COMPARISON OF THE DOMINANT FREQUENCY OF VENTRICULAR-FIBRILLATION, INDUCED UNDER DIFFERENT CONDITIONS IN THE ANESTHETIZED DOG

AAJ ADGEY, JD ALLEN, J ANDERSON, EJF CARLISLE, George Kernohan

Research output: Contribution to journalArticle

Abstract

Using power spectral analysis, we have examined the frequency content ofdifferent types of ventricular fibrillation (VF). Greyhound dogs were anaesthetizedwith sodium pentobarbitone (30-35 mg/kg i.v.) and ventilated with room air. Thee.c.g. of VF was recorded (lead 2, Hellige) with an A-D converter on cassette tape(Loughlin, 1983), and analysed offline by use of the Fast Fourier Transform (Brueland Kjaer Spectrum Analyzer Type 2031). The frequency limits (-3 dB) for thesystem were 04-55 Hz. The dominant frequency of the VF (1-41 s), induced in thespecified way, is given for each group (mean+s.E. of mean).In Group 1 the dominant frequency of VF after rapid electrical stimulation of thenormal heart was initially 99 ±0 7 Hz (N = 5: limb lead II), remained above 9 Hzfor 70 s, and then fell in the next 20 s to about 5 Hz. In contrast the frequency ofVF recorded from an endocardial catheter in the right ventricle (Group 1) remainedhigh for several minutes.In VF induced by the slow i.v. administration of ouabain (6-8 ± 1-3 Hz, N = 4), orthe rapid administration of KCl into the pulmonary artery (4-8 ± 0-8 Hz, N = 5), thedominant frequencies were always significantly lower than in Group 1 (P <0 05).When VF developed after acute coronary occlusion (12-3 ±02 Hz, N = 9) thefrequency of VF recorded from an epicardial electrode over the ischaemic zone wassignificantly lower than that recorded from lead II. VF after reperfusion of acutelyischaemic myocardium (I2-2 ±04 Hz, N = 5), or electrical stimulation of the heartin the presence of acute ischaemia (11-7 ±0-5 Hz, N = 4), showed similar frequencies.Hyperkalaemia and toxic doses of ouabain, which reduce membrane potential,cause lower frequencies of fibrillation. This suggests that ionic movements throughfast Na channels may be required for the initially high frequencies seen in the otherforms of VF. As VF persists in the normal heart, a difference in frequency developsbetween the endocardium and the myocardium.
LanguageEnglish
PagesP24
JournalJournal of Physiology
Volume381
Publication statusPublished - Dec 1986

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Ventricular Fibrillation
Dogs
Ouabain
Electric Stimulation
Myocardium
Endocardium
Hyperkalemia
Poisons
Coronary Occlusion
Fourier Analysis
Pentobarbital
Membrane Potentials
Pulmonary Artery
Reperfusion
Heart Ventricles
Electrodes
Ischemia
Catheters
Extremities
Sodium

Cite this

@article{320d816ffeec4977ad15316a6779be22,
title = "COMPARISON OF THE DOMINANT FREQUENCY OF VENTRICULAR-FIBRILLATION, INDUCED UNDER DIFFERENT CONDITIONS IN THE ANESTHETIZED DOG",
abstract = "Using power spectral analysis, we have examined the frequency content ofdifferent types of ventricular fibrillation (VF). Greyhound dogs were anaesthetizedwith sodium pentobarbitone (30-35 mg/kg i.v.) and ventilated with room air. Thee.c.g. of VF was recorded (lead 2, Hellige) with an A-D converter on cassette tape(Loughlin, 1983), and analysed offline by use of the Fast Fourier Transform (Brueland Kjaer Spectrum Analyzer Type 2031). The frequency limits (-3 dB) for thesystem were 04-55 Hz. The dominant frequency of the VF (1-41 s), induced in thespecified way, is given for each group (mean+s.E. of mean).In Group 1 the dominant frequency of VF after rapid electrical stimulation of thenormal heart was initially 99 ±0 7 Hz (N = 5: limb lead II), remained above 9 Hzfor 70 s, and then fell in the next 20 s to about 5 Hz. In contrast the frequency ofVF recorded from an endocardial catheter in the right ventricle (Group 1) remainedhigh for several minutes.In VF induced by the slow i.v. administration of ouabain (6-8 ± 1-3 Hz, N = 4), orthe rapid administration of KCl into the pulmonary artery (4-8 ± 0-8 Hz, N = 5), thedominant frequencies were always significantly lower than in Group 1 (P <0 05).When VF developed after acute coronary occlusion (12-3 ±02 Hz, N = 9) thefrequency of VF recorded from an epicardial electrode over the ischaemic zone wassignificantly lower than that recorded from lead II. VF after reperfusion of acutelyischaemic myocardium (I2-2 ±04 Hz, N = 5), or electrical stimulation of the heartin the presence of acute ischaemia (11-7 ±0-5 Hz, N = 4), showed similar frequencies.Hyperkalaemia and toxic doses of ouabain, which reduce membrane potential,cause lower frequencies of fibrillation. This suggests that ionic movements throughfast Na channels may be required for the initially high frequencies seen in the otherforms of VF. As VF persists in the normal heart, a difference in frequency developsbetween the endocardium and the myocardium.",
author = "AAJ ADGEY and JD ALLEN and J ANDERSON and EJF CARLISLE and George Kernohan",
note = "abstract only",
year = "1986",
month = "12",
language = "English",
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journal = "Journal of Physiology",
issn = "0022-3751",

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COMPARISON OF THE DOMINANT FREQUENCY OF VENTRICULAR-FIBRILLATION, INDUCED UNDER DIFFERENT CONDITIONS IN THE ANESTHETIZED DOG. / ADGEY, AAJ; ALLEN, JD; ANDERSON, J; CARLISLE, EJF; Kernohan, George.

In: Journal of Physiology, Vol. 381, 12.1986, p. P24.

Research output: Contribution to journalArticle

TY - JOUR

T1 - COMPARISON OF THE DOMINANT FREQUENCY OF VENTRICULAR-FIBRILLATION, INDUCED UNDER DIFFERENT CONDITIONS IN THE ANESTHETIZED DOG

AU - ADGEY, AAJ

AU - ALLEN, JD

AU - ANDERSON, J

AU - CARLISLE, EJF

AU - Kernohan, George

N1 - abstract only

PY - 1986/12

Y1 - 1986/12

N2 - Using power spectral analysis, we have examined the frequency content ofdifferent types of ventricular fibrillation (VF). Greyhound dogs were anaesthetizedwith sodium pentobarbitone (30-35 mg/kg i.v.) and ventilated with room air. Thee.c.g. of VF was recorded (lead 2, Hellige) with an A-D converter on cassette tape(Loughlin, 1983), and analysed offline by use of the Fast Fourier Transform (Brueland Kjaer Spectrum Analyzer Type 2031). The frequency limits (-3 dB) for thesystem were 04-55 Hz. The dominant frequency of the VF (1-41 s), induced in thespecified way, is given for each group (mean+s.E. of mean).In Group 1 the dominant frequency of VF after rapid electrical stimulation of thenormal heart was initially 99 ±0 7 Hz (N = 5: limb lead II), remained above 9 Hzfor 70 s, and then fell in the next 20 s to about 5 Hz. In contrast the frequency ofVF recorded from an endocardial catheter in the right ventricle (Group 1) remainedhigh for several minutes.In VF induced by the slow i.v. administration of ouabain (6-8 ± 1-3 Hz, N = 4), orthe rapid administration of KCl into the pulmonary artery (4-8 ± 0-8 Hz, N = 5), thedominant frequencies were always significantly lower than in Group 1 (P <0 05).When VF developed after acute coronary occlusion (12-3 ±02 Hz, N = 9) thefrequency of VF recorded from an epicardial electrode over the ischaemic zone wassignificantly lower than that recorded from lead II. VF after reperfusion of acutelyischaemic myocardium (I2-2 ±04 Hz, N = 5), or electrical stimulation of the heartin the presence of acute ischaemia (11-7 ±0-5 Hz, N = 4), showed similar frequencies.Hyperkalaemia and toxic doses of ouabain, which reduce membrane potential,cause lower frequencies of fibrillation. This suggests that ionic movements throughfast Na channels may be required for the initially high frequencies seen in the otherforms of VF. As VF persists in the normal heart, a difference in frequency developsbetween the endocardium and the myocardium.

AB - Using power spectral analysis, we have examined the frequency content ofdifferent types of ventricular fibrillation (VF). Greyhound dogs were anaesthetizedwith sodium pentobarbitone (30-35 mg/kg i.v.) and ventilated with room air. Thee.c.g. of VF was recorded (lead 2, Hellige) with an A-D converter on cassette tape(Loughlin, 1983), and analysed offline by use of the Fast Fourier Transform (Brueland Kjaer Spectrum Analyzer Type 2031). The frequency limits (-3 dB) for thesystem were 04-55 Hz. The dominant frequency of the VF (1-41 s), induced in thespecified way, is given for each group (mean+s.E. of mean).In Group 1 the dominant frequency of VF after rapid electrical stimulation of thenormal heart was initially 99 ±0 7 Hz (N = 5: limb lead II), remained above 9 Hzfor 70 s, and then fell in the next 20 s to about 5 Hz. In contrast the frequency ofVF recorded from an endocardial catheter in the right ventricle (Group 1) remainedhigh for several minutes.In VF induced by the slow i.v. administration of ouabain (6-8 ± 1-3 Hz, N = 4), orthe rapid administration of KCl into the pulmonary artery (4-8 ± 0-8 Hz, N = 5), thedominant frequencies were always significantly lower than in Group 1 (P <0 05).When VF developed after acute coronary occlusion (12-3 ±02 Hz, N = 9) thefrequency of VF recorded from an epicardial electrode over the ischaemic zone wassignificantly lower than that recorded from lead II. VF after reperfusion of acutelyischaemic myocardium (I2-2 ±04 Hz, N = 5), or electrical stimulation of the heartin the presence of acute ischaemia (11-7 ±0-5 Hz, N = 4), showed similar frequencies.Hyperkalaemia and toxic doses of ouabain, which reduce membrane potential,cause lower frequencies of fibrillation. This suggests that ionic movements throughfast Na channels may be required for the initially high frequencies seen in the otherforms of VF. As VF persists in the normal heart, a difference in frequency developsbetween the endocardium and the myocardium.

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SP - P24

JO - Journal of Physiology

T2 - Journal of Physiology

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