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Control of Blood Pressure in Hypertensive Neurological Emergencies

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Control of Blood Pressure in Hypertensive Neurological Emergencies Curr Hypertens Rep (2014) 16:436 DOI 10.1007/s11906-014-0436-x HYPERTENSIVE EMERGENCIES (BM BAUMANN, SECTION EDITOR) Control of Blood Pressure in Hypertensive Neurological Emergencies Lisa Manning & Thompson G. Robinson & Craig S. Anderson Published online: 26 April 2014 # Springer Science+Business Media New York 2014 Abstract Neurological hypertensive emergencies cause sig- Introduction nificant morbidity and mortality. Most occur in the setting of ischaemic stroke, spontaneous intracerebral hemorrhage Hypertensive emergencies are defined as large elevations in (ICH), or subarachnoid hemorrhage (SAH), but other causes systolic and/or diastolic BP (usually >180 or >120 mmHg, relate to hypertensive encephalopathy and reversible cerebral respectively) in association with impending or progressive vasoconstriction syndrome (RCVS). Prompt and controlled cerebral and other end organ damage [1, 2•]. Most occur in reduction of blood pressure (BP) is necessary, although there the setting of any of the major types of acute stroke, namely remains uncertainty as to the optimal rate of decline and ideal ischemic stroke, spontaneous ICH, or SAH, but other causes antihypertensive agent. There is probably no single treatment relate to hypertensive encephalopathy and a related disorder, strategy that covers all neurological hypertensive emergen- RCVS or Call-Flemming syndrome. Prompt diagnosis of the cies. Prompt diagnosis of the underlying disorder, recognition underlying disorder, recognition of its severity, and appropri- of its severity, and appropriate targeted treatment are required. ate targeted treatment are required, although not all neurolog- Lack of comparative-effectiveness data leaves clinicians with ical hypertensive emergencies require prompt lowering of BP, limited evidence-based guidance in management, although as such treatment may increase the risk of cerebral ischemia. significant developments have occurred recently in the field. Of the 1 billion people affected with hypertension world- In this article, we review the management of specific neuro- wide, it is estimated that 1 to 2 % will have a hypertensive logical hypertensive emergencies, with particular emphasis on emergency at some time in their life [2•, 3]. Of all the causes of recent evidence. neurological hypertensive emergencies, the majority are due to cerebral infarction (accounting for 25 % of all hypertensive emergencies), with hypertensive encephalopathy (15 %) and Keywords Hypertension . Emergencies . Critical care . ICH (5 %) accounting for most of the rest [4]. The great Neurological . Subarachnoid hemorrhage . Stroke . majority of patients who present with a hypertensive emer- Intracerebral hemorrhage . Encephalopathy gency have prior known hypertension (80 – 90 %), often with This article is part of the Topical Collection on Hypertensive Emergencies poor adherence and/or inadequate treatment, and they are : more often of non-white background, elderly and male [2•, L. Manning T. G. Robinson 5, 6]. Department of Cardiovascular Sciences and NIHR Biomedical Research Unit in Cardiovascular Disease, University of Leicester, Treatment recommendations depend on the type of associ- Leicester, UK ated organ damage. If the patient has raised intracranial pres- L. Manning sure (ICP) and/or neurological deterioration, they require e-mail: [email protected] close monitoring in an intensive care or high dependency T. G. Robinson setting to ensure careful control of BP. The lack of e-mail: [email protected] comparative-effectiveness data leaves clinicians with limited evidence-based guidance in their management of many hy- C. S. Anderson (*) pertensive emergencies [2•, 3]. Short-acting, titratable, intra- The George Institute for Global Health, University of Sydney and Royal Prince Alfred Hospital, Sydney, Australia venous antihypertensive agents are generally recommended, e-mail: [email protected] where guideline recommendations are generally based on 436, Page 2 of 11 Curr Hypertens Rep (2014) 16:436 experience and physiological rationale rather than hard evi- Conversely, persistently high BP may increase the risk of dence, but there have been some significant recent develop- ongoing bleeding in SAH and ICH, promote hemorrhagic ments [1, 7, 8]. In this review, we review the management of transformation of cerebral infarction in ischemic stroke, and specific neurological hypertensive emergencies, with particu- increase the risk of cerebral edema in all neurological hyper- lar emphasis on recent evidence. We begin with background tensive emergencies [15]. Mass effect related to hemorrhage information on the regulation of cerebral blood flow and and cerebral edema in ICH, ischemic stroke, SAH and hyper- potential implications for rapid BP lowering on the injured tensive encephalopathy, leads to elevations in ICP. In this brain. setting cerebral perfusion pressure may be compromised by high levels of MAP [16]. Whether the monitoring of cerebral perfusion pressure in such situations improves outcomes is uncertain, but this is often used to ensure that BP is not Cerebral Autoregulation and Implications for Treatment lowered disproportionate to maintaining adequate cerebral perfusion [17, 18]. Hence, while lowering BP is essential in An underlying hypothesis is that cerebral autoregulation is hypertensive neurological emergencies, it is also a complex altered in the context of hypertensive neurological emergen- and potentially harmful therapy that necessitates careful cies, which complicates the balance of potential benefits and monitoring. harms of BP-lowering treatment. Under normal circum- stances, cerebral autoregulation is organized to maintain a constant cerebral blood flow in the capillary bed to a mean Specific Conditions arterial pressure (MAP) of between 60 and 150 mmHg [9]. As BP progressively increases, vasoconstriction occurs within Acute Ischemic Stroke cerebral arterioles resulting in BP exceeding the upper limit of autoregulation,. This produces breakthrough vasodilatation Stroke is the second leading cause of death and the leading and increased cerebral blood flow, with disruption of the cause of long-term disability worldwide, with acute ischemic blood brain barrier and cerebral edema [10]. To complicate stroke accounting for approximately 70 % of all strokes [19]. matters further, intracerebral pathology, for example, acute Elevated BP is common in those presenting with acute stroke, stroke, in itself may alter cerebral autoregulation (Fig. 1) where approximately 75 % have a BP >140/90 mmHg, and [12–14]. In an altered, and increasingly pressure dependant, 50 % and 15 % have systolic BP (SBP) >160 mmHg and cerebral circulation, therapeutic reduction in BP may increase >184 mmHg, respectively [20, 21]. The natural history is for the risk of cerebral ischemia, particularly in ‘at risk’ penum- BP to decline spontaneously over the subsequent several days bral areas. after the event. Elevated BP is associated with poor short- and 120 long-term outcomes [22–25]. Data from the first International Stroke Trial suggested a U-shaped relationship between base- 100 line SBP (within 48 h of stroke) and short-term mortality and long-term death and dependency; the lowest risk of a poor 80 outcome was in patients with a SBP of 150 mmHg, with very high and very low BP associated with worse outcome [26]. 60 However, other studies have found a more linear relationship between elevated in-hospital BP and poor outcomes [27–30]. 40 Among patients receiving thrombolysis treatment, elevated Normal BP is associated with a near linear increase in the risk of symptomatic ICH, with a U-shaped trend in the risk of death 20 Cerebral ischaemia Cerebral Blood Flow (ml/100g) and dependency at 3 months [22]. Based on these observa- Chronic hypertension tional data, the ideal SBP is 140-150 mmHg in the context of 0 0 50 100 150 200 250 acute ischemic stroke. Cerebral Perfusion Pressure (mmHg) There is limited and conflicting evidence regarding the benefits of BP-lowering treatment in acute ischemic stroke, Fig. 1 The cerebral autoregulation curve in normal individuals, and in patients with chronic hypertension and cerebral ischemia. The in part due to the heterogeneity of time to treatment, entry autoregulatory curve is shifted to the right in chronic hypertension, criteria, type and severity of stroke, and degree and speed of maintaining constant CBF at higher CPP than normal. Therefore, in those BP control across clinical trials. Table 1 describes important with chronic hypertension, greater elevations in blood pressure than those trials in this area and their key findings. The totality of the in non-hypertensive individuals, may be required before cerebral auto- regulation is overwhelmed. In the setting of cerebral ischemia, autoreg- evidence to date is that modest BP lowering with oral agents ulation is impaired, and CBF becomes proportional to CPP [11] within the first 48 h after the onset of ischemic stroke is safe, Curr Hypertens Rep (2014) 16:436 Ta b l e 1 Important Randomized, Controlled Trials of Intervention versus Control in BP Management Following Stroke. All trials included patients with ischaemic stroke and ICH Name (year) Number of Initial median Time to Treatment Outcome measures Key findings participants SBP (mmHg) treatment (hours) SCAST (2013) 2,029 171 17.8 Candesartan PO* Composite endpoint of vascular death, No beneficial effect seen in treatment group [31•] myocardial infarction, or stroke during the first 6 months Functional outcome at 6 months COSSACS
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