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Four thousand years ago, the medical knowledge of the Indian subcontinent was codified into a system called the Ayurveda. Ayurveda remains a vital system of medicine and drug therapy in India and elsewhere. Plant alkaloids are the primary active ingredients of Ayurvedic drugs. Today the pharmacologically active ingredients of many Ayurvedic medicines are being identified and their usefulness in drug therapy being determined.
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Management of medical emergencies requires a thorough knowledge of specific medications and their routes of administration. This article briefly discusses the medications that should be included in a basic emergency cart and routes in which to administer them.
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Drug treatment of status epilepticus is reviewed. Tonic-clonic, focal motor, complex partial and absence status epilepticus are discussed. In managing tonic-clonic status epilepticus one should: (1) maintain vital functions at all times, (2) identify and treat precipitating factors and (3) administer an intravenous loading dose of phenytoin sodium or phenobarbital sodium. Careful use of i.v. diazepam sometimes helps to achieve these objectives. Intravenous phenytoin sodium and phenobarbital sodium provide definitive, long-term control of tonic-clonic seizures but must be administered slowly and require time to reach peak brain concentrations. Intravenous diazepam appears to enter and exit from the brain rapidly and may control seizures while therapeutic brain concentrations of long-acting drugs are being achieved. Phenytoin, phenobarbital and diazepam should not be administered intramuscularly in treating status epilepticus. Treatment of focal motor and complex partial status epilepticus is similar to that of tonic-clonic status epilepticus, but i.v. diazepam is required less frequently and loading doses of phenytoin and phenobarbital sometimes can be given more slowly. Status epilepticus of the absence type is managed with i.v. acetazolamide sodium or diazepam. Paraldehyde, muscle relaxants, general anesthesia and lidocaine may be tried when conventional therapies fail.
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Drug therapy has traditionally been the mainstay of treatment for both ventricular and supraventricular arrhythmias. However, increasing knowledge about the potentially significant adverse effects of these medications, together with the emergence of new, nonpharmacological approaches to the treatment of arrhythmias, has led some to question the future of antiarrhythmic drug therapy. Antiarrhythmic drugs are quite effective in terminating a variety of arrhythmias, including atrioventricular (AV) node re-entrant and AV tachycardias (particularly calcium antagonists and adenosine), atrial flutter (class III agents) and atrial fibrillation (class IA and IC drugs. The chronic use of antiarrhythmic drugs has been increasingly limited by a fear of adverse effects (especially proarrhythmia) and the availability of highly effective nonpharmacological alternatives (particularly ablation for re-entrant tachycardias involving the AV node and bypass tracts and cardiovertor/defibrillators for malignant ventricular arrhythmias. Atrial fibrillation (AF) continues to be a therapeutic challenge for which there is no safe and curative nonpharmacological therapy. Antiarrhythmic drugs of classes IA, IC and III show efficacy in preventing recurrence of AF but there are concerns about possible pro-arrhythmic complications. In the future, antiarrhythmic agents will continue to be used acutely to terminate a broad range of sustained arrhythmias. Chronic use is likely to depend on the development of safer and/or more effective compounds, as well as on improved ways of predicting which patients are likely to develop pro-arrhythmic reactions. The development of molecular electrophysiology will allow for the identification of agents with selected ion channel blocking profiles which may prove efficacious with a lower risk of complications. Finally, an improved understanding of arrhythmia substrates may permit the identification of therapy that prevents arrhythmias by acting on the underlying substrate, rather than simply trying to modify the electrical end product.
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Drug therapy to prevent hip fractures may be considered for postmenopausal women with low bone mass and elderly people with risk factors for hip fracture. As most hip fractures occur 25 years or more after menopause, drug therapy may have to be prescribed for many years to be effective. A preventative drug should be effective, safe, and without side effects. Estrogen therapy decreases bone loss and hip fracture incident, but the effect wears off when treatment is stopped. The positive effect of estrogens on cardiovascular disease should be balanced against the increased risk of breast cancer with long-term use. The newer bisphosphonates are potent inhibitors of bone resorption and decrease bone loss substantially. Again, the effect may wear off after the drug is stopped. The bisphosphonates appear to be safe, but long-term data are lacking. Calcium and/or vitamin D may prevent bone loss in late postmenopausal women and elderly people. The combination was shown to prevent hip fractures and other peripheral fractures in elderly nursing home residents. No single drug will be used more than 10-15 years. Therefore, a public health strategy should be developed with a logical sequence of drug and nondrug interventions for the successful prevention of hip fractures.