CPM 1st Ed Hypertension

Philippine Society of Hypertension
Affiliated with the International Society of Hypertension

and World Hypertension League
Unit 33,2/F, Facilities Centre, 548 Shaw Boulevard, Mandaluyong City
Tel. Nos. 531-1204,531-1265; Fax No. (632) 531-1281
Officers and Board of Trustees 1997

President
Vice-President
Secretary
Treasurer
Trustees
Ramon F. Abarquez, Jr., M.D.

Yolando Q.M. Sulit, M.D.
Gregorio B. Patacsil, Jr., M.D.
Agnes D. Mejia, M.D.
Esperanza I. Cabral, M.D.
Rody G. Sy, M.D.
Nelson S. Abelardo, M.D.
Francis M. Domingo, M.D.
Mr. Gerry S. Arnedo
Mr. Elmer F. Deles
Multi-Sectoral Task Force on the Detection and

Management of Hypertension
Technical Research Committee

Co-chair
Co-chair
Antonio L. Dans, M.D.

Bemadette A. Tumanan, M.D.
Cristina R. Larracas, M.D.
Felix Eduardo R. Punzalan, M.D.
Eugenio B. Reyes, M.D.
Luciene Lourdes C. Villacin, M.D.
Maria Vanessa C. Villaruz, R.N.
HYPERTENSION
CPM 1ST EDITION
Panelists
Ramon F. Abarquez, Jr. M.D.
Ma. Lourdes E. Amarillo
Joselito L. Atabug, M.D
Eliseo Banaynal, M.D.
Annette P. Borromeo, M.D.
Esperanza I. Cabral, M.D
Ma. Delta A. Canela, M.D
Edeliza D. Carandang, M.D.
Virgilio Castro, M.D.
Jayvee G. Cruz, R.N.
Antonio L. Dans, M.D.
Liberty Fajutrao, M.D.
Ms. Mayeth Go
Leni Iboleon, M.D.
Dean Artemio 0. Isidro
Ranulfo Javelosa, M.D.
Anthony B. King, M.D.
Cristina R. Larracas, M.D.
Agnes Mejia, M.D.

Dante D. Morales, M.D.
Oscar D. Naidas, M.D.
Desiree M. Narvaez, M.D.
Victoria Pacardo, M.D.
Elizabeth Paz-Pacheco, M.D.
Mayos Pe, M.D.
Ms. Marisol L. Policarpio
Felix Eduardo R. Punzalan, Jr., M.D.
Eugenio B. Reyes, M.D.
Leonardo Rolle, M.D.
Allan B. Ruales, M.D.
Bernadette Tumanan, M.D.
Ms. Felicidad V. Velandria
Luciene Lourdes C. Villacin, M.D.
Maria Vanessa C. Villarruz, R.N.
Amariles 0. Yazon, M.D.
Ms. Clarissa G. Yu
Organizations Represented
Department of Health, Republic of the Philippines
Fetus as a Patient Institute Philippines
Food and Nutrition Research Institute
Occupational Safety and Health Center
Philippine Obstetrics and Gynecology Society
Philippine College of Occupational Medicine
Philippine Diabetes Association
Philippine Heart Association
Philippine Lipid Society
Philippine Medical Association
Philippine Nurses Association
Philippine Society of Nephrology
Sports Medicine Association of the Philippines
Stroke Society of the Philippines
Philippine Society of Ophthalmology
University of the Philippines, College of Human Kinetics
U.P. College of Medicine, Clinical Epidemiology Unit and Cardiovascular Section
University of the Philippines, College of Nursing
Funding Sources
Department of Health
National Academy of Science and Technology
Philippine Council for Health Research and Development
Philippine College of Physicians
Thesis grant to Bernadette A. Tumanan M D from PCHRD
32
CPM 1ST EDITION
Plans and Programs of the Philippine Society of

Hypertension
The Philippine Society of Hypertension (PSH) was
incorporated on January 24,1994 and is affiliated with
the International Society of Hypertension (ISH) and
the World Hypertension League (WHL). Its vision is to
control the hypertension epidemic. It is a multisectoral
group composed of various medical, surgical and pediatric specialists as well as paramedical, pharmaceutical
and lay professionals whose shared responsibility is the
control of the hypertension epidemic.
Hypertension related mortality of 7/100,000 adults in
the 80's has increased to 21/100,000 in the 90's, second
only to Indonesia. The Philippines is third to Singapore
in coronary artery disease and fourth to Japan in stroke
mortality. These are statistics we do not intend to surpass. The treatment of hypertension is costly. In one
industrial corporation, it amounted to 50% of total drug
expenditures for its employees every year.
After an agenda setting workshop, existing hypertensive programs and data from varied other sources were
collated. A knowledge attitude and practice survey was
also conducted addressing the health providers and the
clients. The data was presented during the first annual
convention of the PSH. The updates and new concepts
on hypertension control were presented by a faculty
organized by Dr. Stevo Julius. This conference was
simultaneously telecast to Cebu, Davao and Legaspi
cities.
The next agenda is to "teach the teacher". A multi-sectoral task force was convened for a formal consensus
development program utilizing evidence based data
systematically collated by a technical group from the
Clinical Epidemiology Unit of the UP-PGH Department
of Medicine. Funding was provided by the Department
of Health (DOH), National Academy of Science and
Technology (NAST), Philippine Council on Health
Research and Development (PCHRD), Philippine
College of Physician (PCP), and Philippine Society of
Hypertension (PSH). The methodology was presented
during the 2nd Annual Meeting of the PSH.
HYPERTENSION
The PSH president presented the Paradigm Shift in

Hypertension Control in a plenary session. From the
70's to the 90's, hypertension awareness, compliance and
desirable BP control have improved by a mere 1% or
5% every 5 years. Althought the target adult population
for hypertension control represents a minority, this is
admittedly the productive sector of the country. Strategies beyond BP control that were discussed included 1)
implications of genetic, gestational, and developmental
characteristics as predictive factors for future hypertension; 2) risk multiplier implications of co-morbid
factors in the development of adverse clinical events;
3) surrogate endpoints particularly LVH, microalbuminuria, or congestive heart failure that occur and are
modulated by factors independent of BP levels; 4) current anti-hypertensive agents that have reduced stroke
by 29%, CAD by 14%, CHF by 49% (mostly) in the
elderly, and LVH regression by 45%. These meta-analysis data suggest that a program is needed to motivate
the non- hypertensive population to submit to regular
BP check-ups and apply lifestyle modifications. More
importantly, BP management should include strategies
beyond BP control.
On-going agenda for health providers includes the dissemination of the practice guidelines on hypertension
management and evaluation of the impact of the practice
guidelines on the actual practice of physicians. Programs
for the public will include self BP monitoring and assessment of cardiovascular disease risk factors as well
as lifestyle modification particularly related to smoking,
obesity and physical inactivity.
Our expectation therefore, on a short-term basis, is to
increase the awareness of the hypertension problem and
its implications, to implement routine BP monitoring
for children and adults who are at risk for hypertension
and to carry out co-morbid risk management with the
hypertensive patients. On a long-term basis, reduction
of hospitalization and death related for CHF, CVA, CAD
and renal failure are to be expected.
The 3rd Annual Meeting of the PSH was held in conjunction with the 2nd Pacific Rim Conference on Hypertension Control. This event was hosted and organized
by the PSH and PCP and was held at the PICC last May
1997. There were over 150 foreign delegates representing 23 countries and over 1,000 Filipino physicians who
participated in the meeting. Over 25 foreign speakers
participated in the scientific sessions. Highlights of this
conference was the presentation of commonalities and
differences in guidelines as well as hypertension control
programs from different countries.
33
HYPERTENSION
Foreword
The Philippine Society of Hypertension Inc. (PSH),
affiliated with the International Society of Hypertension
(ISH) and the World Hypertension League (WHL), has
a multi-sectoral individual and corporate membership.
Its vision is the control of the hypertension epidemic. Its
mission is to "teach the teacher" by evolving together
"shared responsibilities" in the development of programs
and strategies.
This "Clinical Practice Guidelines in the Detection
& Management of Hypertension" is the output of a
Multi-Sectoral Task Force representing 20 organizations
among the panelists and at least 50 organizations in the
public forum. Major contributors to the grant-in-aids
are the National Academy of Science and Technology (NAST), Department of Health (DOH), Philippine Council for Health Research and Development
(PCHRD), Philippine College of Physicians (PCP), and
the Philippine Society of Hypertension (PSH).
The special features of the guidelines are:
1) A multi-sectoral formal consensus development
methodology;
2) Specified levels of evidence-based documentation
for each recommendation given;
3) Risk stratification of hypertensives in relation to
target organ involvement and co-morbid events;
4) Emphasis on local problems like pregnancy-related
hypertensive problems, role of herbal and non-traditional approaches and;
5) Emphasis on primordial preventive measures.
The recommendations given are based on the
assumptions that:
1) Patients to be treated meet the inclusion criteria
of the various studies used in the evidence-based
guidelines;
2) Local clinical endpoints approximate the extrapolated morbid and mortality prevalences used in the
study populations;
3) Health providers will avail of the voluminous references cited;
4) Sound clinical judgement should prevail since the
attending physician has more information available
to him than what the guidelines can supply.
PSH recognizes that about 12% of the adult population or 4.2 million Filipinos have hypertension. Only
50 % of this group are aware of the problem, among
those who are being treated, only about 50% are getting
advice and treatment. However, only about 25% will
have acceptable BP control. Thus, 3.6 million adults
can benefit from monitored management. This number
34
CPM 1ST EDITION
represents a considerable proportion of the productive

sector of the country.
The Board of Trustees of the Philippine Society of Hypertension & all those who contributed to the realization
of the Guidelines express their sincere appreciation to
all who join us in our efforts to control the hypertension
epidemic in our country.
The Philippine Society of Hypertension

Officers and Board of Trustees
CPM 1ST EDITION
HYPERTENSION
HYPERTENSION
The recommendations contained in this CLINICAL

PRACTICE GUIDELINES are intended to GUIDE
practitioners in the detection and management of
hypertension in adult patients. In no way should the
guidelines be regarded as absolute rules, since nuances and
peculiarities in individual cases or particular communities
may entail differences in the specific approach. In the end,
the recommendations should supplement, and not replace
sound clinical judgement.
35
HYPERTENSION
CPM 1ST EDITION
The Philippine Clinical Practice Guidelines on the

Detection and Management of Hypertension
Report of the Multisectoral Task Force on the Detection and Management
of Hypertension Convened by the Philippine Society of Hypertension
Introduction
The multi-sectoral task force for the Control of Hypertension was convened by the Philippine Society of
Hypertension. During the agenda-setting conference
held on August 12, 1995 at the Development Academy
of the Philippines, Pasig City, the need for local guidelines on the detection and management of hypertension
was identified. The multi-sectoral task force was thus
formed to address this need. Thirty-six (36) participants
representing 20 governmental & non-governmental
organizations participated in the guideline development process, which took place in 4 phases, outlined
as follows:
Phase 1 - Preparation of the Evidence Based Report
(EBR).

This initial draft of the manuscript was
prepared by a Technical Research Committee whose members tracked, retrieved, and
appraised current evidence pertaining to
the detection and management of hypertension.
Phase 2 - Preparation of the Intermediate Report.

The 2nd draft of the manuscript was prepared
by all members of the multi-sectoral task
force, based on their criticism and appraisal
of the initial EBR. This was achieved in a
2-day meeting which was held at Corregidor
from January 12-14 1996. A consensus was
defined as 75% of votes cast during any
circulation.
The following 6 questions are addressed by the

present guidelines:
A. How should blood pressure be measured?
B. How should hypertension be diagnosed?
C. How should hypertension be worked up?
D. What advice should hypertensive patients receive
regarding lifestyle modifications?
E. How should hypertension be treated?
F. How can hypertension be prevented among normotensives?
Assessment of Evidence from the Medical Literature:
Evidence addressing these 6 problems were classified according to a system adopted by the Canadian
Hypertension Society [1]. This system allows rating of
studies on a scale of 1 to 6 (best to worst, respectively),
using standardized criteria to assess methodologic rigour (see appendix). Recommendations throughout the
guidelines are then graded from A to D depending on
the best evidence that supports them (Table 1). Thus,
grade A recommendations are based on the strongest
evidence from properly conducted randomized controlled trials. On the other hand. Grade D recommendations
are based on weaker study designs including expert's
opinions, clinical experience and common sense. Grade
D recommendations often address practical issues of
implementation and other factors existing in the local
setting which are not addressed in clinical trials.
Table 1. Grading system for recommendations
Grade A The recommendation is based on one or
more studies at level 1.
Grade B The best evidence available is at level 2.
Grade C The best evidence is at level 3.
Grade D The best evidence available is lower than
level 3, and included expert's opinions,
clinical experience and common sense.
These recommendations address practical
issues of implementation and other factors
existing in the local setting.
Phase 3 - Preparation of the Penultimate Report.

The 3rd draft was prepared after 3 circulations of intermediate versions by mail
(modified Delphi technique), with panelists
requested to vote and comment on specific
statements, until a consensus was reached
on the various issues raised.
Phase 4 - Preparation of the Final Report.

The final draft was prepared after consideration of the comments and feedback of
non-panelists. These non-panelists included
representatives of pharmaceutical companies, heads of related societies, and other
educational influentials.
36
Recommendations
A. HOW SHOULD BLOOD PRESSURE BE
MEASURED?

1. The most accurate and reliable technique for
CPM 1ST EDITION
indirect blood pressure measurement is the

auscultatory method using a mercury manometer (Grade A Recommendation).

Summary of Evidence: Previous technical publications[2,3] and consensus statements [4-6]

have adequately described the technique of
indirect blood pressure measurement using the
auscultatory method. The method described in
Table 2 highlights technical requirements which
are common to these statements.
Table 2. Methods for Indirect Measurement of
Blood Pressure
1. A mercury manometer is ideal for accurate
measurement. Aneroid, digital or other automated devices provide reasonable alternatives,
provided that they satisfy technical requirements
for accuracy, and are calibrated and tested on a
regular basis.
2. The manometer cuff should cover at least 2/3 of
the length of the patient's arm, while the bladder
should cover at least 80% of the arm circumference.
3. The patient should be seated (or supine) with
arms bared, supported, and at heart level. They
should have rested for at least 5 minutes, and
should not have smoked or ingested caffeine
within 30 minutes before measurement.
4. The edge of the cuff should be placed 1 inch
above the elbow crease, with the bladder directly
over the brachial artery.
5. The bladder should be inflated to 30 mmHg
above the point of radial pulse extinction as
determined by a preliminary palpatory determination. It should then be deflated at a rate of
2 mmHg/beat, with the stethoscope bell placed
directly over the brachial artery.
6. Systolic pressure should be recorded at the
appearance of the 1st clear tapping sound
(Korotkoff phase 1). Diastolic blood pressure
should be recorded as disappearance of these
sounds (Korotkoff phase V), unless these are still
present near 0 mmHg in which case, softening of
the sounds should be used as diastolic pressure
(Korotkoff phase IV).
7. For every visit, the mean of 2 readings, taken
at least 2 mins apart, should be regarded as the
patient's blood pressure. If the first 2 readings
differ by 5 mmHg or more, a third reading
should be included in the average.
8. If blood pressure is being taken for the first time,
the procedure should be repeated with the other
arm. Subsequent determinations should then be
performed on the arm with a higher pressure
reading.
HYPERTENSION
2. In the absence of a mercury manometer, aneroid, digital and other self-monitoring devices
may provide acceptable alternatives, provided
they have passed technical requirements for
accuracy, and are calibrated or checked regularly (Grade D Recommendation).
Summary of Evidence: Economical self-monitoring

devices have flooded the market. Although some
doubt has been raised regarding their accuracy [7},
these instruments may provide the only options for
screening and follow-up in many situations.
B. HOW SHOULD HYPERTENSION BE DIAGNOSED?

1. Strategies for Detection
a. Case Finding - Opportunities for case-finding

abound in daily practice. Health practitioners from all fields should be encouraged to
take BP measurements at each patient visit if
the patient consults for unrelated symptoms
(Grade A Recommendation).
b. Mass Screening - In developing countries,

many individuals have limited access to health
care. Consequently, hypertension cannot be
detected by the method of case-finding. In
such situations, an alternative may be mass
screening programs, where health care providers conduct household visits to measure
blood pressure. Such programs may be justified, as long as diagnosis can be confirmed &
treatment is provided (Grade D Recommendation).
Summary a/Evidence: The validity of recommendations to detect for hypertension finds support in
largescale randomized clinical trials which demonstrate that subsequent treatment leads to a reduction
in vascular events [8]. In addition, cost-effectiveness
studies have shown that the benefits achieved from
screening asymptomatic adults for hypertension
outweighs the risks & costs [9,10].
2. Strategies for Confirmation
The diagnosis of hypertension should be based

on repeated measurements (at least 2 visits)
showing sustained elevation. It should not
be based on single determination (Grade A
Recommendation). A proposed schedule for
confirmation based on initial BP readings is
summarized in Table 3 [4]. This schedule is
based on recommendations of the fifth report
of the Joint National Committee on Hyperten37
HYPERTENSION
sion (JNC V) (Grade D Recommendation).

Summary of Evidence: Variability in blood pressure
determination has been well-documented [11-17].
This variability stems from several factors which
include a) natural fluctuation or variability and b)
variation brought about by the technique of blood
pressure determination. The latter source of variability can be minimized by use of proper technique
as described in Table 2. Natural variability, on the
other hand, is best handled by repeated measurements, that is, through a confirmation schedule.
Table 3. Recommended confirmation schedule

for hypertension based on initial levels of blood
pressure.q
Initial level of BP
Recommended confirmation

in mmHg*
schedulef
systolic diastolic
<130
<85
Recheck in 2 years
130-139
85-89
Recheck in 1 year
140-159
90-99
Confirm in 2 months
160-179 100-109 Evaluate or refer to source

of care within 1 month
180-209 110-119 Evaluate or refer to source

of care within 1 week
210
120
Evaluate or refer to source

of care immediately
q These recommendations hold for patients who are not
presently on treatment for hypertension. If doubt exists
regarding the diagnosis in patients already on treatment,
drugs may be stopped for an appropriate period before
commencing with a confirmation schedule.
* If systolic and diastolic categories are different, follow
recommendations for the higher level.
f Scheduling of follow-up should be modified by reliable
information on past BP measurements, seventy of target
organ damage, and presence of other risk factors.
Definition
Hypertension is defined as sustained systolic BF
elevation of 140 mmHg or more, OR sustained diastolic BP elevation of 90 mmHg or more, based on
measurements done during at least 2 visits taken at
least 1 week apart (Grade A Recommendation).
Patients with intermittent elevation in blood pressure should not be labeled as hypertensives. An
example would be "white-coat" hypertension,
which is defined as BF elevation in the clinic setting
but repeatedly normal out of the office (Grade A
Recommendation).
Isolated systolic hypertension is defined as systolic
blood pressure of 140 mmHg or more and a diastolic pressure of less than 90 mmHg (Grade B
Recommendation).
38
CPM 1ST EDITION
Summary of Evidence: The advocated definition of

hypertension is "therapeutic" in nature [18], in that
it identifies a population that can benefit from subsequent therapy. Studies have shown that medical
treatment decreases the incidence of cardiovascular
events, when administered to patients with diastolic
blood pressure of 160 mmHg or more [19-23]. A
lower systolic level of 140 mmHg was accepted by
the panelists, although only 1 RCT used such a cut-off
[24]. This was deemed necessary in order to adhere
with internationally accepted standards [4,6].
Classification
Hypertensive individuals should be classified according to severity of blood pressure, target organ damage, and presence of other risk factors. The system of
classification recommended by JNC V is summarized
in Tables 4, 5 and 6 (Grade D Recommendation).
Summary of Evidence: Severity of hypertension is a
major determinant of the probability of developing a
vascular event in the future [25]. Thus, clinical classification of severity may have important implications
on urgency of treatment, the choice of drugs, the number
of medications given initially, and the frequency of follow-up. Further refinement by classification according to
target organ damage provides an idea of disease chronicity as well as severity, and gives an insight on the stage
of disease progression. Final clarification by inclusion
of other risk factors in the final classification furnishes
a master plan for subsequent management. Tables 5 and
6 list the risk factors for coronary artery disease and
manifestations of target organ damage by hypertension.
Table 4. Classification of Blood Pressure for
Adults Aged 18 years or older *
Mean BP in mmHgf
systolic diastolic
<130
<85
130-139
85-89
140-159
90-99
160-179 100-109
180-209 110-119
210
120
Classificationq
Normal
High normal
Stage 1 (Mild)
Stage 2 (Moderate)
Stage 3 (Severe)
Stage 4 (Very severe)
* This classification holds true for patients who are not acutely
ill and are not currently taking antihypertensive medications.
f Classification should be based on the average of two or more
readings taken at each of 2 or more visits after an initial
screening. If systolic and diastolic categories are different,
follow recommendations for the higher level.
q In addition to classification based on severity, patients
should be classified according to the presence or absence
of target organ damage and additional risk factors. Thus,
a patient with diabetes and a BP of 142/94 mmHg plus left
ventricular hypertrophy should be classified as having "stage
1" hypertension with target organ disease (LVH) and with
another major risk factor (diabetes).
CPM 1ST EDITION
HYPERTENSION
Table 5. Risk factors for Coronary Artery Disease

odifiable risk
M
Non-modifiable risk

factors
factors
Smoking
Age
Hypertension
Male sex
Dyslipidemia
Family history of premature CAD
Diabetes Mellitus
Obesity
Physical inactivity
Table 6. Manifestations of Target-Organ Disease
Organ system
Organ System
Cardiac

Cerebrovascular

Peripheral
Vascular

Renal

Retinopathy

Manifestations
Clinical, electrocardiographic or
radiologic evidence of coronary
artery disease
Left ventricular hypertrophy by
electrocardiography or cardiac
failure
Transient ischemic attack
or stroke
Absence of one or more major
pulses in the extremities (except
in the dorsalis pedis) with or
without intermittent claudication;
arterial aneurysms.
Serum creatinine 130 mmol/L
(1.5 mg/dL) Proteinuria
(1 + or greater)
Retinal arteriolar attenuation;
Hemorrhages &/or exudates,
with or without papilledema/
optic nerve edema
Source: The Fifth Report of the Joint National Committee on

Detection, Evaluation, and Treatment of High Blood
Pressure (JNC V). Arch Intern Med 1995; 153; 154-183.
Diagnosis
c. H O W S H O U L D H Y P E RT E N S I O N B E
WORKED UP ?
The objectives of a thorough hypertension work-up
include the following:
a) To determine the etiology of hypertension,
b) To determine the extent of target organ damage,
c) To detect (and possibly treat) other risk factors for
cardiovascular disease, and
d) To determine if there are contraindications to the use
of certain drugs.
With these objectives in mind, physicians should pay
close attention to all aspects of the clinical evaluation,
including extraction of a detailed history, performance
of a thorough physical examination, and requisition of
relevant laboratory tests.
1. A detailed history and physical examination

should be done in all patients with hypertension
(Grade A Recommendation). Aspects of the history and PE which should be emphasized are
summarized in Table 7.

Summary of Evidence: Effectiveness of treatments

used in randomized controlled trials depends on duplication of the quality of care which was rendered
during the trial period. The medical history and
physical examination were carefully conducted in
hypertension trials in order to search for other risk
factors, evidence of target organ damage, evidence
of secondary hypertension, and possible contraindications to use of certain drugs [23-30]. This
quality of care thus becomes imperative, in order
to maximize the benefits of treatment.
Table 7. Items to emphasize in the clinical history
and physical examination of hypertensive patients.
CLINICAL HISTORY
1. Previous symptoms of cardiovascular, cerebrovascular, pulmonary, or renal disease, diabetes
mellitus, gout, or dyslipidemia;
2. Family history of hypertension, premature cardiovascular death, stroke, diabetes mellitus, or
dyslipidemia;
3. Personal and social history of smoking or tobacco
use, occupational or domestic stress;
4. Usual BP range with and without medication;
5. Medications tried for hypertension, including
response and adverse effects;
6. Other medications being taken which may affect
BP or response to treatment (e.g. contraceptives,
steroids, NSAIDs, decongestants, appetite suppressants, cyclosporin, erythropoietin, TCAs, and
MAO-inhibitors.
PHYSICAL EXAMINATION
1. Height and weight measurement;
2. Head and Neck - funduscopic examination, examination of the neck for bruits, distended veins
or thyroid enlargement;
3. Chest and Lungs - examination of the heart for increased heart rate, increased size, heaves, clicks,
murmurs, arrhythmias, gallops; examination of
the lungs for wheezing and other signs of chronic
lung disease;
4. Abdomen - examination of the abdomen for truncal obesity, purple striae, bruits, enlarged kidneys,
masses, and abnormal aortic pulsation;
5. Examination of the extremities for diminished
or absent peripheral arterial pulsations, bruits,
and edema; arm blood pressure discrepancies
greater than 10 mmHg, or when indicated, similar
discrepancies between leg blood pressures; examination of presence of postural hypotension in
the elderly, i.e., decrease in blood pressure greater
than 10 mmHg on assumption of upright position
from recumbent position.
6. Neurologic assessment for stroke residuals or
encephalopathy.
39
HYPERTENSION
2. The following tests should be routinely performed

in newly diagnosed hypertensives (Grade A
Recommendation):

a. fasting plasma glucose

b. serum creatinine,
c. serum potassium, and
d. urinalysis
Summary of Evidence: All the tests listed above were

used in various trials to screen for conditions which,
even in their asymptomatic phase, have an effect on
the choice of antihypertensive medication [4]. Additional benefits include a) detection and early treatment of diabetes with a screening FPG, b) detection
of asymptomatic renal disease with a serum creatinine
and urinalysis and, c) detection of possible secondary
hypertension with a serum potassium.
3. The following examinations may be performed
only if there are specific indications (Grade D
Recommendation):

a. ECG
b. chest X-ray
c. determination of lipid profile
d. uric acid
e. hematocrit
Summary of Evidence: Because of a very low sensitivity

and specificity in the detection of myocardial ischemia
[31], the usefulness of a resting 12-lead ECG is limited
in asymptomatic patients. On the other hand, when
symptoms of ischemia are present (e.g. in the presence of chronic stable angina pectoris), the test may
be useful as a screening test for severe disease, usually
manifested by resting ST segment depression. Other
uses of the ECG include the detection or clarification
of dysthymias as well as detection of LVH. For the latter, its usefulness is limited by high false positive and
negative rates [32,33]. Chest X-ray may contribute to the
detection of hypertrophy but again it is limited by its low
sensitivity and specificity The other examinations - uric
acid, hematocrit and total cholesterol can be requested
if there are clinical features suggesting that these may
be elevated. Specific indications for determination of
lipid profile, are addressed by the multisectoral task
force on the detection and management of hypercholesterolemia [34].
4. 2D echocardiography is not required for the
routine evaluation of all hypertensive patients
(Grade D Recommendation). Use should be
restricted to patients in whom anatomic or functional abnormalities are suspected.
Summary of Evidence: The echocardiogram is more
40
CPM 1ST EDITION
sensitive than both the ECG and chest radiogram in the

detection of left ventricular hypertrophy [35]. Although
studies suggest that some drugs are more effective than
others in effecting regression of LVH [36,37], there is
no evidence yet that such an effect leads to a reduction
in mortality or cardiovascular events.
5. Ambulatory BP monitoring is not routinely
required for the work-up of all hypertensive
patients (Grade D Recommendation).
Summary of Evidence: The clinical utility of ambulatory
BP monitoring has been well-summarized in various
documents [7,38]. Major problems need to be resolved
before they become more widely used. These problems
include: 1) evaluation of accuracy and precision of various monitoring devices, 2) definition of hypertension
based on 24-hour results, and 3) evaluation of cost-effectiveness compared to standard office measurement.
6. Confirmatory tests for secondary hypertension
should be performed only when clinical clues
to their existence are present (Grade D Recommendation). Physical findings which should lead
to the suspicion of these rare conditions are summarized in Table 8.
Summary of Evidence: When the pre-test probability of
a condition is extremely low (i.e., when the condition is
very rare), tests that detect it, need to be extremely sensitive to be of any use [39]. This principle holds true in
the case of testing for secondary hypertension. Routine
conduct of such tests is of little use, because the conditio
ns are rare. On the other hand, when clinical clues are
present, the probability of some conditions increase, thus
allowing maximization of the operating characteristics
of the diagnostic tests. Physicians unfamiliar with such
tests should refer patients with suspected secondary
hypertension to specialists for further work-up.
Table 8. Clinical clues to secondary causes of
hypertension

CLINICAL clues

abdominal or flank masses, family
history of adult polycystic kidney
abdominal bruits, especially if a
diastolic component is present
delayed or absent femoral pulses,
or decreased BP in the lower
extremities
truncal obesity w/purple striae

tachycardia, tremor, orthotastic
hypotension, sweating, flushing
SUSPECTED
CONDition
polycystic
kidney
renovascular
disease
aortic
coarctation
Cushing's
syndrome
pheochromo
cytoma
CPM 1ST EDITION
and pallor
anemia, edema, azotemia, casts
Chronic renal

disease
pulse discrepancy
Takayasu's arteritis
cramps, body malaise,
Hyperhypokalemia
aldosteronism
use of contraceptive pills
Contraceptive
induced HPN
neck mass w/ bruit, lid lag with
Thyrotoxicosis
or without exophthalmos
poor BP control w/ drug therapy
any of the above
sudden onset of hypertension
any of the above
sudden deterioration of BP
any of the above
control
Precautions
D. WHAT ADVICE SHOULD BE GIVEN TO
HYPERTENSIVE PATIENTS REGARDING
LIFESTYLE MODIFICATIONS?
1. All smokers should stop smoking (Grade A Recommendation).
Summary of Evidence: Several cohort and case-control
studies provide unquestionable proof of the hazards of
smoking [40], As a recognized risk factor for the deve
lopment of coronary artery disease, smoking aggravates
this risk in a hypertensive patient.
2. a. Overweight patients (excess of > 10% of ideal
body weight) should attempt weight reduction
at a rate of 1.0 Ib or 0.5 Kg per week (Grade
B Recommendation).

b. Weight reduction can be achieved by caloric

reduction and regular in aerobic activities (see
item 3). Caloric reduction can be achieved
through dietary prescriptions from a nutritionist. However, in the absence of a professional nutritionist, patients can be advised to
decrease their saturated fat intake to 15%
or less of their total caloric intake (Grade D
Recommendation).
Summary of Evidence: No trials have shown that

weight reduction actually translates to a decrease in
cardiovascular events. Nevertheless, weight reduction
in overweight hypertensive patients can lead to substantial declines in blood pressure, and can enhance
the blood pressure-lowering effect of antihypertensive
agents [41-42].
3. Hypertensive patients should engage in regular
aerobic physical activity unless contraindicated (Grade A Recommendation). This may
HYPERTENSION
be achieved by lower extremity aerobic exercise

such as brisk walking, jogging, or cycling for
30-60 minutes 3-4 times per week.
Summary of Evidence: Regular aerobic physical activity
can reduce blood pressure in hypertensive patients [43].
In addition, it facilitates weight reduction, improves
functional status, and leads to a decrease in CVD and
all-cause mortality [43]. These gains are attained even
at moderate levels representing 40-60% of maximum
oxygen consumption. Thus, an exercise program need
not be expensive or complicated. Brisk walking for
30-60 mins three to 4 x a week is simple and attainable
by most patients. However, patients with suspected or
confirmed cardiovascular disease may need a thorough
evaluation before exercise is prescribed.
4. Alcohol drinkers should moderate their consumption. A reasonable limit would be 30 cc (1 oz or 28
grams) of ethanol per day (equivalent to 60 cc or
2 jiggers of 100-proof whiskey, 240 cc or 1 glass
of wine, or 720 cc or 2 bottles of beer) (Grade D
Recommedation).
Summary of Evidence: Excessive alcohol intake can lead
to blood pressure elevation and resistance to antihypertensive therapy [44]. Table 5 (See Appendix) gives the
alcohol content of common alcoholic drinks.
5. Moderation of dietary sodium to 100 mmol/day
(2.3 g Na, 6 g NaCI) may be attempted in all
hypertensive subjects to see if this can lead to
significant BP reduction (Grade B Recommendation). However, such restriction is absolutely
necessary among patients with Chronic Renal
Disease & Congestive Heart Failure (Grade D
Recommendation).
Summary of Evidence: Considerable controversy exists
regarding the usefulness of sodium restriction among
all hypertensive patients [44]. While trials have shown
that it can lead to appreciable declines in mean blood
pressure [45,46], such declines are experienced by
only 25 to 33% of subjects (salt-sensitive individuals).
Generalizing these results to all hypertensives, where
salt consumption is relatively high, can lead to major
problems in quality of life. Moreover, no trial has
demonstrated that salt reduction can lead to a decline
in cardiovascular events.
6. There are no good studies to justify recommendations regarding relaxation and biofeedback nor
an increase in dietary K, Ca, or Mg.
Summary of Evidence: Recent meta-analysis on relaxation and feedback showed that these non-pharmacologic
measures were not successful in decreasing blood pres41
HYPERTENSION
sure [47]. The same finding were also seen in interventions involving dietary K, Ca, or Mg content [48].
Treatment
E. H O W S H O U L D H Y P E RT E N S I O N B E
TREATED?
The goal of treatment is to normalize blood pressure. The
following recommendations suggest priority therapeutic
options, depending on the underlying circumstances.
When contraindications exist for these options, or when
they fail to control hypertension, other drugs may be
tried (see Table 6 of Appendix for list of drugs).
Another consideration which may affect drug selection
is patient compliance. In some situations, this may take
precedence over the given recommendations. When this
becomes a problem, maneuvers to improve compliance may take into consideration 1) the drug's dosing
schedule, 2) cost, 3) side effects or 4) an individual's
preference for a particular regimen.
Lastly, patient's education must include the need for
maintenance medications despite normalization of blood
pressure as well as regular follow-ups.
1. Uncomplicated Hypertension

a. In uncomplicated mild hypertension (Stage

I), lifestyle modification measures may be
attempted for 3 months before commencing
pharmacologic treatment (Grade D Recommendation).
Summary of Evidence: The TOMH study showed that

pharmacologic treatment and lifestyle modification was
superior to lifestyle modification alone [23]. The 4-year
incidence of death or vascular events in the treatment
group was 11.08% compared to 16.24% in the group
that received lifestyle modification alone (p=0.03). Thus
events were prevented in 5.6% of patients, that is, 1 of
every 20 who were treated. Nevertheless, a 3- month
trial of lifestyle modification alone was advocated by
the consensus panelists, since previous studies have
demonstrated that normalization of mild hypertension
can occur, even without pharmacological intervention
[50].

42
b. All classes of antihypertensive agents (Table

6, Appendix) have been shown to lower blood
pressure with varying degrees of effectiveness
and side effects. However, in uncomplicated
hypertension, unless contraindications exist for their use, -blockers or diuretics are
recommended as the initial agents for monotherapy (Grade A Recommendation).
CPM 1ST EDITION
Summary of Evidence: This recommendation is based

on the results of several overviews and meta-analysis
which showsignificant reduction in stroke and coronary
artery disease with the use of diuretics (chlorthalidone,
or thiazides) or - blockers [1, 4, 5, 8, 50-52]. On the
other hand, the dreaded side effects of diuretic use, that
of cardiac dysrhythmias associated with hypokalemia &
low levels of serum magnesium were seen in sub-group
analyses of studies which use high doses of diuretics in
combination with other drugs with negative inotropic
effects. These results were not duplicated when the sa
me type of sub-group analysis was done on the Hypertension Detection & Follow-up Program (HDFP)
[50]. In addition, these 2 classes of drugs are the most
economical agents in the market. Their use has been
shown to profoundly improve the cost-effectiveness of
CAD & CVD prevention [9, 52-54].
Although other agents have also been found to decrease
blood pressure, no long-term studies assessing their
effects on clinical end-points such as strokes, coronary
events or mortality were done. TOMHS evaluted the
use of an ACE-inhibitor, alpha-blocker, fi-blocker, Ca
antagonist or diuretic in mild hypertension. However,
as a consequence of the size & duration of follow-up
of TOMHS, there was inadequate power for comparing
drug treatments with one another for efficacy in preventing cardiovascular events [23].
2. Hypertension complicated by Ischemic Heart
Disease.

a. In patients with ischemic heart disease, fiblockers or ACE-inhibitors are the drugs
of choice depending on the clinical presentation (Grade A Recommendation). Certain calcium antagonists provide reasonable alternatives but short-acting nifedipine should be avoided. Specific recommendations are summarized in Table 9.
Table 9. Choices for initial monotherapy of
hypertension in patients with various ischemic
syndromes.
CONDITION

1. Q wave
acute MI

2. NON-Q wave
acute MI
(Grade A)
3. UNSTABLE
ANGINA
4. STABLE
ANGINA
DRUG OF
ALTERNATIVE
CHOICE*
DRUGS
BETA-BLOCKERS VERAPAMIL**
and ACE-inhibitors
(Grade A)
BETA-BLOCKERS
DILTIAZEM**
& ACE-inhibitors
BETA-BLOCKERS
No specific
(Grade A)
recommendations***
BETA-BLOCKERS
No specific
(Grade A)
recommendations* * *
CPM 1ST EDITION
* In secondary prevention trials (patients with stable and

unstable angina and acute myocardial infarction), the use
of fi-blockers resulted in a reduction in morbidity and
mortality. ACE-inhibitors, on the other hand have also
been shown to decrease mortality in patients with acute
myocardial infarction 159].
** In post-MI patients in whom fi-blockers or ACE-inhibitors
are contraindicated, verapamil 160] or diltiazem may
be used. This is based from the results of a trial using
verapamil which showed reduction of coronary events
and total mortality in patients after Q infarction. The
use of diltiazem in non-Q infarction 161], on the other
hand, resulted to a decrease in reinfarction rate although
mortality was not reduced. Benefits from either verapamil
or diltiazem are seen only in post-Mi patients without
heart failure.
*** No specific recommendations are given for alternative
drugs for unstable and stable angina except for the non-use
of nifedipine. This is based on the present controversy
with regards its use on patients with ischemic syndromes
(see next item).
b. In patients with ischemic syndromes, shortacting nifedipine should be used with caution
(Grade B Recommendation).
Summary of Evidence: A meta-analysis by Furberg [63]
showed increased mortality in patients with coronary
heart disease (stable and unstable angina and acute
myocardial infarction) who were given nifedipine. It
is in this regard that questions were raised on its use in
such patients [64-66]. Because of some methodologic
flaws of this meta-analysis, its validity was doubted [6769]. Furthermore, ill effects were said to be statistically
significant only with the use of higher doses, i.e., >80
mg/day. In view of this, Opie & Messerii re-analyzed
the data, and still, the possibility of harm i.e., increase
in mortality, could not be eliminated [66]. The relative
risk (RR) with regards the use of 30-60 mg/day was 1.1
with the 95% confidence interval ranging from 0.95 to
1.27 (effect ranging from a 5% reduction in mortality
to a 27% increase in mortality). When all studies were
combined, Messerli's recalculation showed a trend
towards increased mortality, p=0.07 [70].
HYPERTENSION
dinitrate and hydralazine may be used (Grade

A Recommendation).
Summary of Evidence: The first V-Heft trial showed that
the combination of isosorbide dinitrate and hydralazine
was better than placebo in patients with mild to moderate
congestive heart failure treated with digoxin and diuretics [74]. The V-Heft II trial however, showed superiority
of the ACE-inhibitors over this combination [73]. The
use of a 3rd-generation Ca antagonist, Amiodipine as
an alternative based on a recent study could not be
advocated because of the following reasons: 1) improvement in functional capacity was seen only in a subgroup
analysis - group of patients with cardiomyopathy; 2) no
significant reduction in mortality was found, thus one
cannot eliminate harm, and 3) the study is not yet published, thus peer-review has not been completed.
4. Hypertension complicated by Diabetes Mellitus

a. In hypertensive diabetic patients with good

glycemic control, -blockers and diuretics are
the preferred antihypertensive agents (Grade
A Recommendation).
3. Hypertension complicated by Congestive Heart

Failure
Summary of Evidence: Diabetic patients were included

in the trials, using fi-blockers and diuretics which
showed decreased in mortality rates, stroke and coronary
artery disease. These studies were the First Veterans
Administration Study, (VA I), Oslo Study, International
Prospective Primary Prevention Study in Hypertension
(IPPSH), Metoprolol Atherosclerosis Prevention in Hypertension Study (MAPHY), European Working Party
on High Blood Pressure in the Elderly Trial (EWPHE),
Systolic Hypertension in Elderly Program (SHEP), &
the Swedish Trial in Old Patients with Hypertension
(STOP) [22, 27, 50, 75]. The overall increase in fasting
blood glucose during the follow-up period, (2-5 years)
was 0.2 to 0.6 mmol/L. In another study by Lewis [76]
on insulin-dependent diabetics, -blockers and diuretics
were also the principal agents used to control hypertension. ACE-inhibitors were added to address the problem
of proteinuria [76].
a. In the setting of congestive heart failure,

hypertensive patients may receive ACE-inhibitors with or without diuretics (Grade A
Recommendation).
Summary of Evidence: ACE-inhibitors are indicated in

patients with congestive heart failure even without hypertension. This is supported by numerous randomized
controlled trials showing reductions in total mortality
as well as coronary events [71-73].

b. When the use of ACE-inihibitors are contraindicated, a combination of isosorbide
b. In hypertensive diabetic patients with poor glycemic control, -blockers and diuretics should
be avoided (Grade A Recommendation).
Summary of Evidence: In stated trials using fi-blockers and diuretics, patients with uncontrolled diabetes
mellitus were excluded, because of the dangers of 1)
worsening glycemic control and 2) the possibility of
masking hypoglycemia.

c. In hypertensive insulin-dependent diabetics

with urinary excretion of 500 mg/24 hours
or more and a serum creatinine of 2.5 mg/dL
43
HYPERTENSION
or less, the addition of ACE-inhibitors to the

regimen, particularly captopril, can lead to
additional benefits - i.e. decrease in mortality rate, need for dialysis or transplantation
Summary of Evidence: This statement is based on
randomized controlled trial by Lewis et. al. [76] on
insulin-dependent diabetics. Included in the study were
patients who are 18-49 years old who had IDDM for at
least 7 years with an onset before the age of 30 years
and with urinary protein excretion of 500 mg/24 hours
or more and a serum creatinine or 2.5 mg/dL or less.
It was shown that the addition of captopril at 25 mg
TID to existing anti-hypertensive medication resulted
in a 48% relative risk reduction or a 10% absolute risk
reduction in the combined endpoints of death, or need
for dialysis, or transplantation. This means that for every
10 patients treated, 1 event will be avoided. Moreover,
it also led to a 43% relative risk reduction in the risk of
doubling of serum creatinine. It must be noted that in
this trial, captopril was not given as the drug to control
hypertension. It was given to treat proteinuria. Seventyfive percent of the patients, both from the control as
well as the treatment group were receiving diuretics
or -blockers before the study and their usage even
increased further during the study period. The median
follow-up of patients was 3 years.

d. In non-insulin dependent diabetics, ACE-inhibitors (especially captopril and enalapril)

may be used to decrease proteinuria or
improve glomerular filtration rate (Grade
B Recommendation); if ACE-inhibitors are
contraindicated, nondihydropyridine Ca antagonists (especially verapamil and diltiazem)
may be used as alternative agents (Grade B
Recommendation).
CPM 1ST EDITION
without stroke, i.e. -blockers or diuretics (Grade

B Recommendation).
Summary of Evidence: There are few trials done on
hypertensive patients with stroke. Most of them used
-blockers or diuretics. The results of these studies
[24,79] show that a) antihypertensive treatment reduces
the incidence of congestive heart failure among stroke
survivors and b) antihypertensive therapy is more effective in preventing the first stroke than a recurrent stroke.
6. Hypertension complicated by Dyslipidemia
In hypertensive patients with dyslipidemia, the
recommended drugs are also the same as those
without dyslipidemia, i.e., -blockers or diuretics
Summary of Evidence: The occurence of dyslipidemia
was not a reason for exclusion in -blocker and diuretic
trials. Adverse effects on lipid profile are theoretically
hazardous, but these should be weighed against proven
benefit in terms of mortality reduction or prevention of
cardiovascular events [80]. Surprisingly, the expected
magnitude of deterioration in the lipid profile was not
demonstrated in large randomized controlled trials such
as the VAII, USPHS, Oslo, MRC, ANBPS, IPPSH,
HAPPHY, MAPHY, SHEP, EWPHE, & HEP [49]. The
mean increase in total cholesterol ranged from 0.2 to
0.4 mmol/L while the influence on LDL-cholesterol &
triglycerides were unclear.
7. Hypertension complicated by Peripheral Vascular Disease

In hypertensive patients with peripheral vascular

disease, -blockers should be used with caution
Summary of Evidence: A meta-analysis of 14 randomized controlled trials by Maki, et al [77] concluded

that the use of ACE-inhibitors (particulary captopril and
enalapril) in diabetics, resulted to a greater decrease in
proteinuria and improvement in glomerular filtration rate
as compared to other classes of antihypertensive agents.
However, unlike the Lewis study, none of the included
studies monitored clinical endpoints such as mortality
and transplantation rates. Other studies [29,78] also
reported the same favorable results in terms of reduction
in proteinuria using calcium antagonists, particulary
diltiazem and verapamil, although to a lesser extent.
Thus, these two drugs are offered as alternatives.
Summary of Evidence: The use of fi-blockers in

these patients may exacerbate symptoms of the
disease. However, Radack and Beck reported in
their meta-analysis that these drugs could be used
safely in most patients with mild peripheral vascular disease, even if accompanied by intermittent
claudication. However, the study was limited by a
small sample size (n=127) [80-81]. Thus, up to the
present time, there is no evidence for or against the
use of vasodilators in this subset of patients.
5. Hypertension complicated by Stroke

44
In hypertensive patients with stroke, the choice

of antihypertensive agents is the same as those
8. Hypertension complicated by Chronic Obstructive Pulmonary Disease and Asthma

a. In hypertensive patients with chronic obstructive pulmonary disease (COPD), -blockers
should be avoided (Grade A Recommendation). ACE-inhibitors may be used but they
CPM 1ST EDITION
may aggravate cough already existing in these

patients (Grade B Recommendation).
Summary of Evidence: -blockers are generally contraindicatedin patients with chronic obstructive pulmonary disease [83]. This is particularly applicable to
COPD patients with functional airflow obstruction [83].
The MAPHY study, in particular, excluded patients
with obstructive lung disease whose symptoms were
not controlled by stimulants [27]. On the other hand,
ACE-inhibitors may cause cough in 10-15% of patients,
thus its use may produce effects that could interfere with
control of the respiratory disorder.

b. In patients with bronchial asthma, -blockers are

contraindicated (Grade A Recommendation).
Summary of Evidence: fi-blockers, especially nonselective -blockers will precipitate or exacerbate the
symptoms of bronchial asthma [83], thus asthmatics
were excluded from -blocker trials.
SPECIAL CONDITIONS:
9. Hypertension in the Elderly

In hypertensive elderly patients, low dose thiazide diuretics are the preferred agents (Grade
A Recommendation). -blockers may be used as
alternative agents (Grade B Recommendation).
Summary of Evidence: The use of low dose thiazide

diuretics in the elderly (age range=60-84) has been
shown to decrease cardiovascular morbidity and mortality as well as all-cause mortality in several metaanalyses [84-86]. Although hydrochlorothiazide 25 mg
or Chlorthalidone was used, most of the effects can be
achieved with lower doses, e.g. hydrochlorothiazide
12.5 mg/day [84].
-blockers in the above age group has also been shown
in meta-analyses to decrease the same clinical endpoints.
However, they are less effective than diuretics [85-86].
10. Hypertension in Pregnancy

a. In pregnant patients with Stage I (mild) or

Stage II (moderate) hypertension, treatment
can be started using oral medications. Alpha
methyldopa is the preferred agent (Grade
A). When methyldopa alone is ineffective,
-blockers provide a 2nd option (Grade B
Recommendation).
Summary of Evidence: The diagnosis of hypertension in

pregnancy may be made using standard criteria used to
diagnose hypertension in general. Classification of sever-
HYPERTENSION
ity can likewise be made based on Table 4. In addition to

classification according to etiology as having 1) chronic
hypertension or 2) pregnancy-induced hypertension
(also known as pre-eclampsia). A combination of the 2
conditions may occur, & is referred to as "superimposed
pre-eclampsia" [87]. The 2 conditions may not always be
easy to diffrentiate but clinical clues are summarized in
Table 10. As the table indicates, distinguishing between
the 2 causes of hypertension is important mainly for
purposes of prognostication. Although both can lead
to eclampsia (development of seizures) Pregnancyinduced hypertension often disappears after delivery.
A meta-analysis of trials using alpha methyldopa [88] in
pregnant hypertensives (mostly pregnancy-induced hypertension) shows that the drug can effect 1) a reduction of
the incidence of severe hypertension (OR=0.33; 95% Cl:
0.17, 0.63) and 2) a possible reduction in perinatal deaths
(OR=0,58; 95% CL0.18,0.83. However, the possibility
of harm has not been excluded with regards other endpoints such as maternal death and ceasarian section rate.
A meta-analysis of trials using fi-blockers [89] in pregnant hypertensives (mostly pregnancy-induced hypertension) shows that the drug can effect 1) a reduction in
the incidence of severe hypertension (OR = 0.37; 95%
Cl: 0.25, 0.53), 2) a possible reduction in hospitalization
(OR = 0.51, 95% Cl: 0.32, 0.82), and 3) a possible reduction in the incidence of respiratory distress syndrome
(OR = 0.29,95% Cl: 0.14,0.63). However, the incidence
of low birth weight infants was increased (OR = 1.55;
95% Cl: 1.1,2.2). In addition, the possibility of harm has
not been excluded with regards to other endpoints such
as maternal death and caesarian section rate/s.
Table 10. Differences between Pregnancy Induced
Hypertension and Chronic Hypertension.

PREGNANCY-

INDUCED
Age
Usually young (<30)
Parity
Usually primigravid
Onset
After 2 wks AOG
Weight
Sudden
gain and
edema
SystolicBP
<160
Funduscopic Spasm, edema
findings
Proteinuria
Present
Plasma
Elevated
Uric acid
Eclampsia
Possible
(seizures)
BP after
Normal
delivery
CHRONIC
Usually older (>30)
Usually multigravid
Before 20 wks AOG
Gradual
>160
AV nicking, exudates
Absent
Normal
Possible
Elevated
45
HYPERTENSION
b. Pregnant patients with Stage III (severe)

or Stage IV (severe or very severe), or with
symptoms of impending target-organ damage
(see Table 10) should be admitted and started
first on IV therapy, while oral medications are
titrated. The drugs may be used are hydralazine, clonidine, methyldopa, and labetalol
Summary of Evidence: Drugs that have been used for

the treatment of severe pregnancy-induced hypertension
and pre-eclampsia include hydralazine, clonidine, methyldopa, -blockers, nifedipine and rarely, diazoxide.
Although comparisons between these drugs have been
made, there is no strong evidence to justify preference
for any. It is generally recommended that an individual
physician's familiarity should play a crucial role in the
choice of a drug [90].
With regards to adverse effects, hydralazine has been
reported to be relatively safe. The use of labetalol may
lead to severe fetal and neonatal bradycardia. Diazoxide, on the other hand, may lead to serious reduction in
uteroplacental or even cerebral perfusion and hyperglycemia in the newborn. Thus, the use of this drug is not
advised. Fetal or neonatal effects of the maternal use of
Ca antagonists is not yet known.

c. Data is insufficient to support calcium supplementation among non-pregnant women

to prevent hypertension.
Summary of Evidence: Ca supplementation may reduce

the risk of women developing HPN. However, the
evidence is insufficient regarding important outcomes,
such as caesarian section rates, intrauterine growth
retardation or perinatal death. Further trials are needed
to define its role in antenatal care.
11. Hypertension in Emergency and Urgent
Situations

a. Hypertension may be complicated by acute

life-threatening conditions such as those listed
in Table 10. In such setting/s, there is a need
for immediate blood pressure reduction. The
agents that can be used for rapid control of
hypertension are listed in Table 12 (Grade D
Recommendation).
Summary of Evidence: Immediate reduction of BP in

emergency situations may beneficially alter the course
of the confounding disease. This is based on experts'
opinions and pathophysiologic reasoning, rather than on
actual randomized control trials. However, these assertions are so strong that a trial may never get underway
because of the ethical constraints.
46
CPM 1ST EDITION
Oral preparations are now available for the emergency

control of hypertension. These include captopril, clonidine & nifedipine (punctured, squeezed & swallowed).
However, these drugs do not provide good control of
the rate of BP reduction, a disadvantage blamed for
numerous reports of unexpected myocardial or cerebral
hypoperfusion [4,92,93]. Thus, the parenteral agents
listed in Table 10 are preferred, specifically because of
a more controlled rate of reduction of BP [94].

b. In Stage IV or very severe hypertension

uncomplicated by situations listed in Table
11, oral antihypertensive agents should be
given and control of blood pressure should
be achieved within 3 days (Grade A Recommendation).
Summary of Evidence: One of the first RCT's conducted

among American Veterans randomized patients with
very severe hypertension [95]. The study was prematurely terminated because patients in the placebo group
suffered strokes in significant numbers. The earliest
occured 3 days after randomization.
Table 11. Hypertension and Target Organ Disease.
ORGAN NOT ACUTELY
SYSTEM
LIFE

THREATENING
ACUTELY LIFE
THREATENING
Cardiac
LVH

Coronary

atherosclerosis

Acute coronary
events:
AMI
Unstable angina
Acute LV failure
Pulmonary
congestion
or Edema
Cerebro- TIA
vascular

Intracranial
hemorrhage
Thrombotic stroke
Hypertensive
encephalopathy
Peripheral Peripheral
Dissecting
Vascular
occlusive disease aneurysms
Renal
Nephrosclerosis Malignant

nephrosclerosis
Ophthalmic Retinopathy

Papilledema/
Optic nerve
head edema
CPM 1ST EDITION
HYPERTENSION
Table 12. Drugs for Treatment of Hypertensive Crisis

Drugs*
Dose**

Onset of
Action,
min.
Adverse
Reactions
Special
Indications
PARENTERAL DRUGS
VASODILATORS
Sodium
0.3-10 ug/kg/min
Instan-
Nausea, vomiting,
nitroprusside
as IV infusion,
taneous
muscle twitching,

maximal dose for
methemoglobinemia,

no more than 10
cyanide toxicity,

minutes
hypotension

Hypertensive
encephalopathy, acute
intracranial hemorrhage, acute cerebral
infarction, acute left
ventricular failure,
acute coronary insufficiency, dissecting
aneurysm, catecholamine crisis, head
injury, extensive
body burns, malignant
hypertension, postoperative hypertension
Nitroglycerine
5-100 ug/min
2-5
Headache,

as IV infusion
tachycardia, vomiting,

methemoglobinemia

Acute left ventricular

failure, acute coronary
insufficiency, postoperative hypertension
(especially coronary
bypass)
Hydralazine
10-20 mg IV
10
HC1
10-50 mg IM
20-30

Eclampsia,
extensivebody burns,
malignant
hypertension, postoperative hypertension
Tachycardia,
headache, vomiting,
aggravation of angina
pectoris, fluid
retention
ADRENERGIC INHIBITORS
Methyldopa

250-500 mg IV
30-60
Drowsiness
infusion
Eclampsia, peri-op
hypertension
ORAL DRUGS
Nifedipine
5-10 mg PO, repeat 15-30
(not extended
after 30 min
release)

Rapid uncontrolled
reduction in blood
pressure may precipitate circulatory
collapse in patients
with aortic stenosis
Captopril
25 mg PO, repeat
15-30

as required

Hypotension, renal
failure in bilateral
renal artery stenosis
Clonidine

Hypotension,
drowsiness, dry
mouth
0.1-0.2 mg PO,
30-60
repeated every
hour as required
to a total dose of 0.6
* Drugs such as Diazoxide, Phentolamine mesylate, Trimethaphan canisylate, and Labetalol hydrochloride are also used for
hypertensive emergencies but are not available locally.
** IV indicates intravenous; IM intramuscular, PO per orem
Modified from: 1. afford RW, Management of hypertensive crises, JAMA 1991; 266(6):83

2. The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High
Blood Pressure (JNC V), Ardi
47
HYPERTENSION
CPM 1ST EDITION
Table 13. Summary of Pharmacologic Recommendations

CONDITION
DRUG OF CHOICE
ALTERNATIVE DRUGS
1) Uncomplicated
Beta-blocker or Diuretic
Hypertension
ACE-inhibitor or Calcium
channel blocker
2) Hypertension +
Ischemic Syndrome

3) Hypertension + CHF
See Table 9
See Table 9
ACE-inhibitor
ISDN + Hydralazine combination
4) Hypertension +
a) IDDM
Beta-blocker or Diuretic;

Addition of ACE-inhibitor
b) NIDDM
Beta-blocker or Diuretic;

Addition of ACE-inhibitor

5) Hypertension + Stroke
Beta-blocker or Diuretic

6) Hypertension + Dyslipidemia Beta-blocker or Diuretic

7) Peripheral Vascular Disease
Any*

8) Hypertension + COPD
Any*
or Asthma

9) Hypertension in the Elderly
Diuretic

10) Hypertension + Pregnancy
a) Stage I and II
Methyldopa

b) Stage III
IV Hydralazine or IV

Clonidine or Methyldopa or

Labetalol or Nifedipine

11) Hypertension in Emergency/ See Table 12
Urgency Situations

Verapamil or Diltiazem
Beta-blocker
Beta-blocker, Calcium
antagonist (Nifedipine)
See Table 12
* Caution on the use of Beta-blocker
12. Current Status of Herbal Preparations

No indigenous herbal preparations have been

adequately tested.
Summary of Evidence: Among the many herbal preparations being speculated as having anti-hypertensive
properties, only "sambong" is undergoing a rigorous
evaluation. At present, a randomized, double-blind
crossover study is ongoing to test the efficacy of this
herbal medicine among mild hypertensives [reference
unpublished].
Previous studies on garlic failed to demonstrate a significant effect on blood pressure [96].
48
F. HOW CAN HYPERTENSION BE PREVENTED AMONG NORMOTENSIVES ?

Weight reduction among overweight individuals

through moderate physical activity and reduced
total caloric intake can decrease the incidence of
hypertension (Grade B Recommendation).
Summary of Evidence. A significant risk reduction in

the incidence of hypertension was demonstrated among
normotensives subjected to weight reduction [97-99].
Specifically, the trials of Hypertension Prevention, Phase
I reported an odds ratio of 0.66 (96% Cl:0.46-0.94) [99].
The weight reduction program involved a moderate
increase in physical activity by brisk walking for 45
minutes 4-5 times a week as well as reduction in total
caloric intake [99].
CPM 1ST EDITION
HYPERTENSION
Appendix
SUMMARY OF CRITERIA FOR
RATING EVIDENCE
Table 1. Levels of Evidence for Rating Studies on
the Accuracy of Diagnostic Tests
Level 1 ALL 5 OF THE FOLLOWING CRITERIA
ARE SATISFIED

(a) There was an independent interpretation
of the result of the diagnostic test (without
knowledge of the result of the gold standard).
(b) There was an independent interpretation
of the result of the gold standard (without
knowledge of the result of the diagnostic
test).

(c) The study patients consisted of patients suspected (but not known) to have the disorder
of interest.
(d) The diagnostic test & gold standard are
both described in sufficient detail to allow
reproducibility.

(e) The study population consists of at least
50 patients with, & 50 patients without the
disorder of interest
Level 2 4 OF THE 5 CRITERIA ARE MET.
Level 6 NONE OF THE 5 CRITERIA ARE MET.
Table 2. Levels of Evidence for Rating
Studies on the Effectiveness of Treatment
Level 1 A randomized controlled trial (RCT) that
demonstrates a statistically significant difference in at least one major outcome - e.g.,
survival or major illness,

OR

if the difference is not statistically significant,
an RCT of adequate sample size to exclude
25% difference in relative risk with 80%
power, given the observed results.
Level 2 An RCT that does not meet the level 1 criteria.
Level 3 A non-randomized trial with concurrent
controls selected by some systematic method
(i.e., not selected on the basis of perceived
suitability for one of the treatment options).
Level 4 Before-after study or case series (at least 10
patients) with historical controls or controls
drawn from other studies.
Level 5 Case series (at least 10 patients) without
controls.
Level 6 Case series (fewer than 10 patients) or case
reports.
Table 3. Levels of Evidence for Rating

Studies on Prognosis or Causation
ARE SATISFIED

(a) An inception cohort was formed.

(b) Reproducible inclusion & exclusion criteria
were used.

(c) Follow-up was complete for at least 80% of
subjects.

(d) Statistical adjustment was carried out for
extraneous factors (confounders).

(e) Reproducible descriptions of outcome
measures were used.
Level 2 An inception cohort was formed but only 3
of the 4 remaining criteria were satisfied.
Level 5 An inception cohort was formed but none
Level 6 NONE OF THE 5 CRITERIA WERE
MET.
Table 4. Levels of Evidence for Rating Review
Articles
ARE MET

(a) Comprehensive search for evidence.

(b) Avoidance of bias in the selection of articles.

(c) Assessment of the validity of each cited
article.

(d) Conclusions supported by the data & analysis
presented.
Level 2 3 of the 4 criteria are met.
Level 5 NONE OF THE 4 CRITERIA ARE MET.
49
HYPERTENSION
CPM 1ST EDITION
Table 5. ALCOHOL EQUIVALENTS AND SUGGESTED DAILY ALLOWANCE

LIQUOR
WHISKEY
J&B
Johnny Walker (Black)
Chivas Regal
Johnny Walker (Red)
Jim Beam
Cutty Sark
BRANDY
Carlos I
Emperador
Fundador
Napoleon
VOS
RHUM
Tanduay (Dark)
Tanduay ESQ
Tanduay 65
Aejo Rhum
Tanduay (White)
GIN
Gilbey's
SM
Gin Kelly
McKevin's
Duncan
BEER
Premium SMB
Bartles & Jaymes
Heineken
Stag
COGNAC
Camus
Hennesey
TEQUIIA
Cuervo
VODKA
Smirnoff
Absolute
SIOKTONG
Kungfu
Vino Kulafu
Vino de Chino
Anis
WINE
Carlo Rassi
Mompo mass wine
Maria Clara Sangria
Martini Bianci
Andre
Blue Nun
Le Piat dor
Red Rose California
Burgundy
Asti Martini
Mateus
PROOF/VOLUME
G/SHOT**, G/GLASS**
DAILY ALLOWANCE
43% volume
86 proof
40% volume
43% volume
80 proof
80 proof
10 g/shot
10 g/shot
9.6 g/shot
10 g/shot
9.6 g/shot
9.6 g/shot
3 shots
3 shots
3 shots
3 shots
3 shots
3 shots
40% volume
80 proof
40% volume
36% volume
80 proof
9.6 g/shot
9.6 g/shot
9.6 g/shot
8.6 g/shot
9.6 g/shot
3 shots
3 shots
3 shots
3 shots
3 shots
80 proof
65 proof
65 proof
80 proof
80 proof
9.6 g/shot
7.8 g/shot
7.8 g/shot
9.6 g/shot
9.6 g/shot
3 shots
3.5 shots
3.5 shots
3 shots
3 shots
90 proof
80 proof
80 proof
90 proof
90 proof
10.8 g/shot
9.6 g/shot
9.6 g/shot
10.8 g/shot
10.8 g/shot
3 shots
3 shots
3 shots
2.5 shots
2.5 shots
5% volume
5% volume
5% volume
3.9% volume
14g/355 ml bottle
13 g/320 mL bottle
13.2 g/330 mL bottle
10 g/320 mL bottle
2 bottles
2 bottles
2 bottles
3 bottles
40% volume
40% volume
9.6 g/shot
9.6 g/shot
3 shots
3 shots
40% volume
9.6 g/shot
3 shots
80 proof
80 proof
9.6 g/shot
9.6 g/shot
3 shots
3 shots
50 proof
50 proof
50 proof
70 proof
6 g/shot
6 g/shot
6 g/shot
8 g/shot
4.5 shots
4.5 shots
4.5 shots
3 shots
10% volume
13.8% volume
10% volume
16% volume
11% volume
11% volume
9.5% volume
9.5% volume
12.5% volume
7% volume
10% volume
16 g/glass
22 g/glass
16 g/glass
26 g/glass
18 g/glass
18 g/glass
15 g/glass
15 g/glass
20 g/glass
ll g/glass
16 g/glass
2 glasses
l glasses
2 glasses
1 glass
l glasses
l glasses
2 glasses
2 glasses
l glasses
2 glasses
2 glasses
*Shot = 30 cc **Glass = 200 cc

PROOF
: is defined as mixture of Ethanol & water containing 50% by volume of Ethanol
FORMULA
: Grams of ethanol/serving = (% volume) or (proof/2) X cc/serving X 0.8 (density of ethanol)
50
CPM 1ST EDITION
HYPERTENSION
Table 6. Antihypertensive Agents as Listed in the

Philippine Pharmaceutical Directory (PPD), 1996.
ACE-INHIBITORS

Benazepril

Captopril

Cilazapril

Delapril

Enalapril

Lisinopril

Perindopril

Quinapril

Ramipril

CALCIUM
ANTAGONISTS
Amiodipine
Diltiazem
Felodipine
Isradipine
Lacidipine
Manidipine
Nicardipine
Nifedipine
Nimodipine
Nitrendipine
Verapamil

DIURETICS

Acetazolamide

Bumetamide

Furosemide
Hydrochlorothiazide

Indapamide

Spironolactone

BETA-BLOCKERS
Atenolol
Betaxolol
Bisoprolol
Carteolol
Esmolol
Metoprolol
Nadolol
Oxprenolol
Pindolol
Propranolol
CENTRALLY ACTING
DRUGS
Clonidine
Guanfacine
Methyldopa
Reserpine
A2 ANTAGONIST
Losartan
VASODILATORS
Doxazocin
Hydralazine
Prazosin
Sodium Nitroprusside
References
1. Carruthers SG, Larochelle P, Haynes RB, et al. Report
of the Canadian Hypertension Society Consensus
Conference: 1. Introduction. Can Med Assoc J 1993;
149: 289,1993.
2. American Society of Hypertension. Recommendations
for Routine BP Measurement by Indirect Cuff
Sphygmomanometry. Am J Hypertens 1992; 5:207.
3. Frohlich ED, Grim C, Labarhte DR, et al. Recommen
dations for Human Blood Pressure Determinations
bySphygmomanometers: Report of a Special Task Force
Appointed by the Steering Committee, American Heart
Association. Hypertension; 11:209A, 1988.
4. The Fifth Report of the Joint National Committee on
Detection, Evaluation, & Treatment of High BP (JNC
V). Arch Intern Med; 153:154,1993.
5. Whetworth JA, et al. Australian Consensus Conference
on Hypertension. Med J Aust; 160:s2sl6,1994.
6. Haynes RB, Laucourciere Y, Rabkin SW, et al. Report
of the Canadian Hypertension Society Consensus
Conference: 2. Diagnosis of Hypertension in Adults. Can
Med Assoc J; 149:409,1993.
7. Appel LJ, Stason WB. Ambulatory Blood Pressure
Monitoring & Blood Pressure Self-measurement in the
Diagnosis & Management of Hypertension. Ann Intern
Med; 118:867, 1993.

8. Collins R, Peto R, MacMahon S, et al. Blood Pressure,
Stroke, & Coronary Heart Disease. Part 2, Short Term
Reductions in BP: Overview of Randomized Drug Trials
in the Epidemiological Context. Lancet; 335:827, 1990.
9. Littenberg B, Garber AM, Sox HC. Screening for
Hypertension. Ann Intern Med; 122:192, 1990.
10. Littenberg B. A Practice Guideline Revisited: Screening
for Hypertension. Ann Intern Med; 122:937, 1995.
11. Rosner B, BF. Screening for hypertension - Some
Statistical Observations. J Chron Dis; 30:7,1977.
12. Rosner B, Polk BF. The Implications of Blood Pressure
Variablity for Clinical & Screening Purposes. J Chron
Dis; 32:451, 1979.
13. Idem. The Instability of BP Variability Over Time. J Chron
Dis; 34:135,1981.
14. Idem. Predictive Values of Routine Blood Pressure
Measurements in Screening for Hypertension. Am J
Epidemiol 1983; 117:429-442.
15. Shepard DS. Reliability of BP Measurements: Implications
for Designing & Evaluating Programs to Control
Hypertension. J Chron Dis;34:191,1981.
16. Donner AD, Young C, Bass M. Sequential screening
for hypertension in primary care. J Chron Dis; 32:577,
1979.
17. Donner A, Bull S. The Mean Versus the Minimum as
a Criterion for Hypertension Screening. J Chron Dis;
34:527, 1981.
18. Fletcher R.H. Clinical Epidemiology: A Basic Science
for Clinical Medicine, 2nd ed. Boston: Little Brown &
Co., 1991.
19. Veterans Administration Cooperative Study Group on
Anti-hypertensive Agents. Effects of Treatment on
Mortality in Hypertension: II Results in Patients with
Diastolic BP Averaging 90 through 114 mmHg. JAMA;
213:1143, 1970.
20. Medical Research Council Working Party. MRC Trial of
Treatment of Mild Hypertension: Principal Results. Br
Med J; 291:97, 1985.
21. Coope J, Warrender TS. Randomized Trial of Treatment
of Hypertension in the Elderly in Primary Care. Br Med
J; 293:1145, 1986.
22. Dahlof B, Lindholm L, Hansson L, et al. Morbidity &
Mortality in the Swedish Trial in Old Patients with Mild
Hypertension (STOP-HPN). Lancet; 338:1281, 1991.
23. Neaton JD, Grimm RH, Prineas RJ, et al. Treatment
of Mild Hypertension Study (TOMHS) Final Results.
JAMA; 270:713,1993.
24. Hypertensive-Stroke Cooperative Study Group. Effect
of Anti-hypertensive Treatment on Stroke Recurrences.
JAMA; 229:409,1974.
25. D'Agostino RB: Risk Factors for Coronary Heart Disease.
BMJ; 303:385, 1991.
26. Wassertheil-Smoller S, Blaufox MD, Oberman AS,
et al. The Trial of Antihypertensive Interventions &
Management (TAIM) Study: Adequate Weight Loss
Alone & Combined with Drug Therapy in the Treatment
of Mild Hypertension. Arch Intern Med; 152:131,
1992.
27. Wikstrand J, Warnold I, Disson G, et al. Primary Prevention
with Metoprolol in Patients with Hypertension. Mortality
Results from the MAPHY Study. JAMA; 259:1976,
1988.
28. -blocker Heart Attack Trial Research Group. A
Randomized Trial of Propranolol in Patients with AMI.
I. Mortality Results. JAMA;247:1707,1982.
29. Bakris GL. Hypertension in Diabetic Patients: An
Overview of Interventional Studies to Preserve Renal
Function. Am J Hypertens; 6:140s, 1993.
51
HYPERTENSION
30. McCormick KA, Moore SR, Seigel RA (eds). Clinical

Practice Guideline Development Methodology
Perspectives. US Department of Health & Human
Services. Nov 1994; AHCPr Pub No. 95-009.
31. Sox HC, Garber AM, Littenberg B. The Resting ECG as
a Screening Test. A Clinical Analysis. Ann Intern Med;
iii:489,1989.
32. Pornhlit DW, Bove KE, Norris RJ. A Critical Appraisal
of the Electrocardiographic Criteria for the Diagnosis of
LVH. Circulation; 40:185,1969.
33. Reichek N, Devereux RB. LVH: Relationship of
Anatomic, Echocardiographic & Electrocardiographic
Findings. Circ ;63:1391,1981.
34. The Multi-Sectoral Task Force on the Detection and
Management of Hypercholesterolemia. Clinical Practice
Guidelines on the Detection and Management of
Hypercholesterolemia. PJC; 24(4):127, 1996.
35. Woythaler JN, Singer SL, Kwan OL, et al. Accuracy
of Echocardiography versus Electrocardiography in
Detecting LV Hypertrophy: Comparison with Postmortem
Measurements. J Am Coll Cardiol;2:305,1983.
36. Devereux RB, Koren M), De Simone G, Okin PM,
Kligfield P. Methods for Detection of Left ventricular
Hypertrophy: Application of Hypertensive Heart Disease.
Eur H J; 14 Suppi D:8, 1993.
37. Dahlof B. Pennert K, Hansson L. Reversal of left
Ventricular Hypertrophy in Hypertensive Patients: A
Meta-analysis of 109 Treatment Studies. Am J Hypertens;
5:95,1992.
38. Sheps GS, Pickering TG, White WB, et al. Ambulatory
Blood Pressure Monitoring (ACC Position Statement).
JACC; 23:1511,1994.
39. Sackett D.L. Clinical Epidemiology: The Essentials, 2nd
ed. Baltimore: Williams & Wilkins, 1988.
40. Pooling Project Research Group. Relationship of Blood
Pressure, Serum Cholesterol, Smoking Habit, Relative
Weight & ECG Abnormalities to Incidence of Major
Coronary Events: Final Report of the Pooling Project. J
Chron Dis; 31:201, 1978.
41. Langford HG, Davis BR, Blaufox MD, et al. Effect of
Drug & Diet Treatment of Mild Hypertension on Diastolic
BP. Hypertension; 17:210-217, 1991.
42. Schotte DE, Stunkard AJ. The Effects of Weight
Reduction on Blood Pressure in 301 Obese Patients. Arch
Inern Med; 150:1701, 1990.
43. Kelly G & McClellan P. Antihypertensive Efects of
Aerobic Exercise. A Brief Meta-analytic Review of
Randomized Trials. Am J Hypertens; 7:115,1994.
44. World Hypertension League. Alcohol & hypertension
- Implications for Management: A Consensus Statement
by the World Hypertension League. J Hum Hypertens;
5:1854,1991.
45. Kaplan MM. Moderate Sodium Restriction. Am J
Hypertens; 3:518,1990.
46. Cutler JA, Follman D, Elliot P, Suh I. An Overview
of Randomized Trials of Sodium Reduction and BP.
Hypertension; 17 (Suppi I): 1-27-1-33,1991.
47. Law MR, Frost CD, Wald NJ. By How Much Does
Dietary Dalt Reduction Lower Blood Pressure? Ill:
Analysis of Data from Trials of Salt Reduction. BMJ;
302:819,1991.
48. Behavior Changes & the Prevention of High Blood
Pressure: Workshop II. Circulation; 88(3): 1387, 1993.
49. Elliot P. Nutritional Factors in BP. J Hum Hypertens;
8(8):595,1994.
50. Swedish Consensus Statement (Journal of Internal
Medicine/Acta Scandinavia).
51. Ogilvie RI, et al. Report of the Canadian Hypertension
Society Consensus Conference: 3. Pharmacologic
52
CPM 1ST EDITION
Treatment of Essential Hypertension. Can MedAssoc J;

149:575, 1993.
52. Wikstrand J, Berglund G, Tuomilehto J. -blockade in
the Primary Prevention of Coronary Heart Disease in
Hypertensive Patients. Review or Present Evidence. Circ;
84 (Suppi VI): VI-93 - VI-100,1991.
53. Edelson JT, Weinstein MC, Tosteson AN, et al. Long-term
Cost- Effectiveness of Various Initial Monotherapies
for Mild to Moderate Hypertension. JAMA; 263:408,
1990.
54. Pepine CJ, Cohn PP, Deedwania PC, et al. Effects of
Treatment on Out-come in Mildly Symptomatic Patients
with Ischemia During Daily Life. The Atenolol Silent
Ischemia Study (ASIST). Circulation; 90(2):762, 1994.
55. Yusuf S, Wittes J, Friedman L. Overview of Results of
Randomized Clinical Trials in Heart Disease II: Unstable
Angina, Heart Failure, Primary Prevention with Aspirin
& Risk FactorModification. JAMA; 260:2259.
56. ISIS I (1st International Study of Infarct Survival)
Collaborative Group. Randomized Trial of IV Atenolol
Among 16,027 Cases of Suspected Acute Myocardial
Infarction: ISIS-I. Lancet; 2:57, 1986.
57. Pedersen TR. The Norwegian Multicenter Study of
Timolol after MI. Circ; (Suppi I) 67:49.1983.
58. Lau J, Amman EM, Jimenez-Silva J, et al. Cumulative
Meta-analysis of Therapeutic Trials for Myocardial
Infarction. NEJM; 248,1992
59. Yusuf S, Wittes J, Probstfield. Evaluating Effects of
Treatment in Subgroups of Patients Within Clinical
Trial: The Case of Non-Q wave MI & fi-blockers, AJC;
66:220,1990.
60. ISIS-4: A Randomised Factorial Trial Assessing Early
Oral Captopril; Oral Mononitrate, & Intravenous
Magnesium Sulphate in 58,050 Patients with Suspected
Acute Myocardial Infarction. ISIS-4 (Fourth International
Study of Intact Survival) Collaborative Group. Lancet;
345:669, 1995.
61. The Danish Study Group on Verapamil in Myocardial
Infarction. Effect of Verapamil on mortality & major
events after AMI (The Danish Verapamil Infarction Trial
II - DAVIT II). Am J Cardio; 66:779,11990.
62. The Multicenter Diltiazem Post-Infarction Trial Research
Group. The Effect of Diltiazem on Mortality & Reinfarction After Acute Myocardial Infarction. N Engi J
Med; 319:385, 1988.
63. Furberg CD, Psaty BM, Meyer JV. Nifedipine DoseRelated Increase in Mortality in Patients with CHD.
Circulation; 92:1326, 1995.
64. Yusuf S. Calcium Antagonists in Coronary Artery Disease
& Hypertension - Time for Reevaluation? Circulation;
92:1079,1995.
65. Fagan TC. Calcium Antagonist and Mortality. Another
Case of the Need for Cinical Judgement. Arch Intern
Med; 155:2145, 1995.
66. Furberg CD, Psaty BM. Should Dihydropyridines be Used
as First-line Drug in Hypertension? The Con side. Arch
Intern Med; 155:2157,1995.
67. Opie LH, Messerii FH. Nifedipine and Mortality: Grave
Defects in the Dossier. Circulation; 92:1068-1073,
1995.
68. Kloner RA. Nifedipine in Ischemic Heart Disease. Circ;
92:1074,1995.
69. Epstein M. Calcium Antagonists Should Continue to
be Used for First-line Treatment of Hypertension. Arch
Intern Med; 155:2150,1995.
70. Messerii, FH. Case-control Study, Meta-Analysis, &
Bouillabase: Putting the Calcium Antagonist Scare into
Context. Ann Int Med; 123:888, 1995.
CPM 1ST EDITION
71. The SOLVD Investigators. Effect of Enalapril on Survival

in Patients with Reduced Left Ventricular Ejection
Fraction & Congestive Heart Failure. N Engi J Med;
325:293, 1991.
72. The Consensus Trial Study Group. Effect of Enalapril on
Mortality in Severe Congestive Heart Failure: Results of
t he Cooperative North Scandanavian Enalapril Survival
Study (Consensus). N Engi J Med; 316:1429,1987.
73. Cohn JN, Johnson G, Ziesche S. et al. A Comparison of
Enalapril with Hydralazine-Isosorbide Dinitrate in the
Treatment of Chronic Congestive heart failure. N Engi
Med; 325:303, 1991.
74. Cohn JN, et al. Effect of Vasodilator Therapy on Mortality
in Chonic Congestive Heart Failure. N Engi J Med;
314:1547, 1986.
75. SHEP Cooperative Research Group. Systolic Hypertension
in the Elderly Program. JAMA; 265:3255, 1991.
76. Lewis EJ, Hunsicker LG, Bain RP, et al. The effect of
ACE Inhibitor in Diabetic Nephropathy. N Eng J Med;
329: 1456, 1993.
77. Maki DD, Ma JZ, Louis TA, Kasiske BL, et al. Longterm Effects of Antihypertensive Agents on Proteinuria
& Renal Function. Arch Intern Med;155:1073, 1995.
78. Slataper R, Vicknair N, Sadler LRD, Bakris GL, et
al. Comparative Effects of Different Antihypertensive
Treatments on Progression of Diabetic Renal Disease.
Arch Intern Med; 153:973, 1993.
79. Carter AB. Hypotensive Therapy in Stroke Survivors.
Lancet; 485, 1970.
80. McCormick KA, Moore SR, Siegel RA (eds). Clinical
Practice Guideline Development Methodology
Perspectives. US Dept. of Health & Human Services;
AHCPR Publ No. 95-009, Nov 1994.
81. Radack K, Deck C. C-adrenergic Blocker Therapy
does not Worsen Intermittent Claudication in Subjects
with Peripheral Arterial Disease. A Meta-Analysis of
Randomized Clinical Trials. Arch Intern Med; 151:1769,
1991.
82. Thadani U, Whitsett TL. fi-adrenergic Blocker &
Intermittent Claudication: Time for Reappraisal. Arch
Intern Med; 151:1705,1991.
83. ATS Statement: Standards for the Diagnosis & Care of
Patients with Chronic Obstructive Pulmonary Disease.
Official Statement of the American Thoracic Society.
American Journal of Respiratory & Critical Care
Medicine; 152(5)Suppl:578 & 587, 1995.
84. Beard K, Bulpitt C, Mascie-Taylor H, et al. Management
of Elderly Patients with Sustained Hypertension. BMJ;
304:412, 1992.
85. Thijs L. Fagard R, Lijnen, et al. Why is Antihypertensive
Drug Therapy Needed in Elderly Patients with
Systodiastolic Hypertension? J Hypertens Suppi; 12(6):
s25, 1994.
86. Insua JT, Sacks HS, Tai-Shing, et al. Drug Treatment of
Hypertension in the Elderly: a Meta-analysis. Ann Intern
Med; 121(5):355,1994.
87. Collins R, Wallenberg HCS. Hypertension in Pregnancy.
Effective Care in Pregnancy & Childbirth. The Cochrane
Pregnancy & Childbirth Database. Issue 2, 1995.
88. Collins R, Duley L. Methyldopa-based therapy in the
treatment of pre-eclampsia. m: Pregnancy & Childbirth
Module (eds, Enkin MW, Keirse MJNC, Renfrew
MJ, Neilson JP), "Cochrane Database of Systematic
Reviews": Review No. 03997, 29 July 1992. Published
thru "Cochrane Updates on Disk", Oxford: Update
Software, Spring, 1993.
89. Collins R, Duley L. fi-blockers in the treatment of preeclampsia. In Pregnancy & Childbirth Module (eds, Enkin
MW, Keirse MJNC, Renfrew MJ, Neilson JP), "Cochrane
HYPERTENSION
Database of Systematic Reviews": Review No. 03998,

20 April 1993. Published through "Cochrane Updates
on Disk", Oxford: Update Software, Spring, 1993.
90. Duley L. Calcium channel blockers in pregnancy
hypertension. In: Pregnancy & Childbirth Module (eds,
Enkin MW, Keirse MJNC, Renfrew MJ, Neilson JP),
"Cochrane Database of Systemic Reviews": Review
No. 07075, 30 July 1992. Published through "Cochrane
Updates on Disk", Oxford: Update Software, Spring
1993.
91. Collins R, Duley L. IV Labetalol vs IV Diazoxide in
severe pre-eclampsia. In: Pregnancy & Childbirth Module
(eds, Enkin MW, Keirse MJNC, Renfrew MJ, Neilson
JP), "Cochrane Database of Systemic Reviews": Review
No. 04400,20 April 1993. Published through "Cochrane
Updates on Disk", Oxford: Update Software, Spring
1993.
92. O'Mailia JJ, Sander GE, Giles TD. Nifedipine-associated
Myocardial Ischemia or Infarction in the Treatment of
Hypertensive Urgencies. Ann Intern Med; 107(2): 185,
1987.
93. Messerii FH, Kowey P, Grodzicki T. Sublingual nifedipine
for hypertensive emergencies. Lancet; 338:881,1991.
94. Giffoid, RW. Management of Hypertensive Crises.
JAMA; 266:829,1991.
95. Veterans Administration Cooperative Study Group on
Anti-hypertensive Agents. Effects of Treatment on
Morbidity in Hypertension: Results in Patients with
Diastolic Blood Pressure Averaging 115 through 129
mmHg. JAMA; 202:1028, 1967.
96. Silagy CA, Neil HAW. A Meta-analysis of the Effects of
Garlic on Blood Pressure. J Hypertens; 12:463, 1994.
97. National High Blood Pressure Education Program
Working Group on Primary Prevention of Hypertension.
Arch Intern Med; 153:186,1993.
98. Hypertension Prevention Trial Research Group. The
Hypertension Prevention Trial: Three Year Effects of
Dietary Changes in Blood Pressure. Arch Intern Med;
150:153,1990.
99. The Trials of Hypertension Prevention Collaborative
Research Group. The Effects of Non-pharmacologic
Interventions in Blood Pressure in Persons with High
Normal Levels: Results of the Trials of Hypertension
Prevention Phase I. JAMA: 267:1213, 1992.
53
HYPERTENSION
CPM 1ST EDITION
Acknowledgements
Critiques of Draft
Milagros Arroyo, MD, Philippine Society of Ophthalmology
Renato Dantes, MD, Medical Director, Boehringer Ingelheim
Conrado Dayrit, MD, VP - Medical Affairs, United Laboratories Inc.
Mario Festin, MD, U.P. Coll. of Medicine, Clinical Epidemiology Unit
Jesus Fojas, MD, Dean, MCU-FDTMF College of Medicine
Mr. Rene Martinez, VP-Marketmg Services, GX Intl.
Caesar L. Mendoza, MD, Medical Center Manila
Sandra Tankeh-Torres, MD, Medical Director, Pfizer
Cecilia Tomas, MD, U.P. College of Medicine, Dept. of Physiology
Participants in the First Public Forum
Mr. Jorge Maravilla, LR Imperial, Inc.
Mr. Frederick Farol, Therapharma, Inc.
Ms. Shirly Fuentes, Pfizer Inc.
Ms. Dory Guerrero, Boehringer Ingelheim, Inc.
Mr. Gerry Arnedo, Pfizer, Inc.
Dr. Renato Dantes, Boerhinger Ingelheim, Inc.
Mr. Gilbert Donato, Merck, Inc.
Ms. Jeanette Rogacion, Warner-Lambert (Parke-Davis)
Dr. Virgilio Castro, UST Hospital/Philippine Obstetrics and Gynecology Society
Mr. Carlo Estrada, Hoechst Marion Roussel
Mr. Romeo Albornoz, Hoechst Marion Roussel
Dr. Francis Domingo, Servier, Inc. (Med-Asia)
Ms. Odette Magno, Bristol-Myers Squibb, Phils.
Mr. Henry Lim, Roche, Phils.
Dr. Felicidad Cua-Lim, Philippine College of Physicians
Dr. Ronald Yutangco, Philippine Association of Ophthalmology
Dr. Joel Elises, Philippine Pediatrics Society
Sister Francesca San Diego, Philippine Nurses Association
Ms. Precy Cruz, Occupational Health Nurses Assoc. of the Phils.
Dr. Florencio Pine, Philippine Society of Nephrology
Dr. Eugene Ramos, Phil. Col. of Physicians/Bristol-Myers Squibb, Phils.
Dr. Albert Bautista, Synthelabo, Inc.
Dr. Corazon Almirante, Fetus as a Patient Institute of the Philippines
Dr. Raffy Castillo, Phil. Society of Hypertension / Phil. Heart Assoc.
Dr. Ma. Antonia Yamamoto, Phil. Association of Family Physicians
Dr. Tes Somera-Cucueco, DOLE
Dr. Allan Ruales, Philippine Medical Association / MCU-FDTMF
Dr. Liberty Fajutrao, U.P. Coll. of Medicine Clinical -Epidemiology Unit
Dr. Elias Imperial, Bicol Heart Center
Dr. Luciene Villacin, Cardiovascular Research Group
Mr. Gerry Macutay, Medical Clerk, U.P. College of Medicine
Ms. Josephine Manansala, Medical Clerk, U.P. College of Medicine
Myrna Abello, WVSU College of Medicine
Dr. Felix Eduardo Punzalan, Cardiovascular Research Group
Dr. Armando Bolivar, Philippine College of Occupational Medicine
Dr. Conrado Dayrit, National Academy of Science and Technology
Dr. Joselito Atabug, UST- Dept. of Medicine / PHA
Prof. Maria Lourdes Amarillo, UP -College of Medicine, Clinical Epidemiology Unit
Dr. Paul Salandanan, FEU Hospital
Dr. Adriano dela Paz, Philippine Heart Center
Dr. Vie Fileto Chua, FEU Hospital
Dr. Romiro Babanan, FEU Hospital
Dr. Amaryllis 0. Yazon, Fetus as a Patient Institute of the Phils.
Mr. Jayvee Cruz, UP College of Nursing / Phil. Nurses Association
Dr. Oscar Naidas, St. Luke's Medical Center/Philippine Society of Nephrology
Dr. Leni Iboleon, St. Luke's Medical Center/PMA
Dr. Ofelia P. Borje, Philippine Society of Pediatric Cardiology / PHA
Ms. Ma. Patrocinia de Guzman, Food & Nutrition Research mst./DOST
Dr. Ramon Abarquez, Jr., Philippine Society of Hypertension
Dr. Esperanza Cabral, Philippine Society of Hypertension

Dr. Gregorio Patacsil, Jr., Philippine Society of Hypertension
Dr. Antonio Dans, Cardiovascular Research Group
Dr. Desiree Narvaez, Department of Health
Dr. Bernadette Tumanan, Philippine Society of Hypertension
Ms. Felicidad Velandria, Food and Nutrition Research Institute
Dr. Elizabeth Pacheco, Philippine General Hospital/ Philippine Society of Endocrinology and Metabolism
54
CPM 1ST EDITION
HYPERTENSION
Drugs Mentioned in the Treatment Guideline

The following index lists therapeutic classifications as recommended by the treatment guideline. For the prescriber's
reference, available drugs are listed under each therapeutic class.
ACE Inhibitors
Benazepril
Cibacen................................139
Captopril
Capoten...............................140
Cilazapril
Vascace................................140
Delapril
Cupressin.............................140
Enalapril
Renitec.................................140
Lisinopril
Zestril..................................140
Perindopril
Coversyl............................. 140
Quinalapril
Accupril.............................. 142
Ramipril
Ramace............................... 142
Tritace ................................142
Spirapril
Wandopres.......................... 142
Captoprill
Hydrochlorothiazide
Capozide............................. 142
Cilazapril/
Hydrochlorothiazide
Capozide............................. 142
Hydrochlorothiazide
Vascace Plus....................... 142
Angiotensin II Antagonist
Losartan
Cozaar.................................142
Valsartan
Diovan ............. ..................NP"
Beta-Blockers
Atenolol
Serten...................................129
Tenormin............................ 130
UL Atenolol........................ 130
Betaxolol
Kerlone............................... 130
Bisoprolol
Concore.............................. 130
Carteolol
Mikelan.............................. 130
Metoprolol
Betaloc .............................. 130
Betazok.................................l31
Cardiosel............................ 131
USA Metoprolol............ .....131
Nadolol
Corgard............................... 131
Pindolol
Visken................................. 131
Propranolol
Bedranol............................. 131
Duranol............................... 131
Inderal................................ 132
Propranolol Phoenix............................ 132
Propranolol Scanpharm....................... 132
UL Propranolol . .................132
Sotalol
Sotalex................................ 132
AtenolollChlorthalidone
Tenoretic.......... .................. 132
Metoprololl
Hydrochlorothiazide
Betazide.............................. 132
Pindololl /Clop amide
Viskaldix............................ 132
Calcium Channel Blockers
Amiodipine
Norvasc.............................. 132
Diltiazem
Dilatam............................... 134
Diltelan . ............................ 134
Dilzem/DilzemSA/SR.........134
Servazen..............................134
Tildiem............................... 134
Zilden................................. 134
Felodipine
Munobal............................. 134
PlendilER........................... 134
Isradipine
Dynadrc ............................. 134
IcazSRO............................. 136
Lacidipine
Lacipil................................ 136
Manidipine
Caldine............................... 136
Minadil............................... 136
Nicardipine
Cardepine........................... 136
Selevax............................... 136
Nifedipine
Adalat................................. 136
Calcibloc............................ 136
Cardionorm........... ............ 138
Darat................................... 138
Fedcor................................. 138
Nifelan ............................... 138
Nitrendipine
Baypress............................. 138
Verapamil
Hinorm............................... 138
Isoptin/Isoptin SR ..............138
Verelan.................................139
AtenolollNifedipine
Niften.................................. 139
Centrally-Acting Drugs
Clonidine
Catapres.............................. 126
Catapres TTS ..................... 126
Melzin................................ 127
Guanfacine
Estulic................................. 127
Methyldopa
Aldomet.............................. 127
Dopetens ........................... 127
Meldopa ............................ 127
Mendonil............................ 127
UL Methyldopa............. .....127
Moxonidine
Cynt.................................... 127
Physiotens.......................... 129
Reserpine
Rauverid............................. 129
ReserpinelClopamidel
Dihydroergocristine mesylate
Brinerdin/
Brinerdin Mite................. 129
ReserpinelHydralazinel
Hydrochlorothiazide
Ser-Ap-Es........................... 129
Diuretics
Acetazolamide
Diamox............................... 124
Bumetanide
Burinex............................... 124
Furosemide
Aquadrine........................... 124
Flexamide........................... 124
Fretic.................................. 124
Frusema.............................. 124
Furoscan............................. 124
55
HYPERTENSION
Lasix................................... 124
Lasix High Dose ............... 125
Lasix Long 30............,........125
USALab
Furosemide...................... 125
YSP Furosemide...................l25
Hydrochlorothiazide
Dichlotride.......................... 125
Indapamide
Natrilix............................... 125
Spironolactone
Aldactone........................... 125
AmiloridelFurosemide
Frumil................................. 126
AmiloridelHydrochlorothiazide
Moduretic........................... 126
SpironolactonelButizide
Aldazide............................. 126
SpironolactonelFurosemide
Lasilactone......................... 126
Vasodilators
Doxazosin
Carduran............................. 129
Hydralazine
Apresoline.......................... 129
Prazosin
Minipress............................ 129

56
CPM 1ST EDITION

CPM 1st Ed Hypertension

Uploaded by

Copyright:

Available Formats

CPM 1st Ed Hypertension

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

CPM 1st Ed Hypertension

Uploaded by

Copyright:

Available Formats

Philippine Society of Hypertension

Affiliated with the International Society of Hypertension

Officers and Board of Trustees 1997

Ramon F. Abarquez, Jr., M.D.

Multi-Sectoral Task Force on the Detection and

Technical Research Committee

Antonio L. Dans, M.D.

CPM 1ST EDITION

Agnes Mejia, M.D.

CPM 1ST EDITION

Plans and Programs of the Philippine Society of

The PSH president presented the Paradigm Shift in

CPM 1ST EDITION

represents a considerable proportion of the productive

The Philippine Society of Hypertension

CPM 1ST EDITION

The recommendations contained in this CLINICAL

CPM 1ST EDITION

The Philippine Clinical Practice Guidelines on the

The following 6 questions are addressed by the

Phase 3 - Preparation of the Penultimate Report.

1. The most accurate and reliable technique for

CPM 1ST EDITION

indirect blood pressure measurement is the

Summary of Evidence: Previous technical publications[2,3] and consensus statements [4-6]

Summary of Evidence: Economical self-monitoring

B. HOW SHOULD HYPERTENSION BE DIAGNOSED?

1. Strategies for Detection

a. Case Finding - Opportunities for case-finding

b. Mass Screening - In developing countries,

2. Strategies for Confirmation

The diagnosis of hypertension should be based

sion (JNC V) (Grade D Recommendation).

Table 3. Recommended confirmation schedule

CPM 1ST EDITION

Summary of Evidence: The advocated definition of

CPM 1ST EDITION

Table 5. Risk factors for Coronary Artery Disease

Source: The Fifth Report of the Joint National Committee on

1. A detailed history and physical examination

Summary of Evidence: Effectiveness of treatments

2. The following tests should be routinely performed

a. fasting plasma glucose

Summary of Evidence: All the tests listed above were

Summary of Evidence: Because of a very low sensitivity

CPM 1ST EDITION

sensitive than both the ECG and chest radiogram in the

CPM 1ST EDITION

b. Weight reduction can be achieved by caloric

Summary of Evidence: No trials have shown that

be achieved by lower extremity aerobic exercise

a. In uncomplicated mild hypertension (Stage

Summary of Evidence: The TOMH study showed that

b. All classes of antihypertensive agents (Table

CPM 1ST EDITION

Summary of Evidence: This recommendation is based

CPM 1ST EDITION

* In secondary prevention trials (patients with stable and