TY - JOUR
T1 - Comparison of epinephrine with vasopressin on bone marrow blood flow in an animal model of hypovolemic shock and subsequent cardiac arrest
AU - Voelckel, Wolfgang G.
AU - Lurie, Keith G.
AU - McKnite, Scott
AU - Zielinski, Todd
AU - Lindstrom, Paul
AU - Peterson, Colleen
AU - Wenzel, Volker
AU - Lindner, Karl H.
PY - 2001
Y1 - 2001
N2 - Objective: The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow. Design: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. Setting: University hospital laboratory. Subjects: Fourteen pigs weighing 30 ± 3 kg. Interventions: Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 μg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation. Measurements and Main Results: Mean ± SEM bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 ± 4.1 to 3.7 ± 1.8 ml·100 g-1·min-1 in the vasopressin group and from 18.2 ± 4.0 to 5.2 ± 1.0 ml·100 g-1·min-1 in the epinephrine group (p = .025 in both groups). Five minutes after return of spontaneous circulation, mean ± SEM bone marrow blood flow was 3.4 ± 1.1 ml·100 g-1·mi-1 after vasopressin and 0.1 ± 0.03 ml·100 g-1·min-1 after epinephrine (p = .004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p = .004) higher in the epinephrine group when compared with vasopressin (1455 ± 392 vs. 43 ± 19 mm Hg· ml-1·100 g·min, respectively). Conclusions: Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resus-citation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.
AB - Objective: The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow. Design: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. Setting: University hospital laboratory. Subjects: Fourteen pigs weighing 30 ± 3 kg. Interventions: Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 μg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation. Measurements and Main Results: Mean ± SEM bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 ± 4.1 to 3.7 ± 1.8 ml·100 g-1·min-1 in the vasopressin group and from 18.2 ± 4.0 to 5.2 ± 1.0 ml·100 g-1·min-1 in the epinephrine group (p = .025 in both groups). Five minutes after return of spontaneous circulation, mean ± SEM bone marrow blood flow was 3.4 ± 1.1 ml·100 g-1·mi-1 after vasopressin and 0.1 ± 0.03 ml·100 g-1·min-1 after epinephrine (p = .004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p = .004) higher in the epinephrine group when compared with vasopressin (1455 ± 392 vs. 43 ± 19 mm Hg· ml-1·100 g·min, respectively). Conclusions: Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resus-citation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.
KW - Blood flow
KW - Bone marrow
KW - Cardiac arrest
KW - Cardiopulmonary resuscitation
KW - Epinephrine
KW - Hemorrhagic shock
KW - Intraosseous infusion
KW - Vascular resistance
KW - Vasopressin
KW - Ventricular fibrillation
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U2 - 10.1097/00003246-200108000-00015
DO - 10.1097/00003246-200108000-00015
M3 - Article
C2 - 11505132
AN - SCOPUS:0034883020
SN - 0090-3493
VL - 29
SP - 1587
EP - 1592
JO - Critical care medicine
JF - Critical care medicine
IS - 8
ER -