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abductor pollicis muscle after ulnar nerve stimulation. A mixture of neostigmine (2.5 mg) and glycopyrrolate (0.4 mg) was given IV to reverse neuromuscular blockade. Two to 3 minutes later, the patient's heart rate dropped to 32 beats/min and his ECG revealed a Mobitz type I atrio-ventricular (AV) block. Atropine (0.6 mg) was draw but not given as the patient blood pressure and oxygen saturation remained stable. His heart rate gradually returned to a prereversal range of 63 to 70 beats/min over a 6-minute period and remained stable over the next 10 minutes. The

with cardiovascular disease appear to be particularly prone to severe arrhythmias as a result of dental stress or vasopressor-containing local anesthesia. 9 Atrioventricular (AV) block is a type of bradyarrhythmia. Common causes of AV block include ischemic heart disease, various drugs (eg, digitalis and calcium channel blockers), connective tissue disorders, and rheumatic fever. 10 , 11 Second-degree atrioventricular (AV) block involves partial interruption of impulse transmission from the atria to the ventricles and is rarely seen during dental

. Atrial fibrillation is a condition in which numerous ectopic foci in the atria attempt to take over control of rate from the SA node. Collectively these foci fire as many as 300 times per minute and initiate impulses that spread throughout atrial tissues and toward the ventricles. Fortunately, the AV node blocks most of these impulses from entering the ventricles; otherwise, the ventricles would also fibrillate! In some cases, however, too many impulses reach the ventricle causing a rapid ventricular response. This rapid ventricular rate reduces the time for the

block; or (e) a combination of causes (b) and (d). 4 , 5 Breslow et al 6 reported a case in which an accelerated junctional rhythm (ventricular rate >60 bpm) during general anesthesia returned to sinus rhythm following intravenous injection of propranolol (a nonselective β-adrenergic blocking agent). They suggested that the accelerated junctional rhythm resulted from acceleration of AV nodal pacemaker cells, as noted in cause (c), above. The increased automaticity of AV nodal cells is mediated by increased sympathetic activity. Breslow et al 6 presumed that the

appears to have produced a depolarization by proxy, but no QRS complexes were noted, likely due to poor atrioventricular conduction capacity. It was difficult to completely diagnose Mobitz type II second-degree AV block from this ECG strip alone due to the brief timeframe of the event. Normal sinus rhythm reappeared following administration of atropine. Intraoperative TCR is often corrected by prompt disruption of the surgical stimulation. In addition, nerve blocks 4 and administration of atropine 2 have been reportedly effective. CONCLUSION

delayed or absent, eg, AV blocks. The correct explanation is that atrial repolarization is too minor in amplitude to be recorded by surface electrodes. 5 6 The QRS complex represents depolarization of ventricular muscle cells. The Q portion is the initial downward deflection, the R portion is the initial upward deflection, and the S portion is the return to the baseline, or the so-called isoelectric point. Often, the Q portion is not evident and the depolarization presents as only an “RS” complex. In any case, the complex does not represent ventricular

atrioventricular (AV) nodes, allowing for the ventricles to become the dominant pacemaker. 3 Furthermore, abnormal automaticity of the ventricular myocardium is necessary for this rhythm to emerge, as ventricular myocardial cells do not normally exhibit spontaneous diastolic depolarization. 3 , 4 The main electrophysiological mechanism underlying the ectopic automaticity in AIVR is abnormal calcium-dependent automation that affects the phase 4 action potential of diastolic depolarization. 3 Many medications have been reported to precipitate AIVR, including digoxin

6 ablation surgeries for atrioventricular (AV) node reentrant tachycardia, inappropriate sinus tachycardia, and junctional tachycardia. No other relevant medical history, medications, or allergies were reported. Eight months before the scheduled dental treatment, ablation near the sinus node and superior vena cava isolation was performed, resulting in severe sinus bradycardia with almost no intrinsic automaticity; thus, a permanent pacemaker was implanted. Two months prior to the dental treatment, AV node ablation was performed because of junctional

referred to the Nagoya City University Graduate School of Medical Sciences Department of Oral and Maxillofacial Surgery for evaluation of right mandibular tenderness diagnosed as osteomyelitis. Preoperative evaluation revealed moderate cardiac enlargement by chest radiograph (cardiothoracic ratio: 52%). Table 1.  Medical History Timeline* Sinus bradycardia (heart rate: 44 beats/min) and negative T waves (II, III, aV F , V3–6) were observed by 12-lead electrocardiogram

by several types of dysrhythmia in the medical history, including complete right bundle branch block, mitral valve prolapse with second-degree atrioventricular block, third-degree atrioventricular block, sick sinus syndrome requiring pacemaker insertion, and paroxysmal atrial flutter. 3 , 15 Other reports of arrhythmic events during surgical procedures suggest that premature ventricular contraction gives rise to monofocal or multiple QT prolongation. 5 , 15 Concerning respiratory function, patients with CMTD may have disorders of diaphragmatic function