Hypertensive Emergencies
Trevor Langhan PGY-3November 10, 2005
Objectives
Discuss cases of hypertension in ED How to lower BP and when not to do it How low is too low? Or too fast?
Receptor sites
alpha-receptor Vasoconstriction iris dilation intestinal relaxation intestinal sphincter
contraction bladder sphincter
contraction
beta-receptor vasodilation (b2) cardioacceleration
(b1) intestinal relaxation
(b2) uterus relaxation(b2) bronchodilation (b2)
quiz
Nitroprusside
PRO Vasodilator Direct effect on smooth
muscle Dose related BP
reduction Drug of choice for most
HTN emergencies Rapid onset Short duration
CON Increase ICP Metabolized to thiocyanate
by KD cyanide can build up ARF and prolonged use Avoid in pregnancy
Must be IV Unstable in UV light Must be wrapped
Supine to prevent orthostasis
S/E due to decreased BP and vasodilation
Fenoldopam
PRO Peripheral dopamine
agonist Improves renal function Rapid action Does not cross blood
brain barrier Hypotension less often
CON Tachycardia, flushing and
h/a may occur
nitroglycerin
PRO Vasodilating agent
venous Decreases LVEDP Reduces BP by
decreasing preload and CO
Sublingual or IV
CON Limit to pts with cardiac
ischemia or pulmonary edema
Hypotension with pts who have RV dysfunction
hydralazine
PRO Direct arterial vasodilator Historically used ++ in
PIH and eclampsia
CON Reflex tachycardia May provoke angina Flushing, n/v, h/a Chronic use results in
lupus like syndrome
Beta-blockers - labetalol
PRO Selective alpha1 and
non-selective beta blocker
IV or oral No reflex tachycardia Less uncontrolled drops
in BP May not need ICU Good for aortic dissection
or cardiac ischemia
CON IV use has deep
orthostasis Supine post admin x 2-3
hours No effect on renal or
cerebral blood flow Contraindicated:
Heart block CHF Asthma pheo
Beta-blockers - esmolol
PRO Ultra short acting Selective beta1 Little BP effects Good for reflex tachy
CON Thrombophlebitis Tissue necrosis Contraindicated:
Heart block CHF Asthma Pheo cocaine
alpha-blockers - phentolamine
PRO Alpha-blocker Use in catecholamine
HTN crisis: Pheo MAOI crisis cocaine
CON Reflex tachycardia
nicardipine
PRO IV CCB Titratable Less negative inotropy Less tachycardia Mostly vasodilator Safe in pregnancy
CON Caution in poor LV fxn Liver metabolism H/a, flushing, tachycardia
Enalaprilat/enalipril
PRO IV ace-I Infrequent hypotension Increasing evidence for
use in cardiac Remodeling
CON Not dose related May precipitate ischemia
if MAP drop too steep Angioedema Cough ARF Toxic in 1st trimester
quiz - fin
Hypertension
What is normal BP? SBP < 140 DBP < 90
What is hypertension? SBP >160 DBP >100
Anything in between GRAY.
Hypertension
Possible cardiovascular causes of increased BP: Loss of vessel elasticity with age Coarctation of aorta
Delayed femoral pulses Hypertensive upper extremities Bruit in upper back
Hypertension
Endocrine causes for elevated BP: Pheo Excess steroids
Often iatrogenic Cushings
Look for hypokalemia Volume overload from Na retention
Hypertension
Other causes include: Withdrawal of sedative drugs
EtOH, benzo Tyramine toxicity in MAO-I patients Aortic dissection Sympathomimmetic drug intoxication Withdrawal of clonidine or beta blocking
agents Reno-vascular disease Renin-angiotensin system abnormality
Hypertension
HTN will present to the ED in a variety of ways: 1. Hypertensive crisis/emergency 2. Hypertensive urgency 3. Mild hypertension without EOD 4. Transient hypertension
Malignant hypertension
Malignant hypertension: Term no-longer used Prognosis of this d/o has changed much since
first introduced in 1928 1-2/100 000 people in developed countries 1 year survival has increased
<22% in 1939 – 90 % in recent series Only age and renal function at presentation
are independent markers of prognosis
Hypertensive Emergency
Also called hypertensive crisis Elevated blood pressure
signs of acute damage to target organs Brain Eyes Heart kidneys
Hypertensive Emergency
Malignant hypertension Hypertensive encephalopathy Microangiopathic hemolytic anemia Acute renal failure
Eclampsia/preeclampsia Aortic dissection HTN in setting of:
MI Left ventricular failure Bleeding Thrombolytic therapy
Hypertensive Urgency
Blood pressure elevation is an imminent risk for target-organ damage
No acute end organ damage but risk is high if BP elevation continues
Relative increase in BP more important than specific numbers
•Hypertensive Emergency
Rosen’s states: True medical emergencies Immediate reduction of BP in 1 hour
Pathophysiology
Mild to moderate increase in BP leads to initial vasoconstriction
“autoregulation” Maintains perfusion at relatively stable level Prevents increased pressure from being
transmitted downstream to smaller vessels As BP further increases, autoregulation fails Elevated BP disrupts vasc endothelium,
causing narrowing
Pathophysiology
Chronic increase in BP causes arteriolar hypertrophy
Will decrease the amount of pressure passed on to more distal vessels Chronically hypertense people need
diastolic BP’s >130 for symptoms Normotensive people can have hypertensive
crisis at DBP > 100
Case 1
45 y male c/o 12 hour history of SOBOE, mild chest heaviness
Vomiting, drowsy Bi-frontal headache Blurred vision both eyes BP 240/150, HR 102, RR 16, sats 95%
Case 1
PMHx: ? HTN, was on a “water pill” many years ago. No DM, no CAD, generally healthy
Labs normal, except Creat: 150 Inx? DDx? Mgnt?
Hypertensive Emergency
Hypertensive Emergency
Hypertensive Encephalopathy
Cerebral edema: breakthrough hyper-perfusion from severe and
sudden increase BP BP has exceeded the capacity of autoregulation vessels that can’t accommodate the pressure leakage and edema (fibrinoid necrosis)
Autoregulation must be considered during treatment Hypertrophied vessels can’t vasodilate caution with lowering blood pressure Avoid relative hypoperfusion
Hypertensive Encephalopathy
True medical emergency Is an acute presentation, but reversible Progression of untreated cerebral edema leads
to coma and death Admission and invasive BP monitoring is the
recommended mainstay of therapy
Hypertensive Encephalopathy
Test: 1) BP 140/90
What is MAP? What is goal MAP
2) BP 240/140 What is MAP? What is goal MAP?
Approx- 110
Goal – 85
Approx – 175
Goal - 130
Hypertensive Encephalopathy
First hour goals: Reduce MAP by 25% Keeping DBP > 110 mmHg
Goal at 4-6 hours: Reduction to pt’s normal BP
What agents? Nitroprusside - titratable, easy off, potential
toxicity labetalol – alpha and beta blocker
Case 2
67 y female known CAD, DM, smoker, atrial fib.
Presents with c/o weakness left side BP 160/100, HR 94, RR 14, sats 99% O/E left facial droop, markedly weak left
upper/lower extremity EKG: a fib, nil acute Chest exam unremarkable
Case 2
Management? How do you treat her elevated BP?
Stroke syndromes
Most patients with this presentation are ischemic strokes (85%) not hemorrhagic
Likely don’t have acutely elevated BP May have mild to moderate BP elevation ***CAUTION***
lowering BP as watershed area sensitive to hypoperfusion
Lowering BP may worsen ischemic brain injury
Stroke syndromes
Rarely stoke with grossly elevated DBP > 140
But a contraindication to tPA is a BP >185/110 Patients receiving reperfusion therapy may
require a lowering of BP
Titrate labetalol slowly to achieve decrease in MAP by a max of 20%
Stroke syndromes
What if on CT it is an ICH? Little data about acute BP lowering in ICH Many centers lower MAP 20%
May be a negative thing to do CPP depends on BP in setting of increased ICP Most ICHs have elevations of ICP
If lowering is done, use an agent that dose not vasodilate Avoid nitrates Labetolol is best (ACE-I have some benefit)
Case 3
55 year male known LV dysfunction (EF 30%) Chronic HTN On low dose lasix and daily asa, metoprolol Was off his low Na+ diet over all-inclusive
vacation to Mexico Weighs 8 pounds more than usual Legs swollen HR 95, BP 190/120, sats 89%, RR 25
Case 3
Chronic pulmonary edema results in increased PVR and HTN
Acute decompensation in setting of CHF can have marked increase in BP due to catecholamines
Case 3
Standard treatment of CHF: Morphine Oxygen Nitrates (nitroprusside better than NTG) lasix
Improving evidence for use of ACE-I in setting of acute LV dysfunction and CHF
Be on lookout for stroke syndrome as result of acutely lowered BP in someone chronically HTN
Case 4
32 y female awaiting “sweatgland” surgery from plastics for hyperhydrosis, c/o H/A, palpitations
BP 170/90, HR 150 sinus, RR 18 Otherwise healthy Treatment:
Nitroprusside if emergency Phentolamine – 1-5 mg IV boluses (alpha-
block) Followed by beta-blockade
Case 4
Pheochromocytoma Rare tumor – 0.2% of pts with essential HTN Episodic H/A, tachycardia, sweating, HTN Tumor secreting norepinephrine and
epinephrine Diagnosis:
Radiographic measurement of urinary and plasma levels
of catecholamines and metabolites
Case 5 Hypertension in pregnancy
25 y G2P1, LMP 6 months ago When do you treat HTN in pregnancy?
SBP > 160 Treat to goal of 140-155 5-10% of all pregnancies
Any acute DBP elevation >100 is a true HTN emergency
Eclampsia and preeclampsia may occur without extreme elevation of BP
Treatment: Prevention and control of seizures Early obs consult
Ecclampsia Dx: Elevated BP in late 2nd or 3rd trimester
SBP > 140, DBP >90 Elevated urine proteins Pedal edema
No mortality benefit treating SBP 140-170 Expert consensus that SBP > 160 need treatment Methyldopa, CCB, acute episodes with lobetolol or
hydralazine Eclampsia seizure risk peaks during delivery and
24-48 hours after – prevention of seizures with prophylaxis recommended
Case 6
33 year male stock broker. Snorted a “couple of rails” of cocaine ½ hour ago.
Presents with crushing retrosternal chest pain, diaphoresis and H/A
BP 190/100, HR 130, RR 28, sats 96% EKG ST segment elevation V1-V3 Nurse asks “what do you want to give?”
Case 6
Beta blocker contraindicated Beta antagonism will decrease heart rate,
but will also block B2 receptors Will have unopposed alpha agonism by
cocaine toxicity – dangerous HTN crisis Need alpha blockade first Like pheo can use phentolamine, some
sources say hydralazine benzo dosing to decrease BP, HR and battle
sympathetic tone of cocaine
Case 7
55 year male smoker, HTN, DM, unstable angina getting worse.
Shoveling snow and developed left RSCP that radiated to his jaw.
HR 120, BP 190/90, RR 19, sats 99% EKG obvious ant/lateral infarct How do you treat his pressure?
Case 7
Agents of choice in HTN during ACS Immediate lowering of BP indicated to prevent
myocardial damage Also lower BP if pt to undergo reperfusion tx
NTG agent of choice Beta block ACE-I (shown improvement in mortality) CCB (if BB is contraindicated)
Contraindicated agents include: Hydralazine – reflex tachycardia Nitroprusside – reflex tachycardia
Key concepts
Presence of acute target organ damage determines HTN crisis
All pts with persistent elevation of BP should be investigated for EOD
ER doc should be familiar with indications and contraindications of meds to treat HTN crisis
Goal of treat is relative decrease in MAP of 25% in first hour, DBP should not fall <110 mmHg
Pts without EOD rarely require urgent management of HTN
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