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Calcium intravenous

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). [Pg.64]

If die nitrates are administered witii the antihypertensives, alcohol, calcium channel blockers, or the phe-notiiiazines, there may be an increased hypotensive effect. When nitroglycerin is administered intravenously (IV), die effects of heparin may be decreased. Increased nitrate serum concentrations may occur when the nitrates are administered witii aspirin. [Pg.384]

Dantrolene is the mainstay of MH treatment. It has long been available for the treatment of muscle spasm in cerebral palsy and similar diseases. It is a hydantoin derivative that was first synthesized in 1967, and reported to be effective in the treatment of porcine MH in 1975. Also in 1975, dantrolene was shown to be more effective than procainamide in the treatment of human MH, which until that time was the drug of choice. However, the intravenous preparation was not made available until November 1979. It significantly lowered mortality. The half-life of dantrolene is estimated to be 6-8 hr. Dantrolene s primary mode of action is the reduction in calcium release by the sarcoplasmic reticulum. Dantrolene also exerts a primary antiarrhythmic effect by increasing atrial and ventricular refractory periods. Side effects of dentrolene include hepatotoxicity, muscle weakness, ataxia, blurred vision, slurred speech, nausea, and vomiting. Dantrolene is not contraindicated in pregnancy, but it does cross into breast milk and its effect on the neonate is unknown. [Pg.406]

Other electrolytes of importance include calcium (especially if the patient is receiving a calcium channel blocker, such as nicardipine) and magnesium, as hypomagnesemia may predispose the patient to seizures, further complicating the ICP management. If the patient received intravenous iodinated contrast as part of their stroke evaluation, then careful monitoring of the blood urea nitrogen (BUN) and creatinine levels is necessary to detect contrast nephropathy. [Pg.166]

Severe hyperphosphatemia, presenting as hypocalcemia and tetany should be treated with hemodialysis and possibly careful intravenous calcium administration (see management of hypocalcemia)... [Pg.175]

Intravenous diltiazem can be used cautiously for up to 24 hours in patients with non-decompensated heart failure, bpm, beats per minute CCB, calcium channel blocker (diltiazem or verapamil) HF, heart failure LV, left ventricular LVEF, left ventricular ejection fraction. [Pg.119]

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. [Pg.382]

For women whose breast cancer has metastasized to bone, bisphosphonates are recommended, in addition to chemotherapy or endocrine therapy, to reduce bone pain and fractures.28,64 Pamidronate (90 mg) and zoledronate (4 mg) can be given intravenously once each month. These bisphosphonates are given in combination with calcium and vitamin D. [Pg.1321]

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. [Pg.1488]

Calcium and Phosphate Needs of Preterm Infants Requiring Prolonged Intravenous Feeding... [Pg.44]

Our simple approach to determining the optimal Ca/P ratio for intravenous feeding solutions was to simply alter the ratio of calcium to phosphate in these solutions and measure the only external loss of calcium and phosphate which was in the urine. We initially assumed that the difference between the intake and urinary loss of calcium and phosphate would measure the retention of these elements. The results of seven balance studies at varying Ca/P ratios are shown in Figure 5. [Pg.49]

Figure 5. The areas above the measured calcium and measured phosphate retention curves represent the percent of the intravenously administered calcium and phosphate that was lost in the urine. The combined percent losses (Ca + P) are minimized at the intercept of the curves. The dotted line represents an assumed endogenous fecal loss of 20% of the infused calcium added to the measured urinary calcium losses. The Ca/P ratio that minimizes the percent calcium and phosphate losses is then approximately 3.0. (Reproduced with permission from Ref. 4. Copyright 1983 American Society for Parenteral and Enteral Nutrition.)... Figure 5. The areas above the measured calcium and measured phosphate retention curves represent the percent of the intravenously administered calcium and phosphate that was lost in the urine. The combined percent losses (Ca + P) are minimized at the intercept of the curves. The dotted line represents an assumed endogenous fecal loss of 20% of the infused calcium added to the measured urinary calcium losses. The Ca/P ratio that minimizes the percent calcium and phosphate losses is then approximately 3.0. (Reproduced with permission from Ref. 4. Copyright 1983 American Society for Parenteral and Enteral Nutrition.)...
The usual intravenous dose of pentetate calcium trisodium Yb 169 injection for brain and kidney imaging is the equivalent of 0.037 GBq. Express this dose in terms of millicuries. [Pg.308]

Several uses have been suggested for levulinic acid and its salts. Thus, calcium levulinate seems to have advantages as a calcium carrier in tuberculosis therapy, and it is said to be more suitable than calcium gluconate for intravenous injection. A mercury salt, phenyl mercury... [Pg.311]

Magnesium sulfate, applied intravenously is often used as tocolytic. The mechanism of action is not completely clear but might involve a competition with calcium on the cellular level. Precautions in the sense of magnesium plasma level monitoring must be taken in patients with renal insufficiency since this divalent kation is eliminated by the kidneys. Relatively high plasma concentrations are necessary to achieve a sufficient tocolysis. The relatively frequent side effects are respiratory depression, depressed reflexes, headaches, palpitation and skin flushing in the mother and muscle relaxation and, rarely, CNS depression in the fetus. [Pg.306]

Adenosine reduces heart rate and AV conduction, although it is not a calcium antagonist. It is administered intravenously for the acute treatment of paroxysmal supraventricular tachycardia. Adenosine displays a rapid onset and short duration of action. Apart from its antiarrhythmic activity it is also a vasodilator, in particular in the coronary system. [Pg.341]

All patients with methanol toxicity should be given folic acid 50 milligrams intravenously every 4 hours to increase the metabolism of formic acid. In ethylene glycol ingestion, folate, thiamine and pyri-doxine should all be administered, to enhance the metabolism of the poison to non-toxic products, and minimize oxalic acid production. Calcium supplements are required for symptomatic hypocalcaemia. [Pg.512]


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