Nodal rhythm

The sequence of cardiovascular signs as serum magnesium increases from 3 mEq/L to 15 mEq/L is hypotension, cutaneous vasodilation, QT-interval prolongation, bradycardia, primary heart block, nodal rhythms, bundle branch block, QRS- and then PR-interval prolongation, complete heart block, and asystole. 

The a wave This is caused by atrial contraction and is, therefore, seen before the carotid pulsation. It is absent in atrial fibrillation and abnormally large if the atrium is hypertrophied, for example with tricuspid stenosis. Cannon waves caused by atrial contraction against a closed tricuspid valve would also occur at this point. If such waves are regular they reflect a nodal rhythm, and if irregular they are caused by complete heart block. 

Cardiovascular Effects. Epidemiologic studies indicate that chloroform causes cardiac efiects in patients under anesthesia. In a cohort of 1,502 patients (exposure less than 22,500 ppm), dose-related bradycardia developed in 8% of the cases, and cardiac arrhythmia developed in 1.3% of the cases (Whitaker and Jones 1965). Hypotension was observed in 27% of the patients and was related to the duration of the anesthesia and to pretreatment with thiopentone. Chloroform anesthesia (exposure 8,000-10,000 ppm) caused arrhythmia (nodal rhythm, first degree atrio-ventricular block, or complete heart block) in 50% of the cases from the cohort of 58 patients and hypotension in 12% (Smith et al. 

The side-effects are associated with vagal effects on the gastrointestinal tract (anorexia, abdominal discomfort/pain, vomiting and diarrhoea), while cardiotoxic effects include premature ventricular depolarizations, nodal rhythms and AV dissociation, Toxicity is enhanced by hypokalaemia, and this may predispose to more complex arrhythmias. 

Halothane has the highest blood/gas partition coefficient of the volatile anaesthetic agents and recovery from halothane anaesthesia is comparatively slow. It is pleasant to breathe and is second choice to sevoflurane for inhalational induction of anaesthesia. Halothane reduces cardiac output more than any of the other volatile anaesthetics. It sensitises the heart to the arrhythmic effects of catecholamines and hypercapnia arrhythmias are common, in particular atrioventricular dissociation, nodal rhythm and ventricular extrasystoles. Halothane can trigger malignant hyperthermia in those who are genetically predisposed (see p. 363). 

In adults, atrioventricular dissociation was common and in children atrial rhythm disturbances (1). In volunteers, atropine in doses of 1.6 mg/70 kg/minute causes episodes of nodal rhythm with absent P waves on the electrocardiogram (2) the episodes occurred before the heart rate had increased under the influence of the drug. In healthy men being anesthetized for dental surgery a dose of only 0.4 mg atropine intravenously 5 minutes before induction caused reductions in mean arterial pressure, stroke volume, and total peripheral resistance (3). 

The safety and efficacy of mibefradil in association with beta-blockers was assessed in 205 patients with chronic stable angina, randomized to placebo or mibefradil 25 or 50 mg/day for 2 weeks (6). Besides an improvement in angina with mibefradil, it dose-dependently reduced heart rate and increased the PR interval. One patient taking mibefradil had an escape junctional rhythm 26 hours after the last dose of 50 mg. The nodal rhythm disappeared on withdrawal of mibefradil, but based on the overall results it was concluded that mibefradil was safe and effective when given for a short time with beta-blockers. 

Occasionally nodal rhythm, atrioventricular dissociation, and tachydysrhythmias (such as ventricular extra beats or even bigeminy) develop, but these usually occur in association with halothane. 

Nodal rhythm can occur after injection of pancuronium. This dysrhythmia and bradycardia appear to be more common when neostigmine (plus atropine) is given for reversal of pancuronium-induced neuromuscular blockade than for reversal of D-tubocurarine or alcuro-nium (17) cholinesterase inhibition by pancuronium may contribute to the bradycardia in these circumstances. 

Green DH, Townsend P, Bagshaw O, Stokes MA. Nodal rhythm and bradycardia during inhalation induction with sevoflurane in infants a comparison of incremental and high-concentration techniques. Br J Anaesth 2000 85(3) 368-70. 

Bradycardia and other dysrhythmias are common (80% in some series) and occur after the first and subsequent injections of suxamethonium in infants and children. In adults, these effects are seen more commonly after second or later injections, particularly when the interval between the doses is 2-5 minutes. However, it has been suggested that bradycardia and asystole may now be more frequently seen than previously in adults after a single injection of suxamethonium, as a result of the increased use of fentanyl or the omission of atropine beforehand (6). Nodal rhythm and wandering pacemaker are frequent. The bradycardia is sometimes extreme (asystoUc periods of 15-30 seconds duration have been reported). Usually these minor dysrhythmias revert to normal after a few minutes. Halothane can prolong their presence. The incidence of bradycardic asystole is not known, as atropine (the effective therapy) is usually quickly given. 

Inhalational agents potentiate muscle relaxants, which is of more clinical importance with regard to non-depolarizing agents. Tachyphylaxis and phase II block develop earlier and after smaller total doses of suxamethonium when volatile agents such as halothane, enflurane, or isoflurane (306,307) are used instead of balanced anesthesia. Halothane can increase the incidence of cardiac dys-rhjdhmias, especially bradycardia and nodal rhythm, after suxamethonium. Atropine and glycopyrrolate, particularly when given intravenously just before, afford some protection (SEDA-5,136) (308). 

Bundle branch block Nodal rhythms Primary heart block Bradycardia QT interval prolongation - 5 - -4- Sedation... 

Eight out of 17 digitalised patients (anaesthetised with thiamylal and then maintained with nitrous oxide and oxygen) developed serious ventricular arrhythmias following the intravenous injection of suxamethonium (suc-cinylcholine)40 to 100 mg. Four out of the 8 patients reverted to their previous rhythm when they were given tubocurarine 15 to 30 mg, with one patient returning to a regular nodal rhythm from ventricular tachycardia. ... 

In a review of 47 patients who had ingested mad honey 0.5-9 (mean 2.8) hours before presentation, the heart rate was 30-77 (mean 47) per minute and the systolic blood pressure was 50-140 (mean 47) mmHg [105"]. Cardiac rhythms on arrival were sinus bradycardia (n = 37), nodal rhythm (6), sinus rhythm (3), and complete atrioventricular block (1). AU were given atropine 0.5-2 mg. 

In a prospective study of 42 patients (33 men median age 49 years) who had been hospitalized with mad honey intoxication, all had nausea, vomiting, dizziness, fainting, and sweating five had syncope [106"]. The mean blood pressure was 73/52 mmHg and the mean heart rate 38/minute 18 had sinus bradycardia, 15 had complete atrioventricular block, and nine had nodal rhythm. None needed temporary pacing and all were discharged without complications. 

Aliyev F, Turkoglu C, Celiker C. Nodal rhythm and ventricular parasystole an unusual electrocardiographic presentation of mad honey poisoning. Clin Cardiol 2009 32(11) E52-4. 

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