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The Role of Hypoxemia in Determining the Cardiovascular Response to Beta Receptor Agonist Drugs
Published in Richard Beasley, Neil E. Pearce, The Role of Beta Receptor Agonist Therapy in Asthma Mortality, 2020
During the past 30 years, beta adrenoceptor agonists have been increasingly used in the treatment of bronchial asthma especially with the introduction of pressurized aerosols delivering a metered dose of drug. The first drug to be extensively prescribed using this type of administration was isoprenaline, but during the past 15 years it has been largely replaced by drugs that selectively stimulate beta2 adrenoceptors, for example, salbutamol and terbutaline. Isoprenaline is an agonist at beta1 and beta2 receptors with stimulation of beta1 receptors in the heart producing positive chronotropic and inotropic effects, although these effects are less marked when the drug is given in therapeutic doses using an aerosol. The increase in deaths from asthma in England and Wales in young people in the early 1960s was attributed to excessive use of aerosols containing isoprenaline and in those delivering a large dose.1,2 The association between the use of isoprenaline forte and this epidemic of deaths is reviewed in Chapters 2 and 3. It was thought that the increase in deaths with isoprenaline resulted from its cardiac effects and that the introduction of beta2-selective agonists would enable a comparable degree of bronchodi-lation to be achieved with much less effect on the heart.
Drug therapy in the cardiac catheterisation laboratory: A guide to commonly used drugs
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
John Edward Boland, Fuyue Jiang, Andrew Fenning
Isoprenaline is a chronotrope used for diagnosis of hypertrophic obstructive cardiomyopathy (HOCM). HOCM is a disease that causes ventricular hypertrophy, particularly the interventricular septum, resulting in a left ventricular cavity of reduced volume and compliance. The thickened septum may obstruct the outflow tract during systole, causing a drop in aortic pressure and a corresponding rise in ventricular pressure. The hypertrophy may cause obstruction with a pressure gradient even at rest and is especially pronounced after an ectopic beat with a longer filling time. It is important to distinguish between obstructive and non-obstructive disease. Isoprenaline increases heart rate and may increase the amount of obstruction. The drug is diluted to a 1 mcg/mL solution and is usually given as 1–3 mcg injections until a positive or negative result is determined from intracardiac pressure recordings.
Sympathomimetic Amines: Actions and Uses
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
Stimulation of the force of cardiac contractions via cardiac β-adrenoceptors has been a target of drug discovery for the treatment of cardiac failure for the past decade. The potent full agonists at cardiac β-adrenoceptors, such as isoprenaline, are inappropriate since they also stimulate cardiac rate and thereby increase metabolic demands of an already compromised heart. Modest cardiac stimulation by means of a partial agonist may provide some inotropic support to the failing heart. The major problem with this approach, however, is that in chronic cardiac failure β-adrenoceptors are down-regulated (see Chapter 3), thus reducing the effectiveness of β-agonists. As discussed earlier, the β2-adrenoceptor population of the human heart appears to be spared from this down-regulation and it has been argued that selective β2-agonists may be of more value. A further complication is that chronic long-term use of β-agonists will lead to desensitization of β-adrenoceptors with consequent tolerance to their cardiotonic action. However, a range of orally active partial agonists has been introduced over the past few years as potential positive inotropic agents for treating congestive cardiac failure (Table 4.5). It is argued that the degree of down-regulation by partial agonists may be less than with full agonists.
Extracorporeal treatment for calcium channel blocker poisoning: systematic review and recommendations from the EXTRIP workgroup
Published in Clinical Toxicology, 2021
Anselm Wong, Robert S. Hoffman, Steven J. Walsh, Darren M. Roberts, Sophie Gosselin, Timothy E. Bunchman, Sofia Kebede, Valery Lavergne, Marc Ghannoum
Management of patients with CCB poisoning includes airway protection as indicated and treatment of bradycardia, hypotension, and myocardial depression [147]. Gastrointestinal decontamination includes activated charcoal [126] and whole bowel irrigation in those with large ingestions, especially modified release preparations [148,149]. Bradycardia may respond to atropine or isoprenaline (isoproterenol) infusion. Management of hypotension includes intravenous crystalloid infusion, calcium boluses, catecholamines, vasopressors and high dose insulin euglycemic therapy [133,135,150]. In patients with refractory bradycardia and hypotension, mechanical pacing has been performed [151,152]. In addition, extracorporeal membrane oxygenation (ECMO) has been used in patients who are refractory to the aforementioned measures e.g., if there is evidence of cardiogenic shock [153]. The Lipid Emulsion Workgroup concluded that there is insufficient evidence to recommend lipid emulsion therapy in the routine management of CCB poisoning [154].
Paradigm shift in the management of mild asthma: Focus toward a patient centered approach
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2020
I. Satia, R. P. Cusack, P. M. O’Byrne
With the discovery of epinephrine in the late 1890s, the use of subcutaneous epinephrine for the treatment of acute asthma became common. Isoprenaline was discovered in 1940, and was shown to be highly effective by inhalation, but with alarming cardiac side effects.7 The concept that stimulation of an adrenergic receptor might be mediated through several subtypes of specific adrenoceptors was posited in 1948 by Ahlquist8 and later by Lands et al. in 1967,9 with the subsequent discovery of α and β adrenoceptors and their respective subtypes. Improvements in aerosol technology and delivery systems in combination with specific β2 receptor agonists led to the introduction of salbutamol and terbutaline, resulting in immediate bronchodilation with limited systemic and cardiovascular side effects.
Yellow Oleander Seed, or “Codo de Fraile” (Thevetia spp.): A Review of Its Potential Toxicity as a Purported Weight-Loss Supplement
Published in Journal of Dietary Supplements, 2018
Armando González-Stuart, José O. Rivera
Pirasath and Arulnithy (2013) studied 65 cases of yellow oleander poisoning in eastern Sri Lanka to determine the clinical manifestations, cardiac and electrolyte abnormalities, and outcome of management employing locally available treatment. Most of the patients were women (38) compared to men (27). The poisoned individuals were young (median age 23 years), presenting the usual symptoms, including emesis, abdominal pain, and diarrhea. Upon examination, cardiac dysrhythmias such as bradycardia, for example, were a usual finding. The majority of the patients were treated with activated charcoal, and those presenting with bradycardia arrhythmias were treated with intravenous boluses of atropine and intravenous slow injections of isoprenaline. For those individuals who did not respond to pharmaceutical intervention, a cardiac pacemaker was temporarily installed. Although under detoxification treatment, two patients died, presenting a third-degree heart block. Regarding the 63 surviving patients, 83.1% required treatment, 18.4% showed life-threatening arrhythmias, 29 were treated with only atropine and/or isoprenaline, and only one required a cardiac pacemaker. A salient result of the study was that the risk of toxicity was negatively correlated with the number of seeds ingested.