Spatial-temporal filter effect in a computer model study of ventricular fibrillation.

Prediction of countershock success from ventricular fibrillation (VF) ECG is a major challenge in critical care medicine. Recent findings indicate that stable, high frequency mother rotors are one possible mechanism maintaining VF. A computer model study was performed to investigate how epicardiac sources are reflected in the ECG. In the cardiac tissues of two computer models - a model with cubic geometry and a simplified torso model with a left ventricle - a mother rotor was induced by increasing the potassium rectifier current. On the epicardium, the dominant frequency (DF) map revealed a constant DF of 23 Hz (cubic model) and 24.4 Hz (torso model) in the region of the mother rotor, respectively. A sharp drop of frequency (3-18 Hz in the cubic model and 12.4-18 Hz in the torso model) occurred in the surrounding epicardial tissue of chaotic fibrillatory conduction. While no organized pattern was observable on the body surface of the cubic model, the mother rotor frequency can be identified in the anterior surface of the torso model because of the chosen position of the mother rotor in the ventricle (shortest distance to the body surface). Nevertheless, the DFs were damped on the body surfaces of both models (4.6-8.5 Hz in the cubic model and 14.4-16.4 Hz in the torso model). Thus, it was shown in this computer model study that wave propagation transforms the spatial low pass filtering of the thorax into a temporal low pass. In contrast to the resistive-capacitive low pass filter formed by the tissue, this spatial-temporal low pass filter becomes effective at low frequencies (tens of Hertz). This effect damps the high frequency components arising from the heart and it hampers a direct observation of rapid, organized sources of VF in the ECGs, when in an emergency case an artifact-free recording is not possible.

Frequency distribution effects of anchored mother rotors--a computer model study.

Recent findings indicate that major organized centers (mother rotors) can maintain ventricular fibrillation (VF). In computer models the mother rotors can be induced by local shortening of the action potential duration (APD) in the cardiac tissue. Because of the fact that these rotors tend to drift away towards regions with longer APD, an additional heterogeneity (e.g. bundle) has to be included in the model for stabilizing the activation. Thus, the rotor anchors on this bundle and yields to interesting frequency distribution effects. In the dominant frequency (DF) map of a simplified computer model of the left ventricle it can be observed that the anchoring site of the rotor produces a slightly lower DF than in the surrounding cardiac tissue. That means that due to the load effect of the bundle the frequency is decreased. Furthermore the meandering of the mother rotor around this anchor site is reflected in the spectra of signals taken randomly in the organized region. These effects are both detected with two different independent spectral estimators with different resolutions.

Influence of negative expiratory pressure ventilation on hemodynamic variables during severe hemorrhagic shock.

OBJECTIVE: Outcome after trauma with severe hemorrhagic shock is still dismal. Since the majority of blood is present in the venous vessels, it might be beneficial to perform venous recruiting via the airway during severe hemorrhagic shock. Therefore, the purpose of our study was to evaluate the effects of negative expiratory pressure ventilation on mean arterial blood pressure, cardiac output, and short-term survival during severe hemorrhagic shock. DESIGN: Prospective study in 21 laboratory animals. SETTING: University hospital research laboratory. SUBJECTS: : Tyrolean domestic pigs. INTERVENTIONS: After induction of controlled hemorrhagic shock (blood loss approximately 45 mL/kg), 21 pigs were randomly ventilated with either zero end-expiratory pressure (0 PEEP; n = 7), 5 cm H2O positive end-expiratory pressure (5 PEEP; n = 7), or negative expiratory pressure ventilation (up to -30 cm H2O at the endotracheal tube during expiration; n = 7). MEASUREMENTS AND MAIN RESULTS: Mean (+/-sd) arterial blood pressure was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (38 +/- 5 vs. 27 +/- 3 mm Hg; p = .001) and the 5 PEEP animals (38 +/- 5 vs. 20 +/- 6 mm Hg; p < .001) after 5 mins of the experiment. Cardiac output was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (3.1 +/- .4 vs. 1.9 +/- .9 L/min; p = .001) and 5 PEEP animals (3.1 +/- .4 vs. 1.2 +/- .8 L/min; p < .001) after 5 mins of the experiment. All seven negative expiratory pressure ventilation animals, but only three of seven 0 PEEP animals (p = .022), survived the 120-min study period, whereas all seven of seven 5 PEEP animals were dead within 35 mins (p < .001). Limitations include that blood loss was controlled and that the small sample size limits the evaluation of survival outcome. CONCLUSIONS: When compared with pigs ventilated with either 0 PEEP or 5 PEEP, negative expiratory pressure ventilation during severe hemorrhagic shock improved mean arterial blood pressure and cardiac output.