Apart from essential hypertension and secondary hypertension resulting from renal parenchymal/vascular disease, endocrine and cardiac disorders, certain secondary factors may cause acute elevation of BP in the hospitalized patient8,9 (Table 1).

There is no universally acceptable guideline for BP measurement in bed-ridden hospital patients. An audit at a single centre in UK which closely observed practice of in-patient BP measurement (IPBPM) noted 100% deviation in IPBPM technique compared to BP measurement guidelines recommended by the National Institute for Healthcare Excellence (NICE) and European Society of Hypertension (ESH) for office BP monitoring which resulted in frequent overestimation of BP in the hospital setting.10 Measures to standardize IPBPM have been proposed which need further validation10 (Table 2).

Preliminary history and physical exam should be focused on identification of underlying hypertensive emergency. Once the possibility of hypertensive emergency has been excluded, history should be directed to understand the background for current admission, duration of hypertension, presence of pertinent symptoms, concurrent medication, alteration in treatment regimen, presence of comorbidities and any substance abuse (Table 3). A systematic physical exam can assist in confirming diagnosis of hypertension, possible duration (acute/chronic), HMOD and evidence of a cause of identifiable hypertension (Table 3).

Routine diagnostics are performed to evaluate for any underlying causes, end-organ damage and ascertain cardiovascular risk. These include glucose, urinalysis, creatinine with an estimated glomerular filtration rate (eGFR), electrolytes, thyroid profile, lipid profile and electrocardiogram (ECG). Ancillary testing is not recommended when managing acute hypertensive episodes unless indicated for other clinical reasons.11

When confronted with a hypertensive emergency there is a perceived need for intensification of antihypertensive therapy. The estimated in-hospital and one-year mortality for those with hypertensive emergency is 13% and 39%, respectively.13 All such patients need to be closely monitored in intensive care and treated with intravenous antihypertensives. The optimal therapy, choice of drug and goal of BP depends on etiologic factors causing the hypertensive emergency. However, there is insufficient evidence to conclude that lowering BP in hypertensive emergency reduces morbidity or mortality, except in conditions of abdominal aortic dissection and cerebrovascular accident.14–16 A Cochrane systematic review in 2008 found insufficient evidence to determine which drug or drug class is most effective for reducing mortality and morbidity due to hypertensive emergency.16 Rate of BP reduction is guided by autoregulatory principles and guidelines recommend BP to be reduced no more than 20–25% during the first hour and to be maintained at 160/100–110mm Hg during the next 6h.17 Therapy should be gradually transitioned from intravenous therapy to long acting antihypertensives to minimize risk of rebound hypertension.

The one-year mortality of hypertensive urgency is around 9%.13 A retrospective propensity matched cohort study in patients with hypertensive urgency showed no significant difference in major adverse cardiac events (MACE) between those managed as out-patient compared to those referred to a hospital over 1week, 1 month and 6 month period.18 Another study of 549 patients with hypertensive urgency attending emergency room, reported a reduction in BP (20mm Hg decrease in systolic and 10mm Hg decrease in diastolic BP) in 32% patients with a 30-min rest period alone. The remaining patients who did not have reduction in BP with rest had satisfactory response with oral anti-hypertensives in a 2-h average follow-up period.19 In a retrospective cohort of 1016 adult primary hypertension patients, presenting with an initial BP>180/100mm Hg and no HMOD there was no difference between hospital revisits and mortality over a follow up of 30 days whether they were treated with anti-hypertensives or not.20 However, even in the absence of acute HMOD, hypertensive urgency has long term implications with increased risk of cardiovascular events in 2 years and five times higher risk of stroke in 3 years.21,22

Despite the lack of evidence to support reduced short term morbidity and mortality with antihypertensives in acute elevated BP>180/100mm Hg, without target organ damage physicians feel compelled to treat the numbers, often with intravenous antihypertensives.12 There are concerns that using the term “hypertensive urgency” has led to overly aggressive management of severe uncomplicated hypertension.23 The 2017 American guidelines on hypertension advocate reinstitution or intensification of anti-hypertensive drugs with treatment of anxiety in treatment of hypertensive urgency.17 There is no indication for intravenous antihypertensives or immediate reduction of BP in such patients.17,24 We propose the approach shown in Fig. 1 for the management of acute severe hypertension in the hospitalized patient.

Fig. 1.

Management of acute severe hypertension in the hospitalized patient (Pathway 1).

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According to statistics of the American heart association (AHA), in 2005 there were 301,000 with a primary diagnosis of essential hypertension compared to 9,000,300 hospitalizations as a secondary diagnosis.25 Patients admitted for reasons other than a primary diagnosis of hypertension frequently have transient elevations in BP which are not categorized as acute severe hypertension (<180/110mm Hg). This often results in modification of their out-patient anti-hypertensive regimen or new prescriptions “as needed”. There are no studies designed to evaluate if this practice improves outcomes.

A study reported that 11% patients admitted to ICU with ≥1 episode of asymptomatic hypertension (BP>160/90mm Hg) were treated inappropriately with intravenous antihypertensives with a converse increase in BP in 14% of them.26 A report estimates 8.3 inappropriate intravenous anti-hypertensive orders per 1000 patient days with nearly half of them having an adverse event. They also designed an intervention by providing guidance for nurses on assessment for precipitating factors of hypertension such as anxiety, pain and HMOD through specific guided algorithms before contacting physicians. This intervention reduced intravenous hypertensive orders by 60% and number of adverse events (defined as>25% reduction in BP, change in heart rate by>20 beats per minute, or need for IV fluids) by 57% per 1000 patient days.27

In a retrospective propensity matched cohort of 4056 older adults (>65 years) with admission for three non-cardiac conditions (pneumonia, urinary tract infection or venous thromboembolism), discharge with intensified anti-hypertensive regimen was associated with increased risk of re-admissions and serious adverse events defined as hypotension, syncope, electrolyte abnormalities or acute kidney injury (AKI) at 30 days.28 Moreover there was no reduction in cardiovascular events or BP at 1-year follow-up.

Overall current evidence does not support use of intravenous antihypertensives or intensive lowering of BP in these patients and suggests potential harm if BP is lowered rapidly. When considering treating acute hypertension in hospital physicians should meticulously exclude secondary factors (Table 1) resulting in increased BP followed by rest for at least 30min. The BP should be measured by correct technique and if the patient remains hypertensive, and likely to remain hypertensive post hospitalization, oral antihypertensives should be optimized. We propose the approach shown in Fig. 2 for the management of non-emergent hypertension in hospital.

Fig. 2.

Management of nonemergent elevated BP in hospitalized patient (Pathway 2).

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Overwhelming majority of physicians believe that is appropriate to discharge patients on the final anti-hypertensive regimen established during hospital course.12 Though this practice is reasonable for a diagnosis of ‘de novo’ hypertension during hospitalization, changing a previously established antihypertensive regimen prescribed by out-patient care provider may disrupt continuity of care.29 Patients may also stop the new medications due to adverse effects, unawareness of new regimen, pill burden or based on the advice of out-patient care provider who felt they were not indicated. Application of evidence-based knowledge by treating clinician, anti-hypertensive medication reconciliation at discharge, accurate communication between care providers with active patient and family involvement will ensure optimal transition of care.30