Heart-rate slowing and junctional rhythm following intravenous succinylcholine with and without intramuscular atropine preanesthetic medication.

The incidence of heart-rate slowing (greater than 15 percent) and junctional rhythm after two injections of succinylcholine (1 mg/kg), separated by 5 minutes, was determined in adult patients. All patients received intramuscular morphine as preanesthetic medication 60 to 90 minutes before intravenous thiamylal anesthetic induction. Intramuscular atropine (mcg/kg) 60 to 90 or 15 to 20 minutes before anesthetic induction did not alter the incidence of first or second succinylcholine dose heart-rate slowing or junctional rhythm as compared with patients receiving only morphine premedication.     

Dose-response for atropine and heart rate in infants and children anesthetized with halothane and nitrous oxide

The dose recommendations for atropine in anesthetized children vary, and the dose-response for heart rate has not been defined. We determined the dose-response for atropine and heart rate in 181 healthy children anesthetized with halothane and nitrous oxide. After induction of anesthesia, atropine in a dose of 5, 10, 20, 30, or 40 micrograms.kg-1 was administered by rapid intravenous infusion of each subject. The effects of atropine on heart rate, heart rhythm, and systolic blood pressure were compared among dosage groups, and a dose-response curve for peak heart rate was constructed. The effects of atropine were compared also between younger and older subjects. For the group of all 181 subjects, atropine increased heart rate in a dose-related manner up to 30 micrograms.kg-1. Fifty percent maximal response corresponded to 9 micrograms.kg-1, and 90% maximal response corresponded to 26 micrograms.kg-1. Some subjects had nonsinus supraventricular rhythms before atropine, but none had nonsinus rhythm after atropine except after the smallest dose, 5 micrograms.kg-1. Systolic blood pressure increased significantly after all doses of atropine except 5 mu.kg-1. Subjects less than 6 months old had higher control and peak heart rates than did subjects greater than or equal to 2 yr old, but the older subjects had greater change in heart rate after atropine. For subjects greater than or equal to 2 yr old, all doses of atropine produced a significant increase in heart rate. The same was true for younger subjects, less than 6 months old, except that 5 micrograms.kg-1 did not increase heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of remifentanil with and without atropine on heart rate variability and RR interval in children

Remifentanil can cause bradycardia either by parasympathetic activation or by other negative chronotropic effects. The high frequency (HF) component of heart rate variability (HRV) is a marker of parasympathetic activity. This study aimed to evaluate the effect of remifentanil on RR interval and on HRV in children. Forty children ASA I or II were studied after approval by the human studies committee and informed parental consent was obtained. After stabilisation at sevoflurane 1 MAC, they were randomly divided into two groups: one received a 20 microg.kg(-1) atropine injection (AT + REMI) and the other ringer lactate solution (REMI). Three minutes later, a 1 microg.kg(-1) bolus of remifentanil was administered over 1 min, followed by a continual infusion at 0.25 microg.kg(-1).min(-1) for 10 min increased to 0.5 microg.kg(-1).min(-1) for a further 10 min. A time varying, autoregressive analysis of RR sequences was used to estimate classical spectral parameters: low (0.04-0.15 Hz; LF) and high (0.15-0.45 Hz; HF) frequency, whereas the root mean square of successive differences of RR intervals (rmssd) was derived directly from the temporal sequence. Statistical analyses were conducted by means of the multiple correspondence analysis and with non parametrical tests. Remifentanil induced an RR interval lengthening, i.e. bradycardia, in both groups compared to pretreatment values and was associated with an increase of HF and rmssd only for the REMI group. The parasympathetic inhibition by atropine did not totally prevent remifentanil's negative chronotropic effect. A direct negative chronotropic effect of remifentanil is proposed.     

The effects of succinylcholine on heart rate and rhythm in infants]

The authors examined the possible variations of cardiac activity in 91 infants aged between a few days and six months in order to study the changes following administration of succinylcholine during general anaesthesia. No variations in rhythm and/or heart rate occurred, not even in those children to whom atropine had not been injected intravenously before succinylcholine.     

Heart rate and cardiac output after atropine in anaesthetised infants and children

Purpose

Heart rate is considered to be a major determinant of cardiac output in infants and small children but the relationships between age, heart, rate and cardiac output in humans have never been clearly established. This study was designed to determine the change in cardiac output following atropine iv to anaesthetised infants and small children. Methods: Following-,Institutional Ethics Committee approval and written-informed consent, 20 ASA l or ll unpremeditated patients aged from 1 to 36 mo were studied. Anaesthesia was induced with 5 mg · kg^?1 thiopentone, 2 μg · kg^?1 fentanyl and maintained with halothane 0.5% in nitrous oxide 66% in oxygen. Vecuronium, 0.1 mg · kg^?1 was used to provide muscular relaxation. Cardiac output was measured by non-invasive transthoracic blind continuous-wave Doppler echocardiography before and after the administration of 0.02 mg·kg^?1 atropine iv.

Resulits

Atropine increased both heart rate and cardiac index by 31.1 ± 12.8% and 29.4 ± 17.3% respectively (P < 0.05). The cardiac index before atropine was 5.1 ± 1.2 L.min^?1m^?2 and the increase after atropine varied widely from 1,4 to 52.1%. Although atropine did not alter the overall stroke index the recorded changes ranged from -20.8 to + 18.0%. There was no association between age and either cardiac index or % change in cardiac index after atropine. However, there was a positive but weak correlation between percentage change in heart rate and cardiac output (r²=0.46).

Conclusion

Atropine causes a variable increase in cardiac output in infants and children aged between 1 and 36 mo. The change in cardiac,output, considering the limits of the transthoracic echocardiography methodology, suggests that this is related to the increase in heart rate but is not dependent of age.     

Effects on cardiac rhythm of premedication with atropine or glycopyrrolate

The effect of the premedicants atropine and glycopyrrolate on the cardiac dysrhythmic response to instrumentation and intubation was investigated. No significant increase in cardiac dysrhythmias such as bradycardia, atrial and ventricular extrasystoles was found (P greater than 0,01), but a significant increase in tachycardia occurred during induction (P less than 0,05) and intubation (P less than 0,01).     

Hemodynamic responses during induction of anesthesia with halothane-nitrous oxide in children with or without atropine premedication

Forty three children ranged from 1yr. to 6yr. were randomly assigned to non-atropinized group (n = 20; A(–)) and atropinized group (0.015mg·kg^–1 i.m., n = 23; A(+)). Control hemodynamics were measured under 0.5% halothane and 67% nitrous oxide and 33% oxygen for three minutes, and then halothane was increased to 2.5% and maintained for 15min. In the A(–) group, stroke volume (SV) decreased to 64%, heart rate (HR) increased from 100/min to 111/min, and blood pressure (BP) decreased from 65mmHg to 62mmHg. Skin blood flow (SBF) concomitantly measured by a laser doppler flowmeter decreased to 48% and total peripheral resistance (TPR) increased to 128%. In the A(+) group, HR increased from 117/min to 132/min (P 0.05, vs. A(–) group), BP decreased from 67mmHg to 66mmHg. SV decreased to 71% (P 0.05, vs. A(–) group). Changes in SBF and TPR were 68% and 128% respectively. End-expired halothane concentration in the A(+) group increased slower than in the A(–) group but not significantly. The results indicate increased sympathetic tone would work as a compensating mechanism for decreased SV and CO. Atropine premedication attenuated cardiovascular depression by maintaing HR and possibly by delaying induction speed of anesthesia. In conclusion, halotane-nitrous oxide anesthesia decreased SV without a marked decrease in heart rate and blood pressure in children. This decrease in SV and BP was attenuated by atropine premedication.(Kawana S, Namiki A, Morita Y, et al.: Hemodynamic responses during induction on anesthesia with halothane-nitrous oxide in children with or without atropine premedication. J Anesth 6: 63–68, 1992)     

Should the routine use of atropine before succinylcholine in children be reconsidered?

It is common practice to administer atropine before a first dose of succinylcholine in infants and children. However, the administration of succinylcholine without atropine has not been investigated in children. This study was designed to compare cardiovascular changes after the administration of either atropine with succinylcholine or succinylcholine alone. In 41 ASA I or II patients aged from 1 to 12 yr anaesthesia was induced with thiopentone 5 mg · kg^?1. Patients were randomly allocated to receive either atropine 20μg · kg^?1 and succinylcholine 1.5 mg · kg^?1 (n = 20) or succinylcholine 1.5 mg · kg^?1 alone (n = 21). Heart rate and rhythm were recorded continuously from two minutes before induction until two minutes after tracheal intubation. Blood pressure was measured non-invasively before and after induction of anaesthesia and both immediately and two minutes after laryngoscopy. One self-limiting episode of bradycardia was recorded during laryngoscopy in a child who received atropine. Heart rate increased in both groups compared with baseline values (108 ± 25), with a greater increase in patients who had received atropine (150 ± 13) than in those who had not (128 ± 18) (P < 0.05). There was no difference in mean arterial pressure or incidence of arrythmias between the two groups. No recorded arrythmias were judged to be clinically important by a cardiologist. The incidence of bradycardia after succinylcholine in the absence of atropine in children aged from 1 to 12 yr appears to be lower than previously estimated. The use of atropine before a single dose of succinylcholine in children deserves to be reconsidered.     

The heart rate response to succinyl-choline in children: A comparison of atropine and glycopyrrolate

To determine whether intravenous atropine and glycopyrrolate are equally effective in preventing succinyl-choline-induced heart rate changes, we studied the heart rate during the first 78 seconds of anaesthesia in 40 children anaesthetized with either thiopemone, atropine (0.02mgkg~’jandsuccinylcholine(2 mg.kg^-1), orthio-pentone, glycopyrrolate (0.01 mg.kg^-1) and succinylcholine (2 mg.kg^-1 ). Each treatment group was divided into four subgroups which differed only in the interval (6, 10, 15, 20 seconds) between injection of atropine or glycopyrrolate and succinylcholine. During the 54 seconds after succinylcholine, the mean heart rate of each subgroup decreased transiently and then returned to the pre-induclion heart rate or higher. There was no difference in either the magnitude or the duration of the decrease in heart rate or the subsequent increase in heart rate between respective subgroups. Bradycardia occurred in only two patients, both of whom received glycopyrrolate. We conclude that atropine (0.02 mg.kg^-1) and glycopyrrolate (0.01 mg.kg^-1) are equally effective in attenuating succinylcholine-induced changes in heart rate in children.     

Plasma concentration following oral and intramuscular atropine in children and their clinical effects

In a paediatric population, we compared i.m. v oral atropine pre-medication to a control group without atropine and determined atropine plasma concentrations (APC). Forty-five children were randomly assigned to one of three groups. Group I received atropine, 20 μg·kg⁻¹ i.m., 15 min prior to induction. Group II received atropine, 30 μg·kg⁻¹ orally, group III received no atropine. APC (expressed as percent of muscarine-2 receptor subtype occupancy), heart rate, rectal temperature, and salivation were determined before atropine, and 15, 25, 45, 60, 90, 120 (no APC), and 150 min following atropine. Only 10–20% of the M2-cholinoceptors were occupied after oral atropine with a peak at 90 min compared to 60–70% occupancy with a peak 25 min after i.m. atropine. The peak in M2-cholinoceptor occupation in group I was paralleled by a peak percentage change in heart rate of 15% from baseline. The peak in receptor occupation in group II did not correspond to the peak increase in heart rate. The percentage change of heart rate over time was not significantly different from baseline values in any of the groups. Bradycardia or temperature changes did not occur in any of the groups. Antisialogogue effects were observed only in group I. We conclude that atropine, 30 μg·kg⁻¹ orally is not an equipotent dosage to atropine, 20 μg·kg⁻¹ i.m.     

Parasympathetic nervous activity after administration of atropine and neostigmine using heart rate spectral analysis

Recently, heart rate spectral analysis has become recognized as a powerful tool for quantitatively evaluating autonomic nervous system activity. The purpose of this study was to analyze parasympathetic nervous activity by heart rate spectral analysis after administration of atropine and neostigmine for reversal of residual neuromuscular blockade. For our study, 36 female patients (26–37 years of age), ASA physical status (PS) I, who were scheduled for laparoscopic examination, were randomly allocated to one of the following four groups: In group A (1∶1), 9 patients received 1.0mg atropine followed 4 min later by 1.0 mg neostigmine. In group B (1∶2), 9 patients received 0.5 mg atropine followed 4 min later by 1.0 mg neostigmine. In group C (1∶2.5), 9 patients received 1.0 mg atropine followed 4 min later by 2.5 mg neostigmine. In group D (1∶2 mix), 9 patients received a mixed solution of atropine 0.5 mg and neostigmine 1.0mg. After finishing the laparoscopic examination, additional anesthesia was maintained with 70% nitrous oxide, 30% oxygen, and 0.5% isoflurane. The control data were obtained 10 min after finishing the laparoscopic examination. After that, the data on atropine were obtained between 2 and 4min after administration of atropine, and the data on neostigmine were obtained between 5 and 7 min after administration of neostigmine. We selected power spectral density of the high-frequency component (HF-p) in heart rate spectral analysis as an index to assess parasympathetic activity. In groups A, B, and C, the HF-p decreased after administration of atropine. In groups B and C, the HF-p increased after administration of neostigmine as compared to the control. In group A, the HF-p increased after neostigmine but did not differ from the control. The difference between groups D and B was not statistically significant. From the results of this study, we concluded that the muscarinic effect of neostigmine could not be sufficiently blocked by atropine at 1/2 dosages of neostigmine, but could be sufficiently blocked by atropine at equivalent dosages of neostigmine, under light isoflurane anesthesia.     

Neuromuscular blockade in infants following intramuscular succinylcholine in two or five per cent concentration

This study determined the characteristics of the neuromuscular block which followed intramuscular succinylcholine 4 mg.kg^-1 in 20 infants during halolhane anaesthesia. The infants were divided into two groups of ten; the first received succinylcholine in two per cent solution and the second in five per cent solution. The mean maximum depression of the first twitch of the train-of-four (TI) was 89.7 ± 5.0 per cent in 4.0 ± 0.6min, and the mean full recovery of TI occurred in 15.6 ±0.9 min after injection. The maximum block achieved and the onset and recovery times were not affected by the concentration used. Depolarizing block, with equal depression of all twitches of the train-of-four was observed during the onset of neuromuscular blockade. During recovery, phase II block, as determined by a train-of-four ratio (T4/T1) of 0.5 or less, occurred frequently at TI recovery of 25–50 per cent, but was not associated with prolonged paralysis. It is concluded that the onset time of 4 min for intramuscular succinylcholine 4 mg.kg^-1 may be too long for emergency use in infants, and no improvement is obtained by increasing the concentration of injected succinylcholine from two to five per cent.

     

Effects of glycopyrrolate and atropine on heart rate variability

Analysis of heart rate variability, combined with physiological tests (deep breathing and tilt tests) was used to characterise the effects of atropine and glycopyrrolate on the parasympathetic nervous tone of the heart in healthy male volunteers. The low dose of atropine (120 micrograms) administered as a continuous infusion in 15 min was associated with parasympatomimetic effects estimated by the slowing of the heart rate and an increase of the mean and beat-to-beat heart rate variability. The bradycardia and increase of heart rate variability following infusion of glycopyrrolate (50 micrograms) was less marked and did not differ significantly from that of placebo. The higher doses of atropine (720 micrograms) and glycopyrrolate (300 micrograms) administered as a continuous infusion in 15 min produced an equal vagal cardiac blockade characterised by significant tachycardia and a decrease in overall and beat-to-beat heart rate variability. It is concluded that at low doses the parasympatomimetic action of glycopyrrolate is less marked than that of atropine; and at higher doses only small differences exist between these two muscarinic antagonists in their effects on cardiac vagal outflow, assessed by heart rate and heart rate variability.