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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Additional treatments are based on the cause of pulmonary edema. If there is rapid atrial fibrillation, cardioversion is done. Intravenous beta-blockers, digoxin, or careful use of calcium channel blockers can slow the ventricular rate. Intravenous vasodilators are used for severe hypertension. For acute MI or another acute coronary syndrome, treatments include thrombolysis or direct percutaneous coronary angioplasty, with or without stenting. The fluid status is usually normal before pulmonary edema develops. Therefore, diuretics may be not useful when patients have acute decompensation of chronic HF, and can precipitate hypotension. When systolic BP is lower than 100 mg Hg or there is shock, IV dobutamine and counterpulsation with an intra-aortic balloon pump may be needed. Direct-current cardioversion is used for ventricular or supraventricular tachycardia. Newer drugs are available but do not improve outcomes greatly, and can even be implicated in the death of the patient. These include intravenous BNP (nesiritide), ibopamine, levosimendan, pimobendane, and vesnarinone. Once the patient is stabilized, long-term treatment for HF is started.
Pharmacokinetic/Pharmacodynamic Correlations of Selected Vasodilators
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Tsang-Bin Tzeng, Ho-Leung Fung
There are a variety of vasodilators currently in use today. Their mechanisms of action are as diverse as their chemical structures, which range from the simplest of molecules such as nitric oxide (NO), to the more complex macromolecules such as calcitonin-gene-related peptide and atrial natriuretic factor. These agents can cause vasodilation by acting directly on the vasculature, such as in the cases of the nitric oxide donors and calcium channel blockers, or indirectly by diminishing the physiologic constrictive forces that are normally at work. Examples of the indirect vasodilators are the α1-adrenergic antagonists and angiotensin-converting enzyme (ACE) inhibitors (Table 1). The definition of vasodilator is therefore broad and often nonexclusive. Thus, Carvedilol, a ß-adrenergic antagonist, is also a vasodilator1 and the phosphodiesterase inhibitor and inotropic agent, pimobendan, is also classified as a vasodilator. Because of this broad definition for vasodilators, it becomes necessary to restrict our discussion here to selected members. The term vasodilator therapy, in cardiovascular medicine, is generally associated with the treatment of congestive heart failure, and it is generally meant to include direct vasodilators such as organic nitrates on the one hand, and ACE inhibitors on the other. These compounds are therefore chosen for discussion here, with particular focus on the organic nitrates, for which mathematical pharmacokinetic/pharmacodynamic models have been developed. Other vasodilators in clinical use today include hydralazine, minoxidil, and prazosin; unfortunately, pharmacokinetic/pharmacodynamic relationships have not been established for these compounds.
Exercise testing and training in heart failure
Published in ILEANA PIÑA, SIDNEY GOLDSTEIN, MARK E DUNLAP, The Year in Heart Failure, 2005
STEVEN KETEYIAN, ILEANA PIÑA, MATT SAVAL
be identified that can be used clinically to help guide risk stratification or need for transplant. In addition to exercise testing, the role of exercise training has been extensively investigated over the past 15 years, to the extent that we know that exercise tolerance is improved 15-35%, quality of life is enhanced, no further worsening of left ventricular function appears likely and many of the physiological and histochemical abnormalities that occur in conjunction with the disorder are partially reversed with training. Some of those histochemical changes include improvement in mitochondria density, changes in skeletal muscle fibre types and increases in capillary density. In addition, exercise training appears to be safe and free of major complications. All of these beneficial findings related to exercise training should nonetheless be defined as surrogates. Should peak V0 2 improve with exercise training, there is no guarantee that it will translate to improvements in survival, in spite of the powerful predictive value of peak V0 2 . The literature on heart failure is replete with instances of improvements in exercise function which have not translated to improvements in survival. Typical examples are flosequinan, pimobendan, and hydralazine nitrate versus ACE inhibitor. All these agents improved exercise function but were either neutral on mortality or actually increased mortality. At present, definitive, large trial exercise training evidence does not exist for safety and clinical outcomes such as deaths and hospitalizations. Numerous smaller trials suggest that it is safe, and one trial has shown improved clinical outcomes such as hospitalizations and deaths 131. (Most of these trials have been small and single centre and, thus, these important findings need to be confirmed in a large randomized, controlled trial which would include a broad-based group of patients including the elderly and women, as well as diverse racial groups.) Fortunately, such a trial is presently underway. Heart Failure-A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) is a multisite trial study which proposes to enrol 3000 patients to usual care or usual care plus supervised and then home-based exercise training. The study is planned to continue into 2006 and is scheduled to report its findings in 2007. The primary end-points are combined allcause mortality and all-cause hospitalization. With strong penetration of 13 blockers and ACE inhibitors, this trial will be applicable to accepted current clinical care. The inclusion of academic medical centres as well as smaller community practices will make the findings applicable to a general population of heart failure patients. Most patients enrolled into HF-ACTION are on 13-adrenergic blockade therapy, so the generalizability of this trial to other patients with New York Heart Association class II-IV heart failure due to systolic dysfunction will be intact.
Human exposures to veterinary pharmaceutical products reported to Australia’s largest poison information centre
Published in Clinical Toxicology, 2019
Claire E. Wylie, Rose Cairns, Jared A. Brown, Nicholas A. Buckley
Self-administration of prescribed veterinary products due to mistaken identity further accounted for a considerable proportion of adult exposures. In the current study, pimobendan was the most common individually identified product. A phosphodiesterase-inhibitor used as a cardiac inotrope and vasodilator in dogs, over 81% of pimobendan exposures were reported to be either the meat-flavored oblong, chewable orange/brown solid tablet or orange/white hard capsule formulations of the brand “Vetmedin”, produced by Boehringer Ingelheim (North Ryde, NSW). Human exposure to veterinary pimobendan has only been previously described once, identified as the second most commonly reported adult veterinary product exposure reported to the New Zealand PIC in a conference proceeding [36]. Strategies to reduce therapeutic error necessitate future work to investigate risk factors for these common unintentional exposures, including how pet owners store medications at home, aspects of the packaging products are dispensed in, the similarity in appearance to commonly ingested human medicines (including complementary medicines), and product palatability. Future studies exploring mistaken identity of common veterinary pharmaceutical exposures should also investigate the possibility of undisclosed intentional exploration or off-label intentional use to derive primary or perceived beneficial side-effects of veterinary products.
A case of significant hypotension following a human ingestion of veterinary pimobendan
Published in Clinical Toxicology, 2020
Jonathan Brett, Claire Wylie, Jared Brown
Pimobendan is an inotropic drug with a dual mechanism of action consisting of myofilament calcium sensitization and phosphodiesterase 3 (PDE3) inhibition [1]. Pimobendan showed a strong trend towards increase in mortality and was withdrawn from the human market in most countries [2]. Use in veterinary medicine has persisted and pimobendan is one of the most common treatments for canine heart failure which affects up to 10% of dogs [1]. While acute human toxicity is thought to be low, this perception has been extrapolated from animal studies and overdoses with other PDE3 inhibitors and may be inaccurate [3]. We present a case of human pimobendan poisoning reported to the New South Wales Poisons Information Centre (NSWPIC) resulting in significant toxicity.