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David Benditt

Publications and source records attributed to David Benditt.

7 recordsLinked to original sources

Improving SVT discrimination in single-chamber ICDs: a new electrogram morphology-based algorithm.

INTRODUCTION: Wide-spread adoption of ICD therapy has focused efforts on improving the quality of life for patients by reducing "inappropriate" shock therapies. To this end, distinguishing supraventricular tachycardia from ventricular tachycardia remains a major challenge for ICDs. More sophisticated discrimination algorithms based on ventricular electrogram morphology have been made practicable by the increased computational ability of modern ICDs. METHODS AND RESULTS: We report results from a large prospective study (1,122 pts) of a new ventricular electrogram morphology tachycardia discrimination algorithm (Wavelet Dynamic Discrimination, Medtronic, Minneapolis, MN, USA) operating at minimal algorithm setting (RV coil-can electrogram, match threshold of 70%). This is a nonrandomized cohort study of ICD patients using the morphology discrimination of the Wavelet algorithm to distinguish SVT and VT/VF. The Wavelet criterion was required ON in all patients and all other supraventricular tachycardia discriminators were required to be OFF. Spontaneous episodes (N = 2,235) eligible for ICD therapy were adjudicated for detection algorithm performance. The generalized estimating equations method was used to remove bias introduced when an individual patient contributes multiple episodes. Inappropriate therapies for supraventricular tachycardia were reduced by 78% (90% CI: 72.8-82.9%) for episodes within the range of rates where Wavelet was programmed to discriminate. Sensitivity for sustained ventricular tachycardia was 98.6% (90% CI: 97-99.3%) without the use of high-rate time out. CONCLUSIONS: Results from this prospective study of the Wavelet electrogram morphology discrimination algorithm operating as the sole discriminator in the ON mode demonstrate that inappropriate therapy for supraventricular tachycardia in a single-chamber ICD can be dramatically reduced compared to rate detection alone.

Algorithms↗

Atrial fibrillation associated with hypokalemia due to primary hyperaldosteronism (Conn's syndrome).

Aldosterone is a major regulator of the body potassium stores through its role in potassium excretion by the kidney. However, it is unclear whether aldosterone affects transcellular distribution of potassium in atrial myocytes, and whether hypokalemia associated with primary hyperaldosteronism increases susceptibility to atrial fibrillation (AF). We report a case of a 58-year-old male with Conn's syndrome in whom symptomatic AF was related to hypokalemia.

Atrial Fibrillation↗

Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest.

INTRODUCTION: Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival. HYPOTHESIS: 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. METHODS: 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 was >0.90. RESULTS: 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. CONCLUSIONS: 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.

Animals↗

Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest.

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.

Animals↗

Combination drug therapy with vasopressin, adrenaline (epinephrine) and nitroglycerin improves vital organ blood flow in a porcine model of ventricular fibrillation.

There is increasing evidence that the combination of epinephrine (adrenaline) with vasopressin may be superior to either epinephrine or vasopressin alone for treatment of cardiac arrest. However, the optimal combination, and dosage of cardiovascular drugs to minimize side effects, and to improve outcome has yet to be found. We therefore evaluated whether the combination of vasopressin plus epinephrine plus nitroglycerin (EVN), would improve vital organ blood flow during cardiopulmonary resuscitation (CPR) when compared with epinephrine (EPI) alone. After 4 min of ventricular fibrillation (VF) and 4 min of standard CPR, pigs were randomized to the combination of epinephrine (45 microg/kg) plus vasopressin (0.4 U/kg) plus nitroglycerin (7.5 microg/kg; n=12), or epinephrine (40 microg/kg; n=12) alone. Cerebral and myocardial blood flow was measured with radiolabeled microspheres. Defibrillation was attempted after 19 min of VF including 15 min of CPR. Mean+/-SEM coronary perfusion pressures were significantly (P < 0.01) higher 5 min after EVN vs. EPI alone (34+/-3 vs. 24+/-3 mmHg, respectively). At the same time, mean+/-SEM left ventricular, and global cerebral blood flow was also significantly (P < 0.05) higher after EVN vs. EPI alone (0.78+/-0.11 vs. 0.48+/-0.08 ml/min/g; and 0.37+/-0.05 vs. 0.22+/-0.0 3 ml/min/g, respectively). Spontaneous circulation was restored in 11 of 12 animals in the EVN group vs. 6 of 12 swine after EPI alone (P = N.S.). In conclusion, the combination of EVN significantly improved vital organ blood flow during CPR compared with EPI alone. Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.

Animals↗

Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation.

OBJECTIVE: We recently demonstrated that vasopressin alone resulted in a poorer outcome in a pediatric porcine model of asphyxial cardiac arrest when compared with epinephrine alone or with epinephrine plus vasopressin in combination. Accordingly, this study was designed to differentiate whether the inferior effects of vasopressin in pediatrics were caused by the type of cardiac arrest. DESIGN: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: After 8 mins of ventricular fibrillation and 8 mins of cardiopulmonary resuscitation, either 0.4 units/kg vasopressin (n = 6), 45 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered. Six minutes after drug administration, a second respective bolus dose of 0.8 units/kg vasopressin, 200 microg/kg epinephrine, or a combination of 200 microg/kg epinephrine with 0.8 units/kg vasopressin was given. Defibrillation was attempted 20 mins after initiating cardiopulmonary resuscitation. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem left ventricular myocardial blood flow 2 mins after each respective drug administration was 65 +/- 4 and 70 +/- 13 mL x min(-1) x 100 g(-1) in the vasopressin group; 83 +/- 42 and 85 +/- 41 mL x min(-1) x 100 g(-1) in the epinephrine group; and 176 +/- 32 and 187 +/- 29 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p <.006 after both doses of epinephrine-vasopressin vs. vasopressin and after the first dose of epinephrine-vasopressin vs. epinephrine, respectively). At the same times, mean +/- sem total cerebral blood flow was 73 +/- 3 and 47 +/- 5 mL x min(-1) x 100 g(-1) after vasopressin; 18 +/- 2 and 12 +/- 2 mL x min(-1) x 100 g(-1) after epinephrine; and 79 +/- 21 and 41 +/- 8 mL x min(-1) x 100 g(-1) after epinephrine-vasopressin (p <.025 after both doses of vasopressin and epinephrine-vasopressin vs. epinephrine). Five of six vasopressin-treated, two of six epinephrine-treated, and six of six epinephrine-vasopressin treated animals had return of spontaneous circulation (nonsignificant). CONCLUSIONS: In this pediatric porcine model of ventricular fibrillation, the combination of epinephrine with vasopressin during cardiopulmonary resuscitation resulted in significantly higher levels of left ventricular myocardial blood flow than either vasopressin alone or epinephrine alone. Both vasopressin alone and the combination of epinephrine with vasopressin, but not epinephrine alone, improved total cerebral blood flow during cardiopulmonary resuscitation. In stark contrast to asphyxial cardiac arrest, vasopressin alone or in combination with epinephrine appears to be of benefit after ventricular fibrillation in the pediatric porcine model.

Animals↗