RESUMEN
The purpose of this study was to compare the benefit of small volume hypertonic saline/dextran (HSD) versus the risk of obligatory time to administer it on-scene in a model of acute hemorrhagic shock. Dogs were bled to a mean arterial pressure (MAP) of 20 mmHg and then randomized to either: a) direct transport to the emergency department (ED) or b) 10 min delay to insert an iv HSD (4 ml/kg) infusion over 5 min, and then transport. The animals receiving HSD had improved (P less than 0.05) cardiac work and oxygen consumption during transport (MAP = 59 +/- 3 vs 38 +/- 4 mmHg; cardiac index (CI) = 3.2 +/- 0.2 vs 1.3 +/- 0.1 L min-1 M-2; O2CI = 115 +/- 7 vs 104 +/- 7 ml min-1 M-2), paralleled by reduced serum lactate (5.3 +/- 0.8 vs 7.0 +/- 2.3 mmol/L) and decreased metabolic acidosis. The benefits of HSD in attenuating shock-induced oxygen debt were corroborated by lower O2CI (98 +/- 4 vs 112 +/- 5 ml min-1 M-2) and higher pH (7.30 +/- 0.01 vs 7.24 +/- 0.02) in the postresuscitation period.
Asunto(s)
Servicios Médicos de Urgencia , Fluidoterapia , Consumo de Oxígeno , Resucitación , Choque Hemorrágico/terapia , Transporte de Pacientes , Animales , Modelos Animales de Enfermedad , Perros , Humanos , Factores de TiempoRESUMEN
The purpose of this study was to compare the benefit of small volume hyperonic saline/dextran (HSD) versus the risk of obligatory time to administer it on-scene in a model of acute hemorrhagic shock. Dogs were bled to a mean arteiral pressure (MAP) of 20 mmHg and the randomized to either: a) direct transport to the emergency department (ED) or b) 10 min delay to insert an iv HSD (4 ml/Kg) infusion over 5 min, and then transport. The animals receiving HSD had improved (P<0.05) cardiac work and oxigen consumption during transport (MAP = 59 ñ 3 vs 38 ñ 4 mmHg; cardiac index (CI) = 3.2 ñ 0.2 vs 1.3 ñ 0.1 L min-1 M-2; O2CI = 115 ñ 7 vs 104 ñ 7 mlmin-1M-2), paralleled by reduced serum lactate (5.3 ñ 0.8 vs 7.0 ñ 2.3 mmol/L) and decreased metabolic acidosis. The benefitsof HSD in attenuating shock-induced oxygen debt were corroborated by lower O2CI(98 ñ 4 vs 112 ñ 5 ml min-1 M-2) and higher pH (7.30 ñ 0.01 vs 7.24 ñ 0.02) in the postresuscitation period