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Patricia A. Penkoske

Bio: Patricia A. Penkoske is an academic researcher from University of Alberta. The author has contributed to research in topics: Ventricular fibrillation & Defibrillation. The author has an hindex of 12, co-authored 26 publications receiving 1019 citations.

Papers
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Journal ArticleDOI
05 Mar 1998-Nature
TL;DR: High spatial and temporal resolution mapping of optical transmembrane potentials can easily detect transiently erupting rotors during the early phase of ventricular fibrillation, characterized by a relatively high spatiotemporal cross-correlation.
Abstract: Sudden cardiac death is the leading cause of death in the industrialized world, with the majority of such tragedies being due to ventricular fibrillation1. Ventricular fibrillation is a frenzied and irregular disturbance of the heart rhythm that quickly renders the heart incapable of sustaining life. Rotors, electrophysiological structures that emit rotating spiral waves, occur in several systems that all share with the heart the functional properties of excitability and refractoriness. These re-entrant waves, seen in numerical solutions of simplified models of cardiac tissue2, may occur during ventricular tachycardias3,4. It has been difficult to detect such forms of re-entry in fibrillating mammalian ventricles5,6,7,8. Here we show that, in isolated perfused dog hearts, high spatial and temporal resolution mapping of optical transmembrane potentials can easily detect transiently erupting rotors during the early phase of ventricular fibrillation. This activity is characterized by a relatively high spatiotemporal cross-correlation. During this early fibrillatory interval, frequent wavefront collisions and wavebreak generation9 are also dominant features. Interestingly, this spatiotemporal pattern undergoes an evolution to a less highly spatially correlated mechanism that lacks the epicardial manifestations of rotors despite continued myocardial perfusion.

448 citations

Journal ArticleDOI
TL;DR: The hypothesis that a critical mass of myocardium must be affected for successful defibrillation is supported and that unsuccessful defibrillillation is always accompanied by residual fibrillating activity in at least one site.
Abstract: The automatic implantable cardioverter-defibrillator has been shown to dramatically improve survival The future refinement of these devices requires a clear understanding of their mechanism of action We performed the following study to test two hypotheses: 1) When defibrillation is successful, fibrillating activity must be annihilated in a critical mass of both ventricles; and 2) when defibrillation is unsuccessful, at least one area of the ventricular mass has been left fibrillating Unipolar Ag/AgCl sintered electrodes were directly coupled from triangular arrays at 40 epicardial locations (total, 120 recording sites) that covered both right and left ventricular surfaces and were designed to measure the voltage gradient generated by the shock at each triangular array as well as the underlying myocardial electrical activity before and immediately after the shock An algorithm was developed and tested that reliably scored whether a postshock activation was a continuation of the immediately previous fibrillating activity This technique was applied to 203 defibrillation attempts in six open-chest dogs during electrically induced ventricular fibrillation There were 139 successful defibrillation attempts and 64 unsuccessful attempts Monophasic truncated exponential 10-msec defibrillation shocks (05-35 J) were delivered through an anodal patch on the right atrium and a cathodal patch on the left ventricular apex In all cases of unsuccessful defibrillation, at least one ventricular site could be clearly identified that failed to be defibrillated In cases of successful defibrillation two distinct patterns were observed: 1) complete annihilation of fibrillating activity at all sites or 2) nearly complete cessation of fibrillating activity with a single area of persistent fibrillation that subsequently self-extinguished within one to three activations This single site in the second form of successful defibrillation was located in the region of minimum voltage gradient produced by the defibrillating waveform and was occasionally accompanied by dynamic encapsulation with refractory tissue as a result of a wavefront emanating from a region that had undergone successful defibrillation These results support the hypothesis that a critical mass of myocardium must be affected for successful defibrillation and that unsuccessful defibrillation is always accompanied by residual fibrillating activity in at least one site The results also demonstrate that the size of the critical mass required for successful defibrillation can be less than 100%

166 citations

Journal ArticleDOI
TL;DR: Using a recently formulated technique for in vivo cardiac transmembrane current estimation and a newly formulated measure of nonlinear determinism, ventricular fibrillation in vivo exhibits deterministic dynamics similar to those previously used in chaos control.
Abstract: Using a recently formulated technique for in vivo cardiac transmembrane current estimation, we examined ventricular fibrillation for evidence of deterministic linear and nonlinear structure. Both unstable fixed point analysis and a newly formulated measure of nonlinear determinism indicated that ventricular fibrillation in vivo exhibits deterministic dynamics similar to those previously used in chaos control.

73 citations

Journal ArticleDOI
TL;DR: A remarkably simple in vivo technique that incorporates an electrode array with cellular dimensions to continuously estimate the extracellular counterparts of cardiac Ims, culminating in either severely depressed Na(+)- mediated or Ca(2+)-mediated activations.
Abstract: The ionic currents that cross the myocardial membrane during cardiac activation have a corresponding return path in the extracellular space. The transmembrane current (Im) during activation of cardiac cells in situ has previously been envisioned only in mathematical models. We have developed a remarkably simple in vivo technique that incorporates an electrode array with cellular dimensions to continuously estimate the extracellular counterparts of cardiac Ims. Mathematical modeling was performed for uniform plane wave propagation to clarify the biophysical basis and underlying assumptions inherent in this approach. Five-element electrode arrays incorporating 75-microns-diameter silver electrodes with center-to-center distances of 210 microns were experimentally verified to provide spatially sufficient samples for voltage gradient determinations of myocardial activation. Similar results were obtained with 25-microns-diameter electrodes at a center-to-center spacing of 65 microns. An estimate of Im was obtained from the derivative of the magnitude of the voltage gradient of the measured interstitial potentials. The inward component of Im generated by normal Na+ channel activation at 37 degrees C was measured in vivo to be less than 1 msec in duration, consistent with previously known voltage-clamp and simulation results. Intravenous KCl bolus injection was used to demonstrate the voltage-dependent depression of Na(+)-mediated Im in vivo, culminating in either severely depressed Na(+)-mediated or Ca(2+)-mediated activations. Normal Na(+)-, depressed Na(+)-, and possibly Ca(2+)-mediated currents can be recorded in vivo using this technique.

65 citations

Journal ArticleDOI
TL;DR: The hypothesis that the presence of a balanced inwardly and outwardly directed transmembrane charge, obtained from the ratio of the inward to outward area under the cardiac trans Membrane current curve, could reliably differentiate propagating from electrotonic deflections during VF was tested.
Abstract: Ventricular fibrillation (VF) is the principle cardiac rhythm disorder responsible for sudden cardiac death in humans. The accurate determination of local cardiac activation during VF is essential for its mechanistic elucidation. This has been hampered by the rapidly changing and markedly heterogeneous electrophysiological nature of VF. These difficulties are manifested when attempting to differentiate true propagating electrical activity from electrotonic signals and when identifying local activation from complex and possibly fractionated electrograms. The purpose of this investigation was to test the hypothesis that the presence of a balanced inwardly and outwardly directed transmembrane charge, obtained from the ratio of the inward to outward area under the cardiac transmembrane current curve (-/+ Im area), could reliably differentiate propagating from electrotonic deflections during VF. To test this hypothesis, we applied a recently described technique for the in vivo estimation of the transmembrane current (Im) during cardiac activation. A 17-element orthogonal epicardial electrode array was combined with an immediately adjacent optical fiber array to record electrical and optically coupled transmembrane potential signals during VF. Recordings were obtained during electrically induced VF in six dogs to determine the Im associated with activation and the time course of repolarization, as well as unipolar electrograms and bipolar electrograms recorded at multiple center-to-center interelectrode distances from 0.2 to 3 mm. Propagating local activations were associated with the presence of an easily identified inwardly directed Im, with a balanced inward and outward charge (-/+ Im area approximately 1.0). Electrotonic wave-forms lacked this inward Im (-/+ Im area approximately 0.0). Normal Na(+)-mediated inward currents were directly demonstrated to be responsible for some activations during VF.

43 citations


Cited by
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Journal ArticleDOI
TL;DR: The newly inaugurated Research Resource for Complex Physiologic Signals (RRSPS) as mentioned in this paper was created under the auspices of the National Center for Research Resources (NCR Resources).
Abstract: —The newly inaugurated Research Resource for Complex Physiologic Signals, which was created under the auspices of the National Center for Research Resources of the National Institutes of He...

11,407 citations

Journal ArticleDOI
TL;DR: The guidelines for the prevention of surgical wound infections (SSI) were published by the Centers for Disease Control and Prevention (CDC) in 1999 as discussed by the authors, with the goal of reducing infectious complications associated with these procedures.

4,730 citations

Journal ArticleDOI
TL;DR: The “Guideline for Prevention of Surgical Site Infection, 1999” presents the Centers for Disease Control and Prevention's recommendations for the prevention of surgical site infections (SSIs), formerly called surgical wound infections, and replaces previous guidelines.
Abstract: The “Guideline for Prevention of Surgical Site Infection, 1999” presents the Centers for Disease Control and Prevention (CDC)'s recommendations for the prevention of surgical site infections (SSIs), formerly called surgical wound infections. This two-part guideline updates and replaces previous guidelines.Part I, “Surgical Site Infection: An Overview,” describes the epidemiology, definitions, microbiology, pathogenesis, and surveillance of SSIs. Included is a detailed discussion of the pre-, intra-, and postoperative issues relevant to SSI genesis.

4,059 citations

Journal ArticleDOI
01 Feb 2012-Chest
TL;DR: The evidence supporting most recommendations for antithrombotic therapy in neonates and children remains weak and Studies addressing appropriate drug target ranges and monitoring requirements are urgently required in addition to site- and clinical situation-specific thrombosis management strategies.

1,174 citations

Journal ArticleDOI
TL;DR: The association between aprotinin and serious end-organ damage indicates that continued use is not prudent, and the less expensive generic medications aminocaproic acid and tranexamic acid are safe alternatives.
Abstract: Background The majority of patients undergoing surgical treatment for ST-elevation myocardial infarction receive antifibrinolytic therapy to limit blood loss. This approach appears counterintuitive to the accepted medical treatment of the same condition — namely, fibrinolysis to limit thrombosis. Despite this concern, no independent, large-scale safety assessment has been undertaken. Methods In this observational study involving 4374 patients undergoing revascularization, we prospectively assessed three agents (aprotinin [1295 patients], aminocaproic acid [883], and tranexamic acid [822]) as compared with no agent (1374 patients) with regard to serious outcomes by propensity and multivariable methods. (Although aprotinin is a serine protease inhibitor, here we use the term antifibrinolytic therapy to include all three agents.) Results In propensity-adjusted, multivariable logistic regression (C-index, 0.72), use of aprotinin was associated with a doubling in the risk of renal failure requiring dialysis am...

1,089 citations