J Geriatr Cardiol 2018; 15: 504?512. doi:10./

1 Introduction

Hypertension (HTN) remains a common illness around the World.[1] Uncontrolled HTN can lead to hypertensive crises. These are divided into two groups, urgencies and emergencies.[2] Both of them involve severe elevations of blood pressure (BP) more than 180/120 mmHg.[3] The core difference between them is whether severe HTN causes any organ dysfunction (hypertensive emergency) or not (urgency).[1,3] These crises are common among the elderly.

Management of hypertensive crises in elderly patients should integrate a comprehensive set of pharmacological strategies, depending on the core pathophysiological changes related to aging, preexisting risk factors, coexistent comor-bidities, speed of progression of the condition, and the ex-tensiveness of organs involvement. Failure to successfully manage these crises in the elderly is associated with significant morbidity and mortality.[4]

2 Epidemiology and pathophysiology

HTN is one of the most important diseases among in the elderly population. According to the National Health and Nutrition Examination Survey during 2015–2016, 63.1% of American people aged > 60 years have elevated blood pressure.[5] The vast majority of these patients have essential HTN.[6] In addition, HTN remains a major risk factor for cerebrovascular as well as cardiovascular diseases, two of the leading causes of death in the United States causing about 770,000 deaths only in 2016.[7]

The incidence of HTN, and hence, its complications such as hypertensive crises, is different among different groups, and is higher in the elderly and African-Americans.[8–11] Hypertension is not just more prevalent in elderly people, but mortality and morbidity are more significant as well.[12] The investigators of the multicenter STAT registry reported a hospital mortality rate of 6.9% among patients with acute hypertensive crises requiring hospitalization and a cumulative 90 day mortality of 11% among these patients.[13]

Severe HTN is predominant among patients with history ofHTN in the majority of cases.[10] Many of them have inadequate previous medical management, or poor compliance to treatment.[12] Those preventable causes should be addressed and treated, as the recurrence rate of acute hypertensive crises is high. The STAT investigators reported a 90-day readmission rate of 37%, of which, 25% were due to recurrent acute hypertensive crises.[13]

To understand the extent of HTN among the elderly, one must be aware of the pathophysiology of this entity. The regulation of BP is a concert of several organs/systems. The most important mechanisms are the cardiac output and systemic vascular resistance (SVR).[14] Elderly people suffer increased SVR and, hence, elevated BP.[15] Several mechanisms have been suggested to explain the increase in SVR, such as endothelial dysfunction, neuro-hormonal dysregulation, and a reduction in renal homeostatic mechanisms due to decreased glomerular filtration rate (Figure 1).[14,16,17]

3 Clinical manifestations

Many elderly patients with severe uncontrolled HTN are totally asymptomatic. Pinna and collaborators, in a study of 1,546 patients (mean age = 69 years) presented with acute hypertensive crises, reported that 55.6% of the patients referred non-specific symptoms such as dizziness, palpitations, and headache.[18] Whereas symptoms related to end-organ damage, such as chest pain and focal neurologic deficits, were evident in 28.3% and 16.1% of patients, respec-tively.[18] Elderly patients are more likely to have hypertensive emergencies, rather than urgencies, than the general population.[13]

The most frequent end-organ damage associated with hypertensive emergencies are cerebral infarction, acute pulmonary edema, and hypertensive encephalopathy (24%, 23%, and 16%, respectively).[2]

4 Management

The management of hypertensive crises in elderly re-quires prompt understanding of the pathophysiology of the disease, the physiological changes among them, and me-chanism of action and side effects of the medications available (See Table 1). Most experts advise to generally reduce the mean arterial pressure by approximately 10%–15% during the first hour, and another 10%–15% during the next 2 to 4 hours due to the risk of hypoperfusion if the BP is lowered too suddenly or too far (e.g., into the range of < 140/90 mmHg).[19–21] However, faster drop in BP is required in certain conditions, such as aortic dissection, in which BP should be kept between 100 and 120 mmHg systolic and less than or equal to 60 to 70 mmHg diastolic as fast as possible.[20,22,23] While in the acute phase of ischemic stroke, it has been recommended that lowering of BP should be delayed unless BP is > 220/120 mmHg or > 200/100 mmHg with end organ damage or if the patient will receive thrombolytics.[24] In hemorrhagic stroke, the target BP is variable but generally systolic blood pressure (SBP) can be reduced safely to ￡ 140 mmHg.[25] The INTERACT2 trial showed that a rapid decrease of BP does not have a representative reduction in primary outcome of mortality or severe disability in patients with an acute intracerebral hemorrhage, however, their analysis of modified Rankin scores revealed that patients had a better functional outcome when their BP was intensively decreased.[26]