Severe Hypertension in Hospitalized Patients: To Treat or Not to Treat?

Hypertension (HTN) is highly prevalent among hospitalized patients and ranges from about 50% to 70%.1 Moreover, roughly 10% of hospitalized patients develop incident severe HTN [sHTN; blood pressure (BP) >180/110 mm Hg] after admission.2,3 Previous studies suggest that intermittent treatment of severe incident HTN in the hospital setting could result in acute target organ damage (i.e., acute kidney and myocardial injury) and increase the length of hospital stay.3–5 Although this adverse health outcome may be related to an antihypertensive drug-induced precipitous drop in BP,6–8 many patients may develop spontaneous reduction in BP without drug treatment. However, previous studies have not systematically identified predictors of spontaneous reduction in BP. In the present issue of American Journal of Hypertension, Garg et al.9 performed a retrospective study in patients who were initially hospitalized without a cardiovascular or hypertensive emergency as the admitting diagnosis. The authors included a large cohort of over 12,000 patients who developed sHTN in a tertiary care hospital system setting. Information related to medications that may influence BP such as nonsteroidal anti-inflammatory drugs, narcotics, sedatives, and corticosteroids administered before the onset of sHTN was extracted from the electronic medical record (EMR) and included in the analysis. More importantly, the presence or absence of pain was obtained from the chart review. Of the entire cohort, 44.2% experienced spontaneous BP reduction without the use of antihypertensive therapy. Although numerous factors were identified in the univariate model, multivariable logistic regression analyses only identified the presence of chronic obstructive pulmonary disease (COPD) or cardiac arrhythmia, with a spontaneous fall in BP during hospitalization. Moreover, higher age, serum potassium, white blood cell count, heart rate, and body mass index were likewise found to be associated with a spontaneous fall in BP during hospitalization. Among these factors, recent exposure to steroids within 6 hours of having sHTN were found to be associated with the highest odds of experiencing a spontaneous BP reduction [1.30 (95% CI: 1.09, 1.56)]. Overall, there were several interesting correlates disclosed in these analyses. However, these correlations cannot be regarded as causation. Particularly, steroid use in the general population is expected to elevate, rather than reduce, BP. It is plausible that steroid use may be a surrogate for unmeasured confounders such as an acute exacerbation of COPD, which was not captured in the EMR for the present study. Development of hypoxia during a COPD exacerbation may lead to activation of the chemoreflex with a resultant increased sympathetic vasoconstrictor discharge,10 while treatment with bronchodilators and corticosteroids may lead to improvement in oxygenation and a subsequent fall in BP. Moreover, systemic steroid use maybe a surrogate for underlying arthritic pain related to a variety of connective tissue diseases, which may be improved once pain severity has subsided. Similarly, the presence of an elevated heart rate and cardiac arrhythmia may indicate stress or anxiety as a cause of the BP surge, which may be resolved spontaneously after environmental or behavioral intervention that does not require medication use. Unfortunately, details regarding treatment of COPD exacerbation by respiratory therapist, the type (oral vs. inhaled) of steroid use, or nursing intervention to calm down agitated patients are not readily available from the study to provide further clarification. In addition, these correlates had contestably minimal differences between those who experienced a spontaneous BP drop and those who did not. For example, steroid use was present in only 5.1% of patients with spontaneous BP drop vs. 3.4% of patients in the group without a spontaneous BP reduction. Similarly, COPD was identified in 38% of patients with a spontaneous fall in BP vs. 35% of patients without a BP reduction. More importantly, these predictors have not been subjected to external validation by another cohort. The cardiovascular outcomes and hospital length of stay among patients with and without spontaneous vs. drug-induced BP reductions were not reported, which limits ability to inform clinical practice. Despite these limitations, this study demonstrated that almost half of patients who developed severe incident HTN after admission had a spontaneous BP reduction without the use of antihypertensive therapy. Future studies should be aimed at identifying and understanding the mechanistic underpinnings of patients who experience spontaneous BP reductions to better inform clinical practice guidelines with the goal to mitigate the use of unnecessary antihypertensive medications. In the meantime, based on other studies,3–5 the pro re nata use of antihypertensive medication in hospitalized patients with acute sHTN without active target organ damage should not be considered standard of care and should generally be avoided to minimize hypoperfusion of vital organs and potential higher risk for serious cardiovascular adverse events. The authors declared no conflict of interest.