Profound bradycardia with lidocaine during anesthesia induction in a silent sick sinus syndrome patient

Kim, Kyoung Ok; Chung, Sung-Soo; Lee, Kyoungjin; Cho, Hun

doi:10.1016/j.jclinane.2010.01.008

Cited by 11 publications

(7 citation statements)

References 14 publications

(14 reference statements)

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“…before propofol for pain reduction. 84 a-2 adrenoreceptor agonists are better avoided, as they may induce sinus arrest, junctional bradycardia, and atrioventricular block. 44 85 In most of the case reports of SSS-related complications, vecuronium was used for neuromuscular block.…”

Section: Anaesthetic Considerationsmentioning

confidence: 99%

Perioperative management of hereditary arrhythmogenic syndromes

Staikou

Chondrogiannis

Mani

2012

British Journal of Anaesthesia

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Patients with inherited cardiac channel disorders are at high risk of perioperative lethal arrhythmias. Preoperative control of symptoms and a multidisciplinary approach are required for a well-planned management. Good haemodynamic monitoring, adequate anaesthesia and analgesia, perioperative maintenance of normocarbia, normothermia, and normovolaemia are important. In congenital long QT syndrome, torsades de pointes should be prevented with magnesium sulphate infusion and avoidance of drugs such as droperidol, succinylcholine, ketamine, and ondansetron. Propofol and epidural anaesthesia represent safe choices, while caution is needed with volatile agents. In Brugada syndrome, β-blockers, α-agonists, and cholinergic drugs should be avoided, while isoproterenol reverses the ECG changes. Propofol, thiopental, and volatiles have been used uneventfully. In congenital sick sinus syndrome, severe bradycardia resistant to atropine may require isoproterenol or epinephrine. Anaesthetics with vagolytic properties are preferable, while propofol and vecuronium should be given with caution due to risk of inducing bradyarrhythmias. Neuraxial anaesthesia should produce the least autonomic imbalance. Arrhythmogenic right ventricular dysplasia/cardiomyopathy induces ventricular tachyarrhythmias, which should be treated with β-blockers. Generally, β-adrenergic stimulation and catecholamine release should be avoided. Halothane and pancuronium are contraindicated, while large doses of local anaesthetics and epinephrine should be avoided in neuraxial blocks. In catecholaminergic polymorphic ventricular tachycardia, β-blocker treatment should be continued perioperatively. Catecholamine release and β-agonists, such as isoproterenol, should be avoided. Propofol and remifentanil are probably safe, while halothane and pancuronium are contraindicated. Regional anaesthesia, without epinephrine, is relatively safe. In suspicious cardiac deaths, postmortem examination and familial screening are recommended.

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Section: Anaesthetic Considerationsmentioning

confidence: 99%

Perioperative management of hereditary arrhythmogenic syndromes

Staikou

Chondrogiannis

Mani

2012

British Journal of Anaesthesia

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“…18) , suggesting that functional voltage-gated Na + current (I Na ) may be necessary for maintaining human SAN pacemaking and conduction. Furthermore, although antiarrhythmic drugs that block Nav have been shown to inadvertently unmask SND in patients predisposed to the arrhythmia [19][20][21] , no study has determined the specific Nav isoform(s) mediating this detrimental effect on the human SAN. Hence, there is a critical need to determine the functional contributions of Nav channels in maintaining SAN robustness, by studying their role directly in the unique 3D human SAN complex [2][3][4] .…”

mentioning

confidence: 99%

Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

Kalyanasundaram

Hansen

et al. 2020

Nat Commun

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Mechanisms for human sinoatrial node (SAN) dysfunction are poorly understood and whether human SAN excitability requires voltage-gated sodium channels (Nav) remains controversial. Here, we report that neuronal (n)Nav blockade and selective nNav1.6 blockade during high-resolution optical mapping in explanted human hearts depress intranodal SAN conduction, which worsens during autonomic stimulation and overdrive suppression to conduction failure. Partial cardiac (c)Nav blockade further impairs automaticity and intranodal conduction, leading to beat-to-beat variability and reentry. Multiple nNav transcripts are higher in SAN vs atria; heterogeneous alterations of several isoforms, specifically nNav1.6, are associated with heart failure and chronic alcohol consumption. In silico simulations of Nav distributions suggest that I Na is essential for SAN conduction, especially in fibrotic failing hearts. Our results reveal that not only cNav but nNav are also integral for preventing disease-induced failure in human SAN intranodal conduction. Disease-impaired nNav may underlie patient-specific SAN dysfunctions and should be considered to treat arrhythmias.

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“…[ 8 ] Profound bradycardia was observed with a small dose of lignocaine given intravenously prior to propofol. [ 18 ] Hence, we chose to use morphine and thiopentone for induction and sevoflurane for maintenance of anesthesia. Muscle fasciculation produced by succinylcholine can be avoided by using nondepolarizing muscle relaxants.…”

Section: Discussionmentioning

confidence: 99%

Role of temporary pacing at the right ventricular outflow tract in anesthetic management of a patient with asymptomatic sick sinus syndrome

et al. 2015

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A 60-year-old woman posted for percutaneous nephrolithotomy with ureterolithotripsy was found to have a history of hypertension and ischemic heart disease from past 6 months on regular treatment. Pulse rate was irregularly irregular in a range of 56–60/min, unresponsive to atropine, with a sinus pause on the electrocardiogram. Although the patient was asymptomatic, anticipating unmasking of the sick sinus syndrome during general anesthesia in the prone position, a temporary pacemaker was implanted at right ventricular outflow tract (RVOT) septum before the scheduled surgery. A balanced anesthesia technique with endotracheal intubation was administered. There were several episodes of continuous pacing by the temporary pacemaker intraoperatively, which may be attributed to unmasking of the sinus node dysfunction due to general anesthesia. At the end of surgery, patient was extubated after adequate reversal from neuromuscular blockade. Postoperative period remained uneventful, and the pacemaker wires were removed on the 2nd postoperative day. With this case report, we highlight the importance of inserting a temporary pacemaker prior to anesthesia even in an asymptomatic patient if a sinus node dysfunction is suspected preoperatively and if intraoperative access to transvenous pacing is difficult such as in prone position. Pacing at RVOT septum minimizes ventricular dyssynchrony and improves hemodynamic parameters.

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Profound bradycardia with lidocaine during anesthesia induction in a silent sick sinus syndrome patient

Cited by 11 publications

References 14 publications

Perioperative management of hereditary arrhythmogenic syndromes

Perioperative management of hereditary arrhythmogenic syndromes

Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

Role of temporary pacing at the right ventricular outflow tract in anesthetic management of a patient with asymptomatic sick sinus syndrome

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