The classification and approach to hypertension undergoes periodic review by the Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure with the most recent report (JNC 8) having been released in 2014 [3]. This most recent report is quite controversial and unlike previous reports did not provide a classification of hypertension. The previous report published in 2003 (JNC 7) recognized two stages of hypertension (compared to the previous four stages in JNC 6), namely, Stage 1 with a Systolic BP (SBP) of 140–159 and a diastolic BP (DBP) of 90–99 and Stage II hypertension with a SBP ≥ 160 or a DBP ≥ 100 mmHg [4]. Although not specifically addressed in the JNC 7 report, patients with a systolic blood pressure of greater than 179 mmHg or a diastolic that is greater than 109 mmHg are usually defined as having a “hypertensive crisis”. The 1993 report of the JNC proposed an operational classification of hypertensive crises as either “hypertensive emergencies” or “hypertensive urgencies” [5]. This classification remains useful today. Severe elevations in BP were classified as:

Distinguishing hypertensive urgencies from emergencies is critically important in formulating a therapeutic plan. Patients with hypertensive urgency should have their BP reduced within 24–48 h (with PO medication), whereas patients with hypertensive emergencies should have their blood pressure lowered immediately (in the ICU), although not to “normal” levels. The term “malignant hypertension” has been used to describe a syndrome characterized by elevated BP accompanied by encephalopathy or acute nephropathy. This term, however, has been removed from National and International Blood Pressure Control guidelines and is best referred to as a hypertensive emergency.

The vast majority of patients presenting with a hypertensive emergency to an emergency department (ED) have previously been diagnosed with HTN and have been prescribed antihypertensive agents [6, 7]. However, in many of these patients BP control prior to presentation was inadequate [7]. The lack of a primary care physician as well as the failure to adhere to prescribed antihypertensive regimens has been associated with the development of a hypertensive emergency [6, 8]. In the prospective study by Saguner and colleagues, female sex, high grades of obesity, coronary artery disease and non-adherence to medications were associated with hypertensive crisis [9]. In both major metropolitan areas and smaller communities, illicit drug use has been reported to be a major risk factor for the development of hypertensive emergencies [8].

The Studying the Treatment of Acute hypertension (STAT) is a 25-institution US registry of 1,588 patients with severe acute hypertension enrolled between January 2007 and April 2008 who were treated with intravenous therapy [10]. The mean age of the patients was 53 years, 49 % were women and 56 % were African American with a median admission BP of 200/100 mmHg. In the STAT registry the hospital mortality was 6.9 % with an aggregate 90-day mortality of 11 % and a 90-day readmission rate of 37 %.

The factors leading to the severe and rapid elevation of BP in patients with hypertensive emergencies are poorly understood. The rapidity of onset suggests a triggering factor superimposed on pre-existing hypertension. Hypertensive emergencies are thought to be initiated by an abrupt increase in systemic vascular resistance likely related to humoral vasoconstrictors [11]. The subsequent increase in BP generates mechanical stress and endothelial injury leading to increased permeability, activation of the coagulation cascade and platelets, and deposition of fibrin (See Fig. 28.1). With severe elevations of BP, endothelial injury and fibrinoid necrosis of the arterioles ensue. This process results in ischemia and the release of additional vaso-active mediators generating a vicious cycle of on-going injury. The volume depletion that results from pressure natriuresis further simulates the release of vasoconstrictor substances from the kidney. These collective mechanisms can culminate in end-organ hypoperfusion, ischemia and dysfunction that manifests as a hypertensive emergency.

The clinical manifestations of a hypertensive emergency are directly related to the particular end-organ dysfunction that has occurred, and includes:

The signs and symptoms of a hypertensive crisis vary from patient to patient. In the STAT registry the most common presenting symptoms included shortness of breath (29 %), chest pain (26 %), headache (23 %) altered mental status (20 %) and focal neurologic deficit (11 %) [10]. Microangiopathic hemolysis has been reported in up to 27 % of patients presenting with a hypertensive crisis [12]. It is important to make this diagnosis as it is usually associated with reversible renal insufficiency. No particular BP threshold has been associated with the development of a hypertensive emergency. However, organ dysfunction is uncommon with a DBP less than 130 mmHg (except in children and pregnancy) [13]. The absolute level of BP may not be as important as the rate of increase [14–16]. For example, in patients with long-standing hypertension, SBP of 200 mmHg or a DBP up to 150 mmHg may be well tolerated without the development of hypertensive encephalopathy, whereas in children and pregnant women encephalopathy may develop with a DBP of only 100 mmHg [17].

The majority of patients in whom severe hypertension (SBP > 160, DBP > 110 mmHg) is identified on initial evaluation will have no evidence of acute end-organ damage and thus have a hypertensive urgency. Since no acute end-organ damage is present, these patients may present for evaluation of another complaint and the elevated BP may represent an acute recognition of chronic hypertension. In these patients, oral medications to lower the BP gradually over 24–48 h is the best approach to management [11]. Rapid reduction of BP may be associated with significant morbidity in hypertensive urgency due to a rightward shift in the pressure/flow auto-regulatory curve in critical arterial beds (cerebral, coronary, renal) (see Fig. 28.2). Rapid correction of severely elevated BP below the autoregulatory range of these vascular beds can result in marked reduction in perfusion causing ischemia and infarction. Therefore, although the BP must be reduced in these patients, it must be lowered in a slow and controlled fashion to prevent organ hypoperfusion.