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PubMed1989

Atropine-neostigmine mixture: a dose-response study.

The dose-response relationship and the doses of atropine required to prevent neostigmine from lowering heart rates below baseline in 50 per cent (ED50) and 95 percent (ED95) of patients after antagonism of pancuronium-induced neuromuscular blockade were determined in 70 patients with neostigmine-atropine mixtures. Neostigmine 0.04 mg.kg-1 (group A, n = 35) or 0.06 mg.kg-1 (group B, n = 35) was randomly mixed with one of seven doses of atropine (ranging from 0.014 to 0.04 mg.kg-1) in group A and from 0.02 to 0.04 mg.kg-1 in group B), with dose-response curves for atropine being constructed for both groups 5 and 10 min after injection of the mixture. These dose-response curves were found to be parallel in both groups. The calculated ED50 and ED95 values of atropine were similar in both groups. The estimated ED50 doses of atropine in groups A and B at 5 min were 0.031 and 0.033 mg.kg-1 respectively, and at 10 min the ED50 doses were 0.037 and 0.037 mg.kg-1 respectively. The calculated ED95 doses of atropine in groups A and B at 5 min were 0.05 and 0.046 mg.kg-1, and at 10 min the ED95 doses were also similar, being 0.06 and 0.055 mg.kg-1 respectively. Under the conditions employed in this study it would seem that in order to prevent late reductions in heart rates, the appropriate doses of atropine when used with neostigmine should be greater than that commonly used.

Adult↗
PubMed1995

It is not necessary to administer more than 10 micrograms.kg-1 of atropine to older children before succinylcholine.

It is common practice at the Hospital for Sick Children, Toronto, to administer atropine 20 micrograms.kg-1 prior to succinylcholine in infants and children. It is unclear whether "prophylactic" administration of this dose of atropine to older children (6-16 yr) is necessary. This study was designed to compare the changes in heart rate, rhythm and mean arterial pressure after administration of either atropine 10 or 20 micrograms.kg-1 with succinylcholine or vecuronium (control group) to older children anaesthetized with thiopentone. Thirty-six ASA I or II patients (6-16 yr) were studied. Anaesthesia was induced with thiopentone 5 mg.kg-1. Patients were randomly assigned to receive: (a) atropine 10 micrograms.kg-1 and succinylcholine 1.5 mg.kg-1 (n = 12), (b) atropine 20 micrograms.kg-1 and succinylcholine 1.5 mg.kg-1 (n = 13) or (c) vecuronium 0.1 mg.kg-1 (n = 11) to facilitate tracheal intubation. Heart rate and rhythm were recorded continuously using a computerised analogue interface whereas blood pressure was monitored non-invasively before induction of anaesthesia, immediately before and at one and three minutes after laryngoscopy. No difference was observed between patients who received atropine 10 or 20 micrograms.kg-1 prior to succinylcholine. No episode of sinus bradycardia occurred. Premature atrial contractions were observed in two patients (one succinylcholine/atropine 20 micrograms.kg-1, one vecuronium). Administration of atropine 20 micrograms.kg-1 prior to succinylcholine provides no advantage over atropine 10 micrograms.kg-1 in older children in terms of cardiovascular stability.

Adolescent↗
PubMed1995

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 20 micrograms.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.

Adjuvants, Anesthesia↗
PubMed1997

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 I or II unpremedicated patients aged from 1 to 36 mo were studied. Anaesthesia was induced with 5 mg.kg-1 thiopentone, 2 micrograms.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. RESULTS: 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-1.m-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.

Anesthesia↗
PubMed1994

Treatment of tabun poisoned guinea-pigs with atropine, HLö 7 or HI 6: effect on respiratory and circulatory function.

The oxime HI 6 (in combination with atropine) is considered to be an effective antidote in soman intoxication but was shown to be less effective in tabun poisoning. In contrast to HI 6, first in vitro studies with HLö 7 demonstrated a reasonable reactivating potency at acetylcholinesterase (AChE) inhibited by soman and tabun. Therefore, the therapeutic efficacy of HLö 7, HI 6 and obidoxime (with and without atropine) was compared in tabun poisoned guinea-pigs. In addition, the therapeutic effect of atropine in guinea-pigs poisoned by various doses of tabun was investigated. Female Pirbright-white guinea-pigs were anaesthetized with urethane (1.8 g/kg) and the carotid artery, jugular vein and trachea were cannulated. After baseline measurements the animals received tabun, 60, 180 or 300 micrograms/kg, and 2 min later the antidotes (all i.v.): obidoxine, HLö 7, or HI 6 (30 or 100 mumol/kg, each) or atropine 10 mg/kg or a combination of atropine and one of the oximes. Respiratory and circulatory parameters were recorded for 60 min or until the death of the animal. Erythrocyte, brain and diaphragm AChE activity was determined in every animal after the experiment. Poisoning by tabun resulted in a rapid deterioration of respiratory function and respiratory arrest within 5 min. Atropine treatment was very effective in improving the respiratory function after tabun 60 micrograms/kg but was ineffective after tabun 300 micrograms/kg. However, circulatory parameters were restored almost completely in all atropine therapy groups. Therapy of tabun 300 microns/kg poisoned animals with atropine plus oxime (30 micromol/kg) improved respiration to a variable extent and restored circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction.

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.

Adult↗
PubMed1980

Age-related hypotensive effect of atropine in unanesthetized spontaneously hypertensive rats.

Intravenous injection of atropine (0.5-20 mg/kg) produced a dose- and age-dependent decrease in the mean arterial pressure (MAP) of conscious spontaneously hypertensive (SH) rats 11-20 weeks of age. No effect on blood pressure occurred in age-matched Wistar-Kyoto (WKY) controls; however, heart rate was increased in both groups. In contrast to atropine, the same doses of methylatropine increased MAP and heart rate in both SH and WKY rats. Methylatropine also failed to modify the hypotensive effect of atropine in SH rats. The difference between the effects on blood pressure of atropine and methylatropine in SH rats was not seen when the animals were anesthetized with pentobarbital. In this case both agents reduced MAP. Intracerebroventricular (i.c.v.) injection of atropine in doses up to 200 microgram in SH rats failed to modify MAP and was without effect on the hypotensive response to intravenous injection of atropine. Likewise, i.c.v. injection of hemicholinium-3 (which reduces MAP in SH rats) failed to modify the hypotensive effect of atropine. However, intravenous injection of atropine (10 mg/kg) prevented the hypotensive effect of hemicholinium-3. Thee results are discussed in terms of central and peripheral muscarinic mechanisms.

Aging↗
PubMed1994

Determination of atropine and obidoxime in automatic injection devices used as antidotes against nerve agent intoxication.

A capillary gas-liquid chromatographic (GLC) and an ion-pair high performance liquid chromatographic (HPLC) method were developed for the assay of atropine sulphate and obidoxime chloride from a parenteral solution in commercial automatic injection devices. The injectors are aimed for the emergency treatment of poisoning by nerve agents. The two-step GLC method consists of extraction of atropine as a free base prior to GLC analysis using scopolamine as an internal standard. Obidoxime is determined directly in a diluted sample solution by reversed-phase HPLC using sodium 1-heptanesulphonate as a counter ion in the mobile phase. The relative standard deviation (R.S.D.) was 1.81% for the GLC procedure with injectors containing only atropine and 2.37% for the GLC of atropine in atropine-obidoxime injectors. The R.S.D. for the HPLC procedure of obidoxime in atropine-obidoxime injectors was 0.82%. The corresponding R.S.D.s for the sampling of atropine-obidoxime injectors were 0.36% and 0.27%. The coefficient of determination (r2) was 1.000 for both methods. The recoveries at the target concentration averaged 101.0% and 98.7% with a standard error of the mean of 0.30 for both methods. The retention times for atropine and obidoxime were 6.27 and 4.29 min, respectively.

Atropine↗
PubMed1984

Variable inhibition of histamine-induced bronchoconstriction by atropine in subjects with asthma.

To determine whether treatment with atropine causes dose-dependent inhibition of histamine-induced bronchoconstriction, we constructed dose-response curves to inhaled histamine after inhalation of placebo and 0.26 and 2.08 mg of atropine in eight subjects with mild asthma. Both doses of atropine significantly inhibited histamine-induced bronchoconstriction, and 2.08 mg caused significantly greater inhibition than 0.26 mg. Baseline specific airway resistance was significantly reduced by both doses of atropine but was no different after 2.08 mg than after 0.26 mg. There were considerable differences in the efficacy of atropine among individuals. We conclude that atropine causes dose-dependent inhibition of histamine-induced bronchoconstriction and that this effect is not merely a function of the atropine-induced in baseline airway caliber. The large magnitude of the atropine effect in some subjects and the small magnitude of the effect in others suggest that there is variability in the degree of involvement of muscarinic mechanisms in the exaggerated bronchomotor response to histamine in asthmatic subjects.

Adult↗
PubMed1994

The effect of atropine on the activation of 5-hydroxytryptamine3 channels in rat nodose ganglion neurons.

It has been suggested that changes in brain 5-hydroxytryptamine3 receptor function may contribute to some behavior disorders, such as anxiety, schizophrenia and drug abuse. We are using the whole-cell version of the patch-clamp technique to study the function of 5-hydroxytryptamine3 channels in neurons freshly dissociated from rat nodose ganglion. In these cells, 5-hydroxytryptamine elicits an inward current over the concentration range of 0.25-100 microM (EC50 = 2.62 microM) by activating 5-hydroxytryptamine3 receptors. The muscarinic cholinergic antagonist atropine reduced the amplitude of 5-hydroxytryptamine activated inward current in a concentration-dependent manner. Other muscarinic antagonists, scopolamine, dexetimide, the M1 muscarinic receptor antagonist pirenzepine, the M2 receptor antagonist methoctramine and the M3 receptor antagonist 4-DAMP methiodide also inhibited 5-hydroxytryptamine-induced inward current. Atropine did not appear to change the reversal potential of this current. In the presence of 5 microM atropine, the concentration-response curve for 5-hydroxytryptamine current was shifted to the right in a parallel fashion. The EC50 value for 5-hydroxytryptamine was increased from 2.62 to 8.76 microM. Schild plots of increasing atropine and 5-hydroxytryptamine concentrations revealed a pA2 value of 5.74 for atropine (apparent KD = 1.8 microM). These observations suggest that atropine competitively antagonizes the activation of a receptor for the neurotransmitter serotonin, a novel action of muscarinic antagonists in the nervous system. This effect of atropine may contribute to the clinical symptoms seen in severe atropine intoxication.

Animals↗
PubMed1991

Cholinergic actions of diazepam and atropine sulfate in soman poisoning.

The effectiveness of diazepam alone or in the presence of atropine sulfate in reversing soman-induced convulsions, inhibition of blood and brain cholinesterase (ChE) activity, and elevation of brain acetylcholine (ACh) and choline (Ch) concentrations in rats was studied. Diazepam (5 mg/kg, IM) blocked the convulsive activity of soman (100 micrograms/kg, SC) whereas atropine sulfate (12 mg/kg, IM) did not. Inclusion of atropine sulfate enhanced the anticonvulsant effects of diazepam. Neither diazepam nor atropine sulfate alone affected ChE activity in the blood and brain of rats, nor did they alone, or in combination, reverse the ChE inhibition induced by soman. Diazepam by itself caused an increase in ACh concentrations in the striatum and a decrease in Ch concentrations in the cortex and striatum. On the other hand, atropine sulfate produced a decrease in ACh and an increase in Ch concentrations in these two brain regions. With combined treatment, diazepam reversed the effect of atropine sulfate on brain ACh and Ch concentrations. Diazepam attenuated the soman-induced elevation of ACh and Ch concentrations in most of the brain regions studied, while atropine sulfate did not. Only when diazepam was given concurrently with atropine sulfate did the elevated brain ACh or Ch concentrations induced by soman return to normal. These results suggest that the anticonvulsant activity of diazepam in soman poisoning may be partially related to its action on presynaptic cholinergic mechanism.

Acetylcholine↗
PubMed1987

Plasma atropine concentrations via intravenous, endotracheal, and intraosseous administration.

To date, there have been limited studies on the pharmacokinetics of intravenous atropine and no pharmacokinetic studies on the endotracheal or intraosseous administration of atropine. This study examines the time to peak plasma concentration of atropine following intravenous, endotracheal, and intraosseous administration in anesthetized monkeys using a triple crossover design. Plasma atropine was assayed by a radioreceptor method. The time to peak plasma concentration of atropine was shortest with intravenous administration; and longest with endotracheal administration. The mean plasma concentration of atropine was significantly higher in intravenous administrations than in endotracheal administrations at 0.75 and 2 minutes; compared to that noted in intraosseous administrations, the concentration was significantly higher only at 0.75 minutes. The mean plasma concentration of atropine administered intraosseously was significantly higher than that of endotracheal administrations at 5 minutes and was greater than that of intravenous and endotracheal administrations for the samples collected from 5 to 30 minutes. The endotracheal and intraosseous routes provide alternatives to the intravenous administration of atropine when intravenous access is limited or not available.

Animals↗
PubMed2005

Effects of HI 6, diazepam and atropine on soman-induced IL-1 beta protein in rat brain.

The current treatment for soman-intoxication is the oxime HI 6 together with the anticholinergic drug atropine. This antidote combination is known to have effects on seizures, respiratory system, blood pressure and animal survival in experiments. However, the inflammatory responses following soman-intoxication leading to neuronal damage have not been fully evaluated. In this paper we focus on the cytokine IL-1beta induction in the rat brain after soman-intoxication (1.0 x LD50 and 1.1 x LD50) and during antidote treatment. We analyzed the IL-1beta levels in rat brain to determine the effects of time of antidote HI 6 and atropine; the effects of different combinations of HI 6 and atropine; and also the effects of antidotes diazepam and atropine following soman-intoxication. We observed that the initiation of the antidote combination of HI 6 and atropine following soman-intoxication was crucial for successful treatment. The study also demonstrated that atropine alone was more effective against IL-1beta up-regulation after soman-intoxication within the 2-h time frame, than the combination of the HI 6 and atropine, the therapy of choice in many countries. Furthermore, treatment with a combination of diazepam and atropine maintained IL-1beta levels at normal when administered at the onset of the seizures following soman exposure. Soman-intoxicated groups without seizures did not have an elevated cytokine level. This corroborates our earlier studies where soman-intoxicated animals with seizures had high levels of IL-1beta, while animals without seizures had normal values. Our results show that both time and the antidote regime are crucial to the success of treatment.

Animals↗
PubMed1998

Usefulness of adenosine triphosphate-atropine stress echocardiography for detecting coronary artery stenosis.

There have been few studies on adenosine triphosphate (AT) stress echocardiography. The AT stress test may have fewer adverse effects than the adenosine stress test. The addition of atropine to AT echocardiography may enhance the sensitivity for detection of coronary artery disease (CAD). The purpose of this study was to determine the utility of AT-atropine echocardiography for detection of CAD. The group studied consisted of 112 patients with suspected CAD. Sixty-one patients did not have a history of prior myocardial infarction (group I) and 51 patients did (group II). AT was infused intravenously at 180 microg/kg/min for 14 minutes. Atropine (0.25 mg intravenously, repeated up to maximum total dose of 1 mg) was administered starting after 8 minutes of AT infusion. Ischemic response was defined as new or worsening wall motion abnormality occurring during the infusion. The sensitivity and specificity for detection of CAD were assessed using the representative echocardiograms during single AT infusion and AT-atropine infusion. Sixty-two patients had CAD. Fifty-eight patients (52%) developed minor side effects that resolved promptly. The rate-pressure product (10(3)/mm Hg beats/min) was significantly increased at 12 minutes of infusion (12.4+/-3.2) compared with that at baseline (9.1+/-2.3) and that at 6 minutes of infusion (9.4+/-2.1). The sensitivity for detection of CAD was 45% for AT echocardiography and 74% for AT-atropine echocardiography. The specificity was 94% for AT echocardiography and 90% for AT-atropine echocardiography. The sensitivity and specificity of AT-atropine echocardiography was 78% and 93%, respectively, in group I, and 70% and 86%, respectively, in group II. In conclusion, AT-atropine stress echocardiography seems to be well tolerated, safe, and useful for detection of CAD.

Adenosine Triphosphate↗
PubMed1999

Comparison of bicycle, heavy isometric, dipyridamole-atropine and dobutamine stress echocardiography for diagnosis of myocardial ischemia.

Several stress echocardiography (SE) modalities have been introduced for diagnosing coronary artery disease (CAD). Exercise and dobutamine SE are considered to have better diagnostic accuracy than vasodilator or isometric SE, but there are no studies in a single group of patients comparing these 3 tests with heavy 2-arm isometric SE. The purpose of this study was to determine the diagnostic characteristics of 4 SE methods in patients with chest pain. Altogether, 60 patients (age +/- SD 55.1 +/- 2.1 years) were tested with bicycle, heavy 2-arm isometric, dipyridamole-atropine and dobutamine SE. CAD (>50% stenosis) was present in 44 patients; 26 patients had 1-vessel disease. During bicycle SE, the double product at peak stress was higher than during dobutamine and dipyridamole-atropine SE (26.5 x 10(3), p <0.005 vs dobutamine and dipyridamole-atropine SE), and peak wall motion score index (1.40) was higher than during dipyridamole-atropine and isometric SE (1.26 and 1.07, respectively, p <0.05 vs bicycle SE). Bicycle, dipyridamole-atropine, and dobutamine SE had higher sensitivity than isometric SE (90%, 93%, 95%, and 30%, respectively, p <0.05 isometric SE vs others). There were no statistically significant differences with regard to specificity. Similarly, bicycle, dipyridamole-atropine, and dobutamine SE had a higher diagnostic accuracy than isometric SE (78%, 88%, 87% and 47%, respectively, p <0.05 isometric SE vs others). We conclude that bicycle, dipyridamole-atropine, and dobutamine SE have an equal diagnostic accuracy in detecting CAD despite higher double product and ischemic burden at peak stress during bicycle and dobutamine SE over dipyridamole-atropine SE. Heavy isometric SE is inaccurate.

Adult↗
PubMed1981

Use of atropine for brady-asystolic prehospital cardiac arrest.

The efficacy of atropine in treating prehospital cardiac arrest patients developing asystole slow pulseless idioventricular rhythms (PIVR) was evaluated in a controlled, prospective study. Twenty-one prehospital cardiac-arrested patients developing asystole or PIVR (less than 40) were divided into atropine-treated or non-atropine (control) groups. Control group patients received treatment including bicarbonate, epinephrine, calcium, isoproterenol, dexamethasone, and transthoracic pacing. Atropine-treated patients received 1 mg atropine intravenously with a repeat dose at one minute if no rhythm change occurred. These patients then received the same therapy as the control group. In both groups, rhythm changes were treated as appropriate for the specific circumstances. No differences in mortality or effected rhythm changes were observed. Ten of the 11 controls and eight of 10 atropine patients developed rhythms other than asystole or PIVR less than 40. However, only two patients in each group were successfully resuscitated in the emergency department and only one control group patient was discharged alive. Our findings are not in agreement with those of previous authors who have advocated the use of atropine in cardiac arrest patients with these arrhythmias. We question the usefulness of atropine in this setting. More study is necessary in order to clearly define its role in the resuscitation of patients who have sustained brady-asystolic arrests.

Adolescent↗
PubMed1999

Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine.

The purpose of this study was to investigate the therapeutic response to atropine of patients experiencing hemodynamically compromising bradyarrhythmia related to acute myocardial infarction (AMI) in the prehospital (PH) setting and the therapeutic impact of the PH response to atropine on further Emergency Department (ED) care. In addition, the prevalence of AMI in patients presenting with atrioventricular block (AVB) is noted. Retrospective review of PH, emergency department (ED), and hospital records. PH patients, with hemodynamically compromising bradycardia or AVB with evidence of spontaneous circulation, who received atropine as delivered by emergency medical services (EMS) personnel, were used. Urban/suburban fire department-based emergency medical services (EMS) system with on-line medical control serving a population of approximately 1.6 million persons. Hemodynamic instability was defined as the presence of any of the following: ischemic chest pain, dyspnea, syncope, altered mental status, and systolic blood pressure less than 90 mm Hg. Bradycardia was defined as sinus bradycardia, junctional bradycardia, or idioventricular bradycardia (grouped as bradycardia), whereas AVB included first-, second- (types I and II), or third-degree (grouped as AVB). The response that occurred within 1 minute of atropine dosing was recorded as none, partial, complete, or adverse. Comparisons were made between patients with AMI and non-AMI hospital discharge diagnoses. The diagnosis of AMI was confirmed by abnormal elevations in creatinine phosphokinase MB fraction. One hundred seventy-two patients meeting entry criteria were identified. Of these, 131 (76.1%) had complete PH, ED, and hospital records and were used for data analysis. Forty-five patients (34.3%) had a primary hospital discharge diagnosis of AMI; the remaining patients had a non-AMI discharge diagnosis. AMI patients were significantly younger (67 +/- 12 v 73 +/- 13 years, P = .025), were less likely to have a history of heart disease (35.5% v54.7%, P = .038), and were more likely to present with chest pain (68.9% v24.4%, P < .001) or hypotension (60% v37.2%, P = .013) compared with non-AMI patients. Forty-five of 131 patients presented with AVB, of which 25 had a hospital discharge diagnosis of AMI (55.6%). The mean time from first dose of atropine to ED arrival and the total dose of atropine received in the PH setting did not differ between AMI and non-AMI groups (15.2 +/- 7.7 v 16.2 +/- 8.7 minutes, P= .5; and 0.9 +/- 0.49 v 1.0 +/- 0.58 mg, P = .25). The likelihood of achieving normal sinus rhythm in the PH setting did not differ between AMI and non-AMI groups (40% v 18.6%, P = .07). No differences were found between AMI and non-AMI groups in the amount of additional atropine given (1.2 +/- 0.58 v 1.3 +/- 1.1 mg, P = .58) or the use of other resuscitative therapies after ED arrival (isoproterenol, 13.3% v12.8%, P = .93; dopamine, 28.9% v26.7% P = .79; transcutaneous pacing, 26.7% v26.7%, P = .99; transvenous pacing, 8.9% v5.8%, P = .51), with the exception of thrombolytic therapy (24.4% v 0%, P< .001) and cardiac catheterization (22.2% v3.4%, P = .001). Despite a lack of significant difference in achieving a normal sinus rhythm in the prehospital or ED setting, AMI patients were more likely to achieve a normal sinus rhythm over the total course of PH and ED care than non-AMI patients (44.4% v24.4%, P = .019). Hemodynamically unstable (by ACLS criterion) AVB presenting in the PH setting is associated with a hospital diagnosis of AMI in most (55.6%) patients in this study. AMI patients with hemodynamically unstable AVB or bradycardia are no more likely to respond to atropine therapy in the PH setting than patients with non-AMI hospital diagnoses. Finally, although there is no difference in the treatment of compromising AVB or bradycardia received by AMI versus non-AMI patients in the PH or ED setting, AMI patients are more likely to achieve a normal sinus rhythm over the t

Age Distribution↗
PubMed1990

Evaluation of transmitral pressure gradients at different heart rates: divergent action of isoprenaline and atropine.

STUDY OBJECTIVE: The aim was to record diastolic transmitral pressure gradients at high sensitivity to quantitate the effect on transmitral pressure gradients of changing the heart rate. DESIGN: Diastolic left atrial and left ventricular pressures were recorded at high sensitivity (40 mm Hg = 10 mm recorded deflection) in control conditions (heart rate 70 beats.min-1) and after intravenous administration of atropine or isoprenaline (heart rate 110 beats.min-1). A special ventricular extrasystole protocol enabled the zero level of the transmitral pressure gradients to be unequivocally determined at high heart rates. The effect of atropine and isoprenaline on the pressure gradients, absolute diastolic pressures, and diastolic time intervals was investigated. EXPERIMENTAL MATERIAL: 16 mongrel dogs, 16-25 kg, were used. MEASUREMENTS AND RESULTS: Below a heart rate of 110 beats.min-1, four distinct periods were identified, during which a pressure gradient existed. During early and late diastole, a positive pressure gradient was consistently followed by a negative pressure gradient. Mean negative pressure gradient during early diastole correlated with the pressure difference of rapid filling wave (r = 0.72, p less than 0.01) and with mean positive pressure gradient during early diastole (r = 0.66, p less than 0.01). At a heart rate of 110 beats.min-1, isoprenaline augmented, while atropine reduced, the mean positive pressure gradient during early diastole without affecting the time interval over which the gradient occurred. This divergent action of the two drugs was related to their different effects on the decay of left ventricular pressure, which fell faster and deeper with isoprenaline but not with atropine. Both drugs shortened the time interval of the negative pressure gradient in early diastole without significantly affecting the mean negative pressure gradient during this period. In late diastole, atropine augmented the mean positive pressure gradient more than isoprenaline, reflecting the higher afterload after administration of atropine. Neither drug affected the time interval of the positive pressure gradient. As a result of a shortening of the P-R interval, isoprenaline shortened the time interval of the negative pressure gradient and reduced its mean value. Such an effect was not observed with the dose of atropine used. CONCLUSIONS: We conclude that a pressure gradient reversal in early diastole is always observed below a heart rate of 110 beats.min-1 and that isoprenaline and atropine affect the pattern of transmitral pressure gradients in a different way.

Animals↗