β-Receptor Blocker Withdrawal. A Preoperative Problem in General Surgery?

1982 ◽  
Vol 26 ◽  
pp. 32-37 ◽  
Author(s):  
J. Pontén ◽  
B. Biber ◽  
T. Bjurö ◽  
B-Å. Henriksson ◽  
Å. Hjalmarson
2011 ◽  
Vol 140 ◽  
pp. 244-247
Author(s):  
Zhao Heng Lin

OBJECTIVE: To investigate the clinical efficacy and safety of low-energy direct current defibrillation combined with intravenous application of β-receptor blocker in the treatment of ventricular tachycardia storm (VTS). METHODS: A total of 59 patients with VTS were randomly divided into two groups. In the control group (n = 31), intravenous administration of Lidocaine or Amiodarone and routine electrical defibrillation were performed. In the esmolol group (n = 28), intravenous administration of esmolol and low-energy electrical defibrillation were performed in addition to the same drug treatment as the control group.RESULTS: The success rate of terminating recurrent ventricular tachycardia or ventricular fibrillation was significantly higher in the esmolol group than in the control group (89.71% vs. 39.89%, P < 0.05). The necessary discharge times and average discharge energy to terminate ventricular tachycardia or ventricular fibrillation were significantly decreased in the esmolol group compared with control (5.69 ± 1.34 times vs. 8.63 ± 3.79 times, 95.32 ± 13.21J vs. 185.39 ± 25.63J, both P < 0.05). There was no significant difference in the incidence of hypotension (45.16% vs. 39.29%), sinus bradycardia (3.23% vs. 3.57%), and junctional/ventricular escape (38.71% vs. 39.29%) between the esmolol and control groups (all P > 0.05). The mortality was significantly lower in the esmolol group than in the control group (21.43%, 6/28 vs. 77.42%, 24/31, P < 0.01).CONCLUSION: Compared with conventional treatment, intravenous administration of a β-receptor blocker combined with low-energy electrical defibrillation could be a safe and effective therapy to treat VTS.


1976 ◽  
Vol 51 (s3) ◽  
pp. 509s-511s ◽  
Author(s):  
I. McD. G. Stewart

1. After some exclusions, 169 severe uncomplicated essential hypertensive patients presenting consecutively were divided into two groups according to their treatment. Of these, 121 had been given long-term treatment containing propranolol (PC group) and forty-eight had been treated with hypotensive agents excluding any β-receptor-blocker group, the non-β-receptor-blocker (NBB) group. 2. There were no significant differences in myocardial infarction risk factors between the two groups. 3. After a mean follow-up of 5·25 years, nine of the 121 subjects (7·5%) in the PC group had suffered first infarctions and fifteen of the forty-eight subjects (31%) in the NBB group, a significant difference (P < 0·01). 4. It was concluded that the presence of propranolol had prevented more or caused fewer infarctions, perhaps a combination of both, than had the older hypotensive agents unsupported by β-receptor blockade.


2017 ◽  
Vol 8 (2) ◽  
pp. e2634-e2634 ◽  
Author(s):  
Yuan Cao ◽  
Rahul Agarwal ◽  
Francesco Dituri ◽  
Luigi Lupo ◽  
Paolo Trerotoli ◽  
...  

2010 ◽  
Vol 158 (6) ◽  
pp. 2059-2066 ◽  
Author(s):  
Valeska Contardo-Jara ◽  
Stephan Pflugmacher ◽  
Gunnar Nützmann ◽  
Werner Kloas ◽  
Claudia Wiegand

1988 ◽  
Vol 67 (3) ◽  
pp. 561-564 ◽  
Author(s):  
J.R. Martinez ◽  
P. Reed

Dispersed salivary acini isolated from the rat submandibular gland by enzymatic digestion were used to study the effects of a-receptor stimulation on transmembrane transport of 36Cl. In the absence of secretagogue, the tracer accumulated in the cells in a time-dependent manner until a steady-state content of 6.8 ± 0.1 nmol/mg protein was attained after 3-5 min of incubation. Epinephrine (1 μmol/L) alone did not modify 36Cl accumulation but in the presence of the β-receptor blocker propranolol (1 μmol/L) caused a significant (21%) reduction in the isotope content of the cells to 5.2 ± 0.1 nmol/mg protein. In acini pre-loaded with 36Cl for 12 min, 1 μmol/L epinephrine caused a rapid but transient net efflux of tracer, but the isotope content subsequently increased to pre-stimulation levels. In the presence of propranolol, however, the efflux of 36Cl induced by epinephrine was larger and more sustained and was partially inhibited by the K-channel blocker quinidine (1 mmol/L) and significantly by the absence of Ca2+ in the incubation medium. The a-agonist phenylephrine (10 μmol/L) also significantly reduced the steady-state 36Cl content of tracer-pre-loaded cells. By contrast, exposure of the acini to epinephrine in the presence of the a-receptor blocker phentolamine, or the β-agonist isoproterenol, increased the tracer content of the cells, whether the drugs were added at time zero or to tracer-pre-loaded cells. The results indicate that stimulation of a-receptors in salivary acinar cells causes a Ca2+-dependent efflux of Cl which seems to be functionally linked to K release. These effects are similar to those observed following stimulation of cholinergic receptors. The lack of effect of β-receptor stimulation on Cl efflux suggests that this response is not regulated by a cAMP-mediated pathway in salivary cells. The extent of stimulation-induced Cl efflux is likely to be relevant in terms of the amount of saliva secreted upon stimulation.


Neonatology ◽  
2021 ◽  
pp. 1-10
Author(s):  
Tatjana Welzel ◽  
Birgit Donner ◽  
Johannes N. van den Anker

Pregnant women with inherited long QT syndrome (iLQTS) are at an increased risk for preterm delivery and intrauterine growth retardation (IUGR) due to their underlying disease. Additionally, they are at a risk of arrhythmogenic events, particularly during the postpartum period because of physiological changes and increased emotional/physical stress. β-receptor blockers can effectively prevent life-threatening Torsades de Pointes ventricular tachycardia and they are the treatment of choice in iLQTS. Use of β-receptor blockers in pregnancy is recommended, although IUGR is commonly reported for prenatally exposed infants. IUGR, particularly in preterm infants, can result in adverse neonatal outcomes. This review was performed to support clinicians in their selection of β-receptor blocker treatment for their pregnant iLQTS women by (i) summarizing the available literature addressing the impact of different β-receptor blockers on IUGR and (ii) reporting additional aspects which might influence the β-receptor blocker selection. In general, experts recommend to use nonselective β-receptor blockers, such as nadolol and propranolol, for iLQTS management as these drugs seem to be superior in effectiveness. However, β-1-selective receptor blockers, such as bisoprolol or metoprolol, seem to affect less likely uterine contraction, peripheral vasodilation, and are associated with lower IUGR rates and fetal hypoglycemia. They are therefore recommended, except atenolol, as first-line therapy for pregnant women. Additionally, maternal factors such as iLQTS genotype, other underlying comorbidities (e.g., diabetes mellitus type 1, asthma bronchiale), and uteroplacental dysfunction or fetal factors have to be taken into account. Therefore, each woman with iLQTS who wants to become pregnant should be well-advised for a personalized β-receptor blocker therapy according to the individual risk-benefit evaluation by a multidisciplinary team of cardiologists, gynecologists, pediatric cardiologists, neonatologists, and clinical pharmacologists. During pregnancy, a close monitoring of IUGR and, after birth, monitoring of bradycardia, hypoglycemia, and respiratory depression in the neonate is mandatory. This review summarizes available data on β-receptor blocker-related risk for IUGR in prenatally exposed infants and illustrates which factors might influence β-receptor blocker selection with the aim to support clinicians in their pharmacological management of their pregnant iLQTS patients.


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