Vulnerability of Canine Ventricle to Fibrillation During Hypoxia and Respiratory Acidosis

Rogers, Robert M.; Spear, Joseph F.; Moore, E. Neil; Ln, Horowitz; Sonne, J.E.

doi:10.1378/chest.63.6.986

Cited by 42 publications

(18 citation statements)

References 29 publications

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“…Hypoxemia and hypercapnia themselves are arrhythmogenic. 22,23 Nocturnal increases in sympathetic activation persist during wakefulness in patients with OSA, 24 and increased sympathetic drive is associated with AF. 25,26 The forceful ventilatory efforts against upper airway obstruction during apneas result in dramatic shifts in transmural pressures and measurable changes in cardiac chamber dimensions.…”

Section: Discussionmentioning

confidence: 99%

Association of atrial fibrillation and obstructive sleep apnea

Gami¹,

Pressman²,

Caples³

2004

ACC Current Journal Review

178

213

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Background-Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion.OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown. Methods and Results-We prospectively studied consecutive patients undergoing electrocardioversion for AF (nϭ151) and consecutive patients without past or current AF referred to a general cardiology practice (nϭ312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and 2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, Pϭ0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, Pϭ0.0006). Conclusions-The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.

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Section: Discussionmentioning

confidence: 99%

Association of atrial fibrillation and obstructive sleep apnea

Gami¹,

Pressman²,

Caples³

2004

ACC Current Journal Review

178

213

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“…During asphyxia spontaneous ventricular fibrillation occurs in about one-third the number of trials (Coffman & Gregg, 1960). On the other hand systemic hypoxaemia neither predisposes to spontaneous ventricular fibrillation (Badeer & Howarth, 1959) nor does it lower the VFT (Rogers et al, 1973). As indicated by this study, lack of 02 induced by gassing the McEwen's solution with 5% CO2 in N2 or air lowers the VFT in the rabbit isolated perfused heart.…”

Section: Discussionmentioning

confidence: 57%

“…Coffman & Gregg (1960) showed that asphyxia induced by tracheal occlusion produced ventricular fibrillation in one third of their dogs and Szekeres & Papp (1967) found that ventilation with 5-10% 02 lowered the VFT in the cat. On the other hand Badeer & Howarth (1959) showed that ventilation with 100% N2 failed to induce ventricular fibrillation in dogs and Turnbull, MacLean, Dobell & Demers (1965) ventilating dogs with 5-10% 02 and Rogers, Spear, Moore, Horowitz & Sonne (1973) using 10-16% 02 could detect no significant change produced on the VFT. These results appear to confirm the suggestion that a boundary or trigger zone between normal and hypoxic myocardium was important for initiating and maintaining cardiac arrhythmias (Harris, 1948).…”

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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“…The resistance of the heart to these disorders is dependent on its electrical stability, which can be measured by several parameters such as the duration of the vulnerable period (Wegria et al, 1941;Axelrod et al, 1975), ventricular flutter threshold (Szekeres & Papp, 1967), excitability threshold (Jones & Klein, 1982), or ventricular fibrillation threshold (Wegria et al, 1941;Gerst et al, 1966). Factors that contribute to the development of various cardiac disorders not only include local myocardial ischemia (Ferrier et al, 1985;Saint et al, 1992), but also hypoxia (Nishimura et al, 1989) and respiratory and metabolic acidosis (Gerst et al, 1966;Rogers et al, 1973;Kujanik et al, 1984;1985). It is generally accepted that some disorders of pulmonary ventilation belong to the group of proarrhythmogenic factors.…”

Section: Introductionmentioning

confidence: 99%

“…In experiments conducted by Gerst et al (1966) using dogs, pH changes owing to respiratory acidosis and alkalosis did not affect the electrical stability of the heart, measured by VFT. Neither respiratory acidosis nor hypoxia alone significantly changed the VFT, but together they increased the followed parameter in the canine ventricle (Rogers et al, 1973). Kujanik et al (1985) described dynamic changes of the VFT in rats with various types of ventilation, but not its circadian dependence.…”

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confidence: 99%