Mechanism of Ventricular Fibrillation in Hypothermia

Covino, Benjamín G.; D'Amato, Henry E.

doi:10.1161/01.res.10.2.148

Cited by 57 publications

(18 citation statements)

References 7 publications

(1 reference statement)

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“…In accordance with these findings, hypothermia of 30°C increased the vulnerability to pacing‐induced ventricular fibrillation by facilitating wave breaks and promoting the onset of ADP alternans in Langendorff‐perfused isolated rabbit hearts . The increased incidence of ventricular fibrillation, which is frequently observed in patients suffering from accidental hypothermia, was also experimentally confirmed in vivo in a porcine model …”

Section: Discussionsupporting

confidence: 73%

Mild hypothermia (33°C) increases the inducibility of atrial fibrillation: An in vivo large animal model study

Manninger

Alogna

Zweiker

et al. 2018

Pacing Clinical Electrophis

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Section: Discussionsupporting

confidence: 73%

Mild hypothermia (33°C) increases the inducibility of atrial fibrillation: An in vivo large animal model study

Manninger

Alogna

Zweiker

et al. 2018

Pacing Clinical Electrophis

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“…Since hypothermia clearly affects the vulnerability of the heart to various arrhythmias (Holland and Klein, 1958;Covino and Damato, 1962;Nielsen and Owman, 1968), it is of interest to know the influence of changes in temperature on the length of the excitation wave. It is well known that cooling prolongs the refractory period and depresses conduction of the cardiac impulse.…”

Section: The Effects Of Temperaturementioning

confidence: 99%

The wavelength of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium. The role of heart rate, autonomic transmitters, temperature, and potassium.

Smeets¹,

Allessie²,

Lammers³

et al. 1986

Circulation Research

288

136

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We measured the wavelength of the cardiac impulse, defined as the distance traveled by the depolarization wave during the functional refractory period, in isolated narrow strips of rabbit atrium. During control, wavelength was 42 mm during pacing with 2 Hz, and was 28 mm at the maximum pacing rate; early premature beats had a wavelength as short as 23 mm. Administration of carbamylcholine (4 X 10(-7) g/ml) shortened the wavelength to 21 mm during 2 Hz, 18 mm at the maximum pacing rate Fmax, and 16 mm during an early premature impulse, respectively. The effects of epinephrine (6 X 10(-7) M) were strongly rate dependent. At slow heart rates, epinephrine clearly prolonged the wavelength (58 mm), whereas, during maximum pacing, wavelength remained unchanged (28 mm). Hypokalemia (2 mM) decreased the length of the impulse at all stimulation frequencies. Moderate hyperkalemia (5.6 and 7.0 mM) did not modify wavelength because refractoriness and conduction velocity were affected proportionally. Above 7.0 mM potassium, the wavelength became progressively prolonged because of the development of post-repolarization refractoriness. Cooling to 27 degrees C resulted in a slight lengthening of the impulse. At lower temperatures, however, wavelength prolonged significantly because of a relatively strong prolongation of the refractory period. In separate experiments in 15 X 20 mm segments of atrium, reentrant tachyarrhythmias were induced and the circuit size compared with the wavelength. The size of intraatrial circuits was similar to the magnitude of the measured wavelength during maximum pacing. Carbamylcholine and hypokalemia, both of which shorten the impulse length, also clearly decreased the size of reentrant circuits. Cooling to 27 degrees C, which affects both refractoriness and conduction velocity, only slightly prolonged the wavelength; accordingly, the size of reentrant circuits at 27 degrees C was only slightly longer than at 37 degrees C. These experiments emphasize the importance of the wavelength of the cardiac impulse in relation to the occurrence of intramyocardial reentry.

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“…The use of hypothermia in clinical practice has, since 1940, been supported by numerous reports from the 50s and 60s [1][2][3][4] . however, the side effects occurred due to its use such as coagulopathy, cardiac arrhythmias, severe pneumonia and metabolic disturbances, led to a decrease in the number of hypothermia procedures as therapeutic practice and a decline in the conventional therapeutic arsenal 5,6 .…”

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confidence: 97%

Selective hypothermia: an experimental study on traumatic brain injury in rats

Dvilevicius

Prandini

2008

Arq. Neuro-Psiquiatr.

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-Objective:To evaluate the efficiency of selective hypothermia in the treatment of the traumatic brain injury in rats. Method: After the trauma produced for the model of cortical impact, a small craniectomy in the right frontoparietal region was carried through; after the procedure the animals had been divided in two groups of 15 each. Group A, without treatment with hypothermia (control group) and group B, treated with selective hypothermia for a period to 5 to 6 hours. After this time all the animals were sacrificed, their brains had been removed and histopathological analysis was carried through. Results: Comparison between both groups was done using the counting of neurons injured for field. Counting in the control group n=15 had an average of 70.80 neurons injured for field against an average of 21.33 neurons injured for field in group B (submitted to the treatment with hypothermia), with n=15 also. The difference was statiscally significant. Conclusion: Based in the quantification of the neurons injured for field, the effectiveness of the treatment with selective hypothermia was demonstrated.Key Words: selective hypothermia, hypothermia, neuroprotection, traumatic brain injury. Hipotermia seletiva: estudo experimental de traumatismo crânio-encefálico em ratosResumo -Objetivo: Avaliar a eficiência da hipotermia seletiva no tratamento do traumatismo crânio-encefálico (TCe) em ratos. o trauma foi produzido por um modelo de impacto cortical desenvolvido exclusivamente para o estudo. Método: Após o TCe produzido pelo modelo de impacto cortical, foi realizada pequena craniectomia na região fronto-parietal direita; após o procedimento os animais foram divididos em dois grupos de 15 cada um. o grupo A, sem tratamento com hipotermia (grupo controle) e grupo B, tratado com hipotermia seletiva por período de 5 a 6 horas. depois deste tempo todos os animais foram sacrificados, seus encéfalos foram removidos e realizada a análise anatomopatológica. Resultados: Na comparação entre o grupo tratado com hipotermia e o grupo controle utilizou-se a contagem de neurônios lesados por campo. Tal contagem no grupo A (controle/sem tratamento) com n=15 teve media de 70,80 neurônios lesados por campo contra a media de 21,33 nerônios lesados por campo no grupo B (submetido ao tratamento com hipotermia), com n=15 também. diferença estatísticamente significativa pôde ser demonstrada. Conclusão: A análise anatomopatológica dos encéfalos dos animais estudados, baseada na quantificação dos neurônios lesados por campo demonstrou efetividade do tratamento com hipotermia seletiva com diferença estatística significativa.PAlAvrAs-ChAve: hipotermia seletiva, hipotermia, neuroproteção, traumatismo crânio-encefálico.

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Mechanism of Ventricular Fibrillation in Hypothermia

Cited by 57 publications

References 7 publications

Mild hypothermia (33°C) increases the inducibility of atrial fibrillation: An in vivo large animal model study

Mild hypothermia (33°C) increases the inducibility of atrial fibrillation: An in vivo large animal model study

The wavelength of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium. The role of heart rate, autonomic transmitters, temperature, and potassium.

Selective hypothermia: an experimental study on traumatic brain injury in rats

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