Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade

Alboni, Paoló; Shantha, Narasimhan; Filippi, Laura; Pirani, Roberto; Preziosi, S; Tomasi, A; Masoni, A

doi:10.1016/0002-8703(84)90750-6

Cited by 20 publications

(5 citation statements)

References 31 publications

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“…Bradycardia and atrioventricular block are thought to be mediated by the autonomic nervous system, via vagotonic effects, anti-adrenergic effects, or both [14,15]. There also appears to be a depressant effect on intrinsic sinus nodal automaticity not accounted for by pharmacologic blockade of the sympathetic and parasympathetic nervous systems [16].…”

Section: Is This Patient's Cardiotoxicity a Results Of Digoxin? Hyperkmentioning

confidence: 99%

Case files of the medical toxicology fellowship of the California poison control system—San Francisco: Calcium plus digoxin—More taboo than toxic?

Erickson

Olson

2008

J. Med. Toxicol.

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What are the effects of elevated potassium on the heart? As in other tissues, most sodium in the myocardium is extracellular, and most potassium is intracellular. The concentrations of each are maintained by the Na ϩ -K ϩ -ATPase pump and are also dependent on the relative permeability of the cell surface to migration of Na ϩ or K ϩ down their respective concentration gradients. In a normal cardiac cell, the resting potential during diastole is approximately Ϫ90 mV. If Na ϩ enters the cell, the electrical potential becomes less negative; conversely, if K ϩ leaves the cell the transmembrane potential becomes more negative [1,2].Electrical signals are propagated through the heart by action potentials that open voltage-gated sodium channels, allowing rapid influx of Na ϩ and depolarization of the cell (phase 0), as depicted in Figure 1. The rate of rise of phase 0 is directly proportional to the number of sodium channels that are opened during depolarization. The more negative the resting membrane potential at the start of phase 0, the greater the number of Na ϩ channels in the "ready-to-open" state. Conversely, if the resting membrane potential is less negative than normal, fewer Na ϩ channels are ready to open and depolarization will be less robust, with reduced upstroke velocity (V max ), reduced action potential amplitude, and reduced conduction velocity.As the membrane potential reaches Ϫ40 to Ϫ45 mV during phase 0 depolarization, voltage-gated calcium channels are opened, allowing calcium entry. At about the same time, potassium channels open and allow potassium to exit the cell, balancing the influx of calcium. Together, the opposing effects of calcium influx

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Section: Is This Patient's Cardiotoxicity a Results Of Digoxin? Hyperkmentioning

confidence: 99%

Case files of the medical toxicology fellowship of the California poison control system—San Francisco: Calcium plus digoxin—More taboo than toxic?

Erickson

Olson

2008

J. Med. Toxicol.

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“…The trial demonstrated reduced hospitalizations in patients with reduced LVEF and SR but no reduction in mortality was confirmed [117]. When administrated to AF patients, ventricular rate slowing is caused by a parasympathetic effect [118]. A multivariate analysis of the AFFIRM trial, after correcting for clinical characteristics and comorbidities, regardless of gender and the presence or absence of HF, revealed a significant increase in all-cause mortality in AF patients [119].…”

Section: Pharmacological Rate Control Therapymentioning

confidence: 91%

Pharmacologic Rate versus Rhythm Control for Atrial Fibrillation in Heart Failure Patients

et al. 2022

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Atrial fibrillation (AF) and Heart failure (HF) constitute two frequently coexisting cardiovascular diseases, with a great volume of the scientific research referring to strategies and guidelines associated with the best management of patients suffering from either of the two or both of these entities. The common pathophysiological paths, the adverse outcomes, the hospitalization rates, and the mortality rates that occur from various reports and trials indicate that a targeted therapy to the common background of these cardiovascular conditions may reverse the progression of their interrelating development. Among other optimal treatments concerning the prevalence of both AF and HF, the introduction of rhythm and rate control strategies in the guidelines has underlined the importance of sinus rhythm and heart rate control in the prevention of deleterious complications. The use of these strategies in the clinical practice has led to a debate about the superiority of rhythm versus rate control. The current guidelines as well as the published randomized trials and studies have not proved that rhythm control is more beneficial than the rate control treatments in the terms of survival, all-cause mortality, hospitalization rates, and quality of life. Therefore, the current therapeutic strategy is based on the therapy guidelines and the clinical judgment and experience. The aim of this review was to elucidate the endpoints of pharmacologic randomized clinical trials and the clinical data of each antiarrhythmic or rate-limiting medication, so as to promote their effective, individualized, evidence-based clinical use.

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“…15 Among unoperated adults with sinus bradycardia, the sinus node-depressant effects of antiarrhythmic drugs may vary depending upon whether intrinsic sinus node function is normal or abnormal.12, [41][42][43] Previous discussion of patients postoperative Mustard, Senning, or Fontan operation who present with sinus node dysfunction has focused upon the possibility of direct or indirect injury to the sinus node during operation-at the time of cannulation or during atrial surgery. 1 -4 , 4 4 , 4 5 It is interesting that in a recent report only one of seven adults who underwent sinus node resection or isolation as treatment for atrial tachycardia required pacing for symptomatic b r a d y~a r d i a .~~ It may be that a wider area of atrial tissue excision or injury is necessary to cause sinus brady~ardia.~' With regard to the occurrence of autonomic dysfunction following atrial surgery, experimental excision of the sinus node and crista terminalis or chronic embolization of the sinus node artery in the dog have been shown to alter parasympathetic control of subsidiary pacemaker f u n~t i o n .~~-~O It is conceivable that the extensive intra-atrial surgery involved in the Mustard/Senning and/or Fontan procedures may induce changes in cardiac autonomic control o r response.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade–B. Marcus Et Al.: Postoperative intrinsic sinus node evaluation

Marcus

Gillette

Garson

1991

Clinical Cardiology

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Summary:Sinus node dysfunction is a recognized problcni following surgery for congenital heart disease. Seven postoperative patients with sinus node dysfunction (5 Mustard, 1 tetralogy of Fallot, 1 Fontan) underwent electrophysiology study of sinus node function during combined autonomic blockade (CAB) utilizing propranolol 0.2 nigikg iv and atropine 0.04 mg/kg iv to evaluate intrinsic sinus node function isolated from autonomic control. During CAB, intrinsic heart rate, intrinsic corrected sinus node recovery time, and intrinsic sinoatrial recovery time were measured. These results were compared with age-matched normal intrinsic data from our lab [normal (n=7, mean age 9 years) IHR 128f24, intrinsic corrected sinus node recovery time 135_+40 ms, intrinsic sinoatrial conduction time 86 f 19 ms]. Among postoperative Mustard patients (n=S, mean age 13 years, mean years postoperative 11) 2 of 5 had clearly abnormal intrinsic sinus node function with nonsinus rhythm during CAB: 3 of S had sinus rhythm during CAB with normal or mildly abnormal intrinsic sinus node function. The postoperative case of tetralogy of Fallot (age 20 years, postoperative 14 years) had mildly abnormal intrinsic sinus node electrophysiology study. The postoperative case of Fontan (age 16 years, postoperative 1 .S years) had sinus rhythm at rest but left atrial rhythm during CAB. Different aspects of sinus node dysfunction may be expressed during resting electrophysiology study vs. electrophysiology study utilizing CAB. The pathophysiology of sinus node dysfunction among postoperative pediatric patients is not homogeneous with regard to the contribution of intrinsic sinus node dysfunction. In those patients with normal or mildly abnormal intrinsic sinus node function, an important pathophysiologic influence of the autonomic nervous system is implicated.

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Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade

Cited by 20 publications

References 31 publications

Case files of the medical toxicology fellowship of the California poison control system—San Francisco: Calcium plus digoxin—More taboo than toxic?

Case files of the medical toxicology fellowship of the California poison control system—San Francisco: Calcium plus digoxin—More taboo than toxic?

Pharmacologic Rate versus Rhythm Control for Atrial Fibrillation in Heart Failure Patients

Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade–B. Marcus Et Al.: Postoperative intrinsic sinus node evaluation

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