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PubMed1984

Prognostic assessment of survivors of ventricular tachycardia and ventricular fibrillation with ambulatory monitoring.

The ability to assess prognosis in patients with serious ventricular arrhythmias treated with antiarrhythmic drugs by the degree of complexity on the 24-hour ambulatory electrocardiogram was evaluated in 59 survivors of ventricular tachycardia (VT) and ventricular fibrillation. After conventional therapy had failed, patients were treated with investigational drugs until symptomatic VT was abolished. A Holter monitor recording, obtained once the therapeutic regimen was established, was graded for the presence or absence of asymptomatic VT. Fifty-two patients were asymptomatic at discharge and were followed for 700 days. Of 44 patients followed for 1 year, none had recurrent syncope or died if asymptomatic VT was absent at 1 month (p less than 0.002). After 700 days, 27 patients (82%) without asymptomatic VT at 1 month were doing well, compared with 11 patients (58%) with asymptomatic VT at 1 month (p less than 0.002). In patients at risk for sudden cardiac arrest, early abolition of asymptomatic VT on ambulatory monitoring can be used to predict a good long-term clinical response.

Adolescent↗
PubMed2003

Clinical efficacy of a wearable defibrillator in acutely terminating episodes of ventricular fibrillation using biphasic shocks.

The Wearable Cardioverter Defibrillator (WCD) automatically detects and treats ventricular tachyarrhythmias without the need for assistance from a bystander, while at the same time allowing the patient to ambulate freely. It represents an alternative to emergency medical services for outpatient populations with a temporary risk of sudden cardiac death. While the original devices used a monophasic truncated exponential waveform for cardioversion/defibrillation shocks, a new, biphasic shock was developed for the next device generation. In 12 patients undergoing electrophysiological testing for ventricular tachyarrhythmias, termination of electrically induced ventricular fibrillation (VF) was attempted via the WCD. In 22 episodes, induced VF was promptly terminated by the first 70 J (n=12) or 100 J (n=10) biphasic shocks. Time between arrhythmia initiation and shock delivery was 22 +/- 6 seconds (70 J) and 21 +/- 6 seconds (100 J) (P=NS). The measured transthoracic impedance was 71 +/- 5 Ohms (64-79 Ohms) for the 70 J shock and 64 +/- 8 Ohms (47-72 Ohms) for the 100 J shock. The present study demonstrates that a single low energy biphasic shock delivered by the WCD, reliably terminates electrically induced VF (100% of episodes). The results of this study suggest that there is an acceptable safety margin to the maximum output of the device (150 J). Despite our promising data, we recommend that programming all shocks for maximum energy output should be done when using the WCD in ambulatory patients.

Ambulatory Care↗
PubMed1981

QT prolongation and ventricular fibrillation in acute myocardial infarction.

Fourteen acute myocardial infarction (AMI) patients with early ventricular fibrillation (VF) were compared to 27 control patients without VF with regard to the corrected QT interval (QTc) and the QRS duration. Patients with complete bundle branch block (BBB) had been excluded. The QTc tended to be longer in the VF group than in the controls, but the difference, 13 msec, disappeared after exclusion of a further 5 VF patients and one control with QRS duration greater than 0.10 sec of other configurations than complete BBB. In the long QT syndrome of various types, VF is characteristically preceded by diastolic waves (DW) with larger amplitudes than the preceding T waves. None of the 5 AMI patients with an evaluable recording of the onset of VF, showed DWs preceding the arrhythmia. The results of this study do not support the opinion that VG is associated with a prolonged QT interval in AMI in the same way as in the long QT syndrome. The longer QT interval in patients with VF seems to be mainly secondary to the longer QRS duration.

Adult↗
PubMed1976

[Experimental electric and biochemical data on ventricular fibrillation due to ischemia].

The author presents the results of prolonged research into ventricular fibrillation during myocardial ischaemia, both from the electrocardiographic and biochemical standpoints. - He emphasises the successive tonic and atonic features of VF due to ischaemia, and the difference between the fibrillation in an ischaemic area and in a control area. The most original concept is that there is often a difference between the onset of VF in an ischaemic zone and in a control zone. This study has been carried out with both acute and progressive ischaemia. - The biochemical studies were carried out on blood samples taken from the origin of the coronary arteries, the coronary veins, and from the saphenous veins. An important finding was the definite increase in the potassium level of the coronary venous blood in proportion to the degree of ischaemia; the sodium level showed little change, and if anything tended to fall. But the most important and distinctive finding was that at the onset of VF the sodium and potassium concentrations in the coronary venous blood suddenly increase. As the VF continues, there is a progressive increase in lactic acid and a fall in pH, which is maximal at the onset of the VF. These findings are valid under normothermic conditions, and when there is no extracorporeal circulation. - The physiopathological and practical implications of these facts are discussed.

Animals↗
PubMed1997

Shock-induced dispersion of ventricular repolarization: implications for the induction of ventricular fibrillation and the upper limit of vulnerability.

INTRODUCTION: Shock-induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction; however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear. METHODS AND RESULTS: In eight Langendorff-perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV, SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 +/- 15 msec for shocks inducing VF. SIDR was 41 +/- 17 msec for shocks delivered above the ULV, and 33 +/- 14 and 27 +/- 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P < 0.01 vs VF-inducing shocks). Although SIDR was larger for shocks delivered below the LLV (93 +/- 24 msec, P < 0.01 vs VF-inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3% +/- 3.9% vs 16.3% +/- 4.9%, P < 0.01). CONCLUSION: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.

Action Potentials↗
PubMed2006

Familial sudden death is an important risk factor for primary ventricular fibrillation: a case-control study in acute myocardial infarction patients.

BACKGROUND: Primary ventricular fibrillation (VF) accounts for the majority of deaths during the acute phase of myocardial infarction. Identification of patients at risk for primary VF remains very poor. METHODS AND RESULTS: We performed a case-control study in patients with a first ST-elevation myocardial infarction (STEMI) to identify independent risk factors for primary VF. A total of 330 primary VF survivors (cases) and 372 controls were included; patients with earlier infarcts or signs of structural heart disease were excluded. Baseline characteristics, including age, gender, drug use, and ECG parameters registered well before the index infarction, as well as medical history, were not different. Infarct size and location, culprit coronary artery, and presence of multivessel disease were similar between groups. Analysis of ECGs performed at hospital admission for the index STEMI revealed that cumulative ST deviation was significantly higher among cases (OR per 10-mm ST deviation 1.59, 95% CI 1.25 to 2.02). Analysis of medical histories among parents and siblings showed that the prevalence of cardiovascular disease was similar between cases and controls (73.1% and 73.0%, respectively); however, familial sudden death occurred significantly more frequently among cases than controls (43.1% and 25.1%, respectively; OR 2.72, 95% CI 1.84 to 4.03). CONCLUSIONS: In a population of STEMI patients, the risk of primary VF is determined by cumulative ST deviation and family history of sudden death.

Adult↗
PubMed2003

Blockade of the inward rectifying potassium current terminates ventricular fibrillation in the guinea pig heart.

INTRODUCTION: Stable high-frequency rotors sustain ventricular fibrillation (VF) in the guinea pig heart. We surmised that rotor stabilization in the left ventricle (LV) and fibrillatory conduction toward the right ventricle (RV) result from chamber-specific differences in functional expression of inward rectifier (Kir2.x) channels and unequal IK1 rectification in LV and RV myocytes. Accordingly, selective blockade of IK1 during VF should terminate VF. METHODS AND RESULTS: Relative mRNA levels of Kir2.x channels were measured in LV and RV. In addition, LV (n = 21) and RV (n = 20) myocytes were superfused with BaCl2 (5-50 micromol/L) to study the effects on IK1. Potentiometric dye-fluorescence movies of VF were obtained in the presence of Ba2+ (0-50 micromol/L) in 23 Langendorff-perfused hearts. Dominant frequencies (DFs) were determined by spectral analysis, and singularity points were counted in phase maps to assess VF organization. mRNA levels for Kir2.1 and Kir2.3 were significantly larger in LV than RV. Concurrently, outward IK1 was significantly larger in LV than RV myocytes. Ba2+ decreased IK1 in a dose-dependent manner (LV change > RV change). In baseline control VF, the fastest DF domain (28-40 Hz) was located on the anterior LV wall and a sharp LV-to-RV frequency gradient of 21.2 +/- 4.3 Hz was present. Ba2+ significantly decreased both LV frequency and gradient, and it terminated VF in a dose-dependent manner. At 50 micromol/L, Ba2+ decreased the average number of wavebreaks (1.7 +/- 0.9 to 0.8 +/- 0.6 SP/sec x pixel, P < 0.05) and then terminated VF. CONCLUSION: The results strongly support the hypothesis that IK1 plays an important role in rotor stabilization and VF dynamics.

Animals↗
PubMed2005

Repolarization dynamics in patients with idiopathic ventricular fibrillation: pharmacological therapy with bepridil and disopyramide.

The electrocardiographic parameters relating occurrence of ventricular fibrillation (VF) episodes in patients with idiopathic VF (IVF) are still unknown. The aim of this study was to clarify efficacy of pharmacological therapy in patients with IVF with respect to repolarization dynamics. The study group consisted of 8 men (age 43.6 +/- 9.1 years) with IVF (Brugada type 5 patients, prominent J wave in the inferior leads 3 patients) who had documented spontaneous episodes of VF, 7 of whom had implantable cardioverter defibrillators. The relation between QT and RR interval was analyzed from 24-hour Holter ECG using an automatic analyzing system before and after pharmacological therapy (bepridil 5 and disopyramide 3). From QT-RR linear regression lines, QT intervals were determined at RR intervals of 0.6 second [QT(0.6)], 1.0 second [QT(1.0)], and 1.2 seconds [QT(1.2)]. Pharmacological therapy increased the slope of QT-RR regression line from 0.105 +/- 0.020 to 0.144 +/- 0.037 (P < 0.05). Accordingly, QT(1.0) and QT(1.2) became longer after drug therapy [QT(1.0), 0.382 +/- 0.016 seconds vs 0.414 +/- 0.016 seconds (P < 0.01); QT(1.2), 0.403 +/- 0.017 seconds vs 0.442 +/- 0.021 seconds (P < 0.01)]. However, QT(0.6) did not change after drug administration. Before drug therapy the average episodes of VF were 5.5 +/- 5.8 (range 1 to 17) during the observation period of 19.3 +/- 17.6 months (range 6 to 60 months). After drug therapy, 6 patients had no episode of VF for 24 to 120 months (66.0 +/- 38.5 months). Two patients had a single episode of VF for 12- and 96-month follow-ups. Pharmacological therapy decreased the frequency of VF episodes in association with prolongation of QT intervals at slower heart rates. Not only J wave and ST elevation but also shorter QT intervals at slower heart rates may represent an electrophysiological substrate for development of VF episodes in these specific IVF patients.

Adult↗
PubMed1975

Observations on patients with primary ventricular fibrillation complicating acute myocardial infarction.

UNLABELLED: In order to evaluate the events preceding primary ventricular fibrillation (PVF), continuous tape recording was performed in 262 patients consecutively admitted to the hospital within six hours of infarction in whom antiarrhythmic therapy was withheld. Warning arrhythmias (defined as ventricular ectopic beats occurring with a frequency of more than five beats per minute, in runs, falling in the vulnerable phase of the cardiac cycle or being multiformed) were registered in an equal percentage in patients who did or did not develop PVF. Immediately prior to PVF seven patients showed sinus tachycardia, 10 a sinus rate ranging from 60 to 100 beats per minute and two bradycardia due to complete atrioventricular block. The ventricular ectopic beat initiating PVF had a late coupling interval (QR'/QT larger than or equal to 0.85) in 11 patients and a left bundle branch block configuration as frequent as a right bundle branch block. CONCLUSIONS: 1) Warning arrhythmias are not considered good criteria for institution of antiarrhythmic therapy in order to prevent PVF. 2) In patients with sinus rhythm there may be an association between heart rate and onset of PVF. 3) The malignancy of a ventricular ectopic beat is not determined by its coupling interval or its configuration.

Acute Disease↗
PubMed1994

Recurrent cardiac events in survivors of ventricular fibrillation or tachycardia. Implications for driving restrictions.

OBJECTIVE: To determine when survivors of ventricular tachycardia (VT) or ventricular fibrillation (VF) might most safely return to driving. DESIGN: Consecutive case series of 501 VT and VF survivors discharged alive between August 1978 and October 1989 and followed from 0 to 117 months (mean, 26 months). SETTING: Cardiac arrhythmia service of a university hospital. PATIENTS: The study group comprised 290 consecutive patients with sustained VT and 211 patients with VF who underwent electrophysiological studies and were discharged alive (78% male; mean age, 59 years). The mean ejection fraction (available in 338 patients) was 0.42. INTERVENTIONS: Antiarrhythmic drug testing for all patients was guided by serial electrophysiological testing. Overall, 227 patients (45%) were discharged on conventional antiarrhythmic agents, 115 (23%) on amiodarone, 39 (8%) received an implantable defibrillator, and 120 (24%) received no specific antiarrhythmic therapy. MAIN OUTCOME MEASURES: Main outcomes included any event that could hamper a patient's ability to operate a motor vehicle. Specifically, these events included recurrent VF, poorly tolerated, hemodynamically unstable VT, syncope, sudden cardiac death, and implantable defibrillator discharge. RESULTS: Event risks were assessed during the first year after hospital discharge because that is when most patients decide whether to begin driving again. The 1-year outcome event rate for all 501 patients was 17%. Three distinct periods of risk were identified. The monthly hazard rate was highest in the first month after hospital discharge (4.22% per month), intermediate in months 2 through 7 (1.81% per month), and lowest in months 8 through 12 (0.63% per month). The 191 patients for whom no successful conventional antiarrhythmic drug could be found during electrophysiological testing experienced a persistently high monthly event risk (1.6%) during months 8 through 12. CONCLUSIONS: All survivors of VT or VF should refrain from driving during the first month after hospital discharge when the hazard for events that could impair their ability to drive is greatest. Our data would support restricting driving for most patients until the eighth month after hospital discharge, when risk becomes lowest. Restriction might be lengthened in patients for whom electrophysiological testing finds no satisfactory conventional antiarrhythmic agent because their risk remains higher than average even after 7 months. Individualized recommendations should be allowed because the accident rate for patients who actually suffer sudden death is low.

Accidents, Traffic↗
PubMed1998

Quantification of the modifications in the dominant frequency of ventricular fibrillation under conditions of ischemia and reperfusion: an experimental study.

The characteristics of ventricular fibrillatory signals vary as a function of the time elapsed from the onset of arrhythmia and the maneuvers used to maintain coronary perfusion. The dominant frequency (FrD) of the power spectrum of ventricular fibrillation (VF) is known to decrease after interrupting coronary perfusion, though the corresponding recovery process upon reestablishing coronary flow has not been quantified to date. With the aim of investigating the recovery of the FrD during reperfusion after a brief ischemic period, 11 isolated and perfused rabbit heart preparations were used to analyze the signals obtained with three unipolar epicardial electrodes (E1-E3) and a bipolar electrode immersed in the thermostatized organ bath (E4), following the electrical induction of VF. Recordings were made under conditions of maintained coronary perfusion (5 min), upon interrupting perfusion (15 min), and after reperfusion (5 min). FrD was determined using Welch's method. The variations in FrD were quantified during both ischemia and reperfusion, based on an exponential model deltaFrD = A exp (-t/C). During ischemia deltaFrD is the difference between FrD and the minimum value, while t is the time elapsed from the interruption of coronary perfusion. During reperfusion deltaFrD is the difference between the maximum value and FrD, while t is the time elapsed from the restoration of perfusion. A is one of the constants of the model, and C is the time constant. FrD exhibited respective initial values of 16.20 +/- 1.67, 16.03 +/- 1.38, and 16.03 +/- 1.80 Hz in the epicardial leads, and 15.09 +/- 1.07 Hz in the bipolar lead within the bath. No significant variations were observed during maintained coronary perfusion. The fit of the FrD variations to the model during ischemia and reperfusion proved significant in nine experiments. The mean time constants C obtained on fitting to the model during ischemia were as follows: E1 = 294.4 +/- 75.6, E2 = 225.7 +/- 48.5, E3 = 327.4 +/- 79.7, and E4 = 298.7 +/- 43.9 seconds. The mean values of C obtained during reperfusion, and the significance of the differences with respect to the ischemic period were: E1 = 57.5 +/- 8.4 (P < 0.01), E2 = 64.5 +/- 11.2 (P < 0.01), E3 = 80.7 +/- 13.3 (P < 0.01), and E4 = 74.9 +/- 13.6 (P < 0.0001). The time course variations of the FrD of the VF power spectrum fit an exponential model during ischemia and reperfusion. The time constants of the model during reperfusion after a brief ischemic period are significantly shorter than those obtained during ischemia.

Animals↗
PubMed1989

Surgery of ventricular tachycardia and ventricular fibrillation in patients with coronary artery disease and LV-aneurysms.

In 26 patients with left ventricular aneurysm and ventricular tachycardia and/or ventricular fibrillation following myocardial infarction, coronary angiography, left ventriculography and electrophysiologic examination were performed preoperatively. Surgery in all cases consisted of aneurysmectomy and mapping-guided endocardial resection of the area found to be the arrhythmogenic center. Four patients died peroperatively or during the postoperative hospital stay. The 22 survivors were followed up for 3-48 (mean 22) months postoperatively. There were no late deaths. Repeated electrophysiologic studies were performed in 18 of the survivors. Freedom from ventricular tachycardia and fibrillation was achieved in 21 patients, 17 after surgery alone and four after combined surgical and medical treatment. The remaining patient still has ventricular tachycardia despite combined treatment.

Adult↗
PubMed2005

The duration of ventricular fibrillation required to produce pulseless electrical activity.

The duration of untreated (no cardiopulmonary resuscitation) ventricular fibrillation (VF) needed to produce postdefibrillation pulseless electrical activity (PEA) was determined in 9 anesthetized swine ranging in weight from 20 to 30 kg. VF was induced electrically by a right ventricular catheter electrode, while arterial pressure and the electrocardiogram were recorded. VF was confirmed by the presence of VF waves in the electrocardiogram and a loss of pulsatile arterial pressure. VF was allowed to persist for 15-second increments (eg, 15, 30, 45, etc), after which defibrillation was achieved with transchest electrodes and the presence or absence of PEA was noted. If PEA was present, rhythmic chest compressions were applied to rescue the animal. Just after initiation of VF and just before defibrillation, VF wave frequency was measured. PEA was encountered in 100% of the trials after 180 seconds of VF. The threshold duration for PEA was 60 seconds. VF wave frequency decreased with the passage of time. At VF initiation, VF wave frequency (f0) ranged from 6 to 15 per second, with a mean of 10.1+/-2.1 per second. At 180 seconds (f180), the mean frequency was 4.0+/-0 per second. It was only possible to eliminate PEA and restore pumping in 1 animal when untreated VF lasted more than 180 seconds. There was no clear transition in the frequency of the VF waves with the passage of time that could predict the possibility of postdefibrillation PEA. Moreover, because of the different initial VF wave frequencies and the different rates of decrease with time, a measurement of VF wave frequency is unlikely to be informative on how long VF had been present. A consistent finding in this swine study of prolonged untreated VF was a rise in blood K+ which increased from a normal prefibrillation value of about 4 mEq/L to 8 to 12 mEq/L at 180 seconds. The longer the duration of VF, the higher the K+.

Animals↗
PubMed1994

Contrast media-induced ventricular fibrillation: an experimental study of the effects of dimeric contrast media during wedged catheter injection in dogs.

RATIONALE AND OBJECTIVES: We investigated the cardiac effects of an ionic dimer, ioxaglate and two nonionic dimers, iotrolan, and iodixanol. METHODS: During a simulated wedged catheter situation, 22 ml of each contrast medium was injected into the left anterior descending branch of the left coronary artery in seven open-chested, anesthetized dogs. RESULTS: Of 13 injections with each contrast medium, ioxaglate induced ventricular fibrillation in 11 after 34 +/- 5 sec, iotrolan in 6 after 42 +/- 4 sec, and iodixanol in 3 after 61 +/- 1 sec. Ioxaglate markedly lengthened monophasic action potential duration in contrast medium-perfused myocardium. Iotrolan, and iodixanol induced biphasic changes, first lengthening and then shortening action potential duration. The electrophysiological changes occurred later when using iodixanol. CONCLUSIONS: The risk of ventricular fibrillation during long-lasting contrast media exposure to the myocardium, as in a wedged catheter situation, appears to be much lower with iodixanol compared with ioxaglate and also lower than when using iotrolan.

Animals↗
PubMed2003

Effects of heart isolation, voltage-sensitive dye, and electromechanical uncoupling agents on ventricular fibrillation.

We tested whether the interventions typically required for optical mapping affect activation patterns during ventricular fibrillation (VF). A 21 x 24 unipolar electrode array (1.5 mm spacing) was sutured to the left ventricular epicardium of 16 anesthetized pigs, and four episodes of electrically induced VF (30-s duration) were recorded. The hearts were then rapidly excised and connected to a Langendorff perfusion apparatus. Four of the hearts were controls, in which 24 additional VF episodes were then mapped. In the remaining 12 hearts, four VF episodes were mapped after isolation, four more episodes were mapped after exposure to the voltage-sensitive dye di-4-ANEPPS, and six more episodes were mapped after exposure to the electromechanical uncoupling agents diacetyl monoxime (DAM; 20 mmol/l, n = 6) or cytochalasin D (CytoD; 10 micromol/l, n = 6). VF episodes were separated by 4 min. VF activation patterns were quantified using custom pattern analysis algorithms. From comparisons with time-corrected control data, all interventions significantly changed VF patterns. Most changes were broadly consistent with slowing and regularization due to loss of excitability. Heart isolation had the largest effect on VF patterns, followed by CytoD, DAM, and dye.

Animals↗
PubMed1999

Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation.

BACKGROUND: Whether antiarrhythmic drugs improve the rate of successful resuscitation after out-of-hospital cardiac arrest has not been determined in randomized clinical trials. METHODS: We conducted a randomized, double-blind, placebo-controlled study of intravenous amiodarone in patients with out-of-hospital cardiac arrest. Patients who had cardiac arrest with ventricular fibrillation (or pulseless ventricular tachycardia) and who had not been resuscitated after receiving three or more precordial shocks were randomly assigned to receive 300 mg of intravenous amiodarone (246 patients) or placebo (258 patients). RESULTS: The treatment groups had similar clinical profiles. There was no significant difference between the amiodarone and placebo groups in the duration of the resuscitation attempt (42+/-16.4 and 43+/-16.3 minutes, respectively), the number of shocks delivered (4+/-3 and 6+/-5), or the proportion of patients who required additional antiarrhythmic drugs after the administration of the study drug (66 percent and 73 percent). More patients in the amiodarone group than in the placebo group had hypotension (59 percent vs. 48 percent, P=0.04) or bradycardia (41 percent vs. 25 percent, P=0.004) after receiving the study drug. Recipients of amiodarone were more likely to survive to be admitted to the hospital (44 percent, vs. 34 percent of the placebo group; P=0.03). The benefit of amiodarone was consistent among all subgroups and at all times of drug administration. The adjusted odds ratio for survival to admission to the hospital in the amiodarone group as compared with the placebo group was 1.6 (95 percent confidence interval, 1.1 to 2.4; P=0.02). The trial did not have sufficient statistical power to detect differences in survival to hospital discharge, which differed only slightly between the two groups. CONCLUSIONS: In patients with out-of-hospital cardiac arrest due to refractory ventricular arrhythmias, treatment with amiodarone resulted in a higher rate of survival to hospital admission. Whether this benefit extends to survival to discharge from the hospital merits further investigation.

Aged↗
PubMed1997

Dose-response relationship between aortic infusions of polymerized bovine hemoglobin and return of circulation in a canine model of ventricular fibrillation and advanced cardiac life support.

OBJECTIVES: Return of spontaneous circulation after cardiac arrest may be a function of vital organ perfusion. Selective aortic perfusion and oxygenation with oxygenated ultrapurified polymerized bovine hemoglobin improves vital organ perfusion and is an effective adjunct in the treatment of cardiac arrest. This study determined the dose-response relationship between intra-aortic oxygenated ultrapurified polymerized bovine hemoglobin and return of spontaneous circulation. DESIGN: Randomized, interventional study, using a clinically relevant model of ventricular fibrillation with a prolonged arrest time and cardiopulmonary resuscitation based on external chest compression and aortic occlusion with oxygenated ultrapurified polymerized bovine hemoglobin infusion. SETTING: University, resuscitation research laboratory. SUBJECTS: Fasted, mongrel dogs (> 20 kg). INTERVENTIONS: After alpha-chloralose anesthesia, blood gases and vital signs were normalized. Electrocardiogram, aortic arch, and intraesophageal pressures were measured continuously. A descending aortic occlusion-infusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced and basic life support was begun after 10 mins. Interanimal differences in basic life support were minimized by standardization of the esophageal pulse pressure and aortic blood gases. At 13 mins, the aortic occlusion balloon was inflated and a dose of 10, 20, or 30 mL/kg of ultrapurified polymerized bovine hemoglobin was infused at 300 mL/min. Defibrillation was attempted at the end of the infusion. MEASUREMENTS AND MAIN RESULTS: Only two of five animals given 10 mL/kg of ultrapurified polymerized bovine hemoglobin had return of spontaneous circulation, vs. four of five animals given 20 mL/kg, and all seven animals given 30 mL/kg. All resuscitated animals were alive at 1 hr after return of spontaneous circulation. CONCLUSIONS: There is a dose-response relationship between the volume of oxygenated ultrapurified polymerized bovine hemoglobin administered by selective aortic perfusion and oxygenation and return of spontaneous circulation after prolonged cardiac arrest. This result supports the hypothesis that vital organ flow is causally related to improved outcome.

Animals↗
PubMed1999

Incidence, evolution, and spatial distribution of functional reentry during ventricular fibrillation in pigs.

Functional reentry has been hypothesized to be an underlying mechanism of ventricular fibrillation (VF); however, its contribution to activation patterns during fully developed VF is unclear. We applied new quantitative pattern analysis techniques to mapping data acquired from a 21 x 24 unipolar electrode array (2-mm spacing) located on the ventricular epicardium of 7 open-chest, unsupported pigs. Data epochs 4 seconds long beginning 1, 10, 20, 30, and 40 seconds after electrical induction were analyzed. Reentrant circuits were automatically identified and quantified. We found that 2.3% of activation pathways could unambiguously be classified as reentrant. From scaling analysis, an additional 28% of the pathways may also have been reentrant. Reentry was short-lived with 1.5+/-1.5 (mean+/-SD) complete cycles per circuit. The fraction of reentrant pathways, number of cycles per circuit, cycle duration, and area and perimeter of the cores all increased significantly as VF progressed. Core drift speed decreased significantly. Neither the orientation of the cores nor the direction of drift was well predicted by the epicardial fiber orientation (r2=0.108 and 0.138, respectively, by linear regression). Reentrant circuits were clustered in regions of the epicardium. We conclude the following: (1) Epicardial reentry is relatively uncommon and short-lived during VF, suggesting either that sustained reentry is transmural or that mechanisms governing sustained reentry are relatively unimportant to the dynamics of VF. (2) Reentrant circuits become more common, larger, and longer-lived as VF progresses, which may explain a recently observed increase in VF organization during the first minute of VF. (3) The conditions necessary to induce and sustain reentry are distributed nonuniformly.

Animals↗