A Case of Fatal Felodipine Overdose

2008 ◽  
Vol 7 (1) ◽  
pp. 39-42
Author(s):  
Harpreet Lota ◽  
◽  
Natalie Powell ◽  
Rupert Negus ◽  
Richard Leonard ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Channel Blocker ◽  
Management Strategies ◽  
Therapeutic Modality ◽  
High Dose ◽  
Channel Blockers ◽  
Modified Release ◽  
Initial Management ◽  
Whole Bowel Irrigation ◽  
Very High

A 54 year gentleman was admitted to hospital within four hours of taking an overdose of modified release felodipine tablets, with a total dose of approximately 250 mg. The initial management comprised fluid resuscitation, calcium chloride and glucagon. He remained hypotensive and was commenced on hyperinsulinaemia-euglycaemic therapy. Hypotension persisted with the development of progressive metabolic acidosis despite increasing inotropic support, haemofiltration and high dose insulin-dextrose infusions. The patient died 60 hours post overdose. The case highlights the profound, refractory circulatory collapse and lethal consequences of significant calcium channel blocker overdose and also reviews potential management strategies to attempt to reverse these changes. Despite the lack of evidence of whole bowel irrigation in overdose per se, its role in the removal of modified release compounds has not been studied. We would strongly urge emergency departments to consider this therapeutic modality, especially in overdoses involving delayed release preparations of calcium channel blockers, which are extremely toxic in overdose and are associated with very high mortality.

β-Blocker and Calcium Channel Blocker Poisoning: High-Dose Insulin/Glucose Therapy

2016 ◽  
Vol 36 (2) ◽  
pp. 45-50 ◽  
Author(s):  
Dana Bartlett
Keyword(s):  
Calcium Channel ◽  
Channel Blocker ◽  
Case Reports ◽  
Mechanisms Of Action ◽  
Critical Care Nurses ◽  
Poison Control ◽  
High Dose ◽  
Channel Blockers ◽  
Β Blocker ◽  
Glucose Therapy

Overdoses of β-blockers and calcium channel blockers can produce significant morbidity and mortality, and conventional therapies often do not work as treatments for these poisonings. High-dose insulin/glucose therapy has been successful in reversing the cardiotoxic effects of these drugs in cases where the standard therapies have failed, and it appears to be relatively safe. Many successes have been well documented, but the clinical experience consists of case reports, the mechanisms of action are not completely understood, and guidelines for use of the therapy are empirically derived and not standardized. Regardless of these limitations, high-dose insulin/glucose therapy can be effective, it is often recommended by clinical toxicologists and poison control centers, and critical care nurses should be familiar with when and how the therapy is used.

Management of β‎-blocker and calcium channel blocker poisoning

2016 ◽  
Author(s):  
Geoffrey Isbister ◽  
Colin Page
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Calcium Channel Blockers ◽  
Channel Blocker ◽  
Phosphodiesterase Inhibitors ◽  
Blood Glucose Measurement ◽  
Response To Treatment ◽  
Glucose Measurement ◽  
High Dose ◽  
Channel Blockers

β‎-blocker and calcium channel-blockers can cause life-threatening toxicity due to cardiogenic shock. Both β‎-blockers and calcium channel-blockers are heterogenous groups of drugs and particular drugs, such as propranolol, diltiazem, and verapamil are far more toxic than the others in their class. The most important investigations in β‎-blocker and calcium channel-blocker overdose are an electrocardiogram, blood glucose measurement, and electrolytes. Like most overdoses, supportive treatment is the most important, with emphasis on the primary pathophysiology. Early decontamination should be considered based on the severity of the poisoning. Treatment of β‎-blockers and calcium channel-blockers poisoning, using absolute blood pressure as an endpoint can be misleading and measuring cardiac output can be more informative in gauging response to treatment. There are no specific antidotes, although β‎-agonists may be effective in β‎-blocker overdose and calcium has been shown to be effective in calcium channel-blocker overdose. The choice of inotropes and/or vasopressors will differ for β‎-blockers and calcium channel-blockers. These include isoprenaline, high dose insulin euglycaemia, phosphodiesterase inhibitors, and other catecholaminergic inotropes for β‎-blocker poisoning and adrenaline, high dose insulin euglycaemia and vasopressors for calcium channel-blocker poisoning.

Electroanalytical Methods for Determination of Calcium Channel Blockers

2019 ◽  
Vol 15 (3) ◽  
pp. 207-218 ◽  
Author(s):  
Fatma Ağın
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Channel Blocker ◽  
Heart Diseases ◽  
Dosage Forms ◽  
Channel Blockers ◽  
Electroanalytical Methods ◽  
Pharmaceutical Dosage Forms ◽  
Ischemic Heart Diseases

Background:Calcium Channel Blockers (CCBs) are widely used in the treatment of cardiovascular and ischemic heart diseases in recent years. They treat arrhythmias by reducing cardiac cycle contraction and also benefit ischemic heart diseases. Electroanalytical methods are very powerful analytical methods used in the pharmaceutical industry because of the determination of therapeutic agents and/or their metabolites in clinical samples at extremely low concentrations (10-50 ng/ml). The purpose of this review is to gather electroanalytical methods used for the determination of calcium channel blocker drugs in pharmaceutical dosage forms and biological media selected mainly from current articles.Methods:This review mainly includes recent determination studies of calcium channel blockers by electroanalytical methods from pharmaceutical dosage forms and biological samples. The studies of calcium channel blockers electroanalytical determination in the literature were reviewed and interpreted.Results:There are a lot of studies on amlodipine and nifedipine, but the number of studies on benidipine, cilnidipine, felodipine, isradipine, lercanidipine, lacidipine, levamlodipine, manidipine, nicardipine, nilvadipine, nimodipine, nisoldipine, nitrendipine, diltiazem, and verapamil are limited in the literature. In these studies, DPV and SWV are the most used methods. The other methods were used less for the determination of calcium channel blocker drugs.Conclusion:Electroanalytical methods especially voltammetric methods supply reproducible and reliable results for the analysis of the analyte. These methods are simple, more sensitive, rapid and inexpensive compared to the usually used spectroscopic and chromatographic methods.

scholarly journals L-type calcium channel blocker increases VEGF concentrations in retinal cells and human serum

2021 ◽  
Author(s):  
Anmol Kumar ◽  
Stefan Mutter ◽  
Erika Parente ◽  
Valma Harjutsalo ◽  
Raija Lithovius ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Human Serum ◽  
Channel Blocker ◽  
Channel Blockers ◽  
Vascular Endothelial ◽  
Retinal Cells ◽  
Diabetic Eye Disease ◽  
Design And Methods ◽  
Endothelial Growth Factor

Objective: Vascular endothelial growth factor (VEGF) plays a key role in diabetic retinopathy (DR). L-type calcium channel blockers (LTCCBs) have been widely used as antihypertensive medication (AHM), but their association with VEGF and DR is still unclear. Therefore, we explored the effect of LTCCBs compared to other AHMs on VEGF concentrations in retinal cells and human serum. Furthermore, we evaluated the association between the use of LTCCBs and the risk of severe diabetic eye disease (SDED). Research design and methods: Muller cells (MIO-M1) were cultured as per recommended protocol and treated with LTCCBs and other AHMs. VEGF secreted from cells were collected at 24 hours intervals. In an interventional study, 39 individuals received LTCCBs or other AHM for four weeks with a four-week wash-out placebo period between treatments. VEGF was measured during the medication and placebo periods. Finally, we evaluated the risk of SDED associated with LTCCB usage in 192 individuals from the FinnDiane Study in an oberservational setting. Results: In the cell cultures, medium VEGF concentration increased time-dependently after amlodipine (p<0.01) treatment, but not after losartan (p>0.01), or lisinopril (p>0.01). Amlodipine, but no other AHM, increased serum VEGF concentration (p<0.05) during the interventional clinical study. The usage of LTCCB was not associated with the risk of SDED in the observational study. Conclusions: LTCCB increases VEGF concentrations in retinal cells and human serum. However, the usage of LTCCBs does not appear to be associated with SDED in adults with type 1 diabetes.

Severe beta blocker and calcium channel blocker overdose: Role of high dose insulin

2018 ◽  
Vol 36 (4) ◽  
pp. 736.e5-736.e6 ◽  
Author(s):  
Karan Seegobin ◽  
Satish Maharaj ◽  
Ansuya Deosaran ◽  
Pramod Reddy
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Beta Blocker ◽  
Channel Blocker ◽  
High Dose

Influence of Nifedipine on the Visual Fields of Patients with Optic-Nerve-Head Diseases

1994 ◽  
Vol 4 (1) ◽  
pp. 24-28 ◽  
Author(s):  
A.Z. Gaspar ◽  
J. Flammer ◽  
PH. Hendrickson
Keyword(s):  
Optic Nerve ◽  
Visual Field ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Optic Nerve Head ◽  
Channel Blocker ◽  
Glaucoma Patient ◽  
Visual Fields ◽  
Visual Field Defects ◽  
Channel Blockers

Calcium-channel blockers have long been employed in coronary disease, and recent investigations have indicated their efficacy in improving the visual field in low-tension glaucoma or presumed vasospasm, possibly by enhancing ocular circulation. We evaluated the short-term influence of a typical calcium-channel blocker, nifedipine, on 59 patients with visual-field defects, some with optic-nerve-head pathology (n = 38) and some with normal-appearing optic nerve heads (n = 21). On the average, a statistically significant improvement of 1.2 dB was observed. Different types of patients, however, behaved quite differently. The younger the patient, the greater the improvement. Patients with normal optic nerve heads improved by 1.54 dB, whereas patients with optic-nerve-head excavation improved by only 0.66 dB. No response was observed in patients with anterior ischemic neuropathy. Marked deterioration was noted in one glaucoma patient with low systemic blood pressure. The visual-field changes were observed in the scotomatous and non-scotomatous areas. Thus, the calcium-channel blocker nifedipine can be effective in some selected diseases whose pathogenesis probably involves vascular dysregulation though it may even be contraindicated in others

scholarly journals Aberrant Exon 8/8a Splicing by Downregulated PTBP (Polypyrimidine Tract-Binding Protein) 1 Increases Ca V 1.2 Dihydropyridine Resistance to Attenuate Vasodilation

2020 ◽  
Vol 40 (10) ◽  
pp. 2440-2453
Author(s):  
Jianzhen Lei ◽  
Xiaoxin Liu ◽  
Miaomiao Song ◽  
Yingying Zhou ◽  
Jia Fan ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Binding Protein ◽  
Expression Patterns ◽  
Mesenteric Arteries ◽  
Channel Blockers ◽  
Polypyrimidine Tract ◽  
Polypyrimidine Tract Binding ◽  
Polypyrimidine Tract Binding Protein

Objective: Calcium channel blockers, such as dihydropyridines, are commonly used to inhibit enhanced activity of vascular Ca V 1.2 channels in hypertension. However, patients who are insensitive to such treatments develop calcium channel blocker-resistant hypertension. The function of Ca V 1.2 channel is diversified by alternative splicing, and the splicing factor PTBP (polypyrimidine tract-binding protein) 1 influences the utilization of mutually exclusive exon 8/8a of the Ca V 1.2 channel during neuronal development. Nevertheless, whether and how PTBP1 makes a role in the calcium channel blocker sensitivity of vascular Ca V 1.2 channels, and calcium channel blocker-induced vasodilation remains unknown. Approach and Results: We detected high expression of PTBP1 and, inversely, low expression of exon 8a in Ca V 1.2 channels (Ca V 1.2 E8a ) in rat arteries. In contrast, the opposite expression patterns were observed in brain and heart tissues. In comparison to normotensive rats, the expressions of PTBP1 and Ca V 1.2 E8a channels were dysregulated in mesenteric arteries of hypertensive rats. Notably, PTBP1 expression was significantly downregulated, and Ca V 1.2 E8a channels were aberrantly increased in dihydropyridine-resistant arteries compared with dihydropyridine-sensitive arteries of rats and human. In rat vascular smooth muscle cells, PTBP1 knockdown resulted in shifting of Ca V 1.2 exon 8 to 8a. Using patch-clamp recordings, we demonstrated a concomitant reduction of sensitivity of Ca V 1.2 channels to nifedipine, due to the higher expression of Ca V 1.2 E8a isoform. In vascular myography experiments, small interfering RNA-mediated knockdown of PTBP1 attenuated nifedipine-induced vasodilation of rat mesenteric arteries. Conclusions: PTBP1 finely modulates the sensitivities of Ca V 1.2 channels to dihydropyridine by shifting the utilization of exon 8/8a and resulting in changes of responses in dihydropyridine-induced vasodilation.

408: High-Dose Insulin for Calcium Channel Blocker Overdose in a Pediatric Patient

2020 ◽  
Vol 49 (1) ◽  
pp. 193-193
Author(s):  
Mohammad Sallam ◽  
Divij Parsrija ◽  
Rozaleen Phaltas ◽  
Christine Koshel ◽  
Ritesh Korumilli ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Pediatric Patient ◽  
Channel Blocker ◽  
High Dose
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