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ORIGINAL ARTICLE
Blood Pressure Management in Acute
Stroke: Comparison of Current
Guidelines with Prescribing Patterns
Salmann Kanji, Céline Corman, Andre G. Douen ABSTRACT: Objective: Current recommendations for treating elevated blood pressure (BP) in the acute stroke are based largely on
expert opinion and vary with regard to treatment thresholds and choice of antihypertensive agents. In this study we investigate the
influence of these recommendations by comparing the management of hypertension in acute stroke at a tertiary care hospital with
current guidelines. Method: Retrospective chart review of patients admitted with acute stroke at The Ottawa Hospital-General Campus
over six consecutive months. The use of antihypertensive medications (type, dose, routes of administration, BP recordings) in the first
seven days after admission was noted. Results: Transdermal nitroglycerin paste was the most commonly used antihypertensive agent.
In contrast to the 15% reduction in BP over 24 hours recommended for lowering BP in hypertensive patients with ischemic stroke,
nitroglycerin caused a >15% reduction of BPover the first 24 hours on 60% of the occasions used. Furthermore, despite concerns about
sublingual nifedipine, this was the second most commonly prescribed agent. Surprisingly, the mean time to first BP measurement
following initiation of antihypertensive therapy was 117 ± 43 minutes in ischemic stroke and 88 ± 89 minutes in hemorrhagic strokes.
Conclusions: The current guidelines for management of acute poststroke hypertension appear to have little influence on prescribing
patterns, leading to considerable variations in practice. Such variations, likely due to uncertainty caused by lack of evidence from
randomised controlled trials, are intolerable as patients maybe submitted to nonstandardised, potentially harmful care such as
inappropriate choice of antihypertensives and inadequate BP monitoring as observed in this study.
RÉSUMÉ: La prise en charge de la tension artérielle dans le traitement de l’accident vasculaire cérébral aigu: comparaison des lignes
directrices actuelles et des modes de prescription. Objectif: Les recommandations en vigueur pour le traitement de l’hypertension artérielle (HTA)
dans l’accident vasculaire cérébral aigu (AVCA) sont basées en grande partie sur l’opinion d’experts et varient quant aux niveaux où un traitement est
indiqué et au choix d’agents antihypertenseurs. Dans cette étude, nous évaluons l’influence de ces recommandations sur la pratique en comparant la
prise en charge de l’hypertension dans l’AVCAdans un hôpital de soins tertiaires et les lignes directrices en vigueur. Méthode: Il s’agit d’une revue de
dossiers de patients présentant un AVCA admis à l’Hôpital Général d’Ottawa sur une période de six mois. L’utilisation de médicaments
antihypertenseurs (type, dose, voie d’administration, lectures de tension artérielle (TA)) pendant les sept premiers jours après l’admission ont été relevés.
Résultats: La nitroglycérine administrée par voie transdermique était l’agent antihypertenseur le plus souvent utilisé. Alors que la baisse de la TA
recommandée chez les patients hypertendus présentant un AVCAischémique est de 15% sur 24 heures, la nitroglycérine a causé une baisse de plus de
15% de la TA sur 24 heures dans 60% des cas où elle a été utilisée. De plus, malgré les préoccupations quant à l’utilisation de la nifédipine sublinguale,
c’était le deuxième agent le plus souvent prescrit. Il était étonnant de constater que l’intervalle moyen entre la première lecture de TA suivant le début
de la médication antihypertensive était de 117 ± 43 minutes dans l’AVC ischémique et de 88 ± 89 minutes dans l’AVC hémorragique. Conclusions: Les
lignes directrices actuelles pour la prise en charge de l’hypertension post AVCA semblent avoir peu d’influence sur le mode de prescription, ce qui
entraîne des variations considérables dans la pratique. De telles variations, probablement dues à l’incertitude causée par le manque de données provenant
d’études contrôlées randomisées, sont intolérables parce que les patients peuvent être soumis à des soins non standardisés potentiellement nocifs tels
des choix inappropriés d’agents antihypertenseurs et une surveillance inadéquate de la TA comme on l’a observé dans cette étude.
Acute hypertension is observed in approximately 80% of ischemic penumbra, observations have been made linking early patients with acute stroke.1,2,3 Average systolic blood pressure hypertension with poor outcome assessed as death, dependence (SBP) and diastolic blood pressure (DBP) can rise 20 and 10 or disability.5-7 However, other studies have argued against such mmHg respectively, during the first ten days following a stroke.4 The mechanism underlying this acute elevation of blood pressure(BP) appears to be multifactorial, and includes rise in plasmacatecholamines, increased sympathetic discharge, as well asactivation of the renin-angiotensin and adrenocorticotrophic/ From the Department of Pharmacy (SK, CC) and Division of Neurology, (AGD), The cortisol systems, among others.5 Although BP elevation in acute Ottawa Hospital - General Campus, University of Ottawa, Ottawa, ON Canada.
stroke is thought useful in the maintenance of cerebral perfusion ECEIVED MARCH 13, 2001. ACCEPTED INFINALFORM OCTOBER 5, 2001.
Reprint requests to: Andre G. Douen, Division of Neurology, The Ottawa Hospital, pressure and encouragement of collateral blood flow into the General Campus, 501 Smyth Rd., Ottawa, ON K1H 8L6 Canada.
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Situations that clearly necessitate treatment of hypertension ment of poststroke hypertension revealed that these guidelines during an acute stroke include the need for thrombolytic therapy, are poorly supported by strong levels of evidence. One example and life threatening end organ damage such as concurrent of this is the recommendation of a ‘Special Writing Group’of the myocardial infarction, hypertensive encephalopathy, aortic Stroke Council, American Heart Association, that antihyper- dissection, renal failure secondary to accelerated hypertension, tensive agents should be used in acute ischemic stroke for SBP or intraparenchymal hemorrhage.1 , 4 , 9 Furthermore, while >220 mmHg or mean arterial pressure (MAP) >130 mmHg elevated BP might assist cerebral perfusion pressure, a rapid (levels of evidence III through V, grade C).15 This expert panel increase in perfusion pressure above the upper autoregulatory did not provide recommendations for management of DBP. In limits, could result in worsening cerebral edema and contrast, other experts have opined that in acute ischemic stroke hemorrhagic transformation secondary to increased micro- treatment should be initiated for SBP >200 mmHg2,17 and/or vascular pressures.4,5,10 Consequently, the goal of drug therapy in DBP >120 mmHg.1,2 Others still have suggested that acceptable ischemic stroke should be aimed at preventing further brain BP ranges in acute ischemic stroke should be SBP 160 ± 20 injury due to excessive hypertension without compromising cerebral perfusion pressure. However, the lack of clinical trials in With regard to hemorrhagic stroke, the ‘Special Writing this area has led to discrepancies regarding the best way to G r o u p ’ for the American Heart Association balanced two theoretical rationales (decreasing BP decreases risk of ongoing Although there are guidelines, based largely on expert bleeding but may also decrease cerebral perfusion pressure and opinion, for treatment of hypertension in acute stroke, it is worsen brain injury) to recommend the maintenance of MAP unknown how well these recommendations are adopted in actual below 130 mmHg, using the weakest levels of evidence (V, grade practice. We undertook a retrospective chart review to compare C).16 This writing group also used similar weak levels of current recommendations13-18 with actual prescribing patterns for evidence to suggest BP treatment in hemorrhagic stroke of SBP treatment of hypertension in acute stroke, at a large tertiary care >180 or DBP >105 (level V, grade C).16 In contrast, others have suggested that BP should be lowered in the presence ofintracerebral hemorrhage if SBP >200 mmHg or DBP >120 It is clear that there are no concrete guidelines for We conducted a retrospective observational chart review of management of acute poststroke hypertension. In the absence of patients admitted with a diagnosis of stroke to the Ottawa a definitive study, we extrapolated from the existing Hospital-General Campus, over six consecutive months from reports,1,2,13,15-18 to identify compromise ranges in BPparameters June 1 to November 30, 1997. Patients admitted with the primary to define poststroke hypertension as follows: SBP >200 mmHg, diagnosis of acute ischemic stroke or hemorrhagic stroke over DBP >110 mmHg (>105 mmHg for hemorrhagic stroke) or a six consecutive months were identified from a stroke registry.
MAP >130 mmHg, during the first seven days of admission.
Hemorrhagic stroke and intracerebral hemorrhage were Similar parameters are currently being used by one larg e considered to be synonymous. Data collection included multicentre clinical trial evaluating the efficacy of the documenting the type of stroke, past history of hypertension, antihypertensive medications prescribed prior to and following m a n a g e m e n t .1 9 Patients were subdivided into two groups admission, and use of anticoagulation prior to admission. The depending on whether the stroke was ischemic or hemorrhagic.
highest and lowest daily BP readings for the first seven days The highest and lowest independent SBP, DBP, and MAP were following admission were recorded. Any antihypertensive agents recorded on a daily basis for the first seven days of hospital stay.
used acutely to treat high BP, and BP before and after treatment If patients were treated for acute hypertension their SBP, DBP were noted. Complications arising from treatment and failure to and MAP were recorded prior to and after administration of the treat were documented. Patients were excluded if they were antihypertensive agent. The drug used, together with the dose, diagnosed with a subarachnoid hemorrhage, treated with route of administration and time to the first measured post-dose thrombolytics, enrolled in another study, or required only BP was recorded. Treatment failure was defined as failure to palliative care. Unavailability of charts also led to exclusion decrease BPbelow the defined parameters for SBP(200 mmHg), DBP (110 mmHg, ischemic; 105 mmHg, hemorrhagic), MAP The definition of poststroke hypertension is not clearly (130 mmHg), or to within 15% (ischemic)1 7 , 2 0 and 20% defined in the literature. Furthermore, the lack of clinical trials in (hemorrhagic) of initial BP over the ensuing 24 hours.1,21 By this area has led to a number of unsubstantiated opinions from comparison, an excessive drop in BP was defined as a reduction individual experts and special writing groups, who base their in SBP, DBPor MAPby >15% in ischemic strokes17,20 and >20% guidelines from nonrandomized trials on weak levels of in hemorrhagic1,21 strokes, within 24 hours. Although we cannot evidence. With regard to the latter, levels of evidence are usually be entirely sure that an excessive drop in BP is solely due to the ranked I – V, with level I and II based on randomized trials, use of antihypertensive agents, the temporal relationship of the levels III – IV are based on nonrandomized cohort studies and fall in BP to the initiation of therapy, implicates the level V based on anecdotal reports.15,16 In addition, the strength antihypertensive agent in the excessive lowering of the BP.
of a recommendation is graded A to C, with A being supported Complications assessed included hypersensitivity reactions to by level I evidence, B, supported by level II evidence, while C is the medication, tachycardia defined as an increase in heart rate supported by levels III, IV and V evidence.15,16 >20% of baseline, extension or secondary infarctions confirmed A review of the literature regarding guidelines for manage- by computerized tomography of the head, and excessive drop in LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES BP (defined above). We also assessed renal impairment, defined Table 1: Patient demographics
as an increase in serum creatinine greater than 40% (not due toother identifiable cause) or myocardial infarction (assessed by Ischemic (n=109)
Hemorrhagic (n=23)
electocardiogram changes and elevated serum creatin kinaseisoenzyme MB (CK-MB)), in order to determine if BP was lowered sufficiently to avoid end-organ damage. Complications secondary to failure to treat included detection of hemorrhagic transformation of ischemic stroke, renal impairment and myocardial infarction (as defined above).
One hundred and twenty-seven patients were admitted with a diagnosis of ischemic stroke. Of these, 18 patients were excludedfrom the study because of unavailability of charts from medicalrecords (12 patients), enrolment in other studies (two patients),misclassification (two patients), and two were excluded as their Table 2: Average BP on admission
therapy was documented as palliative only. Twenty-six patientswere admitted with a diagnosis of hemorrhagic stroke during this BPon admission
Ischemic Stroke
Hemorrhagic Stroke
period. Of these 26 patients, three charts were excluded from review because of chart unavailability (two charts) and 165 (range: 110-228) 167 (range: 110-210) misclassification (one chart). Patient demographics are shown in Table 1. In the ischemic group, 55% had a prior history of hypertension compared to 48% in the hemorrhagic group.
In the ischemic stroke group (n=109), the mean SBP, DBP and MAP on admission were 165 ± 28 mmHg, 89 ± 20 mmHgand 113 ± 19 mmHg, respectively (Table 2). Thirty-nine of the109 patients (36%) had at least one reading of elevated BP that Table 3: Patients with increased SBP, DBP, MAPwithin the first
met the predefined criteria for acute poststroke hypertension (Table 3). Of those 39 patients, 28 patients (72%) had a historyof hypertension prior to admission. Eleven of these 39 patients Ischemic Stroke (n=109)
(28%) were treated for elevated BPa total of 29 times. The drugs used for acute intervention of BP management within the first seven days, exclusive of regular premorbid antihypertensive medications, were transdermal nitroglycerin paste, sublingual patients with at least one elevated reading and oral nifedipine, propranolol, and captopril. The percent patients with at least one elevated reading reduction in BPaccording to drug and time to recorded effect are shown in Table 4. The time to the recorded effect reflects the firstBPmeasurement recorded by the nurse after drug administration.
Hemorrhagic Stroke (n=23)
On average, the time for this first BP measurement for patients with ischemic stroke was 117 ± 43 minutes. Target SBP, DBP and MAP of < 200, 110, and 130 mmHg respectively, were not patients with at least one elevated reading met six of the 29 times that acutely high BP were treated. Four patients with at least one elevated reading were treated with nitroglycerin paste, three times with the one inch dose and once with the 1.5 inch dose; once with oralnifedipine 10 mg and the other with oral propranolol 40 mg.
There was an excessive (>15%) drop in BP within 24 hours, 15times (twice with captopril, three times with sublingualnifedipine 10 mg, nine times with nitroglycerin paste one inch the 23 (48%) met our criteria for poststroke hypertension (Table and once with nitroglycerin paste 1.5 inches) (Table 4).
3). Seven of these 11 patients had a history of hypertension prior Antihypertensive medications were reordered within 24 hours of to admission. Three of the 11 patients (27%) with elevated BPin admission in 41 of 46 patients (89%) who were taking these hospital were treated for acute hypertension 24 times. The drugs medications prior to admission. Twenty-eight patients with a used were nitroglycerin paste, metoprolol, sublingual nifedipine, history of hypertension prior to admission and having one and intravenous labetalol. The percent reduction in BP for each episode of elevated BP in hospital, were restarted on their pre- drug and the time to the lowest recorded BP after treatment are admission antihypertensive medications within the first 24 hours.
tabulated in Table 5. The average time for first BP measurement In patients with hemorrhagic stroke (n=23), the average SBP, in patients with hemorrhagic stroke was 88 ± 89 minutes. There DBP, and MAP on admission were 167 ± 31 mmHg, 89 ± 19 were seven treatment failures in total, three attributed to mmHg and 115 ± 21 mmHg, respectively (Table 2). Eleven of nitroglycerin paste one inch, three to nitroglycerin paste two THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Table 4: Percent reduction in BP for each drug and time to lowest BP in patients with ischemic stroke treated for acute poststroke
hypertension
number of patients
number of
% reduction
time to recorded
number of times
treated (n=11)*
times used
effect (min)
target BP not reached**
BP>15%***
Some patients used more than one agent.
Target BPfor ischemic stroke is MAP<130 mmHg, SBP<200 mmHg, DBP<110 mmHg.
*** Excessive drop in BPfor ischemic stroke considered to be >15% within 24 hours.
Table 5: Percent reduction in BP for each drug and time to lowest BP in patients with hemorrhagic stroke treated for acute poststroke
hypertension
number of patients
number of
% reduction
time to recorded
number of times
treated (n=3)*
times used
effect (min)
target BPnot reached**
BP>20%***
Some patients used more than one agent.
Target BPfor hemorrhagic stroke is MAP <130 mmHg, SBP<200 mmHg, DBP<105 mmHg.
Excessive drop in BPfor hemorrhagic stroke considered to be >20% within 24 hours. inches, and one to metoprolol. Excessive reduction in BP DISCUSSION
occurred eight times and three of these were attributed to The relative dearth of clinical trials addressing patient sublingual nifedipine 10 mg, two to nitroglycerin paste one inch, outcome following management of elevated BP in acute stroke and one each to nitroglycerin paste two inches, intravenous has led to considerable controversy and reliance on recom- metoprolol and intravenous labetalol. A n t i h y p e r t e n s i v e mendations based largely on expert opinion. A review of the medications were reinitiated on the first day of hospital stay in current literature suggests different thresholds for treatment of eight of nine (89%) patients taking medications prior to hypertension following both ischemic and hemorrhagic strokes.9- 18 It has been previously suggested that treatment of elevated BP In this small study, no acute complications were observed in in ischemic strokes is only warranted if MAP is >130 mmHg or treated or untreated groups, apart from asymptomatic excessive SBP >220 mmHg, or DBP>120 mmHg (Levels of Evidence III drop in BP >15% (ischemic stroke) or >20% (hemorrhagic through IV).16 While these recommendations were upheld more stroke) observed in a small number of cases. However, the full recently in the National Institute of Neurological Disorders and impact of treatment of hypertension in acute stroke can only be Stroke (NINDS) guidelines for treatment of hypertension in accurately assessed through prospective randomised studies with acute stroke,2 2 others have advocated lower thresholds for treatment, SBP >200 mmHg,2,17 and others still have suggested LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES that a SBP of 160 ± 20 mmHg, and DBP of 110 ± 10 mmHg of early BP treatment in hemorrhagic stroke to control bleeding would be acceptable ranges during acute ischemic stroke.13 and hence hematoma expansion. However, the natural history of However, the decision to lower BPduring an acute stroke may be the hemorrhage must always be considered and elevated blood warranted even below these suggested parameters if there is pressures might be warranted in some circumstances e.g. risk of evidence of end organ damage.4,11,12,14 A 15% or less reduction of vasospasm in patients with subarachnoid hemorrhages. As with BPhas been suggested during the first 24 hours,17 consistent with ischemic stroke, evidence of end-organ injury secondary to the observation that in ischemic stroke, a >16% decrease in SBP hypertension will also favor treatment of elevated BP.
from baseline over a 24 hour period results in decreased cerebral C o n s e q u e n t l y, management of acute hemorrhagic strokes should be assessed carefully with particular On the other hand, The Sixth Report of the Joint National attention to the clinical scenario and neuroimaging.
Committee on Prevention, Detection, Evaluation, and Treatment The suggested thresholds for treatment of elevated BP in of High Blood Pressure (JNC-VI)14 does not provide specific acute hemorrhagic strokes are also quite varied. One source parameters and only suggests that in ischemic stroke, it is recommends intervention if SBP is >200 mmHg or DBP i s appropriate to withhold treatment unless BP is very high. The >120 mmHg,1 while others recommend lower thresholds, SBP JNC-VI does, however, recommend maintenance of SBP and >180 mmHg or MAP>130 mmHg.16,18 Furthermore, a suggested D B P below 180 mmHg and 105 mmHg, respectively, if moderate reduction in BP of up to 20% during the first 24 treatment with thrombolytics is indicated, consistent with the hours,1,21 is contrasted by alternate recommendations for BP NINDS randomised study on the use of recombinant tissue reduction of no more than 25% within minutes to two hours, with plasminogen activator (rtPA) in acute stroke.22 However, it is a suggested target SBP of 160 mmHg and DBP of 100 mmHg unclear how guidelines were established in the latter study.
Although specific treatment was not clearly defined in the In our study, ~ 72% of all stroke patients, ischemic and NINDS rtPA study protocol, agents used to achieve target BP of hemorrhagic, who were hypertensive at some point during their less than 185 mmHg systolic and 110 mmHg diastolic were first seven days in hospital did not receive treatment. This thought to include administration of intravenous nitroprusside, or tendency to withhold treatment is likely due to the widely-held repeated doses of labetalol, enalaprilat and sublingual view that actively decreasing BPin an acute stroke will decrease nifedipine.18 Consequently, because antihypertensive therapy cerebral perfusion pressure and could extend the area of was not clearly decided upon a priori in the NINDS rtPA trial, infarction. When hypertension was treated, nitroglycerin paste there is little useful information about the management of stroke was the most commonly prescribed drug. In the ischemic stroke patients that can be derived from this study. Moreover, patients group nitropaste induced an excessive >15% reduction in BP who received acute antihypertensive treatment post- within 24 hours ~ 60% of times administered and did not achieve thrombolysis had worse outcomes than those who did not.23 The t a rget BP on four occasions. In the hemorrhagic stroke latter might indicate that specific thresholds exist for BP population studied, nitroglycerin paste was used 17 times and lowering in acute stroke, as previously suggested.20 produced a BP reduction of >20% within 24 hours on three The management of acute hypertension in hemorrhagic stroke occasions and was ineffective in reaching target BP six times.
is somewhat more complex, since the treatment of hypertension Although there are valid concerns regarding unpredictable in hemorrhagic stroke depends on a number of factors including decreases in BPwith sublingual nifedipine,20,26 this agent was the (i) the underlying mechanism, e.g. aneurysmal rupture versus second most commonly prescribed first line drug. Sublingual hypertensive hemorrhage; (ii) the need to maintain adequate nifedipine was used seven times in ischemic stroke and resulted perfusion pressure and to prevent vasospasm (in cases of in >15% reduction BP on three of these seven occasions. In the subarachnoid hemorrhages); (iii) need to control hematoma hemorrhagic group studied, sublingual nifedipine was expansion and rebleeding that might result from sustained administered four times in the same patient, and on three of these elevated BP. The JNC-VI classifies intracranial hemorrhage as a occasions reduced BP by >20% within 24 hours. The other hypertensive emergency with recommendations for immediate antihypertensive medications prescribed included captopril, reduction in BP (not necessarily to normal range). While this propranolol and oral nifedipine during ischemic stroke, and view is supported by others,13 it is not universal.12 Although it intravenous labetalol and metoprolol in hemorrhagic stroke.
has been suggested that physical disruption and local tissue However, these medications were used too infrequently to pressure caused by intraparenchymal hemorrhages produces a zone of ischemia surrounding the clot which might benefit from One important observation in this study is the length of time elevated BP,12 this needs to be weighed against the risk of to first BP recording following administration of antihyper- hematoma expansion, increased risk of herniation and/or tensive therapy. The average length of time was almost two hours extension into ventricles. Indeed, a SBP of ≥200 mmHg on in the ischemic group and 1.5 hours in the hemorrhagic group.
admission is a predisposing factor to enlargement of a This observation is indeed disturbing as it might suggest spontaneous intracerebral hematoma.24 In addition, hematoma inappropriate follow-up of BP after initiation of treatment, in size is directly linked to patient 30-day mortality, i.e. larger acutely ill stroke patients, and might reflect the lack of evidence- intraparenchymal hemorrhages have worse prognosis.
based guidelines in these patients. On the other hand, our study Furthermore, recent studies in an experimental model of collected data on the time to first recorded BP, and did not intracerebral hemorrhage using autologous blood injection in account for unrecorded BP measurements, that might have been mongrel dogs did not show any evidence of an ischemic made at an earlier time than that recorded in the chart.
penumbra.25 Taken together, these studies strongly argue in favor In variance to the prescribing patterns observed in this study, THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES angiotensin-converting enzyme (ACE) inhibitors, which have an majority of patients within the first 10 days1 has been used to onset of action within minutes, duration of action of a few hours, argue for a conservative approach to treating hypertension in and have been recommended as first-line therapy for the acute stroke. However, the full impact of hypertension on treatment of hypertensive urg e n c i e s ,2 7 might be useful in functional recovery is unknown. Although a review of the managing acute poststroke hypertension. Captopril, which has a published literature in this area has led some to conclude that peak hypotensive effect within 1-2 hours, 28 may be a reasonable there is not enough evidence to fully evaluate the effect of choice. Initial doses of 12.5 to 25 mg, could be followed by a altering BP after an acute stroke,33 others have reported an second or third dose at 0.5-1 hour intervals if necessary.
association between early hypertension (SBP >180 mmHg) and Sublingual captopril may also be an option,29-31 but no studies poor outcome.5 In addition, a negative effect on functional have demonstrated the superiority of sublingual captopril over outcome has been observed in stroke patients with markedly oral administration.32 In contrast to ACE inhibitors, calcium elevated MAP ≥145 on admission.3 4 The latter study also antagonists such as nifedipine or nicardipine should be avoided reported that persistent inadequate control of BP adversely because of unpredictable absorption and possible precipitous fall affected the prognosis in hypertensive intracerebral hemorrhage.
in BP.2 0 , 2 6 In addition, reflex tachycardia with increased Moreover, improved outcome in both mortality and morbidity myocardial oxygen demand and peripheral vasodilation causing was observed in stroke patients whose MAP was ≤145 on steal in certain vascular beds has also been attributed to calcium admission or had BPcontrol such that MAPwas ≤ 125 during the first two to six hours. Consistent with this observation, Patients who do not respond to oral agents or have a MAP ≥ Chamorro et al,3 5 in a study of 481 patients, observed a 130 mmHg or SBP ≥ 220 mmHg may benefit from parenteral correlation between the odds of full neurologic recovery and a antihypertensive agents.14 Parenteral enalaprilat is an acceptable 20-30% decrease in MAP within 48 hours of an acute stroke.
choice and does not require cardiac monitoring. It may be given However, the positive findings in favour of BP management 1.25 mg IVevery six hours as needed and doses up to 5 mg have during an acute stroke is contradicted by earlier studies been used.14 The onset of action is 15 to 30 minutes and the suggesting that higher BP on admission reduces the risk of duration of action is six hours. A 50% dose reduction is required ischemic stroke progression.8 Nevertheless, we do not truly for those with renal insufficiency or a creatinine clearance less know the extent to which untreated hypertension exacerbates than 0.5 mL/second.2 8 The mixed alpha and beta blocker, microvascular injury and edema in an ischemic brain, and labetalol, which has a short half life and may be consequently should not assume that lack of neurologic cardioprotective,18 may be a good alternative to enalaprilat as it worsening implies that elevated BPshould not be treated. Hence, induces a relatively mild decrease in arterial pressure. In we cannot rule out the possibility that thresholds exist for addition, labetalol’s response time is 5 to 10 minutes, with a treatment of poststroke hypertension that may have a positive duration of action for three to six hours. 2 8 The dose recommended by the JNC-VI is 20 to 80 mg IV bolus every 10 In this study we investigated the extent to which current minutes to a maximum of 300 mg or 0.5 to 2.0 mg per minute via recommendations for management of hypertension in acute continuous infusion;14 cardiac and frequent BP monitoring are stroke influences clinical practice. In general, we found n e c e s s a r y. If these measures are ineffective, then sodium tremendous variability in prescribing practices that generally did nitroprusside can be used, provided that elevated intracranial not follow current recommendations, particularly with regard to pressure is not suspected. Nitroprusside requires cardiac thresholds for initiating treatment and choice of medication.
monitoring and thus admission to an intensive care unit.
Variations in practice were also reflected in the choice of Although nitroglycerin paste has been suggested as a possible antihypertensive agent. Despite the lack of support for using alternative in the NINDS guidelines, and is commonly used at calcium channel blockers to reduce BP during an acute stroke36 this institution, there is no literature supporting its use in and grave concerns surrounding adverse events from nifedipine antihypertensive therapy during an acute stroke. Overall, we in hypertensive emergencies,20,26 this agent was the second most observed a relatively excessive reduction in BP in 50% of commonly used antihypertensive. The most commonly used patients treated with antihypertensive agents in the ischemic agent was trandermal nitropaste, which precipitated an undesirable drop in BP by >15% within 24 hours ~ 60% of the The treatment of acute hypertension following hemorrhagic times used for treatment of hypertension in ischemic stroke. This stroke involves similar principles. Oral captopril, at similar doses is particularly worrisome since blood flow to the ischemic suggested for ischemic strokes, may be a reasonable first choice affected area is compromised as BP decreases below 16% of if hypertension is considered moderate (i.e. SBP between 200 baseline over a 24-hour period in patients with ischemic stroke.20 and 220 mmHg, or DBP between 110 and 120 mmHg or MAP Overall, the excessive decrease in BP observed in 50% of ≥130). However, intravenous agents should be considered for patients treated with antihypertensives may, in part, have been hypertensive emergencies (situations requiring immediate BP due to the alarming lack of documented BP recordings after reduction to prevent or limit end organ damage, including initiation of antihypertensive medications.
hypertensive encephalopathy).14 Agents which have unfavorable This study shows an inconsistent, nonstandardized approach e ffects on cerebral perfusion pressure should be avoided, to treatment of hypertension in acute stroke and indicates that the including hydralazine, which can cause cerebral vasodilation1,9 current guidelines have little influence on prescribing patterns and clonidine and methyldopa which may depress higher leading to considerable variations in practice. Such variations, cerebral functions and thus are not good choices.1,4 undoubtedly due to uncertainty caused by lack of evidence from The observation that elevated BP spontaneously remits in the randomised controlled trials, are intolerable as it means that a LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES substantial proportion of patients may be mismanaged. It is clear 17. Adams HP. Acute treatment of cerebral infarction. Therapy in there is a need for definitive criteria for BPmanagement in acute Neurology II. 1995. American Academy of Neurology AnnualMeeting. Seattle, Washington, USA. 1995.
stroke patients that can only be obtained through large pragmatic 18. Broderick JP. Guidelines for medical care and treatment of blood randomised trials of BP management in acute stroke. Two pressure in patients with acute stroke. In: Marler JR, Winter Jones randomised clinical trials assessing BP lowering following acute P, Emr M, eds. Proceedings of a National Symposium on Rapid stroke using transdermal nitroglycerin (ENOS:efficacy of nitric Identification and Treatment of Acute Stroke. The National oxide in stroke trial),37 and candesartan cilexetil (ACCESS: Institute of Neurological Disorders and Stroke; Bethesda,Maryland: December 12-13, 1996; 63-68.
acute canadersartan cilexetil evaluation in stroke survivors)19 are 19. Acute candesartan cilexetil stroke survivor (ACCESS) study. Stroke currently ongoing, which will hopefully provide substantive data that will help define BPparameters and treatment in acute stroke 20. Lisk DR, Grotta JC, Lamki LM, et al. Should hypertension be treated after acute stroke? A randomized controlled trial usingsingle photon emission computed tomography. Arch Neurol1993; 50: 855-862.
ACKNOWLEDGEMENTS
21. Kaneko T, Sawada T, Niimi T, et al. Lower limit of blood pressure André G. Douen was supported by an award from the Heart and in treatment in acute hypertensive intracranial hemorrhage Stroke Foundation of Ontario. We thank Dr. S. Venance for helpful (AHCH). J Cerebral Blood Flow Metab 1983;3:S51.
comments and review of the manuscript.
22. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acuteischemic stroke. N Engl J Med 1995; 333: 1581-1587.
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