Caffeine – Nursing Research (Chapter 2 of 5)


Chapter 2


This chapter is a review of some existing literature and studies on the effects of caffeine which are related to the present study.

Related Literature & Studies

Murdoch (1975) described the pharmacological effects of caffeine. The largest sources of caffeine are from the plants used to make coffee, tea, cocoa and kola (the basis of cola beverages), although it is also found in Latin America as mate’ and guarana. Caffeine particularly has a profound effect on the central nervous system, but it also affects, to a lesser degree the heart muscle, gastric secretion and diuresis. Interestingly, caffeine is ingested daily by a vast number of people and is unique in that it is a potent drug, considered to be part of our normal diet.

Leinart (1966) stated that caffeine stimulates the central nervous system first at the higher levels, the cortex and medulla, and finally the spinal cord at higher doses. Mild cortex stimulation appears to be beneficial resulting in more clear thinking and less fatigue. Caffeine has been shown to improve attention in a study which simulated night driving. The onset of the effect of caffeine occurs within one hour and lasts for three to four hours.

The equivalent of one or two cups of coffee (150 to 250 mg of caffeine) is sufficient to induce adverse effects. The occurrence of hyperesthesia, an unpleasant sensory sensation, can be stimulated by large doses of caffeine.

Ritchie (1975) stated in his study that the medullary, respiratory, vasomotor and vagal centers are stimulated by caffeine. This effect is due to an increased sensitization to carbon dioxide but needs large doses to elicit this effect, 150 to 250 mg, parenterally. The spinal cord is stimulated at higher doses and convulsions and death may result. More than 10 g are needed for such toxicity to occur in man.

Abrams (1977) and Dowell (1965) cited that stimulation of the CNS is followed by depression although the effect is small at low doses e.g. a single cup of coffee. After two hours, males (but not females) showed a lower CNS stimulation compared to placebo. The post stimulation “let down” with caffeine results in fatigue and lethargy and the constant stimulation caused by chronic caffeine dosing could be disastrous.

Children, because of their smaller size, are more susceptible to caffeine. One report noted that hyperactivity and insomnia observed in children could be attributed to excess caffeine intake from cola drinks.

According to Dr. Page, “There is no doubt that children should be kept from using coffee and the popular caffeine containing soft drinks.”    Ritchie (1975) mentioned on his study that caffeine’s effect on the cardiovascular system is less profound than its central nervous system action. Its direct stimulatory effect on the heart may be neutralized by its central vagus stimulation. The direct effect predominates at very large doses with tachycardia and, eventually, arrythmias resulting. Caffeine’s ability to potentiate cyclic AMP can explain its ability to potentiate ionotropic responses to B-adrenergic agonists and glucogon.

Peach (1972) and Poisner (1973) theorized that although caffeine dilates blood vessels by a direct action, its central effect is one of constriction. At higher doses, the dilating effect is apparent .

Similarly, because its direct and central effects are antagonistic, the resultant effect of caffeine on blood pressure is unpredictable. The net effect is usually of less than 10 mm of Hg in blood pressure. Caffeine’s purported efficacy in hypertensive headaches may be due to a decrease in blood flow as a result of the increased cerebral resistance.    Caffeine also stimulates releases of catecholamines from the adrenal medulla and norepinephrine is released from nerve endings in the isolatA heart. It has been shown that prolonged augmentation of gastric secretion results from caffeine administration and that ulcer patient have sustained elevation of acid as opposed to normal.

Gleason (1969) cited that although a dose of approximately 10 g or more taken orally can be fatal, an oral (3.2 g IV) one gram dose will cause adverse effects. The toxic effects are due to CNS and circulatory system stimulation and include some well recognized prominent symptoms in addition to those which can result at high doses or in hypersensitive persons: insomnia, restlessness, excitement, tinnitus, flashes of light, quivering muscles, tachycardia, extrasystoles, and even low grade fever and mild delirium have been observed.

Harrie (1970) described a patient whose constant headaches were due to excessive caffeine consumption. He states, “I suspect that the condition is much more common than supposed and could well be one of the more frequent causes of chronic recurrent headache.” Headaches can also be precipitated by caffeine withdrawal especially by those who have the “habit”.

Ritchie (1975) stated that although caffeine is well absorbed when taken orally, its absorption may be erratic because of its low solubility and because it may cause gastric irritation. Caffeine is principally metabolized with only 10 percent excreted in the urine unchanged.

Parsons and Neims (1978) also cited that caffeine has a physiological half-life of three and a half hours to six hours (Aranda et al., 1979). Its physiological effects are observed in less than one hour. Infants do not metabolize caffeine as well as adults and thus have a half-life of about four days (Aranda et al., 1975). Certainly, continuous ingestion of caffeine by infants can be dangerous. If a cup of coffee is consumed by an adult six or seven times a day it would result in a high steady concentration of caffeine in the blood. As little as four cups a day can result in appreciable omnipresent amounts of caffeine in the body.

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