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Background: Dexmedetomidine, an alpha 2 agonist, has emerged as a desirable sedative agent in the pediatric intensive care unit due to its minimal effect on respiratory status and reduction in delirium. Bradycardia and hypotension are common side effects, however there are emerging reports of more serious cardiovascular events, including sinus arrest and asystole. These case reports have been attributed to high vagal tone or underlying cardiac conduction dysfunction. Objectives: To describe the development of sinus arrest during sedation with dexmedetomidine in a patient without clinical features of high vagal tone, underlying cardiac conduction dysfunction, or intervening episodes of bradycardia. Case Presentation: An 11 month-old patient requiring sedation during mechanical ventilation for acute respiratory failure secondary to Adenovirus. To facilitate sedation, a dexmedetomidine infusion was initiated at .5 mcg/kg/hr and increased to maximum 1 mcg/kg/hr. Within 8 hours of initiating therapy, the patient had three episodes of sinus arrest. There was no intervening bradycardia between episodes and no further episodes occurred following discontinuation of dexmedetomidine. The patient did not have any clinical features associated with high vagal tone or underlying cardiac conduction dysfunction. Conclusions: As result of these findings, understanding risk factors for bradycardia, or more serious hemodynamic instability with dexmedetomidine infusions, is important to help identify high risk patients and weigh the associated risks and benefits of its administration., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ticagrelor is a potent reversible P2Y12 inhibitor with proven superiority over clopidogrel. Ticagrelor increases the tissue concentration of adenosine, thereby leading to bradyarrhythmia. This complication is reported to occur very early after initiating the drug. A randomized controlled trial reported that ticagrelor-induced pauses have an early onset without much clinical impact. However, our patient developed ticagrelor-induced hemodynamically significant sinus arrest 10 months after coronary artery stenting, which improved after stopping the drug. Ticagrelor should be considered as one of the uncommon reasons for late-onset sinus pause or bradyarrhythmia.

Background: Patients with kidney disease may have concurrent hypertension and infection. Dihydropyridine calcium-channel blockers (CCB) are the most popular class of antihypertensive drugs used in clinical settings and can be metabolized by cytochrome P450 isoenzyme 3A4 (CYP3A4). Voriconazole is a commonly used antifungal treatment and a CYP3A4-inhibitor. Insufficient attention to drug interactions from the concomitant use of CCB and voriconazole may result in serious adverse reactions., Case Presentation: Here, we report a patient with acute kidney injury on stable anti-neutrophil cytoplasm antibody associated vasculitis who developed hyperkalemia resulting in sinus arrest with junctional escape rhythm attributed to drug interactions of CCB with voriconazole. This is a very rarely reported case and may be an under-recognized complication. After continuous renal replacement therapy and changing the anti-hypertensive drugs, symptoms, and laboratory abnormalities of the patient fully recovered., Conclusions: This case warns us of severe consequences of drug interactions. Co-prescription of CYP3A4-inhibitors with calcium-channel blockers increases the risk of hypotension and acute kidney injury, which may further induce hyperkalemia and arrhythmia.

Classically, phenytoin (PTN) infusion for the treatment of status epilepticus has been proven to be associated with cardiovascular toxicity, including dysrhythmias, hypotension, and cardiovascular collapse. Subsequently, fosphenytoin (FOS) was introduced on the market in 1997 with claims of having less cardiac toxicity. However, since then, many accounts of cardiac events have been reported undermining these claims. FOS gained popularity due to its water solubility, which allows 3 times faster infusion in comparison with PTN with less venous irritation and local toxicity. FOS is the phosphate ester prodrug of PTN and is rapidly converted to PTN independent of the dose and rate of administration. Intravenous FOS and PTN are bioequivalent. Adverse cardiac effects of both intravenous FOS and PTN have been correlated to the rate of infusion, concentration of the agent, known risk factors, or pre-existing hypersensitivity, and most cases have been identified after infusing a loading dose of these medications. This case report is unique, in that, the patient developed sinus arrest while concurrently receiving oral PTN and intravenous FOS. Clinicians should be more cognizant of the association of FOS and PTN with adverse cardiac events. Baseline electrocardiogram should be obtained on all patients prescribed FOS or PTN to identify underlying cardiac problems that may place the patient in a higher risk category. Telemetry should be performed on all patients receiving PTN in an inpatient setting.

An 88-year-old man was admitted with fatigue, dizziness, and heart palpitations. Both the electrocardiogram and Holter confirmed the existence of sinus bradycardia and sinus arrest. One hour prior to the onset of symptoms, he received levobunolol hydrochloride solution topically. The levobunolol hydrochloride solution was discontinued and the bradycardia resolved. He was diagnosed as having intermittent sinus bradycardia and sinus arrest, induced by topical β-blocker therapy. Levobunolol hydrochloride solution is an effective therapy for ocular hypertension, probably by reducing aqueous fluid production. However, it can induce cardiac side effects such as bradyarrhythmia and should be used with caution in elderly patients or patients with cardiac disease.

A 52-year-old man with Turkish background presented with nausea, emesis, one experience of syncope with loss of consciousness for a few seconds, and documented sinus bradycardia. During monitoring, several phases of bradycardia were observed. After 24 h of monitoring, the patient was free of complaints. The patient's wife reported regular consumption of pontin honey. Because of the anamnesis and the typical characteristics, grayanotoxin poisoning was diagnosed. Typical symptoms of this poisoning are hypotension, bradycardia, syncope, and loss of consciousness. When these symptoms are found and a typical anamnesis exists, this kind of intoxication has to been taken into consideration as part of the differential diagnosis.

Background: Lithium is widely used to treat bipolar disorders. Lithium toxicity is generally caused by inappropriately high doses of lithium or impaired lithium excretion. Most lithium is eliminated via the kidneys and, since thyroid hormone increases tubular reabsorption of lithium, thyrotoxicosis could contribute to the development of lithium toxicity. We report a case of severe lithium toxicity that was apparently precipitated by the onset of thyrotoxicosis resulting from silent thyroiditis and dehydration., Patient Findings: The patient was a 64-year-old woman who was admitted for muscle weakness in the lower extremities, diarrhea, and palpitations. She had bipolar disorder and was being treated with lithium carbonate, which she discontinued one week before admission. Her circulating lithium levels had been monitored yearly. Early in her admission she was dehydrated and had febrile episodes, paroxysmal atrial fibrillation, and muscle weakness. Initially, fluid therapy was started, but she lost consciousness and had a cardiac arrest for 2 minutes due to prolonged sinus arrest. Chest compression and manual artificial ventilation were performed, and body surface pacing was started. Serum lithium was markedly elevated to 3.81 mEq/L (therapeutic range, 0.4-1.0 mEq/L), and thyroid hormone levels were increased (free triiodothyronine, 8.12 pg/mL; free thyroxine, 4.45 ng/dL), while thyrotropin (TSH) was suppressed (<0.01 μIU/mL). Hemodialysis was performed, and a temporary pacemaker was inserted for severe sinus bradycardia. The serum thyroglobulin was 4680 ng/mL (reference range, <32.7 ng/mL). A TSH receptor antibody test was negative. Glucocorticoid therapy and inorganic iodine (100 mg) were administered and continued until day 11. However, her neurological symptoms deteriorated with floppy quadriplegia and deep coma. She gradually recovered. On day 36, she was discharged without any neurological symptoms or thyrotoxicosis., Summary: A 64-year-old woman taking lithium for bipolar disorder developed lithium toxicity in the setting of what seemed likely to be a recent onset of thyrotoxicosis due to silent thyroiditis., Conclusions: Thyrotoxicosis may be a contributing cause of lithium toxicity, particularly if it is abrupt in onset and even with cessation of lithium therapy if renal function is compromised. Thyroid function should be assessed immediately in patients with suspected lithium toxicity.

Cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage is still a leading cause of morbidity and death. This 50-year-old man underwent surgery for aneurysm clipping. After the aneurysm was clipped, papaverine was instilled into the surgical area. Bradycardia, hypotension, and sinus arrest developed in the first minute after applying the papaverine. Thus, the authors concluded that the application of papaverine to the surgical area can result in fatal bradycardia and hypotension.

Sertraline is a selective serotonin reuptake inhibitor with established safety for the treatment of depression. Among the common adverse effects associated with sertraline are nausea, insomnia, diarrhea, somnolence, and dizziness. Cardiac arrest had not been reported in the literature, although tachycardia was frequently seen. In this case report, a patient was presented who had adverse reactions such as nausea, dizziness, insomnia under citalopram treatment, and after his drug was changed to sertraline, developed sinus arrest on the fourth day of treatment.

Pyrethroids are common household insecticides. Even though they are less toxic to humans, reports of accidental and suicidal poisoning are not uncommon. Cardiotoxicity due to pyrethroid poisoning is rare. We report a case of cardiac conduction disturbance due to a pyrethroid, prallethrin. A 28-year-old female presented after a suicidal consumption of prallethrin. Her clinical and laboratory parameters were normal during the first 24 h of hospital stay. On the second hospital day, she developed metabolic acidosis and sinus arrest with escape junctional rhythm. Despite correction of metabolic acidosis, the sinus arrest persisted for 3 days. She reverted back to sinus rhythm with bradycardia after this period and was discharged on the seventh hospital day. Her follow-up was uneventful. Pyrethroid poisoning can affect the gastrointestinal, respiratory, and nervous system. Most serious effects of the toxin in humans are seizures and coma. Mechanism of pyrethroid neurotoxicity is believed to be due to its ability to modify sodium, chloride, and calcium channels of the neurons. Our case raises the possibility that cardiac arrhythmia due to pyrethroid poisoning can occur due to its effect on sodium channels in the heart.