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Aim The optimal head and thorax position after return of spontaneous circulation (ROSC) following cardiac arrest (CA) is unknown. This study examined whether head and thorax elevation post-ROSC is beneficial, in a porcine model. Methods Protocol A: 40 kg anesthetized pigs were positioned flat, after 7.75 min of untreated CA the heart and head were elevated 8 and 12 cm, respectively, above the horizontal plane, automated active compression decompression (ACD) plus impedance threshold device (ITD) CPR was started, and 2 min later the heart and head were elevated 10 and 22 cm, respectively, over 2 min to the highest head up position (HUP). After 30 min of CPR pigs were defibrillated and randomized 10 min later to four 5-min epochs of HUP or flat position. Multiple physiological parameters were measured. In Protocol B, after 6 min of untreated VF, pigs received 6 min of conventional CPR flat, and after ROSC were randomized HUP versus Flat as in Protocol A. The primary endpoint was cerebral perfusion pressure (CerPP). Multivariate analysis-of-variance (MANOVA) for repeated measures was used. Data were reported as mean ± SD. Results In Protocol A, intracranial pressure (ICP) (mmHg) was significantly lower post-ROSC with HUP (9.1 ± 5.5) versus Flat (18.5 ± 5.1) (p Conclusion Post-ROSC head and thorax elevation in a porcine model of cardiac arrest resulted in higher CerPP and lower ICP values, regardless of VF duration or CPR method. IACUC Protocol Number 19-09.

Aim Controlled sequential elevation of the head and thorax (CSE) during active compression–decompression (ACD) CPR with an impedance threshold device (ITD) augments cerebral (CerPP) and coronary (CorPP) perfusion pressures. The optimal CSE is unknown. Methods After 8 minutes of untreated VF, 40 kg anesthetized female pigs were positioned on a customized head and thorax elevation device (CED). After 2 min of automated ACD + ITD-16 CPR to ‘prime the system’, 12 pigs were randomized to CSE to the highest CED position over 4-min or 10-min. The primary outcome was CerPP after 7 minutes of CPR. Secondarily, 24-sec (without a priming step) and 2-min CSE times were similarly tested (n = 6 group) in a non-randomized order. Values expressed as mean ± SD. Results After 7 min of CPR, CerPPs were significantly higher in the 4-min vs 10-min CSE groups (53 ± 14.4 vs 38.5 ± 3.6 mmHg respectively, p = 0.03) whereas CorPP trended higher. The 4-min CSE group achieved 50% of baseline (50% BL) CerPP faster than the 10-min group (2.5 ± 1.2 vs 6 ± 3.1 minutes, p = 0.03). CerPP values in the 2-min and 4-min CSE groups were significantly higher than in the 24-sec group. With CSE, CerPPs and CorPPs increased over time in all groups. Conclusions By optimizing controlled sequential elevation timing, CerPP values achieved 50% of baseline within less than 2.5 minutes and >80% of baseline after 7 minutes of CPR. This novel CPR approach rapidly restored CerPPs to near normal values non-invasively and without vasopressors.

Background The prevalence of coronary artery disease (CAD) among patients with refractory out-of-hospital (OH) ventricular fibrillation (VF)/ventricular tachycardia (VT) cardiac arrest is unknown. Objectives The goal of this study was to describe the prevalence and complexity of CAD and report survival to hospital discharge in patients experiencing refractory VF/VT cardiac arrest treated with a novel protocol of early transport to a cardiac catheterization laboratory (CCL) for extracorporeal life support (ECLS) and revascularization. Methods Between December 1, 2015, and December 1, 2016, consecutive adult patients with refractory OH VF/VT cardiac arrest requiring ongoing cardiopulmonary resuscitation were transported by emergency medical services to the CCL. ECLS, coronary angiography, and percutaneous coronary intervention were performed, as appropriate. Functionally favorable survival to hospital discharge (Cerebral Performance Category 1 or 2) was determined. Outcomes in a historical comparison group were also evaluated. Results Sixty-two (86%) of 72 transported patients met emergency medical services transport criteria. Fifty-five (89%) of the 62 patients met criteria for continuing resuscitation on CCL arrival; 5 had return of spontaneous circulation, 50 received ECLS, and all 55 received coronary angiography. Forty-six (84%) of 55 patients had significant CAD, 35 (64%) of 55 had acute thrombotic lesions, and 46 (84%) of 55 had percutaneous coronary intervention with 2.7 ± 2.0 stents deployed per patient. The mean SYNTAX score was 29.4 ± 13.9. Twenty-six (42%) of 62 patients were discharged alive with Cerebral Performance Category 1 or 2 versus 26 (15.3%) of 170 in the historical comparison group (odds ratio: 4.0; 95% confidence interval: 2.08 to 7.7; p Conclusions Complex but treatable CAD was prevalent in patients with refractory OH VF/VT cardiac arrest who also met criteria for continuing resuscitation in the CCL. A systems approach using ECLS and reperfusion seemed to improve functionally favorable survival.

Chest compliance plays a fundamental role in the generation of circulation during cardiopulmonary resuscitation (CPR). To study potential changes in chest compliance over time, anterior posterior (AP) chest height measurements were performed on newly deceased (never frozen) human cadavers during CPR before and after 5min of automated CPR. We tested the hypothesis that after 5min of CPR chest compliance would be significantly increased.Static compression (30, 40, and 50kg) and decompression forces (-10, -15kg) were applied with a manual ACD-CPR device (ResQPUMP, ZOLL) before and after 5min of automated CPR. Lateral chest x-rays were obtained with multiple reference markers to assess changes in AP distance.In 9 cadavers, changes (mean±SD) in the AP distance (cm) during the applied forces were 2.1±1.2 for a compression force of 30kg, 2.9±1.3 for 40kg, 4.3±1.0 for 50kg, 1.0±0.8 for a decompression force of -10kg and 1.8±0.6 for -15kg. After 5min of automated CPR, AP excursion distances were significantly greater (p0.05). AP distance increased to 3.7±1.4 for a compression force of 30kg, 4.9±1.6 for 40kg, 6.3±1.9 for 50kg, 2.3±0.9 for -10kg of lift and 2.7±1.1 for -15kg of lift.These data demonstrate chest compliance increases significantly over time as demonstrated by the significant increase in the measured AP distance after 5min of CPR. These findings suggest that adjustments in compression and decompression forces may be needed to optimize CPR over time.

Objective Ischemic postconditioning (PC) using three intentional pauses at the start of cardiopulmonary resuscitation (CPR) improves outcomes after cardiac arrest in pigs when epinephrine (epi) is used before defibrillation. We hypothesized PC, performed during basic life support (BLS) in the absence of epinephrine, would reduce reperfusion injury and enhance 24h functional recovery. Design Prospective animal investigation. Setting Animal laboratory Subjects Female farm pigs ( n =46, 39±1kg). Interventions Protocol A: After 12min of ventricular fibrillation (VF), 28 pigs were randomized to four groups: (A) Standard CPR (SCPR), (B) active compression-decompression CPR with an impedance threshold device (ACD-ITD), (C) SCPR+PC (SCPR+PC) and (D) ACD-ITD CPR+PC. Protocol B: After 15min of VF, 18 pigs were randomized to ACD-ITD CPR or ACD-ITD+PC. The BLS duration was 2.75min in Protocol A and 5min in Protocol B. Following BLS, up to three shocks were delivered. Without return of spontaneous circulation (ROSC), CPR was resumed and epi (0.5mg) and defibrillation delivered. The primary end point was survival without major adverse events. Hemodynamic parameters and left ventricular ejection fraction (LVEF) were also measured. Data are presented as mean±SEM. Measurements and Main Results Protocol A: ACD-ITD+PC (group D) improved coronary perfusion pressure after 3min of BLS versus the three other groups (28±6, 35±7, 23±5 and 47±7 for groups A, B, C, D respectively, p =0.05). There were no significant differences in 24h survival between groups. Protocol B LVEF 4h post ROSC was significantly higher with ACD-ITD+PC vs ACD-ITD alone (52.5±3% vs. 37.5±6.6%, p =0.045). Survival rates were significantly higher with ACD-ITD+PC vs. ACD-ITD alone ( p =0.027). Conclusions BLS using ACD-ITD+PC reduced post resuscitation cardiac dysfunction and improved functional recovery after prolonged untreated VF in pigs. Protocol number 12-11.

Survival rates after cardiac arrest have shown minimal improvement in the last 60 years. However, in some forward-thinking cities and hospitals, out-of and in-hospital cardiac arrest survival rates exceed 20% and 40% respectively. These beacons of hope can enlighten us, providing a clearer vision of what it takes to provide Ideal cardiopulmonary resuscitation. To make progress in a field that has seemingly stagnated for too many decades, we must be open to new ideas and develop bundles of care that work in communities with varying EMS systems and various existing infrastructure to bring the best practices to the rest of the country.

Background A recent out-of-hospital cardiac arrest (OHCA) clinical trial showed improved survival to hospital discharge (HD) with favorable neurologic function for patients with cardiac arrest of cardiac origin treated with active compression decompression cardiopulmonary resuscitation (CPR) plus an impedance threshold device (ACD+ICD) versus standard (S) CPR. The current analysis examined whether treatment with ACD+ITD is more effective than standard (S-CPR) for all cardiac arrests of non-traumatic origin, regardless of the etiology. Methods This is a secondary analysis of data from a randomized, prospective, multicenter, intention-to-treat, OHCA clinical trial. Adults with presumed non-traumatic cardiac arrest were enrolled and followed for one year post arrest. The primary endpoint was survival to hospital discharge (HD) with favorable neurologic function (Modified Rankin Scale score≤3). Results Between October 2005 and July 2009, 2738 patients were enrolled (S-CPR=1335; ACD+ITD=1403). Survival to HD with favorable neurologic function was greater with ACD+ITD compared with S-CPR: 7.9% versus 5.7%, (OR 1.42, 95% CI 1.04, 1.95, p =0.027). One-year survival was also greater: 7.9% versus 5.7%, (OR 1.43, 95% CI 1.04, 1.96, p =0.026). Nearly all survivors in both groups had returned to their baseline neurological function by one year. Major adverse event rates were similar between groups. Conclusions Treatment of out-of-hospital non-traumatic cardiac arrest patients with ACD+ITD resulted in a significant increase in survival to hospital discharge with favorable neurological function when compared with S-CPR. A significant increase survival rates was observed up to one year after arrest in subjects treated with ACD+ITD, regardless of the etiology of the cardiac arrest.

OBJECTIVES: Ischemic postconditioning (PC) with “stuttering” reintroduction of blood flow after prolonged ischemia has been shown to offer protection from ischemia reperfusion injury to the myocardium and brain. We hypothesized that four 20-s pauses during the first 3 min of standard CPR would improve post resuscitation cardiac and neurological function, in a porcine model of prolonged untreated cardiac arrest. METHODS: 18 female farm pigs, intubated and isoflurane anesthetized had 15 min of untreated ventricular fibrillation followed by standard CPR (SCPR). Nine animals were randomized to receive PC with four, controlled, 20-s pauses, during the first 3 min of CPR (SCPR + PC). Resuscitated animals had echocardiographic evaluation of their ejection fraction after 1 and 4 h and a blinded neurological assessment with a cerebral performance category (CPC) score assigned at 24 and 48 h. All animals received 12 h of post resuscitation mild therapeutic hypothermia. RESULTS: SCPR + PC animals had significant improvement in left ventricular ejection fraction at 1 and 4 h compared to SCPR (59 ± 11% vs 35 ± 7% and 55 ± 8% vs 31 ± 13% respectively, p < 0.01). Neurological function at 24 h significantly improved with SCPR + PC compared to SCPR alone (CPC: 2.7 ± 0.4 vs 3.8 ± 0.4 respectively, p = 0.003). Neurological function significantly improved in the SCPR + PC group at 48 h and the mean CPC score of that group decreased from 2.7 ± 0.4 to 1.7 ± 0.4 (p < 0.00001). CONCLUSIONS: Ischemic postconditioning with four 20-s pauses during the first 3 min of SCPR improved post resuscitation cardiac function and facilitated neurological recovery after 15 min of untreated cardiac arrest in pigs.

Active compression-decompression cardiopulmonary resuscitation (CPR) with decreased intrathoracic pressure in the decompression phase can lead to improved haemodynamics compared with standard CPR. We aimed to assess effectiveness and safety of this intervention on survival with favourable neurological function after out-of-hospital cardiac arrest.In our randomised trial of 46 emergency medical service agencies (serving 2·3 million people) in urban, suburban, and rural areas of the USA, we assessed outcomes for patients with out-of-hospital cardiac arrest according to Utstein guidelines. We provisionally enrolled patients to receive standard CPR or active compression-decompression CPR with augmented negative intrathoracic pressure (via an impedance-threshold device) with a computer-generated block randomisation weekly schedule in a one-to-one ratio. Adults (presumed age or age ≥18 years) who had a non-traumatic arrest of presumed cardiac cause and met initial and final selection criteria received designated CPR and were included in the final analyses. The primary endpoint was survival to hospital discharge with favourable neurological function (modified Rankin scale score of ≤3). All investigators apart from initial rescuers were masked to treatment group assignment. This trial is registered with ClinicalTrials.gov, number NCT00189423.2470 provisionally enrolled patients were randomly allocated to treatment groups. 813 (68%) of 1201 patients assigned to the standard CPR group (controls) and 840 (66%) of 1269 assigned to intervention CPR received designated CPR and were included in the final analyses. 47 (6%) of 813 controls survived to hospital discharge with favourable neurological function compared with 75 (9%) of 840 patients in the intervention group (odds ratio 1·58, 95% CI 1·07-2·36; p=0·019]. 74 (9%) of 840 patients survived to 1 year in the intervention group compared with 48 (6%) of 813 controls (p=0·03), with equivalent cognitive skills, disability ratings, and emotional-psychological statuses in both groups. The overall major adverse event rate did not differ between groups, but more patients had pulmonary oedema in the intervention group (94 [11%] of 840) than did controls (62 [7%] of 813; p=0·015).On the basis of our findings showing increased effectiveness and generalisability of the study intervention, active compression-decompression CPR with augmentation of negative intrathoracic pressure should be considered as an alternative to standard CPR to increase long-term survival after cardiac arrest.US National Institutes of Health grant R44-HL065851-03, Advanced Circulatory Systems.

ObjectivesWe sought to identify the impact of cardiac resynchronization therapy (CRT) on atrial tachyarrhythmia (AT) susceptibility in patients with left ventricular (LV) systolic dysfunction in whom worsening heart failure (HF) resulted in upgrade from conventional dual-chamber pulse generator to cardiac resynchronization therapy-defibrillator (CRT-D).BackgroundCardiac resynchronization therapy with a defibrillator improves survival rates and symptoms in patients with LV systolic dysfunction but little is known about its effects on AT incidence in the same patient population.MethodsTwenty-eight consecutive HF patients who underwent device upgrade to CRT-D were included. Patients had ≥2 device interrogations in the 1 year before upgrade and ≥3 interrogations in the 18- to 24-month follow-up after upgrade. Echocardiographic parameters were assessed before and at 3 to 6 months after CRT-D. Additional observations included number of hospital stays, HF clinical status, and concomitant pharmacological therapy. By virtue of this study design, each patient served as his/her own control. Statistical analysis was performed by 2-tailed paired ttest and with nonparametric tests where appropriate.ResultsWithin 3 months after CRT, the number of HF patients with documented AT decreased significantly from the immediate pre-CRT value and tended to decline with time. At 1-year follow-up, 90% of patients were AT-free compared with 14% of patients 3 months before CRT (p < 0.001). Furthermore, the number of AT episodes/year and their maximum duration decreased after CRT (mean ± SD; 181 ± 50 vs. 50 ± 20.2, p < 0.05, and 220.8 ± 87 s vs. 28 ± 21 s, p < 0.05, respectively). Finally, CRT was associated with improved LV ejection fraction (mean ± SD; from 26 ± 5.3% to 31 ± 7%, p < 0.001) and reduced number of HF or arrhythmia hospital stays (p < 0.05).ConclusionsOur findings support the view that CRT might decrease AT susceptibility in HF patients with LV systolic dysfunction.

The inspiratory impedance threshold device (ITD) has been shown to improve hemodynamic variables and survival outcomes during cardiopulmonary resuscitation in animals and humans. We hypothesized that use of an ITD, with a resistance of -10 cm H2O, will improve hemodynamics and short-term survival rates during hypovolemic hypotension in spontaneously breathing pigs.Female farm pigs ( approximately 26 kg) were intubated and anesthetized with propofol with the dose adjusted to permit spontaneous respirations. They were bled to 50% of calculated blood volume through an arterial catheter and then prospectively randomized to either treatment with an ITD or observation alone. Arterial and intratracheal pressures as well as arterial blood gases were measured. After 90 min the ITD was removed, normal saline was administered to all surviving animals, the anesthetic was discontinued, and animals were allowed to recover. Statistical analysis was performed with one-way repeated ANOVA and survival rates were calculated with Kaplan-Meier analysis.Treatment with the ITD resulted in lower intratracheal inspiratory pressure in the treatment group (-11+/-0.4 mmHg versus -4+/-0.7 mmHg, respectively, P0.005). Mean arterial pressure after 30 min of treatment with the ITD was higher in the treatment group (61.1+/-5.5 mmHg versus 37.4+/-2.1 mmHg, respectively, P0.005). All pigs in the control group died within 65 min of the initial bleed, whereas 7/8 (87%) treated with an ITD survived for90 min (P0.001). During the recovery phase, 6/8 (75%) in the ITD group survived for3h and awoke without neurological deficit; one surviving animal in the ITD group never woke up. Arterial oxygenation was not compromised in the ITD group.Use of an ITD improved blood pressure and short-term survival rates in a spontaneously breathing porcine model of hypovolemic hypotension.

ObjectivesA rapid, ice-cold saline flush combined with active compression-decompression (ACD) plus an inspiratory impedance threshold device (ITD) cardiopulmonary resusitation (CPR) will cool brain tissue more effectively than with standard CPR (S-CPR) during cardiac arrest (CA).BackgroundEarly institution of hypothermia after CPR and return of spontaneous circulation improves survival and outcomes after CA in humans.MethodsVentricular fibrillation (VF) was induced for 8 min in anesthetized and tracheally intubated pigs. Pigs were randomized to receive either ACD + ITD CPR (n = 8) or S-CPR (n = 8). After 2 min of CPR, 30 ml/kg ice-cold saline (3°C) was infused over the next 3 min of CPR via femoral vein followed by up to three defibrillation attempts (150 J, biphasic). If VF persisted, epinephrine (40 μg/kg) and vasopressin (0.3 U/kg) were administered followed by three additional defibrillation attempts. Hemodynamic variables and temperatures were continuously recorded.ResultsAll ACD + ITD CPR pigs (8 of 8) survived (defined as 15 min of return of spontaneous circulation [ROSC]) versus 3 of 8 pigs with S-CPR (p < 0.05). In survivors, brain temperature (°C) measured at 2-cm depth in brain cortex 1 min after ROSC decreased from 37.6 ± 0.2 to 35.8 ± 0.3 in ACD + ITD CPR versus 37.8 ± 0.2 to 37.3 ± 0.3 in S-CPR (p < 0.005). Immediately before defibrillation: 1) right atrial systolic/diastolic pressures (mm Hg) were lower (85 ± 19, 4 ± 1) in ACD + ITD CPR than S-CPR pigs (141 ± 12, 8 ± 3, p < 0.01); and 2) coronary perfusion pressures (mm Hg) were higher in ACD + ITD CPR (28.3 ± 2) than S-CPR pigs (17.4 ± 3, p < 0.01).ConclusionsA rapid ice-cold saline infusion combined with ACD + ITD CPR during cardiac arrest induces cerebral hypothermia more rapidly immediately after ROSC than with S-CPR.

"Cough syncope" is uncommon, and its mechanism remains controversial.This study evaluated susceptibility to cough-triggered neural reflex hypotension-bradycardia among cough syncope patients. We hypothesized that individuals with cough syncope would manifest not only more profound cough-triggered hypotension than do other fainters but also an inappropriate chronotropic response accompanying cough-induced hypotension, thereby supporting the notion that a neural reflex hypotension-bradycardia contributes to the condition.Three patient groups were studied. Group 1 patients (n = 9) had "cough syncope." The remaining patients had recurrent faints of other causes: group 2 (n = 13) had a positive head-up tilt test, and group 3 (n = 18) had a negative tilt test. With cough, group 1 patients exhibited a greater drop in systolic pressure (-51 +/- 19.3 mmHg) than did either group 2 (-23 +/- 11.1 mmHg, P.04) or group 3 patients (-28 +/- 12.4 mmHg, P.05). Recovery time to normalization of systolic pressure was greater in group 1 (25 +/- 9.1 seconds) than in group 2 or 3 (8 +/- 2.7 seconds and 9 +/- 6.1 seconds, respectively, both P.01 vs group 1). The expected positive chronotropic response accompanying cough-induced hypotension was diminished in group 1 patients (0.16 +/- 0.21 bpm/mmHg) compared with that in either group 2 (0.74 +/- 0.60 bpm/mmHg, P.05 vs group 1) or group 3 (0.33 +/- 0.15 bpm/mmHg, P = .06 vs group 1).Cough syncope patients not only exhibit more pronounced hypotension in response to cough than other fainters, but they also manifest an inappropriate cough-triggered blood pressure-heart rate relationship. These findings argue in favor of the importance of a neurally mediated reflex contribution to symptomatic hypotension in cough syncope.

Implantable cardioverter defibrillators have been shown to provide similar survival benefits for patients who have left ventricular dysfunction due to ischemic heart disease and for subsets of patients who have nonischemic cardiomyopathy. Findings in this study extend these observations by showing that patients who have ischemic or nonischemic heart disease and receive implantable cardioverter defibrillators not only have comparable mortality rates but also similar tachyarrhythmia frequencies during follow-up; further, mortality and tachyarrhythmia outcomes are independent of initial arrhythmia indication.

Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival.Incomplete chest wall recoil during the decompression phase of standard CPR increases intrathoracic pressure and right atrial pressure, impedes venous return, decreases compression-induced aortic pressures and results in a decrease of mean arterial pressure, coronary and cerebral perfusion pressure.Nine pigs in ventricular fibrillation (VF) for 6 min, were treated with an automated compression/decompression device with a compression rate of 100 min(-1), a depth of 25% of the anterior-posterior diameter, and a compression to ventilation ratio of 15:2 with 100% decompression (standard CPR) for 3 min. Compression was then reduced to 75% of complete decompression for 1 min of CPR and then restored for another 1 min of CPR to 100% full decompression. Coronary perfusion pressure (CPP) was calculated as the diastolic (aortic (Ao)-right atrial (RA) pressure). Cerebral perfusion pressure (CerPP) was calculated multiple ways: (1) the positive area (in mmHg s) between aortic pressure and intracranial pressure (ICP) waveforms, (2) the coincident difference in systolic and diastolic aortic and intracranial pressures (mmHg), and (3) CerPP = MAP--ICP. ANOVA was used for statistical analysis and all values were expressed as mean +/- S.E.M. The power of the study for an alpha level of significance set at 0.05 was0.90.With CPR performed with 100%-75%-100% of complete chest wall recoil, respectively, the CPP was 23.3 +/- 1.9, 15.1 +/- 1.6, 16.6 +/- 1.9, p = 0.003; CerPP was: (1) area: 313.8 +/- 104, 89.2 +/- 39, 170.5 +/- 42.9, p = 0.03, (2) systolic aortic minus intracranial pressure difference: 22.8 +/- 3.6, 16.5 +/- 4, 23.7 +/- 4.5, p = n.s., and diastolic pressure difference: 5.7 +/- 3, -2.4 +/- 2.4, 3.2 +/- 2.5, p = 0.04 and (3) mean: 14.3 +/- 3, 7 +/- 2.9, 12.4 +/- 2.9, p = 0.03, diastolic aortic pressure was 28.1 +/- 2.5, 20.7 +/- 1.9, 20.9 +/- 2.1, p = 0.0125; ICP during decompression was 22.8 +/- 1.7, 23 +/- 1.5, 19.7 +/- 1.7, p = n.s. and mean ICP was 37.1 +/- 2.3, 35.5 +/- 2.2, 35.2 +/- 2.4, p = n.s.; RA diastolic pressure 4.8 +/- 1.3, 5.6 +/- 1.2, 4.3 +/- 1.2 p = 0.1; MAP was 52 +/- 2.9, 43.3 +/- 3, 48.3 +/- 2.9, p = 0.04; decompression endotracheal pressure, -0.7 +/- 0.1, -0.3 +/- 0.1, -0.75 +/- 0.1, p = 0.045.Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures.

Aims: The purpose of this multicentre clinical randomized controlled blinded prospective trial was to determine whether an inspiratory impedance threshold device (ITD), when used in combination with active compression–decompression (ACD) cardiopulmonary resuscitation (CPR), would improve survival rates in patients with out-of-hospital cardiac arrest. Methods and results:Patients were randomized to receive either a sham (n = 200) or an active impedance threshold device (n = 200) during advanced cardiac life support performed with active compression–decompression cardiopulmonary resuscitation. The primary endpoint of this study was 24 h survival. The 24 h survival rates were 44/200 (22%) with the sham valve and 64/200 (32%) with the active valve (P = 0.02). The number of patients who had a return of spontaneous circulation (ROSC), intensive care unit (ICU) admission, and hospital discharge rates was 77 (39%), 57 (29%), and 8 (4%) in the sham valve group versus 96 (48%) (P = 0.05), 79 (40%) (P = 0.02), and 10 (5%) (P = 0.6) in the active valve group. Six out of ten survivors in the active valve group and 1/8 survivors in the sham group had normal neurological function at hospital discharge (P = 0.1). Conclusion: The use of an impedance valve in patients receiving active compression–decompression cardiopulmonary resuscitation for out-of-hospital cardiac arrest significantly improved 24 h survival rates. © 2004 Elsevier Ireland Ltd. All rights reserved.

Background:The basic premise that frequent ventilations during cardiopulmonary resuscitation (CPR) are a necessity for tissue oxygenation has recently been challenged. An inspiratory impedance threshold device (ITD) recently has also been shown to increase CPR efficiency, principally by augmenting circulation with little impact on ventilation. The optimal compression to ventilation (C/V) is not known for this new device. The purpose of this study was to compare the currently recommended C/V ratio of 5:1 with a 10:1 ratio, ± the ITD, to optimize circulation and oxygenation during CPR. Methods: Thirty-two adult pigs weighing 26–31 kg were randomized to CPR with varying C/V ratios ± the ITD as follows: A = 5:1, B = 5:1 + ITD, C = 10:1, D = 10:1 + ITD. After 6 min of untreated ventricular fibrillation (VF), closed-chest standard CPR was performed with an automatic piston device that does not impede passive chest wall recoil, at a continuous compression rate of 100 min −1 . Synchronous breaths were given every 5 or 10 compressions during the decompression phase depending on the group. CPR was performed for 6 min and physiological variables were measured throughout the experimental protocol. Results: A reduction in the frequency of ventilation from 5:1 to 10:1 resulted in significantly improved arterial and coronary perfusion pressure in a pig model of cardiac arrest. Addition of an ITD resulted in further increases in arterial and coronary perfusion pressures with both 5:1 and 10:1 C/V ratios, without compromising oxygenation. Conclusion: CPR efficiency can be optimized by changing the compression: ventilation ratio from 5:1 to 10:1 and with concurrent use of the inspiratory threshold device. © 2004 Published by Elsevier Ireland Ltd.

The implantable loop recorder (ILR) has become an important tool for evaluating patients with recurrent syncope. Second generation ILRs have the ability to record events either automatically (auto activated) or by manual activation (patient activated). In an attempt to evaluate the relative utility of the auto-activation feature, this study stratified ILR events based on a grading system designed to classify detected arrhythmias in terms of the likelihood that they provide a diagnostic basis for syncope. Data from 50 patients (27 men, mean age 64 +/- 22 years) who underwent ILR implantation for investigation of recurrent syncope were assessed. The arrhythmia syncope grading system used 5 levels, ranging from grade 0 (rhythm recorded during syncope) to grade IV (rhythm unlikely to provide a diagnostic basis for syncope). Thirty-six patients (72%) demonstratedor =1 auto-activated or patient-activated recording during a follow-up of 14.3 +/- 7.9 months. Of the total of 529 recordings, 223 (194 after auto activation [86.9%]) from 30 patients showed a rhythm abnormality. Auto activation was more effective for documenting arrhythmias that were recorded during syncope or those with highest probability of providing a syncope diagnosis (grade 0 or I arrhythmias: auto activated, 19 patients, patient activated, 3 patients). Times from ILR implantation to first grade 0 and grade I arrhythmias were 13.4 and 7.8 months, respectively. The ILR auto-activation feature proved effective in providing a high probability basis for syncope (196 arrhythmia recordings [87.1%] in 27 patients) and enhanced the diagnostic effectiveness of the device compared with patient activation alone (29 arrhythmia recordings [12.9%] in 6 patients).

Midodrine hydrochloride is a peripheral -receptor agonist capable of inducing venous and arterial vasoconstriction.[1, 2, 3, 4, 5, 6, 7, 8, 9 and 10] As a result of this action, midodrine has been approved in the United States for treatment of orthostatic hypotension, and several reports attest to its effectiveness in that setting. [6 and 7] In addition, other studies suggest that, at least during short-term follow-up, midodrine may also be effective as a preventive measure in patients with vasovagal syncope. [3, 4, 5 and 10] This report extends prior experience with midodrine as a therapeutic measure in patients with refractory recurrent vasovagal syncope.

In an attempt to improve upon the currently poor outcomes for patients in cardiac arrest, new methods and devices have been developed to enhance the efficiency and efficacy of standard cardiopulmonary resuscitation (CPR). One new approach, active compression-decompression (ACD) CPR was developed to lower the intrathoracic pressure during the decompression phase of CPR, thereby enhancing venous blood return to the thorax. Over the past decade the ACD CPR device has been extensively evaluated in animals and humans. ACD CPR is the only new approach for improving CPR efficacy with a mechanical device that has achieved clinical relevance. More recently, an inspiratory impedance threshold valve (ITV ™ ) has been developed that causes a further reduction in intrathoracic pressures, augmenting the efficiency of both standard and ACD CPR. Consequently, ACD CPR and the impedance valve were recently recommended by the American Heart Association. Clinical trials are underway to determine the long-term, potential value of these new technologies.

m-(Iodobenzyl)trozamicol (MIBT) is a recently discovered vesamicol analogue. It has been shown that radiolabelled [125I]MIBT can be used as a marker of cholinergic innervation in the heart as well as in the brain. The purpose of this study was to analyze the direct effects of MIBT on the atrioventricular and intraventricular conduction in addition to the coronary blood flow using the canine isolated, blood-perfused atrioventricular node preparation. Intracoronary administration of MIBT suppressed the atrioventricular and intraventricular conduction, while it increased the coronary blood flow. The effect and duration of action on the intraventricular conduction was less pronounced compared with other effects. Moreover, the doses of MIBT needed to cause negative dromotropic and coronary vasodilator effects in this study was much greater than those needed for imaging the cardiac cholinergic innervation. Pretreatment of the preparations with a muscarinic receptor antagonist, atropine, did not block these effects of MIBT, suggesting that MIBT may possess muscarinic receptor-independent ion channel activity in the cardiac conduction system and coronary arteries.

Use of an inspiratory impedance valve has recently been shown to increase the efficacy of standard and active compression-decompression cardiopulmonary resuscitation. We evaluated the effects of a prototypic impedance valve on the relationship between the active decompression and intra-thoracic pressure using a mechanical model lung system. Intermittent impedance to inspiratory flow of respiratory gases during the decompression phase of active compression-decompression cardiopulmonary resuscitation significantly decreased the intra-thoracic pressure, while the pressure was almost zero cm H2O during the cardiopulmonary resuscitation cycle when the impedance threshold valve was not functioning. Thus, this mechanical model will help in evaluating the valve as well as in optimizing its function by simulating various forms of lung disease.

Active compression decompression resuscitation (ACD-CPR) has been developed as an alternative to standard cardiopulmonary resuscitation (S-CPR). To determine the effect of ACD-CPR on survival and neurologic outcome in patients with out-of-hospital cardiac arrest, this combined analysis involved individual patient data from 2866 patients from seven separate randomized prospective prehospital studies who had received ACD-CPR or S-CPR after out-of-hospital cardiac arrest in seven international sites. Significant improvement in 1-h survival (odds ratio (OR) = 0.83; confidence interval (CI): 0.695-0.99; P0.05) was found with ACD-CPR (n = 1410) versus S-CPR (n = 1456). The odds ratio for hospital discharge after ACD-CPR was similar (OR = 0.82; CI: 0.609-1.107, P = NS), but this finding was not statistically significant. Using the chi2-test for trend, there was a significant improvement in overall survival with ACD-CPR (P0.05) versus S-CPR. This improvement was largely due to the influence of results from one study site. Neurological outcome and complication rates were comparable between groups. Further study is needed to determine which emergency medical services systems may benefit from out-of-hospital use of ACD-CPR.

We prospectively studied the efficacy of pindolol, a beta-adrenergic blocker with intrinsic sympathomimetic activity (ISA), for the prevention of syncope recurrences in 31 patients with recurrent neurocardiogenic syncope. Pindolol proved to be an effective treatment, even in patients who had previously failed treatment with conventional beta blockers, suggesting a clinical benefit from addition of ISA to beta blockade in this setting.

Both epinephrine (Epi) and vasopressin (VP) increase coronary perfusion pressure (CPP) when administered during cardiac arrest. Given their different mechanisms of action we tested the hypothesis that during cardiopulmonary resuscitation (CPR) a combination of VP plus Epi would be superior to either agent alone. Epi(40 microg/kg), VP(0.3 U/kg) and the combination of both agents were assessed in a porcine model of ventricular fibrillation (VF). Maximum CPP (diastolic aortic-right atrial pressures) during CPR was similar among the groups but the time course of action was different in each group: with Epi + VP the increase in CPP was significantly more rapid than with VP alone whereas the CPP remained significantly higher for a longer periods of time with VP or VP + Epi versus Epi alone. Left ventricular blood flow (ml/min per g) determined during CPR two min after drug administration was similar between groups: Epi 1.06 +/- 0.16; VP 0.82 +/- 0.26; Epi + VP 0.83 +/- 0.14 (P = N.S.). Post drug administration. 2 min, cerebral blood flow (ml/min per g) in the VP group (0.76 +/- 0.15) was more than two times higher compared with Epi alone (Epi:0.30 +/- 0.08, P0.01 versus VP) and Epi plus VP (Epi + VP:0.23 +/- 0.03, P0.01 versus VP). We conclude that combination of VP + Epi during cardiac arrest results in a more rapid rise in CPP when compared with VP alone and a more sustained elevation in CPP than observed with Epi alone. Thus, the synergistic effects of these two potent vasopressor agents may be of benefit during CPR.

Atrial fibrillation is the most common cardiac arrhythmia requiring treatment. Limitations of medical treatment have prompted development of nonpharmacologic therapies for this arrhythmia. These are aimed at ventricular rate control during atrial fibrillation, termination of the arrhythmia, and/or prevention of recurrences. Ventricular rate control can be achieved with transcatheter ablation or modification of the atrioventricular node. The MAZE operation is effective in preventing arrhythmia recurrence, but because it requires cardiac surgery, its appeal is limited. Development of the technique for direct transcatheter ablation of atrial fibrillation is eagerly anticipated and may represent the standard curative treatment of the future. In appropriately selected patients, implantable device therapy may play an important role in the treatment of paroxysmal atrial fibrillation.

Effective management of the syncope patient is critically dependent on excluding conditions in which altered consciousness is not due to syncope (e.g., seizure and sleep disorders) then establishing the basis for syncopal symptoms. The initial diagnostic step in syncope patients is differentiation of those individuals with normal cardiovascular status from those with structural heart disease. In the former, tilt-table testing and related studies of autonomic nervous system function are usually the most productive direction in which to proceed. In patients with structural heart disease, a functional assessment of the suspected structural disturbance (i.e., hemodynamic, angiographic, imaging as appropriate) and evaluation for susceptibility to symptomatic arrhythmias by monitoring or conventional electrophysiologic testing is appropriate. Autonomic function testing should follow if the diagnosis remains unclear. In only a few instances should specialized neurologic studies be undertaken as an initial step. The ultimate objective is always to obtain a sufficiently strong correlation between syncopal symptoms and detected abnormalities to feel confident in the diagnosis, permit an accurate assessment of prognosis, and develop an appropriate treatment plan.

In an effort to reduce energy requirements for atrial defibrillation to a level low enough to perform painless electrical cardioversion with an implantable atrial defibrillator, we tested the hypothesis that drug therapy with the class III agent d-sotalol, when used concurrently with a low-energy shock, reduces atrial defibrillation threshold. In a nonthoracotomy canine model of atrial fibrillation, intracardiac shocks were delivered between the distal coronary sinus and the mid-right atrium. Based on a step-up energy delivery protocol the atrial defibrillation threshold was defined as the least amount of energy that resulted in a >10% and

Objective: This study was designed to assess whether median frequency of ventricular fibrillation (VF) correlates with myocardial blood flow and defibrillation success during cardiopulmonary resuscitation (CPR) after epinephrine or vasopressin administration. Methods and results: After 4 min of VF and 3 min of CPR, 14 pigs received 0.045 mg/kg epinephrine or 0.4 U/kg vasopressin. Using radio-labeled microspheres, median myocardial blood flow during CPR before, and 90 s and 5 min after drug administration (DA) was 15.5 (12.6, 23.1; 25th percentile, 75th percentile), 26.4 (18.5, 29.1), 16.9 (14.9, 19.1) ml min−1 100 g−1, respectively, in the epinephrine, and 16.9 (15.4, 18.9), 48.1 (36.9, 68.9) (P < 0.05 vs. before DA), 52.3 (38.5, 65.0) ml min−1 100 g−1,respectively, in the vasopressin group. Using spectral analysis of VF, median frequency of VF was 11.0(10.7, 11.8), 11.3(9.6, 13.1), 10.2, (8.8, 11.4) Hz, respectively, in the epinephrine, and 10.1 (10.0, 10.5), 11.7 (11.1, 14.2) (P < 0.05 vs. before DA), 13.2 (11.5, 13.9) Hz, respectively, in the vasopressin group at the same points in time. Median frequency correlates significantly with myocardial blood flow in the epinephrine (n = 21; rs = 0.772; P < 0.001) and in the vasopressin group (n = 21; rs = 0.905; P < 0.001). Median fibrillation frequency before the first defibrillation was 13.0 (12.2, 13.2) Hz in resuscitated (n = 8) and 9.2 (8.3, 10.2) Hz (n = 6) in non-resuscitated animals (P < 0.01). Conclusions: We conclude that median frequency of VF reflects myocardial blood flow and the chance of successful defibrillation during closed-chest CPR after vasopressor treatment in a porcine model of VF.

This study compared alterations in arterial catecholamine concentrations associated with tilt-induced vasovagal syncope that differed in older (>65 years) and younger patients (

A retrospective review of patients evaluated at a university-based referral hospital was performed to assess the basis for syncope associated with exercise in young patients. Over an 8-year period, 54 consecutive young patients (aged 12 to 30 years) were referred for evaluation of frank syncope. Twelve patients had syncope associated with exercise (group I) and 42 patients had syncope not associated with exercise (group II). Patients underwent physical examination, chest x-ray, 2-dimensional echocardiography, and in selected cases, cardiac catheterization. Head-up tilt-table testing was performed in 11 of 12 group I patients. Ten group I patients had no evidence of structural heart disease: 9 of these 10 (90%) developed syncope with tilt-table testing. Head-up tilt-table testing was performed in 41 of 42 group II patients: 34 (83%) developed syncope with tilt-table testing. Standard cardiac electrophysiologic study was performed in 9 of 12 group I and in 30 of 42 group II patients, and identified a basis for syncope in only 2 group I and 1 group II patients. Among 9 group I patients with a positive result on head-up tilt-table testing and no evidence of structural heart disease (mean follow-up 4.3 years), 7 are without further episodes of syncope; 3 have discontinued medication and 5 have resumed at least limited exercise. In conclusion, susceptibility to tilt-induced syncope was the most frequent finding in young patients without structural heart disease referred for evaluation of exercise-associated syncope. Tilt-table testing may be an important diagnostic tool for the evaluation of these patients.

Within the last several years a new method of CPR, termed active compression-decompression (ACD) CPR was developed. Based upon the theory that active rather than passive chest wall decompression would augment venous return and ventilation by causing an increase in negative intrathoracic pressure during the decompression phase of CPR, a hand-held device was designed and is now being used clinically. Studies in dogs and pigs in ventricular fibrillation have demonstrated a significant improvement in systolic blood pressure, coronary perfusion pressure and total brain and myocardial blood flow with ACD CPR compared with standard CPR. Animal and human studies suggest that the mechanism of ACD CPR is complex, with coronary perfusion occurring during both the compression and decompression phases. Clinical studies comparing ACD to standard CPR in patients in cardiac arrest demonstrate that immediate resuscitation rates are nearly doubled when ACD CPR is started within 10 min after cardiac arrest. The potential long term benefits of ACD CPR remain under investigation.

Prevention of recurrent atrial fibrillation and flutter remains a difficult clinical problem. Consequently, development of an easily implantable automatic atrial cardioverter defibrillator is appealing. In this context we have examined the feasibility of intracavitary low-energy shocks delivered via transvenously positioned electrodes for termination of induced atrial tachyarrhythmias in canine models. This study extends these observations with use of single-pathway (5 msec pulse duration) and dual-pathway sequential (55msec, 0.2 msec separation) shocks of varying leading edge voltages (100 to 400 V) in a closed-chest canine talc-pericarditis model. Bipolar 9.5 French electrode catheters (electrode surface areas, 0.62 cm 2 ) were positioned at the superior vena cava-right atrium (SVC-RA) junction (labeled SVC) and right ventricular (RV) apex, with a subcutaneous plate over the chest wall. For single-pathway shocks, overall treatment effectiveness was comparable among the three vectors tested (RV apex to SVC, 35%; RV apex to subcutaneous plate, 17%; and SVC to subcutaneous plate, 35%). Furthermore, there was no evident relationship between leading edge voltage and shock effectiveness. In conrast, although each of the dual-pathway shock vector combinations tested also showed similar overall effectiveness, there was an apparent dose-response effect as leading edge voltage increased. The SVC (common) to RV apex (pulse 1) and subcutaneous plate (pulse 2) achieved 60% effectiveness at 400 V (approximately 4 joules). Thus this study provides additional evidence favoring feasibility of low-energy transvenous atrial cardioversion defibrillation. However, further refinement of energy delivery is essential for the implantable automatic atrial cardioverter defibrillator concept to become clinically accepted.

An enzymatic assay for adenosine 3':5'-monophosphate (cAMP) is described. Current measurement techniques can be expensive, time-consuming, and lack versatility. The critical step of this new method is the enzymatic destruction of endogenous purinergic noncyclic nucleotides. The diester linkage of cAMP is then cleaved and AMP is phosphorylated to ATP. Newly formed ATP is amplified using ATP-ADP cycling reactions and NADPH is measured fluorometrically. cAMP was measured in neonatal rat ventricular myocytes cultured on standard 100-mm dishes and treated with 2 microM 3-isobutyl-1-methylxanthine +/- 1 microM isoproterenol. When the enzymatic fluorometric assay was compared with an immunocolorimetric assay and a radioimmunoassay, cAMP content (pmol/plate mean +/- SE) was 124.3 +/- 6.7, 130.6 +/- 3.9, and 144.0 +/- 4.4 without isoproterenol and 656.4 +/- 23.5, 659.5 +/- 54.1, and 677.1 +/- 48.9 with isoproterenol, respectively. The standard curve with the enzymatic fluorometric assay is linear, in contrast to the curves of the nonlinear immunocolorimetric assay and radioimmunoassay. The enzymatic fluorometric assay can be used to detect < 20 fmol of cAMP/sample and can be adapted to measure < 1 fmol/sample. It can also be used to measure the activities of adenylate cyclase and phosphodiesterase. In summary, this enzymatic cAMP assay is sensitive, safe, versatile, and inexpensive and has multiple potential applications.

Vasovagal syncope after head-up tilting is thought to be secondary to a complex, neurally-mediated reflex with both vasodepressor and cardioinhibitory efferent components. The efficacy of edrophonium, an acetylcholinesterase inhibitor, as a provocative agent for triggering syncope during head-up tilt testing was evaluated. Forty-five consecutive patients (22 female and 23 male) with history of recurrent unexplained syncope received edrophonium (10 mg intravenous) after 30 minutes of 60 degrees head-up tilting alone. Twenty normal control subjects (9 female and 11 male) were tested with head-up tilt testing and edrophonium. Syncope was induced in 19 of 45 patients with the diagnosis of unexplained syncope. In 9 patients who developed syncope with head-up tilting alone, the predominant hemodynamic finding was marked vasodepression. In contrast, in 10 patients who developed syncope only after head-up tilting and edrophonium, the predominant hemodynamic findings were marked vasodepression and bradycardia. Syncope was induced in 1 of 20 normal subjects after head-up tilting and edrophonium. There was no long-term complication from using edrophonium. It is concluded that head-up tilt testing with edrophonium: (1) significantly increases the identification of patients with vasovagal syncope, (2) may be particularly useful when provocation with isoproterenol is undesirable, and (3) may be an effective method to help differentiate patients with a significant reflex cardioinhibitory component from those with a predominantly reflex vasodepressor component.

Patients with accessory pathway-mediated supraventricular tachycardia have typically been treated with drugs or surgery. Although catheter ablation using high voltage direct current shocks has been used to treat patients with drug-refractory supraventricular tachycardia, there are associated disadvantages, including damage due to barotrauma as well as the need for general anesthesia. Recently, transcatheter radiofrequency energy has evolved as an alternative to direct current shock or surgery to ablate accessory pathways.Percutaneous catheter ablation of 109 accessory pathways with use of radiofrequency energy was attempted in 100 consecutive patients. Patient age ranged from 3 to 67 years. The patients had been treated for recurrent tachycardia with a mean of 2.7 ± 0.2 antiarrhythmic agents that either proved ineffective or caused unacceptable side effects. In seven patients previous attempts at accessory pathway ablation with use of direct current shock had been unsuccessful. Forty-five (41%) of the pathways were left free wall, 43 (40%) were septal and 21 (19%) were right free wall.Eighty-nine (89%) of the 100 patients had successful radiofrequency ablation at the time of hospital discharge. In all but 12 patients the ablation was accomplished in a single session. Complications attributable to the procedure, but not to the ablation itself, occurred in four patients (4%). No patient developed atrioventricular block or other cardiac arrhythmias. Over a mean follow-up period of 10 months, nine patients had some return of accessory pathway conduction; a repeat ablation procedure was successful in all five patients in whom it was attempted.It is concluded that a catheter ablation procedure using radiofrequency energy can be performed on accessory pathways in all locations. The procedure is effective and safer, less costly and more convenient than cardiac surgery and can be considered as an alternative to lifelong medical therapy in any patient with symptomatic accessory pathway-mediated tachycardia.

Seven of 120 consecutive patients with inducible sustained ventricular tachycardia (from September 1, 1988 to January 1, 1991) had bundle branch reentrant tachycardia and underwent percutaneous radiofrequency ablation of the right bundle branch. The seven patients had been unsuccessfully treated with a mean of 3 ± 1 drugs. Four patients presented with syncope and three with aborted sudden death. The baseline electrocardiogram revealed a left bundle branch block pattern in three patients and an intraventricular conduction defect in four.The baseline HV interval was prolonged in each case (79 ± 2 ms). With use of programmed ventricular extrastimuli, sustained bundle branch reentrant tachycardia was inducible in all patients at a mean cycle length of 283 ± 17 ms (range 230 to 350). Bundle branch reentrant tachycardia characteristics included atrioventricular dissociation, a His deflection that preceded each QRS complex and spontaneous His to His variation that preceded changes in ventricular tachycardia cycle length.A quadripolar catheter was positioned across the tricuspid valve with the distal electrode tip of the catheter near the right bundle branch. One to three applications of continuous unmodulated radiofrequency current at 300 kHz between the distal electrode and a large posterior skin patch resulted in complete right bundle branch block in all patients, after which none had inducible bundle branch reentrant tachycardia on restudy. On restudy, three of the seven patients had ventricular tachycardia of myocardial origin (not bundle branch reentry). One patient required no therapy; drug or defibrillator therapy was used in the others. After a mean follow-up interval of 12 ± 3 months (range 6 to 29) complete right bundle branch block persisted, there were no spontaneous episodes of ventricular tachycardia and no patient required a permanent pacemaker.Radiofrequency catheter ablation of the right bundle branch is easily performed and is a safe and effective treatment for bundle branch reentrant tachycardia. It is probably the procedure of choice for these highly symptomatic patients.

Introduction La recuperation cerebrale etait consideree comme impossible apres 12 min d’ischemie globale jusqu’a recemment. Le Poloxamer 188 (P188) est un tensioactif synthetique connue pour minimiser les lesions de reperfusion. Il a ete montre que le postconditionnement ischemique (PCI) et le sevoflurane (SEV) reduisent les lesions de reperfusion secondaires a un arret cardiaque. Nous emettons l’hypothese qu’une therapie multiple (M-RCP) avec la combinaison de P188, PCI et SEV au debut de la reanimation cardiorespiratoire (RCP) ameliore l’hemodynamique durant la RCP, reduit la dysfonction ventriculaire post-reanimation, ameliore la survie sans sequelle neurologique a 24 h et reduit les dommages des organes vitaux apres un arret cardiaque prolonge dans un modele porcin. Materiel et methodes Apres une fibrillation ventriculaire (FV) de 15 min, une RCP standard a ete realisee chez les animaux temoins (n = 8) et comparee aux animaux du groupe M-RCP (n-13) qui ont subi une VF non traitee 17 min. La M-RCP etait constituee : a) P188 : bolus IV (250 mg/kg) au debut de la RCP suivie d’une perfusion de 250 mg/kg de P188 en 4 h apres le retour a une circulation spontanee (RACS), b) PCI : reanimation cardiopulmonaire avec compression decompression active, valve d’impedance inspiratoire pendant 20 s, puis 20 s de pause pendant 3 cycles et c) SEV : insufflation de SEV 2 % pendant les 3 premieres min. L’adrenaline (0,5 mg) a ete utilisee chez tous les animaux. La survie et le score de categorie de performance cerebrale (CPC) ont ete evalues a 24 h. La Troponine, CK-MB, creatinine et fonction hepatique ont ete evaluees a 4 h. Un test exact de Fischer et un test t non apparie ont ete utilises pour l’analyse statistique. Resultats L’hemodynamique est ameliore durant la M-RCP ( Fig. 1 ) durant la RCP. Tous les animaux atteints ont eu un RACS. La FEVG etait ameliore (63 ± 13 a 1 h, 61 ± 8 a 4 h) vs temoins (38 ± 12 a 1 h, 36 ± 18 a 4 h) (p Fig. 1 ). Discussion Une therapie multiple qui cible les lesions de reperfusion au niveau des membranes mitochondriale et cellulaire ameliore les parametres hemodynamiques au cours de RCP et facilite la reanimation cerebrale, cardiaque et des organes vitaux apres un arret cardiaque non traitee prolongee.

transfer in swine Patrick Shanley1, MS; Erik Kulstad2, MD, MS; Melissa Naiman3, PhD; D. Mark Courtney1, MD, MS; Anja Metzger4,6, PhD; Tim Matsuura4, PhD; Scott McKnite5, BS, Jennifer Rees6, PhD; Keith Lurie4,6, MD 1. Northwestern University; 2. Advocate Christ Medical Center; 3. U. of Illinois at Chicago; 4. U. of Minnesota; 5. Minneapolis Medical Research Foundation; 6. Advanced Circulatory Systems, Inc.

Although essential to cardiac conduction, little is known about the biochemistry underlying post-receptor adrenergic, cholinergic. and purinergic processes in the AV node. To study these mechanisms, we developed a highly sensitive fluorometric assay for cAMP and used it to characterize regional adenylyl cyclase activity (ACA) (pmollmin/mg of protein) in membrane preparations made from freeze-dried 20 micron thick micro-dissected pieces of canine (n = 6) right atrium (RA), AV nodal region (AVN), and left ventricle (LV). Adjacent sections were stained for acetylcholinesterase activity to identify the AVN. Basal and NaF-stimulated ACAs (mean ± SEM) were 7.2 ± 0.4 and 72.4 ± 7.5 in RA, 15.6 ± 1.3 and 58.8 ± 4.7 in AVN. and 6.4 ± 0.9 and 66.7 ± 5.0 in LV, respectively. Isoproterenol (10 –7 –10 –4 M) increased ACA in a dose-dependent fashion and the increment of cAMP production rate was similar in three different regions. Adenosine (10 –3 M) and carbachol (10 –5 M) inhibited isoproterenol (10 –6 M)-stimulated ACA as follows: Download high-res image (64KB) Download full-size image Results of this study demonstrate for the first time that (l) there are significant regional differences in ACA under basal conditions and after adrenergic, purinergic, and cholinergic stimulation in the heart. and (2) adenosine inhibits ACA in the RA, AVN and LV, whereas the inhibitory effects of cholinergic stimulation are more specific for the AVN.

B on extensive experience with implantable cardioverter-defibrillators and automatic external defibrillators, the utility of biphasic transthoracic shock has been demonstrated in the setting of lifethreatening ventricular tachyarrhythmias. These observations have led to the application of biphasic waveforms during elective transthoracic cardioversion for atrial fibrillation (AF). The present report compares cardioversion outcomes in 2 sequential groups of patients with AF undergoing transthoracic cardioversion. It was undertaken in an attempt to ascertain the extent to which biphasic waveform technique enhances transthoracic AF cardioversion success rates. • • • Records of 145 patients were reviewed. The patients were referred to our center for elective transthoracic cardioversion between January 1999 and September 2001, and had undergone this procedure in the electrophysiologic laboratory. Patients with atrial flutter (20 patients, 14%) were also included because of the similarity of the arrhythmia and the treatment required. Demographic and clinical data—including arrhythmia type and duration, underlying disease, and concomitant medications—were documented, along with echocardiographic data including left atrial diameter and left ventricular ejection fraction. Procedural data—including the number of cardioversion attempts made, energy levels used, and anesthetic employed— were documented. Similarly, complications were recorded, particularly skin irritation. A successful cardioversion procedure was defined as restoration of sinus rhythm for 1 cycle after energy application. Recurrence of the arrhythmia 2 hours after a successful cardioversion (i.e., before the patient left the observation unit) was deemed an “early recurrence.” The statistical significance of the efficacy of biphasic waveform cardioversion compared with monophasic waveform shock cardioversion was evaluated using chi-square and Fisher’s exact tests. A p value of 0.05 was considered statistically significant. Data were obtained in 145 sequential patients who underwent elective electrical cardioversion for AF or atrial flutter. Eighty-two patients (mean age 67 15 years) received biphasic waveform cardioversion, and the remaining 63 patients (mean age 66 14 years) underwent cardioversion with a monophasic waveform device. The ratio of men to women was 1.8:1 and 2:1 for the biphasic and monophasic waveform cardioversion study groups, respectively. The presenting arrhythmia was AF in 70 patients (85%) in the biphasic group and in 55 patients (87%) in the monophasic group. Atrial flutter was present in 12 patients (15%) in the biphasic group and in 8 patients (13%) in the monophasic group. The mean duration of patients’ treatment for the arrhythmia event was 36 56 and 60 106 days (p NS) for the biphasic and monophasic groups, respectively. Baseline clinical characteristics for patients in each treatment group are listed in Table 1. Underlying disease processes (i.e., cardiomyopathy, coronary artery disease, valvular heart disease, lung disease, and other structural heart disease) were found to be similarly prevalent in both treatment groups. Patients in the monophasic waveform group tended to use more digoxin, amiodarone, and other antiarrhythmic medications compared with biphasic group patients. The frequencies of usage of blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors were similar in both groups. The mean left atrial diameter was 46 10 mm in the biphasic group and 45 12 mm in the monophasic waveform group. Mean left ventricular ejection fraction was similar for the biphasic and monophasic groups (49 13% and 49 15%, respectively). Procedure success rate was 99% (81 patients) in the biphasic waveform cardioversion group compared with 81% (51 patients) in the group treated with monophasic waveform (p 0.001). The mean energy required for procedural success was 126 46 J and 228 83 J for the biphasic and monophasic waveform groups, respectively (p 0.001). The mean number of attempts before achieving procedural success was 1.3 0.8 for the biphasic cardioversion group and 1.2 0.4 for the monophasic cardioversion group. The treated arrhythmia recurred in 10 biphasic group patients (12%) and in 6 monophasic group patients (12%). All recurrences were in patients with AF. Skin irritation was not observed in any of the patients who received biphasic waveform shock, whereas 2 patients (3%) who received monophasic waveform shock required topical treatment for irritation at patch sites. • • • From the Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine, Minneapolis, Minnesota. Dr. Ermis is supported in part by a grant from the Midwest Arrhythmia Research Foundation, Minneapolis, Minnesota. Dr. Benditt’s address is: Cardiac Arrhythmia Center, MMC 508, 420 Delaware Street, Minneapolis, Minnesota 55455. Manuscript received April 9, 2002; revised manuscript received and accepted June 7, 2002.

In all, 18 consecutive patients with atdoventricuiar nodal reentry tachycardia (AVNRT) underwent right ventricular (RV) stimulation duling AVNRT from either the RV apex or summit. Stimulation from the RV apex advanced the tachycardia with the same atrial sequence in 8 of 18 patients (33%), hut never concl@vely excluded the m ence of a low atrial tachycardia. RV summit stimulation resulted in direct stimulation of the low septal rim atrium in 8 patients. RV summit stim ulaticn advanced the tachycardia in 4 patients, de layed it in 2 and terminated R in 3 without an atrial electrogram. The latter 2 fmdings exclude the presence of a low atrial tachycardia. Thus, in ps tients with AVNRT, application of extrastimuli closer to the putative reentrant site enables greater efficacy in tachycardia resetting and in excluding a low septal atrial tachycardia. (AmJCardiol1993,72:1299-1273) trioventricular nodal reentrant tachycatdia (AVNRT) A is 1 of the most common causes of supraventricular tachycardia.’ AVNRT remains a diagnosis of exclusion, and the differentiation of AVNRT from other forms of tachycardia, particularly low atrial tachycardia, can be difficult. The effect of programmed ventricular premature depolarizations during tachycardia has been shown to be critical in helping to establish diagnosis.2 Ventricular premature depolarizations inserted during AVERT, which either terminate the tachycardia without retrograde atrial activation or result in delay of the succeeding atrial impulse, exclude the diagnosis of atria1 tachycardia. Furthermore, a ventricular premature depolarization that advances the tachycardia without change in the atrial activation sequence strongly suggests AVNRT However, because of the short excitable gap and refractoriness of intervening tissue, ventricular premature depolarizations inserted from the right ventricular apex frequently do not enter the tachycardia circuit in patients with AVNRT. We hypothesized that activation closer to the putative reentrant circuit by stimulation near the His bundle would facilitate access into the circuit. Therefore in this study, we compared stimulation of the right ventricular (RV) apex with that of the RV summit in patients with AVNRT.