Trends in Hypertension Hypertensive Emergency Case Decision and Classification
Define hypertensive urgency (HU) & emergency (HE) · Define hypertensive urgency (HU) & emergency...
Transcript of Define hypertensive urgency (HU) & emergency (HE) · Define hypertensive urgency (HU) & emergency...
Define hypertensive urgency (HU) & emergency (HE)
Discuss the pathophysiology of hypertensive
urgency/emergency
Identify signs and symptoms associated with hypertensive urgency/emergency
Choose appropriate pharmacologic agents to treat
hypertensive urgency/emergency
Develop treatment goals for specific disease states related to
or caused by hypertensive urgency/emergency
Recognize possible adverse complications of
antihypertensive medications in certain hypertensive
emergencies
75 million adults in US affected by HTN
32% of the US population is diagnosed with HTN.
1 in 3 American adults has prehypertension.
54% of those diagnosed with HTN are adequately controlled.
High blood pressure costs the US about $48.6 billion each year
www.CDC.gov
Occurs in 1-2% patients with HTN
If untreated, carries a 70-90% 1-year
mortality and 100% 5-year mortality rate
Laragh J. Am J hypertens 2001.
Terminology for hypertensive
urgency/emergency is not consistent,
making data variable in published studies.
Billing codes make it difficult.
› Accelerated HTN
› Hypertensive crisis
› Malignant HTN
› HU/HE down-code to Essential HTN
Severe Hypertension is defined as:
BP ≥180/≥120 mmHg
Asymptomatic
Hypertensive Urgency is defined as:
BP ≥180/≥120 mmHg
Largely asymptomatic
Hypertensive Emergency is defined as:
Acute/rapidly evolving end-organ damage
(EOD)
BP ≥220/≥140 mmHg
Exact BP can vary
Bob is a 50-year-old man who comes to the ER complaining of a
headache. He has “no medical history” but also tells you he
hasn’t seen a doctor for over 20 years. Exam reveals BP 210/120
in the R arm and 216/118 in the L arm. ECG shows NSR 80 with
LVH. No other abnormal PE or diagnostic findings.
What does he have?
A. Severe hypertension
B. Hypertensive crisis
C. Hypertensive urgency
D. Hypertensive emergency
Blood volume
Cardiac Factors
•Heart rate
•Contractility
Humoral Factors
Constrictors Dilators
•Angiotensin II Prostaglandins
•Catecholamines
•Thromboxane
•Leukotrienes
•Endothelin
BP = Cardiac output x TPR
Neural Factors
Constrictors Dilators
α –Adrenergic β-Adrenergic
Sodium & H2O Retention
Potassium Excretion
Aldosterone
Volume Peripheral
vasoconstriction
Angiotensin II
Angiotensin I
AngiotensinogenRenin
ACE
Failure of the normal autoregulatory function
Increase in systemic vascular resistance
Endovascular injury and fibrinoid necrosis of arterioles
Cycle of ischemia & platelet deposition release vasoactive substances
The exact BP at which EOD begins is
different for everyone.
Patients who chronically have poorly
controlled BP have more compensatory
mechanisms to protect against EOD.
Treatment is guided by EOD.
SBP(mmHg)
220
200
180
160
140
120
100
Hyperperfusion
Perfusion
Hypoperfusion
Average SBP
Upward Shift of
Autoregulatory Mechanism
Prevailing BP
▪Normal Physiology
▪HTN Emergency
Perfusion
Hypoperfusion
Abrupt stop in prescribed BP meds
Elicit drugs
Secondary HTN causes
Neurologic insult
Undiagnosed HTN + OTC medication
Previous dx of HTN
Current medications/changes
Compliance
Risk factors
Elicit or OTC medications
Salt, alcohol intake
Other comorbidities
› CAD, CVA, DM, CKD
FH
Eyes› Blurred vision, papilledema, hemorrhages, venous
tapering, exudates
Heart› Chest pain, palpitations, dyspnea, displaced apical
pulse, S3/S4, JVD
Lungs› Dyspnea, crackles
Brain› Headache, stroke sx, ALOC
Kidney› Renal artery bruit, pulsatile abdominal mass
BMP: elevated BUN/creat
UA: protein
CXR: cardiomegaly, pulmonary edema
ECG: LVH, T-wave inversion, ACS
CT Head: small vessel ischemic changes,
hemorrhage
CT Chest: aortic dissection
Acute coronary syndrome
Acute heart failure
Aortic dissection
Hypertensive encephalopathy
Intracerebral hemorrhage
Ischemic stroke
Hemorrhagic stroke
Head trauma
Acute kidney injury
Acute increase in sympathetic activity
Eclampsia
“First Do No Harm”
No EOD, asymptomatic
BP ≥180/≥120 mmHg
Per ACC/AHA & JNC: Treat as Stage II
BP should be reduced over hours to days to
avoid ischemic events.
BP goal <160/<100 mmHg
MAP should not be lowered more than 25-
30% in first few hours to days.
Rapid control of HTN w/o symptoms =
increased adverse outcomes
Treat patients, not numbers!
Accurate BP readings
Reactive HTN?
“Without presence of acute EOD, no literature
demonstrated that patients receiving
pharmacologic interventions had better
outcomes than patients referred for BP
monitoring/close follow-up.”
Annals Emergency Medicine, March 2006
Can be treated as outpatient or
observation admission
PO medications in low doses with titration
preferred.
› Clonidine
› Captopril
› Furosemide
Ideal medication will lower BP without
adverse side effects.
Bob is a 50-year-old man who comes to the ER complaining of a headache. He has “no medical history,” but also tells you he hasn’t seen a doctor for over 20 years. Exam reveals BP 210/120 in the R arm and 216/118 in the L arm. ECG shows NSR 80 with LVH. No other abnormal PE or diagnostic findings.
What is your treatment plan?
A. Administer SL nifedipine
B. Dismiss to F/U w/PCP in 2 days on PO meds
C. Administer PO labetalol and admit to obs
D. Administer IV nitroprusside and admit to ICU
“Short-acting nifedipine should be used in
great caution (if at all), especially at higher
doses, in the treatment of hypertension.”
National Heart, Lung, & Blood Institute, ad hoc panel, 1995
ICU admission
Arterial line for BP monitoring
IV medications
Initiate goal-directed treatment even
before work-up is complete
Goal is to preserve kidney, brain, and
cardiac function
Severe acute HTN can cause ischemia/MI or may be the result
BP reduction is combined with reperfusion/antithrombotic therapies.
Beta-blockers (Labetalol) in conjunction with nitroglycerin preferred agents
Goals of therapy: treat until symptoms subside or DBP 100 mmHg
Can cause both systolic & diastolic HF
Reduction of afterload & preload with Nitroglycerin or Nitroprusside
Adjuncts include loop diuretic, morphine, and oxygen
ACE-I also 1st line agents for CHF
Goals of therapy: reduce sympathetic tone and filling pressures
Nitroprusside end product is thiocyanate
› Precursor to cyanide!
Extreme caution in patients with renal
insufficiency
Cyanide toxicity can be fatal.
Beta-blockers and calcium channel
blockers are NOT recommended in acute
decompensated heart failure.
› Further reduce SV and CO
Most rapidly fatal of HTN emergencies
Risk factors › Untreated HTN, advanced age, disease of aortic
wall
Type A surgical management.
Type B medical management.
Labetalol followed by Nitroprussidepreferred agents
SBP goal <100-120 mmHg within 20 minutes
Goal of therapy: reduce shearing forces caused by BP & tachycardia
Occurs from hyperperfusion of brain
Labetalol, Nicardipine, and Fenoldopamrecommended agents
If neurologic function worsens, suspend treatment.
Goals of therapy: reduce MAP no more than 10-20% in the first hour of treatment and no more than 25% at 24 hours
A 76-year-old male presents to the ED with
acute onset aphasia and R-sided weakness
upon awakening this AM. Serial blood
pressures are 180-195/95-105, HR 90s. He is
not a candidate for thrombolytics.
Would you treat this BP?
If so, what agent would you use?
HTN is single most identifiable risk factor for
acute stroke.
Management of HTN in acute stroke
remains controversial.
Long-term control of HTN for secondary
prevention of stroke confirmed literature
› HOPE, CAMELOT, PROGRESS trials
www.strokecenter.org
AHA recommends treatment of SBP > 220 mmHg or DBP >120 mmHg in patients not receiving thrombolytics.
Preferred agents are Labetalol (first-line) and Nicardipine (second-line)
Nitroprusside can be used to augment BP control.
Cautious reduction of BP by 15% in first 24 hours for those who require treatment.
Stead et al performed meta-analysis of 65
trials (11,500 patients) involving acute stroke
and HTN treatment within 1 week (2004).
› Results: insufficient evidence to evaluate effect
of altering BP on outcomes after stroke
ENOS trial showed higher rates of death or
disability in patients who continued blood
pressure treatment within 48 hours of stroke
(2015).
A cause or result of acute severe HTN?
HTN is the single most important risk factor for
cerebral bleed.
In ICH, use Esmolol or Labetalol.
In SAH, use Nimodipine (prevention of
vasospasm).
Goals of therapy: MAP 110 mmHg, BP 160/90
mmHg and adjust for patient mental status
If ↑ ICP is suspected, consider ICP monitoring.
To keep CPP adequate MAP must
exceed ICP.
CPP = MAP – ICP
Lowering BP even in ICH may cause
hypoperfusion of brain.
Goal CPP is 50-70 mmHg.
Cause and result of acute HTN
Fenoldopam preferred agent due to
increased renal perfusion while lowering BP
Goal of therapy: prevent further renal
damage
Pheochromocytoma, autonomic
dysfunction, sympathomimetic drug use,
and MAO-I use + tyramine ingestion
Recommended agents are Nitroprusside
and Phentolamine
Avoid beta-blocker alone d/t unopposed
alpha-adrenergic vasoconstriction.
Due to preeclampsia or exacerbation of
preexisting HTN
Preferred agents are Hydralazine and
Labetalol
Acute Disease State BP Goal Treatment
HTN Encephalopathy 10-20% reduction* Labetalol, Nicardipine, Fenoldopam
ACS 10-20% reduction* Labetalol, NTG
AKI 10-20% reduction* Fenoldopam
ICH/SAH MAP 110mmHg Labetalol, Esmolol,
Nimodipine (SAH)
Aortic Dissection
(Type B)
SBP <100-120mmHg in 20 min
Labetalol, Nitroprusside
Acute Ischemic Stroke Do not treat unless
SBP >220mmHg
Nicardipine, Labetalol
Acute Heart Failure 10-20% reduction* NTG, Nitroprusside, diuretic, ACE, Morphine
*In 1st hour, then additional 5-15% over next 24 hours.
Which of the following best classifies a
blood pressure of 148/92 mmHg?
A. Normal blood pressure
B. Prehypertension
C. Stage 1 hypertension
D. Stage 2 hypertension
E. Hypertensive urgency
In a patient with hypertensive emergency, in general, which of the following is the most appropriate blood pressure reduction goal within the first few hours?
A. 0-5%
B. 10-20%
C. 30-50%
D. 60-75%
E. 80-90%
Which of the following pharmacologic agents is preferred for the treatment of aortic dissection?
A. Furosemide
B. Labetalol
C. Lisinopril
D. Nicardipine
E. Nitroglycerine
HTN urgency BP ≥180/≥120 mmHg and NO end organ damage
HTN emergency = EOD
In most HE, no more than 10-20% reduction in BP in 1st hour
Treatment of HE directed by type of EOD
Treat BP in acute stroke only if >220 mmHg (DBP > 120 mmHg)
Treat the patient, not the numbers, when
it comes to severe hypertension.
Choose the appropriate drug for the
hypertensive condition you are treating.
Choose the appropriate level of care
when treating a hypertensive patient.
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