OBJECTIVES: We attempted to determine the effects of beta-adrenergic blockade during cardiopulmonary resuscitation (CPR) on defibrillation rates and postresuscitation left ventricular function. BACKGROUND: The results of previous studies suggest that propranolol administration can both reduce myocardial oxygen requirements and increase coronary perfusion pressure during CPR. METHODS: Left ventricular pressure and segment length were measured before and after 5 min of CPR in 22 dogs either given epinephrine (0.015 mg/kg body weight at the onset and after 4 min) or pretreated with propranolol (2 mg/kg) and given epinephrine during CPR. RESULTS: Despite identical epinephrine doses, coronary perfusion pressure during CPR was higher in the epinephrine plus propranolol group (p < 0.05), and defibrillation was successful in 9 of 11 dogs given both epinephrine and propranolol versus 6 of 11 dogs given epinephrine alone (p = NS). Peak and developed left ventricular pressures, left ventricular end-diastolic pressure and the peak rate of left ventricular pressure development (+dP/dt) did not differ between study groups when measured either 5 or 15 min after successful defibrillation. However, when survivors in the epinephrine group were given propranolol after CPR to eliminate compensatory sympathetic stimulation, left ventricular developed pressure and peak +dP/dt were lower (p < 0.05) despite trends toward higher left ventricular end-diastolic pressures and normalized end-diastolic segment lengths compared with dogs given propranolol before CPR. CONCLUSIONS: These findings suggest that beta-adrenergic blockade reduces myocardial injury during CPR without decreasing the likelihood of successful defibrillation or compromising spontaneous postresuscitation left ventricular function.
OBJECTIVES: We attempted to determine the effects of beta-adrenergic blockade during cardiopulmonary resuscitation (CPR) on defibrillation rates and postresuscitation left ventricular function. BACKGROUND: The results of previous studies suggest that propranolol administration can both reduce myocardial oxygen requirements and increase coronary perfusion pressure during CPR. METHODS: Left ventricular pressure and segment length were measured before and after 5 min of CPR in 22 dogs either given epinephrine (0.015 mg/kg body weight at the onset and after 4 min) or pretreated with propranolol (2 mg/kg) and given epinephrine during CPR. RESULTS: Despite identical epinephrine doses, coronary perfusion pressure during CPR was higher in the epinephrine plus propranolol group (p < 0.05), and defibrillation was successful in 9 of 11 dogs given both epinephrine and propranolol versus 6 of 11 dogs given epinephrine alone (p = NS). Peak and developed left ventricular pressures, left ventricular end-diastolic pressure and the peak rate of left ventricular pressure development (+dP/dt) did not differ between study groups when measured either 5 or 15 min after successful defibrillation. However, when survivors in the epinephrine group were given propranolol after CPR to eliminate compensatory sympathetic stimulation, left ventricular developed pressure and peak +dP/dt were lower (p < 0.05) despite trends toward higher left ventricular end-diastolic pressures and normalized end-diastolic segment lengths compared with dogs given propranolol before CPR. CONCLUSIONS: These findings suggest that beta-adrenergic blockade reduces myocardial injury during CPR without decreasing the likelihood of successful defibrillation or compromising spontaneous postresuscitation left ventricular function.
Authors: Scott T Youngquist; Atman Shah; Christian McClung; Joseph L Thomas; John P Rosborough; James T Niemann Journal: Resuscitation Date: 2010-11-03 Impact factor: 5.262
Authors: Hilde Karlsen; Harald Arne Bergan; Per Steinar Halvorsen; Kjetil Sunde; Eirik Qvigstad; Geir Øystein Andersen; Jan Frederik Bugge; Theresa Mariero Olasveengen Journal: Intensive Care Med Exp Date: 2019-12-04