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PubMedDate not supplied

Vector magnitude using orthogonal ECG leads during ventricular fibrillation is associated with defibrillation outcome.

Random fluctuations of ventricular fibrillation (VF) affect defibrillation; in addition, the heart is more susceptible to defibrillation at a higher absolute VF voltage (AVFV). Shocks delivered at higher AVFV waveforms from a single lead of the electrocardiogram (ECG) are more effective than conventional shocks. The authors investigated a new sensing method using multiple leads for better representation of the depolarization state of the heart. In this non-thoracotomy defibrillation study, a vector waveform derived from three orthogonal surface leads X, Y, and Z was analyzed in real time using two distinct defibrillation lead configurations, P1: RV-coil electrode (-) <--> (SVC-coil electrode + SCP) (+); and P2: RV-coil electrode (+) <--> (SVC-coil electrode + SCP) (-), where (-) represents cathode and (+) anode for the first phase of biphasic shock (RV = right ventricle, SVC = superior vena cava, SCP = subcutaneous patch). A PC-based closed-loop waveform-processing system, the peak-shock method (PSM), was developed to analyze the vector waveforms and trigger a biphasic shock at an AVFV peak. In using this defibrillation technique, an empirical threshold was applied to a weight function consisting of short-term and long-term moving averages of the vector VF waveform. A total of 340 shock trials in nine canine studies resulted in a significantly higher defibrillation success rate for the PSM compared with the conventional random-shock method (RSM), which involved shocking after a fixed VF time (54% for the PSM versus 42% for the RSM, p < 0.03). This further confirms that a susceptible period for defibrillation occurs during VF. The hardware/software design satisfied the requirements for processing the VF vector waveform in real time, and with the help of signal-processing techniques the high VF voltage could be detected at it occurred in real time. In addition, the P2 defibrillation lead configuration was significantly better than the P1 (p < 0.006).

Algorithms↗

PubMed2005

Intraoperative bypass flow measurement reduces the incidence of postoperative ventricular fibrillation and myocardial markers after coronary revascularisation.

OBJECTIVE: Sudden ventricular fibrillation (VF) and myocardial infarction (MI) are life-threatening complications after coronary artery bypass grafting (CABG). We prospectively analysed the impact of intraoperative bypass flow measurement with the transit time flow Doppler method (TTFD) on the incidence and outcome of postoperative VF and MI. METHODS: In 1995 a standardized algorithm for the treatment of postoperative VF was introduced in our institution. The rate of postoperative VF was therefore exactly registered. In 1998 the TTFD method was implemented as a standard in all CABG cases. Whenever insufficient bypass graft flow was detected, anastomoses were redone and technical problems affecting the grafts were excluded. The incidence of postoperative VF and CK/CK-MB fraction was observed prospectively and the new data was compared to the data from 1995 to 1998. RESULTS: From 1/95 to 7/98 a total of 4321 patients (group A) were operated on with isolated CABG procedures using extracorporeal circulation. In the period from 8/98 to 10/02 a total of 3421 patients (group B) was operated on with isolated CABG procedures under the same conditions, except that the TTFD method was used in every case. The treatment of VF was standardised in both groups according to the algorithm. The most striking effect was the significant reduction of VF from 0.66% to 0.44% when TTFD was introduced and the steep decrease in mortality from 30% to 12.2% in patients with VF when the algorithm and TTFD were routinely applied. Furthermore the rate of insufficient bypass flow detected by angiography was reduced by 66%. CONCLUSION: Routinely the use of TTFD significantly reduced the incidence of postoperative VF, postoperative CK/CK-MB fraction, and angiographically detected bypass malfunction. A simultaneously implemented algorithm reduced the mortality with VF after CABG. The consequent use of TTFD intraoperatively reduced the incidence of postoperative anastomosis and technically related complications of bypass surgery and led to a significant reduction of postoperative mortality in CABG procedures.

Algorithms↗

PubMed1999

Cardioprotection: intermittent ventricular fibrillation and rapid pacing can induce preconditioning in the blood-perfused rat heart.

The aim of the study was to use the isolated blood-perfused rat heart to: (i) determine whether brief intermittent rapid pacing and ventricular fibrillation are able to mimic preconditioning by ischemia and thereby protect the isolated blood-perfused heart against ischemia-induced injury and (ii) characterize the effects of these interventions on cardiac metabolism. To this end, isolated, blood-perfused (2.4 ml/min), paced (360 beats/min) rat hearts (n = 6/group), were aerobically perfused for 20 min. Hearts were then randomized to four groups: (i) a further 16 min aerobic perfusion (UC, untreated controls), (ii) ischemic preconditioning (IP, 3 min ischemia + 3 min reperfusion followed by 5 min ischemia + 5 min reperfusion), (iii) electrically induced ventricular fibrillation (VF, 3 min fibrillation + 3 min sinus rhythm followed by 5 min fibrillation + 5 min sinus rhythm) and (iv) rapid pacing at > or = 600 beats/min (RP, 3 min rapid pacing + 3 min normal heart rate followed by 5 min rapid pacing + 5 min normal heart rate). Hearts were then subjected to 35 min of zero-flow, global ischemia (37 degrees C) and 40 min reperfusion. In parallel studies, blood samples were collected during the first 3 min of treatment and plasma taken for the analysis of noradrenaline. The hearts were then immediately frozen and assayed for high energy phosphates and noradrenaline content. Time-to-50% contracture during ischemia was 13.2 +/- 0.8 min in controls; this was reduced to 6.3 +/- 1.1 min by IP but was unaffected by VF or RP (12.4 +/- 1.1 and 12.8 +/- 1.2 min respectively). Post-ischemic left ventricular developed pressure (LVDP) in untreated controls recovered to only 19.9 +/- 8.4% of its pre-ischemic value whereas with IP, VF and RP substantial and similar improvements were observed (60.3 +/- 7.4, 56.2 +/- 5.7 and 45.3 +/- 10.3%, respectively, P < 0.01). This protection was achieved without any significant depletion of high energy phosphates during VF or RP. Noradrenaline was essentially unchanged in controls and with RP, but VF caused a loss from tissue and a large elevation in the plasma. Our results suggest that both RP and VF are as effective as brief ischemia in protecting the heart against injury during ischemia and reperfusion. In contrast to IP, this protection can be achieved without the exacerbation of ischemic contracture and without inducing ischemia during the preconditioning period.

Adenine Nucleotides↗

PubMed1993

Usefulness of CKMB and troponin T determinations in patients with acute myocardial infarction complicated by ventricular fibrillation.

The usefulness of creatine kinase (CK) time activity curves for diagnosis of acute myocardial infarction in patients who have been defibrillated for ventricular fibrillation is limited due to the release of the enzyme as a result of the countershock. The present study of four patients with acute infarction complicated by primary ventricular fibrillation indicates that analysis of CKMB and even more so of troponin T, a specific cardiac antigen, permits reliable diagnosis of acute myocardial infarction in this particular setting. Furthermore, the data indicate that noninvasive assessment of coronary artery patency may be also possible in these patients by means of these two serum markers.

Acute Disease↗

PubMed1980

Time dependency of ventricular fibrillation thresholds determined using trains of stimuli.

When determining ventricular fibrillation threshold (VFT), considerable time elapses from beginning a VFT measurement until the actual occurrence of ventricular fibrillaion (VF). We have defined this elapsed time as the "time to VF" and examined the effect of varying time to VF on the measured value of VFT. We induced VF in anesthetized dogs with a 100-Hz train of 16 4-ms stimuli applied to the right ventricular epicardium. The time to VF was varied by changing either the increment of fibrillation current increase (0.5, 1.0, or 2.0 mA) from one train to the next and/or the number of atrial paced beats between trains (6-192 beats). For 0.5-mA current increments, as time to VF increased from 66 to 454 s, VFT fell progressively from 15.3 +/- 4.8 to 6.7 +/- 1.1 mA. When time to VF exceeded 454 s, VFT increased again. Current increments of 1.0 and 2.0 mA had a similar time dependency of VFT. For any time to VF the VFT was lower when small current increments (i.e., more trains) were used to induce VF. Pretreatment with reserpine in six dogs abolished the time dependency. We conclude that time elapsed from the beginning of a VFT determination until VF actually occurs and the total number of trains used are important determinants of the VFT, probably because of local catecholamine release by the stimuli.

Animals↗

PubMedDate not supplied

Ventricular fibrillation. A complication and hazard of transcatheter obliteration of the renal artery with absolute ethanol in dogs.

Selective renal artery embolization with absolute ethanol was performed without balloon occlusion in a series of 11 healthy mongrel dogs. Electrocardiogram, blood ethanol level, heart rate, and blood pressure of the aorta and pulmonary artery were monitored. Ventricular extrasystoles and/or ventricular fibrillation occurred in six of the 11 dogs, to which absolute ethanol in doses ranging from 0.09 to 0.40 ml/kg was administered. In three of these six animals, the electrocardiograms showed only ventricular extrasystoles after intra-arterial bolus injection of absolute ethanol at doses of less than 0.15 ml/kg and subsequent recovery to a normal sinus rhythm. Ventricular fibrillation subsequent to ventricular extrasystoles immediately after intra-arterial injection of absolute ethanol at doses of more than 0.18 ml/kg occurred in three. In five of eight dogs that survived after alcohol injection in this series, a severe hypertensive response was observed. Absolute ethanol has the potential hazard of causing ventricular arrhythmia. Thus, careful observations should be undertaken in clinical therapeutic application of this agent, particularly in the absence of balloon occlusion, absolute ethanol should never be used without monitoring the electrocardiogram.

Animals↗

PubMed1996

[Prognostic factors after sustained ventricular fibrillation or tachycardia. A multivariate study apropos of 160 cases].

The authors analysed survival of 160 patients (121 men and 31 women; average age 57.2 +/- 12.5 years; follow-up 29 +/- 20 months) treated for malignant ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation, syncope with inducible ventricular tachycardia). The therapeutic evaluation was frequently invasive (145 patients underwent at least programmed ventricular stimulation, 108 patients underwent full endocavitary electrophysiological studies) and non-pharmacological therapy was widely used (defibrillator n = 44; antiarrhythmic surgery n = 28; ablative procedures n = 19; transplantation n = 7). The following underlying pathologies were observed: ischaemic heart disease n = 120; non-ischaemic left heart disease n = 19; right heart cardiac disease n = 4; and apparently normal hearts n = 17). The average ejection fraction was 40.5 +/- 15.5% and 29 patients were in the NYHA functional classes III or IV. Fifty-five patients had life-threatening arrhythmias whilst receiving amiodarone. At 2 years, the actuarial sudden death rate was 5.9 +/- 2.1% and the actuarial total cardiac mortality rate was 13.1 +/- 2.9%. Univariate analysis showed age, the presence of underlying cardiac disease, the presence of dilated cardiomyopathy, the absence of an invasive approach, the need for basal pacing in electrical cardioversion, the absence of betablocker therapy, a decreased left ventricular ejection fraction and a high NYHA functional class, to be predictive of sudden death. In multivariate analysis, age, the NYHA class for total cardiac mortality and the NYHA class for sudden death, were the only independent predictive factors. The authors conclude that in the era of invasive methods of evaluation and widespread use of non-pharmacological therapeutic methods, the symptomatology of cardiac failure assessed by the NYHA classification remains the most powerful independent prognostic factor after an episode of malignant ventricular arrhythmia.

Actuarial Analysis↗

PubMed1999

[Ventricular fibrillation during mild hypothermic therapy in a patient undergoing neurosurgery].

A 35 year old male for mild hypothermic therapy for neurosurgery, developed ventricular fibrillation. Total resection of cerebral arteriovenous malformation was performed under mild hypothermic therapy, with the target core temperature of 33 degrees C. Intraoperatively cooling rate was low and a reduction of peripheral temperature associated with metabolic acidosis was noted. After the conclusion of the operation and during transferring the patient to an intensive care unit, multiple ventricular premature beats were noted. Thereafter, ventricular tachycardia developed proceeding ventricular fibrillation. We suggest that careful management of thermal and cardiovascular systems is required to prevent adverse events during mild hypothermic therapy.

Adult↗

PubMed1996

Tedisamil Attenuates Ventricular Fibrillation in a Conscious Canine Model of Sudden Cardiac Death.

BACKGROUND: The electrophysiologic and antifibrillatory properties of tedisamil (KC-8857;3,7-di-(cyclopropylmethyl)-9,9-tetramethylene-3,7-diazabicyclo[3.3.1]-nonane dihydrochloride) were studied in a conscious canine model of sudden cardiac death. METHODS AND RESULTS: Three to five days after surgically induced myocardial infarction (2-hour occlusion of the left anterior descending coronary artery), animals were subjected to programmed electrical stimulation to identify those at risk for ischemia-induced ventricular fibrillation. Sixty minutes after tedisamil (10 mg/kg, administered orally) PES was repeated. Tedisamil increased the ventricular effective refractory period from 106 +/- 6 to 134 +/- 7 ms (P <.05) compared to placebo treatment, which did not alter the ERP (123 +/- 6 to 116 +/- 5 ms). Tedisamil prolonged the QTc interval, from a predrug value of 308 +/- 14 to 327 +/- 14 ms, postdrug. The extent of the surgically induced anterior wall myocardial infarct did not differ between groups, tedisamil, 29 +/- 2%, and placebo, 28 +/- 2% of the left ventricle. CONCLUSIONS: Tedisamil conferred protection against ischemia induced ventricular fibrillation; 7 of 10 tedisamil-treated dogs survived, compared to 4 of 14 surviving in the vehicle treated group (P <.05). Although we observed instances of vomiting and/or diarrhea in several dogs after a single oral administration of tedisamil, the data indicate that oral administration of tedisamil provides protection from ischemia-induced ventricular fibrillation in the postinfarcted conscious canine. The mechanism by which tedisamil achieves its antifibrillatory effect may be related to its ability to prolong the ERP of the ventricular myocardium without altering ventricular conduction velocity.

Journal Article↗

PubMed1978

Ventricular refractoriness during acute myocardial ischaemia and its relationship to ventricular fibrillation.

Studies were made in anaesthetised dog of the effects of repeated acute occlusions of a branch of the anterior descending coronary artery on ventricular refractory periods in adjacent ischaemic and non-ischaemic myocardium. Differences occurred in refractoriness between normal and ischaemic areas in the ventricle. This was greatest 2.5 min after occlusion, and on release of occlusion, ventricular refractory periods reverted to normal within 5 min. Spontaneous ventricular fibrillation was directly and significantly related to the degree of dispersion of refractoriness in a given dog immediately preceding release and following release of occlusion. Infusion of isoprenaline caused significant shortening of refactory period and increased dispersion of refractoriness during ischaemia. Studies of dispersion of refractoriness should prove valuable in assessing the efficiency of metabolic or antiarrhythmic protection against ventricular fibrillation.

Animals↗

PubMed1990

Effect of duration of ventricular fibrillation on defibrillation efficacy in humans.

The currently available automatic implantable cardioverter-defibrillator has proven highly successful for termination of ventricular tachycardia and fibrillation. Newer devices, however, permit lower energy shocks to be delivered initially and longer episodes of arrhythmia to occur before shocks are delivered. These changes may result in longer durations of arrhythmia before successful termination. Little is known about the effects of the duration of ventricular fibrillation on the efficacy of defibrillating shocks. In this study, we examined the efficacy of defibrillating shocks in 22 patients undergoing automatic implantable cardioverter-defibrillator implantation or generator change. Defibrillating shocks ranging from 300 to 600 V (5.9-24.2 J) were delivered in matched pairs after 5 and 15 seconds of ventricular fibrillation. For the 300-V shocks (5.9 J), defibrillation was accomplished in 82% of patients when the shocks were given after 5 seconds of ventricular fibrillation and in only 45% of patients when the shocks were delivered after 15 seconds (p less than 0.01). At higher energies, there was no difference in the efficacy of defibrillation shocks delivered after 5 compared with 15 seconds of ventricular fibrillation. The postshock aortic, systolic, and diastolic blood pressures were significantly lower when the shocks were given after 15 seconds of ventricular fibrillation than after only 5 seconds. We conclude that the duration of ventricular fibrillation affects defibrillation efficacy especially at energies that are relatively low compared with maximal device outputs and that longer episodes of ventricular fibrillation cause more postshock hemodynamic depression. These observations have implications for defibrillation threshold testing at the time of device implantation and for the design and programming of future automatic implantable antitachycardia devices.

Adult↗

PubMed1988

Susceptibility of hypertrophied rat hearts to ventricular fibrillation during acute ischemia.

This study compared arrhythmias induced by acute ischemia in Langendorff preparations of normal and hypertrophied rat hearts. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 6 to 8 weeks prior to study. The ratio of left ventricular weight to body weight (LVW/BW) and systolic blood pressure (SBP) were significantly higher in two groups of rats with hypertrophied hearts (moderate hypertrophy: 2.68 +/- 0.06 mg/g, 182 +/- 3 mmHg; severe hypertrophy: 3.31 +/- 0.03 mg/g, 238 +/- 5 mmHg) than in normal hearts (2.18 +/- 0.03 mg/g, 125 +/- 3 mmHg), while there were no differences in body weights. During 30 min of ischemia produced by left coronary artery occlusion in the Langendorff preparations, ventricular fibrillation occurred in six of 20 (30%) normal, six of nine (67%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied preparations (P less than 0.001 normal vs severely hypertrophied). Tachyarrhythmias occurred in 15 of 20 (75%) normal, eight of nine (89%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied hearts. Heart rate and coronary efflux before and during the ischemic period did not differ between normal and hypertrophied hearts. The ratio of non-perfused to perfused areas of the left ventricle, measured by Evans blue dye staining and with computerized planimetry, also was not different for normal (57.6 +/- 2.3%) and hypertrophied hearts (moderate hypertrophy 62.5 +/- 3.3%, and severe hypertrophy 59.1 +/- 2.0%). Additional control studies using larger hearts from older rats also indicate that myocardial mass was not an important determinant of ischemic arrhythmias in hypertrophy. Prolongation of endocardial and epicardial conduction time during 30 min of ischemia was not different between normal and hypertrophied hearts. Action potential duration and refractory periods were significantly longer in ventricular cells of hypertrophied hearts than in normals, and superfusion with hypoxia/zero glucose solution shortened these parameters to a greater extent in hypertrophied cells. These results lead us to conclude that hypertrophied hearts have a greater susceptibility to ventricular fibrillation during acute ischemia, and that dispersion of refractoriness may play a role in this phenomenon.

Action Potentials↗

PubMed2005

[Characterization of premature ventricular contraction initiating ventricular fibrillation].

UNLABELLED: The aim of this study is to characterize the electrocardiographic features of premature ventricular contractions (PVC) from different anatomical region that trigger ventricular fibrillation (VF). METHODS AND RESULTS: 36 consecutives patients (20 males, 42+/-14 yrs) undergoing VF ablation from 7 centres were studied (22 with idiopathic VF, 4 associated with a long QT syndrome, 3 with Brugada syndrome, 4 with ischaemic cardiomyopathy and 3 associated with other substrate). Mapping of these PVC showed 2 different origins, which were then confirmed by ablation: right ventricular outflow tract (RVOT) (22%) and peripheral Purkinje network (81%). One patient had PVC from both origins (Brugada). RVOT PVC were frequent but had triggered only 5+/-5 episodes of VF for 26+/-33 months. Purkinje PVC were more likely to be present during electrical storm with 18+/-28 episodes of VF for 33+/-45 months. Right Purkinje PVC have a left bundle branch block with superior axis morphology whereas left Purkinje ones have a right bundle branch block. The axis of activation showed variation from inferior to superior depending on the area of origin from the Purkinje network and the exit site to the myocardium. However Purkinje PVC were characterized by short QRS duration (126+/-18 vs 145+/-13ms for RVOT PVC; p=0.05). In addition the coupling interval was significantly shorter compared to RVOT PVC (292+/-45 vs 358+/-37ms respectively; p=0.005). CONCLUSION: PVC initiating VF demonstrate specific electrocardiographic features that facilitate determination of their origin. Ablation of these typical PVC is feasible in order to reduce ICD shock.

Adult↗

PubMed1986

Prevention of ventricular fibrillation by metoprolol in a pig model of acute myocardial ischaemia: absence of a major arrhythmogenic role for cyclic AMP.

Absence of a Major Arrhythmogenic Role for Cyclic AMP. Journal of Molecular and Cellular Cardiology (1986) 18, 375-387. We examined the mechanism whereby beta-adrenoceptor antagonism exerts an antiarrhythmic effect in early myocardial ischaemia. Ligation of the anterior descending coronary artery in the anaesthetized open-chest pig resulted in severe transmural anteroseptal ischaemia. Blood flow in the mid-ischaemic zone 20 min after ligation was decreased to 5.7 +/- 0.7% of the preligation control value. Epicardial ST-segment deflections of 6.7 +/- 0.4 mV were recorded over this zone. A distinct phase of ventricular arrhythmias was evident about 10 to 30 min after ligation. A high incidence of ventricular fibrillation (14/16 pigs) was associated with a circumstantial increase in levels of cyclic AMP in ischaemic tissue. Twenty minute values were: 1.10 +/- 0.06, P less than 0.05 v. the non-ischaemic tissue level of 0.86 +/- 0.05 nmol/g. Propranolol 3 mg/kg IV, metoprolol 20 mg/kg IV or sotalol 10 mg/kg IV were given between 30 min prior to and 10 min after ligation. Adequate beta-adrenoceptor antagonism by each agent could be proven. Metoprolol decreased the incidence of ventricular fibrillation (2/13, P less than 0.0005 v. control group), while propranolol or sotalol did not. All three beta-antagonists decreased tissue levels of cyclic AMP prior to ligation. However, the temporary increase in ischaemic tissue after ligation could not be prevented. Furthermore, cyclic AMP in ischaemic tissue 20 min after ligation was higher in the metoprolol group than in the propranolol or sotalol group (0.94 +/- 0.04 v. 0.81 +/- 0.02 P less than 0.05, and 0.79 +/- 0.03 nmol/g P less than 0.01, respectively). Blood flow in the mid-ischaemic zone of the metoprolol group was increased to 8.6 +/- 0.6% of preligation control value (P less than 0.0001 v. control group). In contrast, blood flow in the mid-ischaemic zone of the propranolol or sotalol group was decreased. Metoprolol also reduced epicardial ST-segment deflections over the mid-ischaemic zone to 3.5 +/- 0.2 mV (P less than 0.0001 v. control group). ST-segment deflections in the propranolol group were increased. The mechanism whereby metoprolol prevented ventricular fibrillation may be explained by a decrease in the severity of ischaemia but not in terms of changes of tissue levels of cyclic AMP.

Acute Disease↗

PubMed1996

Ventricular premature beat-driven intermittent restoration of coronary blood flow reduces the incidence of reperfusion-induced ventricular fibrillation in a cat model of regional ischemia.

With a cat model of regional cardiac ischemia, we examined whether the incidence of reperfusion-induced ventricular fibrillation (VF) could be reduced by ventricular premature beat (VPB)-driven intermittent reperfusion. In addition, we assessed whether the effect of the intermittent reperfusion was comparable with that of ischemic preconditioning in suppressing the VF. Of 15 cats subjected to uninterrupted reperfusion after 20-minute occlusion of the left anterior descending coronary artery, 13 (86.70%) had VF, whereas only 1 (7.1%) of 14 cats subjected to the VPB-driven intermittent reperfusion had VF. This incidence of VF was significantly lower than that of the animal group subjected to uninterrupted reperfusion. However, it was not statistically different from that (3 of 15) of the group subjected to a 10-minute episode of the coronary artery occlusion before the 20-minute occlusion (i.e., "ischermic preconditioning"). Our results suggest that the VPB-driven intermittent reperfusion (i.e., "postconditioning") is very effective in preventing reperfusion-induced VF and as good as, if not better than, ischemic preconditioning.

Animals↗

PubMed2006

Catheter ablation for an incessant form of antiarrhythmic drug-resistant ventricular fibrillation after acute coronary syndrome.

A 77-year-old man was admitted with an acute coronary syndrome (ACS), severe heart failure (HF), and repeated ventricular fibrillation (VF) episodes. A single premature ventricular complex (PVC) induced ventricular tachycardia (VT), which degenerated to VF reproducibly. This PVC was eliminated by catheter ablation at the left ventricular posteroseptal region where double Purkinje potentials preceding the ventricular wave had been recorded. The electrical storm disappeared, and programmable stimulation failed to induce any tachyarrhythmias after the ablation. A Purkinje fiber network-related PVC served as a trigger and as a substrate for VT and VF in a case of ACS with HF.

Aged↗

PubMed1972

Effect of physostigmine on ventricular fibrillation and myocardial glycogen in hypothermic dogs.

1. Physostigmine (0.1 mg/kg i.v.) given at 37 degrees C and 25 degrees C rectal temperatures, completely protected the hypothermic dog heart against ventricular fibrillation.2. Pentolinium, atropine, vagotomy and reserpine did not significantly alter the incidence of ventricular fibrillation.3. The incidence of ventricular fibrillation under hypothermia could be significantly increased by ligating the anterior descending branch of the left coronary artery. The incidence of ventricular fibrillation in coronary ligated hypothermic dogs was reduced to half by physostigmine pretreatment.4. Hypothermia produced ventricular glycogen depletion and physostigmine prevented ventricular glycogenolysis under hypothermia. However, in the normothermic state physostigmine itself produced a significant decrease in cardiac glycogen.5. The relation between the antifibrillatory and antiglycogenolytic effects of physostigmine under hypothermia are discussed.

Animals↗

PubMed1996

Treatment of refractory ventricular fibrillation by combined internal (epicardial) and external (transthoracic) defibrillation.

This report describes a modified defibrillation technique used successfully in a patient with an implanted epicardial cardioverter defibrillator who developed refractory ventricular fibrillation. During operative testing at the time of generator replacement, two episodes of intractable ventricular fibrillation were terminated by using a combined internal (epicardial)-external (transthoracic) defibrillation system that delivered a 360-J shock between the anterior epicardial patch and a large posterior skin electrode.

Defibrillators, Implantable↗