Transcript Hypertension in the ED

HYPERTENSION IN THE ED
Treat now, later or never?
2012
Dr Peter Jordan
Registrar Teaching
Northern ED
Case 1
 58-year-old man c/o left temporal
headache – Gradual onset, mod severity
 No history of hypertension
 BP 146/96 mm Hg – Mildly tender L)
temporal area otherwise NAD
Case 2
 71-year-old woman sent in by her LMO
who noted an elevated BP 190/100. Triage
BP 190/110 mm Hg.
 Asymptomatic
 ?Ix/ Treatment
Case 3
 0600 - 96-year-old woman from home
presents in pulmonary oedema.
 ? pMHx - diltiazem 240 and frusemide
80/40
 Resus - BP 220/130 mm Hg, RR 28 sitting
in a tripod position.
 BP treatment required
Background
 Physicians definitions of HT are generally not useful
in ED
 Overtreatment may convert patients from a stable,
asymptomatic, hypertensive state to an unstable,
symptomatic, normotensive or hypotensive state.
 Historically, nifedipine was used routinely for
hypertensive states, urgencies and emergencies,..
Grossman E, et al..Should a moratorium be placed on
sublingual nifedipine capsules given for hypertensive
emergencies and pseudoemergencies? JAMA.
1996;276(16):1328-1331. (Review)
BP Screening
 25% to 75% of patients with elevated systolic
or diastolic BP in the ED remain hypertensive
at follow-up.
Central Questions When Treating
Hypertension In The ED
 Are ED measurements of blood pressure accurate in
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determining if the patient is truly hypertensive?
Is there any evidence that the patient’s current blood
pressure is contributing to the acute condition?
Is there any evidence that the patient’s current blood
pressure is contributing to active end-organ
damage?
How aggressively should the patient’s blood
pressure be managed?
What is the appropriate disposition and follow-up?
Evidence
Hoekstra J, Qureshi A. Management of
hypertension and hypertensive emergencies
in the emergency department: the EMCREGinternational consensus recommendations.
Ann Emerg Med. 2008;51(3):S1-S38.
(Consensus guideline)
National Guidelines Clearinghouse
(www.guidelines.gov) = 400 guidelines
for the management of hypertension - focus
on chronic disease and do not address
immediate evaluation and management in
any depth
Chobanian AV, Bakris GL, Black HR, et al. Seventh report
of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):12061252. (Report)
“Patients with marked BP elevations and acute target
organ damage (eg, encephalopathy, myocardial
infarction, unstable angina, pulmonary oedema,
eclampsia, stroke, head trauma, life-threatening
arterial bleeding, or aortic dissection) require
hospitalization and parenteral drug therapy. Patients
with markedly elevated BP but without acute targetorgan damage usually do not require hospitalization,
but they should receive immediate combination oral
antihypertensive therapy. They should be carefully
evaluated and monitored for hypertension-induced
heart and kidney damage and for identifiable causes
of hypertension.”
Only 1 guideline (ACEP) specifically directed at
ED management of hypertension.
ACEP Clinical policy: critical issues in the
evaluation and management of adult patients
with asymptomatic hypertension in the
emergency department. Ann Emerg Med.
2006;47(3):237-249. (Clinical policy)
End-organ effects:
 Stroke (29%)
 Pulmonary oedema (23%)
 encephalopathy (18%)
 congestive heart failure (15%)
 Acute Coronary Syndrome (13%)
Prospective studies of triage vital signs show
20 - 28% hypertensive (140 syst or 90 diast)
- 6% having an SBP > 180 or Diastolic >
110mm Hg
Essential hypertension (90%) progresses in
varying degrees through interactions among
the cardiovascular, renal, and central
nervous systems. Cardiac remodeling then
occurs secondary to increased afterload.
Secondary HT (approx 10%)- primary
aldosteronism, Cushing syndrome,
pheochromocytoma, renovascular
Hypertensive emergencies or urgencies
generally occur after an abrupt increase in
systemic vascular resistance, resulting in
endothelial injury, fibrin deposition, and
arteriolar necrosis.
Differential Diagnosis Of Hypertension In
The ED
Acutely Dangerous
Less Acute
 Stroke
 Obstructive uropathy
 Aortic dissection
 Hyperthyroidism/hyperparathy
 Drug intoxication: cocaine,
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amphetamine, monoamine
oxidase inhibitor
Drug withdrawal:
antihypertensives, alcohol,
other sedative hypnotics
Renal failure
Pheochromocytoma or other
tumor
Thyroid storm
roidism
 Sleep apnea
 Cushing syndrome
 Primary hyperaldosteronism
 Renovascular hypertension
 Essential hypertension
 Causes of secondary hypertension need to be
specifically identified because their
treatments differ substantially from the
treatment of essential hypertension.
 CVA - BP is permitted to remain elevated for
cerebral protection (consensus)
 Aortic Dissection - BP is aggressively
controlled to avoid rupture or propagation
Key Questions
Have you ever been told you have high blood pressure?
Concern(s)?
Do you have any chest pain?
Do you have any shortness of breath?
Are you on any medications, or are you using any recreational
drugs or herbal medicines?
Have you recently stopped taking any medications or
recreational
drugs or herbal medicines?
Have you had any focal weakness, slurring of speech,
numbness, or clumsiness?
Do you snore or wake up during sleep? Do you feel tired
throughout the day?
Have you had high blood pressure in the past that has not
responded to multiple medications?
Clonidine etc
Examination
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Systematic/ Complete
Vital signs
Cardiovascular
Fundoscopy
Cognitive state/ focal neurology
Thyroid/ reflexes
Toxidromes
Abdominal aorta/ Peripheral pulses
Investigations
 Should be tailored to the individual patient
 FBE – rarely useful
 K+ low in 45% of patients with primary
hyperaldosteronism
 ECG - specific, but not very sensitive
Cornell criteria: Sum of R wave in aVL and S
wave in V3, >2.8 mV in men or >2.0 mV in
women = best predictor of future
cardiovascular mortality.
Investigations (cont.d)
 Urinalysis - Renovascular hypertension,
nephrotic syndrome, nephritic syndrome,
preeclampsia
 Pregnancy test - Possible preeclampsia;
(avoid ACEIs)
LVH
Treatment - Asymptomatic Patients With BP
Less Than 180/110 mm Hg
ED BP readings—especially persistently
high ones—are good indicators of chronic HT
If BP < 180/110 mm Hg - Follow-up with LMO
1 wk to 1 month
Asymptomatic patients with BP >180/110
and a History of Hypertension on
Antihypertensive Medications
 Non compliant – restart
 Compliant – adjust meds – preferably in
consultation with LMO
Asymptomatic Patients with BP over
180/110 and No History of Hypertension
 Commence antihypertensive medication if
they cannot see a primary care provider the
next day
 The choice of initial agent is multifactorial
Antihypertensive options
Agent
Starting Dose
Indications
Negatives
ACEIs e.g.
Lisinopril
5-10mg daily
CCF, DM, Post MI Renal artery
stenosis,
dehydration,
hyperkalaemia
Angiotensin
receptor
blockers (eg
Irbesartan)
75-150mg daily
As per ACEI – if
intolerant of or in
addition to
See above
β-Blockers (eg,
metoprolol) 25-50
mg bd
25-50 mg bd
Patients with
coronary artery
disease; longterm
management of
CHF; rate control;
hyperthyroidism
Not a good
monotherapy;
heart block;
bradycardia; sick
sinus syndrome;
bronchospasm;
decompensated
CHF
Agent
Start dose
Indications
Negatives
Calcium channel
Blockers (eg.
diltiazem)
180-240 mg daily
Rate control or
coronary artery
disease in patients
who cannot take βblockers
Not a good
monotherapy,
oedema; may lower
heart rate
works well
with other agents
Gout, hypokalemia,
Hypercalcemia,
Diminishing
effectiveness
as GFR decreases;
electrolyte
disturbances;
Thiazide
12.5 mg daily
diuretics (eg.
hydrochlorothiazid
e)
Hypertensive Emergencies
 Cerebral infarction or haemorrhage
 Acute pulmonary oedema
 Hypertensive encephalopathy
 acute CHF
 aortic dissection
 (Pre Eclampsia)
CVA - Ischaemic
 Treatment guidelines based on expert
opinion:
 BP> 220/120 suggests IV Rx (SNP)
 Thrombolysis cut-off 185/110 – many titrate
to just below but monitor tightly
 No increase in adverse events
CVA - Haemorrhagic
Classic tightrope – Adequate Perfusion pressure v increasing haemorrhage
No prospective or efficacy data –
1. If SBP is > 200 mm Hg or MAP is > 150 mm Hg, consider aggressive
reduction of BP with continuous IV infusion, with BP
monitoring every 5 minutes.
2. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there is
evidence for or suspicion of elevated intracranial pressure,
consider monitoring intracranial pressure and reducing BP using
intermittent or continuous IV medications to keep cerebral perfusion
pressure > 60-80 mm Hg.
3. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there is
no evidence for or suspicion of elevated intracranial pressure,
consider a modest reduction of BP (eg, MAP of 110 mm Hg or
target BP of 160/90 mm Hg) using intermittent or continuous IV
medications; clinically re-examine the patient every 15 minutes.
APO
 Mortality inversely proportional to BP levels
(during Tx)
 Mortality Proportional to hypotension, renal
failure, cardiacischaemia and arrhythmia
 Evidence positive for CPAP, weakly positive
for GTN and neutral/ mixed for Frusemide in
severe APO only
Hypertensive Encephalopathy
Sx - headache, seizures, visual disturbances,
nausea, vomiting.
Diagnosis made only after other potential
hypertensive emergencies are excluded
Nitroprusside – avoid - decreased systemic
pressure and preserved intracranial perfusion
pressures
(Consensus) goal = 20% to25% reduction in
MAP or Diastolic BP 100 to 110.
Aortic Dissection
Standard Tx: titratable IV B-blocker (eg,
Esmolol/ metoprolol), and nitroprusside for BP
control.
Second line – Calcium channel blockers
Theory = reducing the force of left ventricular
contractions enhances laminar flow and lessen
stress on the aortic wall. Turbulent flow is
increased by using a vasodilator alone.
Target pressure is the lowest pressure tolerated by
the patient: (100 to 120 systolic )
Beware B Blocker if acute AI
Sympathetic Crisis
 BDZs and Vasodilators
 Theoretical risk of unopposed alpha
activation but evidence suggests nil harm and
reduced incidence AMI.
Unstable Angina/NSTEMI
 Nitroglycerin can be used to control both
symptoms and BP
 Other therapies are more likely to have a
beneficial effect on outcomes.
 oralb-blockers < 24/24.
 ACEIs and/ or angiotensin receptor blockers If
HT and LVF or APO < 24/24.
Renal Failure
 If low GFR - treatment of hypertension
should involve an ACE inhibitor, especially
for patients on hemodialysis
 Cr and K need close monitoring initially
Pre Eclampsia/ Eclampsia
 Many common drugs contraindicated
because of the potential for toxic effects on
the fetus
 Goal is a reduction in SBP to 140 and DBP of
90
 Classic therapy hydralazine/ Mg – beware
precipitous drops in BP
Case 1 conclusion 58 YO - headache
Headache responded to Ibuprofen, Paracetamol
and metoclopramide.
CRP <10. HT was being followed by his LMO , so
no further investigations or Mx
for BP was undertaken.
Case 2: 96-year-old woman
incidental finding BP 190/110
ECG - normal sinus rhythm
Creatinine 80 / K+ 4.1 mEq/L
After discussion with her LMO
lisinopril and hydrochlorothiazide combination
prescribed and review in 5 days arranged.
Case 3 96-year-old woman –
APO hypertensive 210/130
Chest Auscultation - Basal creps
Med reg requested BNP level (elevated).
CXR - Pulmonary oedema.
Mx: GTN infusion /CPAP/ Frusemide 40 mg IV .
BP eased to 175/110 mm Hg – Weaned off GTN
infusion in ED and ward admitted