Download Hypertensive Urgency/Emergency Module

Resident Version
Hypertensive Urgency/Emergency Module
created by Dr. Teodora Konstantinova
Objectives:
1) You will be able to understand the difference between hypertensive urgency and
hypertensive emergency.
2) You will be able to recognize important markers in the patient history and
physical exam when evaluating patients with markedly elevated blood pressure.
3) You will learn the appropriate management strategies for the hypertensive
urgency/emergency.
A. Overview of hypertensive urgency/emergency
Hypertensive crisis is defined as a critical elevation in blood pressure in which
DBP > 120 mmHg. The severity of the condition, however, is not determined by the
absolute blood pressure level but by the magnitude of the acute increase in blood
pressure. As far as the seriousness of the situation is concerned two forms were defined:
Hypertensive emergency and hypertensive urgency.
The presence of acute or ongoing end-organ damage constitutes a hypertensive
emergency, whereas the absence of such complications is known as a hypertensive
urgency.
Hypertensive emergencies generally require a reduction in blood pressure within a few
hours, usually using IV medications given in ICU. Hypertensive urgencies also require
prompt medical attention, but BP can be lowered over 24 to 48 hours, sometimes in a
closely monitored outpatient setting.
True hypertensive emergencies
Acute Aortic Dissection
Angina or Acute MI
CHF
ARF
Microangiopathic Hemolytic Anemia
Eclampsia
Hypertensive Encephalopathy
Intracerebral or Subarachnoid hemorrhage
Pheochromocytoma Crisis
Severe HTN in patients requiring Urgent Surgery
Interactions with MAO-I Inhibitors
The exact pathophysiology underlying the development of hypertensive crisis is
unknown. It is mostly due to an acute elevation of systemic vascular resistance. Humoral
factors (particularly the renin angiotensin aldosterone system) and the local products
produced by the vasculature (prostaglandins, free radicals) may be involved. The net
effect is a decrease in oxygen and nutrient supply to target organs which causes endorgan damage. The primary sites are CNS, cardiovascular system, ophthalmic and renal
vascular systems.
B. Clinical assessment
The history and physical examination determine the nature, severity, and hypertensive
event. The history should focus on the presence of TOD (target organ damage), the
circumstances surrounding the identifiable etiology.
1) Medications (compliance; intake of over-the-counter preparations; use of recreational
drugs; MAO inhibitors)
2) Degree of BP control
3) Presence of previous TOD, particularly renal and cardiovascular disease
4) Date of last menstrual period
5) Other medical problems (prior HTN, thyroid disease, Cushing disease, SLE)
6) Assess whether specific symptoms suggesting TOD are present (chest pain, back pain,
dyspnea, neurologic symptoms)
Physical examination
BP should be measured with a cuff of the appropriate size for the patient.
Measure BP in both arms and legs, and palpate pulses in all extremities.
Focus the physical examination on the detection of TOD and determine the acuity.
ENT: Careful fundoscopic examination may reveal acute changes such as hemorrhages,
cotton-wool exudates, or disk or retinal edema.
Cardiovascular: JVD; crackles, peripheral edema, carotid bruits, R or L sided murmurs,
S3, S4, and a pericardial rub.
Abdomen: examine for a bruits and a palpable mass that may indicate the presence of an
abdominal aortic aneurysm.
CNS: level of consciousness, visual fields, focal neurological signs (may indicate
hypertensive encephalopathy, subarachnoid hemorrhage, or stroke).
Diagnostic studies
BUN, creatinine, electrolyte, glucose levels, CBC, EKG, UA, CXR should be obtained in
cases of suspected hypertensive emergencies to look for evidenceTOD.
Renal impairment may present as hematuria, proteinuria, or elevations of BUN/creatinine
and K levels
Blood glucose is important, because hypoglycemia may simulate encephalopathy or
stroke
CBC: may reveal microangiopathic hemolytic anemia
EKG: evidence of ischemia, electrolyte abnormalities or LVH
CXR: CHF or aortic dissection
CT scan of the head: should be performed in patients with neurologic symptoms
Treatment
The treatment goal in hypertensive emergency is the immediate reduction of mean
arterial pressure (MAP=[ 1/3(SBP-DBP)+DBP]) in a controlled, graded manner, using
improvement in the patient’s condition as a guide. BP reduction should not exceed a 20 to
25 % reduction within the first 30 to 60 min.
The treatment goal in hypertensive urgencies is the gradual reduction of BP
within 24h by using oral antihypertensive medications. The recommended duration to
achieve BP reduction varies from a few hours to 48h in the literature. Follow-up in 24 h
should be arranged. Admission decisions depend on the patient’s co-morbid conditions,
and the clinician’s impression of the patient’s anticipated response to therapy.
Specific agents in hypertensive emergency:
A) Sodium Nitroprusside: iv 0.25 mcg/kg/min (rapidly acting arteriolar dilator and
venodilator is the drug of choice for hypertensive emergencies. The rate of onset is
extremely rapid, with duration of action of 1-2 min and a plasma half-life of 3-4 min.
This drug is an excellent choice for all hypertensive emergencies except eclampsia prior
to delivery (because it crosses the placenta). Caution: metabolizes to cyanide- cyanide or
thiocyanate toxicity (MS changes, lactic acidosis)
B) Labetalol: this agent is a competitive, selective alpha 1 blocker and a competitive,
non-selective beta blocker. It can be used iv for hypertensive emergencies and be easily
converted to oral agent as the first line of therapy for hypertensive urgencies. It can be
safely used in patients with CVA and CAD. It is ideal for use in syndromes associated
with excessive catecholamine stimulation, such as pheochromocytoma, MAO inhibitorinduced emergency and abrupt clonidine withdrawal. It has also been used in pregnancyinduced HTN.
After an iv bolus, the BP falls in 5 min, with a max response in 10 min, and an effect
lasting up to 6h. Only BB useful in hypertensive emergency
C) Esmolol: this is an ultra-short-acting beta 1 selective adrenergic blocker. It has been
used in the treatment of SVT, MI, unstable angina and thyrotoxicosis.
D) IV NTG: causes both arteriolar dilatation and venodilation with a greater effect on the
venous system (preload) than on the arterial vasculature (after-load). The main indication
for NTG is in the setting of myocardial ischemia.
E) Hydralazine: this agent acts as a direct arteriolar dilator. The main indication is
pregnancy-induced HTN.
F) Enalapril: iv prep of ACE inhibitor; improves cardiac index and stroke volume
without affecting HR, start at 1.25 mg iv and up to 5 mg iv q6h. onset of action 15 min.
G) Nicardipine: dihydropyridine Ca ++ channel blocker, decreases after-load, maintains
cardiac output, no reflex tachycardia, onset: 5-15 min, duration: 4-6h.
H) Fenoldopam: peripheral dopamine 1 receptor agonist; shown to improve renal
function in hypertensive emergencies.
Special Clinical Situations
CHF: enalaprilat, diuretics, NTG
Coronary ischemia: NTG + BB
Aortic dissection: Block first (Esmolol, metoprolol) plus Nitroprusside (goal SBP < 100)
ARF and CRF: Fenoldopam
CVA: Goals of therapy, if initiated should be gradual reduction of SBP < 220 and DBP
< 110 mmHg. Short acting agents as Fenoldopam, Nicardipine or Labetalol are preferred
agents
Hypertensive encephalopathy: Nitroprusside, Nicardipine, Labetalol
Hypertensive Urgency
Medications: use short acting agents that you can titrate quickly.
Felodipine 5 mg po; Captopril 12.5 mg po; Hydralazine 10 mg po; Lopressor 25 mg po
All patients with hypertensive urgency being discharge home should be placed on
combination treatment and have rapid follow-up.
Case
HPI: 55 yo male presented to the ER with complain of severe bifrontal headache for he
last 3 days, which was getting progressively worse. He noted blurred vision, and stated
that he feels like he is in a fog. He also reports that in the last few days he felt very tired
and SOB and noticed swelling of his LE.
PMHs: HTN, hypercholesterolemia
Medications: Norvasc and Lipitor
Social: denies smoking, ETOH and IVDU
PE: vitals - BP 250/140 in both arms, HR= 96; RR-24, T-37 C, Pox-88% on RA
General: in moderate distress
HEENT: PERLA. No nystagmus, fundi with papilledema
Neck: + JVP 6cm above the sternal angle
Lungs: bibasilar crackles
CVS: RR S1, S2, + S4
Abdomen: NT/ND + BS
Extr: pulses are equal and full, no bruits 1+ edema of LE, around the ankles
Neuro: A & O x 3, CN II to XII: normal, sensory and motor exam: normal; deep tendon
reflexes: normal
EKG: NSR, no sign. ST/T changes
CXR: b/l interstitial markings
Labs: CBC: wbc: 10, H/H: 13/40, plt: 150
BMP: Na 136, K-4.0, Cl-109, CO2-23, BUN/creat: 24/1.8, glucose-129
UA: 0 rbc, 0 wbc, no protein
Does this patient meets the criteria for hypertensive emergency?
Do I need to lower the BP?
How much do I lower the BP?
Review questions
1. A 48 yo male presents to the ER with 2 days history of worsening occipital headache
and blurred vision in his right eye. His BP found to be 220/130 mm/Hg and HR- 78 bpm.
On fundoscopic exam, the physiologic cup of the optic disk in the right eye is obscured.
Flamed shaped hemorrhages are noted. The remainder of the physical exam is normal.
Laboratory findings include hematuria (2+) and serum creatinine of 2.1 mg/dL
Optimal management of this patient would be:
A) Gradual reduction of diastolic BP to 90 to 100 mm/Hg over 2 days
B) Reduction of DBP to 90 over 2 to 3 hours
C) Reduction of the MAP to 120 mm/Hg over 2 to 3 hours
D) Reduction of MAP to 120 mm/Hg over 6 to 12 hours
E) Measurement of intracranial pressure prior to lowering the BP
2. A 50 yo male with long standing history of HTN presents to the ER with complain of
severe mid-sternal chest pain with radiation to the back. The pain started 1 hour ago. The
physical exam reveals BP 230/130, P-110/min, right carotid pulse is weaker than left. An
early diastolic murmur is heard over the left sternal border. The ECG shows evidence of
LVH. CXR shows widening of the mediastinum.
What is the best approach at this time?
A)
B)
C)
D)
Give sublingual Nifedipine
Start IV BB and IV Nitroprusside
Start IV Diazoxide
Start Thrombolytic therapy
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
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