Duricef
Peter J. Cawley, MD
- Acting Assistant Professor of Medicine
- Division of Cardiology, University
- of Washington School of Medicine
- Seattle, Washington
The exudative stage is sometimes subdivided into an early phase premonitory symptoms 500 mg duricef amex, which occurs hours after the insult medications you can give your cat order duricef 250mg visa, and in which endothelial cell edema medications 2 times a day purchase duricef 500mg on line, capillary congestion medications for schizophrenia order duricef with visa, interstitial edema medications jamaica purchase generic duricef on-line, and hemorrhage occur medications canada discount duricef 500mg with amex. Later in the exudative phase, multifocal bilateral patchy opacities, usually ground-glass opacity and air space consolidation, will be seen. These opacities may be accompanied by air bronchogram formation (generally uncommon in patients with hydrostatic pulmonary edema). These opacities progress over the following days, and become increasingly confluent until the involved portions of all lobes bilaterally. Pleural effusions are uncommon and, when present, are smaller than in patients with hydrostatic pulmonary edema. The positive pressure used during mechanical ventilation will increase lung volumes and create the appearance of improvement in the radiographic opacities, but usually this finding does not reflect true clearing of fluid from the alveoli. Because the alveoli are filled with protein-rich fluid, numerous inflammatory cells, and hyaline membranes, true radiographic clearing will be prolonged. Patchy multifocal opacities may rapidly evolve to diffuse opacities later in the exudative phase and as the proliferative phase progresses. Mild interlobular septal thickening may occur, but is less pronounced than in patients with hydrostatic pulmonary edema. Neutrophilic infiltration, hemorrhage, epithelial cell injury, and macrophage accumulation are also seen. During this phase, hyaline membranes become organized, pulmonary capillaries are obliterated, and collagen deposition begins. Groundglass opacity may persist, but is often associated with coarse reticulation architectural distortion, and reflects the presence of fibrosis rather than edema, hyaline membrane formation, and inflammatory cell infiltration, as in the exudate and proliferative phases. The imaging findings are not specific, but indicate development of a coarser, more organized appearance, which tends to reflect the underlying histopathologic changes. Traction bronchiectasis and bronchiolectasis and architectural distortion may appear. Interlobular septal thickening is often a prominent feature, whereas air space consolidation is less conspicuous or absent altogether. Because the alveolar edema fluid is protein-rich and pulmonary capillary wedge pressures are often normal, some element of capillary leak is also present. Therefore, neurogenic pulmonary edema shows a histopathologic pattern of both hydrostatic and permeability pulmonary edema, representing a mixed edema pattern. Manifestations of Disease Clinical Presentation the edema fluid may appear very quickly, within minutes to hours of the responsible episode. This pattern of edema may be seen in patients with re-expansion pulmonary edema, high-altitude pulmonary edema, and neurogenic pulmonary edema, among other less commonly encountered situations (Box 100-5). Imaging Techniques and Findings Radiography Chest radiographs show multifocal, bilateral air space consolidation. Imaging Techniques and Findings Radiography Chest radiography in patients with conditions producing mixed edema shows features typically associated with hydrostatic pulmonary edema as well as the multifocal or diffuse lung opacities typically encountered in permeability edema. This frontal chest radiograph in a patient with subarachnoid hemorrhage shows bilateral pulmonary opacity without widening of the vascular pedicle or features suggesting hydrostatic edema. Manifestations of Disease Clinical Presentation Re-expansion pulmonary edema usually occurs within 2 to 4 hours of lung re-expansion, often after rapid removal of the space-occupying process within the pleural space, but may progress for 1 to 2 days. Etiology and Pathophysiology the mechanism of re-expansion pulmonary edema includes a combination of several factors. First, diminished perfusion in the collapsed lung results in decreased surfactant production and decreased pulmonary compliance, requiring a more negative intrapleural pressure to achieve inflation of the collapsed lung. These factors favor the production of hydrostatic pulmonary edema when the pulmonary collapse is relieved. Additionally, the hypoxemia that accompanies the prolonged pulmonary collapse and hypoperfusion results in the release of free radicals that produce capillary endothelial injury, causing permeability edema that worsens from the increased perfusion that occurs with reperfusion. The production of free radicals that gain access to the blood stream may also explain the occasional occurrence of reexpansion pulmonary edema that develops in regions of lung that were not severely collapsed, and even pulmonary parenchyma on the contralateral side. Temporarily decreased pulmonary lymphatic or venous return may also play a role in re-expansion pulmonary edema. Risk factors for the development of re-expansion pulmonary edema include prolonged pulmonary collapse (usually at least 72 hours), a large-volume pleural spaceoccupying process (>1500 mL fluid), and coexistent cardiovascular disease. The history will usually suggest that a large volume of fluid or air was removed, and that the pleural process has usually been present for a number of days. Within hours of the drainage procedure, increased opacity, usually ground-glass opacity or air space consolidation, develops within the expanded lung. The pathologic and radiographic findings associated with re-expansion pulmonary edema usually resolve within a few days to a week. Treatment of re-expansion pulmonary edema is usually supportive, with supplementary oxygen and ventilatory support as required. Prevention of re-expansion pulmonary edema revolves around slow removal of the pleural effusion or pneumothorax over a period of days, as well as optimization of cardiovascular disease treatment before thoracentesis. As a general rule, for long-standing pleural effusions, one should avoid removing more than 1500 mL during the first thoracentesis procedure. Pulmonary edema usually develops between 12 hours and 3 days after ascent,1 usually in the first day. Less commonly, high-altitude pulmonary edema develops in people with prolonged residence at a high altitude. The drop in partial pressure of oxygen that occurs at high altitude produces severe hypoxic vasoconstriction in the pulmonary arterial bed but, in susceptible individuals, this vasoconstriction is nonuniform. This inhomogeneous vasoconstriction response results in highvolume shunting of blood into pulmonary vessels unprotected by hypoxic vasoconstriction, producing severe elevations in pulmonary arterial pressure and resulting in pulmonary edema. Suggestive clinical context I Neurogenic pulmonary edema (intracranial pathology) I Re-expansion edema (rapid drainage of pneumothorax or pleural effusion) I High-altitude pulmonary edema I Reperfusion edema following lung transplantation I Edema associated with tocolytic therapy (preterm labor treatment) I Postpneumonectomy or postvolume reduction edema, air embolism. Imaging Techniques and Findings Radiography Chest radiographs show patchy air space consolidation, which may be unilateral (often the right side) or bilateral, usually without pleural effusion or cardiomegaly. From Imaging Findings Differentiating among the various histopathologic patterns of edema on imaging studies can be challenging. Often, presumptive treatment for hydrostatic pulmonary edema with radiographic reassessment is useful-hydrostatic pulmonary edema will improve rapidly, whereas the time course to resolution for permeability edema with diffuse alveolar damage is prolonged. Synopsis of Treatment Options Supplemental oxygen administration or return to sea level results in resolution within 1 to 2 days,1 and radiographic findings clear rapidly with appropriate treatment. Hydrostatic pulmonary edema is typically characterized on thoracic imaging studies by findings suggesting pulmonary I venous hypertension and interstitial edema: peribronchial cuffing, perihilar indistinctness and vascular haze, subpleural edema and, in particular, interlobular septal thickening. Imaging features of interstitial edema are less prominent in nonhydrostatic causes of pulmonary edema. Gotway A large number of conditions may result in pulmonary hemorrhage (Table 101-1). Broadly speaking, pulmonary hemorrhage may originate in the airways or lung parenchyma. Airway-related pulmonary hemorrhage is commonly the result of bronchitis, bronchiectasis, or malignancy, whereas parenchymal hemorrhage may result from pulmonary infarction, necrotizing pneumonias, toxic inhalational injury, malignancy, or causes of diffuse alveolar hemorrhage, with or without pulmonary vasculitis. Pulmonary capillaritis refers to alveolar interstitial inflammation consisting of neutrophil accumulation associated with fibrinoid necrosis, producing injury to the basement membrane and resulting in leaky capillaries. Repeated bouts of inflammation and hemorrhage result in the deposition of hemosiderin-laden macrophages. Note that there is occasionally some overlap in this classification system; Goodpasture syndrome, collagen vascular disease, and systemic lupus erythematosus may be associated with pulmonary hemorrhage with or without pulmonary capillaritis. Often, a network pattern of smooth interlobular septal thickening is superimposed in the regions of ground-glass opacity. The histopathologic hallmark of vasculitis is the presence of angiocentric inflammation, usually extending through all layers of blood vessel walls. Fibrinoid necrosis and perivascular fibrosis are also commonly present, and may ultimately lead to vascular obliteration and occlusion. Both leukocytoclastic (neutrophil-predominant) and granulomatous (lymphocyte-predominant) vasculitic patterns may occur. Most pulmonary vasculitides share the common pathogenesis of immune complex deposition in the vessel wall, with activation of complement and cellular chemotaxis, leading to an enzymatic and inflammatory cascade that ultimately produces vascular damage. The whole process may be antigen-driven, which may explain the association of a number of vasculitides with viral infections and collagen vascular disorders. However, some granulomatous vasculitides may be the result of cellmediated immunity rather than immune complex deposition. The main histopathologic derangement of vasculitides affecting the lung is capillaritis, perhaps associated with inflammation of slightly larger vessels (Table 101-2). Findings often predominate in the dependent regions of lung and, in most patients, appear relatively quickly. Shortly after the appearance of lung opacities, a linear and reticular network may be evident superimposed on the regions of ground-glass opacity, representing interlobular septal thickening. The pulmonary opacities clear slowly over a period of 7 to 14 days if there are no superimposed processes or repeated episodes of alveolar hemorrhage. Recurrent bouts of alveolar hemorrhage may produce areas of fibrosis and scarring, manifesting on chest radiography as areas of coarse linear and reticular opacity with architectural distortion. Cough, hemoptysis, shortness of breath and chest pain are common in patients with pulmonary involvement. Occasionally, areas of consolidation may be subpleural or peribronchiolar in distribution, simulating organizing pneumonia; the so-called atoll or reverse halo sign may also be seen. The airway wall thickening is circumferential and often nodular and irregular, occasionally resulting in tracheobronchial stenosis. Manifestations of Disease Clinical Presentation the average age of onset is about 50 years, and men are more commonly affected than women. Patients also often complain of myalgias and arthralgias, and individually affected organ systems may also produce particular symptoms. For example, involvement of the gastrointestinal tract may produce diarrhea and bleeding, whereas involvement of the skin may produce dermatologic manifestations, such as purpura and splinter hemorrhages. Shortness of breath, cough, and hemoptysis are the more common symptoms of thoracic involvement, and hemoptysis may be life-threatening. Poorly defined ground-glass opacity centrilobular nodules, reflecting prior pulmonary hemorrhage and the presence of hemosiderin-laden macrophages, may be seen. Thoracic involvement usually occurs in the setting of established disease, with patients complaining of chest pain, shortness of breath, cough, and hemoptysis. Hemoptysis may be massive and life-threatening and is the cause of death in up to 39% of patients. On chest radiographs, pulmonary artery aneurysms appear as central hilar prominence or perihilar rounded opacity of variable size. The margins of the aneurysms may be poorly defined because of surrounding pulmonary hemorrhage. Differential Diagnosis From Clinical Presentation Patients with microscopic polyangiitis typically have elevated erythrocyte sedimentation rates, and other rheumatologic markers, such as rheumatoid factor and antinuclear antibody, may be elevated. Therefore, a tissue diagnosis, usually obtained from the lung via surgical lung biopsy, is often required. Some have speculated that a virus may be responsible, whereas others have implicated an immunologic mechanism as the cause. Histopathologically, a small-vessel vasculitis is present caused by extensive inflammation of vessel walls with plasma cells and lymphocytes. Several classification schemes for Takayasu arteritis have been advanced (see later), and criteria for diagnosis have also been established (Table 101-3). A, Frontal chest radiograph shows rounded, poorly defined opacity in the left retrocardiac region representing a pulmonary artery aneurysm. Prevalence and Epidemiology Takayasu arteritis usually occurs in patients younger than 40 years and shows a strong predilection for women, who account for 80% to 90% of cases. The highest disease prevalence has been reported in Asia, especially Japan, although it may be underreported in Europe and North America. During the early, inflammatory stage, fever, pain in the region of the inflamed vessels, myalgias, fatigue, and malaise are common. On physical examination, bruits or diminished pulse over the involved vessels may be detected. When the brachiocephalic vessels are involved, neurologic symptoms may dominate the clinical picture. The possibility of a heritable cause or hormonal influences has also been considered. This is especially important because early diagnosis and treatment are associated with improved prognosis in patients with Takayasu arteritis. This postcontrast T1-weighted image shows circumferential intense enhancement of the thickened brachiocephalic artery wall (arrowheads). Angiography Angiography has traditionally been the primary procedure for the diagnostic evaluation of Takayasu arteritis. Angiography often demonstrates long, smooth, tapered stenoses that range from mild to severe. Arterial occlusions may be present, and collateral vessels or the subclavian steal phenomenon may be seen. Angiography is useful for guiding and evaluating interventional procedures, such as angioplasty or stent placement. This catheter pulmonary angiogram shows several stenoses, one high grade (arrow), in the right pulmonary arterial system. Additionally, angiography does not depict changes in wall architecture as well as cross-sectional techniques, and cannot differentiate between vascular narrowing caused by acute mural inflammation from that caused by chronic transmural fibrosis.
These studies indicate that the ventilation scan can be eliminated medicine over the counter generic duricef 250mg on-line, thus reducing cost and radiation dose nature medicine duricef 500mg lowest price. This study used aerosolized technetium 99m (Tc 99m) for the ventilation portion of the V/Q scan instead of the radioisotope xenon 133 medications knee purchase generic duricef. Tc 99m is five times smaller in diameter and has a 20% efficiency of pulmonary deposition in comparison to 2% for xenon 133 treatment junctional rhythm order duricef 500mg line, thus helping improve the results medications via ng tube buy duricef 500 mg overnight delivery. It was usually performed in cases of discrepancy between the clinical suspicion and results of the V/Q scan treatment in spanish order 500 mg duricef fast delivery, or if there were coexisting conditions. Angiography was also often performed prior to interventions such as mechanical clot fragmentation. Major complications (1% to 3%) associated with the procedure include respiratory distress requiring resuscitation, cardiac perforation, contrast reactions, major dysrhythmias, renal failure, and hematomas. Minor complications (5%) are contrast-induced renal dysfunction, respiratory distress, angina, minor contrast reaction, and transient dysrhythmias. An inspiratory breath-hold is desirable because it can increase the pulmonary vascular resistance, leading to better contrast enhancement. Various concentrations of contrast agent and protocols for injection rate have been used, each with its own advantages and disadvantages. High-contrast agent concentration (300 to 360 mg/mL) with a high rate of infusion (3 mL/second or higher) is the most popular, convenient, and effective because it maximizes pulmonary artery opacification and allows the use of preloaded syringes. Typically, 2- to 3-mm collimation imaging is done with or without narrow overlapping reconstruction. This technique provides excellent image quality, but also leads to a larger data storage requirement. Additionally, it is preferable to use larger pitch values with narrower collimation. Also, proper timing of the contrast bolus is extremely important to obtain a high-quality image. Generally, a presumptive scan delay of 20 seconds for upper extremity injections works well to obtain adequate enhancement. Multiplanar reformatted images can be useful to identify small artery abnormalities, which usually follow an oblique course, and three-dimensional reconstructions with volume rendering aid in displaying complex anatomy. Small subsegmental emboli may not be detected, although the advent of faster scanners has allowed even these small and likely clinically insignificant emboli to be readily seen with increasing frequency. It has a reported high accuracy, with sensitivity reported to range from 60% to 100% and specificity from 81% to 100%. When it was first developed it represented an important advance, because it allows over 90% of patients to hold their breaths throughout the study, thus reducing motion artifact from breathing. Eccentric or peripheral intraluminal filling defects form acute angles with the vessel wall. Occasionally, it may be outlined by contrast agent when imaged along its axis (railroad track sign). Saddle embolus bridges can form across the right and left main pulmonary arteries and are a cause of sudden death. This is important, because neither V/Q scan nor pulmonary angiography can detect other conditions reliably. The accuracy of diagnosis depends on the size of the artery affected and the size of the emboli (clot burden). It has also been shown to have higher sensitivity and specificity in comparison to V/Q scintigraphy. A confident diagnosis can be made in 90% of patients because, even in those in whom a scan is interpreted as negative, an alternative diagnosis can be established. Controversies regarding the accuracy for diagnosis have been reflected in various studies in different populations (see further discussion in the next section). In this method, 1 point is given for a clot in each proximal artery, which is equivalent to each segment arising distally, thus resulting in a maximum score of 9 for right lung, 7 for left lung, and 16 total. The sensitivity and specificity rates are particularly diminished (61% to 79% at its best) for small subsegmental emboli, which are usually uncommon in an acute setting. Another limitation to be taken into account is reaction to the contrast medium used. Nearly 15% of patients experience mild reactions such as nausea, vomiting, and flushing. The incidence of these reactions is reduced substantially by using low-osmolality contrast media. Furthermore, patients with preexisting primary conditions such as pregnancy and renal failure are contraindicated from the use of this test. However, that number gradually increased to 64-detector technology, which is widely used currently, and scanners with 256 detectors or more are or will be available in the near future. The increase in the number of detectors has led to a reduction in study time by 10 seconds and slice thickness as low as 0. The coronal, sagittal, and axial reconstructions using thin axial collimation have different sensitivities and may aid in the reduction of artifacts and false-positive rates by threedimensional visualization. The first evaluated patients with high clinical probability or an abnormal D-dimer test by the Geneva score. Limitations Important limitations include unsatisfactory images caused by respiratory and cardiac motion. They may not be of acute danger to the patient but predict a future, more severe embolism. Such a technique not only expedites patient evaluation, but also provides a diagnostic benefit over ultrasound assessment. Hence, it eliminates breath-hold and also produces T-2 weighted images, allowing thrombus imaging without the use of any contrast. Instead of directly imaging the vascular structures, this technique generates a signal based on the volume of blood in that region. The major limitation is its low sensitivity rate but its combination with lower extremity imaging may improve the diagnosis. There have been reports of fatal arrhythmias caused by cardiac pacemaker failure; hence, they are strongly contraindicated. The reduction in breath-hold time to 20 seconds (as a result of the acquisition of all the images in a shorter time) had led to its increased popularity. With thicker image acquisition, adenopathy can often be confused with intraluminal filling defects. In a recent postoperative setting, such as can be seen in pneumonectomy patients, an arterial stump or cutoff can be misconstrued as representing an acute embolus. This frequent diagnostic dilemma is encountered when there is a lack of opacification in multiple pulmonary vessels. The high specificity allows patients with positive results to be treated with confidence. It presents as a lobulated enhancing mass and should be considered when there is an emboli that is unresponsive to standard treatment 5. This tumor phenomenon can metastasize to the pulmonary vasculature and mimic an acute thrombus. However, several areas need further research and properly conducted therapeutic trials. The role of imaging and the optimal duration of anticoagulant therapy in different subgroups of patients with venous thromboembolism require further study. Surgical endarterectomy is usually reserved for chronic organizing pulmonary emboli and not during acute presentation. I the interpreting physician should diagnose and inform the referring physician about the findings of acute pulmonary embolism so that prompt medical treatment can be initiated. He or she should also specify about any right ventricular strain, if any, because this helps establish the severity of the disease. Embolization of thrombi to pulmonary arteries usually occurs from deep veins in lower extremities or pelvis. In addition, tests and pathways in specific patient groups have not been evaluated in detail. For example, there are many studies on the use of D-dimer testing in emergency department patients but few on its use in inpatients or intensive care unit patients. Patients with specific comorbid conditions have not been studied extensively, and preliminary data suggest specific characteristics in oncology patients, patients with chronic obstructive pulmonary disease, and others. It will be of particular importance to resolve disparate assertions regarding radiation exposure from the use of different imaging techniques. Use of multidetector computed tomography for the assessment of acute chest pain: a consensus statement of the North American Society of Cardiac Imaging and the European Society of Cardiac Radiology. Excluding pulmonary embolism with computed topographic pulmonary angiography or ventilation-perfusion lung scanning. The presence of shock defines the threshold to initiate thrombolytic therapy in patients with pulmonary embolism. Assessing clinical probability of pulmonary embolism in the emergency ward: a simple score. Comparison of two clinical prediction rules and implicit assessment among patients with suspected pulmonary embolism. D-dimer for the exclusion of acute venous thrombosis and pulmonary embolism: a systematic review. Normal D-dimer levels in emergency department patients suspected of acute pulmonary embolism. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Correlation of postmortem chest teleroentgenograms with autopsy findings: with special reference to pulmonary embolism and infarction. Long-term followup in patients with suspected pulmonary embolism and a normal lung scan. Clinical validity of a normal perfusion lung scan in patients with suspected pulmonary embolism. A normal perfusion scan in patients with clinically suspected pulmonary embolism: frequency and clinical validity. Usefulness of non-invasive diagnostic tools for diagnosis of acute pulmonary embolism in patients with a normal chest radiograph. Do preliminary chest x-ray findings define the optimum role of pulmonary scintigraphy in suspected pulmonary embolism Value of ventilation/perfusion scans compared to perfusion scans alone in acute pulmonary embolism. Technegas versus 81mKr ventilation-perfusion scintigraphy: a comparative study in patients with suspected acute pulmonary embolism. Performance of helical computed tomography in unselected outpatients with suspected pulmonary embolism. Diagnostic strategy for patients with suspected pulmonary embolism: a prospective multicenter outcome study. Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism. Anatomic distribution of pulmonary emboli at pulmonary angiography: implications for cross-sectional imaging. Comparison of contrast-enhanced magnetic resonance angiography and conventional pulmonary angiography for the diagnosis of pulmonary embolism: a prospective study. When it is severe, pulmonary hypertension can be severely debilitating and even fatal. During the past decade, advances in diagnosis and therapeutics have markedly affected the mortality of pulmonary hypertension. In 2003, an international multidisciplinary conference held in Venice, Italy, revisited the classification of pulmonary hypertension with a goal of classifying pulmonary hypertension into categories based on treatment algorithms that may be beneficial. Of these categories, pulmonary hypertension due to chronic embolic disease is the only one that may benefit from pulmonary thromboendarterectomy and one of the only forms of pulmonary hypertension that may be cured. This is important to consider so that it is not confused with recurrent acute pulmonary embolism, which represents either failure of anticoagulation or a manifestation of a hypercoagulable state. The mean time from onset of symptoms to diagnosis is about 3 years, highlighting the insidious, nonspecific nature of this process. Imaging usually begins with a chest radiograph, which might suggest pulmonary hypertension, and quickly moves to an echocardiogram, which is used to estimate pulmonary pressures and to assess cardiac function. This value is added to an estimate of right atrial pressure, which is based on the size of the inferior vena cava and its variation during respiration. On occasion, echocardiography may be performed with a contrast agent or agitated saline. The left atrium and ventricle are observed to confirm the absence of any echogenic material. If any is seen, this suggests that an intracardiac right-to-left shunt is present and the intravenously injected material is shunting to the left side of the heart. Both chambers tend to be enlarged, and the right ventricle tends to be hypertrophied. The observation of muscle hypertrophy is important because right ventricular enlargement alone may be seen in the setting of acute pulmonary embolism. In this situation, right ventricular enlargement may be a finding of right-sided heart strain and may require more aggressive intervention or closer observation. With right-sided heart enlargement and right ventricle hypertrophy, the interventricular septum tends to straighten at first and then to bow toward the left. The interatrial septum also may eventually straighten and then bow toward the left. Rarely, intravenous contrast material may be seen entering the left atrium through a septal defect, or two thin membranes may be seen in the region of the atrial septum.
Purchase duricef 500 mg. Symptoms and Warning Signs of Depression.
Indications are difficult coronary anatomy ombrello glass treatment buy duricef canada, subaortic stenosis medicine quinidine cost of duricef, and absence of pulmonary stenosis symptoms rheumatoid arthritis generic duricef 250mg line. In patients whose anatomy is amendable medicine for diarrhea order cheap duricef, a reverse switch procedure may be performed to convert the atrial switching to arterial switching symptoms of ebola order duricef with amex. This is accomplished by raising the pulmonary resistance with a pulmonary artery band medicine 834 discount duricef american express. The goals of these procedures are to reduce ventricular workloads and preserve ventricular functions. Most patients undergo reoperation for atrioventricular valve regurgitations and pulmonary stenosis. The overall surgical mortality is 6%; the late survival rate is 55% to 85% at 10 years and 48% at 20 years. Patients are also at risk for the complications associated with the atrial switch procedure. The classic cardiomediastinal silhouette of "egg on a string" is seen only in one third of cases. In the short-axis view, the aorta is anterior and to the right of the pulmonary trunk. In the suprasternal view, the ascending aorta lies parallel to the pulmonary trunk. Doppler technique is used to detect any hemodynamically significant subvalvular and valvular stenoses of the outlet valves. The aortic arch and pulmonary trunk are absent from their normal positions (arrowheads), thereby leaving a thin mediastinum. In the early days, after the development of the arterial switch procedure, catheter coronary angiography was routinely performed in postoperative patients to assess coronary patency. With experience and improved surgical outcome, coronary angiography is now reserved for patients presenting with signs or symptoms of cardiac ischemia. For patients with detected coronary stenoses, a stress test such as a stress myocardial perfusion study or stress echocardiography should be performed to determine the clinical significance of the lesions. On occasion, aortic regurgitation or pulmonary stenosis develops after the arterial switch operation. After the atrial switch procedure, routine echocardiography is needed to assess the integrity of the atrial baffle and ventricular functions. Atrial baffle leak typically occurs at the suture site of the atrial baffle to the atrial wall and is readily detected by color Doppler duplex imaging. Of greater concern is any obstruction of the flow channels created by the atrial baffle. Doppler imaging may detect accelerated flow at the obstruction, which would require further evaluation by catheter measurement of pressure gradient. After pulmonary artery banding for a planned reverse switch procedure, Doppler imaging is used to estimate the pressure gradient at the pulmonary band and the left ventricular systolic pressure from a mitral regurgitant jet. The latter helps monitor whether the trained left ventricle is ready to take on systemic pressure load. Dislodgment of these clots into the baffled channel causes systemic thromboembolism. The right atrium should have a broad-based, pyramidal atrial appendage and the left atrium should have a tubular, crenellated atrial appendage. The right main pulmonary artery should be anterior to the right mainstem bronchus and the left main pulmonary artery should course above the left mainstem bronchus. The right mainstem bronchus should be more vertically oriented than the left mainstem bronchus. If these features are left-right reversed, then the atrial situs is inversed and the positions of the morphologic left and right atria are reversed. In contrast, a left ventricle has fine trabeculations except at the apex, absence of a moderator band, and fibrous continuity of the inletoutlet valves without muscle in between. In addition, it requires that the right ventricle be aligned with the aorta and the left ventricle is aligned with the pulmonary trunk, or ventriculoarterial discordance. The hemodynamic significances of these lesions dictate the proper surgical interventions. When medical management is maximized, cardiac transplantation is the final therapeutic option. Catheter angiography is reserved for coronary imaging and hemodynamic measurements. Genetic basis for congenital heart defects: current knowledge: a scientific statement from the American Heart Association Congenital Cardiac Defects Committee, Council on Cardiovascular Disease in the Young. Balloon atrial septostomy is associated with preoperative stroke in neonates with transposition of the great arteries. Coronary artery obstruction after the arterial switch operation for transposition of the great arteries in newborns. Long-term outcome after the mustard repair for simple transposition of the great arteries: 28-year follow-up. Twenty-five-year experience with rastelli repair for transposition of the great arteries. Combined arterial switch and Senning operation for congenitally corrected transposition of the great arteries: patient selection and intermediate results. Intention-to-treat analysis of pulmonary artery banding in conditions with a morphological right ventricle in the systemic circulation with a view to anatomic biventricular repair. Outcomes of definitive surgical repair for congenitally corrected transposition of the great arteries or double outlet right ventricle with discordant atrioventricular connections: risk analyses in 189 patients. Myocardial density and composition: a basis for calculating intracellular metabolite concentrations. Chan Truncus arteriosus is an uncommon but potentially lethal congenital heart disease that manifests during the neonatal period or early infancy. It is defined by a common origin of the aorta and the pulmonary arteries, resulting from an incomplete embryologic septation and separation of the aorta and the pulmonary trunk. Since then, different classifications had been proposed by Collett and Edwards3 in 1949, by Van Praagh and Van Praagh4 in 1965, and by the Society of Thoracic Surgeons in 2000. Subsequently, Van Praagh and Van Praagh4 proposed a different classification with four types, 1 to 4. Van Praagh and Van Praagh type 1 is identical to Collett and Edwards type I, describing a short pulmonary trunk arising from the common arterial trunk. Van Praagh and Van Praagh type 2 describes separate origins of the left and right branch pulmonary arteries arising from the common arterial trunk, regardless of the distance separating their origins. Van Praagh and Van Praagh type 3 describes one branch pulmonary artery arising from the common arterial trunk and the other connected to a ductus arteriosus or an aorticopulmonary collateral artery. Van Praagh and Van Praagh type 4 describes the coexistence of a common arterial trunk and an interrupted or a severely hypoplastic aortic arch. Van Praagh and Van Praagh type 3 and type 4 have no correspondence in the Collett and Edwards classification. Although the Van Praagh and Van Praagh classification provides a more refined description of truncus arteriosus, it does not completely serve the needs of surgeons. In 2000, the Society of Thoracic Surgeons proposed a uniform reporting system with modifiers that better describe anatomic features useful for surgical outcome studies. Synonyms are common arterial trunk, truncus arteriosus communis, and common aorticopulmonary trunk. Truncus arteriosus is defined by the anatomy: the aorta and the pulmonary arteries arise from a common trunk above a single truncal valve. In Collett and Edwards type I, a common arterial trunk divides into an aorta and a short pulmonary trunk, which divides into the left and right branch pulmonary arteries. Of patients with truncus arteriosus, 34% to 41% harbor a chromosome 22q11 deletion. Today, this chromosomal deletion is readily detected with the fluorescence in situ hybridization technique. Genetic screening is important because 22q11 deletion is inherited in an autosomal dominant fashion from one parent in 6% to 28% of cases. Knowledge of this deletion also heightens clinical suspicions for associated anomalies, including athymia, hypocalcemia, and nasopalatal malformation. Truncus arteriosus is also associated with trisomy 8 and chromosomal 10p deletion. Similar to the closing of a zipper, the fusion proceeds upward through the truncus arteriosus, creating two spiraling lumens that become the ascending aorta and the pulmonary trunk. From this junction, the fusion also travels downward through the conus cordis until it meets the ventricular septum, separating the right and left ventricles. Separation of the systemic and the pulmonary circulations is completed by 9 weeks of gestation. Beginning in the seventh week, specialized tissue swellings from the conotruncal junction evolve into the aortic and the pulmonary semilunar valves; these are also completed by 9 weeks. Persistent truncus arteriosus is the failure of development or fusion of the conotruncal ridges. Second, the failure to form separate aortic and pulmonary valves leave a single truncal valve. All three defects lead to important hemodynamic derangements and their clinical manifestations. The conus cordis is destined to become the ventricular outflow tracts; the truncus arteriosus separates into the ascending aorta and the pulmonary trunk; and the branchial arches evolve into the branch pulmonary arteries and the aortic arch. In normal embryologic development, beginning in the fifth week of gestation, fusion of the endocardial cushions separates the atrioventricular canal into right and left openings, which are destined to become the tricuspid annulus and the mitral annulus. Through these two openings, blood flow develops into two intertwined, spiraling streams that flow out the conus cordis and the truncus arteriosus, or conotruncus for short. The right ventricle, subjected to the systemic pressure generated by the left ventricle, becomes hypertrophic. Uncommonly (11% to 29%), the truncal valve aligns exclusively with the right ventricle. The truncal valve has fibrous continuity with the mitral valve, similar to the normal relationship between the aortic valve and mitral valve. Competency of the truncal valve has important implications to survival and surgical outcome. In most autopsy cases, the truncal valve leaflets are dysplastic and thickened with myxomatous degeneration. In the most common situation, the truncal valve is tricuspid with a posterior cusp, a right anterior cusp, and a left anterior cusp. The right coronary artery usually arises from the right anterior cusp, and the left main coronary artery arises from the posterior cusp. In a quadricuspid valve, the right and left coronary arteries most commonly originate from the opposing right and left cusps. In pathology series, a single coronary artery was seen in 10% to 20% of cases,13 and stenosis at the coronary ostium was found in 7% of cases. B, the coronary arteries are shown originating from the opposite cusps of a quadricuspid valve. Histologic studies have shown tissue pathology similar to that of Marfan syndrome. The most common interruption (84%) occurs between the left common carotid artery and the left subclavian artery (type B interrupted aortic arch). The right subclavian artery may be fed by either of these arteries depending on whether it has a normal or an aberrant origin. Less commonly (16%), the interruption occurs distal to the left subclavian artery (type A interrupted aortic arch). Interruption between the left and right carotid arteries (type C interrupted aortic arch) is rare. The pulmonary arteries usually arise from the left posterior aspect of the common arterial trunk. When the branch pulmonary arteries arise from the common arterial trunk separately, the left branch pulmonary artery is often superiorly related to the right branch pulmonary artery. In the extreme case of aortic arch interruption, blood flow to the descending aorta is carried entirely by a large ductus arteriosus. Other cardiac anomalies associated with truncus arteriosus are secundum atrial septal defect, aberrant subclavian artery, persistent left superior vena cava, and tricuspid stenosis. Frontal view shows prominent peripheral pulmonary arteries from large pulmonary flow and diffuse ground-glass opacity from pulmonary edema. Instead, patients present with symptoms of heart failure a few days after birth and symptoms of pulmonary hypertension in the first year of life. These clinical presentations can be explained by the underlying hemodynamic derangements. In truncus arteriosus, because the pulmonary arteries and the aorta share a common origin, the pressures driving the pulmonary flow and the systemic flow are the same. The shunt ratio, defined as pulmonary flow divided by systemic flow, is equal to systemic vascular resistance divided by pulmonary vascular resistance. During the first week of life, the pulmonary vascular resistance decreases rapidly below the systemic vascular resistance. The shunt ratio can reach 5: 1 or greater, which implies a pulmonary flow five times the systemic flow. This torrential pulmonary flow returns through the pulmonary veins into the left ventricle. Assuming that there is no shunting at the atrial level, the left ventricle must handle this amount of flow by stroking five times the volume of the right ventricle. The left ventricle is severely volume overloaded, leading to congestive heart failure.
The controversy that continues to smolder is the role of balloon dilation or stent for the native coarctation of the aorta medications zanaflex discount 250 mg duricef overnight delivery. Complete repair has become the generally accepted approach to these complex defects because the prior approach of repair of the coarctation of the aorta and pulmonary artery banding has resulted in complications such as double-outlet obstruction early postoperatively and a more complicated medical and surgical management approach long term medicine prescription drugs generic duricef 250 mg visa. The extreme forms of obstructive left-sided heart lesions include hypoplastic left heart syndrome and its many variants medicine 50 years ago order duricef with mastercard. Because these are duct-dependent lesions medicine for runny nose purchase duricef 500mg online, they tend to be manifested in the first few days of life medications epilepsy purchase 500 mg duricef visa, although they may on occasion present late at several weeks of age medicine ball slams buy 250mg duricef visa. It essentially created a hemodynamically stable single ventricle, which could proceed down the single ventricle pathway of palliation with a bidirectional caval anastomosis and a subsequent Fontan procedure. Acyanotic right-sided heart lesions are few in number but tend to be more approachable through interventional cardiac catheterization procedures of balloon pulmonary valvuloplasty, angioplasty, or pulmonary artery stent placement. Anomalies of the tricuspid valve, such as Ebstein anomaly,15 tend to be manifested with cyanosis in the newborn period, and the infants can be quite ill. If acyanotic, they are typically diagnosed after an echocardiogram is obtained as part of evaluation of a murmur. The mean age at diagnosis of the acyanotic forms of this disease is the middle teenage years. Indications and Contraindications Surgical interventions for both aortic and mitral valve disease share similar indications and contraindications. As previously discussed, there are limited options in the smaller patient for operative intervention because mechanical valve replacement is fraught with an extraordinary number of risks and the need for early and repeated surgeries to essentially "up-size" these valves as the patient grows. Catheter-based intervention for severe aortic valve stenosis in the newborn16 is typically the preferred option. However, often less than perfect reduction in the stenosis gradient is tolerated such that one minimizes the risks for significant aortic insufficiency. Aortic insufficiency is a much more difficult disease to treat in infants and children. The Ross procedure has been an effective surgical procedure to provide good relief of aortic valve disease in children while avoiding many of the long-term medical management concerns of a mechanical aortic valve replacement. Mitral valve repair continues to be the optimal goal of most surgeons when possible, secondary to the issues revolving around mitral valve replacement at an early age. Somatic growth and the issues of chronic anticoagulation in the younger and more active patients empower surgeons to continue to develop surgical repair procedures for the mitral valve. The Norwood procedure for the hypoplastic left heart constellation of defects has significantly altered the approach to these formerly uniformly fatal lesions. Modifications of this procedure have resulted in the Sano shunt and a move toward even more creative attempts at palliation, such as the hybrid procedure, or patent ductus arteriosus stent and bilateral pulmonary artery banding. Pulmonary valve stenosis has long been a disease that lends itself to interventional catheterization procedures. Surgical open pulmonary valvotomy is still an option, but it is often reserved for unique circumstances at this time. In combination with newer technologies such as threedimensional echocardiography to evaluate valve morphology, much can be done to mitigate complications of surgery or the natural history of these defects. To help understand the basic physiology involved in these lesions, they are typically classified by degree of pulmonary blood flow (Table 28-6). Complete transposition of the great arteries is the most common cyanotic congenital heart lesion that presents in neonates. However, until the development of the surgical atrial septectomy in the 1950s and the balloon atrial septostomy in the 1960s, early death was expected. These palliative interventions allowed the development of physiologic palliative procedures, such as the atrial switch operation (Mustard and Senning),21 and later the anatomic correction with the arterial switch procedure. Although survival rates for the arterial switch procedure approach 95%, significant anatomic variations influence the outcome. These include associated cardiac anomalies, relationship of the great arteries to each other, and coronary artery anatomy variants. Single-ventricle defects are rare defects and can present with either increased or decreased pulmonary blood flow. Communication between the two circulations must exist after birth to sustain life. Single Ventricle A family of complex lesions with both atrioventricular valves or a common atrioventricular valve opening into a single ventricular chamber Postoperative Surveillance As is repeatedly emphasized in the diagnosis and surveillance of children with cardiac defects, the consideration of noninvasive and radiation-free imaging modalities is mandatory. This differentiates these defects from tricuspid atresia patients, who typically have a smooth inlet of the remaining ventricle. These cardiac defects invariably have other associated cardiac defects, such as complex outflow tract obstruction or interrupted aortic arch. Indications the surgical intervention in these defects depends on the age at presentation, the size and weight of the patient, and the presence of associated congenital cardiac and extracardiac defects. Complete repair of the patient with transposition of the great arteries with the arterial switch operation is the goal of the experienced cardiothoracic surgeon. The age at which to attempt complete repair is generally within the first 1 to 2 weeks of life because the left ventricular function and mass change as pulmonary vascular resistance changes with age. The surgical approach to the patient with single ventricle remains one in which the preoperative medical management and the skill of the congenital cardiac surgeon dictate much of the operative timing and decision-making. The single-ventricle pathway,25 as it has become known, requires careful medical and surgical management of pulmonary vascular resistance and single-ventricle systolic function, with an attempt to preserve single-ventricle diastolic function. The staged approach to ultimate palliation with a Fontan variant repair of these defects is now common. These palliative procedures may include pulmonary artery banding, pulmonary artery transection and creation of systemic-to-pulmonary artery shunt, and the Damus-Kaye-Stansel approach for selected defects. Caval anastomoses, hemi-Fontan, and the Fontan variant are the typical considerations for subsequent surgery for these patients. However, when this palliation fails or the poor hemodynamics of the patient preclude consideration of a Fontan intervention, cardiac transplantation remains a viable option. Abnormal coronary artery patterns, an early contraindication, are no longer considered a contraindication to this operation. Palliative operations for the single ventricle are dependent on preservation of good ventricular systolic and diastolic function as well as a low-resistance pulmonary vascular bed to allow passive return of blood from the pulmonary vascular bed to the receiving atrium of the single ventricle. Problems with either, and often both, may limit the ability to fully palliate these patients. Outcomes and Complications Surgical results of the arterial switch operation are influenced by a large number of factors. However, the simple arterial switch procedure in a patient with an intact ventricular septum has survival results that are above 95%. It is the associated congenital cardiac defects that often increase the potential morbidity and increase the need for a diverse approach to monitoring of these patients postoperatively. The single-ventricle patients have more issues involving close follow-up of the passive cavopulmonary circuits, which are necessary to provide adequate cardiac output and oxygenation of blood. Acyanotic patients can also present these defects, as noted before, and their manifestations are influenced by the degree of pulmonary blood flow. Tetralogy of Fallot represents approximately 7% to 10% of cases of congenital heart disease and is the most common cause of cyanotic congenital heart disease in all ages. The degree of valvular pulmonary stenosis and right ventricular hypertrophy or outflow tract obstruction dictates the time of presentation because these patients may be acyanotic at birth and infancy if this is not significant. However, the natural history of this lesion is progression of the cyanosis as the hypertrophy and pulmonary stenosis worsen with age. Contraindications Pulmonary vascular resistance has a common role for this category of defects, although for different reasons. The ability to perform the arterial switch operation for transposition of the great arteries is influenced by "deconditioning," changes that occur within the left ventricular myocardium as a result of decreasing pulmonary artery resistance, which typically occurs within the first several days after birth. Ebstein Anomaly Downward displacement of tricuspid valve into the right ventricle Caused by anomalous attachment of tricuspid leaflets Valve tissue is dysplastic and results in tricuspid regurgitation. Abnormally situated tricuspid orifice produces "atrialized" portion of the right ventricle between the atrioventricular ring and valve origin, continuous with the right atrium chamber. Tetralogy of Fallot Obstruction to right ventricular outflow, usually infundibular (subpulmonary valvular) stenosis Malaligned ventricular septal defect Aortic override of the ventricular septal defect Right ventricular hypertrophy tion, and elimination of the valvular pulmonary stenosis. Because of the long-term chronic right ventricular volume overload from the common pulmonary insufficiency seen after resection of the right ventricular outflow tract or pulmonary stenosis, there have been recent attempts to preserve some pulmonary valve tissue and to tolerate some degree of pulmonary stenosis. The belief is that this may limit the degree of insufficiency and protect the right ventricle from the damage of chronic volume overload and ventricular dilation. Tricuspid atresia patients are almost always confined to a single-ventricle palliation pathway. This may involve a Blalock-Taussig shunt to augment pulmonary blood flow but limit damage to the pulmonary vascular bed for chronic pressure or volume overload of the pulmonary arteries. In more extreme forms of the lesion, the pulmonary arteries may be very small, noncontinuous, or almost exclusively supplied by systemic collaterals. Much work has been done to try to improve pulmonary blood flow through unifocalization procedures with systemic-to-pulmonary artery shunts. However, these patients have varied native pulmonary architecture, so no absolute surgical options may be available. Patients with tricuspid atresia have contraindications to single-ventricle palliation options similar to those of other single-ventricle patients. Pulmonary vascular resistance and ventricular performance dictate whether these are viable options or if cardiac transplantation is the only endpoint. Again, these patients can present with varying amounts of pulmonary blood flow and a variety of associated congenital cardiac defects. This is a cyanotic defect for which electrocardiography can be quite helpful in the diagnosis because rightsided electrical forces are typically diminished or absent. This presentation is often associated with right ventricular outflow obstruction from the inferiorly displaced septal leaflet of the tricuspid valve, right ventricular hypoplasia, and elevated pulmonary vascular resistance. These are perhaps some of the sickest infants with congenital heart disease because of the associated defects and complicating physiology. Indications Definitive surgical repair for the patients with tetralogy of Fallot has become the goal of the pediatric cardiologist and cardiothoracic surgeon. Some adult patients may have undergone initial palliation with either a Potts shunt (descending aorta to pulmonary artery) or a Waterston shunt (ascending aorta to pulmonary artery) as a method to improve pulmonary blood flow. These carried significant risks for pulmonary artery hypertension and distorted pulmonary artery anatomy. For this reason, these procedures have been abandoned and replaced with the modified Blalock-Taussig shunt (typically Gore-Tex) as a palliative procedure to augment pulmonary blood flow. This procedure often provides several months to years of time to allow other medical issues to be addressed as well as adequate growth to permit corrective surgery. With proper anatomic substrate, surgical survival for definitive repair approaches 95%. Palliative shunts can be associated with pulmonary artery distortion and stenosis at the anastomosis site between the shunt and pulmonary artery. Although uncommon, acute thrombosis of the shunt can precipitate a life-threatening event from a lack of pulmonary blood flow and severe cyanosis. Tricuspid atresia patients tend to do quite well with the single-ventricle pathway for palliation. Because these patients have a normally functioning left ventricle, they tend to be the ideal patients for excellent long-term survival after the Fontan procedure, with a good quality of life. Three patients with tricuspid atresia were the first to undergo the Fontan operation, which he published in 1971. It is not uncommon for these patients who have done well to be able to successfully carry a pregnancy to term with little adverse hemodynamic effect. However, this does require close pre-conception planning and cardiac surveillance during the pregnancy. There is some controversy related to the role of angioplasty and stent placement as a primary treatment. Admixture lesions, such as transposition of the great arteries, are usually treated with a complete repair. To reduce the risk of postoperative pulmonary regurgitation I that can lead to right ventricular volume overload, some surgeons have recently tolerated a degree of postoperative pulmonary stenosis. For congenital heart disease, echocardiography is the mainstay of preoperative planning and postoperative monitoring. The direct vision intracardiac correction of congenital anomalies by controlled cross circulation. Intracardiac surgery with the aid of a mechanical pump oxygenator system (Gibbon type): report of 8 cases. E-type prostaglandin-a new emergency therapy for certain congenital cardiac malformations. Surgical versus medical treatment with cyclooxygenase inhibitors for symptomatic patent ductus arteriosus in preterm infants. Ventricular septal defect and aortic valve regurgitation: pathophysiology and indications for surgery. Atrial septal defect combined with partial anomalous pulmonary venous return: complete anatomic and functional characterization by cardiac magnetic resonance. Controversies, genetics, diagnostic assessment, and outcomes relating to the heterotaxy syndrome. Staged surgical repair of functional single ventricle in infants with unobstructed pulmonary blood flow. The unnatural history of tetralogy of Fallot: surgical repair is not as definitive as previously thought. The mid-to-late 1970s were a period of intense efforts toward the miniaturization of catheter design along with feasibility studies beginning with a canine model and extending to the operating room setting and, finally, the cardiac catheterization laboratory. Consequently, over the next several decades, the promise of this noninvasive approach to the management of patients with symptomatic coronary heart disease was realized with an explosion in the technology of catheter materials and manufacturing. The development of "niche" devices,5,6 each designed for a specific anatomic situation, allowed for broader application in a wider spectrum of lesions and patients.
Image acquisition lasts 5 to 15 minutes symptoms liver disease order cheap duricef on line, and attenuation correction is used in image generation symptoms your period is coming buy genuine duricef line. Unlike 13N-ammonia and 82Rb symptoms questions buy cheap duricef on line, O-water is a diffusible agent that is not extracted by or trapped within the myocytes but rather freely diffuses across membranes treatment brown recluse spider bite discount duricef online american express. The kinetics of 15O-water are dependent only on myocardial perfusion and are not affected by the metabolic rate-limiting steps that affect extracted tracers medications you cant take while breastfeeding buy duricef uk, eliminating the issues with tracer roll-off sewage treatment cheap 500mg duricef free shipping. Application of a single-compartment model to the dynamic image data allows a highly accurate estimation of absolute myocardial flow across a wide range of blood flow rates (0. The advantage of 15O-water as an "ideal" flow tracer is counterbalanced by the complex acquisition protocols and analyses required for use in clinical practice. Because the 15O-water is not extracted from the blood pool, the images are contaminated by the high level of residual activity within the blood pool, which must be subtracted from the final image to properly evaluate myocardial perfusion. Blood pool data obtained during this acquisition can be subtracted from the 15O-water perfusion, eliminating the contribution of the blood pool from the final 15O-water data set. Alternatively, very early acquisitions (20 to 40 seconds after tracer infusion) provide an image of the blood pool before tracer flow has reached the myocardium; these are then used to remove background blood pool signal from the myocardium. This study demonstrates normal myocardial perfusion at stress and rest with homogeneous uptake throughout. The generator is rapidly replenished, with 90% of the maximal activity available after 5 minutes, and full replenishment occurs by 10 minutes. Extraction of 82Rb is similar to that of thallium 201 (201Tl), another potassium analogue,6 but it is less than that of 13N-ammonia7; therefore, the issues associated with roll-off may be present in 82Rb as they are in all other extractable tracers. Extraction of 82Rb is affected by myocardial perfusion as well as by the metabolic milieu. Other processes, including fatty acid metabolism and neurohormonal innervation, have been studied as well. The prolonged half-life of 18F allows local distribution of the agent from a central cyclotron site to regional imaging centers. Myocytes generally favor fatty acids derived from adipose tissue stores as their primary source of energy. However, after a glucose load, glucose becomes the primary metabolic energy substrate as systemic release of insulin limits free fatty acid release and increases transmembrane transport of glucose. Free fatty acids such as acetate and palmitate enter the cell and participate in the betaoxidation pathway. Short-axis images demonstrate a large perfusion defect in the lateral segments (white arrow). An oral glucose load (25 to 100 g) or an intravenous glucose load is administered and followed by insulin as needed before imaging. In diabetic patients, a more rigorous methodology is necessary to produce highquality scans, and a euglycemic hyperinsulinemic clamp is often used. A dose of 5 to 15 mCi is injected, and imaging begins at least 45 minutes after tracer infusion. Acyl coenzyme A enters the mitochondria through the acyl carnitine transport system and becomes part of the betaoxidation pathway. During periods of ischemia, there is a rapid shift away from fatty acid metabolism to increased glucose use. Free fatty acids account for the preponderance of myocardial energy formation, and these pathways are dramatically altered by ischemia. Therefore, free fatty acid imaging is an attractive target for noninvasive imaging of ischemia and the associated alterations in oxidative metabolism. Initially produced in 1934 and first studied in humans in 1945, it has the advantage of being an organic molecule and therefore can potentially be used to target a wide variety of metabolic processes. However, both 11 C-palmitate and 11C-acetate have been effectively employed for the evaluation of myocardial oxidative metabolism. Several studies have evaluated fatty acid metabolism in normal volunteers and patients. Walsh and colleagues17 demonstrated decreased mitochondrial metabolism in infarcted myocardium. In addition, 11C-palmitate infusion during dobutamine stress testing demonstrated the expected rise in fatty acid metabolism in the normal myocardial segments, whereas areas supplied by stenosed vessels did not show a rise in fatty acid use. These effects are broadly divided into two groups: deterministic and stochastic effects. Deterministic effects have a threshold level below which there are no adverse events. When the threshold for biologic effect is reached, the severity of the effect is proportional to the final dose delivered, with increasing doses causing increasingly severe effects. Conditions in which an acute exposure to a high level of radiation leads to cell death are deterministic and include skin toxicity, bone marrow toxicity, gastrointestinal effects, and central nervous system syndrome. These effects are usually seen at doses above those experienced in diagnostic medical procedures. There is no threshold level below which exposure is completely safe, and increasing exposure increases the probability of an adverse effect but not necessarily the severity. The risk of future malignant disease is an important stochastic effect of ionizing radiation and is the focus of concern in diagnostic radiology procedures. Absorbed dose refers to the amount of energy deposited in tissue by the radiation passing through it. The absorbed radiation dose is measured in grays (Gy); 1 Gy corresponds to the amount of radiation required to deposit 1 joule of energy in 1 kilogram of matter. The equivalent dose, expressed in sieverts (Sv), corrects for the different effects that different types of radiation have on tissues, with alpha particles depositing more energy than beta or gamma radiation. This measurement does not take into account the sensitivity of different tissues to radiation. The effective dose, also expressed in sieverts, is the sum of the tissueweighted equivalent doses to all the exposed organs. This measurement is most useful in comparing the risk posed by a nonuniform radiation exposure to the patient through exposure to a diagnostic test or to nuclear medicine staff through occupational exposure. Because tissues such as lung and breast tissue are more sensitive to the effects of ionizing radiation than are other organs such as skin, radiation to those organs is of greater concern. By way of comparison, the average annual background radiation at sea level is about 2. Sympathetic activation leads to increased cardiac activation, an increase in contractility, and an increase in heart rate. The parasympathetic system acts in opposition, slowing heart rate and decreasing contractility. Neurohormonal activation is altered in heart failure, in diabetes, after myocardial infarction, and after cardiac transplantation. In addition, cardiac arrhythmias have been associated with abnormalities of the autonomic nervous system. Therefore, a compelling case can be made for imaging of the cardiac autonomic activation. Multiple tracers have been developed for the evaluation of both the sympathetic and parasympathetic pathways (Table 25-3). This radiopharmaceutical has been studied in multiple conditions including cardiac transplantation, cardiomyopathies, diabetes, and myocardial infarction. Note that with decreasing age and female sex, the risk of malignant transformation increases. Radiation dose and cancer risk estimates in 16-detector computed tomography coronary angiography. The true risk to the patient from exposure to diagnostic medical radiation is difficult to estimate. The relatively low dose of radiation delivered with each exposure and the long latency time before the development of adverse events make it difficult to establish a causal link as large studies with long follow-up times are necessary to evaluate such effects. Therefore, much of the data available is derived from the study of nuclear plant workers involving occupational or accidental exposures or from the atom bomb experience at Hiroshima and Nagasaki. There are increased rates of leukemia and breast, thyroid, colorectal, and lung cancer in the exposed population. In addition, the variable sensitivity of different tissues places women at higher risk from exposure to the thorax as breast tissue is sensitive to the effects of radiation. It is therefore reasonable to exercise greater caution in scanning younger patients, especially a pediatric population. Nuclear cardiology accounted for 57% of all nuclear studies; most of these studies were myocardial perfusion scans. The hybrid procedures also permit the assessment of other functional or physiologic information. This additional information, of course, comes at a cost of additional radiation exposure; therefore, understanding of the mechanisms of dose reduction becomes important in the proper administration of these tests. A, In prospective gating, the patient is scanned only during the short time window effective for coronary imaging. B, In retrospective scans, there is continuous exposure and reconstruction after acquisition eliminates data acquired at times outside of the effective window. The total radiation to which the patient is exposed is determined by the tube current, the voltage applied across the tube, the length of the field scanned, the rotation time, the speed of the table through the scanner, and the x-ray beam width. As exposure increases, the signal-to-noise ratio increases, improving image quality. This requires relatively slow table speed in relation to the rotation of the x-ray tube (pitch), leading to increased exposure when helical scanning techniques are used. In addition, the small size of the coronary arteries requires a high spatial resolution, demanding increased radiation energy and exposure times to maximize the signal-to-noise ratio and to improve image quality. One strategy involves dose modulation, which allows lowering of the tube current during preselected portions of the cardiac cycle that are unlikely to provide diagnostic information. Therefore, data obtained during much of the cardiac cycle are unnecessary for the evaluation of the coronary arteries because the coronaries are in motion and cannot be imaged optimally secondary to throughplane motion. The coronaries are relatively still during endsystole and diastasis, and therefore only information acquired during those two selected phases of the cardiac cycle is generally clinically useful in the evaluation of epicardial coronary arteries. By maximizing the x-ray tube output during those two phases and, importantly, lowering tube output during the rest of the cardiac cycle, dose savings of 30% to 40% can be achieved. This technique allows greater dose savings than those available with helical techniques. This scan uses an axial acquisition as opposed to the helical acquisition in the retrospective technique. This scanning approach requires longer scan times and therefore longer breath-hold times as well as a stable cardiac rhythm. Whereas the main advantage of prospective gating is decreased radiation dose, the primary disadvantage is the loss of functional information as the heart is imaged for only a short period of the entire cardiac cycle. Tube current and tube voltage can and should be adjusted to the lowest levels that produce diagnostic-quality images. These adjustments are especially applicable in smaller and thinner patients because less x-ray attenuation occurs in these patients. Last, the width of the scan field in the z direction should be minimized to include only the heart and coronary arteries to avoid unnecessary radiation to adjacent structures (Table 25-5). Positrons deposit their energy locally, which accounts for much of the radiation exposure to the patient. Radiation dosimetry of nuclear radiopharmaceuticals is calculated by a mathematical biokinetic model that incorporates the tissue biodistribution of the agent as well as biologic and physical decay. As positron annihilation events produce high-energy photons, these photons can travel long distances and affect bystanders. Maintaining an appropriate distance from a recently injected patient reduces occupational exposure. Each technique should be optimized individually, allowing the best results in each portion of the study. The first consideration is whether additional information is gained from combining both modalities. In some cases, a normal or abnormal test result from one of the two imaging techniques may be sufficient to make the diagnosis and to define future management of the patient. In such cases, the second study may be avoided entirely, saving the patient unnecessary cost and exposure. Considering which population of patients will benefit most from the combination of physiologic and anatomic information allows the greatest dose savings overall. When both studies are performed, efforts should be made to reduce exposure with each modality. Tube current should be set at the lowest level that will produce images of diagnostic quality. Measurement of regional myocardial blood flow with N-13 ammonia and positron-emission tomography in intact dogs. Comparison of Rb-86 and microsphere estimates of left ventricular blood flow distribution. Noninvasive assessment of coronary stenoses by myocardial imaging during pharmacologic coronary vasodilation. Detection of coronary artery disease in human beings with intravenous N-13 ammonia and positron computed tomography. Detection of coronary artery disease with 13N-ammonia and high-resolution positron-emission computed tomography. Positron emission tomography for the diagnosis of coronary artery disease: a non-university experience and correlation with coronary angiography.
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