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Correlation among fibrillation, defibrillation, and cardiac pacing.

An electrical stimulus must create an electric field of approximately 1 V/cm in the extracellular space to stimulate myocardium during diastole. To initiate fibrillation by premature stimulation during the vulnerable period or to defibrillate, an extracellular electric field of approximately 6 V/cm is required, a value approximately six times greater than that necessary for diastolic pacing. Yet, the current strength of the pulse given to the stimulating electrode to initiate fibrillation or to defibrillate is much greater than six times the diastolic pacing threshold. The ventricular fibrillation threshold is typically 40 times greater than the diastolic pacing threshold expressed in terms of current. The defibrillation threshold in terms of current is typically thousands of times greater than the diastolic pacing threshold. The reason that these thresholds vary so much more in terms of stimulus current than in terms of extracellular potential gradient is that each of the three thresholds requires creation of the required potential gradient at different distances from the stimulating electrode. Pacing requires a potential gradient of approximately 1 V/cm only in a small liminal volume of tissue immediately adjacent to the electrode. Initiation of ventricular fibrillation by premature stimulation during the vulnerable period requires a potential gradient of approximately 6 V/cm about 1 cm away from the stimulating electrode to allow sufficient space for the central common pathway of a figure-eight reentrant circuit to form. Since the potential gradient falls off rapidly with distance from the stimulating electrode, a stimulating current about 40 times greater than the diastolic pacing threshold is required to generate an electric field of 6 V/cm approximately 1 cm away from the stimulating electrode. Defibrillation requires an electric field of approximately 6 V/cm throughout all or almost all of the ventricular myocardium. Since some portions of the ventricles can be more than 10 cm away from the defibrillation electrodes, a shock of several amps is required to create this field, a current thousands of times greater than the pacing threshold.

Animals↗

Effects of polarity for monophasic and biphasic shocks on defibrillation efficacy with an endocardial system.

Electrode polarity has been reported to be one of the factors that affect defibrillation efficacy. We studied the influence of polarity on defibrillation efficacy when monophasic and biphasic waveforms were used with an endocardial lead system. In six anesthetized pigs, defibrillation catheters were placed in the right ventricular (RV) apex and at the junction of the superior vena cava (SVC) and right atrium. Monophasic shocks were 6 ms in duration, while for biphasic shocks the first phase was 6 ms and the second was 4 ms in duration. Four electrode configurations were tested: R:S, M (the RV electrode, cathode; the SVC electrode, anode, with a monophasic shock); S:R: S, B(the RV electrode, first phase cathode; the SVC electrode, first phase anode, with a biphasic shock); S:R, B. Defibrillation probability of success curves were determined using an up/down protocol requiring 15 shocks for each configuration. For monophasic shocks, total delivered energy at the 50% probability of success point was significantly lower when the RV electrode was an anode than when it was a cathode (R: S, M: 24.4 +/- 7.4 J [mean +/- SD] vs S:R, M: 16.4 +/- 5.5 J; P < 0.05). For biphasic shocks, total energy was not affected by polarity reversal of the electrodes (R:S, B: 8.7 +/- 1.4 J vs S:R, B: 8.4 +/- 2.5 J; P = NS). The endocardial electrode configuration with the RV electrode as an anode requires less energy for defibrillation with a monophasic but not a biphasic waveform.

Animals↗

Spontaneous reinitiation of atrial fibrillation following transvenous atrial defibrillation.

Spontaneous reinitiation of atrial fibrillation (AF) has not been systematically looked at in patients undergoing transvenous AF. This study involved 11 patients, the mean age 60 +/- 8 years, 3 male and 8 female, in whom transvenous atrial defibrillation successfully converted AF to sinus rhythm. Eight patients had paroxysmal AF and three patients had chronic persistent AF for 4 weeks or more. Four patients were taking antiarrhythmic medications at the time of testing. Multipolar transvenous catheters were positioned inside the coronary sinus, right atrium, and the right ventricle. Atrial defibrillation testing was performed using the METRIX atrial defibrillation system in nine patients and the Ventritex HVSO2 in the remaining two patients. A total of 64 therapeutic shocks (range 3-11) were delivered in the 11 patients, and 31 of these successfully converted AF to sinus rhythm. In four patients spontaneous AF was reinitiated following 12 successful transvenous atrial defibrillation episodes. The mean time to reinitiation of AF following shock delivery and restoration of sinus rhythm was 8.26 +/- 5.25 seconds, range 1.8-19.9 seconds. All 12 episodes of spontaneous AF were preceded by a spontaneous premature atrial complex. The coupling interval of the premature atrial complexes was 443 +/- 43 ms, range 390-510 ms. None of the patients taking antiarrhythmic medications or those demonstrating no premature atrial complexes had spontaneous reinitiation of AF. In conclusion, spontaneous reinitiation of AF can occur in a significant proportion of patients with AF undergoing transvenous atrial defibrillation. This phenomenon is preceded by the occurrence of atrial premature complex. Findings of this study may have significant clinical implications.

Adult↗

Effect of rates of perfusion on dominant frequency and defibrillation energy in isolated fibrillating hearts.

This study assessed the influence of rates of reperfusion on excitability of the myocardium using dominant frequency (DF) (in Hz) of VF and the relationship of DF to the minimum defibrillation energy (MDE) (in J). Our hypothesis was that increasing flow during reperfusion increases DF that raises MDE. Initially, six Langendorff perfused swine hearts were serially fibrillated and perfusion arrested for 4 minutes followed by reperfusion and defibrillation to establish reproducibility of the model. The epicardial ECG was analyzed for DF. In subsequent studies (n = 8), no flow VF was followed by 1-minute reperfusion at normal flow or 10% flow (low flow) and shocked with increasing energy via epicardial pads until defibrillation. The DF at onset of no flow VF was 9.5 +/- 1.4 and decreased to 3.6 +/- 1.4 after 4 minutes. Reperfusion at normal flow increased the DF of VF compared to low flow after 1 minute (10.8 +/- 1.1 vs 4.5 +/- 1.1 Hz, P = 0.0002) and was associated with increased defibrillation energy requirements (13.5 +/- 5.0 vs 7.3 +/- 6.2 J, P = 0.047). In summary, defibrillation energy requirements are lower when myocardial excitability is reduced during low flow reperfusion.

Animals↗

A biventricular ICD system with biventricular defibrillation.

We describe the case of a 59-year-old gentleman with severe dilated cardiomyopathy requiring implantation of a dual-chamber biventricular implantable cardioverter-defibrillator (ICD). High defibrillation thresholds (DFT) were encountered at implant with an inadequate defibrillation safety margin. Testing of all possible shock vectors/polarities with and without the SVC coil and optimization of the distal RV coil position all proved inadequate. A satisfactory defibrillation safety margin was achieved following placement of a second lead in the coronary sinus to enable biventricular defibrillation. This case highlights an additional strategy for combating high DFTs and is an option even in dual-chamber biventricular ICD systems.

Electric Countershock↗

The effect of cardiac compression on defibrillation efficacy and the upper limit of vulnerability.

INTRODUCTION: We determined the effects of decreasing the ventricular blood volume and altering cardiac geometry on defibrillation, the upper limit of vulnerability (ULV), and the relationship between them. METHODS AND RESULTS: In six pigs, fibrillation/defibrillation trials were performed with a left ventricular apex patch to a superior vena cava catheter electrode configuration and a biphasic waveform. Thirty trials each were performed on a compressed versus noncompressed (normal) heart. Compression was achieved using direct mechanical ventricular actuation. Dose-response curves were constructed, and the 50% probability points (ED50) were compared for leading edge voltage (LEV), leading edge current (LEI), and total energy (TE). In another 12 pigs, triplicate defibrillation thresholds (DFTs) and ULVs were determined for each heart state. The T wave was scanned with shocks in 10-msec steps for determining the ULV. Compression resulted in decreased ED50s for LEV (delta = 138 +/- 77 V, P < 0.05, mean +/- SD), LEI (delta = 1.57 +/- 0.7 A, P < 0.05), and TE (delta = 4.9 +/- 3.6 J, P < 0.05) compared to normal. In the second study, compression significantly reduced DFT (P < 0.02) and ULV (P < 0.02) for LEV, LEI, and TE compared to normal. The ULV tended to be lower than the DFT for the normal heart state (delta = 23 +/- 46 V LEV: P = NS). However, the ULV was significantly greater than the DFT for the compressed heart state (delta = 19 +/- 25 V LEV; P < 0.03). CONCLUSIONS: Shock delivery during cardiac compression improves defibrillation efficacy. Additionally, cardiac compression decreases both DFT and ULV, which supports the ULV hypothesis of defibrillation. Finally, maintaining the heart's geometric and volumetric state during ULV testing in paced rhythm and DFT testing in ventricular fibrillation moves the ULV higher than the DFT-the position predicted by the ULV hypothesis for defibrillation.

Animals↗

Effect of electrode polarity on internal defibrillation with monophasic and biphasic waveforms using an endocardial lead system.

INTRODUCTION: To test the hypothesis that the effect of shock polarity on defibrillation depends on waveform duration, this study determined strength-duration defibrillation curves of monophasic and biphasic truncated exponential waveforms for both polarities. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were obtained in 32 pigs for catheter electrodes in the right ventricle (RV) and superior vena cava (SVC) using a modified Purdue technique. Both electrode polarities were tested in five different protocols. In part 1, DFTs were determined with 1- to 14-msec monophasic waveforms. In parts 2, 3, and 4, DFTs were determined with two different sizes of SVC electrodes for biphasic waveforms with a phase 1 of 4 or 6 msec and a phase 2 ranging from 1 to 10 msec. In part 5, DFTs were tested for monophasic waveforms ranging from 2 to 11 msec and for biphasic waveforms with a phase 1 duration corresponding to each monophasic waveform and a phase 2 held constant at 1 msec. Mean DFTs for monophasic waveforms were significantly lower when the RV electrode was an anode than when it was a cathode for waveform durations > or = 3 msec. For biphasic waveforms in which phase 2 was < or = phase 1 in duration, no significant difference in mean DFT was observed when polarity was reversed. Even a phase 2 as short as 1 msec could eliminate the DFT difference between polarities observed with monophasic shocks. When phase 2 was > or = 2 msec longer than phase 1, polarity did affect the DFT of biphasic waveforms; it affected the DFT similarly to a monophasic waveform of the same polarity as phase 2. Phase 1 duration and electrode size also affected the difference in DFT produced by changing the electrode polarity. CONCLUSIONS: For phase durations most commonly used clinically because of their low DFTs, reversing polarity changed defibrillation efficacy for monophasic but not biphasic shocks. For inefficient biphasic waveforms with phase 2 > or = 2 msec longer than phase 1, the DFT was lower when the RV electrode was an anode during phase 2, similar to the polarity difference for monophasic waveforms, suggesting that a long second phase of biphasic waveforms defibrillates in a similar fashion to monophasic waveforms.

Animals↗

Sawtooth first phase biphasic defibrillation waveform: a comparison with standard waveform in clinical devices.

INTRODUCTION: A major limitation in a conventional truncated exponential waveform is the rapid drop in current that results in short duration of high current or longer duration with a lower average current. We hypothesized that increasing the first phase average current by boosting the decaying waveform prior to phase reversal may improve defibrillation efficacy. METHODS AND RESULTS: To better simulate a "rectangular" waveform during the first phase, a "sawtooth" defibrillation waveform was constructed using "parallel-series" switching of capacitances (each 30 microF) during the first phase. This permitted a boost in the voltage late in the first phase. This sawtooth biphasic waveform (sawtooth) was compared to two clinical waveforms: a 135-microF capacitance (control-1) and a 90-microF capacitance (control-2) waveform. Defibrillation threshold (DFT) parameters were evaluated in 13 anesthetized pig models using a system consisting of a transvenous right ventricular apex lead (anode) and a left pectoral "hot can" electrode (cathode) system. DFT was determined by a "down-up down-up" protocol. The stored energy for sawtooth, control-1, and control-2 was 10.5 +/- 2.8 J, 12.3 +/- 3.7 J*, and 12.2 +/- 2.8 J*, respectively (*P < or = 0.01 vs sawtooth). The average current of the first phase for sawtooth, control-1, and control-2 was 7.6 +/- 1.3 A, 4.7 +/- 0.9 A*, and 6.2 +/- 0.9 A*, respectively (*P = 0.0001 vs sawtooth). CONCLUSION: A sawtooth biphasic waveform utilizing a "parallel-series" switching system of smaller capacitors can improve defibrillation efficacy. A higher average current in the first phase generated by such a waveform may contribute to more efficient defibrillation by facilitating myocyte capture.

Animals↗

Effect of electrode length on atrial defibrillation thresholds.

INTRODUCTION: Catheter-based electrodes have been used previously to terminate episodes of atrial fibrillation in animals and man. Typically, these electrodes span 6 to 7 cm, and lowest energy requirements are achieved when these electrodes are positioned in the distal coronary sinus and in the right atrium. The purpose of this study was to evaluate the use of longer electrode lengths for atrial defibrillation. METHODS AND RESULTS: In 15 patients, two decapolar catheters were inserted, one into the distal coronary sinus and one in the right atrium. To provide longer electrodes lengths, a third catheter was inserted and alternated positioned in the right atrium or coronary sinus. A 6-cm electrode span was obtained by using the distal 8 rings on the coronary sinus catheter or 8 consecutive electrodes on the right atrial catheter and increased from 6 to 11 cm by connecting 5 consecutive, nonoverlapping rings of the third catheter with the 10 rings of the initial right atrial or coronary sinus catheter. Atrial defibrillation thresholds were determined twice, in a randomized order, in each patient for each of the three combinations of electrode lengths. All 15 patients could be successfully converted to sinus rhythm without complications; however, one patient could be converted reproducibly with only 2 of the 3 electrode combinations. Mean thresholds were 306 +/- 102 V, 5.9 +/- 4.0 J for the 6 cm/6 cm electrode length combination with an impedance of 72 +/- 18 omega. For the electrode combination using the 11-cm electrode in the right atrium, the defibrillation threshold was 296 +/- 107 V, 5.8 +/- 3.9 J with an impedance of 61 +/- 17 omega and was 294 +/- 91 V, 5.6 +/- 3.6 J with an impedance of 55 +/- 11 omega for the 11-cm electrode in the coronary sinus. There were no significant differences in defibrillation voltage or energy (P > 0.05) associated with the longer electrode lengths; however, the longer electrode lengths did significantly lower shock impedance (P < 0.05). CONCLUSION: The use of longer electrodes, when using the right atrium to coronary sinus shock vector, does not lower the defibrillation requirements for restoration of sinus rhythm.

Adult↗

Direct evidence of the role of virtual electrode-induced phase singularity in success and failure of defibrillation.

INTRODUCTION: We recently demonstrated that virtual electrode-induced phase singularity is responsible for arrhythmogenesis during T wave shocks and explains the upper and lower limits of vulnerability. Furthermore, we suggested that the same mechanism might be responsible for defibrillation failure. The aim of this study was to experimentally support this hypothesis. METHODS AND RESULTS: We used the voltage-sensitive dye di-4-ANEPPS and fast imaging to assess electrical activity in Langendorff-perfused rabbit hearts. Ventricular arrhythmias were induced by monophasic shocks applied during T wave. Three types of defibrillation shocks (n = 79) were delivered from an intravenous right ventricular electrode: monophasic (8 msec), optimal biphasic (8/8 msec, 2/1 leading-edge voltage ratio), and nonoptimal biphasic (8/8 msec, 1/1 leading-edge voltage ratio). We found that a monophasic shock extinguished arrhythmic pattern of electrical activity via a virtual electrode polarization effect. However, the virtual electrode polarization was likely to produce phase singularities, leading to another arrhythmia and defibrillation failure. Nonoptimal biphasic shocks produced similar effects. Optimal biphasic shocks were successful because the first phase of the shock erased the arrhythmia via the virtual electrodes effect, whereas the second phase canceled the virtual electrodes, eliminating the substrate for phase singularities and arrhythmia resulting from them. CONCLUSION: Our data provide the first experimental support of the hypothesis implicating virtual electrode-induced phase singularity in defibrillation failure in the Langendorff-perfused rabbit heart. Optimal biphasic shock has a higher defibrillation efficacy because it does not produce virtual electrode-induced phase singularities.

Animals↗

The influence of opening the thorax on defibrillation threshold in canines.

To determine if intraoperative testing is predictive of implantable defibrillator performance postoperatively, we measured sequential pulse defibrillation thresholds (DFTs) in 16 adult canines (28.0 +/- 3.5 kg, mean +/- SD body weight) at the time of epicardial defibrillation electrode implantation. Three epicardial defibrillation electrodes were sutured directly to the anterior, posterior, and left lateral epicardial surfaces of the heart through a left fifth intercostal thoracotomy. The pericardium was sutured closed over the electrodes and DFT was measured first with the thorax open and again after closing all surgical wounds, evacuating the thorax, and reinflating the lungs. Mean +/- SD DFT voltage, current, and impedance (pulse 1), and total delivered energy (both pulses) for the open chest measurements were 321 +/- 87 volts, 4.2 +/- 1.9 amps, 80 +/- 14 ohms and 5.3 +/- 3.7 joules, respectively. The corresponding DFT values for the closed chest measurements were 321 +/- 92 volts, 5.1 +/- 1.9 amps, 64 +/- 10 ohms and 6.1 +/- 3.9 joules, respectively. Paired Student's t-test comparison of open versus closed chest DFT values indicated that there were no significant differences in voltage (P greater than 0.80) or energy (P greater than 0.20), but there were significant differences in both current (P less than 0.01) and impedance (P less than 0.001). It is concluded that despite alterations in impedance and current flow, voltage and energy DFT are not significantly different between open and closed chest animals. This suggests that intraoperative testing of implantable defibrillators is predictive of postoperative performance.

Animals↗

Bispectral energies within electrocardiograms during ventricular fibrillation are correlated with defibrillation shock outcome.

We investigated whether the degree of phase coupling among orthogonal electrocardiograms during ventricular fibrillation (VF) was correlated with defibrillation shock outcome. We used cross bispectrum to estimate the degree of phase coupling. In dogs, VF was electrically induced and terminated with a defibrillation shock with a 50% probability of success. The defibrillation shock was delivered between the right ventricular apex and a subcutaneous patch electrode. Bispectra were integrated within 8.7-11.7, 8.7-11.7 Hz bandwidths and compared between those trials for which the defibrillation shocks were successful (206 trials, 49%) and unsuccessful (221 trials, 51%) in terminating VF. Results showed that between 200 and 1000 ms before defibrillation shock, unsuccessful trials had greater bispectral energy than successful trials (p<0.05). Although correlations between degree of phase coupling and shock outcome do not indicate causal relationship or predictability, they provide further evidence of the organization during fibrillation. We discuss the nonstationary wavelet hypothesis, previously proposed in the literature by other investigators, as one of the possible mechanisms to explain the correlation between bispectral energy and shock outcome.

Animals↗

The automated external defibrillator: critical link in the chain of survival.

Sudden death due to ventricular fibrillation (VF) is the leading cause of death in the United States. Early defibrillation is the most important determinant of survival and is the key element in cardiopulmonary resuscitation. Obstacles to rapid defibrillation by trained emergency personnel persist, but the development of the automated external defibrillator (AED) promises to realize the goal of widespread early defibrillation and translate to an improved chance for survival for the cardiac arrest victim. Technological advancements have made the AED safe, easy to use, accurate, and effective in terminating VF. Use of the AED by trained nontraditional first responders (e.g., firefighters, police officers, flight crews) has improved survival rates in a variety of settings and forms the basis for public-access defibrillation.

Cardiopulmonary Resuscitation↗

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation.

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.

Adrenergic Uptake Inhibitors↗

Temporal stability and precision of ventricular defibrillation threshold data.

Over 200 measurements of the minimum damped sinusoidal current and energy for transchest electrical ventricular defibrillation (ventricular defibrillation threshold) were made to determine the stability and precision of threshold data in 15 pentobarbital-anesthetized dogs. Threshold was determined by repeated trials of fibrillation and defibrillation with successive shocks of diminishing current, each 10% less than that of the preceding shock. The lowest shock intensity that defibrillated was defined as threshold. In three groups of five dogs each, threshold was measured at intervals of 60, 15, and 5 min over periods of 8, 5, and 1 h, respectively. Similar results were obtained for all groups. There was no significant change in mean threshold current with time. Owing to a decrease in transchest impedance, threshold delivered energy decreased by 10% during the first hour of testing. The standard deviations for threshold peak current and delivered energy in a given animal were 11% and 22% of their respective mean values. Arterial blood pH, Pco2, and Po2 averaged change of pH, PCO2 and PO2 were not significantly different from zero. The data demonstrate that ventricular defibrillation threshold is a stable physiological parameter that may be measured with reasonable precision.

Animals↗

Effect of ischemia, hypertrophy, hypoxia, acidosis, and alkalosis on canine defibrillation.

Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not significantly elevated after left anterior descending coronary occlusion, nor was there a relationship between the size of the occluded coronary distribution area (coronary risk area) and the change in DFT in individual animals. Renal hypertension and left ventricular hypertrophy were induced by unilateral nephrectomy and contralateral renal artery stenosis. DFT in left ventricular hypertrophy dogs was not significantly higher than in dogs without hypertrophy. Finally, we induced systemic hypoxia and acid-base abnormalities. Neither respiratory nor metabolic acid-base disturbances affected DFT, but during systemic hypoxia (O2 tension 45 +/- 2) DFT fell from 83 +/- 49 to 58 +/- 28 J (P less than 0.01). Thus in dogs, myocardial ischemia, left ventricular hypertrophy, and acid-base abnormalities do not elevate defibrillation energy requirements, whereas hypoxia reduces the energy needed to defibrillate.

Acidosis↗

Tripling survival from sudden cardiac arrest via early defibrillation without traditional education in cardiopulmonary resuscitation.

BACKGROUND: Early defibrillation is the most important intervention affecting survival from sudden cardiac arrest (SCA). To improve public access to early defibrillation, we established Piacenza Progetto Vita (PPV), the first system of out-of-hospital early defibrillation by first-responder volunteers. METHODS AND RESULTS: The system serves a population of 173 114 residents in the Piacenza region of Italy. Equipment for the system comprises 39 semiautomatic external biphasic defibrillators (AEDs): 12 placed in high-risk locations, 12 in lay-staffed ambulances, and 15 in police cars; 1285 lay volunteers trained in use of the AED, without traditional education in cardiac pulmonary resuscitation, responded to all cases of suspected SCA, in coordination with the Emergency Medical System (EMS). During the first 22 months, 354 SCA occurred (72+/-12 years, 73% witnessed). The PPV volunteers treated 143 SCA cases (40.4%), with an EMS call-to-arrival time of 4.8+/-1.2 minutes (versus 6.2+/-2.3 minutes for EMS, P=0.05). Overall survival rate to hospital discharge was tripled from 3.3% (7 of 211) for EMS intervention to 10.5% (15 of 143) for PPV intervention (P=0.006). The survival rate for witnessed SCA was tripled by PPV: 15.5% versus 4.3% in the EMS-treated group (P=0.002). A "shockable" rhythm was present in 23.8% (34 of 143) of the PPV patients versus 15.6% (33 of 211) of the EMS patients (P=0.055). The survival rate from shockable dysrhythmias was higher for PPV versus EMS: 44.1% (15 of 34) versus 21.2% (7 of 33), P=0.046. The neurologically intact survival rate was higher in PPV-treated versus EMS-treated patients: 8.4% (12 of 143) versus 2.4% (5 of 211), P=0.009. CONCLUSIONS: Broad dissemination of AEDs for use by nonmedical volunteers enabled early defibrillation and tripled the survival rate for out-of-hospital SCA.

Cardiopulmonary Resuscitation↗

Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest.

BACKGROUND: Early defibrillation is considered the most important factor for restoring spontaneous circulation in cardiac arrest patients with ventricular fibrillation. Recent studies have shown that, after prolonged ventricular fibrillation, the rates of return of spontaneous circulation (ROSC) and survival are improved if defibrillation is delayed so that CPR can be given first. To examine whether CPR improves myocardial readiness for defibrillation, we analyzed whether CPR causes changes in predictors of defibrillation success calculated from the ventricular fibrillation waveform. METHODS AND RESULTS: ECG recordings were retrieved for 105 patients from an original study of 200 patients receiving CPR or defibrillation first. Altogether, 267 CPR sequences from 77 patients were identified on which the effect of CPR could be evaluated. Five predictors of ROSC (spectral flatness measure, energy, centroid frequency, amplitude spectrum relationship, and estimated probability of ROSC) were determined from a spectral analysis of the ventricular fibrillation waveform immediately before and immediately after each of the 267 sequences. CPR increased spectral flatness measure, centroid frequency, and amplitude spectrum relationship (P<0.05, P<0.001, P<0.01). In an analysis of the effect of the duration of CPR, the probability of ROSC and amplitude spectrum relationship showed a positive change for CPR sequences lasting >3 minutes (P<0.001, P<0.05). CONCLUSIONS: During resuscitation from ventricular fibrillation, changes in the predictors calculated from the ventricular fibrillation waveform indicated a positive effect of CPR on the myocardium.

Cardiopulmonary Resuscitation↗