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Background Electromagnetic interference (EMI) induced by electrocautery during surgery in patients with cardiac pacemakers or implanted cardioverter-defibrillators (ICDs) may inhibit pacing and cause inappropriate tachyarrhythmia oversensing. In particular, susceptibility to EMI may be enhanced in ICDs by frequently used wide interelectrode sensing (i.e., integrated bipolar sensing). Consequently, ICD function is usually disabled preoperatively and restored later by noninvasive programming. Because sensing by closely spaced electrodes (i.e., true bipolar) may be less susceptible to EMI, preoperative programming to a true bipolar mode may minimize the need for perioperative programming while preserving device function. Methods Our study population consisted of 23 consecutive patients either receiving a new ICD or undergoing ICD pulse generator change. In each patient, electrocautery-induced EMI was initiated with the ICD in the closely spaced sensing configuration and again during widely spaced sensing. Results In comparing the 2 sensing modes, right ventricular electrogram amplitude was significantly greater and EMI noise amplitude tended to be greater with widely spaced bipolar sensing. Furthermore, widely spaced bipolar sensing was associated with ICD pacing inhibition in 22 of 23 patients and incorrect "ventricular fibrillation" detection in 17 of 23 patients. Conversely, closely spaced bipolar sensing was not accompanied by either pacing inhibition or incorrect ventricular fibrillation sensing. Conclusion Closely spaced bipolar sensing (i.e., true bipolar) appropriately rejects electrocautery-induced EMI. Programming implanted devices to closely spaced bipolar sensing may minimize the need for perioperative reprogramming while preserving intraoperative device operation.

UNLABELLED: During normothermic cardiac arrest, a combination of active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) with the inspiratory threshold valve (ITV) significantly improves vital organ blood flow, but this technique has not been studied during hypothermic cardiac arrest. Accordingly, we evaluated the hemodynamic effects of ACD + ITV CPR before, and after, the administration of vasopressin in a porcine model of hypothermic cardiac arrest. Pigs were surface-cooled until their body core temperature was 26 degrees C. After 10 min of untreated ventricular fibrillation, 14 animals were randomly assigned to either ACD CPR with the ITV (n = 7) or to standard (STD) CPR (n = 7). After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after 28 min of cardiac arrest, including 18 min of CPR. Before the administration of vasopressin, mean +/- SEM common carotid blood flow was significantly higher in the ACD + ITV group compared with STD CPR (67 +/- 13 versus 26 +/- 5 mL/min, respectively; P < 0.025). After vasopressin was given at minute 8 during CPR, mean +/- SEM coronary perfusion pressure was significantly higher in the ACD + ITV group, but did not increase in the STD group (29 +/- 3 versus 15 +/- 2 mm Hg, and 25 +/- 1 versus 14 +/- 1 mm Hg at minute 12 and 18, respectively; P < 0.001); mean +/- SEM common carotid blood flow remained higher at respective time points (33 +/- 8 versus 10 +/- 3 mL/min, and 31 +/- 7 versus 7 +/- 3 mL/min, respectively; P < 0.01). Without active rewarming, spontaneous circulation was restored and maintained for 1 h in three of seven animals in the ACD + ITV group versus none of seven animals in the STD CPR group (not significant). During hypothermic cardiac arrest, ACD CPR with the ITV improved common carotid blood flow compared with STD CPR alone. Moreover, after the administration of vasopressin, coronary perfusion pressure was significantly higher during ACD + ITV CPR, but not during STD CPR. IMPLICATIONS: New strategies are needed to improve the efficiency of cardiopulmonary resuscitation (CPR) in hypothermic cardiac arrest. Active compression-decompression CPR with the inspiratory threshold valve improved carotid blood flow (and coronary perfusion pressure with vasopressin) compared with standard CPR.

Exogenous vasopressin is a promising vasopressor when blood pressure is critically threatened, but the role of endogenous vasopressin during cardiopulmonary resuscitation (CPR) is unknown. We assessed the role of endogenous versus exogenous vasopressin in a porcine open chest CPR model. Seven minutes before induction of cardiac arrest, seven pigs received 10 microg/kg of a selective vasopressin V(1)-receptor-antagonist (Blocked Vasopressin group); another 12 pigs in two groups received saline administration only. After 4 min of untreated ventricular fibrillation followed by 3 min of basic life support CPR, six animals received 0.8 U/kg vasopressin (Exogenous Vasopressin group), whereas the blocked vasopressin group (n = 7), and the remaining six animals received saline placebo only (Endogenous Vasopressin group). Defibrillation was attempted after 14 min of CPR. During basic life support CPR, left ventricular myocardial blood flow was significantly (P < 0.05) decreased in the Blocked Vasopressin group compared with the Exogenous Vasopressin group and Endogenous Vasopressin group (42 +/- 5 compared with 64 +/- 6 and 66 +/- 6 mL x min(-1) x 100g(-1)). Left ventricular myocardial blood flow was significantly decreased in the Blocked Vasopressin group versus Exogenous Vasopressin group versus Endogenous Vasopressin group 90 s and 5 min after drug administration, respectively (38 +/- 4 and 27 +/- 3 vs 145 +/- 32 and 110 +/- 12 vs 62 +/- 4 and 56 +/- 6 mL x min(-1) x 100g(-1), respectively). None of seven Blocked Vasopressin animals, six of six Exogenous Vasopressin pigs, and six of six Endogenous Vasopressin swine had return of spontaneous circulation after 14 min of cardiac arrest including 10 min of CPR (P < 0.05). In conclusion, pigs with blocked endogenous vasopressin had poor coronary perfusion pressure and left ventricular myocardial blood flow during open chest CPR, and could not be successfully resuscitated. All pigs with effective endogenous vasopressin or pigs with effective endogenous vasopressin and additional exogenous vasopressin had good left ventricular myocardial blood flow during experimental CPR, and survived the 1-h postresuscitation phase. We conclude that endogenous vasopressin is an adjunct vasopressor to epinephrine and may serve as a back-up regulator to maintain cardiocirculatory homeostasis.

The use of an inspiratory impedance threshold valve (ITV) during active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) improves perfusion pressures, and vital organ blood flow. We evaluated the effects of positive end-expiratory pressure (PEEP) on gas exchange, and coronary perfusion pressure gradients during ACD + ITV CPR in a porcine cardiac arrest model. All animals received pure oxygen intermittent positive pressure ventilation (IPPV) at a 5:1 compression-ventilation ratio during ACD + ITV CPR. After 8 min, pigs were randomized to further IPPV alone (n = 8), or IPPV with increasing levels of PEEP (n = 8) of 2.5, 5.0, 7.5, and 10 cm H(2)O for 4 consecutive min each, respectively. Mean +/- SEM arterial oxygen partial pressure decreased in the IPPV group from 150 +/- 30 at baseline after 8 min of CPR to 110 +/- 25 torr at 24 min, but increased in the PEEP group from 115 +/- 15 to 170 +/- 25 torr with increasing levels of PEEP (P0.02 for comparisons within groups). Mean +/- SEM diastolic aortic minus diastolic left ventricular pressure gradient was significantly (P0.001) higher after the administration of PEEP (24 +/- 0 vs 17 +/- 1 mm Hg with 5 cm H(2)O of PEEP, and 26 +/- 0 vs 17 +/- 1 mm Hg with 10 cm H(2)O of PEEP), whereas the diastolic aortic minus right atrial pressure gradient (coronary perfusion pressure) was comparable between groups. Furthermore, systolic aortic pressures were significantly (P0.05) higher with 10 cm H(2)O of PEEP when compared with IPPV alone (68 +/- 0 vs 59 +/- 2 mm Hg). In conclusion, when CPR was performed with devices designed to improve venous return to the chest, increasing PEEP levels improved oxygenation. Moreover, PEEP significantly increased the diastolic aortic minus left ventricular gradient and did not affect the decompression phase aortic minus right atrial pressure gradient. These data suggest that PEEP reduces alveolar collapse during ACD + ITV CPR, thus leading to an increase in indirect myocardial compression.Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation improves perfusion pressures, and vital organ blood flow during cardiac arrest. Increasing levels of positive end-expiratory pressure during performance of active compression-decompression cardiopulmonary resuscitation with an inspiratory impedance valve improves oxygenation, and increases the diastolic aortic-left ventricular pressure gradient and systolic arterial blood pressure.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n 5 5) or epinephrine (early epinephrine: 45, 45, and 200 mg/kg, respectively, n 5 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0.8 units/kg, respectively, n 5 5) or epinephrine (late epinephrine: 45 and 200 mg/kg, n 5 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 6 1.5 Hz vs 7.0 6 0.7 Hz (P , 0.001), mean amplitude was 0.65 6 0.26 mV vs 0.21 6 0.14 mV (P , 0.001, and coronary perfusion pressure was 27 6 9m m Hg vs 86 4m m Hg (P , 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survive d1h( P , 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation. (Anesth Analg 2000;90:1067‐75)

The purpose of this study was to record median frequency of ventricular fibrillation (VF) in patients undergoing cardiopulmonary bypass for cardiac surgery, and to assess whether defibrillation success depends upon median VF frequency. Data were collected from 20 patients undergoing aortocoronary bypass grafting. Using computerized fast Fourier transformation of the signal from the electrogram, median VF frequency was assessed from onset of VF until aortic cross-clamping and during the 4-s period immediately before each defibrillation during the reperfusion phase. During VF, when an adequate coronary perfusion was maintained by cardiopulmonary bypass prior to aortic cross-clamping, median VF frequency (5.8 +/- 0.1 Hz to 6.2 +/- 0.1 Hz) remained constant for the entire observation interval (96 +/- 25 s; mean +/- SEM). A total of 42 defibrillations were performed: 22 resulted in supraventricular rhythm, 10 in VF, 6 in asystole, and 4 in electromechanical dissociation (EMD). Median VF frequency before defibrillation resulting in supraventricular rhythm was 4.7 +/- 0.17 Hz. In contrast, median VF frequencies before unsuccessful defibrillation resulting in persistent VF (3.5 +/- 0.28 Hz; P0.05), EMD (2.9 +/- 0.15 Hz; P0.01), or asystole (2.8 +/- 0.28 Hz; P0.01) were significantly lower. Above a threshold of 3.0 Hz, the probability of successful defibrillation increased as median VF frequency increased. The probability of success was 100% at a frequency ofor = 5.5 Hz. We conclude that median VF frequency is a reliable noninvasive variable which can be used to predict defibrillation success during the reperfusion phase after cardiac surgery.