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Just as for non ST-segment elevation acute coronary syndrome, risk stratification is important for management of ST-segment elevation acute myocardial infarction GRACE and TIMI risk scores can be helpful tools Patients with recurrent ischemia (spontaneous or provoked), hemodynamic instability, impaired LV function, heart failure, or serious ventricular arrhythmias should undergo cardiac catheterization (Table 10 5) ACE inhibitor (or ARB) therapy is indicated in patients with clinical heart failure or LV EF < 40% For patients not undergoing cardiac catheterization, submaximal exercise (or pharmacologic stress testing for patients unable to exercise) before discharge or a maximal test after 3 6 weeks (the latter being more sensitive for ischemia) helps patients and physicians plan the return to normal activity Imaging in conjunction with stress testing adds additional sensitivity for ischemia and provides localizing information Both exercise and pharmacologic stress imaging have successfully predicted subsequent outcome One of these tests should be used prior to discharge in patients who have received thrombolytic therapy as a means of selecting appropriate candidates for coronary angiography

Patients who sustain substantial myocardial damage often experience subsequent progressive LV dilation and dysfunction, leading to clinical heart failure and reduced longterm survival In patients with EFs less than 40%, longterm ACE inhibitor (or ARB) therapy prevents LV dilation and the onset of heart failure and prolongs survival The HOPE trial, as well as an overview of trials of ACEinhibitors for secondary prevention, also demonstrated a reduction of approximately 20% in mortality rates and the occurrence of nonfatal myocardial infarction and stroke with ramipril treatment of patients with vascular disease and without confirmed LV systolic dysfunction Therefore, ACE inhibitor therapy should be strongly considered in this broader group of patients and especially in diabetics and patients with even mild systolic hypertension, in whom the greatest benefit was observed

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alcoholism or liver failure; and in instances of renal failure, particularly in patients requiring dialysis These conditions are usually obvious, with hypoglycemia being only a secondary feature When fasting hypoglycemia is a primary manifestation developing in adults without apparent endocrine disorders or inborn metabolic diseases from childhood, the principal diagnostic possibilities include: (1) hyperinsulinism, due to either pancreatic B cell tumors or islet hyperplasia or surreptitious administration of insulin (or sulfonylureas), and (2) hypoglycemia due to non insulin-producing extrapancreatic tumors Postprandial (reactive) hypoglycemia may be classified as early (within 2 3 hours after a meal) or late (3 5 hours after eating) Early, or alimentary, hypoglycemia occurs when there is a rapid discharge of ingested carbohydrate into the small bowel followed by rapid glucose absorption and hyperinsulinism It may be seen after gastrointestinal surgery and is particularly associated with the dumping syndrome after gastrectomy In some cases, it is functional and may represent overactivity of the parasympathetic nervous system mediated via the vagus nerve Rarely, it results from defective counterregulatory responses such as deficiencies of growth hormone, glucagon, cortisol, or autonomic responses Alcohol-related hypoglycemia is due to hepatic glycogen depletion combined with alcohol-mediated inhibition of gluconeogenesis It is most common in malnourished alcohol abusers but can occur in anyone who is unable to ingest food after an acute alcoholic episode followed by gastritis and vomiting Immunopathologic hypoglycemia is an extremely rare condition in which anti-insulin antibodies or antibodies to insulin receptors develop spontaneously In the former case, the mechanism appears to relate to increasing dissociation of insulin from circulating pools of bound insulin When antibodies to insulin receptors are found, most patients do not have hypoglycemia but rather severe insulin-resistant diabetes and acanthosis nigricans However, during the course of the disease in these patients, certain anti-insulin receptor antibodies with agonist activity mimicking insulin action may develop, producing severe hypoglycemia Factitious hypoglycemia is self-induced hypoglycemia due to surreptitious administration of insulin or sulfonylureas.

FIGURE 3-19

Alkalinization with intravenous sodium bicarbonate to keep the pH above 72 has been recommended by some in the emergency treatment of lactic acidosis; as much as 2000 mEq in 24 hours has been used However, there is no evidence that the mortality rate is favorably affected by administering bicarbonate, and its use remains controversial Hemodialysis may be useful in cases where large sodium loads are poorly tolerated

The mortality rate of spontaneous lactic acidosis is high The prognosis in most cases is that of the primary disorder that produced the lactic acidosis

Forsythe SM et al Sodium bicarbonate for the treatment of lactic acidosis Chest 2000 Jan;117(1):260 7 [PMID: 10631227] Salpeter S et al Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus Cochrane Database Syst Rev 2006 Jan 25;(1):CD002967 [PMID: 16437448]

Spontaneous hypoglycemia in adults is of two principal types: fasting and postprandial Symptoms begin at plasma glucose levels in the range of 60 mg/dL and impairment of brain function at approximately 50 mg/dL Fasting hypoglycemia is often subacute or chronic and usually presents with neuroglycopenia as its principal manifestation; postprandial hypoglycemia is relatively acute and is often heralded by symptoms of neurogenic autonomic discharge (sweating, palpitations, anxiety, tremulousness)

Differential Diagnosis (Table 27 13)

Fasting hypoglycemia may occur in certain endocrine disorders, such as hypopituitarism, Addison s disease, or myxedema; in disorders related to liver malfunction, such as acute

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