Hypertensive Emergencies On The Cutting Edge by MikeJenny


									         Hy pe r t e n s ive E m ergencies – On The Cu t t ing Edge

Hypertensive Emergencies – On The Cutting                          These data have important implications for clinicians in
Edge                                                               the emergency department (ED) where elevated BP and
Phillip D. Levy, MD, MPH                                           its associated consequences are commonly encountered. 5
Associate Professor of Emergency Medicine                          According to the National Hospital Ambulatory Medical
Associate Director of Clinical Research, Department of             Care Survey, 2.9% of the 115 million ED visits in 2005 were
Emergency Medicine                                                 related to chronic HTN, up from 2.1% in 1995. In 2006,
Wayne State University School of Medicine                          16.2% of those treated in EDs across the US, approximately
Detroit, MI                                                        15 million patients, had an initial BP that was “severely high”,
                                                                   for example ≥ 160/100 mm Hg.6,7 The vast majority of patients
Objectives:                                                        with substantially elevated BP in the ED are asymptomatic
                                                                   and, untreated, their BP will often diminish within a few
 1. Describe severe blood pressure elevation in the emergency
                                                                   hours of ED arrival. 8,9 Yet ED management is frequently
    department, highlighting features which distinguish true
                                                                   directed towards pharmacological reduction of the numerical
    hypertensive emergencies from other conditions
                                                                   BP value.10-12 This may be attributable to confusion regarding
 2. Describe the basic pathophysiology which contributes to        the risk profile of patients with HTN and a consequent failure
    and results from a hypertensive emergency                      to differentiate true hypertensive emergencies which warrant
 3. Describe hypertensive emergency management guided by           immediate intervention to arrest potentially fatal acute end-
    target-organ specific therapeutic intervention and blood        organ damage13 from simple BP elevations that portend long-
    pressure reduction goals                                       term risk but carry a low likelihood of near-term adverse

Introduction                                                       What Is a Hypertensive Emergency?

Hypertension (HTN) is one of the most important chronic           While the term “hypertensive crisis” has been used to
medical conditions, affecting close to 75 million Americans1 and  categorize any patient whose BP exceeds a certain threshold,
approximately 1 billion people worldwide. The current burden      often systolic BP ≥ 180 or diastolic BP ≥ 110-120 mm
of HTN reflects a steady rise in disease prevalence over the past  Hg, 16-18 there is limited evidence to suggest that BP alone
two decades, which, at least in the United                                                provides sufficient granularity to direct
States, has been accompanied by greater                                                   emergent decision making. Moreover,
levels of awareness, treatment and blood      According to the National Hospital as noted by Shayne and Pitts in their
pressure (BP) control. Hypertension Ambulatory Medical Care Survey, comprehensive review, use of this term
is defined by the 7 th Joint National                                                     is misleading as most with a severely
Committee on Prevention, Detection, 2.9% of the 115 million ED visits elevated BP in the ED are not at risk for
Evaluation, and Treatment of High                                                         acute, or even subacute, development
Blood Pressure [JNC 7] as a BP > 140/90       in 2005 were related to chronic of pressure-mediated consequences.19
mm Hg for most and > 130/80 mm Hg
                                              HTN, up from 2.1% in 1995. In Alternative terminology (Table 1)
for individuals with diabetes mellitus                                                    focused on the presence or absence
or chronic kidney disease. Despite the 2006, 16.2% of those treated in of signs or symptoms attributable to

trend towards an increase in BP control,                                                  acute target-organ damage within the
overall rates of HTN remain suboptimal EDs across the US, approximately context of severe HTN has been widely
with persistent elevation in nearly 50%.4                                                 promulgated and serves to distinguish
                                              15 million patients, had an initial those with active vasculopathy from
Among those with poorly controlled
HTN, almost 1 in 5 (11.5% overall) BP that was “severely high”, for those without. 10,19-22 As so defined,
have exceedingly high BPs, defined as >                                                    hypertensive emergencies constitute
160/100 mm Hg, the JNC 7 cut-off for example ≥ 160/100 mm Hg.                             the subset of patients who present
Stage II HTN, a circumstance which is                                                     with acute end-organ damage and
particularly concerning considering that                                                  evidence of organ system dysfunction
the independent risk of pressure-related cardiovascular mortality (Table 2). Though still used by some, often inappropriately,
is known to double with each 20/10 mm Hg rise in BP above the     the terms “accelerated” and “malignant” HTN are applicable
‘‘ideal’’ level of 115 ⁄ 75 mm Hg. 3                              only to those patients with acute BP elevations which are

Hypertensive Emergencies – On The Cutting Edge                                                                                 19
              Advancing the Standard of Care: Cardiovascular and
              Neurovascular Emergencies

  Table 1. Terminology for patients with severely elevated blood pressure

     Term                           Description                 Implications *
     Hypertensive emergency         Presence of acute target-   Requires immediate intervention with
                                                                                                                         Although some hypertensive
                                    organ damage manifest       parenteral therapy and admission to a
                                    by clinical sequelae or     monitored setting                                        emergency patients will
                                    diagnostic test
                                                                                                                         present de novo with
     Hypertensive urgency           Presence of chronic         Requires re-initiation or up-titration of oral
                                    target-organ damage         antihypertensive therapy; acute blood
                                    without evidence of acute   pressure reduction with parenteral or rapid              elevated blood pressure,
                                    deterioration               acting oral agents should be avoided; may
                                                                necessitate serial testing in an observation
                                                                setting                                                  most episodes are triggered
     Uncomplicated hypertension     Asymptomatic without        Requires arrangement of timely follow-up
     with poor control              evidence of acute or        with reinforcement of the need for life-long             by an acute rise in systemic
                                    chronic end-organ           dietary and medication compliance; initiation
                                    damage                      (for new onset), re-initiation or up-titration
                                                                (for chronic hypertensives) of oral
                                                                                                                         vascular              resistance
                                                                antihypertensive therapy may be needed if
                                                                follow-up is uncertain; acute blood pressure             superimposed on underlying
                                                                reduction is unnecessary and may be
                                                                                                                         chronic HTN.
     * Should also prompt a search for potential medications which may increase blood pressure including
     non-steroidal anti-inflammatory drugs, steroids, decongestants, appetite suppressants, over-the-counter
     stimulants, oral contraceptives, and tricyclic antidepressants.

accompanied by retinal hemorrhage or
papilledema, respectively. Regardless, such
ocular findings are still considered target-
organ damage and can be aptly described                             Table 2. Target-organ involvement in hypertensive emergencies
using more generalizable terminology like                            Injury Pattern by Target-Organ                             Estimated Incidence* (%)
hypertensive emergency.
                                                                     Brain                                                              37-45
Pathophysiology                                                        Acute ischemic stroke                                             6-25
                                                                       Hypertensive encephalopathy                                       8-16
                                                                       Intracerebral or subarachnoid bleed                               5-23
Although some hypertensive emergency
patients will present de novo with elevated                          Heart                                                              27-49
blood pressure, most episodes are triggered by                         Acute heart failure syndromes                                    14-37
                                                                       Acute coronary syndrome                                          11-12
an acute rise in systemic vascular resistance
superimposed on underlying chronic HTN.23 In                         Blood vessels
either case, the etiology is usually idiopathic,                        Aortic dissection                                                1-2
such as “primary” or “essential” HTN, with an                        Kidney                                                              ?
identifiable cause, such as “secondary” HTN,                             Acute renal insufficiency                                        22
in fewer than 10% (Table 3).                                            Acute glomerulonephritis                                         ?

                                                                     Other                                                              1.5-2
From a macrocirculatory standpoint,                                     Eclampsia                                                         2
hypertensive emergencies resemble                                       Retinal hemorrhage or papilledema                                0.9
                                                                        Microangiopathic hemolytic anemia                                0.6
uncomplicated instances of uncontrolled
chronic HTN but on a microcirculatory                                * Incidence estimates represent a range based on percentages compiled from Zampaglione (60)
level, they differ greatly. This is due in                             and Katz (21)

large part to the rate of BP rise, which is
more abrupt in those with a hypertensive
emergency and neurohormonal activation,

20                                                                                                               Hypertensive Emergencies – On The Cutting Edge
         Hy pe r t e n s ive E m ergencies – On The Cu t t ing Edge

                                                                     PATIENT EVALUATION:

                                                                     General Approach

                                                                     Hypertensive emergencies are generally accompanied by
                                                                     symptoms related to the target-organ that is acutely involved.
                                                                     Focal neurological deficit or altered mentation point to brain
                                                                     injury while chest pain or shortness of breath are indicative
                                                                     of cardiac or vascular involvement. Though frequently
                                                                     encountered, and potentially worrisome depending on the
                                                                     scenario, symptoms such as headache or dizziness do not, in
                                                                     and of themselves, serve as criterion from which a diagnosis of
                                                                     hypertensive emergency can be established. Retinal or kidney
                                                                     involvement tends to be more cryptic but can, depending
specifically, the sympathetic nervous and renin-angiotensin-          on the degree of associated papilledema, uremia, acidosis
aldosterone systems, which often precipitates the acute event.       or hyperkalemia, present with defining clinical features
The net result is an overwhelming of vascular autoregulation,        such as blurred vision, obtundation, Kussmaul respirations,
which serves to maintain a relatively constant blood flow            palpitations or ventricular dysrhythmias.
when confronted by changing pressure dynamics, with local
mechanical stress and endothelial injury. The latter leads to        The work-up of a hypertensive emergency should be guided
reduced endothelial nitric-oxide synthase (eNOS) function            by symptoms and signs identifiable on clinical examination
and a drop in nitric-oxide mediated vascular smooth muscle           which should include funduscopy. Depending on the case,
relaxation. 24 This, coupled with excess release of endothelin,      the evaluation of HTN can involve the use of one or more
causes a profound increase in systemic vascular resistance           of the following modalities: plain film radiography (chest
through arteriolar constriction. The cycle is thus self-             x-ray), computed tomography, magnetic resonance imaging,
perpetuating with an initial inciting factor setting off a cascade   electrocardiography, or echocardiography. Laboratory testing
of effects that functionally maintains BP at severely elevated       for renal dysfunction including a urinalysis and a basic
levels. Without interruption of microcirculatory dysfunction,        metabolic panel is recommended for most patients regardless
perfusion distal to the arterioles begins to decrease and a          of their presentation. More sensitive novel biomarkers of
proinflammatory, hypercoagulable state with fibrinoid necrosis         acute renal injury such as cystatin-c, neutrophil-gelatinase
and regional ischemia develops.23                                    associated lipocalin (NGAL), and kidney injury molecule-1
                                                                     (KIM-1)29 may be incorporated in the future.
At the macrocirculatory level, sustained elevations in systemic
vascular resistance cause the central aortic pressure and left       Asymptomatic Hypertension
ventricular (LV) load to rise, which, in turn, requires greater
                                                                     The necessity for testing is to identify occult target-organ
contractile force to maintain cardiac output and forward
                                                                     damage in patients who have profound yet asymptomatic HTN
flow.25,26 This manifests as an increase in both the rate and
                                                                     is not clear. In a recent multicenter study of 109 such patients,
magnitude of LV pressure (dp/dt) which, in the absence of
                                                                     clinically meaningful unanticipated test abnormalities were
cardiac dysfunction, imparts greater mechanical stress and
                                                                     detected in only 6%. None of these tests were felt by the
shear force on the aorta. However, when underlying LV
                                                                     treating physician to be definitively attributable to HTN.30
remodeling or overt cardiac dysfunction are present, the
                                                                     Chest x-ray and electrocardiography in particular have
ventricle may be too weak to generate sufficient pumping
                                                                     poor sensitivity for detection of subclinical cardiac disease,
force (systolic dysfunction) or too stiff to accommodate the
                                                                     especially LV hypertrophy, and a low likelihood of altering
necessary increase in LV pressure (diastolic dysfunction).
                                                                     clinical management.31 Investigation of other approaches to
Either may produce a relative decrease in preload recruitable
                                                                     detect clinically silent target-organ cardiac damage such as
stroke work, and thus stroke volume, precipitating back-flow
                                                                     measurement of serum natriuretic peptide (NP) biomarkers
of fluid into the lungs and rapid onset of acute heart failure.
                                                                     such b-type NP (BNP) and n-terminal pro-BNP (NT-proBNP)
This has often been termed “flash pulmonary edema”.27, 28
                                                                     concentration have yielded conflicting results.32,33 Based on

Hypertensive Emergencies – On The Cutting Edge                                                                                    21
           Advancing the Standard of Care: Cardiovascular and
           Neurovascular Emergencies

the findings of a recent study using echocardiography, the          vasodilators and dopamine agonists, concluded that despite
prevalence of subclinical target-organ cardiac damage among         minor differences in the degree of BP lowering with one
those with asymptomatic, severely elevated BP in the ED may         antihypertensive class versus another, there was insufficient
be far greater (approximately ~75%) than previously thought.34      evidence to determine which agent is most effective at reducing
Such data highlight the underlying risk for pressure-mediated       morbidity or mortality.39 More recent data from The ECLIPSE
consequences of poor BP control among these patients and            (Evaluation of CLevidipine In the Perioperative Treatment
suggest a potential benefit from more extensive screening           of Hypertension Assessing Safety Events) trial, 40 which
particularly in the outpatient setting.                             compared clevidipine to nitroglycerin, sodium nitroprusside,
                                                                    and nicardipine in 1512 cardiac surgery patients with acute
While the current approach to routine testing may not impact        HTN and the CLUE (Evaluation of Intravenous niCardipine
acute care in asymptomatic hypertensives, there is value in         and Labetalol Use in the Emergency Department)41 study,
knowing information such as baseline renal function and             which included 226 ED patients with severely elevated
electrolyte levels prior to initiation of antihypertensive therapy. BP, suggest superiority but within class equivalence of IV
Accordingly, the JNC 7 recommends                                                           dihydropyridine calcium channel
that a basic metabolic panel be obtained                                                    blockers for BP reduction, such as more
before prescribing oral BP lowering While some oral or sublingual rapid lowering and greater time spent
medications. 3 It is most appropriate                                                       within prespecified target range, versus
to have such medications initiated or medications have a relatively quick alternative therapy. Although mortality
restarted by the patient’s primary care                                                     was also slightly lower in ECLIPSE with
physician. When follow-up cannot be onset of action, a more predictable, use of clevidipine compared to sodium
ensured, this responsibility may fall on controlled antihypertensive effect nitroprusside only, generalizability of
the ED provider.35 Based on existing                                                        this finding is limited by virtue of the
evidence, first-line therapy for nearly can be achieved with parenteral select patient population enrolled.
all hypertensive individuals should                                                         Because the focus of the CLUE study
involve the use of thiazide or thiazide- agents making them preferable in was immediate BP lowering effects,
like diuretics like chlorthalidone with
                                               the setting of a true hypertensive outcomes beyond 30 minutes were
the addition of a second agent, usually                                                     not assessed. Consequently, the “hard”
an angiotensin converting enzyme emergency.                                                 clinical meaning of observed group-wise
inhibitor (ACE-I) or a calcium channel                                                      differences in BP reduction is unclear.
blocker, if the patient has chronic HTN
which is poorly controlled on monotherapy.36,37                     Given existing data limitations, deciding which parenteral
                                                                    medication is best for an individual patient can be challenging.
MANAGEMENT:                                                         Understanding the pharmacology of differing therapeutic
Antihypertensive Therapy                                            options can facilitate utilization, enhance the ability to
                                                                    direct intervention towards the appropriate precipitant, and
While some oral or sublingual medications have a relatively         help avoid potentially harmful application. As shown in the
quick onset of action, a more predictable, controlled               following equation, mean arterial pressure (MAP) can be
antihypertensive effect can be achieved with parenteral agents      reduced by lowering any of the following parameters: systemic
making them preferable in the setting of a true hypertensive        vascular resistance (SVR) which stems largely from regulation
emergency. According to data from the Studying the                  of vasogenic tone in the arterioles, cardiac output (CO) which
Treatment of Acute hyperTension (STAT) registry, labetalol          is the pumping force of the heart, or central venous pressure
is the most common IV antihypertensive medication used for          (CVP) which represents intravascular volume and, more
management of severely elevated BP, defined in the registry          roughly, hydrostatic force in the circulatory system. As with
as BP > 180/110 mm Hg, and nitroglycerin is the infusion            most physiology, these parameters do not work in isolation
used most frequently.38 Direct comparison data are scant with       and perturbations in one may affect the other. For example
regard to the relative efficacy of differing agents. A Cochrane      reducing CVP causes, by the Frank-Starling principle, a
Review of 15 randomized controlled trials (n = 869) involving       decrease in CO:
7 different drug classes including nitrates, ACE-I, diuretics,
                                                                             MAP = (CO x SVR) + CVP
calcium channel blockers, α1-adrenergic antagonists, direct

22                                                                                    Hypertensive Emergencies – On The Cutting Edge
         Hy pe r t e n s ive E m ergencies – On The Cu t t ing Edge

Most intravenous (IV) antihypertensive agents exert their         and the acute consequences of elevated BP rather than
effect directly either through receptor-mediated activation       the BP itself. As indicated in Table 2, the vast majority of
or inhibition or indirectly through a decrease in production      hypertensive emergencies involve the brain or heart and
or release of endogenous vasoconstrictors. As shown in Table      treatment goals should reflect the specific problems caused
4, the specific hemodynamic response is a function of the         by high pressures. For instance, in acute coronary syndromes
pathway being interrupted. For the                                                      complicated by HTN, the primary
most part, all IV antihypertensives                                                     goal beyond reperfusion is a reduction
produce some decrease in SVR. The M o s t             i n t r a v e n o u s ( I V ) in cardiac work-load and an increase
magnitude of BP reduction is largely a                                                  in coronary artery perfusion. Based on
reflection of the mechanism of action. antihypertensive agents exert respective pharmacodynamic profiles
Intrinsic dose response relationships,
                                          their effect directly either through and existing evidence,                     specific
which often change with aging, are                                                      agents can be aligned with indication
important to consider when using any receptor-mediated activation or driven goals to develop an approach
agent clinically.42                                                                     to management which is likely to yield
                                          inhibition or indirectly through a optimal outcomes (Table 5). While few
Specific Indications
                                          decrease in production or release absolute contraindications exist, nitric
                                                                                        oxide donors do cause greater reduction
In clinical practice, antihypertensive
therapy is often administered simply of endogenous vasoconstrictors.                    in systemic (vs. cerebral) vascular
                                                                                        resistance resulting in relatively greater
to control elevated BP with clinicians
                                                                                        intracranial pressure and the potential
using medications with which they
                                                                  for shunting of blood flow to the peripheral circulation.44
are most familiar. For treatment of a true hypertensive
                                                                  Similar effects may also occur with hydralazine and both
emergency however, therapeutic intervention is best directed
                                                                  classes should be used with caution or avoided in neurologic
towards the precipitant of specific target-organ dysfunction
                                                                  hypertensive emergencies.45,46

                                                                                    Blood Pressure Goals

                                                                                    The long-standing approach to
                                                                                    antihypertensive medication use is to target
                                                                                    a maximal reduction in MAP of 25% within
                                                                                    the first hour and a goal BP of 160/100 mm
                                                                                    Hg by 2-6 hours.3,16 This treatment is based
                                                                                    on existing understanding of the cerebral
                                                                                    pressure-flow autoregulation curve, which
                                                                                    shifts to the right in chronic HTN. An
                                                                                    excessive decrease in BP may lead to a
                                                                                    precipitous decline in cerebral blood flow.19
                                                                                    Given the heterogeneity of acute target-
                                                                                    organ dysfunction, the use of as a singular
                                                                                    goal for BP control in all hypertensive
                                                                                    emergencies makes little physiologic sense.
                                                                                    This is particularly true for conditions such
                                                                                    as aortic dissection, where more aggressive
                                                                                    targets such as a systolic BP < 110 mm Hg
                                                                                    have been recommended to decrease on-
                                                                                    going injury and reduce the likelihood of
                                                                                    perioperative adverse events. 47 Similarly,
                                                                                    reductions in MAP which exceed 30% have
                                                                                    been associated with more rapid symptom
                                                                                    resolution and improved outcomes in acute

Hypertensive Emergencies – On The Cutting Edge                                                                                23
          Advancing the Standard of Care: Cardiovascular and
          Neurovascular Emergencies

                                                                                 state that “aggressive” reduction is warranted
                                                                                 when systolic BP is > 200 mm Hg or MAP
                                                                                 is > 150 mm Hg and more modest decreases
                                                                                 are indicated with target BP 160/90 mm Hg
                                                                                 or MAP 110 mm Hg when lesser elevations,
                                                                                 defined as systolic BP > 180 mm Hg or
                                                                                 MAP > 130 mm Hg, are present.53 The
                                                                                 persistent BP elevation in the setting of acute
                                                                                 intracerebral hemorrhage is associated with
                                                                                 hematoma expansion and worse outcomes
                                                                                 prompted the recent study of the target and
                                                                                 timing of antihypertensive therapy. The
                                                                                 Intensive Blood Pressure Reduction in Acute
                                                                                 Cerebral Hemorrhage Trial (INTERACT; n
                                                                                 = 404) and the Antihypertensive Treatment
                                                                                 of Acute Cerebral Hemorrhage study
                                                                                 (ATACH; n = 60) compared differing BP
                                                                                 goals, finding a strong signal that earlier
                                                                                 intervention with lower BP targets (systolic
                                                                                 BP approximately 140 mm Hg) may attenuate
                                                                                 hematoma expansion without an excess of
                                                                                 adverse events.54-57 To achieve such targets,
                                                                                 nicardipine may be more effective than other
                                                                                 agents including labetalol.58


                                                                                   With little exception, patients with
heart failure patients with a hypertensive phenotype.48,49 A     hypertensive emergency should be admitted to a monitored
recent subanalysis of 302 patients with acute heart failure in   setting. By virtue of the presenting clinical picture and the
the STAT registry found that adverse events were increased       corresponding use of IV antihypertensive medications, some
when systolic BP was lowered beyond 120 mm Hg within 12          of which can produce precipitous drops in blood pressure,
hours. This underscores the need for continued vigilance         many will require on-going treatment in a step-down or
when managing this condition.50                                  intensive care unit. In certain circumstances, such as chest
                                                                 pain with elevated BP or acute deterioration of chronic kidney
Understanding the importance of BP goals may be most
                                                                 disease, short-term management in an observation unit may
critical when treating neurologic hypertensive emergencies.
                                                                 be appropriate. This presumes that timely reassessment and
This is evident on review of the current American Heart
                                                                 expeditious completion of the diagnostic work-up can be
Association/American Stroke Association (AHA/ASA)
                                                                 assured in this setting.59
guidelines for acute ischemic stroke, which call for a BP
reduction to < 185/110 mm Hg when thrombolysis is planned.       Prognosis
Otherwise, antihypertensive therapy is only indicated when
BP is markedly elevated (> 220/120 mm Hg) with a goal to         Outcomes associated with a given hypertensive emergency
decrease by approximately 15% at 24 hours post-onset.51 This     are largely a function of underlying target-organ damage. Data
is supported by a meta-regression of BP control in stroke        from STAT suggest that severe HTN is a high-risk condition
which suggests an association between large falls or increases   with in-hospital and 30-day mortality rates of 6.9% and 11%,
in BP and worse outcome and modest reductions with a             respectively, and a 90-day readmission rate of nearly 40%.21
decrease in death and/or dependency.52 Updated in 2010, the      When associated with moderate to severe acute kidney injury,
AHA/ASA guidelines for acute intracerebral hemorrhage            mortality is even greater (odds ratio = 1.05; p=0.03 per 10-
                                                                 mL/min decline).60

24                                                                                Hypertensive Emergencies – On The Cutting Edge
           Hy pe r t e n s ive E m ergencies – On The Cu t t ing Edge

Conclusion                                                                        14. Effects of treatment on morbidity in hypertension. Results in patients
                                                                                      with diastolic blood pressures averaging 115 through 129 mm Hg. JAMA
Severe BP elevations in the ED are common. Differentiating
a true hypertensive emergency from poorly controlled chronic                      15. Vlcek M, Bur A, Woisetschlager C, Herkner H, Laggner AN, Hirschl
HTN is critical to enable appropriate application of resources.                       MM. Association between hypertensive urgencies and subsequent
                                                                                      cardiovascular events in patients with hypertension. J Hypertens
When indicated, therapeutic intervention should be driven                             2008;26:657-62.
by condition-specific goals using agents appropriate for the
                                                                                  16. Grossman E, Ironi AN, Messerli FH. Comparative tolerability profile of
disease manifestations. Understanding the pharmacology of
                                                                                      hypertensive crisis treatments. Drug Saf 1998;19:99-122.
antihypertensive medications can facilitate management and
better prepare the emergency physician to provide care for this                   17. Varon J, Marik PE. The diagnosis and management of hypertensive crises.
                                                                                      Chest 2000;118:214-27.
important group of patients.
                                                                                  18. Varon J. The diagnosis and treatment of hypertensive crises. Postgrad Med
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             Advancing the Standard of Care: Cardiovascular and
             Neurovascular Emergencies

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26                                                                                                     Hypertensive Emergencies – On The Cutting Edge

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