Large doses of uterotonic drugs caused type II second degree sinoatrial block during cesarean section.

In China, it is a routine procedure to inject 250 µg of hemabate (sterile solution, an oxytocic, contains the tromethamine salt of the (I5S)-15 methyl analogue of naturally occurring prostaglandin F2α in a solution suitable for intramuscular injection) into the myometrium of patients experiencing uterine inertia after delivery, with an additional dose given in the event that the efficacy is not obvious. Although hemabate is prohibited from being used in patients with active liver disease, there are no restrictions regarding the application of hemabate in positive hepatitis B surface antigen (HbsAg)-positive subjects with normal liver function. Here we report adverse effects of hemabate in 1 HbsAg-positive subject with normal liver function. This subject experienced increased blood pressure, chest tightness, and type II second degree sinoatrial block 25 minutes after an additional injection of hemabate. Thus, special attention should be paid when applying hemabate in HbsAgpositive subjects with normal liver function.

Quinine-induced arrhythmia in a patient with severe malaria.

It was reported that there was a case of severe malaria patient with jaundice who presented with arrhythmia (premature ventricular contraction) while getting quinine infusion was reported. A man, 25 years old, was admitted to hospital with high fever, chill, vomiting, jaundice. The patient was fully conscious, blood pressure 120/80 mmHg, pulse rate 100 x/minute, regular. On admission, laboratory examination showed Plasmodium falciparum (++++), total bilirubin 8.25 mg/dL, conjugated bilirubin 4.36 mg/dL, unconjugated bilirubin 3.89 mg/dL, potassium 3.52 meq/L Patient was diagnosed as severe malaria with jaundice and got quinine infusion in dextrose 5% 500 mg/8 hour. On the second day the patient had vomitus, diarrhea, tinnitus, loss of hearing. After 30 hours of quinine infusion the patient felt palpitation and electrocardiography (ECG) recording showed premature ventricular contraction (PVC) > 5 x/minute, trigemini, constant type--sinoatrial block, positive U wave. He was treated with lidocaine 50 mg intravenously followed by infusion 1500 mg in dextrose 5%/24 hour and potassium aspartate tablet. Quinine infusion was discontinued and changed with sulfate quinine tablets. Three hours later the patient felt better, the frequency of PVC reduced to 4 - 5 x/minute and on the third day ECG was normal, potassium level was 3.34 meq/L. He was discharged on 7th day in good condition. Quinine, like quinidine, is a chincona alkaloid that has anti-arrhythmic property, although it also pro-arrhythmic that can cause various arrhythmias, including severe arrhythmia such as multiple PVC. Administration of parenteral quinine must be done carefully and with good observation because of its pro-arrhythmic effect, especially in older patients who have heart diseases or patients with electrolyte disorder (hypokalemia) which frequently occurs due to vomiting and or diarrhea in malaria cases.

Atropine often results in complete atrioventricular block or sinus arrest after cardiac transplantation: an unpredictable and dose-independent phenomenon.

BACKGROUND: A paradoxic response to atropine with development of atrioventricular (AV) block has been described in patients after heart transplantation (HTx). We investigated further the incidence and dose-response relationship of this paradoxic atropine response and explored predictive factors. METHODS: We investigated 25 clinically stable patients (age 55 +/- 2 years) 18 to 126 months after HTx. After endomyocardial biopsy, a temporary pacemaker was introduced and patients were monitored. Atropine was given in ascending doses (0.004 mg/kg body weight initially, total cumulative dose 0.035 mg/kg body weight). Physiologic tests were performed to evaluate the presence of reinnervation. RESULTS: In 20% of the patients (5/25), a paradoxic response to atropine was observed. Four patients exhibited third degree AV block, one of whom also demonstrated sinus arrest. A fifth patient showed sinus arrest only. In all patients but one, there was no ventricular escape rhythm before ventricular pacing was commenced (10 sec after block). The observed adverse effect was not correlated with the applied atropine dosage, and predisposing factors could not be identified, apart from a slightly lower resting heart rate (80 +/- 5 vs. 90 +/- 2 beats/min, P = 0.07). CONCLUSION: A significant proportion of patients respond paradoxically to atropine after HTx, leading to asystole as the result of sinus arrest or AV block. Although a plausible explanation for this effect remains speculative, our data indicate that the use of atropine or other anticholinergic drugs in patients after HTx is contraindicated.

Atrio-sinus interaction demonstrated by blockade of the rapid delayed rectifier current.

BACKGROUND: Proper pacemaking of the heart requires a specific organization of the sinoatrial (SA) node. The SA node drives the surrounding atrium but needs to be protected from its hyperpolarizing influence, which tends to suppress pacemaker activity. It has been suggested that the hyperpolarizing atrial influence is minimal at the site of the central nodal area. METHODS AND RESULTS: Atrio-sinus interaction was assessed by specific depolarization of the SA node by blocking the HERG-encoded rapid delayed rectifier current (I(K,r)) with the drug E-4031. In the SA node, E-4031 (1 micromol/L) changed action potential configuration drastically but never resulted in pacemaker arrest. In the atrium, E-4031 did not affect the membrane resting potential, thereby leaving the normal hyperpolarizing load on the SA node intact. When the SA node was sectioned into strips and subsequently separated from the atrium, spontaneous electrical activity of the strip containing the primary pacemaker ceased on I(K,r) blockade. When not separated from the atrium, I(K,r) blockade never resulted in pacemaker arrest. A similar effective atrio-sinus interaction was demonstrated in computer simulations. CONCLUSIONS: Our results demonstrate that the atrium provides an effective hyperpolarizing load on the central SA nodal area and is at least one of the controlling mechanisms for normal pacemaking function. The present study can be of help in understanding why patients with long-QT2 syndrome secondary to a mutation in HERG do not show sinus arrest.

[Sinoatrial block induced by therapeutic doses of diltiazem. Report of 3 cases]. / Bloc sino-auriculaire induit par le diltiazem aux doses therapeutiques. A propos de trois observations.

We report three observations of Diltiazem intoxication at therapeutic doses with occurence of sino auricular block. The situation evolute favorably for two patients while the third die. The electro systolic stimulate seems to be justified in case of Diltiazem intoxication.

Cardiac electrophysiological actions and interactions of ethanol, cocaine, and the metabolite ethylcocaine.

The influence of ethanol on the actions of cocaine and ethylcocaine on rat sinoatrial preparations was studied. Ethanol did not modify the depressant effect of cocaine or ethylcocaine on sinoatrial rate (SR) in preparations with spontaneous activity. Cocaine produced sinoatrial block only in the presence of ethanol, and the latter accentuated the sinoatrial block produced by ethylcocaine. Ethanol did not modify the depressant effect of cocaine or ethylcocaine on membrane potentials of atrial fibers in preparations driven at a constant rate. In conclusion, ethanol, in a concentration that did not by itself affect SR or produce sinoatrial block, accentuated the effects of cocaine and ethylcocaine on sinoatrial conduction, without modifying the effects on SR. It is proposed that the accentuation of the block was the consequence of the combination of a depressant action on the fast sodium system and a deterioration of the cell-to-cell coupling.

Evidence for sinoatrial blockade associated with high dose cytarabine therapy.

Cytarabine therapy is rarely complicated by cardiotoxicity. The present report describes the clinical course of a 35-year-old female patient with acute myelogenous leukemia in complete remission, who developed sinus bradycardia while on high dose cytarabine as a consolidation therapy. The electrocardiographic findings suggested that bradycardia was most probably the result of sinoatrial blockade. The available information regarding a possible association of cytarabine with disturbances of cardiac rhythm is reviewed.

Irreversible sinus node dysfunction induced by resumption of lithium therapy.

We present the case of a 56-year-old woman with syncope and sinus node dysfunction after long-term lithium therapy. Following lithium discontinuation, sinus node function recovered completely. After resuming low doses of lithium, however, severe sinus node dysfunction recurred. Thereafter, sinus node function did not recover after lithium was discontinued, and a permanent pacemaker was implanted. These findings suggest that irreversible sinus node dysfunction should be recognized as a potentially fatal, albeit rare, risk of lithium therapy, and that previous recovery from sinus node dysfunction after long-term lithium treatment cannot always guarantee the reversible nature of this abnormality after resumption of lithium therapy.

Sinoatrial and atrioventricular block caused by intracoronary infusion of adenosine early after heart transplantation.

Intracoronary adenosine was infused in 22 patients early (less than 2 months) after heart transplantation to study coronary flow reserve in the left anterior descending artery. Potentially serious bradycardia requiring discontinuation of the infusion occurred in three patients. This complication had not been noted when adenosine was given to 84 patients with at least 1 year after transplantation. Newly transplanted hearts may therefore have increased susceptibility to the bradycardic action of adenosine, which should be used with caution in this population.

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 510 to 900 ms (mean 743 +/- 141) and the longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,018 +/- 168). A long sinus or atrial pause occurring at the termination of tachycardia or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 +/- 1,674), was provoked by the administration of various drugs. These included an intravenous bolus injection of adenosine triphosphate (5 mg; one patient), intravenous bolus injection of verapamil (5 mg; one patient), a combination of a single oral dose of diltiazem (120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient). In five patients, low frequency deflections suggestive of sinus node activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing with a long arrest suggesting suppression of sinus automaticity was also noted in three of these five patients; the longest sinus arrest in these three patients was 4,160, 4,800 and greater than 4,910 ms, respectively. The remaining patient with a pause of 6,840 ms had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological mechanisms of cocaine-induced cardiac arrest. A possible cause of sudden cardiac death.

The hypothesis that cocaine intoxication results in cardiac arrest by producing a block of the propagation of the action potential, without loss of pacemaker function, was tested in rat cardiac tissues. In spontaneously active sinoatrial preparations, cocaine exerted a dose-dependent negative chronotropic action, which was not modified by atropine or propranolol. Sinus node arrest was never observed. Instead, cocaine produced sinoatrial block. The mechanism of this block involved a fall in the resting potential and a decrease in the amplitude and Vmax of phase 0 of the action potential of atrial fibers. In sinoatrial preparations and papillary muscles driven at 5 Hz., cocaine depressed the resting potential, the total amplitude, the overshoot of the action potential, and the Vmax of phase 0. Cocaine had a biphasic effect on the atrial action potential duration. The initial shortening was muscarinic. The prolongation was alpha-adrenergic mediated and probably the result of the inhibition of the transient outward current Ito. In papillary muscles, only the prolongation of the action potential occurred. In conclusion, the electrophysiological actions of cocaine can explain cardiac sudden death. The fall in the resting potential associated with the decrease in the amplitude of the action potential of contractile fibers will result in a block of the propagation of the action potential. Quiescence of the contractile fibers will occur while the sinus node is still generating action potentials at a rate compatible with life.