Multiple Failed External Defibrillation Attempts During Robot-Assisted Internal Mammary Harvest for Myocardial Revascularization
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Abstract:
We describe multiple failed external defibrillation attempts via rescue defibrillation pads for ventricular fibrillation that occurred secondary to direct electrical current transmission through the pericardial sac from electrocautery during robot-assisted internal mammary harvest. Only after resumption of two-lung ventilation and decompression of the iatrogenic pneumothorax was the patient successfully defibrillated. Conditions necessary for robotic intrathoracic surgery may make defibrillation and resuscitation difficult if they become necessary.Keywords:
Mammary artery
Myocardial Revascularization
Fibrillation
Coronary perfusion pressure
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Introduction
Transthoracic defibrillation is performed to correct life threatening cardiac arrhythmias of the heart, i.e. ventricular fibrillation (VF) and ventricular tachycardia (VT). These are due to chaotic electrical excitation of the heart chambers and loss of coordinated contraction of myocytes that could induce cardiac arrest. Resuscitation guidelines recommend defined defibrillation energies for patient recovery, research indicates that these techniques may cause myocardial damage. However, there is limited information regarding the defibrillation potentially damaging effects on the tissues of the heart at structural and genomic levels. This study investigates the extent of myocardial injury associated with the use of increasing energies (75J, 150J, 200J and 360J) of defibrillation in a porcine model of cardiac arrest using genomic, histological and ultrastructural analysis techniques.Methodology
General anaesthesia was induced in swine models (≈10–40 kg) in accordance with The Home Office guidelines. VF was induced and defibrillation administered, each animal receiving 20 shocks at the defibrillation energy protocol at 3 min intervals followed by 6 hour recovery period. Upon completion, animals were humanely euthanised. Cardiac tissues were excised and processed for genomic, histological and ultrastructural analyses and examination.Results:Haemodynamic results demonstrated ROSC occurred in all pigs. Troponin I levels were elevated 3–4 hours after the completion of defibrillation protocol. Gross pathological examination demonstrated no unusual changes. Histological and SEM analysis indicate defibrillation causes changes to the porcine cardiac tissue as evidenced by instances of hypereosinophilia, increased collagen-I deposition and areas of multifocal acute subendocardial, epicardial and myocardial necrosis. qPCR analysis indicates defibrillation induces genomic changes, there was an upregulation in the mRNA expression of structural and inflammation related genes such as Collagen-I, IL-6/18 and MCP1. Hydroxyproline analysis and SEM imaging also illustrated minor changes in collagen content and structural appearance of the tissue, further supported with Image J colour hue analysis.Discussion
The current paradox is cardiac defibrillation depends on the successful selection of energy to generate sufficient current flow through the heart to achieve defibrillation, whilst causing minimal injury to the heart. At this acute timeframe (post protocol), the animal models illustrated biological effects from repeated defibrillation upon cardiac tissues at a structural and genomic level and suggests there is a cardioprotective measure taken by the cardiomyocytes due to electrical overstimulation. In conclusion, these results show repeated defibrillation at increasing energies produces immediate changes to the functional myocardium at a genomic, microscopic and ultrastructural level.Fibrillation
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Vulnerability in Ventricular Fibrillation. Introduction: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated Ventricular fibrillation by falling into the vulnerable period of the wave fronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. Methods and Results: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 ± 13 msec to 156 ± 5 msec (P < (0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as post‐shock early sites, the preshock intervals clustered within a narrow range both before (58 ± 14 msec) and during (10l ± 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P< 0.001.). Conclusion: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.
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Out-of-hospital cardiac arrest claims more than 450,000 lives annually in North America. Many communities have dedicated significant resources to provide rapid defibrillator response for patients in ventricular fibrillation. In spite of these efforts, mortality from out-of-hospital cardiac arrest has not improved significantly. Emerging evidence suggests some patients in ventricular fibrillation arrest may be harmed by immediate defibrillation.Recent laboratory studies have shown benefit in performing a period of chest compressions (cardiopulmonary resuscitation) prior to defibrillation in models with more than 4 minutes of induced ventricular fibrillation. During the initial 4 minutes the heart is more amenable to electrical defibrillation. Between 4-10 minutes, chest compressions create some coronary perfusion and fill the left ventricle to prepare the heart for electric shock. These findings, in conjunction with most emergency medical service response times reported to be 5-8 minutes, have prompted human investigation into a strategy of chest compression first. A recent randomized controlled trial reported a fivefold increase in survival for patients with more than 5 minutes of VF who received 3 minutes of chest compressions prior to defibrillation compared with those who had not.Current guidelines call for rapid defibrillation as the most important 'link' in the 'chain of survival'. For most ventricular fibrillation patients who have professional rescuers arrive after 5-8 minutes of ventricular fibrillation, however, immediate defibrillation is likely to be ineffective. Counterintuitively, these patients may benefit from a period of chest compressions prior to being shocked.
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Background: The amplitude spectrum area (AMSA), a frequency-domain ventricular fibrillation (VF) waveform metric, can predict successful defibrillation and the return of spontaneous circulation (ROSC) after defibrillation attempts. We aimed to investigate the validation of Spectral Energy for the quantitative analysis of the VF waveform to guide defibrillation in a porcine model of cardiac arrest and compare it with the AMSA metric. In addition, we sought to determine the effects of epinephrine and cardiopulmonary resuscitation (CPR) on AMSA and Spectral Energy. Methods: Sixty male domestic pigs weighing 35 to 45 kg were involved in this study. VF was initially untreated for 10 min followed by 6 min of CPR. Epinephrine was administered to the animals after 2 min of CPR. After the CPR, a single 120-J biphasic shock was applied to the animals. AMSA and Spectral Energy values were measured every minute from the electrocardiogram (ECG) to defibrillation. Receiver operating characteristic (ROC) curves were calculated for both the Spectral Energy and AMSA methods. Results: Spectral Energy and AMSA values gradually decayed during untreated VF in all the animals. However, after the application of CPR and epinephrine, Spectral Energy and AMSA values were significantly increased in animals which were later successfully defibrillated, but did not increase in animals in which defibrillation was unsuccessful. The ROC curves showed that the Spectral Energy and AMSA methods possessed similar levels of sensitivity and specificity in predicting defibrillation success (P<0.001). Conclusions: Both the Spectral Energy and AMSA methods accurately predict successful defibrillation. Moreover, increases in the value of either Spectral Energy or AMSA after application of CPR and epinephrine may also predict successful defibrillation.
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To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF).Randomized, controlled trial.University animal laboratory.Thirty swine (27 +/- 1 kg).After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks.After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p <.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p <.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation. The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p <.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p <.0001)Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.
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