Chapter 81 Poisoning by Cardiovascular Drugs
1 What are the clinical effects of digoxin toxicity?
Although all nodal agents such as digoxin, β-blockers, and calcium channel blockers delay conduction through the atrioventricular node, each has distinct properties that can help distinguish one from the other in a poisoning or overdose. Because digoxin stimulates automaticity in addition to delaying nodal conduction, frequent junctional or ventricular ectopy may be seen. The appearance of regularized atrial fibrillation, actually an accelerated junctional rhythm, is classic for digoxin poisoning. Bidirectional ventricular tachycardia, though rare, is pathognomonic for digoxin toxicity. Patients poisoned with digoxin may also have characteristic noncardiac symptoms, including scotomata, color aberrancy, confusion, hallucinosis, vomiting, and diarrhea.
2 What is the role of potassium in digoxin overdose?
Digoxin exerts its effects in part by binding to the sodium-potassium–adenosine triphosphatase (Na+, K+–ATPase) pump on cardiac cell membranes, competing with potassium for binding sites. When a patient taking digoxin has hypokalemia, the low serum potassium level decreases the competition for binding, leading to increased effects of digoxin and potentiating toxicity.
Conversely, once a patient is digoxin toxic, the Na+, K+–ATPase pumps are thoroughly bound and inhibited. This leads to decreased uptake of potassium into the cells, with resultant increases in the serum potassium concentration. Therefore hypokalemia can potentiate toxic effects of digoxin, and hyperkalemia is a marker for digoxin toxicity.
3 Should you avoid giving calcium to digoxin-poisoned patients?
Historically, the administration of calcium to treat hyperkalemia in patients with digoxin toxicity was contraindicated. The concern, based on case reports and animal models, was that resulting high levels of myocardial calcium could produce a stone heart by impairing diastolic relaxation and precipitate ventricular dysrhythmias. In recent years, a retrospective study suggests that patients who (possibly inadvertently) received intravenous calcium while digoxin toxic had no increase in mortality or any life-threatening dysrhythmias within 1 hour of administration, a finding supported by more recent animal models. Currently, avoiding calcium in suspected digoxin overdose is still recommended, although this may change in the future as data continue to emerge.
4 What is digoxin immune Fab, and how is it used as an antidote?
Digoxin immune Fab is a preparation of antibody fragments with specificity for digoxin. It is produced by preparing monoclonal antibodies to digoxin and then chemically cleaving off the immunogenic Fc portion. Digoxin immune Fab binds to digoxin, as well as a number of naturally occurring cardiac glycosides, and neutralizes their effects on the myocardium and other end-organs. Dosing of Fab fragments is based on the amount required to neutralize the total body burden of digoxin, which can be estimated on the basis of the amount ingested or on the serum digoxin level, if available. In patients who have chronic toxicity, a smaller dose is sometimes administered initially to avoid fully reversing the therapeutic effects of digoxin while treating toxicity.
5 How can the clinician distinguish between β-blocker and calcium channel blocker poisoning?
β-Blockers and calcium channel blockers may be difficult to distinguish clinically from one another in poisoning. Both classes have similar negative effects on cardiac conduction, inotropy, and blood pressure. Also, many patients with cardiovascular disease are taking medications of both types. However, serum blood glucose determination can help tell the two drug classes apart. β-Blockers may cause and/or mask hypoglycemia by blocking stimulation of hepatic glycogenolysis and the release of pancreatic glucagon in response to falling serum glucose levels. Calcium channel blockers may prevent the release of insulin from the pancreas, a process normally mediated by influx of calcium through voltage-gated calcium channels. The ensuing hypoinsulinemia can lead to impressive hyperglycemia in patients without diabetes.
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