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Response to pinprick discount fosamax 35 mg womens health questionnaire, painful pinch/pressure fosamax 70 mg on line breast cancer radiation, or a cold stimulus on the limbs is the most useful in demonstrating a grossly intact sensory arc purchase online fosamax women's health on birth control. Abnormal autonomic responses in metabolic encephalopathy may demand intervention and can cause significant morbidity and mortality buy fosamax 70mg visa womens healthcare group. Hypotension, unresponsive to volume expansion, points to intoxication with barbiturates or opiates, myxedema, or Addisonian crisis. In this setting, occult sepsis must always be ruled out before treating for specific metabolic derangements. Examination of urine, blood cell counts and coagulation factors, blood and sputum cultures, chest x-ray, and a lumbar puncture are essential to rule out infection. Seizures are another significant symptom of metabolic encephalopathy, especially in uremia, hypoglycemia, pancreatic failure, and various types of metabolic acidosis (e. In renal failure, however, one-third to half of the standard loading doses of phenytoin or phenobarbital may be all that is needed to control seizures. A persistent focus of epileptiform activity on the recording warrants further investigation and anticonvulsant therapy. Careful review of all medications taken before and during hospitalization may direct attention to toxicology screens of blood and urine. The general toxicology screen should be sensitive to opiates, benzodiazepines, caffeine and salicylates, theophylline, barbiturates, and alcohol. If there has been a sudden change in mental status, a bolus of 25 g glucose should be administered intravenously without hesitation to avoid prolonged hypoglycemia. Pharmacogenomic studies have revealed that there are 58 genetic variants in metabolic pathways that play a significant role in drug metabolism and activity at target sites, thus influencing toxicity. Many selective serotonin reuptake inhibitors and cardiovascular agents are metabolized by these two classes of enzymes and the aforementioned variants may cause drug levels to be too high or to be converted to active forms so quickly that peak levels are higher than expected, contributing to the adverse effect profiles. Poor metabolizers may also have more drug–drug interactions because of competitive inhibition of clearance of one drug versus the other when coadministered. Reference lists for problematic pharmacogenomic effects are updated regularly and widely available on websites for pharmacologists and toxicologists. Slow activity that is prominent frontally, with deep triphasic waves (in the 2- to 4-Hz range), is characteristic of hepatic encephalopathy but can be seen in renal failure too . This has also been reported in levetiracetam toxicity , hyperammonemic states due to gastroplasty  and ureterosigmoidostomy , and rare metabolic disorders such as ornithine transcarbamylase deficiency . Spreading of the slow activity toward the occipital leads is a sign of deepening coma in this setting. Bursts of high voltage activity amidst normal background frequencies are also a sign of diffuse metabolic disturbance. Most mass lesions, such as subdural hematomas or brain tumors, are evidenced clinically by a rostrocaudal progression of neurologic signs. The initial picture may be nonfocal with obtundation, but this is followed sequentially by flexor or extensor posturing on one or both sides and then the loss of pupillary or caloric responses. Early consultation by a neurologist is crucial, especially when the cause of impaired consciousness is not clearly due to a metabolic disorder. Lumbar puncture is also indicated when there is a rapid onset of encephalopathy, especially with a fever, headache, or meningismus. Occult subarachnoid hemorrhage, infection, or elevated intracranial pressure may be found in the absence of funduscopic changes or clear-cut clinical history. It is easy to recognize hepatic encephalopathy in an individual with the obvious stigmata of chronic liver disease, such as ascites, varices, or jaundice. In those without apparent liver disease, the mental changes may only appear after an additional metabolic demand on the liver. Such stressors are a high-protein meal, gastrointestinal bleeding with increased blood absorption from the gut, or hepatically metabolized drugs . As the patient progresses into a coma, asterixis may be replaced by muscle spasticity and decorticate or decerebrate posturing to stimulation. The Babinski responses are present (extensor plantar reflexes), and gaze-evoked ocular movements are variable at this stage; pupillary responses are always preserved. Hyperventilation is another consistent sign of hepatic encephalopathy and results in respiratory alkalosis. The ocular, pupillary, and respiratory patterns above help to distinguish severe hepatic encephalopathy from space-occupying lesions of the cortex and brainstem. The pathophysiology of hepatic coma is not certain, but it is thought to be caused by portacaval shunting of neurotoxic substances. These putative toxins include excess ammonia, large molecules normally excluded by the blood–brain barrier , increased water, and the “false” neurotransmitter octopamine . The serum transaminases are usually elevated two- to threefold, and serum ammonia is at least in the high normal range once the patient is lethargic—with a linear correlation thereafter between higher laboratory values and lower cognitive state. Neurologic recovery then depends on the capacity of the liver to regenerate at least 25% of its full function. With prolonged or repeated bouts of hepatic coma, there may be persistent, irreversible signs of basal ganglia dysfunction evidenced by chorea, postural tremors, or a parkinsonian picture (acquired hepatocerebral degeneration) . Reye’s Syndrome Reye’s syndrome is a unique and quite morbid form of acute hepatic encephalopathy seen in children, usually between ages 1 and 10 years. It occurs in the clinical setting of an acute viral infection, for example, chickenpox or influenza A or B, plus aspirin therapy . Approximately 4 to 7 days after the viral symptoms start, the child becomes irritable, with vomiting and sometimes with headache or blurred vision. An agitated delirium, combativeness, and progressive obtundation rapidly ensue over hours, followed by hyperventilation, pupillary dilatation, and generalized seizures. The pathology of Reye’s syndrome includes infiltration of the liver and other visceral organs with small fat droplets and diffuse cerebral edema. In cases that are complicated by severe hypoglycemia and seizures, anoxic damage with laminar necrosis of the cerebral cortex is also found. The cause of these changes is presumed to be mitochondrial poisoning, but the pathogenic agent has not yet been identified. This has led to the standard practice of prescribing acetaminophen instead of aspirin for viral symptoms in children, notably reducing the incidence of Reye’s syndrome . The differential diagnosis relies on measurement of liver function and a high index of suspicion in the appropriate setting. The serum transaminases rise three- to fivefold in the first 48 hours, and the serum ammonia is dramatically increased, sometimes into the 200 μmol per L range. Hypoglycemia is also an early sign, aggravating the lactic acidosis and respiratory alkalosis that are seen later in the course. Treatment for Reye’s syndrome is directed toward diminishing the cerebral edema, controlling seizures, and providing adequate electrolytes and glucose for support while the liver is effectively shut down with respect to oxidative metabolism.
A hospital’s surge capacity refers to “the ability to provide adequate medical evaluation and care during events that exceed the limits of the normal medical infrastructure of an affected community  discount 35mg fosamax otc women's health boutique escondido. Operations—This section oversees and coordinates the immediate response and ongoing operational activities generic fosamax 35mg on line womens health consultants ob gyn. Planning—This section assesses the potential for future events discount fosamax 35mg online menstruation vomiting, develops contingency plans for future events discount fosamax 35mg fast delivery pregnancy jokes, and plans timelines for the deployment of critical resources. These planning activities permit the operations branch to focus on managing the response to active events. Logistics—This section focuses on the logistical support that every event requires, including equipment, personnel, supply, and infrastructure support. Finance—This section accounts for and manages all money that is spent during the response to a disaster. Although immediate costs and purchases during a disaster may be supported by affected communities and hospitals, accurate purchasing records, inventory records, personnel costs, and transportation costs must be carefully managed in order to recoup costs after the event insofar as possible. Surge Capacity Surge capacity refers to the ability of a hospital or other health care system to expand its normal operating capacity in the setting of an emergency. This level would be implemented during major mass-casualty incidents that trigger activation of the hospital emergency operations plan. Contingency capacity: This level would be used temporarily during a major mass-casualty incident, or on a longer-term basis during a disaster whose medical demands exceeded routine hospital and community resources. This level of response implies the need to increase a hospital’s critical care capacity by 100% and may require the use of alternate hospital resources for the provision of critical care, for example, the use of postanesthesia care unit spaces and staff . In general, the level of medical care provided at this degree of surge response would be within the usual community standards. Crisis capacity: This level would be implemented during catastrophic situations that result in a significant impact on the standard of medical care that can be provided. Examples of such an event, which implies a 200% increase of the critical care demand on a hospital, include a prolonged pandemic, a natural disaster with extensive destruction of infrastructure, a large-scale terrorist attack, or a prolonged violent conflict. Severe limitations of space, staff, and supplies would not allow hospitals to provide the usual standard of medical care. At the crisis level, institutions will need to consider triage principles, rationing of care, and other potential ethical challenges while maximizing their ability to provide the best possible care to the greatest number of the patients. Hospitals and their critical care units should develop disaster preparedness plans that contain specific criteria for each level of surge capacity. Identical disasters might have very different effects on different hospitals, depending on an institution’s size and mission. For example, an eight-victim automobile crash may require a conventional level of surge capacity for a large hospital that includes a level 1 trauma center, but could require a contingency or crisis level of surge capacity for a small community hospital. During contigency and crisis capacity scenarios, a hospital may need to optimize its resources in order to maximize its ability to care for those patients in greatest need. By providing temporary facilities for noncritical care, hospitals can redirect resources towards higher-acuity patients. Department of Health and Human Services spends approximately $255 million per year, or over $4 billion since 2002, in grant support to local institutions to enhance their ability to respond to disasters, including improvements of surge capacity . Government Accountability Office indicated that many states were not adequately prepared to respond to a major catastrophe, such as an influenza pandemic . Disasters requiring critical care resources include massive trauma events, such as natural disasters, transportation-related accidents, or violent trauma such as deliberate explosions or mass shootings. Lastly, disasters may affect hospitals through destruction of the hospital infrastructure itself, such as during a hurricane or earthquake, or by illness or injury that afflict the hospital staff; in both scenarios, the mission of the hospital can be impaired at a time when it is needed most. The 2010 earthquake in Haiti led to the immediate death of 230,000 people, but the mass trauma was followed by a cholera epidemic that affected 352,033 during 2011 alone. The devastation to Haiti’s medical system, already fragile before the quake, further impaired that country’s ability to cope with the other two disasters . The bulk of this growth has occurred in academic medical centers and other large hospitals, suggesting that potential surge capacity may be limited at smaller, nonteaching hospitals . Of special note, a disproportionate paucity of pediatric critical care resources would exist should we become resource limited during a disaster. This relative scarcity of pediatric critical care resources may present unequal access to care for children as compared to adults during disasters, a time when children often are disproportionately affected. Overall, these data suggest that hospitals of developed countries have a consistent, although uneven, ability to expand their critical care capacity during a disaster. However, even with normal excess capacity, there may not be a sufficient number of critical care beds to meet the demands of a pandemic that might affect the entire nation at the same time. Thus, if critical care capabilities become overwhelmed by large numbers of critically ill or injured patients during a disaster, high mortality rates will likely occur. Surging Assets to Optimize Critical Care Capability When planning for surge capacity during disasters, hospitals need to prepare for events that have a sudden impact and are of relatively short duration, such as transportation accidents and explosions, as well as more prolonged events, such as natural disasters and pandemics [3,5]. Space: the physical space within (or rarely outside of) the hospital that can be used to provide critical care to a large number of critically ill or injured patients. The provision of mechanical ventilation is the most common requirement needed to manage critically ill patients with respiratory compromise. The main challenge of providing this important therapeutic modality during a disaster is the availability of mechanical ventilators. During a major influenza pandemic, demand for mechanical ventilators in the United States could increase by 60,000, assuming a 30% attack rate and a high case-fatality rate of 0. The United States has approximately 62,000 full-feature ventilators, or 20 of these per 100,000 residents, plus an additional 100,000 ventilators with fewer features but which could be used during a disaster . Thus, in preparing to provide mechanical ventilation to a large number of critically ill disaster casualties, planners need to consider other options, such as high-flow nasal cannula oxygenation or noninvasive positive-pressure ventilation for selected patients. Anesthesia machines and transport ventilators could serve as additional options, although these could be similarly limited by the number of trained personnel and have disadvantages with regard to infection control [29–32]. The provision of critical care during a disaster will also require that a large quantity of supplies and pharmaceuticals be on hand and readily available to critical care providers. The Joint Commission currently requires that accredited hospitals plan for 96 hours of autonomous function, without external resupply, in the event of disaster (although 96 hours of supplies and the ability to function at full capacity are not required). In 2005, during the Hurricane Katrina disaster in New Orleans, the lack of available supplies, pharmaceuticals, and operational equipment forced the dedicated staff at Charity Hospital to improvise critical care practices and deviate from the usual standards of care prior to final evacuation of the hospital . Hospitals in areas affected by the Great East Japan Earthquake and subsequent tsunami of 2011 and by Hurricane Sandy in 2012 showed comparable experiences. In Miyagi Prefecture in Japan, for example, six out of 14 of hospitals had less than 1 day of food on hand at the time of the quake, and another six hospitals had less than 1 day of medical supplies. Just-in-time supply practices at New York City hospitals produced some similar shortages, offset in part by supplies available from elsewhere in the city [34,35]. Shortages of intensivists, critical care nurses, respiratory therapists, critical care pharmacists, and other specially trained personnel may be a limiting factor in caring for large numbers of critically ill patients.
It has been reported that many of the patients with arsenic neuropathy were initially thought to have Guillain–Barré disease [5 order discount fosamax online breast cancer north face,7] cheap fosamax 35mg free shipping menstrual or pregnancy cramps. Because the fundamental lesion in arsenic toxicity is the loss of capillary integrity discount fosamax 35mg fast delivery womens health of westerly, increased glomerular capillary permeability may result in proteinuria buy 35mg fosamax with visa breast cancer pink. Because of shock and decreased glomerular filtration rate and depending on the dose of arsenic ingested, peak urinary arsenic excretion may often be delayed by 2 to 3 days. Accordingly, arsenic removal by hemodialysis has been reported to exceed its daily urinary excretion in patients with acute renal failure. In most cases, a diffuse, branny desquamation develops over the trunk and extremities; it is dry, scaling, and nonpruritic. Patchy hyperpigmentation—dark-brown patches with scattered pale spots, sometimes described as “raindrops on a dusty road”—occurs particularly on the eyelids, temples, axillae, neck, nipples, and groin. Arsenic hyperkeratosis usually appears as cornlike elevations, less than 1 cm in diameter, occurring most frequently on the palms of the hands and on the soles of the feet. Most cases of arsenic keratoses remain morphologically benign for decades, and in other cases, marked atypia (precancerous) develops and appears indistinguishable from Bowen’s disease—an in situ squamous cell carcinoma. Skin lesions take several years to manifest the characteristic pigmented changes and hyperkeratoses, whereas it may take up to 40 years before skin cancer becomes evident. Brittle nails with transverse white bands (leukonychia striata arsenicalis transversus), Reynolds–Aldrich–Mees lines, appearing on the nails have been associated with arsenic poisoning. Leukonychia striata arsenicalis transversus takes about 5 to 6 weeks to appear over the lunulae after an acute poisoning. Diagnostic Evaluation the temporal sequence of organ system injury may suggest acute arsenic intoxication. After a delay of minutes to hours, severe hemorrhagic gastroenteritis becomes evident, which may be accompanied by cardiovascular collapse or death. Bone marrow depression with leukopenia may appear within 4 days of arsenic ingestion and usually reaches a nadir at 1 to 2 weeks. Sensorimotor peripheral neuropathy may become apparent several weeks after resolution of the initial signs (gastroenteritis or shock) of intoxication resulting from ingestion. The differentiation between arsenic neuropathy and Landry–Guillain– Barré disease is based on clinical and laboratory findings in that arsenic neuropathy rarely involves the cranial nerves, sensory manifestations are more prominent, weakness in the distal portions of the extremities is more severe, and the cerebrospinal fluid protein concentrations are usually less than 100 mg per dL [5,6]. Some arsenic compounds, particularly those of low solubility, are radiopaque, and if ingested they may be visible on an abdominal radiograph. Urine arsenic concentrations may be measured as “spot,” that is, the concentration in a single-voided urine specimen, reported in micrograms per liter. Urine arsenic concentrations may also be measured as a timed urine collection, or the concentration in urine collected during a 12- to 24-hour period, reported in micrograms per 12 or 24 hours. In the first 2 to 3 days following acute symptomatic intoxications, total 24- hour urinary arsenic excretion is typically in excess of several thousand micrograms, with spot urine concentration >1,000 mg per L, and depending on the severity, it may not return to background for weeks. Therefore, it is important to take a careful dietary history of the past 48 hours when only total urinary arsenic is measured. However, blood concentrations decline rapidly to normal values despite elevated urinary arsenic excretion and continuing symptoms. Elevated arsenic content in hair and nail segments, normally <1 part per million, may persist for months after urinary arsenic values have returned to background. However, caution should be exercised when interpreting the arsenic content obtained from hair and nails because the arsenic content of these specimens may be increased by external exposure. Treatment begins with eliminating further exposure to the toxin and providing basic and advanced life support. Gastric lavage should be performed following an acute ingestion and should be considered if the ingestion has been within the past 24 hours because some arsenic compounds of low solubility may be retained in the stomach for a prolonged period. Frequently, seriously poisoned patients will have already vomited, evacuating some of their stomach contents. Intravascular volume depletion may require aggressive replacement with crystalloids, colloids, and blood products. There are no good data to indicate that suppression of ventricular dysrhythmias decreases mortality rates. If dysrhythmias occur, they should be treated according to current advanced cardiac life support guidelines. Lidocaine, magnesium, and isoproterenol have been used with limited success in the management of arsenic-induced torsades de pointes. Patients with arsenic polyneuropathy should receive analgesics for pain and physical therapy for rehabilitation. Patients with polyneuropathy associated with severe arsenic poisoning should be observed closely for respiratory dysfunction. In cases in which there is progressive sensorimotor dysfunction, particularly ascending weakness, respiratory muscle function should be monitored carefully. Hemodialysis (initiated 24 to 96 hours postingestion) has been reported to remove about 4 mg of arsenic during a 4-hour period in patients with established renal failure. It should not be surprising that only small amounts of arsenic are removed by dialysis as minimal amounts of arsenic are left in the central compartment once tissue distribution and equilibration is complete. The principle behind chelation therapy is to increase excretion of the metal and decrease the target organ’s metal burden. It competes with tissues and other compounds containing thiol groups for metal ions, removes metal ions that previously have been bound, and binds with the metal ion to form a stable complex (chelate), rendering the metal less reactive and less toxic. The metal–chelator complex is water soluble and can be excreted in the urine, bile, or both, and to some extent it can be removed by hemodialysis. In cases of suspected acute symptomatic intoxication, treatment should not be delayed while waiting for specific laboratory confirmation. The initial dose is 3 to 5 mg per kg every 4 hours, gradually tapering to every 12 hours during the next several days. D-Penicillamine has also been reported to be successful adjunct treatment in cases of acute pediatric arsenic toxicity . Disadvantages in using D-penicillamine include that it is administered only by the oral route, it is usually not well tolerated, it should be used with caution in patients who are allergic to penicillin, and it entails potential enhanced absorption of arsenic-chelate complex. Adverse drug events associated with long-term D-penicillamine treatment include fever, pruritus, leukopenia, thrombocytopenia, eosinophilia, and renal toxicity. A complete blood count and renal function tests should be monitored weekly during D-penicillamine therapy. The reported adverse drug events include pain at the injection site; systolic and diastolic hypertension with tachycardia; nausea; vomiting; headache; burning or constricting sensation in the mouth, throat, and eyes; lacrimation; salivation; rhinorrhea; muscle aches; tingling of the extremities; pain in the teeth; sense of constriction in the chest; abdominal pain; sterile or pyogenic abscesses at the site of injection; and a feeling of anxiety or unrest. The adverse drug events may be lessened by the use of epinephrine or by pretreatment with antihistamine or ephedrine . Usually 24- hour urinary arsenic excretion is followed before, during, and after chelation with continued chelation therapy until the urinary arsenic excretion is <25 μg per 24 hours. This is likely to occur during the recovery period when urinary inorganic arsenic concentration has declined to less than 100 μg per 24 hours or total blood arsenic concentration is less than 200 μg per L . However, the value of chelation in the treatment of an established arsenic neuropathy has not been demonstrated. In cases of chronic symptomatic arsenic intoxication with high urinary arsenic excretion, an empiric course of chelation may be warranted. The garlic-like odor is not a reliable indicator of exposure because hazardous effects may occur below the odor threshold.
In regard to antithrombotic therapy purchase fosamax canada menstrual endometrium, patients with diabetes should be treated similarly to patients without diabetes purchase fosamax 35 mg without prescription breast cancer ribbon template. For patients at low risk buy fosamax on line amex menstruation 3 weeks straight, medical therapy is appropriate generic fosamax 70mg with mastercard menstruation games, and a more conservative ischemia-guided approach is reasonable. Cangrelor is a recently approved intravenous P Y2 12 receptor blocker with a short onset and offset of action [8,106]. Falk E: Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Mizuno K, Satumo K, Miyamoto A, et al: Angioscopic evaluation of coronary artery thrombi in acute coronary syndromes. Arbustini E, De Servi S, Bramucci E, et al: Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty. Reichlin T, Hochholzer W, Bassetti S, et al: Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. Keller T, Zeller T, Peetz D, et al: Sensitive troponin I assay in early diagnosis of acute myocardial infarction. High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. Veretto T, Cantalupi D, Altieri A, et al: Emergency room technetium- 99 m sestamibi imaging to rule out acute myocardial ischemic events in patients with nondiagnostic electrocardiograms. Berning J, Launbjerg J, Appleyard M: Echocardiographic algorithms for admission and predischarge prediction of mortality in acute myocardial infarction. Multicenter Postinfarction Research Group: Risk stratification and survival after myocardial infarction. Nicod P, Gilpin E, Dittrich H, et al: Influence on prognosis and morbidity of left ventricular ejection fraction with and without signs of left ventricular failure after acute myocardial infarction. Validation of the Killip- Kimball classification and late mortality after acute myocardial infarction. A randomized comparison of tissue-type plasminogen activator versus placebo and early invasive versus early conservative strategies in unstable angina and non-Q-wave myocardial infarction. Toss H, Lindahl B, Siegbahn A, et al: Prognostic influence of increased fibrinogen and C-reactive protein levels in unstable coronary artery disease. Is there an association between aspirin dosing and cardiac and bleeding events after treatment of acute coronary syndrome? Simon T, Verstuyft C, Mary-Krause M, et al: Genetic determinants of response to clopidogrel and cardiovascular events. Association of clopidogrel pretreatment with mortality, cardiovascular events, and major bleeding among patients undergoing percutaneous coronary intervention: a systematic review and meta-analysis. Long-term dual antiplatelet therapy for secondary prevention of cardiovascular events in the subgroup of patients with previous myocardial infarction: a collaborative meta-analysis of randomized trials. Tricoci P, Huang Z, Held C, et al: Thrombin-receptor antagonist vorapaxar in acute coronary syndromes. Bivalirudin versus heparin in patients planned for percutaneous coronary intervention: a meta-analysis of randomised controlled trials. Chatterjee S, Chaudhuri D, Vedanthan R, et al: Early intravenous beta- blockers in patients with acute coronary syndrome—a meta-analysis of randomized trials. The Multicenter Diltiazem Postinfarction Trial Research Group: the effect of diltiazem on mortality and reinfarction after myocardial infarction. Yusuf S, Sleight P, Pogue J, et al: Effects of an angiotensin-converting- enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Randomized Aldactone Evaluation Study Investigators: the Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. Scandinavian Simvastatin Survival Study Group: Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian simvastatin survival study (4S). Rosengren A,Wallentin L, Simoons M, et al: Age, clinical presentation, and outcome of acute coronary syndromes in the Euroheart acute coronary syndrome survey. The first priority is, therefore, to determine whether the patient has poor perfusion related to the dysrhythmia and whether emergent management is required . If the patient is sufficiently stable, providers may have time to perform a detailed assessment focusing on a relevant history, including ongoing symptoms, underlying cardiovascular disease, and medications, as well as pertinent laboratory tests. Third-degree atrioventricular block or complete heart block with atrioventricular dissociation and ventricular escape rhythm. After two unsuccessful attempts of defibrillation, epinephrine can be used as a first-line vasopressor agent . Epinephrine intravenous route may not be effective after 15 min of resuscitation, and vasopressin may be successfully used. Providers should anticipate the difficult airway management, and no more than two attempts should be made for intubation. Administration of large, repeated doses of magnesium should be avoided in the presence of severe renal insufficiency because of its potential toxicity. Benzodiazepines the use of flumazenil, as an antidote, in patients with undifferentiated coma is not recommended because it may be associated with seizures, arrhythmias, and hypotension. Many of these drugs also have a characteristic known as use-dependency, such that the administration of β-blockers can decrease their electrophysiologic effect. Digoxin Antidigoxin Fab antibody should be administered to patients with severe life-threatening cardiac glycoside toxicity after resuscitation. Hyperkalemia is a marker of severity in acute cardiac glycoside poisoning and is associated with poor prognosis. Antidigoxin Fab may be administered empirically to patients with acute poisoning from digoxin whose serum potassium level >5. Local anesthetic Guidelines recommend considering intravenous long-chain toxicity fatty acid emulsion as an initial bolus during cardiac arrest, particularly in bupivacian toxicity. The guidelines recommend (class I) controlled temperature management between 32°C and 36°C for a patient with in- hospital arrest, irrespective of initial rhythms (shockable vs. It is noteworthy that a prospective study of targeted temperature for patients with in-hospital cardiac arrest is not available. In hemodynamically stable patients, cardioversion, administration of intravenous magnesium, and lidocaine are initial steps. As for hemodynamically stable patients, intravenous magnesium can be given for the purpose of treatment and prevention, irrespective of serum magnesium level. Its diagnostic performance varies among clinicians with the sensitivity >79% and specificity ~60% [17,19]. All antiarrhythmic drugs can be proarrhythmic, and the decision whether to continue or discontinue therapy should be discussed with a cardiologist. Unstable patients with palpable pulses require immediate cardioversion with appropriate sedation and analgesia.
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