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Abstract. Objectives: To determine whether a hypertonic saline bolus improves cardiac conduction or plasma potassium levels more than normal saline infusion within 15 minutes of treatment for severe hyperkalemia. Previously with this model, 8.4% sodium chloride (NaCl) and 8.4% sodium bicarbonate (NaHCO 3 ) lowered plasma potassium equally effectively. Methods: This was a crossover study using ten conditioned dogs (14-20 kg) that received, in random order, each of three intravenous (IV) treatments in separate experiments at least one week apart: 1) 2 mmol/kg of 8.4% NaCl over 5 minutes (bolus); 2) 2 mmol/kg of 0.9% NaCl over one hour (infusion); or 3) no treatment (control). Using isoflurane anesthesia and ventilation (pCO 2 = 35-40 torr), 2 mmol/kg/hr of IV potassium chloride (KCl) was infused until conduction delays (both absent p-waves and Ն20% decrease in ventricular rate in Յ5 minutes) were sustained for 15 minutes. The KCl was then decreased to 1 mmol/kg/hr (maintenance) for 2 hours and 45 minutes. Treatment (0 minutes) began after 45 minutes of maintenance KCl. Results: From 0 to 15 minutes, mean heart rate increased 29.6 (95% CI = 12.2 to 46; p < 0.005) beats/min more with bolus than infusion and 23.4 (95% CI = 2.6 to 43.5; p < 0.03) beats/min more with bolus than control. No clinically or statistically significant difference was seen in heart rate changes from 0 to 30 minutes. Decreases in potassium from 0 to 15 minutes were similar with bolus, infusion, and control. Conclusions: In this model, 8.4% NaCl bolus reversed cardiac conduction abnormalities within the first 15 minutes after treatment, more rapidly than did the 0.9% NaCl infusion or control. This reversal occurred despite similar reductions in potassium levels. Key words: hypertonic; sodium; hyperkalemia; treatment; animal model. AC-ADEMIC EMERGENCY MEDICINE 2000; 7:965-973 T HERE is controversy regarding the use of sodium bicarbonate (NaHCO 3 ) in the emergency treatment of hyperkalemia. Despite the fact that alkalinization is often taught to be the standard of care, 1,2 most investigations have shown little or no benefit to alkalinization for emergent (i.e., benefits within 15-60 minutes of treatment) treatment of hyperkalemia. Sodium bicarbonate may decrease potassium in hyperkalemia by sodium loading rather than by alkalinization. Janson and Marx speculated that infusion of sodium solutions may be effective in hyperkalemia.7 A recent animal study, using a crossover design in dogs given potassium loads (mean Ϯ SD pretreatment potassium level of 9.06 Ϯ 0.82 mmol/L), compared various treatments matched in sodium and water content.8 A bolus of 8.4% sodium chloride (NaCl) (2 mmol Na/kg) caused potassium to decrease at least as much as a bolus of 8.4% NaHCO 3 (2 mmol Na/kg). Reduction of potassium levels by the concentrated sodium solutions from a mechanism other than alkalinization (for example, hemodilution, ion displacement, or some other mechanism) could not be ruled out. No difference was seen in cardiac conduction between the treatments....

Abstract. Objective: To determine whether pharmacologic antagonism of adenosine A 1 -receptor-mediated cardiovascular changes can improve cardiac function and prolong survival during systemic hypoxia. Methods: Rats were anesthetized with ketamine, instrumented [including left ventricular (LV) pressure transducing catheters], paralyzed with vecuronium, then ventilated to pCO 2 = 35-40 torr. After 10 minutes of equilibration (baseline), treatment commenced with saline (n = 7), NPC-205, an adenosine A 1 receptor selective antagonist, at doses of 1 mg/ kg (n = 10) or 10 mg/kg (n = 10), or drug vehicle (n = 9). Ten minutes later, inspired oxygen was reduced to 5%. Table 1. Activation of the adenosine A 1 receptor, located primarily in cardiomyocytes and the conduction system, results in negative inotropic, negative chronotropic, negative dromotropic, and anti-beta-adrenergic effects.2 Adenosine cardiovascular A 2 receptor agonism results in cor-

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