(Hypertension. 1996;27:144-147.)
© 1996 American Heart Association, Inc.
Articles |
From the Ward of Internal Medicine II and Emergency Department, Martini Hospital, Turin, and Institute of Internal Medicine, University of Turin (Italy).
Correspondence to Paolo Cavallo-Perin, MD, Istituto di Medicina Interna, Corso A.M. Dogliotti, 14, 10126 Torino, Italy.
| Abstract |
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Key Words: hypertension, arterial hypertension, detection and control emergency treatment
| Introduction |
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Epidemiological studies indicate that the prevalence of hypertension in
adults is
15% to 22% depending on the population
considered,4 but data on hypertensive urgencies and
emergencies are lacking both in the general population and emergency
departments.
The aim of the present study was to evaluate the prevalence of hypertensive emergencies and urgencies in an emergency department during 12 months of observation and the frequency of end-organ damage with the related clinical picture during the first 24 hours after presentation of the patient.
| Methods |
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All patients over 18 years of age who presented to the
emergency department with a hypertensive crisis were included in the
study; all patients were white. The criteria used to define
hypertensive crisis were those of the Joint National Committee on
Detection, Evaluation, and Treatment of High Blood
Pressure1 and included diastolic blood
pressure
120 mm Hg, according to previous
reports.5 6 7 8
Both patients previously recognized to be hypertensive (those with
known hypertension) and those who were not previously known to have
hypertension (those with unknown hypertension) were considered. We
classified as hypertensive emergencies all cases in which the increase
in blood pressure was associated with one or more of the following
types of acute or ongoing end-organ damage1 :
hypertensive encephalopathy; stroke (cerebral infarction or
intracerebral or subarachnoid
hemorrhage); acute pulmonary edema, congestive heart
failure, left ventricular failure, or aortic dissection;
acute myocardial infarction or unstable angina pectoris; progressive
renal insufficiency; and eclampsia. All these conditions were diagnosed
clinically and by diagnostic tests (blood and urine
chemistry, eye fundus examination, ECG, roentgenogram, computed
tomography, and ultrasound imaging) as appropriate; computed
tomographic scanning in particular was performed in all patients with
neurological symptoms. In the absence of end-organ damage all other
hypertensive crises were considered by exclusion to be hypertensive
urgencies.1
Each patient underwent a complete history, physical examination, and routine blood and urine chemical analyses. Blood pressure was measured with the patient in the recumbent position by use of a mercury sphygmomanometer according to a standard technique. The average of two consecutive readings taken 30 seconds apart was used. Each patient was monitored at the emergency department for at least 24 hours and treated according to his or her condition with nifedipine, captopril, clonidine, sodium nitroprusside, or furosemide.5 7 9 10 All subjects gave informed consent to participate in the study.
The prevalence of hypertensive crises, urgencies, and emergencies is expressed both as a percentage of the total number of patients applying to the Internal Medicine Section of the Emergency Department and as a percentage of all medical urgencies-emergencies. We included in medical urgencies-emergencies any critically ill patient; that is, any patient with an illness or injury that by its nature and/or severity is a direct threat to life or places the patient at high risk of life-threatening complications.11
All results were expressed as mean±SD. Statistical analysis
was performed by Student's t and
2
tests.
| Results |
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120 mm Hg was 449. No patient showing features of a
hypertensive emergency had a diastolic pressure <120 mm
Hg. The numbers of hypertensive crises, urgencies, and emergencies are
reported in Table 1
|
The Figure
presents the distribution of hypertensive
urgencies and emergencies by age class in men and women: the peaks of
urgencies and emergencies were earlier in men than women (51 to 60
versus 61 to 70 years of age and 61 to 70 versus 81 to 90 years of age,
respectively). The circadian and circannual distributions of
hypertensive urgencies and emergencies showed two peaks during the day
(at 9 AM and 7 to 8 PM) and one peak during the
year (January), respectively.
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Table 2
reports the prevalences of hypertensive crises,
urgencies, and emergencies, whereas Table 3
reports the
frequency of each type of end-organ damage in the group with
hypertensive emergencies. The majority (83%) of the patients with
hypertensive emergencies showed only one type of end-organ damage,
whereas in small groups (14% and 3%, respectively) two or three
types of end-organ damages were present
simultaneously.
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Table 4
reports the frequency of signs and symptoms in
all hypertensive crises, urgencies, and emergencies; headache,
epistaxis, psychomotor agitation, and arrhythmia were more
frequent in urgencies than emergencies (P<.04 to
P<.001), whereas chest pain, dyspnea, and neurological
deficit were more frequent in emergencies (P<.02 to
P<.001).
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| Discussion |
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As far as the time of presentation of hypertensive crises is concerned, as previously noted, we found two peaks during the day (at 9 AM and 7 to 8 PM) and one peak during the year (January). The peaks during the day do not represent the time at which the crises occurred, owing to the variability of the latency period between the appearance of symptoms and arrival at the Emergency Department either by their own choice or having been sent by their doctor (transport time). On the other hand, the circadian and circannual rhythms of hypertensive crises are unknown, even though the Framingham Study showed that sudden cardiac death had a circadian variation with a peak at 7 to 9 AM.12
In our series of patients presenting with a hypertensive crisis,
60% were women (Table 1
). This high percentage of women is
also
present in hypertensive urgencies and probably reflects the
larger number of women than men present in hypertensive
populations.13 However, this excess disappears in
hypertensive emergencies (Figure
), which suggests that
hypertensive men
are more susceptible than hypertensive women to end-organ damage.
In addition, postmenopausal age seems to increase the susceptibility to
end-organ damage.
Approximately one fourth of the patients presenting with
hypertensive crises had unknown hypertension (Table 1
),
indicating that
a hypertensive crisis occurs most commonly in patients with known
hypertension. These data confirm a previous report14 that
suggested that often hypertensive patients did not take medication as
prescribed or received inadequate therapy. Furthermore, the proportion
of our patients with unknown hypertension is higher in hypertensive
urgencies (28%) than emergencies (8%). Another interesting result of
the present study deals with the frequency of signs and symptoms of
hypertensive urgencies and emergencies and the pattern of end-organ
damage in hypertensive emergencies. We found headache and
epistaxis to be the most frequent signs at presentation in
hypertensive urgencies (22% and 17%, respectively), whereas chest
pain, dyspnea, and neurological deficit were the most frequent signs in
hypertensive emergencies (27%, 22%, and 21%) (Table 4
).
Furthermore,
the most frequent end-organ damage associated with hypertensive
emergencies were cerebral infarction, acute pulmonary edema,
and hypertensive encephalopathy (24%, 23%, and 16%, respectively);
cerebral hemorrhage accounted for only 4.5% (Table 3
). The
clinical pattern of presentation of hypertensive crises had
never been studied before and is of some interest in clarifying the
natural history of the disease in this respect.
In conclusion, the present study indicates that hypertensive urgencies and emergencies represent one fourth of all events in emergency medicine, that a quite differentclinical pattern of presentation is present in hypertensive urgencies versus emergencies, and that cerebral infarction and acute pulmonary edema are the most frequent types of end-organ damage in hypertensive emergencies.
| Acknowledgments |
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Received April 27, 1995; first decision June 8, 1995; accepted September 11, 1995.
| References |
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2. Ault M, Ellrodt A. Pathophysiological events leading to end-organ effects of acute hypertension. Am J Emerg Med. 1985;3(suppl):10-15.
3. Vidt D, Gifford R. A compendium for the treatment of hyper-tensive emergencies. Cleve Clin Q. 1984;51:421-430. [Medline] [Order article via Infotrieve]
4. Kaplan NM. Clinical Hypertension. Baltimore, Md: Williams & Wilkins; 1991;329-348.
5. Calhoun DA, Oparil S. Treatment of hypertensive crisis. N Engl J Med. 1990;323:1177-1183. [Medline] [Order article via Infotrieve]
6. Dellinger RP. Hypertensive emergencies and urgencies. In: Civetta JM, Taylor RW, Kirby RR, eds. Critical Care. Philadelphia, Pa: JB Lippincott Co: 1992;1209-1217.
7. Gonzales VM, Ibarra C, Jeries C. Single-dose sublingual nifedipine as the only treatment in hypertensive urgencies and emergencies. Angiology. 1991;42:908-913.
8. Houston MC. Hypertensive emergencies and urgencies: pathophysiology and clinical aspects. Am Heart J. 1986;111:205-210.
9. Pascale C, Zampaglione B, Marchisio M. Management of hyper-tensive crisis: nifedipine in comparison with captopril, clonidine, and furosemide. Curr Ther Res. 1992;51:9-18.
10. Schillinger D. Nifedipine in hypertensive emergencies: a prospective study. J Emerg Med. 1987;5:463-473. [Medline] [Order article via Infotrieve]
11. Hudson LD. Essentials of critical care medicine: approach to the critically ill patient. In: Kelley WN, ed. Textbook of Internal Medicine. Philadelphia, Pa: JB Lippincott Co; 1992;1842-1844.
12. Willick SN. Circadian variation in the incidence of sudden cardiac death in the Framingham Heart Study Population. Am J Cardiol. 1987;60:801-806. [Medline] [Order article via Infotrieve]
13. Julius S. Borderline hypertension: an overview. Med Clin North Am. 1977;61:495-511. [Medline] [Order article via Infotrieve]
14. Kincaid-Smith P. Malignant hypertension. Cardiovasc Rev Rep. 1980;1:42-50.
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