Treat now, later or never?

2012Dr Peter JordanRegistrar TeachingNorthern 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 TreatingHypertension In The ED

Are ED measurements of blood pressure accurate in 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 EMCREG-international consensus recommendations. Ann Emerg Med. 2008;51(3):S1-S38. (Consensus guideline)

National Guidelines Clearinghouse(www.guidelines.gov) = 400 guidelinesfor 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 reportof the Joint National Committee on Prevention, Detection,Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252. (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 target-organ 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 Stroke Aortic dissection Drug intoxication: cocaine,

amphetamine, monoamine oxidase inhibitor

Drug withdrawal: antihypertensives, alcohol, other sedative hypnotics

Renal failure Pheochromocytoma or other

tumor Thyroid storm

Less Acute Obstructive uropathy Hyperthyroidism/

hyperparathyroidism 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 recreationaldrugs or herbal medicines?

Clonidine etc

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 notresponded to multiple medications?

Examination

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 sensitiveCornell 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 β-blockers

Not a good monotherapy, oedema; may lower heart rate

Thiazidediuretics (eg. hydrochlorothiazide)

12.5 mg daily works wellwith other agents

Gout, hypokalemia,Hypercalcemia, Diminishing effectivenessas GFR decreases;electrolyte disturbances;

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

aggressivereduction of BP with continuous IV infusion, with BPmonitoring every 5 minutes.2. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there isevidence for or suspicion of elevated intracranial pressure,consider monitoring intracranial pressure and reducing BP usingintermittent or continuous IV medications to keep cerebral

perfusionpressure > 60-80 mm Hg.3. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there isno evidence for or suspicion of elevated intracranial pressure,consider a modest reduction of BP (eg, MAP of 110 mm Hg ortarget BP of 160/90 mm Hg) using intermittent or continuous IVmedications; 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 EncephalopathySx - 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/LAfter discussion with her LMO lisinopril and hydrochlorothiazide

combinationprescribed 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