Search

Unlabelled: We assessed the effects of a calcium channel blocker versus saline placebo on ventricular fibrillation mean frequency and hemodynamic variables during prolonged cardiopulmonary resuscitation (CPR). Before cardiac arrest, 10 animals were randomly assigned to receive either nifedipine (0.64 mg/kg; n = 5) or saline placebo (n = 5) over 10 min. Immediately after drug administration, ventricular fibrillation was induced. After 4 min of cardiac arrest and 18 min of basic life support CPR, defibrillation was attempted. Ninety seconds after the induction of cardiac arrest, ventricular fibrillation mean frequency was significantly (P < 0.01) increased in nifedipine versus placebo pigs (mean +/- SD: 12.4 +/- 2.1 Hz versus 8 +/- 0.7 Hz). From 2 to 18.5 min after the induction of cardiac arrest, no differences in ventricular fibrillation mean frequency were detected between groups. Before defibrillation, ventricular fibrillation mean frequency was significantly (P < 0.05) increased in nifedipine versus placebo animals (9.7 +/- 1.2 Hz versus 7.1 +/- 1.3 Hz). Coronary perfusion pressure was significantly lower in the nifedipine than in the placebo group from the induction of ventricular fibrillation to 11.5 min of cardiac arrest; no animal had a return of spontaneous circulation after defibrillation. In conclusion, nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR; this was nevertheless associated with no defibrillation success., Implications: This study evaluates the effects of a calcium channel blocker on ventricular fibrillation mean frequency, hemodynamic variables, and resuscitability during prolonged cardiopulmonary resuscitation (CPR) in pigs. Nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR but did not improve resuscitability.

When ventilating an unintubated patient with a self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressure with subsequent stomach inflation; this may occur frequently when rescuers without daily experience in bag-valve-mask ventilation need to perform advanced airway management. The purpose of this study was to assess the effects of a newly developed self-inflating bag (mouth-to-bag resuscitator; Ambu, Glostrup, Denmark) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used, consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100 ml/cm H(2)O)); airway resistance, 0.39 kPa/l per second (4 cm H(2)O/l/s), oesophagus (LESP, 1.96 kPa (20 cm H(2)O)) and simulated stomach. Twenty nurses were randomised to ventilate the manikin for 1 min (respiratory rate: 12 per minute) with either a standard self-inflating bag or the mouth-to-bag resuscitator, which requires the rescuer to blow up a single-use balloon inside the self-inflating bag, which in turns displaces air towards the patient. When supplemental oxygen is added, ventilation with up to 100% oxygen may be obtained, since expired air is only used as the driving gas. The mouth-to-bag resuscitator therefore allows two instead of one hand sealing the mask on the patient's face. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The mouth-to-bag resuscitator versus standard self-inflating bag resulted in significantly (P<0.05) higher mean+/-S.D. mask tidal volumes (1048+/-161 vs. 785+/-174 ml) and lung tidal volumes (911+/-148 vs. 678+/-157 ml), longer inspiratory times (1.7+/-0.4 vs. 1.4+/-0.4 s), but significantly lower peak inspiratory flow rates (50+/-9 vs. 62+/-13 l/min) and mask leakage (10+/-4 vs. 15+/-9%); peak inspiratory pressure (17+/-2 vs. 17+/-2 cm H(2)O) and stomach tidal volumes (16+/-30 vs. 18+/-35 ml) were comparable. In conclusion, employing the mouth-to-bag resuscitator during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate and improved lung tidal volumes, while decreasing mask leakage.

If the airway of a cardiac arrest patient is unprotected, basic life support with low rather than high inspiratory flow rates may reduce stomach inflation. Further, if the inspiratory flow rate is fixed such as with a resuscitator performance may improve; especially when used by less experienced rescuers. The purpose of the present study was to assess the effect of limited flow ventilation on respiratory variables, and lung and stomach volumes, when compared with a bag valve device. After institutional review board approval, and written informed consent was obtained, 20 critical care unit registered nurses volunteered to ventilate a bench model simulating a cardiac arrest patient with an unprotected airway consisting of a face mask, manikin head, training lung [with lung compliance, 50 ml/0.098 kPa (50 ml/cmH(2)O); airway resistance, 0.39 kPa/l/s (4 cmH(2)O/l/s)] oesophagus [lower oesophageal sphincter pressure, 0.49 kPa (5 cmH(2)O)] and simulated stomach. Each volunteer ventilated the model with a self-inflating bag (Ambu, Glostrup, Denmark; max. volume, 1500 ml), and a resuscitator providing limited fixed flow (Oxylator EM 100, CPR Medical devices Inc., Toronto, Canada) for 2 min; study endpoints were measured with 2 pneumotachometers. The self-inflating bag vs. resuscitator resulted in comparable mean +/- SD mask tidal volumes (945 +/- 104 vs. 921 +/- 250 ml), significantly (P < 0.05) higher peak inspiratory flow rates (111 +/- 27 vs. 45 +/- 21 l/min), and peak inspiratory pressure (1.2 +/- 0.47 vs. 78 +/- 0.07 kPa), but significantly shorter inspiratory times (1.1 +/- 0.29 vs. 1.6 +/- 0.35 s). Lung tidal volumes were comparable (337 +/- 120 vs. 309 +/- 61 ml), but stomach tidal volumes were significantly (P < 0.05) higher (200 +/- 95 vs. 140 +/- 51 ml) with the self-inflating bag. In conclusion, simulated ventilation of an unintubated cardiac arrest patient using a resuscitator resulted in decreased peak flow rates and therefore, in decreased peak airway pressures when compared with a self-inflating bag. Limited flow ventilation using the resuscitator decreased stomach inflation, although lung tidal volumes were comparable between groups.

Objective: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) may be more effective than optimal doses of epinephrine. The main purpose of this study was to determine whether intraosseous vasopressin achieves serum drug levels comparable with intravenous doses during CPR and, additionally, to evaluate the effects of intraosseous vasopressin during CPR., Design: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, blood gases, and return of spontaneous circulation., Setting: University hospital laboratory., Subjects: Twelve domestic pigs., Interventions: After 4 mins of untreated ventricular fibrillation and 3 mins of CPR, 12 pigs were randomized to be treated with intravenous administration of vasopressin (0.8 unit/kg vasopressin; n = 6) or intraosseous vasopressin (0.8 unit/kg vasopressin; n = 6). Defibrillation was performed 5 mins after drug administration to attempt the return of spontaneous circulation., Measurements and Main Results: At both 90 secs and 5 mins after drug administration, intravenous and intraosseous administration of vasopressin resulted in comparable mean (+/-SEM) coronary perfusion pressure (43+/-4 vs. 44+/-3 and 30+/-2 vs. 37+/-2 mm Hg, respectively) and vasopressin plasma concentrations (13,706+/-1,857 vs. 16,166+/-3,114 pg/mL and 10,372+/-883 vs. 8246+/-2211 pg/mL, respectively). All animals in both groups were successfully resuscitated; pigs that received intraosseous vasopressin had a significantly higher (p < .05) mean arterial (92+/-6 vs. 129+/-12 mm Hg) and coronary perfusion pressure (84+/-11 vs. 119+/-11 mm Hg) at 5 mins of return of spontaneous circulation., Conclusions: Intraosseous vasopressin resulted in comparable vasopressin plasma levels, hemodynamic variables, and return of spontaneous circulation rates as did intravenous vasopressin. Intraosseous vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.

Background and Purpose: It is unknown whether a combination of vasopressin and epinephrine may be superior to vasopressin alone by targeting both nonadrenergic and adrenergic receptors., Methods: After 15 minutes of cardiac arrest (13 minutes of ventricular fibrillation and 2 minutes of pulseless electrical activity) and 3 minutes of chest compressions, 16 animals were randomly treated with either 0.8 U/kg vasopressin (n = 8) or 0.8 U/kg vasopressin combined with 200 microg/kg epinephrine (n = 8)., Results: Comparison of vasopressin with vasopressin and epinephrine at 90 seconds and 5 minutes after drug administration resulted in comparable mean (+/-SEM) coronary perfusion pressure (54+/-3 versus 57+/-5 and 36+/-4 versus 35+/-4 mm Hg, respectively), cerebral perfusion pressure (59+/-6 versus 65+/-8 and 40+/-6 versus 39+/-6 mm Hg, respectively), and median (25th to 75th percentiles) left ventricular myocardial blood flow [116 (81 to 143) versus 108 (97 to 125) and 44 (35 to 81) versus 62 (42 to 74) mL x min(-1) x 100 g(-1), respectively], but significantly increased (P<0.05) total cerebral blood flow [81 (77 to 95) versus 39 (34 to 58) and 50 (43 to 52) versus 28 (16 to 35) mL x min(-1) x 100 g(-1), respectively]. Return of spontaneous circulation rates in both groups were comparable (vasopressin, 7 of 8; vasopressin and epinephrine, 6 of 8)., Conclusions: Comparison of vasopressin with vasopressin and epinephrine resulted in comparable left ventricular myocardial blood flow but significantly increased cerebral perfusion.