Ventricular Fibrillation Waveform Research Articles

Monitoring the quality of cardiopulmonary resuscitation

Numerous recent reports have described limitations in the quality of cardiopulmonary resuscitation. Thus, there has been increasing interest in the techniques available to monitor quality. This review focuses on the major publications since the review published by the International Liaison Committee on Resuscitation in 2005. Some key articles published prior to this time period have also been included. A number of devices can monitor various components of the quality of cardiopulmonary resuscitation. End-tidal CO2 measurement assists in confirming placement of endotracheal tubes, correlates with cardiac output and detects the return of spontaneous circulation. Turbine flow-meters monitor respiratory rate and tidal volume. Transthoracic impedance monitoring measures respiratory rate, and may assist in confirmation of endotracheal tube placement. A new mechanical device (CPREzy) and a new defibrillator/monitor allow estimation of depth (and rate) of compressions. Ventricular-fibrillation waveform analysis may facilitate better timing of defibrillation. Echocardiography detects conditions that may impair the quality of cardiopulmonary resuscitation. Many options are available to monitor the quality of cardiopulmonary resuscitation. Some have significant limitations, and others are only readily available in hospital. The use of the information from this more intensive monitoring promises to improve outcomes of cardiopulmonary resuscitation.

Ventricular fibrillation frequency characteristics are altered in acute myocardial infarction

Future automated external defibrillators are being designed to direct rescue efforts (chest compressions first vs. defibrillation) by inferring the duration of ventricular fibrillation based on its waveform characteristics such as frequency content. This approach assumes that the ventricular fibrillation waveform is an appropriate surrogate for ventricular fibrillation duration and is not affected by structural heart disease. We hypothesized that an acute myocardial infarction may alter the frequency content of ventricular fibrillation. Animal intervention study with comparison to control group. University animal laboratory. Twenty-seven swine. Acute myocardial infarction was induced by occlusion of the mid-left anterior descending artery. Ventricular fibrillation was induced in swine with acute myocardial infarction and control swine. Ventricular fibrillation was induced in 11 swine with an acute myocardial infarction and in 16 control swine. Ventricular fibrillation waveforms were analyzed for mean, median, and dominant frequency, as well as bandwidth and amplitude. All frequency characteristics were significantly (p < .001) altered in swine with acute myocardial infarction compared with controls. Specifically, these characteristics were significantly depressed and varied little over time in swine with acute myocardial infarction compared with controls. These data establish that ventricular fibrillation during an acute myocardial infarction has an altered frequency content and time evolution compared with ventricular fibrillation without coronary obstruction. Frequency characteristics such as mean, median, dominant, and bandwidth show little variation in time after an acute myocardial infarction and are not suitable surrogates for ventricular fibrillation duration. These findings have important implications for the development of "smart" automated external defibrillators designed to determine duration of ventricular fibrillation from the waveform characteristics.

Analysis of the ventricular fibrillation waveform in refibrillation

Frustrating outcomes are driving investigation of alternative resuscitation protocols. Previous analysis of the ventricular fibrillation (VF) waveform has focused on guiding whether to shock immediately or to delay for delivery of cardiopulmonary resuscitation in the case of presenting VF. The same issues emerge in the case of refibrillation. All cases of witnessed VF cardiac arrest in the Rochester, MN, area in a 9-yr period were analyzed. Rochester rescuers employed an early defibrillation protocol during the study period. A summary measure of the VF waveform before the shock delivered in 35 incidents of refibrillation was compared with the time elapsed from the initial shock, the intervening electrocardiographic rhythm, ambulance response time, and call-to-shock time for prediction of early return of spontaneous circulation and of neurologically intact survival. VF waveform analysis separated patients with good outcomes when treated with early defibrillation of refibrillation from those without good outcomes more clearly than other predictors. Analysis of VF waveform offers promise for real-time guidance of resuscitation efforts on the basis of individual patient characteristics, in refibrillation and in the initial shock. It has advantages over guidance based on individual or aggregate system response times.

Adenosine A 1 receptor antagonism hastens the decay in ventricular fibrillation waveform morphology during porcine cardiac arrest

Endogenous adenosine (ADO) is known to be cardioprotective during acute myocardial ischemia. Coronary sinus ADO concentration has recently been shown to increase nearly 13-fold over baseline levels after 5 min of untreated ventricular fibrillation (VF). The role of ADO in VF has never been previously examined. The objective of this study was to determine the effect of ADO receptor antagonism, as measured by the scaling exponent (ScE), on the degeneration of VF over time during the circulatory phase of cardiac arrest. A well-established swine model of prolonged VF arrest was used for this experiment. Eighteen domestic mixed-breed swine were assigned by block randomization to receive either DTI-0017 (5mg/kg), a potent ADO A(1) receptor antagonist or placebo in a double-blind fashion. The animals were instrumented under general anesthesia and acclimatized. The assigned solution was infused over 5 min. One minute after the infusion was completed, VF was induced with a 3s, 60 Hz, 100 mA transthoracic shock and left untreated. Lead II ECG was monitored continuously and recorded at 1000 samples/s. It was determined a priori that evaluation of the plots would be limited to a previously observed plateau phase historically occurring between 5 and 8 min corresponding to the circulatory phase of cardiac arrest. The scaling exponent values over this period were calculated for each of the 18 recordings using custom MATLAB routines. Using the Wald statistic to produce the Chi square distributions the null hypothesis, that there was no difference between the two groups, was tested. The Wald statistic calculation based on eight epochs from 300 to 475 s in placebo and DTI groups was significant to reject the null hypothesis of no difference in the groupxtime interaction at the 0.015 level (Chi square distribution for Wald=17.49, d.f.=7). In this swine model, adenosine A(1) receptor antagonism accelerated the natural decay in the ECG VF waveform during the circulatory phase of cardiac arrest. Our findings would suggest that endogenous adenosine has cardioprotective effects during sudden cardiac arrest by slowing the time-dependent degeneration of VF.

Ventricular fibrillation waveform characteristics are different in ischemic heart failure compared with structurally normal hearts

For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration. Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency). All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001). VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

Part 3: Defibrillation

The 2005 Consensus Conference considered questions related to the sequence of shock delivery and the use and effectiveness of various waveforms and energies. These questions have been grouped into the following categories: (1) strategies before defibrillation, (2) use of automated external defibrillators (AEDs), (3) electrode-patient interface, (4) use of the electrocardiographic (ECG) waveform to alter management, (5) waveform and energy levels for the initial shock, (6) sequence after failure of the initial shock (ie, second and subsequent shocks), and (7) other related topics. The ECC Guidelines 2000 1 state that defibrillation should be attempted as soon as ventricular fibrillation (VF) is detected, regardless of the response interval (ie, time between collapse and arrival of the AED). If the response interval is >4 to 5 minutes, however, there is evidence that 1½ to 3 minutes of CPR before attempted defibrillation may improve the victim’s chance of survival. The data in support of out-of-hospital AED programs continues to accumulate, and there is some evidence supporting the use of AEDs in the hospital. Analysis of the VF waveform enables prediction of the likelihood of defibrillation success; with this information the rescuer can be instructed to give CPR or attempt defibrillation. This technology was developed by analysis of downloads from AEDs; it has yet to be applied prospectively to improve defibrillation success and is not available outside research programs. All new defibrillators deliver a shock with a biphasic waveform. There are several varieties of biphasic waveform, but the best variant and the optimal energy level and shock strategy (fixed versus escalating) have yet to be determined. Biphasic devices achieve higher first-shock success rates than monophasic defibrillators. This fact, combined with the knowledge that interruptions to chest compressions are harmful, suggests that a 1-shock strategy (1 shock followed immediately by CPR) may be preferable to …

Waveform analysis of ventricular fibrillation to predict defibrillation

Ventricular fibrillation occurs during many cases of cardiac arrest and is treated with rescue shocks. Coarse ventricular fibrillation occurs earlier after the onset of cardiac arrest and is more likely to be converted to an organized rhythm with pulses by rescue shocks. Less organized or fine ventricular fibrillation occurs later, has less power concentrated within narrow frequency bands and lower amplitude, and is less likely to be converted to an organized rhythm by rescue shocks. Quantitative analysis of the ventricular fibrillation waveform may distinguish coarse ventricular fibrillation from fine ventricular fibrillation, allowing more appropriate delivery of rescue shocks. A variety of studies in animals and humans indicate that there is underlying structure within the ventricular fibrillation waveform. Highly organized or coarse ventricular fibrillation is characterized by large power contributions from a few component frequencies and higher amplitude. Amplitude, decomposition into power spectra, or probability-based, nonlinear measures all can quantify the organization of human ventricular fibrillation waveforms. Clinical data have accumulated that these quantitative measures, or combinations of these measures, can predict the likelihood of rescue shock success, restoration of circulation, and survival to hospital discharge. Many quantitative ventricular fibrillation measures could be implemented in current generations of monitors/defibrillators to assist the timing of rescue shocks during clinical care. Emerging data suggest that a period of chest compressions or reperfusion can increase the likelihood of successful defibrillation. Therefore, waveform-based prediction of defibrillation success could reduce the delivery of failed rescue shocks.

Angular velocity: a new method to improve prediction of ventricular fibrillation duration.

Ventricular fibrillation (VF) is a leading cause of sudden death. Electrical defibrillation is the primary modality of treatment, but evidence is accumulating that its use in the late stage of VF prior to providing ventilation, chest compressions and the administration of appropriate medication is detrimental. In VF of <5 min duration a 'shock first' strategy is effective. In VF of 5> min duration a 'perfuse first' approach is more effective. Because of the difficulty in determining the duration of VF in the clinical setting we have sought to develop method which analyze 5 s intervals of VF waveform and quickly provide an estimate of duration. Such methods would be useful in directing clinical interventions. Using methods of nonlinear dynamics and fractal geometry we have previously derived a quantitative measure of VF duration, namely the scaling exponent (ScE). In this study we report on a novel method also based on nonlinear dynamics, the angular velocity (AV). By constructing a flat, circular disk-shaped structure in a three-dimensional phase space and measuring the velocity of rotation of the position vector over time, a statistic is developed which rises from 58 rad/s at 1 min to 79 rad/s at 4 min and then decreases in a linear manner to 32 rad/s at 12.5 min. Using ScE and AV probability density estimated, VF of <5 min duration can be identified with 90% sensitivity on the basis of a single 5 s recording of the waveform. The combination of ScE and AV can be used in developing strategies for the treatment of VF during the different clinical phases of VF.

Clinical review: Reappraising the concept of immediate defibrillatory attempts for out-of-hospital ventricular fibrillation

Despite well developed emergency medical services with rapid response advanced life support capabilities, survival rates following out-of-hospital ventricular fibrillation (VF) have remained bleak in many venues. Generally, these poor resuscitation rates are attributed to delays in the performance of basic cardiopulmonary resuscitation by bystanders or delays in defibrillation, but recent laboratory data suggest that the current standard of immediately providing a countershock as the first therapeutic intervention may be detrimental when VF is prolonged beyond several minutes. Several studies now suggest that when myocardial energy supplies begin to dwindle following more prolonged periods of VF, improvements in coronary artery perfusion must first be achieved in order to prime the heart for successful return of spontaneous circulation after defibrillation. Therefore, before countershocks, certain pharmacologic and/or mechanical interventions might take precedence during resuscitative efforts. This evolving concept has been substantiated recently by clinical studies, including a controlled clinical trial, demonstrating a significant improvement in survival when basic cardiopulmonary resuscitation is provided for several minutes before the initial countershock. Although this evolving concept differs from current standards and may pose a potential problem for automated defibrillator initiatives (e.g. public access defibrillation), successful defibrillation and return of spontaneous circulation have been rendered more predictable by evolving technologies that can score the VF waveform signal and differentiate between those who can be shocked immediately and those who should receive other interventions first.

Dynamic nature of electrocardiographic waveform predicts rescue shock outcome in porcine ventricular fibrillation

Study objective: Survival decreases with duration of ventricular fibrillation, and it is possible that failed rescue shocks increase myocardial damage. Structure in the ECG signal during ventricular fibrillation can be quantified by using the scaling exponent, a dimensionless measure that correlates with ventricular fibrillation duration. This study examined whether the scaling exponent could predict rescue shock success and whether unsuccessful rescue shocks altered the structure of the ventricular fibrillation waveform and the responsiveness to subsequent rescue shocks. Methods: Ventricular fibrillation was electrically induced in 44 anesthetized swine, which were randomly assigned to receive 70-J biphasic rescue shocks at 2, 4, 6, 8, or 10 minutes. If rescue shocks failed, up to 2 subsequent rescue shocks were performed at 2-minute intervals. The scaling exponent was calculated at 1-second intervals from ECG to quantify the organization of the ventricular fibrillation waveform. Results: A total of 92 rescue shocks were delivered, of which 23 successfully converted ventricular fibrillation to an organized rhythm (immediate success). After these 23 rescue shocks, 14 swine sustained organized rhythms for more than 30 seconds (sustained success). Lower scaling exponent values were associated with increased probability of successful rescue shocks. Receiver operating characteristic curves had an area under the curve of 0.86 for immediate rescue shock success and 0.93 for sustained rescue shock success. Failed rescue shocks increased the rate of scaling exponent increase over time but did not appear to affect subsequent rescue shock success when the scaling exponent was taken into account. Conclusion: Highly deterministic ventricular fibrillation, reflected by a low scaling exponent, predicted rescue shock success regardless of antecedent failed rescue shocks. In addition, unsuccessful rescue shocks might decrease post-rescue shock ventricular fibrillation waveform organization. [Ann Emerg Med. 2003;42:230-241.]

Optimal timing for electrical defibrillation after prolonged untreated ventricular fibrillation.

It currently is recommended that electrical shocks be delivered immediately on recognition of ventricular fibrillation. However, decreased effectiveness of this approach has been reported after prolonged intervals of untreated ventricular fibrillation. We investigated the optimal strategy for successful defibrillation after prolonged untreated ventricular fibrillation by using a rat model of ventricular fibrillation and closed-chest resuscitation. Controlled, randomized, laboratory study. Research laboratory at a VA hospital. Seventy pentobarbital anesthetized Sprague-Dawley rats. After 10 mins of untreated ventricular fibrillation, four groups of rats were randomized to receive electrical shocks (which we designated as "experimental shocks") immediately before or at 2, 4, or 6 mins of chest compression. Unsuccessfully defibrillated rats received additional shocks (which we designated as "rescue shocks") after 8 mins of chest compression. The number of rats that restored spontaneous circulation after the experimental shocks increased with increasing duration of the predefibrillatory interval of chest compression (0 of 8, 0 of 8, 2 of 8, and 7 of 8, respectively, p <.005). Two additional groups then were randomized to receive repetitive experimental shocks at 2, 4, and 6 mins or a single attempt at 6 mins of chest compression. Although a comparable number of rats restored spontaneous circulation in each group, rats subjected to repetitive defibrillation attempts had more intense postresuscitation ectopic activity and worse survival. Two final groups were used to investigate whether inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) could facilitate return of spontaneous circulation during repetitive defibrillation attempts. Although spontaneous circulation was restored earlier in more rats subjected to NHE-1 inhibition, the differences were statistically insignificant. NHE-1 inhibition, however, replicated previously reported resuscitation and postresuscitation benefits. The optimal predefibrillation interval of chest compression was approximately 6 mins, and this coincided with partial return of the amplitude and frequency characteristics of the ventricular fibrillation waveform to those present immediately after induction of ventricular fibrillation. Improved outcome after prolonged untreated ventricular fibrillation may result from strategies that provide chest compression before attempting defibrillation and avoid early and repetitive defibrillation attempts. The amplitude and frequency characteristics of the ventricular fibrillation waveform could help identify the optimal timing for attempting electrical defibrillation.

Monitoring during cardiac arrest: are we there yet?

Advancements in electronic data acquisition have translated into improved monitoring of victims of cardiac arrest, but initial techniques remain direct observation of pulses and respirations. The most essential monitor continues to be the electrocardiogram. However, monitoring diastolic blood pressure, myocardial perfusion pressure, and end-tidal carbon dioxide are extremely useful. Most of the current research on monitoring during cardiopulmonary resuscitation focuses on methods for analyzing ventricular fibrillation waveforms. By analyzing the waveform, defibrillation shocks may be delivered at the time when the chance of success is optimal. Low-amplitude and low-frequency fibrillation waveforms are associated with increased rates of asystole and pulseless electrical activity after defibrillation. Methods of analyzing the ventricular fibrillation waveform include measuring the amplitude and frequency and combining the contributions of amplitude and frequency by various methods to improve discrimination. Other types of monitoring being studied for their usefulness during cardiac arrests include sonography, Bispectral Index monitoring, tissue carbon dioxide monitors, and pupil observation. The test of these monitoring techniques is ultimately their ability to improve patient survival to hospital discharge, which is a major challenge for resuscitation researchers.

From Vivendi to Veolia environnement

In retrospective swine and human investigations of ventricular fibrillation (VF) cardiac arrest, the amplitude-spectral area (AMSA), determined from the VF waveform, can predict defibrillation and a return of spontaneous circulation (ROSC).We hypothesized that an algorithm using AMSA in real time to direct postshock chest compression (CC) duration would shorten the time to ROSC and improve neurological outcome in a swine model of VF cardiac arrest with acute myocardial infarction (AMI) or nonischemic myocardium.AMI was induced by occlusion of the left anterior descending artery. VF was untreated for 10 min. Animals were randomized to either traditional resuscitation with 2 min of CC after each shock or to an AMSA-guided algorithm where postshock CCs were shortened to 1 min if the preshock AMSA exceeded 20 mV-Hz.A total of 48 animals were studied, 12 in each group (AMI vs. normal, and traditional vs. AMSA-guided). There was a nonsignificant shorter time to ROSC with an AMSA-guided approach in AMI swine (17.2 ± 3.4 vs. 18.5 ± 4.7 min, p = NS), and in normal swine (13.5 ± 1.1 vs. 14.4 ± 1.2, p = NS). Neurological outcome was similar between traditional and AMSA-guided animals. AMSA predicted ROSC (p < 0.001), and a threshold of 20 mV-Hz gave a sensitivity of 89%, with specificity of 29%.Although AMSA predicts ROSC in a swine model of VF arrest in both AMI and normal swine, a waveform-guided approach that uses AMSA to direct postshock CC duration does not significantly shorten the time to ROSC or alter neurological outcome.

Transthoracic impedance does not decrease with rapidly repeated countershocks in a swine cardiac arrest model

Study purpose: Successful defibrillation is dependent upon the delivery of adequate electrical current to the myocardium. One of the major determinant of current flow is transthoracic impedance. Prior work has suggested that impedance falls with repeated shocks during sinus rhythm. The purpose of this study was to evaluate changes in transthoracic impedance with repeated defibrillation shocks in an animal model of cardiac arrest due to ventricular fibrillation (VF). Methods: VF was electrically induced in anesthetized swine. After 5 min of untreated VF, monophasic or biphasic waveform defibrillation was attempted using a standard sequence of ‘stacked shocks’ (200, 300, then 360 J, if necessary) administered via adhesive electrodes. If one of the first three shocks failed to convert VF, conventional CPR was initiated and defibrillation (360 J) attempted 1 min later. Strength–duration curves for delivered voltage and current were measured during each shock and transthoracic impedance calculated. Animals requiring a minimum of four shocks were selected for study inclusion. Impedance data from sequential shocks were analyzed using mixed linear models to account for the repeated-measures design and the variability of the initial impedance of individual animals. Results: Thirteen animals (monophasic waveform, n=7, biphasic waveform, n=6) required at least four shocks to terminate VF (range 4–6). Transthoracic impedance did not change from the first shock in the 13 animals (46±8 Ω) to the fourth shock (46±9 Ω). In animals receiving more than four shocks, transthoracic impedance likewise did not change significantly from the first to the last shock, which terminated VF. The lack of a significant change in impedance was also observed when animals were analyzed according to defibrillation waveform. Conclusion: Transthoracic impedance does not change significantly with repeated shocks in a VF cardiac arrest model. This is likely due to the lack of reactive skin and soft tissue hyperemia and edema observed in non-arrest models.

Precountershock cardiopulmonary resuscitation improves ventricular fibrillation median frequency and myocardial readiness for successful defibrillation from prolonged ventricular fibrillation: A randomized, controlled swine study

Study objective: After prolonged ventricular fibrillation (VF), precountershock cardiopulmonary resuscitation (CPR) will improve myocardial “readiness” for defibrillation compared with immediate defibrillation. Methods: After 10 minutes of untreated VF, 32 swine (27±1 kg) were randomly assigned to receive immediate countershocks (DEFIB), CPR for 3 minutes followed by countershocks (CPR), or CPR for 3 minutes plus intravenous epinephrine followed by countershocks (CPR+EPI). VF waveform was evaluated by fast Fourier transformation. Results: VF amplitude and median frequency by fast Fourier transformation decreased during the untreated VF interval in all groups, and the median frequency subsequently increased during each minute of precountershock CPR. Although the VF median frequency in the 3 groups did not differ after 10 minutes of untreated VF (8.9±0.8 Hz versus 8.4±0.5 Hz versus 7.3±0.5 Hz, respectively), immediately before the first shock the VF median frequency was much lower in the DEFIB group than in either the CPR or CPR+EPI groups (8.9±0.8 Hz versus 13.1±0.8 Hz versus 13.8±0.9 Hz, respectively; P <.01). None of the 10 animals in the DEFIB group attained return of spontaneous circulation after the first set of shocks versus 5 of 10 animals in the CPR group and 6 of 12 animals in the CPR+EPI group (DEFIB versus each CPR group; P <.05). Cardiac output 1 hour after resuscitation was substantially worse in the DEFIB group than in the CPR or CPR+EPI groups (74±7 mL/kg per minute versus 119±7 mL/kg per minute versus 104±15 mL/kg per minute; P <.05). Conclusion: Precountershock CPR can result in substantial physiologic benefits compared with immediate defibrillation in the setting of prolonged VF. Moreover, these benefits can be attained with or without the addition of intravenous epinephrine. [Ann Emerg Med. 2002;40:563-570.]

Scaling exponent predicts defibrillation success for out-of-hospital ventricular fibrillation cardiac arrest.

-Defibrillator shocks often fail to terminate ventricular fibrillation (VF) in out-of-hospital cardiac arrest (OOHCA), and repeated failed shocks can worsen the subsequent response to therapy. Because the VF waveform changes with increasing duration of VF, it is possible that ECG analyses could estimate the preshock likelihood of defibrillation success. This study examined whether an amplitude-independent measure of preshock VF waveform morphology predicts outcome after defibrillation. Methods and Results-Clinical data and ECG recordings from an automated external defibrillator were obtained for 75 subjects with OOHCA in a suburban community with police first responders and a paramedic-based emergency medical system. An estimate of the fractal self-similarity dimension, the scaling exponent, was calculated off-line for the VF waveform preceding shocks. Success of the first shock was determined from the recordings. Return of pulses and survival were determined by chart review. The first shock resulted in an organized rhythm in 43% of cases, and 17% of cases survived to hospital discharge. A lower mean value of the scaling exponent was observed for cases in which the first defibrillation resulted in an organized rhythm (P:=0.004), for cases with return of pulses (P:=0.049), and for cases surviving to hospital discharge (P:<0.001). Receiver operator curves revealed the utility of the scaling exponent for predicting the probability of restoring an organized rhythm (area under the curve=0.70) and of survival (area under the curve=0.84). -The VF waveform in OOHCA can be quantified with the scaling exponent, which predicts the probability of first-shock defibrillation and survival to hospital discharge.

P HYSICIAN I NTERPRETATION AND Q UANTITATIVE M EASURES OF E LECTROCARDIOGRAPHIC V ENTRICULAR F IBRILLATION W AVEFORM

Objectives. The characteristics of the ventricular fibrillation (VF) waveform may influence treatment decisions and the likelihood of therapeutic success. However, assessment of VF as being fine or coarse and the distinction between fine VF and asystole are largely subjective. The authors sought to determine the level of agreement among physicians for interpretation of varying VF waveforms, and to compare these subjective interpretations with quantitative measures. Methods. Six-second segments of waveform from LIFEPAK 300 units were collected. Fifty segments, including 45 VF and five ventricular tachycardia (VT) distracters, were graphed to simulate rhythm strips. These waveforms were quantitatively described using scaling exponent, root-mean-squared amplitude, and centroid frequency. Thirty-two emergency medicine residents were asked to interpret the arrhythmias as VT, “coarse” VF, “fine” VF, or asystole. Their responses were compared with the qantitative measures. Interphysician agreement was assessed with the kappa statistic. Results. One thousand four hundred forty interpretations were analyzed. There was fair agreement between physicians about the classification of arrhythmias (κ = 0.39). Mean values associated with coarse VF, fine VF, and asystole differed in all three quantitative measure categories. The decision whether to defibrillate was highly correlated with the distinction between VF and asystole (Pearson chi-square = 1,170.40, df = 1, p[two-sided] < 0.001). Conclusions. With only fair agreement on the threshold of fine VF and asystole, defibrillation decisions are largely subjective and caregiver-specific. These data suggest that quantitative measures of the VF waveform could augment the current standard of subjective classification of VF by emergency care providers.

Effects of repetitive electrical shocks on postresuscitation myocardial function.

Whereas myocardial cell injury can occur during electrical defibrillation proportional to the energy level of individual shocks, only minimal (or no) injury seems to develop when the energy is limited to the levels typically required to terminate ventricular fibrillation. During cardiac arrest, however, multiple shocks are often required to terminate ventricular fibrillation or to treat episodes that appear subsequently during the resuscitation effort or the postresuscitation interval. Concern exists because an inverse relationship has been reported between the number of electrical shocks delivered during cardiac resuscitation and both resuscitability and survival. Repetitive electrical shocks can alter diastolic function and prompt leftward shifts of the end-diastolic pressure-volume curves. Repetitive shocks may, therefore, contribute to the recently recognized phenomenon of postresuscitation myocardial dysfunction and hamper efforts to reestablish competent myocardial function after resuscitation. Thus, strategies aimed at limiting the number of electrical shocks during cardiopulmonary resuscitation are highly desirable. These may include real-time ventricular fibrillation waveform analysis to improve targeting of individual shocks and efforts (using mechanical and pharmacologic means) to render the myocardium more responsive to individual shocks and to promote greater electrical stability after successful defibrillation.

Ventricular fibrillation exhibits dynamical properties and self-similarity

Electrocardiographic recordings of ventricular fibrillation (VF) appear chaotic. Previous attempts to characterize the chaotic nature of VF have relied on peak-to-peak intervals [Witkowski et al., Phys. Rev. Lett. 1995;75(6):1230–3; Garfinkel et al., J. Clin. Investig. 1997;99(2):305–314; Hastings et al., Proc. Natl. Acad. Sci. USA 1996;93:10495–9], the frequency spectrum [Goldberger et al., 1986;19:282–289] or other derived measures [Kaplan and Cohen, Circ. Res. 1990;67:886–92], with results that demonstrate some characteristics of chaos. We have sought to determine whether VF is chaotic rather than random and whether the waveform can be described quantitatively using the tools of fractal geometry. We have constructed an attractor, measured the correlation dimensions, estimated the embedding dimension and measured Lyapunov exponents. When the digitized waveform is analyzed directly, VF exhibits nonrandom, chaotic behavior over a decade of sampling frequency. Within the scaling range we have estimated the Hurst exponent, and the self-similarity dimension of the VF waveform, supporting the presence of chaotic dynamics. Furthermore, these characteristics are measurable in a porcine model of VF under different recording conditions, and in VF recordings taken from human subjects immediately prior to defibrillation. Analyses of the Hurst exponents and self-similarity dimensions are correlated with the duration of VF, which may have clinical applications.

Scaling structure of electrocardiographic waveform during prolonged ventricular fibrillation in swine.

Ventricular fibrillation (VF) is the most common arrhythmia causing sudden cardiac death. However, the likelihood of successful defibrillation declines with increasing duration of VF. Because the morphology of the electrocardiogram (ECG) waveform during VF also changes with time, this study examined a new measure that describes the VF waveform and distinguishes between early and late VF. Surface ECG recordings were digitized at 200 samples/s from nine swine with induced VF. A new measure called the scaling exponent was calculated by examining the power-law relationship between the summation of amplitudes of a 1,024-point (5.12 second) waveform segment and the time scale of measurement. The scaling exponent is a local estimate of the fractal dimension of the ECG waveform. A consistent power-law relationship was observed for measurement time scales of 0.005-0.040 seconds. Calculation of the scaling exponent produced similar results between subjects, and distinguished early VF (< 4-minute duration) from late VF (> or = 4-minute duration). The scaling exponent was dependent on the order of the data, supporting the hypothesis that the surface ECG during VF is a deterministic rather than a random signal. The waveform of VF results from the interaction of multiple fronts of depolarization within the heart, and may be described using the tools of nonlinear dynamics. As a quantitative descriptor of waveform structure, the scaling exponent characterizes the time dependent organization of VF.