By W. Tjalf. Missouri Southern State College.
A more recent prospective randomized trial or prednisone in children with persistent myocarditis >3 months found improved function in the treated group at 1 year (161) cheapest nizagara. A review of data regarding immunosuppressant therapy in myocarditis concluded that treatment does not significantly improve outcomes purchase 25mg nizagara with amex, but also acknowledged that most studies in children were underpowered (163) buy nizagara now. Treatment is not without adverse drug effects, reported in 39% of patients in one adult placebo-controlled trial of prednisone/azathioprine (167). This same study also found that although function improved at follow-up, there was no difference in composite outcomes of death, heart transplant, or heart failure admission at 2-year follow- up. Despite other conflicting data in treatment of myocarditis, use of immunosuppressant therapy in giant cell and eosinophilic myocarditis is well established. Eosinophilic myocarditis treatment includes reduced exposure to the inciting exposure or toxin in addition to steroids (30). Mechanical Circulatory Support For myocarditis patients with acute severe cardiogenic shock or progressive heart failure despite optimal medical therapy, mechanical circulatory support may be utilized. As previously mentioned, patients with fulminant myocarditis are more likely to present with severe dysfunction and cardiogenic shock, but have an expected high rate of myocardial recovery and superior long-term outcomes in survivors. In adults, reported survival to discharge ranged from approximately 60% to 70% (64,183,184). Recovery of normal function in nontransplanted survivors at follow-up was the norm in most patients from these series in both children and adults. Observed 1-year transplant-free survival has been reported as 80% to 90% in pediatric myocarditis (76,77,121). Event rates did not differ between biopsy confirmed and clinically diagnosed myocarditis (p ≥0. Ventricular remodeling and survival are more favorable for myocarditis than for idiopathic dilated cardiomyopathy in childhood: an outcomes study from the Pediatric Cardiomyopathy Registry. Patients may develop refractory heart failure unresponsive to medical treatment requiring heart transplantation. The authors hypothesized these findings were related to persistence of infectious and/or immune mechanisms even after transplantation. Myocarditis patients had significantly worse post-transplant survival and lower freedom from rejection death post-transplant compared to patients without a history of myocarditis. Early predictors of survival to and after heart transplantation in children with dilated cardiomyopathy. Clinicians must be aware of the various clinical presentations of myocarditis for accurate diagnosis. Despite controversies in use of immunosuppression and antiviral therapy, the primary therapy for myocarditis remains supportive. However, immune-targeted therapy in specific subsets of patients with chronic disease, especially virus-negative inflammatory cardiomyopathy, has shown some promise. Long-term outcomes in children are also lacking and late cardiac effects of childhood myocarditis are poorly understood. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies. Clinicopathological features of paediatric deaths due to myocarditis: an autopsy series. Demographics, trends, and outcomes in pediatric acute myocarditis in the United States, 2006 to 2011. The effects of gender and age on occurrence of clinically suspected myocarditis in adulthood. Age and gender effects on the extent of myocardial involvement in acute myocarditis: a cardiovascular magnetic resonance study. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Spatiotemporal changes of coxsackievirus and adenovirus receptor in rat hearts during postnatal development and in cultured cardiomyocytes of neonatal rat. Myocarditis in children and detection of viruses in myocardial tissue: implications for immunosuppressive therapy. Critically ill children during the 2009–2010 influenza pandemic in the United States. Early detection and successful therapy of fulminant chlamydia pneumoniae myocarditis. Diphtheritic myocarditis: clinical and laboratory parameters of prognosis and fatal outcome. Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification. Eosinophilic myocarditis temporally associated with conjugate meningococcal C and hepatitis B vaccines in children. Eosinophilic myocarditis in an adolescent: a case report and review of the literature. Diagnosis and classification of eosinophilic granulomatosis with polyangiitis (formerly named Churg-Strauss syndrome). Innate immune receptor activation in viral myocarditis: pathophysiologic implications. Consequences of unlocking the cardiac myosin molecule in human myocarditis and cardiomyopathies. Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. Clinical implications of anti-heart autoantibodies in myocarditis and dilated cardiomyopathy. Autoimmunity against M(2)muscarinic acetylcholine receptor induces myocarditis and leads to a dilated cardiomyopathy-like phenotype. Autoantibodies against M2-muscarinic acetylcholine receptors: new upstream targets in atrial fibrillation in patients with dilated cardiomyopathy. Differential profile and biochemical effects of antiautonomic membrane receptor antibodies in ventricular arrhythmias and sinus node dysfunction. Significance of the adenine nucleotide translocator in the pathogenesis of viral heart disease. Auto-antibody against adenine nucleotide translocator in dilated cardiomyopathy and myocarditis–incidence and relation to cardiac function and morphology. New-onset heart failure due to heart muscle disease in childhood: a prospective study in the United kingdom and Ireland. Clinical features and outcomes of childhood dilated cardiomyopathy: results from a national population-based study. The challenges of prompt identification and resuscitation in children with acute fulminant myocarditis: case series and review of the literature. Management and outcomes in pediatric patients presenting with acute fulminant myocarditis. Favourable clinical outcome in patients with cardiogenic shock due to fulminant myocarditis supported by percutaneous extracorporeal membrane oxygenation.
Further purchase nizagara uk, given that all components of the renin–angiotensin system are expressed within the kidney itself generic nizagara 50mg with amex, the importance of local mechanisms is being increasingly studied safe nizagara 50mg. Every cell type in the kidney can synthesize endothelin and contain abundant endothelin receptors, particularly the vasculature and the medulla. As a result, endothelin not only modulates total and regional renal flow, but also glomerular filtration, Na and H O handling,2 and acid–base regulation. Alterations in the endothelin pathway appear to be central in the pathophysiology of several acute and chronic renal conditions (35). During stress, however, autonomic rather than autoregulatory mechanisms predominate and act primarily to limit renal blood flow. Both α - and α -adrenergic receptors are present in the kidney and stimulation of both by1 2 neural discharge or circulating catecholamines causes renal vasoconstriction, redistributing blood away from the kidney as blood is distributed away from the peripheral circulation. Control over flow to the renal medulla, by contrast, is primarily through the actions of vasopressin, with autoregulation playing only a minor part. As medullary flow decreases in response to release of vasopressin, the osmotic gradient increases and uptake of the resorbate increases. As mentioned, the medulla consists of two distinct zones with complex vasculature to allow the countercurrent multiplication and exchange critical to the reuptake of the vast majority of the ultrafiltrate. It is in the inner medulla that the extreme concentration of the urine occurs and the greatest sensitivity to vasopressin exists. Splanchnic Circulation The splanchnic circulation consists of the vascular beds of the spleen, gastrointestinal tract, and liver. Similar to the renal circulation, the splanchnic circulation receives about 25% of cardiac output in the adult, but it is also a large reservoir of blood, containing about 20% to 25% of total blood volume. Thus, response to stresses such as hemorrhage leads not only to redistribution of blood flow away from the splanchnic circulation but also to mobilization of blood from that vascular bed to the central vessels and other organs. Control over the splanchnic bed in response to stress is primarily central rather than local, with neurohumoral catecholamine stimulation being the major mechanism controlling vasoconstriction (36). Stimulation of both carotid and aortic baroreceptors causes sympathetic neural stimulation of splanchnic resistance and capacitance vessels and large decreases in splanchnic blood flow and volume (37). It appears that approximately half the decrease in splanchnic blood volume is secondary to active vasoconstriction of the capacitance (venous) system and half secondary to its passive decrease in volume. The afferent limbs of these responses are uncertain because, unlike with hemorrhage, stimulation of baroreceptors does not occur. Responses specific to the individual components of the splanchnic vascular bed are discussed next. The spleen has significant sympathetic adrenergic innervation and responds to stimulation with vasoconstriction (38). Although there are β-adrenergic receptors as well as α-adrenergic receptors, the former are less active. In addition to sensitivity to adrenergic stimulation, human splenic arterioles respond to vasopressin and angiotensin with vasoconstriction. There is no evidence of autoregulation or other local controls over splenic blood flow. Thus, in response to stress, central mechanisms direct blood flow away from the spleen. Unlike other mammals, humans do not show significant reduction in splenic venous capacitance with stimulation, so it does not contribute significantly to the blood reservoir when mobilized with stress. It is the other components of the splanchnic circulation that contribute to increasing blood volume during hypovolemic stresses. The gastrointestinal tract has a complex vascular bed, controlled by a greater variety of mechanisms. As in the spleen, mesenteric vessels are richly innervated with sympathetic nerves, which respond to stimulation with vasoconstriction, although there are some vasodilatory β-adrenergic receptors as well. Constriction of the venous effluent vessels in addition to the passive decrease in venous capacitance causes mobilization of blood volume from this large reservoir. However, unlike the splenic circulation, the intestinal circulation escapes from vasoconstriction as vascular resistance decreases and flow increases secondary to autoregulation. This phenomenon is not well defined, but it is probably secondary to sensitivity of the arteriolar bed to vasodilator metabolites such as adenosine, in much the same way that adenosine is involved in local regulation of other vascular beds, such as the cerebral and myocardial circulations. In anticipation of food, the response is central in origin and largely sympathetic, causing vasoconstriction. Once food has been ingested, there are major local vascular responses related to the type of food, the products of digestion in different parts of the intestine, and the secondary effects of various gastrointestinal hormones. The hydrolytic products of carbohydrates and fat are particularly potent local vasodilators and appear to act on a metabolic basis similar to that of autoregulation by increasing local oxygen consumption. Local hormones that may play a role in vasodilation include cholecystokinin, secretin, gastrin, glucagon, and vasoactive intestinal polypeptide. The overall response to feeding yields increases in local blood flow of ≥300% within 60 to 90 minutes. Because of the large increase in oxygen consumption, however, these increases are not enough to meet the increased metabolic demand, so that oxygen extraction also increases. The hepatic circulation receives both highly oxygenated blood from the hepatic arteries and blood of lesser saturation but greater substrate concentrations from the portal vein. The portal vein terminates in the hepatic sinusoids, and the hepatic arterioles split into a complex capillary network that also drains into the sinusoids. These vessels, along with the biliary ductules and lymph vessels and nerves, occupy the portal triad. In these sinusoids, which allow free contact with the hepatic cells, the blood passes radially away from the center of the hepatic glomus to the periphery, where it passes into the hepatic venules on its way to the hepatic veins and inferior vena cava. As the blood passes from the center (zone 1) to the periphery (zone 3), near the hepatic venules, different metabolic activities predominate. As with the kidney, flow to the liver is large (about 25% of cardiac output in the adult) and far exceeds its metabolic demand for oxygen. As with the intestinal circulation, hepatic blood volume is large (about 10% of total blood volume) and is mobilized during periods of stress. Conversely, as hepatic venous pressure increases, hepatic blood volume increases greatly because of the large compliance of these capacitance vessels. There are also sphincters in the hepatic venules that may regulate hepatic blood volume by varying sinusoidal volume and portal resistance. Portal venous blood contributes about 75% of hepatic flow, and this flow is determined primarily by mechanisms that regulate splenic and intestinal flow, although presinusoidal sphincters exist as well. Alterations in hepatic venous pressure affect neither portal flow nor its intrahepatic distribution. Similarly, there are vasodilatory β -adrenergic receptors and there is some responsiveness to vasodilatory gastrointestinal2 hormones such as glucagon, secretin, and pentagastrin. An additional regulatory mechanism of hepatic arterial flow exists that is somewhat analogous to intestinal autoregulation.
Since you have limited ability to communicate with your popula- tion discount nizagara line, you will need to have a stable of couriers as well as a distributed network of command centers that you can not only send messages to cheap nizagara 25mg line, but also receive information on the current hurricane damage and needs of communities for resources purchase nizagara 25 mg fast delivery. Now that people have been injured and killed, you will need more medical person- nel and coroners to recover the bodies to prevent disease and infection from being incurred on your population. The last thing you need now is a pan- demic of bacterial or virus infections to afict the rest of your community that was not directly impacted by the hurricane. How will you coordinate your rescue eforts with your neighboring colony to the north? Tere may be some common resources that could be used by both colonies for rescue and recovery operations. Certain skilled laborers may be available in one colony and not the other that can be sent to the neighboring colony that needs specialized services. The neighboring colony in return may be in a position to send resources to your colony. Stage 3 of the Disaster You are now receiving word that multiple dams have either been broken or are fooding due to the winds and high volume of water that is coming in from the hurricane (U. Department of Commerce, National Oceanic and Atmospheric Administration, 2012; Rufman, 1996). In addition, you are now receiving damage reports that your cornfelds have been laid to waste (U. With the dams breaking you will need to shore up those structures and stop any additional fooding. In addition, you will need to send out inspectors to investigate the status of other dams that have not broken and repair the dams if the situation warrants emergency repair work. Using your communication network, you will need to summon all workers that can possibly work on dam and break- water structures to perform repair work, as well as inspect other structures. In addition, you will now need to communicate to the populations around dams that could break that evacuations should occur for residents in those areas. Your organization has two additional problems to contend with: (1) fnding food for your citizens and (2) fnding engineers and construction workers for the dam projects. If the dams are not repaired or inspected properly, you could even have more agriculture destroyed, more citizens displaced, and possibly more citizens killed if the dams do not hold. However, the dam inspection and construction projects, as well as fnding food for your citizens, should be placed as high-priority problems that need to be resolved. Since the rescue process involves frst responders, the other two issues should not detract personnel from working on resolutions to those issues. Tis situation calls for sending out feelers to surrounding states to see if stockpiles of food may be purchased or donated from other colonial governments. If that approach fails, see how many canned and preserved foods can be gathered up and sent to population centers that will be afected by the food shortage. You are receiving reports that a number of people have been displaced and need both food and shelter (Stone, 2006). You send out riders on horseback to use as couriers for communicating with your various emergency crisis units in the feld, and you attempt to gain the confdence of your citizenry that stability will eventually occur. A major priority at this point in the disaster is to make sure that there is enough temporary housing for all of your displaced citizens. One option is to appeal to neighboring communities to take in dis- placed persons until housing can be provided. You have neighboring colonies that can also be called upon to assist with the recovery of the state after the hurricane. Medical personnel and morticians will be needed to take care of the injured and collect the dead to prevent infection and disease from spread- ing. Tere will still be some ongoing rescue eforts, but at this point in time your resources should shift to more of a recovery nature. Calling up any mili- tary aid would be reasonable at this time to show the citizens that the govern- ment is in control of the situation, and this action would also add additional manpower that would be employed with the recovery efort. The issue of setting up logistics for food, water, and medicine coming from neighboring states would also need to be established to relieve your citizens’ plight. You do not have motorized transport and communication has to occur through couriers that travel either by foot or on Case Studies: Disasters from Natural Causes—Hurricanes ◾ 47 horseback. At this point in the disaster, it would be wise as a leader to make visits to areas where the hurricane has hit and provide confdence to your citizens as well as gain frsthand knowledge of the actual situation. However, even in modern times there is a pos- sibility that electricity could be cut of and refrigeration of food would not be possible. In this situation it is important to get as much cured or preserved food as possible. Having preserved food allows for stockpiles of food to be stored and transported more efectively. Since you have to consider that wag- ons are the best transportation you will have at this point, the food will have to be able to be hauled over long distances in all sorts of climates and still be edible upon delivery. The results will often be based on what resources are available to construct housing (e. Another remedy might be to put up a large amount of tents until more permanent housing can be constructed, but one has to keep in mind that the climate might prove to be too harsh for certain populations, particularly the very old or very young, to tolerate for a great length of time. Key Issues Raised from the Case Study The case study illustrates the challenges of dealing with shelter, supplies, and evacu- ation issues in the absence of modern resources. With no power or modern communications the colonists had to overcome the communication issues by using couriers on foot or on horseback to relay messages. In modern times the infrastructure may exist for more modern communication, but that does not always guarantee it will be working properly during times of crisis. Administrators need to have an alternate plan that will consist of more rudimentary forms of communicating in case modern telecom- munications infrastructure fails. Without having the ability to shore up infrastructure, such as dams, the hur- ricane actually caused more damage than would have occurred naturally. When structures such as dams fail, it can lead to a large amount of fooding that will not only kill or injure people, but also cause damage to other infrastructure, such as bridges, houses, and businesses. Administrators need to be cognizant of the dangers of dams bursting during a hurricane or earthquake and should regularly inspect and upgrade that infrastructure accordingly. In the time of when this crisis occurred, modern communication, transportation, and construction materi- als did not exist, which in many parts of the world may still be the case if a natural disaster occurs. Administrators in underdeveloped parts of the world should take heed of these issues and attempt to reinforce infrastructure as much as possible to weather a natural disaster. Galveston Hurricane, Texas, 1900 Stage 1 of the Disaster You are the city manager of a large coastal city of 42,000 inhabitants (Cline, 2000). You are concerned about the possibility of hurricanes hitting your city and causing widespread death and destruction. You have just witnessed the city of Indianola get hit twice by hurricanes and ultimately abandoned by the resi- dents due to the damage that was inficted upon their community (Texas State Historical Association, 2001). You have some residents that favor building a sea wall to limit the potential damage by a hurricane, but their pleas fall on deaf ears (Cline, 2000). To gain this support, the city manager needs to win over the mayor and the city council to bolster the necessary political support that will be needed to build a seawall.
The right ventricular pressure tracing has a rapid upstroke during isovolumic contraction purchase nizagara 100mg online, a plateau during systolic ejection cheap nizagara 100 mg otc, a decline to near zero during isovolumic relaxation order nizagara 100 mg fast delivery, and a slow rise to the end-diastolic pressure during diastolic filling. Normally, the peak systolic pressure is <30 mm Hg, and the end-diastolic pressure is <8 mm Hg. Except in the context of tricuspid valve stenosis, the end-diastolic pressure corresponds to the right atrial a wave. Right ventricular systolic pressure is elevated in the presence of a large ventricular septal defect, right ventricular outflow tract obstruction, and pulmonary hypertension. Recordings should be obtained in the apex and in the outflow tract to confirm the absence of any intracavitary gradient. The normal pulmonary artery systolic pressure is equal to the right ventricular systolic pressure (<30 mm Hg), and the mean pressure is <20 mm Hg. Pulmonary artery diastolic pressure begins with the dicrotic notch caused by valve closure, and the diastolic pressure is typically no more than 2 to 3 mm Hg higher than the wedge pressure. Increased pulmonary artery pressure occurs with distal obstruction to flow, such as with peripheral pulmonary stenosis, pulmonary arteriolar obstruction, pulmonary thromboembolism, pulmonary venous obstruction, or left atrial hypertension (due to other causes such as cor triatriatum, mitral stenosis, or left ventricular diastolic dysfunction). Pulmonary artery pressure is also elevated in the presence of aorta-pulmonary artery communications (such as patent ductus arteriosus or aortopulmonary window) or a significant ventricular septal defect (if there is no pulmonic stenosis). In the presence of pulmonary hypertension, a pulse pressure of <40% of the peak systolic pressure suggests a fixed resistance, whereas a wide pulse pressure (>60% of the peak systolic pressure) suggests high flow and low resistance. Pulmonary artery diastolic pressure that is significantly higher than mean left atrial or pulmonary artery wedge pressure also suggests an obstructive cause of pulmonary hypertension. Systolic pressure gradients between right ventricle and pulmonary artery are due to right ventricular outflow tract obstruction, although gradients of 5 mm Hg may be normal. Gradients ≤10 mm Hg may be seen with structurally normal pulmonary valves and increased blood flow, as with a large atrial septal defect. In the setting of very severe branch stenosis or a very tight pulmonary artery band, the catheter may produce enough obstruction of the vessel as it crosses the stenosis that the pressure distally resembles the wedge pressure tracing. When an end-hole catheter is appropriately wedged in a pulmonary artery branch, the distal pulmonary venous pressure is transmitted retrograde through the capillary bed and arterioles to the catheter tip. When using a balloon-tipped wedge catheter (end-hole), the catheter is advanced as far as it can into the distal pulmonary artery and the balloon is partially inflated while monitoring the tracing for its characteristic appearance. The wedge tracing should have the characteristic a- and v-wave appearance of an atrial tracing (see Fig. The wedged catheter position is confirmed by observation of the characteristic left atrial waveform or by withdrawal of fully saturated blood. When small catheters are used, it may not be possible to withdraw a blood sample from the wedged position. Interpretation of the wedge pressure must be guided by an understanding of the anatomy. The pulmonary artery wedge pressure does not reflect the left ventricular end-diastolic pressure when there is pulmonary vein stenosis, cor triatriatum, mitral stenosis, or anomalous pulmonary venous return. When the wedge pressure is elevated, these lesions should be confirmed or ruled out by direct measurement of the left atrial or left ventricular end-diastolic pressure. Left Heart Catheterization Characteristic left heart waveforms are shown in Figure 16. The normal left atrial mean pressure is 6 to 10 mm Hg (depending on age), which is several mm Hg higher than the right atrial mean pressure. In contrast to the right atrium, the left atrial v wave is usually higher than the a wave, and neither is >5 mm Hg above the mean pressure. An elevated a wave is seen with defects resulting in left atrial outflow obstruction (mitral stenosis, supravalvar mitral ring) or with diseases that impair left ventricular compliance (aortic stenosis, coarctation of the aorta). The a wave may be dominant with an atrial septal defect, as a large atrial septal defect allows transmission of pressure across the septum, or with diseases that elevate the right atrial a wave. Elevation of the left atrial mean pressure (and both the a and v waves) may be encountered with large left-to-right shunts at the ventricular or great vessel level or as a sign of left ventricular failure. If the end-diastolic pressures in the left atrium and left ventricle are not equal, some form of mitral valve obstruction is present. Higher gradients (>8 to 10 mm Hg) suggest structural mitral stenosis, whereas lower gradients suggest physiologic stenosis due to increased blood flow across the valve, such as from a large ventricular septal defect. When transseptal technique is used to enter the left atrium, one can use a smaller diameter catheter to advance into the left ventricle and simultaneously measure left atrial and left ventricular pressure. The peak systolic pressure in the left ventricle should be equal to or up to 5 mm Hg greater than the peak systolic pressure in the ascending aorta. A gradient between the left ventricle and the aorta is present in dynamic left ventricular obstruction (as in hypertrophic cardiomyopathy), subaortic stenosis, or aortic valve stenosis. The normal aortic pressure is a reflection of left ventricular stroke volume and systemic vascular resistance. Near the aortic valve, the arterial waveform displays a relatively slow upstroke, a broad peak, and a near-linear drop to end-diastole. In the distal arteries, the peak becomes sharper, the dicrotic notch (representing the decrease in pressure with closure of the aortic valve) becomes more obvious, and pulse wave amplification occurs. The pulse pressure in the ascending aorta is usually 25 to 50 mm Hg, or <50% of the peak systolic aortic pressure. A narrow pulse pressure may be encountered in pericardial tamponade or low cardiac output states. A gradient between the ascending and descending aorta suggests coarctation of the aorta. Derived Hemodynamic Variables Measurement of cardiac output, in terms of pulmonary and systemic blood flow, is a necessary first step to quantifying shunt volume and vascular resistance. Because cardiac output cannot be measured directly, it can be estimated using the indicator dilution technique described by Fick (17). The indicators most commonly used are oxygen or cold saline (thermodilution) (18). In one analogy, a coal-bearing train, representing blood, passes through a coal-loading station (capillary bed) at a constant but unknown rate (cardiac output). The train consists of a series of cars (hemoglobin), each of which have a known load of coal (oxygen content). By knowing the rate of delivery of the coal (oxygen uptake) and the amount of coal in the cars before and after the station, one can easily calculate the rate at which the train is moving through the station. In quantitative terms, cardiac output can be calculated according to the following logic: Blood flows at an unknown rate. Because the quantity of oxygen in the blood that is being sampled directly affects the calculation of cardiac flow rates, it is important to be able to accurately measure or estimate the oxygen content of a blood sample. Oxygen is carried in the blood in two forms: either attached to hemoglobin or dissolved in plasma. The amount of oxygen bound to hemoglobin is influenced by many factors including the partial pressure of oxygen (pO ). For example, hemoglobin F (fetal hemoglobin) has a higher affinity for oxygen than the more common hemoglobin A.
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