How does pseudoephedrine raise blood pressure




















Adrenaline raises blood pressure and heart rate. In , the FDA recommended the withdrawal of medications that contained another decongestant in the adrenaline family, phenylpropanolamine, which had been linked to an increased risk of hypertension and stroke. To continue reading this article, you must log in. Already a member? Login ». As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles.

No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. Thanks for visiting. These products will help reduce inflammation of the nasal passages more than non-hypertonic products. Nasal steroid products e. Flonase are effective in relieving nasal congestion.

The effect may not be as immediate as Sudafed pseudoephedrine products , but they gain effectiveness over time. Contents Overview Safety Alternatives. Was this article helpful? We'll never share your email with anyone else. Submit Close. Staiger walrus. Related Articles. View more articles. Future research might examine subsets of the population at risk for autonomic insufficiency, such as diabetic patients, to determine whether exaggerated BP responses to oral pseudoephedrine are present.

Although few patients had extreme elevations in BP, many individual patients had changes, raising the BP from low normal to high normal or slightly hypertensive levels.

Given the uncommon description of adverse effects in the studies we reviewed, it is unlikely that these changes are of clinical significance to most patients. We were also interested in whether the normal elevation of BP and HR during exercise was accentuated by pseudoephedrine.

The medication did not produce significant increases in BP or HR with exercise above the levels in those not exposed to pseudoephedrine in the young, healthy population studied. This study had several limitations. First, the population studied included an insufficient number of older patients to reach conclusions on use in the elderly population. Second, we evaluated only 1 element of safety—BP and HR. Pseudoephedrine may have many other adverse effects, such as drug-drug interactions, that are beyond the scope of this article.

Many of the included studies pooled baseline vital sign data for placebo and treatment groups. Separate analysis of studies with separate baseline data for both groups, and higher-quality studies in general, showed less pronounced effects on vital signs. Therefore, we may have overestimated the effect of pseudoephedrine in our results. However, we believed it was important to highlight the worst-case scenario for patients, and we chose to include the lesser-quality studies.

In addition, the studies reported mean BP and HR responses rather than individual data. Mean results may mask extreme responses. If 40 individuals had only a 1— or 2—mm Hg increase in SBP but 1 increased BP by 30 mm Hg, this would still yield an average response of only 1 to 2 mm Hg. Some studies included a statement that no participant had a marked increase in BP, but most provided no information. Moreover, our total study sample size was patients, which may be too small to detect rare idiosyncratic adverse events.

The emergence of a risk of hemorrhagic stroke and marked BP elevation in postmarketing surveillance with phenylpropanolamine was seen in only a few cases when the total number of prescriptions in the general population was in the millions. Our data cannot be used to fully eliminate the possibility of this risk. In addition, we may have experienced publication bias.

It is likely that studies may have been more likely to report their data when an effect was seen. If so, then our analysis would tend to overstate the mean magnitude of effect. These effects are greatest in magnitude with immediate-release formulations, higher doses of medication, and short-term medication administration. Patients with stable, controlled hypertension do not seem to be at higher risk for BP elevation as a group than other patients when given pseudoephedrine along with their antihypertensive medications.

Effects of pseudoephedrine may be important when considered on a population basis given their widespread use as decongestants. Although we did not find any life-threatening adverse effects of BP elevation in this review, a meta-analysis cannot predict how any individual patient will react. Therefore, the risk-benefit ratio should be evaluated carefully before using sympathomimetic agents in individual patients most at risk for BP and HR elevations.

We encourage physicians to instruct patients with cardiovascular disease to monitor their BP carefully after starting therapy. Correspondence: Stephen M. Disclaimer: The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting those of the Department of the Army or the Department of Defense.

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue. Figure 1. View Large Download. Table 1. Subjects were randomly assigned to receive pseudoephedrine or placebo during the 2nd week of the study, and to receive the opposite during the 4th week of the study.

Blood pressure readings were taken at the beginning and end of each week of the trial, and at a 1-week poststudy follow-up visit. The mean diastolic pressure was 82 mm Hg in patients receiving pseudoephedrine and



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