Download Hypertensive Emergencies - Calgary Emergency Medicine

Hypertensive
Emergencies
Alyssa Morris, R2
March 5, 2009
Objectives
 Definitions
 Pathophysiology
 Secondary causes of HTN
 Cases
 Treatment options and goals
Definitions
 Hypertensive Emergency
• Acute, life threatening, usually a BP> 180/120
• Target organ damage
• Reduce BP in 1-3 hours
 Hypertensive Urgency
• Asymptomatic, severe HTN, usually >180/120
• NO target organ damage
• Usually no need to reduce BP in ED
 Both of these are spectrums and the BP at which they
occur is variable
Hypertensive Emergencies
 Neurological
• Hypertensive
Encephalopathy
• CVA
• SAH
• ICH
 Cardiovascular
• MI/ischemia
• Acute LV dysfxn
• Ao dissection
 Pulmonary
• Acute edema
 Other
• Acute renal
failure/insufficiency
• Retinopathy
• Eclampsia
• MAHA
Hypertensive Emergencies
 Occurs in 1% pts with HTN
 Single organ involvement found in 83%
 Two organ involvement in 14%
 Three or more organs involved in 3%
 Most common presentations:
• Cerebral infarction 24.5%
• Pulmonary edema 22.5%
• Hypertensive encephalopathy 16.3%
• CHF 12%
Pathophysiology
Physiologic Mechanisms Involved
1) Cardiac output
2) Peripheral/systemic vascular resistance
3) Renin-Angiotensin-Aldosterone System
4) Autonomic Nervous System
5) Other: bradykinin, endothelin, etc…
Components of BP
BP= CO x SVR
CO= HR x SV
Think of the components as:
• CO= heart
• BP= arteries
• SVR= arterioles
RAAS
ANS
BP= CO x SVR
CO= HR x SV
 Adrenal medulla
•
Releases catecholamines which act on the adrenergic receptors
 Kidney
•
•
Releases renin in response to increased sympathetic tone
Alpha 1 receptors result in renal artery constriction
 Blood vessels
•
Alpha receptors result in constriction
 Heart
•
B1/2 receptors result in increased CO, chronotropy (HR) and
inotropy (SV)
Case 1
 70M brought in by EMS. Wife called because he had been
complaining of a severe h/a, vomitted and then later
became altered.
 PMHx: HTN, Afib, cataracts, NIDDM
 Meds: HCTZ, Metoprolol, Metformin
 O/E: T= 37.6, P=80, BP= 210/124, 02=94%, altered level of
consciousness, no focal deficits, fundi difficult to see
 Is this a hypertensive urgency or emergency?
 Which major clinical syndrome does this case represent?
Hypertensive Encephalopathy
 Uncommon syndrome
 Acute and reversible
 Results from an abrupt, sustained rise of BP that
exceeds the limits of cerebral autoregulation of
the small resistance arteries in the brain
 Arises from “breakthrough” hyperperfusion and
leakage of fluid thru BBB
CPP=MAP-ICP
Clinical Presentation
 Severe h/a
 Drowsiness
 ALOC
 Vomitting
 Seizures
 Focal neuro deficits
 Blindness
Tx
 How fast would you try to reduce the BP?
 Why do you not want to reduce it too quickly?
 What would you consider using to reduce the
BP?
Drug Options
 VASODILATORS
 CALCIUM CHANNEL
• Nitroprusside
BLOCKERS
• Nitroglycerin
• Enalaprilat
• Fenoldopam
 ALPHA BLOCKERS
• Hydralazine
• Phentolamine
 BETA BLOCKERS
• Labetalol
• Esmolol
• Clonidine
Nitroprusside
 Potent smooth muscle relaxing agent
 Acts on both resistance and capacitance vessels
 Reduces both preload and afterload
 Rate of onset rapid
 Duration of action very short
 Also a cerebral vasodilator
• Can increase ICP secondary to increased cerebral blood flow
 What is an intermediate metabolite?
Nitroprusside
 Complications:
• Hypotension :. Reflex tachycardia and inc SV
• Prolonged use can produce hypothyroidism
• Cerebral edema
• Local necrosis if extravasates from line
 Unstable in UV light, therefore wrapped in tinfoil
 Infusion at 0.25-0.5ug/kg/min -then increase by
0.5mcg/kg/min
 Max of 10 mcg/kg/min
 Is there a group you would not use this in?
Nitroglycerine
1) Activates guanylate cyclase
2) Accumulation of cGMP
3) Sequestration of Ca into SR
4) Relaxation of Vascular smooth muscle
 Dose dependent

Low dose: venodilator (preload)
 High dose: veno and arteriodilator (afterload)
 Therefore, usually reduce BP by reducing preload and CO
 Start with 10-20ug/min infusion
 Titrate up 5-10ug/minQ3-5min
Who would you want to be careful using this drug in?
Fenoldopam
 Trade name is Corlopam
 Peripheral dopamine-1 receptor agonist
 Dop-1 R located postsynaptically in systemic and renal vasculature
• Mediate systemic, renal and mesenteric vasodilation and natriuresis
 Improves renal fxn acutely in malignant htn
 Does not cross BBB
 Rapid onset and elimination ½ life of 9 min
 Hypotension less common side effect
 0.1ug/kg/min, then up by 0.1ug/kg/min every 15 min
 Max dose is 1.6ug/kg/min
Hydralazine
 Direct arteriolar vasodilator
 Used to be used as first line in pregnancy htv emergencies
 Starting dose is 5mg IV
 Repeat doses of 5-10mg IV every 20 mins to maintain
desired BP
 Complications:
• Marked hypotension
• Reflex tachycardia (can give angina)
• Flushing and nausea
• H/a
Labetalol
 Selective α-1 blocker and nonselective β-blocker
 α:β blockade ratio between 1:3 and 1:7
 Not a significant drop in CO like other βB
 Does not affect cerebral blood flow or renal fxn
 BP starts to fall in 5-10 mins
 Max effect at 30 mins
Labetalol
 Start with 10-20mg IV over 2mins
 Repeat dose of 20,40 or 80 mg every 10 mins to
max of 300mg
 Or after loading dose can start infusion at 1-
2mg/min and titrate up
 Contraindicated in patients with CHF, heart block,
asthma, pheo, cocaine
 Give oral when have reached max IV dose
Esmolol
 Selective β-1 blocker
 Very short acting
 Elimination ½ life of 9 minutes
 No intrinsic sympathomimetic activity
 Loading dose of 500 ug/kg over 1 minute
 Follow with infusion of 50-100 υg/kg/min (can rpt Q5min)
 Max dose of 300 ug/kg/min
 Contraindications same as labetalol
Phentolamine
 α-blocking agent
 Used for the Mx of catecholamine-induced HTV
crisis
 What are some examples of this?
 Immediate effect
 Effect lasts up to 15 mins
 1-5mg IV boluses
Nicardipine
 Parenteral dihydropyridine CCB
 More titratable, less negatively inotropic, and induces less
tachycardia than nifedipine
 Acts predominantly as a vasodilator
 Onset of action is 5-15 mins
 Duration of action is 4-6 hours
 Infusions starting at 5 mg/hr
 Increase infusion every 15 mins
 Max dose of 15mg.hr
Case 2
 71F brought in by EMS. Last seen normal 1
hour ago and found aphasic and hemiparetic.
 PMHx: HTN
 Meds: HCTZ
 O/E: T= 37.6, P= 78, BP= 200/110, 02= 95%, R
Hemiparesis, GCS 12
 How do you want to Mx this pt?
HTN Mx in Ischemic Stroke
Stroke. 2007;38:1655-1711.
HTN Mx in Ischemic Stroke
 HTN common in 1st hours after stroke
• SBP>160 found in 60% pts with acute ischemic
stroke
 For every 10mmHg raise >180, risk of neurologic
deterioration increases by 40% and risk of poor
outcome by 23%
 Increased BP may be due to:
•
•
•
•
•
•
CV event and increased ICP
Full bladder
Nausea
Pain
Pre-existing BP
Hypoxia
HTN Mx in Ischemic Stroke
 Theoretical reasons for lowering BP in stroke
• Decrease formation of brain edema
• Lessening risk of hemorrhagic transformation
of infarction
• Preventing further vascular damage
• Forestalling early recurrent stroke
 BUT remember aggressive tx of BP may lead to
neurologic worsening by decreasing perfusion
pressure to ischemic areas of brain
CPP=MAP-ICP
HTN Mx in Ischemic Stroke
 A lot of studies showing harm with reduction of BP
 Most pts have a decrease in BP a few hours post-
stroke w/o intervention
 Oliveira-Filho et al. Neurology. 2003;61:1047-1051
• Found >90% pts had a decrease in SBP by 28% in
24hrs post-stroke with no intervention
 No data define levels of HTN that mandate
emergent tx but many suggest >185/110 b/c greater
than this is a contraindication to tPA
Consensus Statement
 “ emergency administration of antihypertensive
agents should be withheld unless DBP>120 and
SBP>220”
 “reasonable goal to decrease blood pressure by
15-25% within 24 hours”
 This is a case-by-case decision
 More research needs to be done
CHIPPS
Controlling hypertension and hypotension immediately poststroke trial Lancet Neurol. 2009;:48-56.
 Prospective, RCT, pilot study
N=179
 Primary outcome of death or dependency
 ICH or ischemic strokes with SBP>160 randomized to
labetalol, lisinopril or placebo
 Reduced BP on average by 20 systolic
 Death or 61% vs 59% (p=0.82) for tx vs placebo
 No increased serious adverse events or neuro deterioration
Case 3
 Same story as before but has this CT
HTN Bleeds
Where do you get HTN bleeds in the brain?
1) Cerebellum
2) Pons
3) Basal ganglia
4) Thalamus
Stroke, 2007;38:2001-2023
HTN Mx in Hemorrhagic Stroke
 Primary rational for reducing BP is to avoid hemorrhagic
expansion from potential sites of bleeding
• -especially if aneurysm or AVM
 BP is correlated with increased ICP and volume of
hemorrhage
 Difficult to determine whether increased BP is a cause of
hemorrhage growth or an effect of increased volumes of
ICH and increased ICP
 In primary ICH there is little prospective evidence that
exists to support a specific BP threshold
HTN Mx in Hemorrhagic Stroke
Summary of studies
 Isolated SBP<210 is not clearly related to hemorrhagic




expansion or neurologic worsening
Decrease in MAP by 15% does not result in decreased
CBF
Baseline BP was not associated with growth of ICH in
largest prospective study
Hemorrhage enlargement occurs more frequently in pts
with increased SBP but it is not clear if this is an effect
of increased growth of ICH with associated increase in
ICP or a contributing cause to the growth of ICH
Evidence supports maintaining CPP >60mmHg
ATACH Study
Antihypertensive treatment of acute cerebral hemorrhage
 International, multicenter, open-labeled, RCT
 3-dose-tiered trial of lowering SBP to predetermined levels:
170-200, 140-170, 110-140
 Using IV Nicardipine
 Data collection complete
 Inclusion criteria
•
•
•
•
w/I 12h on onset Sxs and ICH on CT
GCS>8
BP on admission >170 on two separate readings
Not surgical candidates
INTERACT I
Intensive blood pressure reduction in acute cerebral hemorrhage.
Lancet Neurol. 2008;7:391-9.
 Phase 1 pilot study, RCT, open-label, safety-efficacy study
 Determine whether lowering BP after ICH will decrease death or
long-term disability
 N= 404
 Target BP of 140 vs 180
 Primary outcome of ICH growth
 Hematoma growth of 13.7% vs 36.3% (p=0.06)
 No difference in secondary outcomes
 Phase 2 ongoing
Case 4
 32F with known bicuspid Ao valve with c/o tearing back
pain radiating into neck
 BP R arm= 220/100
BP L arm= 170/78
 Which BP do you go by? Why?
 What do you want to do?
 What is the factor you want to reduce to avoid
propagation?
 What would be your goal BP? What would you use?
 What if her pulse is now 55 but her SBP is still 150?
HTN Mx in Ao Dissection
 Remember to check BP in legs if you are thinking
dissection b/c the flap can give you falsely low BP in
arms
 Want to avoid shear stress and wide pulse pressures
 Reduce the LV ejection force
 Goal is to get SBP 90-110 but just do what you can
 Use labetalol or esmolol
 Can use nipride after have sufficiently BB b/c will blunt
the reflex tachycardia and increased SV
HTN Mx in Ao Dissection
 Diagnosis and management of aortic dissection. A task
force report. Eur Heart J. 2001;22(18):1642
 Use BB first line
 Lower SBP <110
 HR <60
 Use nipride only after sufficiently beta blocked
 Acute Aortic syndromes. Circulation. 2005;112(24):3802
 Use BB first line
 SBP 100-120
 HR <60
 Role of CCBs unknown if don’t tolerate BB
Case 5
 24F 4 days post-partum from induced twin vaginal
delivery at 36w due to development of PIH called
EMS for increased SOBEMS report
• T= 37.9 P= 115 BP= 200/ 115 RR= 29 O2= 84% BS= 5.6
• En route to hospital patient became increasingly distressed
 On arrival, patient in extremis
• T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB
• Speaking one word sentences, diaphoretic, looking
exhausted. Heart sounds not auscultated, JVP at angle of
jaw, crackles to apices, 2+ edema to shins, abdo soft and not
tender, normal reflexes, no clonus
CASE 5
 EMS report
 T= 37.9 P= 115 BP= 170/ 100 RR= 29 O2= 84% BS= 5.6
 En route to hospital patient became increasingly distressed
 On arrival, patient in extremis
 T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB
 Speaking one word sentences, diaphoretic, looking
exhausted. Heart sounds not auscultated, JVP at angle of
jaw, crackles to apices, 2+ edema to shins, abdo soft and not
tender, normal reflexes, no clonus
Q: What can cause respiratory failure in the post-partum patient?
DDX
 Respiratory Failure in the post-partum patient
 Pulmonary Embolism
 Cardiogenic Pulmonary Edema
 Neurogenic Pulmonary Edema
 Amniotic Fluid Embolism
 Aspiration
 Community or hospital acquired pneumonia
Q: What are some causes of cardiogenic pulmonary edema
in peripartum women?
DDX
 Cardiogenic Pulmonary Edema
 Peripartum cardiomypathy
 Pre-eclampsia/Eclampsia
 Aortic stenosis
 Mitral stenosis
 Other cardiomyopathies
•
•
•
•
•
•
Cocaine
Alcoholic
Diabetic
Hypertrophic
Dilated
Restrictive
Q: What investigations do you
want on this patient?
How do you want to tx her assuming she has htn
induced pulmonary edema?
HTN Mx in Pre-Eclampsia
 Remember they can present weeks after
delivery
 Nitrates, but in her would need to start high and
go up quickly
• Stand by the bed and start at 10ug/min and go
up by 10s quickly until effect- she needed
110ug/min
 Nitroprusside could also be used if post-partum
HTN Mx in Pre-Eclampsia
 BiPAP/CPAP

FRC
Improves V/Q-
adrenergic outflow
HR/BP

preload and afterload b/c raised intrathoracic pressure
 Loop Diuretics
Block Na resorption in Loop of Henle
Na/H20 Excretion
Plasma Volume
Preload
Case 6
 69F presents after a home BP of 200/104. No other
complaints.
 PMHx: Htn, MI 10 years ago
 Meds: HCTZ, metoprolol, lisinopril
 O/E: BP= 200/112
 What do you want to do with this patient?
Drug Summary
 Nitroprusside
• 0.25-0.5ug/kg/min
• Inc by 0.5ug/kg/min quickly
 Nitro
• 10-20ug/min
• Inc by 5-10ug/min Q3-10min
 Labetalol
• 10-20mg IV Q5-10min
• Infusion at 1-2mg/min