DEXTROSE CONTAINING INTRAVENOUS FLUID IMPAIRS OUTCOME AND INCREASES DEATH AFTER 8 MINUTES OF CARDIAC-ARREST AND RESUSCITATION IN DOGS
- 1 September 1986
- journal article
- research article
- Vol. 100 (3) , 505-511
Abstract
Use of dextrose in intravenous resuscitation fluids is common practice; however, this study indicates that 5% dextrose solutions, even if administered in physiologic quantities, greatly worsens the outcome of survivable cardiac arrest. Twelve adult male mongrel dogs were premedicated with morphine, anesthetized with halothane, instrumented, intubated, and ventilated. Each dog was first given 500 ml of either lactated Ringer''s (LR) (n = 6) or 5% dextrose in LR (D5LR) (n = 6). Halothane was stopped and fibrillation was induced (60 Hz). Blood glucose just before cardiac arrest was 129 mg/dl in the LR dogs and was increased to 335 mg/dl in the D5LR dogs. After eight minutes of arrest, resuscitation, including internal cardiac massage and standard advanced cardiac life support drug protocols (modified for dogs), was begun. When stable cardiac rhythm was obtained, the chest was closed, and LR or D5LR continued until a total of 1L was given. A neurologic score (0 = normal to 100 = dead) was assigned at 1, 2, 6, and 24 hours. The LR group did not differ statistically from the D5LR group in operative time, number of defibrillatory shocks, time to spontaneous ventilation, time to extubation, or drugs required. Resuscitation was successful in all six LR and five of six D5LR group; however, by 2 hours after resuscitation and thereafter, D5LR group had a significantly greater neurologic deficit (p < 0.05) than did the LR group. By 9 hours, four of six D5LR dogs displayed convulsive activity and died. At 24 hours the D5LR group had a greater (p < 0.008) neurologic deficit (82 .+-. 11) than did the LR group (21 .+-. 7), which walked and ate. We conclude that the addition of 5% dextrose to standard intravenous fluids greatly increases the morbidity and mortality associated with cardiac resuscitation.This publication has 14 references indexed in Scilit:
- Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic ratsActa Neurologica Scandinavica, 2009
- Moderate hyperglycemia augments ischemic brain damageNeurology, 1982
- The Neurologic Effects of Thiopental Therapy Following Experimental Cardiac Arrest in CatsAnesthesiology, 1982
- Hyperglycemia, recognized and unrecognized, as a risk factor for stroke and transient ischemic attacks.Stroke, 1982
- Ventricular fibrillation in the cat: a model for global cerebral ischemia.Stroke, 1981
- Brain Lactic Acidosis and Ischemic Cell Damage: 2. HistopathologyJournal of Cerebral Blood Flow & Metabolism, 1981
- Brain Lactic Acidosis and Ischemic Cell Damage: 1. Biochemistry and NeurophysiologyJournal of Cerebral Blood Flow & Metabolism, 1981
- Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels.Stroke, 1980
- Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. I. Local cerebral blood flow and glucose utilization.Stroke, 1980
- Nervous System Effects of Cardiac Arrest in MonkeysArchives of Neurology, 1977