myocytes display two types of growth during the fetal and neonatal transitioning from a proliferative phase to a hypertrophic phase. After their formation, the myocardial cells of the primitive heart tube undergo region-specific growth that drives cardiac morphogenesis (115). During this proliferative phase, mitosis and cell division are coupled as the myocardium rapidly expands. A second wave of mitosis without cytokinesis follows this phase and generates binucleated cardiac myocytes (116,117). Thus, myocardial growth transitions from cell division to cell hypertrophy during the perinatal period. An intermediate phase is associated with the binucleation of cardiac myocytes, which are particularly evident in ventricular myocytes (116). As cardiac myocytes are exiting the proliferative growth phase during the postnatal period, the myocardial mass dramatically increases. At the cellular level, cardiac myocytes are growing via hypertrophic mechanisms, adding sarcomeres in series (lengthwise) and in parallel (widthwise) (121). Also during this phase of heart development, interstitial fibroblasts begin to increase in cell number, becoming the predominant cell type of the myocardium (122). The postnatal myocardium has a limited ability to regenerate; however, as mentioned above, data support the concept that, the younger the myocardium, the more plastic and capable of reinitiating cardiac myocyte proliferation. Indeed, studies in neonatal mice found that the ability to regenerate after a traumatic injury (apical dissection) is lost by neonatal day 7, a time point that coincides with the loss of cardiac myocyte proliferative capacity (118,123,124). Neonatal mice are also capable of undergoing cardiac regeneration following myocardial infarction (125). Studies in humans have largely been hampered by the lack of available tissue from normal hearts. As expected, the number of cardiac myocytes in mitosis and cytokinesis were highest in infants and decreased to very low level by 20 years of age (127).
Disadvantages of resection relate primarily to the presence of a circumferential suture line discount vasodilan 20 mg online blood pressure over 160, which led to a high incidence of restenosis in early studies order vasodilan 20mg line hypertension vitals. The use of interrupted and absorbable sutures anteriorly and an extended anastomosis in patients with isthmus or arch hypoplasia have improved clinical outcomes after resection in more recent studies (48 order on line vasodilan hypertension 2 symptoms,49,53,59,67). For infants with arch hypoplasia a technique referred to as aortic arch advancement, similar to that used in interrupted aortic arch repairs, also has led to improved outcomes in some centers (68). Prosthetic patch aortoplasty was the second surgical technique described for coarctation repair, by Vosschulte (69) in 1961. A longitudinal incision is made across the coarctation and the area is enlarged with a patch of prosthetic material such as Dacron or Gore-Tex (Fig. Compared with coarctation resection, patch aortoplasty has the advantages of requiring less extensive aortic mobilization, preserving intercostal arteries, and avoiding a circumferential suture line. The disadvantages of this technique include the use of prosthetic material and a relatively high incidence of late aortic aneurysm formation (37,70,71,72,73). In 1966 Waldhausen and Nahrwold (74) introduced the subclavian flap aortoplasty procedure in an attempt to improve the high P. The left subclavian artery is ligated and divided, and a longitudinal incision is extended through the proximal subclavian artery and beyond the coarctation. The proximal subclavian stump then is turned down onto the coarctation and used as a patch of autologous tissue (Fig. The subclavian flap procedure has the advantages of requiring less extensive aortic mobilization, avoiding a circumferential anastomosis, avoiding prosthetic materials, and using living tissue as a patch with theoretical growth potential. An obvious disadvantage is that the procedure requires sacrifice of the left subclavian artery. Early studies suggested that the subclavian flap operation was the treatment of choice for infants with coarctation because of an apparent reduction in the incidence of late restenosis. Therefore, because of the occasional untoward effects on the left upper extremity (75,76) many centers prefer resection if the anatomy is suitable (51). Transcatheter Therapy Percutaneous balloon angioplasty and stenting offer less-invasive alternatives to surgical repair for patients with coarctation of the aorta. Balloon angioplasty has been used for coarctation since 1982, and subsequent literature documents angioplasty safety and effectiveness in patients with a native coarctation (77,78,79,80,81,82,83,84) and with recurrent postoperative coarctation (84,85,86,87,88,89,90,91). Stenting is a more recent percutaneous option for native and recurrent coarctation, supported by a growing body of evidence (92,93,94,95,96,97,98,99,100,101,102,103,104), that is appropriate in larger patients. The mechanism by which balloon angioplasty relieves coarctation stenosis has been elucidated in several postmortem and experimental studies (105,106,107,108). Angioplasty enlarges the coarctation lumen by expanding the lesion diameter and producing linear intimal and medial tears at the coarctation site (and in the normal distal aorta as well). In most instances, the medial tears are shallow, but rarely some extend to the adventitia. Histologic evaluation in animal models demonstrate vascular healing to occur by 8 weeks after angioplasty (108). Prior to angioplasty (A) there is a severe discrete coarctation completely occluded by the catheter. Immediately after angioplasty (B) the aortogram documents improvement in the stenosis, with an intimal irregularity anteriorly. Angioplasty for Native Coarctation The acute effectiveness of balloon angioplasty for discrete native (unoperated) coarctation has been demonstrated in numerous studies (Fig. Angioplasty acutely decreased the systolic gradient from 48 mm Hg to 12 mm Hg, with an increase in the coarctation diameter from 3. In a follow-up study of 59 children ≥2 years after native coarctation angioplasty, repeat cardiac catheterization found a residual systolic gradient of ≥20 mm Hg or more in 27% of patients (81); in the remaining patients, the mean residual systolic gradient was 6 mm Hg (median 8 mm Hg). Other follow-up studies show similar effectiveness (83), with the residual gradient in some improving over time (84). Recurrent stenosis after an initially successful angioplasty appears to be uncommon during intermediate- term follow-up in children and adolescents, but is relatively common in infants younger than 6 months of age (79,80,81,82,109). The incidence of aneurysm formation at the dilation site varies widely in published reports, possibly reflecting varying definitions of an aneurysm. The larger follow-up studies suggest that the incidence of aneurysm formation is approximately 5% to 16% (81,82,83,84).
Raspy breathing or stridor in a postoperative patient should trigger investigation of the vocal cords that may be injured from direct trauma from endotracheal intubation purchase vasodilan 20mg on-line arrhythmia when i lay down, or paralyzed from injury to the recurrent pharyngeal nerve order 20mg vasodilan with amex blood pressure drops when standing. Asymmetric chest wall movement again may indicate diaphragmatic hemiparesis due to phrenic nerve injury buy vasodilan 20 mg low price hypertension benign essential 4011. Cardiovascular Examination There are three parts to a complete cardiovascular system examination. Percussion is of little value for assessment of heart size and is not commonly performed to evaluate the heart. Observation/Inspection In addition to the general inspection described above, there can be observed findings that are specific to the cardiovascular system. Inspection of the chest wall may reveal chest wall surgical scars that suggest particular lesions. A right thoracotomy is used for placement of a right Blalock–Thomas–Taussig shunt, atrial septal defect repair, or mitral valve surgery. A midline sternotomy is used for most heart operations, especially if cardiopulmonary bypass is used. A left thoracotomy is used for patent ductus ligation, coarctation repair, or placement of a left Blalock–Thomas–Taussig shunt. Pulsations of the suprasternal notch may be visible in the presence of significant aortic runoff lesions such as aortic regurgitation. A left parasternal precordial bulge often is noted in patients with right ventricular volume overload (i. Examining a patient for a precordial bulge is best done with the patient supine, shoulders square on the examination table, with the examiner bending and looking tangentially across the chest. Because the dilated right ventricle is below the left precordium, the developing cartilaginous rib cage will expand to accommodate the structure. With the patient supine and the examiner at the feet of the patient, the point of maximal impulse can sometimes be observed. It is usually located in the left fourth intercostal space in the midclavicular line. Left ventricular hypertrophy does not usually alter the location of the point of maximal impulse. Palpation Palpation of peripheral pulses, the chest, the abdomen, and the back should be included in each cardiac examination. Palpation of the extremities (peripheral) to assess pulses and perfusion and of the precordium (central) to assess activity and thrills should be performed. Peripheral Palpation, Pulses Pulses should be assessed, noting regularity and quality of the pulsations. It is important to palpate pulses simultaneously in the upper and lower extremities, specifically right brachial or radial and right femoral pulses. If there is a delay between the upper- and lower-extremity pulses or absence of femoral pulsations, coarctation of the aorta should be considered. Diminished pulses are ominous in children and may suggest cardiac failure or shock. Absent or weak pulses in the left arm may result from previous subclavian flap repair of a coarctation of the aorta or in the right arm from systemic-to-pulmonary artery shunts (i. Bounding pulses reflect aortic runoff as in aortic regurgitation, patent ductus arteriosus, or arteriovenous malformations. Assessment of tissue perfusion includes determining the quality of the peripheral pulses, as well as skin temperature and capillary refill. Skin temperature should be determined, as should transition of central to peripheral cutaneous temperature. Change in temperature from central to peripheral can be determined by running the backs of the fingers from proximal to distal on the upper or lower extremities. Patients who have cool peripheral extremities who are warm centrally may be volume depleted or have low cardiac output.
Quality assurance data should be vetted at the very least among the entire group of echocardiographers and preferably include some external evaluators who are independent of the laboratory buy 20 mg vasodilan with amex blood pressure chart by who. Quality metrics should be reported on a regular basis not only to the laboratory personnel but also to the entire cardiology group order cheap vasodilan line blood pressure eating. This can take the form of a “dashboard” of these metrics with color coding demonstrating if the laboratory is meeting (green) or falling short of (red) or intermediate in obtaining threshold (yellow) 20 mg vasodilan free shipping hypertension 2 torrent. A key driver diagram is made which includes the primary drivers which the team believes contribute directly to achieving the aim and the interventions which impact those drivers. The Future For years, echocardiography has enjoyed a status to itself as the premier diagnostic modality for pediatric cardiovascular disease. Now echocardiography shares the stage of noninvasive cardiac imaging with magnetic resonance and computed tomographic imaging, positron emission tomography, metabolic imaging, and perfusion imaging. Echocardiographers should understand that these modalities complement, rather than replace, echocardiography. For example, cardiac magnetic resonance imaging excels in imaging both extracardiac anatomy and the spatial relationships within the thoracic cavity. The former has been difficult and the latter impossible for the pediatric echocardiographer. On the other hand, echocardiography excels in the evaluation of intracardiac anatomy where magnetic resonance imaging is inferior to echo. Accepting these complementary uses will allow the pediatric echocardiographer to deliver the best patient care possible. The myriad of diagnostic tests provides echocardiographers with at least two challenges. Echocardiographers must resist the tendency to become less rigorous when performing the echocardiographic examination because other imaging modalities exist as bailout options. If complex, difficult anatomy is possible to be diagnosed by echocardiography, the echocardiographer should make every attempt to do so in order to avoid the expense, inconvenience, and potential risk associated with other imaging modalities. Echocardiography personnel need to continue to bring the same rigor and compulsiveness to the examination that were employed in the past. The second challenge is one of “imaging responsibility” to not only patients and but also the healthcare system. Cardiologists are responsible for recognizing and resisting the lure of employing all of the diagnostic armamentarium at their disposal. Echocardiographers need to lead the charge by partnering with colleagues from other imaging modalities to develop pathways for diagnostic approaches that are age- and disease-specific and bring the greatest value to the patient. Another challenge involves the increasing miniaturization of computer and ultrasound equipment. This trend has provided the exciting development of hand-carried ultrasound devices. Using such devices, cardiologists may be able to provide point-of-service care more effectively and frequently. Evidence shows that these devices also improve diagnostic accuracy by complementing the cardiac physical examination (113,114,115,116). However, the increased availability of echocardiography made possible by hand-carried devices has tempted other noncardiac specialists to practice cardiac ultrasound (117,118). While this has the potential benefit of enhancing overall patient care by improving diagnostic accuracy, it also emphasizes the need for responsible practice of ultrasound. It is the duty of the echocardiography community to develop standards for the practice of hand- carried ultrasound and ensure that they are met. Most physicians who use a stethoscope are not cardiologists, the diagnostic accuracy P. A pediatrician may hear a murmur but may not be able to determine its etiology and therefore refers the patient to a pediatric cardiologist who will not only hear the murmur but will offer a definitive diagnosis. As with the stethoscope, it should be expected and indoctrinated as standard of care, that when a noncardiologist identifies a patient with suspected pathology using a hand-held device, the patient be referred to a cardiologist for further and definitive echocardiographic evaluation.
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