Hypertensive Crises

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Hypertensive Crises Nadim J Lalani 08.03.2007 Thanks to Dr Sarah McPherson Dr Trevor Langhan [who usually presents this talk]

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Hypertensive Crises. Nadim J Lalani 08.03.2007 Thanks to Dr Sarah McPherson Dr Trevor Langhan [who usually presents this talk]. Famous Last words?. “I have a terrific headache” April 12 1945. Clues:. Survived Assassination Feb 1933 “we have nothing to fear but fear itself” - PowerPoint PPT Presentation

Transcript of Hypertensive Crises

Page 1: Hypertensive Crises

Hypertensive Crises

Nadim J Lalani08.03.2007

Thanks to Dr Sarah McPhersonDr Trevor Langhan [who usually presents this

talk]

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Famous Last words?

“I have a terrific headache”

April 12 1945

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Clues:

• Survived Assassination Feb 1933• “we have nothing to fear but fear

itself”• President during Pearl Harbor

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FDR

•Arguably the greatest US President of all time

•Only US President to be elected to 4 terms

•“New Deal” brought the US back from the Great Depression Social Security

•Suffered from complications of GBS and was a paraplegic

•Started the “March of Dimes” is on the dime

•Dies April 12 1945 of ICH from Hypertension

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West J Med. 2001 August; 175(2): 119–124.

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Objectives

• Definitions• Pathophys [briefly]• Cases• Q/A format:

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Definitions?

• Normal BP?– sys BP < 120 mm Hg– dias BP < 80 mm Hg

• Hypertension?– sBP > 140 mm Hg– dBP > 90 mm Hg

• In Between = “prehypertension”• Hypertension acc to Rosen:

– SBP > 160– DBP > 95

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Definitions?

• Hypertensive Crisis?• Hypertensive Urgency?• Hypertensive emergency?• Malignant Hypertension?• Severe Hypertension?

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Definitions

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Malignant/Severe Hypertension

Malignant:• Older term [no longer used] but often

asked for it by attendings• Essentially Hypertensive Emergency

with the end organ effectsSevere:• Sys BP > 180• Dias BP > 120• No end organ effects

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What Counts as “End organ Damage”?

H

E

A

D

T

O

T

O

E

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Hypertensive “syndromes”

• Encephalopathy• Stroke• Pulmonary edema• ACS• Aortic dissection• Pregnant • Renal failure• Other end-organ [retinal findings,

hemolysis]

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BP Measurement

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BP Measurement

If no extinguishment

•NB Cuff Size

•10 minutes in between

•Pt supine/ lights off &c.

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Increased BP in the ED

• Things that cause “reactive” HTN in the ED?– Anxiety– Pain– Drugs (illicit - cocaine, amphetamines,

LSD, PCP & OTC’s)– ETOH withdrawal– BP cuff too small– Machine vs sphygmomanometer

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Hypertension

• Classified into:– Primary = Essential Hypertension [95%]– Secondary [5%]

• Secondary more likely to cause severe HTn

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Essential hypertension

• Cause not entirely understood– Theories….

• Alterations in contractile properties of vascular smooth muscle

• Change in vascular smooth muscle from chronic elevated BP from primary failure of normal autoregulation

• Change in RAAS p-way

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Secondary Hypertension

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Specific 20 causes

1)Renal Disease: [most prevalent]Renal artery stenosis high renin

stateFibromuscular dysplasia of the renal

artery– Young white women– Flank bruits

Primary renal disease (e.g chronic pyelo) ? From local ischemia

Renin secreting tumors

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2) Arterial disease:• large artery abN can lead to HTn• Coarctation of the aorta TRIAD?

• Upper extremity hypertension• Possible delayed femoral pulses• Systolic murmur heard over the back

• Loss of elasticity of the arteries with age

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3) Glucocorticoids: • Iatrogenic• Cushing’s

– 10 Pituitary tumor ACTH– ACTH – secreting tumor [>50% lung]– Adrenal tumors

• Primary hyperaldosteronism [Conn’s]– hypokalemia

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4)Pheochromocytoma: • Catecholamine-secreting tumors• Also w/ Neurofibro & MEN type ii• Clinically

– Paroxysms of HTN– Tachycardia– Fatigue– Malaise– Sweating– Apprehension

• Elevated urine catecholamines and metanephrines• Nb any incidental adrenaloma screen for pheo

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4) Drugs Sympathomimetics &c. MAOI and tyramine Withdrawal

andblockers• ETOH, benzos

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ED Presentation

• Four general ways:– Hypertensive emergencies

• Requires BP reduction in 1h

– Hypertensive urgency– Mild-moderate hypertension– Transient hypertension

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Approach

• ABC’s• Assess whether the reading is correct• Hx &P/E:

– Pulmonary Oedema?– CHF / Ischemia/ dissection? – High ICP/ SAH/ Neuro deficits?

• Diagnostix– Lytes, Urine +/ - TNT, EKG, CXR, +/- CT head

• Is this a Hypertensive Emergency?

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Fundoscopy

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Fundoscopy

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Case 1

• 84 yo F presents to the ED c/o HA feeling unwell for 1 week

• Hx HTn• O/e: BP 190/130, HR 80, rest of exam

N• Approach?

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Hypertensive Urgency

• No benefit to treating in the ED• Real risk of harm even with

appropriate MAP reduction• Most will have lower BP on f/u exams• Bottom Line : DON’T TREAT but

refer

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Recommendations

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Case 2

• 53-year-old M presents To ED w/ increased SOB, headache, N/V and visual changes, worsening for several days.

• O/e: Confused, BP 253/140 mm Hg. • Approach?

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Hypertensive encephalopathy

• Pathophys:– Acute increase in BP [ MAP usually > 160]– Overwhelms cerebral autoregulation

[resistance vessels can’t cope]– Eventually leads to vasospasm & ischemia.– Ischemia leads to leaky capillaries and edema

• Clinically– Acute and reversible– Headache, vomiting, drowsiness, confusion,

seizures, focal neuro deficits blurred vision– Normal CT head and bloodwork, elevated

opening pressure on LP

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• Management:– Sodium Nitroprusside or Labetalol – Goal: decrease MAP by 25% in 1 hour– Keep DBP > 110– Admit

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Case 3

40 y female family hx HTN, CVA Presents w/ L sided weakness BP 190/120, HR 94, RR 14, sats 99% O/E left facial droop, L dense hemi-plegia Considerations?

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Hypertensive Emergency- Stroke

Most (85%) are ischemic not hemorrhagic strokes

Elevated BP usually result of the stroke itself

May have mild to moderate BP elevation NB!!

Lowering BP may worsen ischemic brain injury watershed areas sensitive to hypoperfusion Do not treat [exception is stroke 20 Ao

Dissection]

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Hypertensive Stroke - lytics

BP >185/110 is a contraindication to tPA

Lower BP 1st

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Hypertensive stroke

• Management:– Labetalol agent of choice– Titrate slowly to goal reduction in MAP

by a max of 20%

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Hypertension + hemarrhagic Stroke

No data on acute BP lowering in ICH ICH causes inc ICP So May be inadvertently lowering CPP if

you lower BP My bottom line: treat only in concert with

ICU/Nsx If lowering is done, use an agent that dose

not vasodilate Avoid nitrates Labetolol is best (ACE-I have some benefit)

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Case 4

• 50 yo M at a “rave” comes into ED with ALOC [Pmhx: takes phenelzine]

• O/E: HR 100, BP 190/130, diaphoretic, GCS 9 and rigid extremeties

• Approach?

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MAOI – drug interactions

• sympathetic surge• Avoid B-blockers• Management:• ABCDEF’s of tox

– Phentolamine 5mg IV over 1min repeat Q5-10min

– Sodium nitroprusside 0.3 mcg/kg/min

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Case 5

• 55 year male known LV dysfunction (EF 30%), Chronic HTN , smoker

• Has not been able to buy meds• Presents to ED w/ incr SOB, leg swelling• HR 95, BP 190/120, sats 89%, RR 25,

Rales• Approach?

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Hypertension – Pulmonary edema

• Pts w/ CHF have incr PVR so have HTn

• Poor control LVH LV failure• Management:

– Standard therapy for CHF– NTG / nitroprusside– Low dose ACE-i

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Case 6

32 y female presents to ED c/o H/A, palpitations and feeling uneasy

BP 170/90, HR 150 sinus, RR 18, diaphoretic, pupils 6mm

Approach? Patient leaves AMA

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Case 7

• Same lady comes back the next day with SOB, Palpitations after doing cocaine

• O/E: BP 190/100, HR 130, RR 28, sats 96%

EKG ST segment elevation V1-V3 Considerations?

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Pheochromocytoma/Cocaine

Treatment: Avoid Beta blockade unopposed alpha Nitroprusside if emergency Phentolamine – 1-5 mg IV boluses

(alpha-block) With cocaine can use benzos to

counteract sympathetic drive

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Case 8

55 year male smoker, HTN, DM, c/o left RSCP that radiated to his jaw

after 1st training run for his 10k this summer.

HR 120, BP 190/90, RR 19, sats 99%

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EKG

•Approach?

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HTn + ACS

• Management: Immediate lowering of BP indicated to

prevent myocardial damage NTG agent of choice Beta block [labetalol] CCB (if BB is contraindicated)

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Case 9

19 y pregnant primip presents to ED with increasing swelling to hands and face

O/e: Hr 100 BP 130/80 Approach?

5% pregnacies complicated by PIH Preeclampsia = HTN, proteinuria + edema Eclampsia = preeclampsia + coma/Sz Both are Hypertensive Emergencies

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HTN in pregnancy Defined as BP > 140/90

W/u includes: CBC, Creat, Urinalysis, Liver enzymes

Mild PIH trial bed rest + close follow

If Persistently > 140/90 and symptomatic admit

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When do you need drugs? SBP > 160 DBP > 100 HELLP

Treatment: Hydralazine 5mg Iv bolus + 5-10 mg q15 prn Labetalol Control Sz [Mg IM or Iv protocol] Early Obs consult

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Case 10

• 66 yo M Hx HTN presents to ED c/o ripping CP radiating to back

• O/E: BP 200/100, HR 120 CXR wide mediastinum

• Considerations?

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• Goal is to reduce shear forces • Treat tachycardia and HTN

– Labetalol +– Nitroprusside

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drugsdrug dose onse

tduration

indication Contra-indication

nitroprusside

0.3-10 ug/kg/min

1-2 min

1-2 min Any hypertensive emergency

PregnancyProlong useRenal failure

nitroglycerin

10-100 ug/min

2-5 min

3-5 min AMI, CHF

hydralazine 5 mg5-10mg q20min

10-20 min

3-8 h preganancy AMI, aortic dissection

esmolol 500ug/kg then 50-300 ug/kg/min

1-2 min

10-20 min

CAD, aortic dissection

CHF, heart block, asthma, catecholamine excess

labetalol 20mg then 20-80 q10 min to max 300 OR 1-2 mg/min

2-10 min

2-4 h CAD, aortic dissection, eclampsia, hypertensive crisis

CHF, heart block, asthma, catecholamine excess

phentolamine

5 mg q 1-2 min

1-2 min

10-30 min

Catecholamine excess

AMI

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References

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