Existing hospital policies for monitoring during conscious sedation should be followed purchase 100 mg januvia with amex, including frequent assessment of blood pressure and pulse oximetry januvia 100 mg with amex. Supplemental oxygen is delivered via nasal cannula best 100mg januvia, face mask buy januvia 100 mg with visa, or, in the case of heavier sedation, an Ambu bag. Shock Waveforms Defibrillators that employ biphasic waveforms have largely replaced those utilizing monophasic waveforms. Advantages of biphasic waveforms are lower defibrillation thresholds, meaning shocks using biphasic waveforms require less energy to achieve defibrillation, and they are less likely to cause skin burns and myocardial damage [3]. Biphasic truncated exponential waveform and biphasic rectilinear waveform are both commercially available, with the former being more common. For instance, one study demonstrated the equivalent efficacy of a 120 to 200 J biphasic sequence with a 200 to 360 J monophasic sequence [9]. However, there is evidence that biphasic shocks result in less dermal injury, and no significant difference in myocardial damage [10]. Although an animal model suggested better maintenance of cardiac function after biphasic shocks, human data on myocardial function are not yet available [11]. Whichever modality is used, impedance can be minimized by avoiding positioning over breast tissue, by clipping body hair when it is excessive, by delivering the shock during expiration, and by firm pressure on the pads or paddles. The optimal anatomic placement of pads and paddles is not clear; however, the general principal holds that the heart must lie between the two electrodes [3]. In anterior-lateral placement, the lateral paddle should be located lateral to the left breast and should have a longitudinal orientation, since this placement results in a lower transthoracic impedance than horizontal orientation. After the patient is adequately prepared and the electrodes are applied, attention may be turned to the device itself. If cardioversion—rather than defibrillation—is to be performed, the synchronization function should be selected. One should be aware that the synchronization function is automatically deselected after each shock in most devices, meaning that it must be manually reselected prior to any further shock delivery if another synchronized shock is desired. Recommendations specific to each device are available in the manufacturer manuals and should be consulted by physicians unfamiliar with their particular device. In the 2010 algorithm, vasopressors (epinephrine or vasopressin) may be given before or after the second shock, and antiarrhythmics such as amiodarone and lidocaine may be considered before or after the third shock (Table 15. If there is any uncertainty regarding which energy should be used, it is best to shock with the highest available energy. If signs of instability are present (such as chest pressure, altered mental status, hypotension, or heart failure) and are thought to be secondary to the tachycardia, urgent cardioversion is indicated. If the patient is stable, however, one might consider enlisting the assistance of an expert in distinguishing between ventricular and supraventricular arrhythmia. Adenosine may also be considered for a diagnostic and therapeutic option for a regular, monomorphic, wide complex tachycardia (a new addition to the 2010 guidelines). If the patient exhibits signs or symptoms of hypoperfusion and instability mentioned above, immediate cardioversion is advised. Treatment of Supraventricular Tachycardia the most common narrow complex tachycardia is sinus tachycardia which is an appropriate cardiac response to some other physiologic condition. If these fail, nondihydropyridine calcium channel antagonists or β-blockers may terminate the arrhythmia. Cardioversion is indicated only rarely for clinical instability, usually in patients with underlying heart disease in whom the initial therapies fail. However, a rapid ventricular response is usually secondary to, rather than the cause of, heart failure and ischemia. Many patients become asymptomatic or minimally symptomatic with adequate rate control, allowing the decision about cardioversion to be made electively. The ideal starting energy for biphasic devices has not yet been defined, but should be lower than that of monophasic devices. Current guidelines indicate that peri-cardioversion anticoagulation with unfractionated heparin, low molecular weight heparin, direct thrombin inhibitor, or a factor Xa inhibitor are all acceptable options [2,19]. It is recommended that anticoagulation continue for 3 weeks after cardioversion, as the risk of thromboembolism still exists during this period. Pharmacologic Cardioversion Cardioversion can be achieved not only electrically but also pharmacologically. Although electrical cardioversion is quicker and has a higher probability of success, pharmacologic cardioversion does not require sedation. The risk of thromboembolism with pharmacologic cardioversion has not been well established but is thought to be similar to that of electrical shock because it is the return of sinus rhythm rather than the shock itself that is believed to precipitate thromboembolism [5]. Dofetilide, flecainide, ibutilide, propafenone, amiodarone, and quinidine have been demonstrated to have some degree of efficacy in restoring sinus rhythm [19]. Although β-blockers and calcium channel antagonists are often believed to facilitate cardioversion, their efficacy has not been established in controlled trials. When cardioversion fails to even temporarily terminate the arrhythmia, the operator’s technique should be reviewed and modified. If a device that delivers monophasic waveform shocks is being employed, it may be exchanged for one that delivers biphasic waveform shocks. Sotalol, ibutilide, dofetilide, or amiodarone may be initiated prior to another attempt at cardioversion. Complications of Defibrillation and Cardioversion Burns Shock can cause first-degree burns and pain at the paddle or pad site. One study documented moderate to severe pain in nearly one quarter of patients undergoing cardioversion. Another study showed a lower rate of dermal injury with biphasic rather than monophasic shocks, and is associated with lower energy necessary with biphasic shocks. The lowest effective energy should be used to minimize skin injury; however, this must be balanced against a requirement for multiple shocks when a low energy shock fails to terminate an arrhythmia. In addition, burns are much more common with self-adhesive pads, so that for elective cardioversion, paddles may be preferable. Arrhythmias Bradyarrhythmias such as sinus arrest and sinus bradycardia are common immediately after shock and are almost always short-lived. If cardioversion or defibrillation must be performed urgently, one should anticipate the ventricular arrhythmias to be more refractory to shock than usual. This observation suggests that clinically significant myocardial damage from cardioversion or defibrillation is unlikely. Nonetheless, it has been suggested that any two consecutive shocks be delivered no less than 1 minute apart to minimize the chance of myocardial damage. However, one must be aware of the possibility that external energy delivery may alter the programming of the internal device. Furthermore, energy may be conducted down an internal lead, causing local myocardial injury and a resultant change (typically an increase) in the pacing or defibrillation threshold. In addition, interrogation of the device immediately after any external shock delivery is recommended. For these reasons, chest thump is considered a therapy of last resort, administered only to a pulseless patient when a defibrillator is unavailable and unlikely to become available soon. Cardioversion and Defibrillation in Pregnancy Cardioversion and defibrillation have been performed in all trimesters of pregnancy without obvious adverse fetal effects or premature labor [13]. Part 5: Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing. Neal S, Ngarmukos T, Lessard D, et al: Comparison of the efficacy and safety of two biphasic defibrillator waveforms for the conversion of atrial fibrillation to sinus rhythm. Scholten M, Szili-Torok T, Klootwijk P, et al: Comparison of monophasic and biphasic shocks for transthoracic cardioversion of atrial fibrillation. Lown B, Kleiger R, Williams J: Cardioversion and digitalis drugs: changed threshold to electric shock in digitalized animals. There is no other bedside method of cardiac imaging that is as immediate and relevant for assessment of cardiopulmonary failure. When combined with other aspects of critical care ultrasonography, it is a key element of the whole-body ultrasonography approach to the critically ill patient, because, when combined with the history and physical examination, it affords the intensivist the ability to promptly diagnose and manage hemodynamic failure. In addition, the reader of the echocardiography service study may not be fully aware of the clinical facts of the case.

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An occasional patient presents with fulminating disease; crisis management then coincides with initial evaluation and institution of therapy generic januvia 100 mg on line. Otherwise generic januvia 100mg mastercard, crisis may be precipitated by other illnesses buy cheap januvia online, such as influenza or other infections discount januvia, or by surgery. General Measures the respiratory function of any acutely deteriorating or severely weak myasthenic should be monitored compulsively. When the weakening myasthenic reaches a point at which increased respiratory effort is required, fatigue often prevents the effective use of secondary muscles, and respiratory failure rapidly ensues. Arterial blood gas values and even oxygen saturation are poor indicators of incipient failure in the face of respiratory muscle compromise. If a2 downward trend is noted (greater than 30% decrease) [16], elective intubation should be considered even sooner, unless there is a realistic expectation of rapid reversal. Acute deterioration in a myasthenic always warrants consideration of contributing circumstances or concurrent illness that may accentuate the underlying defect in neuromuscular transmission. The presence of fasciculations, diaphoresis, or diarrhea should alert the clinician to this possibility. In the past, the importance of differentiating between myasthenic crisis and cholinergic crisis was stressed. Edrophonium testing was used to differentiate between the two; abrupt deterioration after a conventional 10-mg test dose indicated overdosage with cholinesterase inhibitors. Because oftentimes it is very difficult to determine the response and because of the potential side effects with overdosage of anticholinesterase drugs of increased pulmonary secretions, many authors now recommend discontinuation of cholinesterase inhibitors at the time of crisis [2,17,18] and reinstituting them when patients are stronger. A brief holiday from cholinesterase inhibition also often results in an enhanced response to therapy when reinstituted. There should be a comprehensive search for systemic infection in the deteriorating patient, particularly the patient receiving immunosuppressive therapy. Otherwise, insignificant electrolyte effects on transmitter release or muscle membrane excitability may be amplified at the myasthenic neuromuscular junction. Myasthenia gravis may also impart enhanced sensitivity to a number of medications that have only minimal effects on neuromuscular function in normal individuals. Aminoglycoside and fluoroquinolone antibiotics, β-blockers, and many cardiac antiarrhythmics may have adverse effects. Anticholinergics, respiratory depressants, and sedatives of any kind should be avoided or used only with great caution. This increased sensitivity occasionally results in postoperative failure to wean in an undiagnosed mild myasthenic patient who has undergone surgery for an unrelated problem. Incentive spirometry should be avoided, because muscular fatigue outweighs any potential benefit, even in the postoperative patient. Careful attention to efficient clearance of respiratory secretions is key and can be complicated by cholinesterase inhibitors, which increase respiratory secretions. Atropine may be used to minimize this effect, but its other autonomic side effects, such as ileus, constipation, and delirium, may limit longer-term use. Symptomatic therapy with cholinesterase inhibitors is now primarily used on a shorter-term basis, pending response to immunomodulating therapies. Plasmapheresis; intravenous human immune globulin; corticosteroids; and longer-term immunosuppressants and cholinesterase inhibitors are discussed individually. The results have been quite favorable, prompting the National Institutes of Health Consensus Conference to support its use despite the lack of controlled trials [20]. Most patients demonstrate a significant clinical response within 48 hours of initiation of plasmapheresis, although the response is short lived unless therapy is continued on an intermittent basis. The rapid response from plasmapheresis can be crucial in the face of crisis, providing a short-term reprieve during which alternative therapy can be initiated or any intercurrent medical problems resolved. Approximately 50 mL per kg should be exchanged per session [21], approximating 60% to 70% of total plasma volume. Plasma removed is replaced by an equal volume of normal saline and 5% albumin, adjusted to maintain physiologic concentrations of potassium, calcium, and magnesium. Many patients develop increased sensitivity to cholinesterase inhibitors after plasmapheresis; dosage should be correspondingly reduced. The major potential complications of plasmapheresis include hypotension; arrhythmia; and hypercoagulability due to hemoconcentration. Although plasmapheresis is too invasive to be used for long-term therapy in the majority of patients, periodic plasmapheresis has been beneficial in some patients with moderate to severe myasthenia refractory to immunosuppressive agents [22]. More recently, a total dose of 1 g per kg was reported to be equally efficacious to 2 g per kg, although there was a trend toward slight superiority of the higher dose [28]. Maximal improvement occurred by the second week after therapy, and the therapeutic response usually persists for several weeks. Patients should be pretreated with acetaminophen and diphenhydramine to prevent flu- like symptoms that commonly occur during infusion. Renal function should be checked prior to initiation of therapy, because renal failure may occur in those with renal insufficiency. Likewise, an IgA level should be obtained,because patients with IgA deficiency may develop anaphylaxis. Longer-Term Immunosuppression Corticosteroids have proven to be an effective long-term therapy for almost all myasthenic patients whose clinical manifestations cannot be well managed with low doses of cholinesterase inhibitors. Despite potential side effects associated with corticosteroid therapy, a response rate of greater than 80% supports its use [29]. Carbohydrate metabolism, electrolytes, blood pressure, and diet should be closely monitored; bisphosphonates (e. Screening for tuberculosis exposure with skin testing and chest radiographs should be done before initiation of therapy. Approximately one-third of patients may become transiently weaker before they improve, if given high doses of prednisone initially [3]. Initiation with relatively low doses of prednisone and increasing in a stepwise manner has been advocated by some clinicians to minimize interim deterioration, especially if the patient is not intubated [17]. The authors prefer to begin with 15 to 25 mg of prednisone or its equivalent as a single daily dose, increasing the dose by 5 mg every second or third day until a dose of 1 mg/kg/d is reached. Oral corticosteroids are preferable, because there is a risk of developing acute steroid-induced myopathy in patients with myasthenia who are given high doses of intravenous corticosteroids [18,30]. Once maximal response is obtained, usually within 2 to 3 months, patients may be gradually shifted to alternate-day therapy by concurrently reducing the off-day dose and increasing the on-day dose, with a 10-mg shift made once each week. Some individuals note a definite off-day adverse effect; this can usually be countered with a 10-mg alternate-day dose. Many patients can be maintained in remission with as little as 20 to 25 mg of prednisone every other day (or alternating with 10 mg). Only rare patients remain in remission if therapy is discontinued, and overenthusiastic tapering of steroids is an all too common precipitant of unnecessary disability or even crisis. Myasthenia sometimes remits spontaneously, and if the patient has undergone thymectomy (see later), the probability of remission increases appreciably, making discontinuation of therapy a more realistic option. It is effective in 70% to 90% of patients with myasthenia gravis [2] and is often initiated in patients with an insufficient response to corticosteroids, as a steroid-sparing agent, or in patients in whom corticosteroids are contraindicated [3]. Azathioprine is limited by a relatively long delay before its effects are clinically evident, up to 6 to 12 months, but its side-effect spectrum compares favorably with steroids over a time frame of many years. If a patient tolerates a 50- mg per day test dose, the daily dose can be increased by 50 mg each week up to 2 to 3 mg/kg/d. The dose is reduced if the white blood cell count is less than 3,000 per μL; an elevated mean corpuscular volume can also be used to assess adequate response [4,31]. In up to 10% of patients, an influenza-like reaction characterized by fever, malaise, and myalgias occurs within the first few weeks of therapy and resolves after discontinuing the drug [2,31]. Concurrent treatment with allopurinol should also be avoided,because it interferes with the degradation of azathioprine, thereby increasing the risk of bone marrow and liver toxicity [31]. Onset of clinical improvement is quicker than with azathioprine, with most patients noticing improvement after 1 to 3 months, and becoming maximal around 7 months [33]. Its major limitations are renal toxicity and hypertension, which are seen in about one-quarter of patients. To minimize side effects, the starting dose of 5 mg/kg/d can be given in two divided doses 12 hours apart, followed by adjustments to maintain a predose trough level in the range of 100 to 150 ng per L. Subsequent adjustments can be made depending on creatinine levels and clinical improvement, with the aim to reduce the dose as much as possible, once maximal improvement is obtained [33]. Significant hypertension and preexisting renal disease are contraindications to the use of cyclosporine. Another agent from the realm of transplant medicine, mycophenolate mofetil (CellCept), has also been used effectively for longer-term therapy. Several case series, retrospective analysis, and a small placebo-controlled, double-blind trial suggested that mycophenolate mofetil is beneficial in patients with myasthenia gravis [34–36].

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