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Current of injury

Fig. 1.9 Atrial and ventricular electrograms (EGM) as obtained through a Medtronic Pacing System Analyser Model 5311. Ventricular. Above A typical rS configuration with a minor current of injury pattern. Below The current of injury pattern is more pronounced. Atrial Above A typical rS pattern. Below Approximately 150ms after the atrial electrogram lies a large far-field ventricular electrogram. Fig. 1.9 Atrial and ventricular electrograms (EGM) as obtained through a Medtronic Pacing System Analyser Model 5311. Ventricular. Above A typical rS configuration with a minor current of injury pattern. Below The current of injury pattern is more pronounced. Atrial Above A typical rS pattern. Below Approximately 150ms after the atrial electrogram lies a large far-field ventricular electrogram.
In addition to statistical probability, several ECG criteria help identify the RCA or the LCX as the artery containing the culprit lesion (Tables 1, 2). Each of these criteria is based on one of two anatomic facts. First, the myocardial distribution of the RCA is slightly rightward in the frontal plane, and consequently the current of injury resulting from its occlusion will be reflected more in lead III than lead II. Conversely the distribution of the LCX is slightly leftward in the frontal plane, and the current of injury from its closure will be seen more in lead II than lead III. Similarly the current of injury with RCA occlusion is more or less perpendicular to the axis of lead aVR, whereas the current of injury resulting from occlusion of the LCX has a mean... [Pg.4]

Fig. 9. Chicago Heart Association Detection Project in Industry one-hour post-load plasma glucose and rate of ECG myocardial infarction, ischemia, or current of injury patterns, whites by age-sex, exclusive of those on antihypertensive medication (29). Fig. 9. Chicago Heart Association Detection Project in Industry one-hour post-load plasma glucose and rate of ECG myocardial infarction, ischemia, or current of injury patterns, whites by age-sex, exclusive of those on antihypertensive medication (29).
Fig. 11. Chicago Heart Association Detection Project in Industry plasma glucose, other risk w factors and myocardial infarction, ischemia, digitalis effect, current of injury white females, > age 45-64 (29). Ri... Fig. 11. Chicago Heart Association Detection Project in Industry plasma glucose, other risk w factors and myocardial infarction, ischemia, digitalis effect, current of injury white females, > age 45-64 (29). Ri...
Despite intensive research on the neurobiological mechanisms of chronic pain, this therapeutic area remains one of the least satisfactorily covered by current drugs. There is considerable preclinical evidence that hyperalgesia and allody-nia following peripheral tissue or nerve injury is not only due to an increase in the sensitivity of primary afferent nociceptors at the site of injury but also depends on NMDA receptor-mediated central changes in synaptic excitabihty (Zieglgansberger and Tolle 1993 Sandkiihler and Liu 1998 Hide 2000 Parsons 2001 Fundytus 2001). [Pg.277]

Janse MJ, van Capelle FJL, Morsink H, Kleber AG, Wilms-Schopman F, Cardinal R, Naumann d Alnon-court C, Durrer D Flow of injury current and patterns of excitation during early ventricular arrhythmias in acute myocardial ischemia in isolated porcine and canine hearts. Circ Res 1980 47 151-165. [Pg.128]

Obtain Hospital Casualty/Fatality Report (HICS Form 259) from the Public Information Officer and Planning Section Chief and report to appropriate authorities the following minimum data Number of casualties received and types of injuries treated. Current patient capacity (census) Number of patients hospitalized, discharged home, or transferred to other facilitie Number dead. Individual casualty data name or ph reical description, sex, age, address, seriousness of injury or condition. ... [Pg.155]

Complement activation also contributes to ischemic injury. Current evidence indicates that ischemia leads to the expression of neoantigen or ischemia antigen on cellular surfaces, and this induces binding of circulating IgM natural antibody. This immune complex causes Cl binding, complement activation and the formation of C3a and C3b. C3b activates the remainder of the complement cascade leading to the formation of the membrane attack complex, which is the principal mediator of injury. Complement inhibition results in less myocardial ischemia and reperfusion injury, reviewed by Chan.38... [Pg.16]

The lack of full reversibility within 21 days of application is a critical parameter to identify substances inducing serious eye damage. If the majority of the models currently accepted from a regulatory point of view (see Section 3) may allow to predict such effects, they were not specifically designed and/or do not specifically address the reversibility/persistence of effects. This may be particularly of relevance depending upon the types of materials to be evaluated, and if in vivo irreversible effects are expected. As such, a number of in vitro test methods have been developed and optimized to distinguish persistent from reversible ocular effects. These include the use of histopathology and Depth of Injury of effects (Dol), the Porcine Corneal Ocular Reversibility Assay (PorCORA) and the Ex-Vivo Eye Irritation test (EVEIT). [Pg.185]


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