DOWNLOAD PDF INFLUENCE OF POST-EXERCISE GLUCOSE INGESTION ON PLASMA POTASSIUM LEVELS AND ECG MEASUREMENTS

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1 Chapter 1 : Salicylate Toxicity Get this from a library! Influence of post-exercise glucose ingestion on plasma potassium levels and ECG measurements. [Hedy Reynolds]. Reye Syndrome Approach Considerations Initial and serial salicylate levels are important in the evaluation of salicylate toxicity. The absolute level should not detract from the importance of careful and repeated clinical evaluation. Immediately begin therapy in symptomatic patients. Do not wait for the salicylate levels to return from the laboratory. If managing an acute or acute-on-chronic ingestion, repeat the salicylate serum level test every 2 hours until the salicylate level falls. If the levels increase, consider the possibility that a sustained-release preparation was ingested or that a concretion in the GI tract has formed. One cautionary note is to always confirm the units of measurement with the laboratory. Traditional units are milligrams per deciliter; however, many laboratories report salicylate concentrations in milligrams per liter or micrograms per milliliter, both of which differ by a factor of 10 from the traditional units. Monitoring peak concentration In overdoses, the peak serum concentration may not occur for hours, so concentrations obtained before that time may not reflect peak levels. Chronic ingestion can increase the half-life to longer than 20 hours. In patients with significant ingestions, serum salicylate levels should be monitored at least every 2 hours until a peak has been reached and then every hours until the peak falls into the nontoxic range. Serum electrolytes and renal function studies BUN and creatinine levels Obtain measurements of serum electrolytes, blood urea nitrogen BUN, creatinine, calcium, magnesium, and glucose. Repeat these tests at least every 12 hours until the salicylate level falls and the acid-base disturbance improves. If hemodialysis is required, testing is needed more frequently. Monitor serum potassium concentrations; normal levels may be difficult to obtain during alkalization therapy. Electrolyte levels should be obtained every hours when the patient is being alkalized because severe hypokalemia and other electrolyte abnormalities can occur. Urinalysis Monitor and maintain an alkaline urine ph every 2 hours during alkalization therapy. Maintain a urine ph of 7. It is important to monitor the serum ph, as well as the urine ph. Consider obtaining a urine specimen for a qualitative toxicology screen. Imaging studies A chest radiograph is indicated if evidence of severe intoxication, pulmonary edema, aspiration pneumonitis, or hypoxemia is present. Consider an abdominal radiograph if an aspirin concretion is suspected. Other methods of identifying gastric salicylate bezoars include the following: Ultrasonography Computed tomography CT scanning of the abdomen Endoscopy Other studies to obtain include the following: Serum glucose level Serum acetaminophen levels - These should always be obtained in any unknown overdose Liver function tests Prothrombin time and activated partial thromboplastin time CBC count Hepatic, hematologic, and coagulation profiles - Obtain for patients with clinical evidence of moderate to severe toxicity eg, those that need to be admitted for inpatient care ECG References Toxicity Versus Serum Level The toxicity of salicylates does not always correlate well with serum levels, and the levels are often less helpful in patients with long term exposure. Serum salicylate levels may correlate only moderately with clinical manifestations. In acute ingestion, levels may sometimes be high without significant clinical signs, whereas levels in patients with chronic ingestion that are in the high therapeutic range may be associated with significant clinical toxicity. Therefore, levels must always be interpreted and correlated with the history and clinical findings. Done nomogram The Done nomogram was formulated in to assist physicians in predicting the severity of salicylate intoxication based on a serum level and a known time of ingestion. The nomogram was based primarily on previously healthy pediatric patients with acute single-salicylate ingestion. However, clinical application of the nomogram has several limitations. The nomogram is used only to evaluate a single acute ingestion. In contrast to the Rumack-Matthew nomogram,[16] the Done nomogram indicates severity of toxicity based on a 6-hour level of nonâ enteric-coated aspirin rather than the need for antidotal therapy. Currently, the Done nomogram is regarded as not very useful and is seldom used by clinicians. Positive results with the urine ferric chloride test only indicate that a salicylate is present; however, even very small amounts Page 1

2 of a salicylate, such as a single ingested aspirin tablet, can give a positive test result. Most emergency departments no longer perform this test and instead obtain a plasma salicylate level because these results are now rapidly available from almost all hospital laboratories and are much more useful clinically. References Arterial Blood Gas Arterial blood gas ABG testing should be performed to evaluate for the presence of acid-base disturbances. Primary respiratory alkalosis may occur, followed by concomitant primary metabolic acidosis resulting from production of lactic acid, metabolites, and other organic acids. Therefore, the most common abnormality, especially in adults, is a mixed acid-base disturbance a primary respiratory alkalosis plus a primary metabolic acidosis. The presence of this finding should raise the suspicion of the possibility of an aspirin overdose. Repeated blood gases and serum salicylate levels should be done every 2 hours, until the acid-base status is improving, levels are falling, and the patient is clinically improving. References Approach Considerations Salicylate toxicity continues to be seen in the emergency department as a result of unintentional ingestions or suicide attempts. A high index of suspicion is necessary, with prompt recognition of clinical signs and symptoms of salicylate poisoning, such as tinnitus, hyperventilation, tachycardia, and metabolic acidosis. Principles of treatment include stabilizing the ABCs as necessary, limiting absorption, enhancing elimination, correcting metabolic abnormalities, and providing supportive care. No specific antidote is available for salicylates. When considering treatment options, the final decision should be individualized according to the clinical status of the patient and should not depend only on a particular salicylate level. Optimal management of a salicylate poisoning depends on whether the exposure is acute or chronic. Gastric lavage and activated charcoal are useful for acute ingestions but not for cases of chronic salicylism. Patients with chronic, rather than acute, ingestions of salicylates are more likely to develop toxicity, especially of the CNS, and require intensive care. Salicylate poisoning has been shown to cause metabolic derangements with significant inhibition of Krebs cycle enzymes. Because of impaired glucose homeostasis, CNS glucose supply is sometimes lowered, which results in hypoglycorrhachia and delirium, even when serum glucose concentration is normal. Glucose boluses in euglycemic patients with salicylate-induced delirium have sometimes caused a prompt improvement in mental status and therefore should be given to any patient with a salicylate overdose who has a change in mental status, despite a serum glucose level within the reference range. This may lead to a vicious cycle of increased salicylate consumption and increased confusion. Similar scenarios occur in persons with underlying psychiatric disorders. Arrange a follow-up for these patients in 24 hours. Also, consultation with a nephrologist is indicated in serious overdoses to arrange for hemodialysis, if it becomes necessary. References Triage Care In one study, authors reviewed US poison center data for and determined that over 40, exposures to salicylate-containing products occurred. Immediate emergency department referral by local poison control centers Patients who state that an intentional ingestion occurred or in whom a large administration is suspected should immediately be referred to the emergency department. In addition, typical symptoms of salicylate toxicity warrant referral to the emergency department for evaluation. Do not induce vomiting for salicylate ingestion. Activated charcoal for acute ingestions of a toxic dose can be administered if no contraindications such as depressed mental status are present. Asymptomatic dermal exposures to methyl salicylate or salicylic acid The skin should be thoroughly washed with soap and water; the patient can be observed at home. Ocular exposure to methyl salicylate or salicylic acid The eye or eyes should be irrigated with room-temperature tap water for 15 minutes. If pain, decreased visual acuity, or persistent irritation is reported after irrigation, referral to an ophthalmologist is recommended. Poison centers should monitor the onset of symptoms at periodic intervals for approximately hours after ingestion. An evidence-based consensus guideline to assist poison center personnel in the appropriate out-of-hospital triage and initial out-of-hospital management of patients with a suspected exposure to salicylates is also available from the Department of Health and Human Services. Large-bore vascular access catheters may be required to facilitate emergent hemodialysis. Endotracheal intubation may be required for the following reasons: As noted above, if they really require intubation and mechanical ventilation, they must be hyperventilated and closely monitored, including frequent checking of their blood gases, or they may rapidly deteriorate. In a recent article Page 2

3 by Dr. McCabe patients who were intubated had much better survival if they had hemodialysis performed early[20]. Protection of patients who are too agitated and delirious for central line placement, hemodialysis, and other necessary medical procedures without therapeutic sedation Protection of the airway against aspiration during lavage or activated charcoal administration or in obtunded patients who cannot protect their own airway ABCs As with all significant overdoses the airway, breathing, and circulation ABC should be evaluated and stabilized as necessary. Dehydration and concomitant electrolyte abnormalities must be immediately corrected. GI tract decontamination Some authorities recommend performing gastric lavage in all symptomatic patients regardless of time of ingestion. Gastric lavage may be beneficial, unless contraindicated, up to 60 minutes after salicylate ingestion. Protect the airway before gastric lavage. Initial treatment should include the use of oral activated charcoal, especially if the patient presents within 1 hour of ingestion. Activated charcoal can limit further gut absorption by binding to the available salicylates. The minimum dose is 30 g. Use of cathartics is not routinely indicated with activated charcoal; however, many clinicians administer the first dose of activated charcoal with sorbitol. Sorbitol should not be used in young children. Repeat cathartic dosing generally should be avoided because of concern over resultant electrolyte imbalances. Repeated doses of charcoal may enhance salicylate elimination and may shorten the serum half-life. Repeated doses of charcoal may remove salicylates from the circulation into the GI tract. Repeated doses of activated charcoal may assist in treating bezoars with ongoing absorption of salicylates, which should be suspected when salicylate levels continue to rise or fail to decrease, despite appropriate management. Repeated doses of activated charcoal have also been used to treat overdoses of enteric-coated or sustained-release aspirin; however, whole-bowel irrigation WBI with polyethylene glycol is probably more effective in this setting, as noted below. The passage of stool with charcoal and the resolution of serious clinical manifestations may be the reasonable criteria for discontinuing multiple doses of activated charcoal. WBI with polyethylene glycol was found to be more effective than single-dose activated charcoal in reducing salicylate absorption. The study was carried out in volunteer subjects 4 hours after they had ingested enteric-coated aspirin. Provide maintenance fluids to maintain urinary alkalization. Forced diuresis is not recommended. The greater the urine flow, the more difficult it is to alkalinize the urine. Be cautious of excessive fluid volumes in cases of salicylate-induced pulmonary edema. Renal excretion of salicylic acid depends on urinary ph. Increasing the urine ph to 7. Concomitant alkalization of blood and urine keeps salicylates away from brain tissue and in the blood, in addition to enhancing urinary excretion. When the urine ph increases to 8 from 5, renal clearance of salicylate increases times. Raising the urinary ph level from 6. Because aspirin is a weak acid, it ionizes when exposed to a basic environment, such as alkaline urine. Page 3

4 Chapter 2 : A primary care approach to sodium and potassium imbalance - best tests September ECG parameters, serum K+, and glucose concentrations were measured preexercise (Time 0), min post-exercise (Time 1), and 25 (Time 2) and 60 (Time 3) min postexercise. Many of the changes may be seen late on head imaging and should not delay administration of hypertonic saline or mannitol in those pediatric cases where cerebral edema is suspected. References Electrocardiography DKA may be precipitated by a cardiac event, and the physiological disturbances of DKA may cause cardiac complications. An ECG should be performed every 6 hours during the first day, unless the patient is monitored. An ECG may reveal signs of acute myocardial infarction that could be painless in patients with diabetes, particularly in those with autonomic neuropathy. An ECG is also a rapid way to assess significant hypokalemia or hyperkalemia. T-wave changes may produce the first warning sign of disturbed serum potassium levels. Low T wave and apparent U wave always signify hypokalemia, while peaked T wave is observed in hyperkalemia. Telemetry Consider telemetry in patients with comorbidities especially cardiac, known significant electrolyte abnormalities, severe dehydration, or profound acidosis. References Approach Considerations Managing diabetic ketoacidosis DKA in an intensive care unit during the first hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: Correction of fluid loss with intravenous fluids Correction of hyperglycemia with insulin Correction of electrolyte disturbances, particularly potassium loss Correction of acid-base balance Treatment of concurrent infection, if present It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, ph exceeds 7. Insulin infusion can be discontinued 30 minutes later. The JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. If neutral protamine Hagedorn NPH insulin was used previously, however, start back at the usual dose only when the patient eats well and is able to retain meals without vomiting; otherwise, the dose should be reduced to avoid hypoglycemia during its peak efficacy period. In newly diagnosed patients with type 1 diabetes, a careful estimate of the long-acting insulin dose should be considered. Starting with smaller doses generally is recommended to avoid hypoglycemia. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones. Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production. Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows: Administer L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings When the patient becomes euvolemic, the physician may switch to half the isotonic sodium chloride solution, particularly if hypernatremia exists. Isotonic saline should be administered at a rate appropriate to maintain adequate blood pressure and pulse, urinary output, and mental status. If a patient is severely dehydrated and significant fluid resuscitation is needed, switching to a balanced electrolyte solution eg, Normosol-R, in which some of the chloride in isotonic saline is replaced with acetate may help to avoid the development of a hyperchloremic acidosis. Insulin should be started about an hour after IV fluid replacement is started to allow for checking potassium levels and because insulin may be more dangerous and less effective before some fluid replacement Page 4

5 has been obtained. Although the incidence of life-threatening hypokalemia due to aggressive insulin administration is very low, there is little to no advantage in starting insulin prior to rehydration and evaluation of serum potassium levels. Initial bolus of insulin does not change overall management of DKA. Fluid administration is as vital in children as in adults. A low-dose insulin regimen has the advantage of not inducing the severe hypoglycemia or hypokalemia that may be observed with a high-dose insulin regimen. Only short-acting insulin is used for correction of hyperglycemia. Subcutaneous absorption of insulin is reduced in DKA because of dehydration; therefore, using intravenous routes is preferable. SC use of the fast-acting insulin analog lispro has been tried in pediatric DKA 0. The results were shown to be comparable to IV insulin, but ketosis took 6 additional hours to resolve. Such technically simplified methods may be cost-effective and may preclude admissions to intensive care units in patients with mild cases. Use of subcutaneous insulin analog aspart has been shown to be effective as well in adults. The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0. Larger volumes of an insulin and isotonic sodium chloride solution mixture can be used, providing that the infusion dose of insulin is similar. Hypoglycemia may develop rapidly with correction of ketoacidosis due to improved insulin sensitivity. Allowing blood glucose to drop to hypoglycemic levels is a common mistake that usually results in a rebound ketosis derived by counter-regulatory hormones. Rebound ketosis necessitates a longer duration of treatment. The other hazard is that rapid correction of hyperglycemia and hyperosmolarity may shift water rapidly to the hyperosmolar intracellular space and may induce cerebral edema. Although DKA was a common problem in patients with diabetes who were treated with continuous subcutaneous insulin infusion through insulin infusion pumps, the incidence of DKA was reduced with the introduction of pumps equipped with sensitive electronic alarm systems that alert users when the infusion catheter is blocked. If the potassium level is 4. If the potassium level is The monitoring of serum potassium must continue even after potassium infusion is stopped in the case of expected recurrence of hypokalemia. In severe hypokalemia, not starting insulin therapy is advisable unless potassium replacement is under way; this is to avert potentially serious cardiac dysrhythmia that may result from hypokalemia. Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Potassium can be given as follows: If sodium bicarbonate is indicated, ml of 1. This may be repeated every half hour if necessary. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis. Bicarbonate typically is not replaced as acidosis will improve with the above treatments alone. Administration of bicarbonate has been correlated with cerebral edema in children. References Treatment of Concurrent Infection In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empiric antibiotics on suspicion of infection until culture results are available may be advisable. Management of Treatment-Related Complications Cerebral edema Cerebral edema is a serious, major complication that may evolve at any time during treatment of DKA and primarily affects children. It is the leading cause of DKA mortality in children. Be extremely cautious to avoid cerebral edema during initiation of therapy. Deterioration of the level of consciousness in spite of improved metabolic state usually indicates the occurrence of cerebral edema. MRI usually is used to confirm the diagnosis. Cerebral edema that occurs at initiation of therapy tends to worsen during the course of treatment. Mannitol or hypertonic saline should be available if cerebral edema is suspected. According to Wolfsdorf et al, 0. Clinical cerebral edema is rare and carries the highest mortality rate. Glaser et al suggested that up to half of children with DKA have subtle brain MRI findings, particularly with respect to narrowing of the lateral ventricles. The risk of cerebral edema is related to the severity and duration of DKA. It is often associated with ongoing hyponatremia. Cerebral edema is correlated with the administration of bicarbonate. Concerns about the role of overaggressive or overly hypotonic fluid resuscitation as a cause of the edema that have been raised in the past correlate more closely with disease severity than with rapid administration of fluids. Usually, correction of the cause is sufficient to treat cardiac dysrhythmia, but if it persists, consultation with a cardiologist is mandatory. Performing cardiac monitoring on patients with DKA during correction of Page 5

6 electrolytes always is advisable. Pulmonary edema Pulmonary edema may occur for the same reasons as cerebral edema in patients with diabetic ketoacidosis. Be cautious of possible overcorrection of fluid loss, though it occurs only rarely. Although initial aggressive fluid replacement is necessary in all patients, particular care must be taken in those with comorbidities such as renal failure or congestive heart failure. Diuretics and oxygen therapy often suffice for the management of pulmonary edema. Acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Coronary arteriography usually is normal, and patients tend to recover fully without further evidence of ischemic heart disease. Diabetic retinopathy Microvascular changes consistent with diabetic retinopathy have been reported prior to and after treatment of diabetic ketoacidosis; the blood-retinal barrier does not experience the same degree of perturbation as the blood-brain barrier does, however. See Diabetic Retinopathy for more complete information on this topic. Hypoglycemia In patients with diabetic ketoacidosis, hypoglycemia may result from inadequate monitoring of glucose levels during insulin therapy. Insulin sensitivity improves after clearance of ketones. Hypokalemia Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration and insulin treatment, which not only reduces acidosis but directly facilitates potassium reentry into the cell. Consultations An endocrinologist also may be consulted to assist with management after the patient has been stabilized adequately. Any mental status change in pediatric patients suggests the possibility of cerebral edema, and when this occurs, a pediatric endocrinologist or pediatric intensivist should be consulted as soon as possible. Psychological counseling of young children and adolescents usually is helpful. References Long-Term Monitoring Frequent blood glucose monitoring at home makes DKA less likely, as this allows them to promptly search for possible reasons for unexpectedly high blood glucose values before the condition progresses to DKA. In a study of patients with DKA who were admitted to a pediatric intensive care unit, Bradley and Tobias concluded that multiple weaknesses existed in the prehospital care of these patients. Page 6

7 Chapter 3 : Holdings : The caloric expenditure of aerobic dance York University Libraries Supervisor, of H. Reynolds master's thesis, "Influence of Post Exercise Glucose Ingestion on Plasma Potassium Levels and ECG Measurements" which was chosen to. Effects of high-intensity exercise on blood glucose in type 2 diabetic patients A single session of continuous high-intensity exercise resulted in 60 minutes of postexercise hyperglycemia, 49 while both a single session of HIT, 50 and a 2-week training program 51 have been shown to improve postprandial glucose control over a hour period following exercise. Little et al 51 evaluated the effects of six sessions of HIT over 2 weeks on glucose regulation 48 to 72 hours after the last training session in people with type 2 diabetes. Most participants engaged in 60 minutes or less of exercise per week prior to entering the study. The HIT protocol required only 30 minutes of high-intensity exercise per week, with a total time commitment including warm-up, cool-down, and rest of 75 minutes. When asked how enjoyable would engaging in HIT three times per week for the next 4 weeks be, the mean response was 7. Additionally, it elicited ratings of perceived exertion of 4 to 8 on a point scale. Before training and from 48 to 72 hours after the last training session, glucose regulation was assessed using hour continuous glucose monitoring under standardized dietary conditions. The results of the two studies might be clinically significant, as controlling postprandial hyperglycemia is a treatment goal with type 2 diabetics. Kjaer et al 49 investigated the effect of 5 minutes of high-intensity exercise on blood glucose control during and for 3 hours immediately following exercise in type 2 diabetic patients two on a sulfonylurea and five on diet only. There was a greater and more sustained rise in glucose levels in type 2 diabetics compared to controls. This value was maintained until 60 minutes postexercise, and then plasma levels decreased over the remainder of the minute recovery period. Glucose concentrations at 60 minutes postexercise did not differ significantly from pre-exercise levels. In both groups, plasma insulin levels increased after exercise above pre-exercise levels, and returned to baseline about minutes postexercise. However, 24 hours after exercise in the type 2 diabetic group and not the controls, there was an increased effect of insulin on glucose uptake compared to the pre-exercise state as estimated by the insulin clamp technique. Other studies have found similar increases in insulin-mediated glucose disposal after short-term high-intensity exercise in insulin-resistant subjects. Harmer et al 54 studied the effects of 7 weeks of SIT. The number of cycle bouts per training session was increased from four in week 1, to six in week 2, eight in week 3, and ten in weeks 4â 7. SIT resulted in a greater rise in plasma glucose during and immediately after exercise a minute period in diabetics compared to nondiabetic controls. This increase was significantly attenuated by 7 weeks of training. HbA1c was not altered. All the other studies involved a single exercise session. Guelfi et al 55 studied the effects of HIT repeated 4-second cycle ergometer efforts separated by rest on blood glucose during exercise and in the immediate 1-hour postexercise period. Participants injected their normal dose of insulin and had breakfast. After the postprandial peak in blood glucose, on alternate days, participants either exercised or rested. During exercise blood glucose declined more rapidly as compared to the nonexercising controls, indicating that high intensity exercise may increase the risk of hypoglcemia. This finding is not supported by the other studies reviewed. However during the recovery period blood glucose levels continued to decline in the controls while remaining stable in the exercise group suggesting a decreased risk of postexercise hypoglycemia. Blood glucose fell to a greater extent in the moderate exercise group compared to the HIT group, and remained stable in the HIT group in the 1-hour recovery period while continuing to fall in the moderate-exercise group. Blood glucose at 1-hour postexercise was 3. However, Maran et al, 56 using a similar exercise protocol, demonstrated that following morning HIT, blood glucose was significantly lower between midnight and 6 AM the next day compared to when only moderate-intensity exercise was done. Thus, unlike moderate-intensity exercise, HIT is unlikely to cause hypoglycemia during or immediately postexercise in type 1 diabetics, but 14 to 20 hours later it may result in lower glucose levels. Summary Clinical practice guidelines typically recommend that people with type 2 diabetes perform moderate Page 7

8 to vigorous aerobic exercise and resistance exercise three to five times per week for a total of at least to minutes per week. Many persons do not achieve the recommended amounts of exercise with lack of time being cited as a reason. Classic SIT protocols can require as little as 2 to 3 minutes of maximal exercise spread over 15 to 30 minutes. With healthy nondiabetic subjects, 2-week protocols have resulted in improvements in muscle GLUT4 content, insulin sensitivity, and FBG. Insulin sensitivity improvement has been sustained up to 3 days post-intervention. Improvements in VO2max were similar to that achieved by much longer sessions of endurance aerobic exercise. In type 2 diabetic patients, a low-volume 2-week HIT program increased GLUT4 protein, a marker of insulin sensitivity, and decreased average blood glucose 48 to 72 hours postexercise. The protocol used was less intense than SIT and was acceptable to study participants. However, unlike with moderate-intensity exercise, blood glucose levels tend to be higher in both type 1 and 2 diabetic patients during and in the 2 hours immediately following intense exercise due to rising catecholamine levels promoting glycogenolysis, and these levels may remain high in the 2-hour post-exercise period. HIT depletes muscle glycogen and it is possible that after catecholamine levels decrease in the post-exercise phase, a period of increased peripheral uptake of glucose follows as glycogen stores are replenished. Conclusion The optimal exercise strategy has not been determined, but low volume SIT with as little as 7. Unlike moderate-intensity exercise, high-intensity exercise decreases the risk of hypoglycemia during and immediately after exercise in diabetic patients. Therefore, there may be no need for well controlled patients on insulin or insulin secretagogues to eat or decrease medication dosage shortly before high-intensity exercise. Both the risks of musculoskeletal injury and cardiovascular complications have to be considered. The cost of exercising and the provision of facilities equipment, supervision, and gyms also have to be taken into account if this form of exercise is to have a mass impact. Studies on the effect of high-intensity exercise on blood glucose have been few and of short duration, and have involved a small number of patients who were probably not representative of the general diabetic population. With diabetics, it is therefore uncertain if any improvements in blood glucose achieved by a brief intervention would be sustained over a longer period, reduce HbA1c levels, improve health outcomes, and can be replicated in the general diabetic population. Similarly, in the nondiabetic population it is not known whether improvements in insulin sensitivity would be sustained and result in a clinically important endpoint such as diabetes prevention. Further studies are needed to determine whether HIT programs, perhaps in the less intense form or as an adjunct to moderate-intensity exercise, would be effective in the long-term and have a high enough adherence rate to be efficacious. Large scale randomized trials lasting years may be necessary to show whether HIT can prevent diabetes, and such trials may be impractical. Footnotes The author reports no conflicts of interest in this work. Lifetime risk for diabetes mellitus in the United States. Rubin RR, Peyrot M. Quality of life and diabetes. Diabetes Metab Res Rev. Global healthcare expenditure on diabetes for and Diabetes Res Clin Pract. American Diabetes Association Standards of medical care in diabetes, Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. Physical activity in US adults with diabetes and at risk for developing diabetes, Low cardiorespiratory fitness in people at risk for type 2 diabetes: Canadian Journal of Diabetes. Exercise prescription for patients with type 2 diabetes and pre-diabetes: J Sci Med Sport. Managing Diabetes in Primary Care in the Caribbean. Caribbean Health Research Council; Differences in perceived barriers to exercise between high and low intenders: Am J Health Promot. Nagi D, Gallen I. ABCD position statement on physical activity and exercise in diabetes. Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus: Physical activity advice only or structured exercise training and association with HbA1c levels in type 2 diabetes: Exercise for type 2 diabetes mellitus. Cochrane Database Syst Rev. Effects of different modes of exercise training on glucose control and risk factors for complications in type 2 diabetic patients: Effect of noninsulin antidiabetic drugs added to metformin therapy on glycemic control, weight gain, and hypoglycemia in type 2 diabetes. Metformin and exercise in type 2 diabetes: Meta-analysis of the effect of structured exercise training on cardiorespiratory fitness in Type 2 diabetes mellitus. Mobilization of visceral adipose tissue related to the improvement in insulin sensitivity in response to physical training in NIDDM. Page 8

9 Effects of branched-chain amino acid supplements. Exercise increases muscle GLUT-4 levels and insulin action in subjects with impaired glucose tolerance. Elevated skeletal muscle glucose transporter levels in exercise-trained middle-aged men. Exercise, glucose transport, and insulin sensitivity. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Marliss EB, Vranic M. Intense exercise has unique effects on both insulin release and its roles in glucoregulation: Glucoregulatory and metabolic response to exercise in obese noninsulin-dependent diabetes. Metabolic adaptations to short-term high-intensity interval training: Exerc Sport Sci Rev. A time-efficient exercise strategy to improve muscle insulin sensitivity. Contribution of energy systems during a Wingate power test. Br J Sports Med. Kavanagh MF, Jacobs I. Breath-by-breath oxygen consumption during performance of the Wingate Test. Can J Sport Sci. Comparison of the aerobic contributions to Wingate anaerobic tests performed with two different loads. J Sports Med Phys Fitness. Muscle power and metabolism in maximal intermittent exercise. Page 9

10 Chapter 4 : Hyperkalemia: Hyperkalemia at The Medical Dictionary Objective. To determine whether ingesting 0, 1, or 2 servings of bananas after 60 minutes of moderate to vigorous exercise in the heat alters [K +] p or [glucose] p and whether changes in [K +] p result from hypotonic fluid effluxes or K + ion changes. Hyperkalemia refers to serum or plasma levels of potassium ions above 5. Both units mean the same thing when applied to concentrations of potassium ions. Description A normal adult who weighs about 70 kg contains a total of about 3. This level is in contrast to the much lower concentration found in the blood serum, where only about 0. Hyperkalemia can be caused by an overall excess of body potassium, or by a shift from inside to outside cells. For example, hyperkalemia can be caused by the sudden release of potassium ions from muscle into the surrounding fluids. In a normal person, hyperkalemia from too much potassium in the diet is prevented by at least three types of regulatory processes. First, various cells and organs act to prevent hyperkalemia by taking up potassium from the blood. It is also prevented by the action of the kidneys, which excrete potassium into the urine. A third protective mechanism is vomiting. Consumption of a large dose of potassium ions, such as potassium chloride, induces a vomiting reflex to expel most of the potassium before it can be absorbed. The most common cause of hyperkalemia is kidney or renal disease, which accounts for about three quarters of all cases. Kidney function is measured by the glomerular filtration rate, the rate at which each kidney performs its continual processing and cleansing of blood. The elderly are at particular risk, since many regulatory functions of the body do not work well in this population. Elderly patients who are being treated with certain drugs for high blood pressure, such as spironolactone Aldactone and triamterene Dyazide, must especially be monitored for possible hyperkalemia, as these medications promote the retention of potassium by the kidneys. The adrenal gland produces the hormone aldosterone that promotes the excretion of potassium into the urine by the kidney. Hyperkalemia can also result from injury to muscle or other tissues. Since most of the potassium in the body is contained in muscle, a severe trauma that crushes muscle cells results in an immediate increase in the concentration of potassium in the blood. Hyperkalemia may also result from severe burns or infections. Acidic blood plasma, or acidosis, is an occasional cause of hyperkalemia. Acidosis, which occurs in a number of diseases, is defined as an increase in the concentration of hydrogen ions in the bloodstream. When acidosis is the cause of hyperkalemia, treating the patient for acidosis has two benefits: Symptoms of hyperkalemia include abnormalities in the behavior of the heart. Heart abnormalities of mild hyperkalemia 5. With severe hyperkalemia over 8. Patients with moderate or severe hyperkalemia may also develop nervous symptoms such as tingling of the skin, numbness of the hands or feet, weakness, or a flaccid paralysis, which is characteristic of both hyperkalemia and hypokalemia low plasma potassium. Diagnosis Hyperkalemia can be measured by acquiring a sample of blood, preparing blood serum, and using a potassium sensitive electrode for measuring the concentration of potassium ions. Alternatively, atomic absorption spectroscopy can be used for measuring potassium. Since high or low potassium levels result in abnormalities in heart function, the electrocardiogram is usually the method of choice for the diagnosis of both hyperkalemia and hypokalemia. Treatment Insulin injections are used to treat hyperkalemia in emergency situations. Insulin is a hormone well known for its ability to stimulate the entry of sugar glucose into cells. It also provokes the uptake of potassium ions by cells, decreasing potassium ion concentration in the blood. When insulin is used to treat hyperkalemia, glucose is also injected. Serum potassium levels begin to decline within 30 to 60 minutes and remain low for several hours. In non-emergency situations, hyperkalemia can be treated with a low potassium diet. If this does not succeed, the patient can be given a special resin to bind potassium ions. One such resin, sodium polystyrene sulfonate Kayexalate, remains in the intestines, where it absorbs potassium and forms a complex of resin and potassium. Eventually this complex is excreted in the feces. A typical dose of resin is 15 grams, taken one to four times per day. The correction of hyperkalemia with resin treatment takes at least 24 hours. Prognosis The prognosis for specifically correcting hyperkalemia Page 10

11 is excellent. However, hyperkalemia is usually caused by kidney failure, an often irreversible and eventually fatal condition. Prevention Healthy people are not at risk for hyperkalemia. Patients with renal disease and those on certain diuretic medications must be monitored to prevent its occurrence. Key Terms Acidosis An abnormally high acid hydrogen ion concentration in blood plasma. The unit of acid content is ph, with a lower value indicating more acidic conditions. Blood plasma normally has a ph of 7. Alkaline blood has a ph value greater than ph 7. When the blood ph value is less than 7. Chapter 5 : The impact of brief high-intensity exercise on blood glucose levels Type I individuals show an increase in the plasma glucose toward normal values during exercise. This causes them to suffer from hyperglycemia as well. This occurs because their muscles do not utilize the glucose normally but the release of glucose from the liver is still normal. Chapter 6 : Diabetic Ketoacidosis blood sugar levels 2-hrs after drining 75 g of glucose; delayed removal of glucose indicates diabetes Hemoglobin A1c Test standard for diagnosing diabetes; 3 month average of what your blood glucose is. Page 11