Acetaminophen is one of the most familiar pain medicines in the world, but researchers have found that it can have a surprising effect when given directly into a vein.
A study from the University of Copenhagen found that intravenous acetaminophen can temporarily lower blood pressure. The effect may be particularly important for critically ill patients, whose blood pressure may already be difficult to keep stable.
Acetaminophen, also called paracetamol in many countries, is used to reduce pain and fever. Most people take it as a tablet or liquid at home, and it is generally considered safe when used at recommended doses.
In hospitals, however, doctors may give the medicine through an intravenous line when a patient cannot easily take medication by mouth.
The way a medicine enters the body can change what happens to it. When acetaminophen is swallowed, it travels through the digestive system and is processed mainly by the liver before its breakdown products circulate more widely. Giving the drug directly into the bloodstream creates a different pattern of processing and exposure.
Doctors have previously noticed that some seriously ill patients experience a fall in blood pressure after receiving intravenous acetaminophen.
This can be more than a minor concern in intensive care, where patients may already have dangerously low blood pressure because of severe infection, surgery, injury or other medical problems. A further decrease can reduce the amount of blood reaching vital organs.
Researchers led by Thomas Qvistgaard Jepps wanted to understand why this happens. Their work focused on potassium channels, tiny structures in the walls of blood vessels that help control whether the vessels tighten or relax. Changes in these channels can alter the width of blood vessels and therefore influence blood pressure.
The researchers found evidence that intravenous acetaminophen can lead to the formation of substances that affect these potassium channels. When the channels are activated, blood vessels can relax and become wider. Wider blood vessels reduce resistance to blood flow, which can cause blood pressure to fall.
This mechanism could help explain an effect that has been observed frequently in critically ill patients. According to the researchers, a drop in blood pressure has been reported in around 60% of critically ill patients receiving intravenous acetaminophen.
Among those affected, roughly one-third have required medical treatment to bring their blood pressure back to a safer level.
To investigate the mechanism more closely, the researchers performed experiments in rats. They found that blocking certain potassium channels could prevent the blood pressure reduction caused by intravenous acetaminophen. This provided evidence that the channels play an important role in the reaction.
The finding could eventually help doctors develop better ways to prevent or manage this side effect. For example, identifying patients who are particularly vulnerable to a sudden blood pressure decrease could allow closer monitoring during treatment. The biological mechanism might also provide a target for future treatments designed to limit the effect.
The results do not mean that ordinary acetaminophen use suddenly needs to be considered dangerous. The research is mainly relevant to intravenous treatment, particularly in seriously ill hospital patients. Taking acetaminophen by mouth does not expose the body to the drug in exactly the same way.
This distinction is important because millions of people safely use oral acetaminophen for headaches, fever and other common forms of pain.
The new findings should not be interpreted as evidence that a normal tablet routinely causes a dangerous fall in blood pressure. Instead, they show that the route used to deliver a medicine can influence its effects.
Intravenous acetaminophen can still be useful in hospitals. It provides pain and fever relief without some of the problems associated with other pain medicines, and it can be given to patients who cannot swallow. Doctors must simply consider its benefits alongside the possibility of a temporary blood pressure decrease.
The study also offers a broader lesson about familiar medicines. A drug can behave differently depending on its dose, how it enters the body and the health of the person receiving it. Effects that are minor in a healthy person may become much more important in someone who is critically ill.
There are also limits to what the research can tell us. Some of the detailed work explaining the potassium-channel mechanism was performed in animals, so further research is needed to establish exactly how the process works in people.
Researchers will also need to determine the best way to predict which hospital patients are most likely to experience a clinically important blood pressure drop.
Overall, the findings provide a biological explanation for a side effect that hospital clinicians have already observed.
They do not challenge the general usefulness of acetaminophen, but they support careful blood pressure monitoring when the drug is given intravenously to vulnerable patients. Better understanding of the mechanism could ultimately make this common treatment even safer.
The study was led by Thomas Qvistgaard Jepps and researchers at the University of Copenhagen. The research was published in the American Heart Association journal Atherosclerosis, Thrombosis, and Vascular Biology.
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