Ventricular fibrillation as a cause of sudden death in coronary artery thrombosis

Smith, Fred. J.

doi:10.1016/s0002-8703(39)90441-2

Cited by 14 publications

(1 citation statement)

References 17 publications

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“…There is a considerable body of undisputed evidence that a localized area of ischaemia with a resultant anoxia of that part of the heart muscle produced experimentally by occlusion of a coronary artery in animals (Harris, 1948;Chardack, Gage, Frederico, Cusick, Matsumoto & Lanphier, 1964) or occurring spontaneously in man (Miller, 1939;Smith, 1939) gives rise to ventricular arrhythmias including fibrillation and also lowers the ventricular fibrillation threshold (VFT) of the infarcted area (Wiggers, Wegria & Pinera, 1940;Shumway, Johnson & Stish, 1957;Han, 1969). However, the experimental results obtained where there is a generalized hypoxia of the animal are contradictory.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Anoxia on the Ventricular Fibrillation Threshold in the Rabbit Isolated Heart

Murnaghan

1975

British J Pharmacology

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The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37° C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. Gassing the McEwen's solution with 5% CO2 in N2 (anoxia) instead of with carbogen caused a negative inotropic and chronotropic effect and significantly lowered the VFT. Although anoxia releases noradrenaline from the heart the effect of anoxia on the VFT was not prevented by β‐adrenoceptor blockade with propranolol or pindolol or by previous treatment with reserpine. Perfusion with adenosine (5 μM) which is released from the heart muscle by anoxia, or with dipyridamole (10 μM) which protects the adenosine from binding or destruction by the tissues, or with both combined failed to alter the VFT significantly. Furthermore neither adenosine nor dipyridamole significantly altered the effect of anoxia on the VFT. Anoxia, adenosine and dipyridamole significantly increased the duration of the induced arrhythmia when compared with that of the controls. Anoxia and adenosine significantly shortened the vulnerable time, i.e. the minimal time after the R‐wave of the ECG at which the pulse had to be applied to induce the arrhythmia. Perfusion with the McEwen's solution gassed with 5% CO2 in air (hypoxia) significantly lowered the VFT but the effect was not as great as with anoxia. Isoprenaline when infused lowered the VFT but this effect was not potentiated by hypoxia. The results indicate that (a) anoxia lowers the VFT in the perfused isolated heart of the rabbit and that this effect is not due to adenosine or noradrenaline released by the anoxia and (b) hypoxia does not sensitize the heart to the arrhythmic effect of isoprenaline.

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Section: Introductionmentioning

confidence: 99%

The Effect of Anoxia on the Ventricular Fibrillation Threshold in the Rabbit Isolated Heart

Murnaghan

1975

British J Pharmacology

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Ventricular Fibrillation Causing Sudden Death of a Patient With Disease of the Left Coronary Artery

Thompson¹

1941

JAMA

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RESULTSIn acute attacks the effect of the treatment is amazing. Patients who have been disabled by acute sprains or acute muscular spasm often regain the full use of the affected parts immediately. The pain frequently does not recur in cases of minor involvement and rarely recurs in full intensity in those of more serious involvement. Two to four treatments usually suffice to bring about, even in more serious cases, a minimum degree of discomfort. Thus, in all cases the period of disability is reduced drastically. Atrophy of the muscles involved does not develop to the same degree as when immobilization is employed. Swelling is more readily absorbed. Patients treated by this method are less apt to sustain the same injury again than those treated by immobilization. The same holds true for chronic and "rheumatic" conditions, although a longer period of treatment is usually required in those cases.As a means of aiding in diagnosis and in the evaluation of roentgenograms, this treatment is of great value. Further analysis and experience will be needed to establish general rules. As compared with the injection of procaine hydrochloride into the muscles and ligaments (Leriche4), this method shows the following advantages :1. Application is simpler.2. Repeated application is possible, with less difficulty and risk.3. Large areas can be controlled which otherwise would call for the use of vast quantities of procaine hydrochloride.4. It does not work when fractures or tears are present ; thus it is less dangerous and more selective.5. It is more advantageous in its use as a diagnostic means, being more selective.6. There is less risk of a local after-effect and no general after-effect such as is sometimes seen after the administration of procaine hydrochloride.7. There is no danger of infection. THEORYPayr 5 described the "chain effect of painful muscle spasm." He described how pain, originating in one portion of the sensory motor chain, leads to reflex muscular spasm and locking of joints. This chain consists of the following elements : sensory nerve, nerve center, motoric nerve, muscle and sensory nerve. Pain originating in the course of this chain leads to muscular spasm. The spasm is in itself painful and leads to more spasm. Elimination of pain at any point of the chain results in the breaking of the chain and therefore in relaxation of the muscular spasm. This may be achieved directly by the injection of an anesthetic into the muscle, joint, ligament, sensory nerve or spinal cord.If the pain-free interval is used to restore the muscle to normal function, the spasm does not recur or recurs with much less intensity. Empirically, on the basis of this chain, cutaneous anesthesia similarly relieves the deep-seated pain in muscular spasm.I have no explanation to offer as to how this deep effect of surface anesthesia works. It seems to be a fact, but the underlying physiologic explanation presents an interesting field for exploration. It must be definitely understood that in no case will the ethyl chloride alone, without a...

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Die Coronarerkrankungen. Coronarinsuffizienz, Angina pectoris und Herzinfarkt

Schimert¹,

Schimmler²,

Schwalb³

et al. 1960

Angeborene Herz- Und Gefässmissbildungen Durchblutungsstörungen Des Herzmuskels

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Ventricular fibrillation as a cause of sudden death in coronary artery thrombosis

Cited by 14 publications

References 17 publications

The Effect of Anoxia on the Ventricular Fibrillation Threshold in the Rabbit Isolated Heart

The Effect of Anoxia on the Ventricular Fibrillation Threshold in the Rabbit Isolated Heart

Ventricular Fibrillation Causing Sudden Death of a Patient With Disease of the Left Coronary Artery

Die Coronarerkrankungen. Coronarinsuffizienz, Angina pectoris und Herzinfarkt

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