• Korean Journal of Veterinary Research
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• v.57 no.1
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• pp.51-54
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• 2017

A 9-month-old intact male Maltese dog (1.52 kg) was diagnosed with a patent ductus arteriosus (PDA). Transcatheter occlusion of the PDA was performed by using the Amplatz canine duct occluder (ACDO). After occlusion, reflex bradycardia occurred and lasted for at least 15 h with normal systolic arterial pressure and slightly increased diastolic arterial pressure. The bradycardia slowly resolved, and the heart rate was normal in re-examinations after 7 and 30 days. This is the first case of reflex bradycardia after ACDO implantation, in which the bradycardia continued for a long time, even after recovery from anesthesia.

• The Korean Journal of Pharmacology
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• v.1 no.1 s.1
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• pp.53-61
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• 1965

Effects of intraventricular norepinephrine (NE) on rabbit blood pressure and heart rate were investigated. 1) Blood pressure was little affected by small doses of NE (below $500{\mu}g$) but showed marked rise by 1 mg. 2) Heart rate was decreased by intraventriccular NE $(200{\sim}500{\mu}g)$. One mg of NE caused less pronounced bradycardia than with smaller doses. The bradycardia could not be observed in vagotomized or atropinized animals. 3) Intraventricular NE potentiated reflexive bradycardia produced by 5-hydroxytryptamine. 4) Cord-sectioned rabbit showed different responses; the smaller doses $(100{\sim}200{\mu}g)$ produced transitory bradycardia and depression of blood pressure, which followed by tachycardia and pressure rise. The transitory bradycardia and depressor effects were not observed in cord-sectioned and vagotomized rabbit. 5) Treatment of animals with reserpine, guanethidine and hexamethonium changed the effects of intraventricular NE on blood pressure, i.e., in these cases the smaller doses of NE caused maked elevation of blood pressure. 6) From these observations it was inferred that central NE caused stimulation of cardioinhibitory and vasomotor center. The former seemed to be more sensitive to NE than the latter. Susceptibility of the vasomotor center to NE seemed to be influenced by peripheral sympathetic tone.

• Journal of The Korean Society of Clinical Toxicology
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• v.11 no.2
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• pp.119-126
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• 2013

Purpose: The aim of this study was to evaluate the clinical characteristics and outcome of patients who presented to the emergency department (ED) with cardiotoxicity caused by ingestion of Himalayan mad honey. Methods: Medical records of 12 patients who presented to the ED from January 1, 2005 to December 31, 2012 with cardiotoxicity caused by ingestion of Himalayan mad honey were retrospectively reviewed. Results: The mean age of patients was 54.5 years and 58.3% were men. The median amount of mad honey ingested was 30.0 cc, and the mean time from ingestion to onset of symptoms was 39.4 minutes. All patients had hypotension and bradycardia upon arrival in the ED. The initial electrocardiogram showed sinus bradycardia in seven patients, junctional bradycardia in four patients, and atrial fibrillation with slow ventricular response in one patient. Four patients were treated with intravenous normal saline solution only. Eight patients were treated with intravenous normal saline solution and atropine sulfate in a dose ranging from 0.5 to 2.0 mg. Blood pressure and pulse rate returned to normal limits within 24 hours in all patients. Conclusion: Our study showed that all patients with cardiotoxicity caused by ingestion of Himalayan mad honey had severe hypotension, bradycardia, and bradyarrythmias, including sinus bradycardia and junctional bradycardia and all patients responded well to conservative treatment, including intravenous normal saline solution and intravenous atropine sulfate.

• Journal of Dental Anesthesia and Pain Medicine
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• v.21 no.5
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• pp.475-477
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• 2021

• The Korean Journal of Physiology
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• v.14 no.1
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• pp.15-23
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• 1980

In an attempt to clarify the influence of lung volume and water temperature on the heart rate response during apneic face immersion in the trained athletes, 10 soccer players were studied while holding their breath as long as possible after full inspiration(TLC), full expiration(RV) or normal breath(FRC) with face immersion in water. The electrocardiogram(Lead II) was recorded before and during each manuever and compared with 20 control subjects. The results are summarized as follows; 1) Resting heart rate was significantly lower in the athletes than that of the control groups. 2) During apneic face immersion, severe bradycardia were observed in both groups and the heart rate was significantly lower in the athletes than that of the control groups. 3) The degree of the bradycardia (maximum percent reduction of heart rate, HRmax.) were inversely propotional to the lung volume and water temperature. In the above results, bradycardial response was more sensitive in the athletes than the control. It was suggested that diving bradycardia was related to the gas content in the lung and reflex from the cold receptor in the face.

• Journal of Yeungnam Medical Science
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• v.6 no.2
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• pp.241-245
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• 1989

Induction of A-V block by tachycardia is a well-known phenomenon. But there are few case reports of bradycardia-dependent A-V block. We report a case of bradycardia-dependent A-V block with review of literatures. This patient was a 52-year-old fe male who complained of dizziness and anterior chest discomfort. Electrocardiographic recording demonstrated complete A-V block. Monitor electrocardiographic recordings during sitting position and after atropine administration demonstrated decrease of degree of block from complete A-V block to first degree A-V block. The occurrence of complete A-V block for bradycardia during supine position suggests a phase 4-dependent block. After a permanent ventricular pacemaker was implanted, the patient recovered and was with out symptoms during 12 months follow up.

• Korean Journal of Veterinary Research
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• v.53 no.2
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• pp.89-93
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• 2013

This study was performed to investigate the effect of Nei Guan (PC-6) moxibustion stimulation on artificial bradycardia of dogs. Xylazine was injected for inducing bradycardia. Rectal temperature, systolic blood pressure, respiratory rate, heart rate were recorded every 10 minutes for 120 minutes. Systolic blood pressure significantly increased on 40 min (p < 0.05) after xylazine injection, compared with those of control group. Heart rate significantly increased on 40 min (p < 0.01), 50 min (p < 0.01), 60 min (p < 0.01), 70 min (p < 0.01), 80 min (p < 0.01), 100 min (p < 0.01), 120min (p < 0.01) after xylazine injection, compared with those of control group. In conclusion, moxibustion of Nei Guan (PC-6) showed recovery effect in xylazine induced bradycardia in dogs.

• Neonatal Medicine
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• v.28 no.1
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• pp.59-63
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• 2021

An important, albeit rare, cause of fetal bradycardia is long QT syndrome (LQTS). Congenital LQTS is an ion channelopathy caused by mutations in genes encoding cardiac ion channel proteins. Fetal onset of LQTS imposes high risk of life-threatening tachyarrhythmias and sudden cardiac death. Here, we report the case of a female newborn with fetal onset of bradycardia and a 2:1 atrioventricular (AV) block. After birth, a 12-lead electrocardiogram (ECG) revealed bradycardia with QT prolongation of a corrected QT (QTc) interval of 680 ms and pseudo 2:1 AV block. Genetic testing identified a heterozygous Gly402Ser (c.1204G>A) mutation in CACNA1C, confirming the diagnosis of LQTS type 8 (LQT8). The patient received propranolol at a daily dose of 2 mg/kg. Mexiletine was subsequently administered owing to the sustained prolongation of the QT interval and pseudo 2:1 AV block. One week after mexiletine inception, the ECG still showed QT interval prolongation (QTc, 632 ms), but no AV block was observed. There were no life-threatening tachyarrhythmias in a follow-up period of 13 months.

• Journal of Veterinary Clinics
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• v.31 no.4
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• pp.350-353
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• 2014

A 13-year-old, castrated male, Shih Tzu dog with a history of acute ataxia was referred to veterinary medical teaching hospital and anesthetized for diagnostic magnetic resonance imaging of cervical intervertebral disk disease. After preanesthetic evaluation including physical examination, blood chemistry, radiography and ultrasound, the patient was premedicated with intravenous butorphanol (0.2 mg/kg). Anesthesia was induced by intravenous propofol (6 mg/kg) and maintained with isoflurane at 1.2 minimal alveolar concentrations. Because the mean arterial pressure (MAP) decreased from 70 to 58 mmHg at 70 minutes after induction, dobutamine was administered by constant rate infusion ($5{\mu}g/kg/min$) to treat hypotension. However MAP did not increase, and heart rate rapidly decreased from 100 to 55 beats per minute (bpm). To treat bradycardia, intravenous glycopyrrolate ($5{\mu}g/kg$) was administered, and heart rate increased to 165 bpm. After extubation of endotracheal tube, the patient showed normal recovery without any problems related to cardiovascular system. Unexpected dobutamine-induced bradycardia was considered as Bezold-Jarisch reflex. It is recommended that clinicians know and prepare the possibility of bradycardia during dobutamine therapy under general anesthesia.

• Journal of The Korean Dental Society of Anesthesiology
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• v.12 no.3
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• pp.151-155
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• 2012

A vasovagal reaction is defined as the 'development of hypotension and bradycardia associated with the typical clinical manifestations of pallor, sweating and weakness'. The most profound degree of vasovagal reaction results in fainting or syncope. Incidence of vasovagal reactions in the local anesthetic department of a dental hospital is around 2%. The pathophysiology of the hypotension/bradycardia reflex responsible for vasovagal syncope is not completely understood. Central as well as peripheral mechanisms have been implicated in its pathogenesis: however their relative contribution is not fully elucidated. Recently, trigeminocardiac reflex, previously known as oculocardiac reflex, may serve as syncope. The management of vasovagal syncope is evolving. Non-pharmacological treatment options are a fundamental first step of all treatment pathways. In this article, we would like to review new mechanism of vasovagal syncope and hope to be of help to manage the syncopal patients.