Sergio L. Zanotti-Cavazzoni

Chapter Outline

Introduction

Hypertension is a common clinical disorder. Estimates indicate that almost 30% of the U.S. adult population suffers from elevated blood pressure.¹ Furthermore, one third of these patients are unaware of their diagnosis, and of those who are diagnosed and treated, only 34% have adequate control of their blood pressure.² Severe elevations in blood pressure, hypertensive crises, will occur in about 1% of patients with chronic hypertension.^1,3 Hypertensive crises constitute a clinical problem that the intensivist will encounter in the hospital setting. Unfortunately, a paucity of clinical studies evaluating optimal therapeutic strategies and a lack of consideration for key pathophysiologic aspects have led to common misunderstandings and pitfalls in the management of patients with hypertensive crises.

Definitions

According to the seventh report of the Joint National Committee (JNC) on Detection, Evaluation, and Treatment of High Blood Pressure, hypertension is classified into three stages: prehypertension, stage 1, and stage 2 (Table 34.1).³ The terms malignant hypertension and accelerated hypertension have been abandoned. These terms were utilized to describe severe elevations in blood pressure associated with advanced retinopathy (Keith-Wagener-Barker stages 3 and 4). Prognosis of these clinical entities has improved dramatically with the advent of effective drugs for hypertension. In addition, studies have demonstrated that retinopathy as measured by the Keith-Wagener-Barker classification does not correlate with severity of hypertension or outcomes.⁴

Hypertensive crises are defined as severe elevations in blood pressure. Although some authors have suggested a diastolic blood pressure (DBP) > 120 mm Hg, it is preferable to evaluate acute elevations of blood pressure within the context of each individual patient and the effects a given blood pressure has on organ function in that patient. For example, an acute raise in diastolic blood pressure to a value of 100 mm Hg can cause significant damage in a previously normotensive individual whereas a diastolic pressure of 130 mm Hg may be tolerated in a patient with a history of uncontrolled hypertension. As we will see, these patients will require different therapeutic approaches. To clarify these situations better, hypertensive crises have been traditionally classified into hypertensive emergencies and hypertensive urgencies.

A hypertensive emergency is a severe elevation in blood pressure associated with the presence of acute end-organ damage. Hypertensive emergencies require immediate control of blood pressure, within 1 to 2 hours, to prevent further organ damage. This will usually require the use of intravenous medications and invasive monitoring (arterial line) in a high-dependency unit such as the intensive care unit. The principal systems susceptible to acute end-organ damage from severe elevations in blood pressure include the central nervous, cardiovascular, and renal systems (Fig. 34.1). Several clinical situations are associated with hypertensive emergencies (Box 34.1). The absolute level of blood pressure and the time course of this elevation will determine the development of a hypertensive emergency. However, acute end-organ damage can occur at different blood pressure values in different patients. Therefore, it is more useful to define hypertensive emergencies with the presence of acute end-organ damage as opposed to specified numbers of systolic or diastolic blood pressure. In addition to initiating immediate therapeutic interventions, patients with a hypertensive emergency may require further diagnostic evaluation to determine the cause of their elevated blood pressure. Depending on the population studied, 20% to 50% of patients presenting with a hypertensive emergency will have a secondary cause of hypertension identified.⁵

A hypertensive urgency occurs when severe elevations of blood pressure occur without evidence of acute end-organ damage. In hypertensive urgencies, the blood pressure can be lowered more gradually, over 24 to 48 hours. This can be accomplished usually with oral medications and does not require invasive hemodynamic monitoring in an intensive care unit. Hypertensive urgencies can be associated with chronic stable organ dysfunction, such as stable angina, chronic renal insufficiency, or previous cerebrovascular accident, without evidence of acute end-organ damage.

Pathophysiology

The underlying pathophysiology of hypertensive crises is still not fully understood. The transition of mild hypertension or normotension to a hypertensive crisis is usually caused by an event that leads to an abrupt increase in blood pressure. Situations associated with this event may include cessation of hypertensive medications with potential rebound effects, consumption of illicit drugs, and severe pain, as well as several clinical syndromes. Blood pressure is determined by the product of cardiac output and systemic vascular resistance (BP = CO × SVR). In most hypertensive crises, the initial rise in blood pressure is secondary to increased systemic vascular resistance. The rise in systemic vascular resistance is believed to be caused by humoral vasoconstrictors.⁶ With the increase in blood pressure, mechanical stress on the arteriolar wall leads to endothelial damage and fibrinoid necrosis of the arterioles.^6,7 Vascular damage leads to loss of autoregulatory mechanisms, ischemia, and acute end-organ damage, which prompts further release of vasoconstrictors and initiates a vicious cycle (Fig. 34.2).^6,7

Approach to Management

Unfortunately there is a paucity of clinical trials to guide the clinician in the optimal management of patients with hypertensive emergencies. However, a systematic approach with consideration of underlying pathophysiology can help the clinician to avoid common pitfalls in the clinical management of patients with hypertensive crises. The most common pitfall in treating patients with hypertensive crises involves treating numbers without evaluating individual patients for acute end-organ damage. This usually is associated with inappropriate use of intravenous drugs with the potential for precipitous and harmful drops in blood pressure. A methodical approach to patients with severe elevations in blood pressure can help establish safe and effective treatment. To that effect, the clinician should address three fundamental questions: