Guidline for managment of Hyperyension in Primary care

Transcription

GUIDELINE FOR MANAGEMENT
OF HYPERTENSION IN PRIMARY
Kingdom of Bahrain
Ministry of Health
CARE SETTINGS AND
OUTPATIENT CLINICS IN THE
KINGDOM OF BAHRAIN
Hypertension
Nov 2014
WORKING & REVIEW GROUP
PRIMARY CARE GROUP
SECONDARY CARE GROUP
Dr. Anwar Jamsheer
Chairman Medical Department,
Consultant Cardiologist, SMC
Dr. Ameera AL-Nooh
Consultant Family Physician
Dr. Wafa AL Sharbati

Dr. Mai Mansoor Mohamed
Dr. Maha Ali Al Mokla
Dr. Maha Al-Tajer
REVIEWED
Dr. Abdul Hussain AL Ajami
Head of Non-Communicable Disease Unit
Dr. Mariam Al-Mulla Harmas
Director of the public health
SUPERVISION
Dr. Mariam Athbi Al-Jalahma
Assistant Undersecretary,
Primary Care and Public Health
2
TABLE OF CONTENTS
Page No
List of Tables
3
List of Figures
7
Abbreviations
8
Introduction
10
Chapter 1: Algorithm Annotations of Hypertension Diagnosis and
Treatment
The Rule of Halves and Staging System
11,13
11,12
Part I: Prevention Stage
1. Screening and Identification of Elevated BP
2. Standardization of BP Measurement
14
14
15
Part II: Diagnostic Stage
3. Accurate Staging
4. Confirm Chronicity of High BP Level
5. Role of Self/ Home Blood Pressure Monitoring and Ambulatory
Blood Pressure Monitoring in Confirming the Chronicity of High
BP Level
6. Initial Clinical Evaluation
7. Is Secondary Cause Suspected?
16
16
17
17
Part III: Control Stage
9. Therapeutic Approaches
a. Lifestyle Modifications
b. Drug Therapy
I. Antihypertensive Drugs
II. Vascular Protection for Hypertensive Patients
c. Target BP Sitting
10. Subsequence Therapeutic Approaches to Achieve Control
a. Drug Manipulation
b. Criteria to Achieve Control
11. Resistant Hypertension
12. Hypertension Consultation
25
25
28
28
28
29
27
36
36
36
37
40
Part IV: Follow-up Stage (Hypertension Continuing Care)
13. Follow-up Criteria and Evaluation
41
41
Chapter 2: Hypertension during Ramadan and Hajj
3
20
22
42
Chapter 3: Hypertension and Co-Morbidities
1. Hypertension and Diabetes Mellitus
2. Hypertension and Chronic Rental Disease
3. Hypertension and Coronary Heart Disease
4. Hypertension and Dyslipidemia
5. Hypertension and Congestive Heart Failure
6. Hypertension and Cerebrovascular Disease
7. Obese Patients
8. Metabolic Syndrome
9. Hypertension after Renal Transplantation
44
44
44
48
49
50
50
52
52
52
Chapter 4: Hypertension in Special Groups
1. Hypertension in Children
2. Hypertension in Women
3. Hypertension in Elderly
4. Minority Populations
55
55
62
63
64
Chapter 5: Hypertensive Crises
1. Hypertensive Urgencies
2. Hypertensive Emergencies
65
66
67
Chapter 6: The Role of Nurses and Nurse Practitioners in Hypertension
Management
70
Appendices
Appendix 1: Initial History, Physical Exam, and Basic Investigation
Appendix 2: Risk Stratification: Major Risk Factors for CVD, TODs
and ACCs
Appendix 3: Etiological Classification of Hypertension with Clinical
Finding and Recommended Evaluation
Appendix 4: Antihypertensive Drugs
Appendix 5: Antihypertensive Drugs Indications, Contraindications,
Interactions and Potential Side Effects
Appendix 6: Adverse Effects of Antihypertensive Drugs
Appendix 7: Recommended Education Messages
Appendix 8: HTN Sheet
73
73
78
97
98
100
References
112
4
87
91
94
LIST OF TABLES
Table 1:
Standardization of BP Measurement: Guidelines for the Measurement of
Blood Pressure to Diagnose and Treat Hypertension…........................... 15
Table 2:
Classification of Blood Pressure for Adults (Aged ≥18 Years)…………16
Table 3:
Recommendations for Follow-up Based on Initial Blood Pressure
Measurements for Adults without Acute TOD…………………………16
Table 4:
Recommended Duration and Tasks during each Visit to Confirm
Chronicity of High BP Level…………………………………………….17
Table 5:
Diagnostic Hypertension Level in Clinics Compare to Self / Home and
Ambulatory Blood Pressure Monitoring…………………………………17
Table 6:
Clinical indications for out-of-office blood pressure measurement for
diagnostic purposes……………………………………………………………………..20
Table 7:
Risk Factors for Secondary Hypertension, Order Additional Work-up and
Consider Referral ……………………………………………………………………….22
Table 8:
Clinical indications and diagnostics of secondary hypertension………….23
Table 9:
Laboratory investigations………………………………………………….24
Table 10:
Lifestyle Modifications to Prevent and Manage Hypertension…………28
Table 11:
Classification and Management of Blood Pressure for Adults………….29
Table 12:
Other Medications Used As Vascular Protection for Hypertensive Patients
Evidenced Based Combinations of Antihypertensive Drugs…………………..……..33
Table 13: Evidence-Based Antihypertensive Drug Treatment for Special
Situations/Populations with Target BP………………………………………………..34
Table 14:
Recommended Duration for Follow-up of Patients on Antihypertensive
Drug Treatment to Achieve Control…………………………………….36
Table 15:
Strategies to Improve Patient Adherence………………………………..39
Table 16:
Suggested Indications for Specialist Referral………………………….40
Table 17:
NKF-K/DOQI* Guidelines on Blood Pressure Management and Use of
5
Antihypertensive Agents in Chronic Kidney Disease…………………48
Table 18:
Definitions of the Cardiometabolic Syndrome…………………………53
Table 19:
Classification of hypertension in children and adolescents……………..56
Table 20:
Blood pressure levels for boys by age and height percentile…………59,60
Table 21:
Blood pressure levels for girls by age and height percentile………….61
Table 22:
Definition and Acute Reductions in BP Duration and Target BP for
Hypertensive Crises……………………………………………………..66
Table 23:
End-Organ Damage Seen in Hypertensive Emergencies………………..67
Table 24:
Preferred Agents Used for the Acute Treatment of Hypertensive
Urgencies……………………………………………………………….69
Table 25:
Recommended Antihypertensive Drugs for Hypertensive Emergencies..71
Table 26:
Strategies to Promote Blood Pressure
Control…………………………..71,72
6
LIST OF FIGURES
Figure 1:
Rule of Halves (a-b)…………………………………………………11,12
Figure 2:
Algorithm Annotations of Hypertension Diagnosis and Treatment……13
Figure 3:
Indirect Method of Measuring BP………………………………………14
Figure 4:
Cardiovascular risk stratification according to SBP and DBP and prevalence
of risk factors……………………………………………………………24
Figure 5:
Initiation of lifestyle changes and antihypertensive drug treatment………26
Figure (6a ) : Algorithm for Treatment of Hypertension……………………………...30
Figure (6b):
Algorithm for Treatment of Hypertension………………………………31
Figure 7:
Possible Combinations of Different Classes of Antihypertensive Agents..32
Figure 8:
Considerations in the Evaluation of Resistant Hypertension and General
Strategy for Diagnosing a Secondary Cause of Hypertension…………38
Figure 9: Algorithm for Treating Patients with Diabetes or Kidney Disease to Goal
BP………………………………………………………………………47
Figure 10: Approach to Hypertensive Crises………………………………………..68
7
ABBREVIATIONS
ACCs
Associated Clinical Conditions
ACEIs
Angiotensin Converting Enzyme-Inhibitors
ABPM
Ambulatory Blood Pressure Monitoring
α-Bs
Alpha-Blockers
ARBs
Angiotensin Receptors Blockers
β-Bs
Beta-Blockers
BP
Blood Pressure
BMI
Body Mass Index
BPH
Benign Prostatic Hypertrophy
CNS
Central Nervous System
COX-2
Cyclooxygenase
CPR
Cardiopulmonary Resuscitation
CVD
Cardiovascular Disease
CCBs
Calcium Channel Blockers
CBC
Complete Blood Count
CHD
Coronary Heart Disease
CHF
Congestive Heart Failure
CRD
Chronic Renal Disease
DASH
Dietary Approaches to Stop Hypertension
DBP
Diastolic Blood Pressure
DM
Diabetes Mellitus
ECG
Electro-cardiogram
FPG
Fasting Plasma Glucose
HB
Hemoglobin
HDL
High density Lipoprotein
H/O
History Of
HTN
Hypertension
INS
Insulin
ISHTN
Isolated Systolic Hypertension
I.V.
Intra-venous
LDL
Low Density Lipoprotein
LV
Left Ventricle
8
MI
Myocardial Infarction
NCEP
National Cholesterol Education Program
NSAIDs
Non-Steroidal Anti-Inflammatory Drugs
No.
Number
OSA
Obstructive Sleep Apnea
PND
Paroxysmal Nocturnal Dyspnea
PVD
Peripheral Vascular Disease
Rx
Treatment
SBP
Systolic Blood Pressure
SCD
Sickle Cell Disease
SE
Side Effect
S/H BPM
Self / Home Blood Pressure Monitoring
TBP
Target Blood Pressure
TG
Triglyceride
TIA
Transient Ischemic Attack
TOD
Target Organ Damage
VOC
Vasoocuulsive Crisis
WHO
World Health Organization
9
INTRODUCTION
Essential hypertension has become one of the most widespread diseases in many countries.
Overall the hypertension prevalence appears around 30-45% of the general population, with
a steep increase with aging. The average BP levels across different European countries are
noticeably different (4,5,13,37,21,27,28,31,42,46,51,59,67,68,74,75,78,85,93). Results from The National NonCommunicable Diseases and Risk Factors Survey conducted in 2007 in the Kingdom of
Bahrain showed that 16.3% (289 out of 1769) of adults aged 20 to 64 years were known
cases of hypertension, and another 26.4% (467 / 1769) had above normal average systolic or
diastolic blood pressure.
In both the known cases and the new potential cases, the
prevalence increases with age from 5% and 17.1% in the age group 20-29 years, to 60.7%
and 27.9% in age group 60-64 years, respectively (3). The treatment of hypertension is the
second most common reason for office visits to physicians in United States and for the use
(91)
of prescription drugs
. Hypertension (HTN) prevalence in the Kingdom of Bahrain is
38.2% (3).
Hypertension is the most important modifiable risk factor for coronary heart disease (the
leading cause of death in North America)
(90)
. It causes stroke (the third leading cause),
congestive heart failure, end-stage renal disease and peripheral vascular disease in the younger
and older population
(80)
. Hypertension is quantitatively the major risk factor for premature
cardiovascular disease, being more common than cigarette smoking, dyslipidemia and diabetes
(90)
. Since obtaining comparable results about the prevalence of hypertension among countries
was difficult, stroke mortality reports were suggested as a surrogate of hypertension status.
(47)
According to World Health Organization (WHO) analysis of the incidence and trends of stroke
mortality in Europe, western countries were found to exhibit downward trend, in contrast to
eastern European countries, which showing a clear-cut increase in death rates from stroke (71).
Active treatment with antihypertensive medications led to statistically significant 16 %
reduction in the number of coronary events and 40 % reduction in stroke (15). Active treatment
with antihypertensive medications led to statistically significant (20-30%) reduction in the
coronary events, and 40-45% reduction in stroke. (38)
There are several evidence based guidelines on prevention, detection, evaluation, and treatment
of high blood pressure.(37,38, 43,47 ) The current management of hypertension is characterized by
underdiagnosis, misdiagnosis, undertreatment, overtreatment, and misuse of medications (84).
10
CHAPTER ONE
ALGORITHM ANNOTATIONS OF HYPERTENSION DIAGNOSIS AND TREATMENT
The Rule of Halves and Staging System (Figures 1a, 1b)
"The rule of halves" stated that half of hypertensive patients were not diagnosed. And out of the
half diagnosed, half not treated and out of the treated patient, half were not controlled. This
leaves us with about 12.5% out of all hypertensive patients were well controlled and followed
(79).
This rule that still exist (68) clearly describes the overall situation of hypertension and draws
more emphasis on drastic measures needed to be taken in order to shift the overall approach to
hypertension (2). (Figure 1a)
Hence, the staging system is arrived to provide comprehensive practical guideline to approach
to hypertension. There are four stages namely the preventive, diagnostic, control and follow up
(Figure 1b). These stages arranged in order to minimize the hazards and maximize the benefits
while encountering any patient. So you can't diagnose any patient without effective preventive
screening tools, neither start controlling hypertensive patients without having established the
accurate diagnosis using validated diagnostic tools. Furthermore, you can't follow patient every
three to six month if they are not well controlled. Hence, the problems of underdiagnosis,
misdiagnosis, undertreatment, overtreatment, and misuse of medications can be handled
perfectly with the staging system (84). (Figure 2)
Figure 1a: Rule of Halves (84)
HTN Role of halves:
12.5%
12.5%
Not Diagnosed
50%
Not Treated
Not Controlled
Controlled
25%
11
Figure 1b: Rule of Halves and Staging System (84)
1. Prevention Stage
Hypertension
50% not
Diagnosed
2. Diagnosis Stage
50% Diagnosed
50% not Treated
50% Treated
3. Control Stage
50% not
Controlled
50% Controlled
4. Follow-up Stage
= 12.5 % of All
Hypertensive
12
1
Screening and Identification of
Elevated
BP > 140/90
Part I:
Prevention
Stage
Figure 2: Algorithm Annotations of
Hypertension Diagnosis and Treatment
2
Standardization of BP Measurement
3
Accurate Staging
Part II:
Diagnostic
Stage
A = Annotation
1-13
5
Is this Patient Hypertensive?
a) Self / Home Blood Pressure
4
Confirm Chronicity of High BP Level
?
Monitoring
b) Ambulatory Blood Pressure
Monitoring
6
Initial Clinical Evaluation
7
Is Secondary Cause
Suspected?
Yes
8
 Order Additional Work-up
 Consider Referral
No
Part III:
Control
Stage
a)
b)
c)
9
Therapeutic Approaches
Lifestyle Modifications
Initial Drug Therapy
Target BP Sitting
C
BP at Goal?
Yes
No
10
Subsequence Therapeutic Approaches
to Achieve Control
a) Drugs Manipulation
b) Criteria to Achieve Control
C
BP at Goal?
Yes
No
11
Resistant
Hypertension
Yes
12
Hypertension Consultation
No
Part VI:
13
Follow-up Criteria and Evaluation
Follow-up
Stage
13
1. Screening and Identification of Elevated BP
a) Hypertension screening age: Preschool and ≥ 18 years old.
b) Follow-up recommendation according to BP level (Table 3)
Every 2 years if less than 120/80.

Every year if 120-139/80-89 Hg.

BP Greater Than or Equal to 140/90 should be followed as table 4.
c) Screening method: Refer to clinics blood pressure measurement (Clinics BPM) - Table 1.
2. Standardization of BP Measurement (Table 1)
a) The Importance of Standardization

Accurate, reproducible blood pressure measurement is important to allow comparisons
between blood pressure values and to correctly classify blood pressure (36,63).

Incorrectly labeling a hypertensive patient as normotensive may increase risk for
vascular events, since risk rises with increasing blood pressure (36,63).

Labeling a patient with normal blood pressure as a hypertensive can affect insurability,
employment, morbidity from medications, loss of time from work, and unnecessary
lab and physician visits (36,63).

Standardized blood pressure technique should be employed when confirming an
elevated reading and for all subsequent readings during follow-up and treatment for
hypertension (36,63).
b) Indirect Method of Measuring BP (36, 63)
Figure 3: Indirect Method of Measuring BP
Standardization of BP Measurement
Mercury Sphygmomanometers: Gold standard(10)
1- Clinics BPM
Aneroid Sphygmomanometers
Automated Devices
14
Out-of-office BP measurement that includes home BP measurement (self-monitoring) and
ambulatory BP monitoring, are now regarded as of strong prognostic for diagnosis and
management of hypertension along with office BP measurement (47).
Table 1: Standardization of BP Measurement: Guidelines for the Measurement of Blood
Pressure to Diagnose and Treat Hypertension (36, 63)
Patient Conditions
Posture
 Initially, check for postural changes ( drop in 20mmHg and above) by taking readings after five minutes
supine, then immediately and two minutes after standing - this is particularly important in patients over age
65, diabetics, or those taking antihypertensive drugs
 Sitting pressures are recommended for routine follow-up; the patient should sit quietly with the back
supported for five minutes and the arm supported at the level of the heart
Circumstances
 No caffeine during the hour preceding the reading and no smoking during the preceding 30 minutes
 No exogenous adrenergic stimulants, such as phenylephrine in decongestants or eye drops for pupillary
dilatation
 A quite, warm setting
 Home readings should be taken upon varying circumstances
Equipment
Cuff Size
 The length of the bladder should be 80 percent and the width of the bladder should be at least 40 percent of
the circumference of the upper arm cuff Bladder encirculating at least 80% the arm
Manometer
 Aneroid gauges should be calibrated every six months against a mercury manometer
Technique
Number of Readings
 Take at least two readings on each visit, separated by as much time as possible; if readings vary by more
than 5 mmHg, take additional reading until two consecutive readings are close
 For the diagnosis of hypertension, take three readings at least one week apart
 Initially, take blood pressure in both arms; if pressures differ, use the higher arm
 If the arm pressure is elevated, take the pressure in one leg, particularly in patients under age 30
Performance
 Inflate the bladder quickly to 20 mmHg above the systolic pressure as estimated from loss of radial pulse
 Deflate the bladder 3 mmHg per second
 Record the Korotkoff phase V (disappearance) as the diastolic pressure except in children in whom use of
phase IV (muffling) may be preferable
 If the Korotkoff sounds are weak, have the patient raise the arm, open and close the hand five to ten times,
and then inflate the bladder quickly.




BP measurement should always be associated with measurement of heart rate (pulse at rest ) because
elevated resting heart rate values independently predict CV morbid or fatal events (2013 ESH/ESC HTN
guideline).
If automated device was used to measure BP palpate the radial pulse for irregularity (Atrial fibrillation)
before measuring BP. If pulse irregularity is present, measure Bp manually , repeatedly using direct
auscultation over the brachial artery. (New 2011 Nice).
In many European countries, BP can no longer be estimated using mercury, but semiautomatic
(47)
sphygmomanometers are used instead
.
If a person is unable to tolerate ABPM, home BP monitoring HBPM is a suitable alternative to confirm
diagnosis of hypertension.
Recordings

Record the pressure, patient position, arm, and cuff size: e.g. 140/90, seated, right arm, large adult cuff
15
Part II: Diagnostic Stage
3. Accurate Grading
Table 2: Classification of Blood Pressure for Adults (Aged ≥18 Years) (47)
Initial Blood Pressure (mmHg)
Category
Optimal
Systolic
Diastolic
<120
And
<80
Normal
120-129
And /Or
80-84
High normal
130-139
And /Or
85-89
Grade I
140-159
And /Or
90-99
Grade 2
160-179
And /Or
100-109
Grade 3
≥180
≥140
And /Or
And
≥110
Hypertension
Isolated systolic BP
<90
The blood pressure (BP) category is defined by the highest level of BP, whether systolic or diastolic. Isolated systolic
hypertension should be graded 1, 2, or 3 according to systolic BP values in ranges indicated.
4. Confirm Chronicity of High BP Level
Criteria for Diagnosis of Hypertension

Level of BP Measurements: Hypertension is defined as persistent elevation of SBP ≥
140 mm Hg and/or DBP ≥ 90 mm Hg in adults not on anti-hypertensive medications(47).

Number of BP Measurements: Three BP reading (Except In Malignant HTN) (47)
Table 3: Recommendations for Follow-up Based on Initial BP Measurements for Adults without
Acute TOD (47)
Initial Blood Pressure (mmHg)*
Systolic
Diastolic
Follow-up Recommended†
Optimal
<120
And
<80
Recheck in 2 years
Normal
120-129
And /Or
80-84
Recheck in 1 year‡
High Normal
130-139
And /Or
85-89
Recheck in 1 year‡
Grade I
140-159
Grade 2
160-179
90-99
Confirm within 2 months‡
And /Or
And /Or 100-109 Evaluate or refer to source of care within 1 month.
Grade 3
>180
And /Or
>110
 Evaluate and treat immediately (if acute emergency) or
 Within 1 week depending on clinical situation and
complications.
≥140
And
<90
Depend on the above Systolic BP reading
Hypertension
Isolated Systolic
Hypertension (>60yrs)
* Not taking antihypertensive drugs and not acutely ill. When systolic and diastolic pressure fall into different categories, the higher category should be
selected to classify the individual’s blood pressure status. (Isolated systolic hypertension [ISH] is defined as SBP greater than or equal to 140 mm Hg and
DBP less than 90 mm Hg and staged appropriately [e.g., 170/82 mm Hg is defined as Grade 2 ISH].) In addition to classifying grades of hypertension on the
basis of average blood pressure levels, clinicians should specify presence or absence of target organ disease and additional risk factors. This information is
(47)
important for risk assessment and treatment (see Figure (4)
.
† Optimal blood pressure with respect to cardiovascular risk is SBP less than 120 mm Hg and DBP less than 80 mm
Hg. However, unusually low readings should be evaluated for clinical significance.
‡ Based on the average of two or more readings taken at each of two or more visits after an initial screening.
16
Table4: Recommended Duration and Tasks during each Visit to Confirm Chronicity of High BP
Level (47)
Recommended Duration of Follow-up to Confirm Chronicity of High BP Level
Hypertension
1st Visit
2nd Visit
Total Duration
3rd Visit
Grade I*
Initial BP
measurement
One month
(After Initial BP
measurement)
One month
(After 2nd BP
measurement )
Two month
Grade 2
Initial BP
measurement
Two weeks
(After Initial BP
measurement )
Two weeks
(After 2nd BP
measurement )
One month
Grade 3
Initial BP
measurement
3rd Day
(After Initial BP
measurement )
7th Day
(After 2nd BP
measurement )
One week
>180 Or >110
(Two Options)
Initial BP measurement:
Evaluate and treat immediately (if acute emergency)
+
+
+
History
Physical exam &
Finalization:
 Confirm chronicity
investigation
 Risk stratification
 Initiation of Rx
 Sitting the target BP
Tasks
Immediately
* Visit 4-5 can be schedule especially in absence of TOD or diabetes and BP still in stage 1 after the third visit
5. Role of Self/Home Blood Pressure Monitoring and Ambulatory Blood
Pressure Monitoring in Confirming the Chronicity of High BP Level (47)
Table 5: Diagnostic Hypertension Level in Clinics Compare to
Self/Home and Ambulatory Blood Pressure Monitoring (47)
Initial Blood Pressure (mmHg) Consistent with Hypertension
Systolic
≥ 140
And /Or
Diastolic
≥ 90
Home Pressure Average
≥ 135
And /Or
≥ 85
Daytime Average ABP
≥ 135
And /Or
≥ 85
Night Time ( or Asleep)
≥ 120
And /Or
≥ 70
24-Hour Average ABP
≥ 130
And /Or
≥ 80
Clinics
BP self measurement may benefit pt. by providing information on:

Response to antihypertensive medicines.

Improve Pt. adherence with them
17

Evaluate white coat hypertension
Person with all average BP >135/85 mmHg, measured at home are generally considered to be
hypertensive home measurement device should be checked regularly for accuracy.
a) Self/Home Blood Pressure Monitoring (S/H BPM)
(47)
Indication for Use of HBPM on a Regular Basis

Diabetes mellitus

CKD

Suspected nonadherence

Demonstrated white coat effect (confirmed with ABPM)

BP controlled in the office but not at home (masked hypertension); the later
condition which carries an elevated cardiovascular risk similar to sustained
hypertension.
When using home blood pressure monitoring (HBPM) to confirm a diagnosis of hypertension
ensure that:

For each blood pressure recording, two consecutive measurements are taken, at
least 1 minute apart and with person seated and

Blood pressure recorded twice daily, ideally in the morning and evening and

Blood pressure recording continues for at least 4 days, ideally for 7 days.

Discard the measurements taken on the first day and use the average value of all
the remaining measurements to confirm a diagnosis of hypertension.

Refer patient to specialist if they have: Accelerated hypertension usually higher
than 180/110 mmHg with sign of papilledema and/or retinal hemorrhage, or
suspected phaeochromocytoma, or need for special investigation for suspected
secondary cause of hypertension (47).
b) Ambulatory Blood Pressure Monitoring (ABPM) (47)

ABPM is performed with the patient wearing a portable BP measuring device, usually
on the non dominant arm, for a 24-25h period, so it gives information on BP during
daily activities and at night during sleep.
18

The patient is instructed to engage in normal activities but to refrain from strenuous
exercise and, at time of cuff inflation, to stop moving and talking and keep the arm
still with the cuff at heart level.

The patient is asked to provide information in a diary on symptoms and events that
may influence BP, in addition to the times of drug ingestion, meals and going to and
rising from bed (in practice, measurements are often made at 15min intervals during
the day and every 30min overnight.

The measurements are downloaded to a computer and a range of analyses can be
performed.
Evidence from meta-analysis of published observational studies and pooled individual data
(16,11,30)
, however, has shown that ambulatory BP in general is a more sensitive risk predictor
of clinical CV outcomes, such as coronary morbid or fatal events and stroke, than office BP.
19
Table6:Clinical
indications
for
out-of-office
BP
measurement
for
diagnosis
Night dipping is the BP drop that occurs normally during the night (by >10% of daytime values).
It is usually measured using a night-day BP ratio. <0.9 is accepted as an arbitrary cut-off to define
subjects as ‘dippers’.
Masked Hypertension is high normal office but a raised out-of-office BP. Masked hypertension
is associated with high CV risk.
White Coat Hypertension is high office BP but normal out-of-office BP. When there is no
diabetes, OD, CVD or CKD, subjects with this type of hypertension have lower risk than who
have sustained hypertension for the same office BP.
6. Initial Clinical Evaluation
Once it has been determined that the patient has persistent hypertension, an evaluation should
be performed to ascertain the following information:

Determine extent of organ damage.

To asses the patients overall cardiovascular risk status.

To rule out identifiable and often curable causes of hypertension.
a. Aims
20
During the initial office evaluation of a person with elevated blood pressure readings, six
important issues must be addressed

Documenting an accurate diagnosis of hypertension (discussed earlier).

Defining the presence or absence of TOD related to hypertension. (Appendix 1-2)
Screening for other cardiovascular risk factors that often accompany hypertension.
(Appendix 1-2)

Assessing future risk for cardiovascular disease, which suggests the appropriate
intensity of treatment. (Appendix 1-2)

Assessing whether the person is likely to have an identifiable cause of
hypertension (secondary hypertension) and should have further diagnostic testing
to confirm or exclude the diagnosis (Appendix 3).

Obtaining data that may be helpful in the initial and subsequent choices of therapy
(Table12/Appendix 3).
b. The Clinical Evaluation includes

History and physical examination (Appendix 1). Should table 8, 9 be added in
Appendix 1 or replace it

BP measurement (Table 1)

Basic investigations
c. Basic Investigation (47)

Urine analysis

Hemoglobin

Fasting plasma glucose

Lipid profile

Creatinine

Uric acid

Potassium

ECG (standard 12-lead)
d. Role of Echocardiography in Hypertension (47)
The gender difference in interpreting the LVH has to be approached with caution. The
LVH in females has to be correlated with the body surface area; otherwise significant
LVH will be missed in women if the interpretation was solely used the absolute
dimensions.
21
Recommendations

Routine echocardiographic evaluation of all hypertensive patients is not
recommended

Indication: Hypertensive patients suspected of having:
o Left ventricular dysfunction
o Coronary artery disease

Echocardiography should not be used to track the therapeutic regression of left
ventricular hypertrophy
7. Is Secondary Cause Suspected?
About 10% of cases of HTN are due to secondary causes such as renovascular and
renoparynchymal diseases. The main causes of secondary HTN with their clinical finding,
recommended tests and referral are shown in Appendix 3. Certain clinical and biochemical
features suggest the presence of a secondary cause for HTN and warrant further investigations
(Appendix 3). Refer to figure 6 for approach to Secondary HTN.
Table 7: Risk Factors for Secondary Hypertension, Order Additional Work-up and
Consider Referral (28-29):
o Poor response to therapy (resistant hypertension)
o Worsening of control in previously stable hypertensive patient
o Grade 3 hypertension (systolic blood pressure > 180 mm Hg or diastolic blood
pressure >110 mm Hg)
o Onset of hypertension in persons younger than age 20
o Significant hypertensive target organ damage
o Lack of family history of hypertension
o Findings on history, physical examination, or laboratory testing that suggest a
secondary cause (Appendix 1-3).
22
Table 8: Clinical indications and diagnostics of secondary hypertension (47)
23
Figure 4 : CV risk stratification according to SBP and DBP and prevalence of risk factors
Table 9: Laboratory investigations (47)
24
(47)
9. Therapeutic Approaches
The primary goal of treatment in hypertensive patients is to achieve the maximum reduction
in the total risk of cardiovascular and renal morbidity and mortality. This requires
identification and treatment of all reversible risk factors such as smoking, dyslipidemia, or
DM and the appropriate management of associated co-morbidities, as well as treatment of the
raised BP per se (47).
Evidence favoring therapeutic reduction of high blood pressure:
Through treatment of hypertension, BP induced regression of organ damage, such as LVH and
urinary protein excretion, may be accompanied by a reduction of fatal and nonfatal outcomes
(24)(261,262 from page 1300 ESH/ESC 2013).
The treatment recommendations are based on available evidence from randomized controlled
trials and focus on important issues for medical practice:

When drug therapy be initiated
The evidence favoring drug treatment in low-to-moderate risk, grade 1 hypertension is
scant. Recent guidelines have also highlighted the lack of evidence for treating grade
1 hypertension, restricting treatment to grade 1 hypertensive patients with signs of OD
or at high total CV risk. (37)
Refer to figure (5), with the recommendation on initiation of lifestyle changes and
antihypertensive drug treatment
25
Figure 5 : Initiation of lifestyle changes and antihypertensive drug treatment

The target BP to be achieved by treatment in hypertensive patients at different
CV risk levels, and therapeutic strategies and choice of drugs in hypertensive
patients with different clinical characteristics.
Refer to table 12 for target BP setting
Refer to Figure 6a, 6b for Algorithm for Treatment of Hypertension and Table 11
Classification
and
management
of
blood
pressure
for
adults(47)
and
Evidence-Based
Antihypertensive Drug Treatment for Special Situations/Populations with target BP , respectively.
Initiate antihypertensive drug treatment immediately in patients with:
-
Grade 3 hypertension (SBP ≥ 180 mmHg and/or DBP ≥110 mmHg)
-
Isolated systolic hypertension and widened pulse pressure (SBP ≥ 160 mmHg and DBP ≤ 70
mmHg (.
-
One or more associated conditions or evidence of end-organ damage
- High absolute risk for cardiovascular disease assessed according to clinical indicators or the
risk calculator.
Monitoring treatment and BP targets
o Use clinic BP measurement to monitor the response to treatment.
26
o Aim for a target clinic BP below 140/90 mmHg in People age under 80
years with treated hypertension.
o Aim for a target clinic BP below 150/90 mmHg in people aged 80 years
and over, with treated hypertension.
o People identified as having a "white –coat effect", consider ABPM or
HBPM as an adjunct to clinic BP measurement to monitor response to
therapy.
o When using ABPM or HBPM ,aim for target BP during the person's usual
waking hours of:
o Below 135/85 mmHg for people aged under 80 years
o Below 145/85 mmHg for people aged 80 years and over.
(NICE, 2011)
Choice of Initial Antihypertensive Drugs
Depend on Two Criteria:
o BP Stage
o Co morbidities
o Target Organ Damage
o A 10 years CV risk equivalent to 20% or greater
a) Lifestyle Modifications
Appropriate lifestyle changes are the cornerstone for the prevention of hypertension
and important for its treatment, but should never delay the initiation of drug therapy in
patients at high level of risk.
27
Table 10: Lifestyle Modifications to Prevent and Manage Hypertension* (47)
Modification
Recommendation
Weight Reduction
Adopt DASH eating
plan
Adopt Mediterranean
type of diet
Dietary sodium
reduction
Physical activity
Moderation of alcohol
consumption
Quit smoking
Maintain normal body weight (body mass
index 18.5–24.9 kg/m2)(Waist circumference
to <102cm in men and <88cm in women)
.The risk of overweight and target body mass
index (BMI) in hypertension.
Consume a diet rich in fruits, vegetables, and
low fat dairy products with a reduced content
of saturated and total fat.
Replace red meat with white one, and eat fish
at least twice per week
Eat 300-400g/day of fruit and vegetables,
peas and beans (legumes), and wholegrain
cereals, Where possible, use monounsaturated olive oil in place of animal fat
such as butter. Eat unsalted nuts (30g).
Reduce dietary sodium intake to no more than
100 mmol per day (2.4 g sodium or 6 g
sodium chloride).(advice to avoid added salt
and high-salt food)
Engage in regular aerobic physical activity
such as brisk walking (at least 30 min per
day, most days of the week).
Limit consumption to no more than 2 drinks
(e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof
whiskey) per day in most men, and to no
more than 1 drink per day in women and
lighter weight persons.
All smokers should be advised to quit
smoking
Approximate SBP
Reduction
(Range)†
5–20 mmHg/10kg339. 356358(25,52,29)
8–14 mmHg339, 356-358
(25,52,29)
2–8 mmHg(25,65,34,17)
4–9 mmHg(18)
2–4 mmHg (25,69,20)
26,48
* For overall cardiovascular risk reduction, stop smoking.
† The effects of implementing these modifications are dose and time dependent, and could be greater for some individuals.
b) Drug Therapy
II. Vascular Protection Drugs for Hypertensive Patients

Types
o Monotherapy
o Combination Therapy
Refer to appendix 4-6 for each major class of antihypertensive drug compelling indications exists
for use in specific groups of patients and also compelling contraindications . Refer to Figure 6a, 6b
28
for Algorithm for Treatment of Hypertension , possible combinations of different classes of
antihypertensive agents, and Recommendations for combining blood pressure lowering drugs,
respectively. Table 10 describes evidenced based combinations of antihypertensive drugs .
II. Vascular Protection Drugs for Hypertensive Patients (47)

Statins

Aspirin
Refer to Table 12 on Other Medications Used as Vascular Protection for Hypertensive
Patients
Table 11: Classification and Management of Blood Pressure for Adults * (47)
Initial Blood Pressure (mmHg)
Systolic*
Optimal
High Normal
<120
120-139
Grade I
140-159
And
And
/Or
And
/Or
Risk-Stratified Drug Choices
Diastolic*
Lifestyle
Modification
<80
80-89
---Yes
90-99
Yes
Yes
Grade 2
160-179
And
/Or
100-109
Yes
Grade 3
>180
And
/Or
>110
* Treatment determined by highest BP category.
† Compelling indications (Table 12).
‡ Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.
† Treat patients with chronic kidney disease or diabetes to BP goal of <140/90 mmHg.
29
Without Compelling
Indication
Other
Than Hypertension
No antihypertensive
drug indicated
With
Compelling
Indications
(See Table 13)
Drug(s) for
compelling
Indications†
Thiazide-type
diuretics for most.
May consider ACEI,
ARB, BB, CCB, or
combination.
Initiate two drugs for
Most‡: diuretic one
of either ACE-I,
ARB, BB, or CCB
two drugs for
Most‡: diuretic one
of either ACE-I,
ARB, BB, or CCB
Appropriate drug
therapy for
compelling
indication† and
diuretic
Appropriate drug
therapy for
compelling
indication† and
diuretic
Figure (6a ) : Algorithm for Treatment of Hypertension
Established HTN
Lifestyle Modifications
BP not at Goal with Lifestyle Measures
Initial Drug Therapy
HTN with
Comorbidities^(Table 13)
HTN without Comorbidities
Grade 1
Hypertension
Grade 2
Hypertension
Two Options (at low dose):
1-Monotherapy^:
o 1-Thiazide-type diuretics (for most)*
o 2-May consider ACEI, ARB, CCB, BB**
2- Combination therapy^: Two drugs at very low dose
(Table)
One Option: Combination therapy (at low dose):
Two-drug combination† for most (usually thiazide
diuretic* and ACEI, or ARB, or BB, or CCB^)
Recheck within 4 weeks‡
BP not at Goal
o
o
o
o
o
o
Increase the dose (full dose)
Change drug
Add second Drug (low dose)
Increase the dose(full dose)
Change drug
Add third Drug (low dose)
Recheck within 4 weeks‡
BP not at Goal
3 Drugs combinations near/at
full dose including diuretics
Recheck within 2-3 weeks
BP not at Goal
Evaluation for Resistant hypertension and Secondary Hypertension
(Figure8)
^ Selection of initial drug either type or number according to table 12 (HTN with Comorbidities- (Table 13) or BP stage
* Select thiazide diuretic for all unless contraindicated (Appendix 5)
** Combination therapy involving B and D may induce more new onset diabetes compared with other combination therapies
‡ Reduces the duration to 2–3 weeks according to Table 13
† Caution is advised in those at risk for orthostatic hypotension, such as patients with diabetes, autonomic dysfunction, and some older persons.
30
Figure (6b) : Algorithm for Treatment of Hypertension
From ASH/ISH Hypertension Guideline
31
Figure (7): Possible Combinations of Different Classes of Antihypertensive Agents (47)
Because of a greater effect of RAS blockers on urinary protein excretion (513) (47), it appears
reasonable to have either an ACE inhibitor or an ARB in the combination. However, the
simultaneous administration of two RAS blockers (including the rennin inhibitor, Aliskiren) should
be avoided in high-risk patients because of the increased risk reported in ALTITUDE and
ONTARGET (433,463) (47).
Fixed-dose or single-pill combinations
Availability extends to the so-called polypill (i.e. a fixed-dose combination of several
antihypertensive drugs with a statin and a low-dose aspirin), with the rationale that hypertensive
patients often present with dyslipidemia and not infrequently have a high CV risk (12, 13). One
study has shown that, when combined into the polypill, different agents maintain all or most their
expected effects (467). The treatment simplification associated with this approach may only be
considered, however, if the need for each polypill component has been previously established (141).
Appendix 4 for Combination Drugs for Hypertension(30)
32
Anti-platelet therapy
Aspirin is not recommended in primary prevention of CV D in low-to-moderate risk patients in
whom absolute benefit and harm are equivalent. (47)
b) Target BP Sitting
Table 12: Other Medications Used as Vascular Protection for Hypertensive Patients (81)
Indications
Drugs
Dose
1. Aspirin
Controlled BP* and :
o Patient is aged ≥ 50 years with blood
pressure controlled to < 150/90 mm Hg
o Target organ damage
o Diabetes mellitus
o 10 year risk of cardiovascular disease of ≥
20%
81mg daily
2. Statin
Same for primary and secondary
prevention.
Use the appropriate intensity of statins
to reduce ASCVD risk in those most
likely to benefit
(4 statin benefit
groups) according to ACC/AHH
Guideline on treatment of blood
cholesterol regardless. No
RCT
evidence to support continued use of
specific LDL-C and/or non-HDL-C
treatment targets*
*Treatment decisions in selected
individuals (not included in 4 statin
benefit groups) may be informed by
other factors such as CRP, Family
history, Ca score, ABI
3. Vitamins
No benefit shown, do not prescribe
Statins are recommended in high-risk
hypertensive patients with established
atherosclerotic disease or with at least 3 of the
following criteria:
o Male
o Age 55 or older
o Smoking
o Type 2 Diabetes
o Total-C/HDL-C ratio of 6 mmol/L or
higher
o Family History of Premature CV disease
o LVH
o ECG abnormalities
o Microalbuminuria or Proteinuria
ASCVD risk reduction using the new Pooled
Cohort Equations to estimate 10-year ASCVD:4
statin benefit groups including individuals with:
1. Clinical ASCVD
2. Primary elevations of LDL-C≥190mg/dL
3. Diabetes aged 40-75 years with LDL-C
70-189mg/dL and without clinical
ASCVD
4. Without clinical ASCVD or diabetes with
LDL-C 70to 189mg/dL and estimated 10year ASCVD risk ≥7.5%
Secondary Prevention
(Including Patients with Type 2 Diabetes)
1. Aspirin
Use for all patients unless contraindicated
2. Statin
As mentioned above
3. Vitamins
No benefit shown, do not prescribe
* Caution should be exercised if BP is not controlled. Low-dose aspirin therapy should be considered only when BP is controlled, because the
risk of hemorrhagic stroke is increased in patients with uncontrolled
33 hypertension.
Table 13: Evidence-Based Antihypertensive Drug Treatment for Special
Situations/Populations with Target BP (47, 43,35)
Health Problem I
Disease
Target BP
Drugs to Use
Drugs to Avoid
African-American
<140/90
Calcium blocker; diuretic
β-Bs, ACEIs, ARBs
Angina
<130/85
β-Bs (A), non-Dihydropyridine-CCBs,
Long Acting DihydropyridineCCBs (B).
Short Acting
Dihydropyridine CCBs
(C).
Asthma / COPD
<140/90
Thiazide diuretics (B), Potassium sparing
Diuretics (B).
β-Bs (A).
Atrial Fibrillation
<140/90
β-B (B), ARBs, non-DihydropyridineCCBs (B).
NSR.
CHF
<130/85
ACEIs (A), Diuretics (A), ARBs (A),
Isosorbide Dinitrate with Hydralazine
(A), Dihydropyridine-CCBs (A).
Non-DihydropyridineCCBs (A).
Conduction Defects
<140/90
NSR.
β-Bs, DihydropyridineCCBs.
Depression
<140/90
NSR.
β-Bs, Reserpine.
DM
<140/85
ACEIs (A), Cardioselective β-Bs (A),
Low Dose-Diuretics (B), Long-Acting
High Dose-Diuretics.
Dihydropyridine-CCBs (B), lndapamide
(C), ARBs (C), α-Bs (C), Loop diuretic
(C).
Dyslipidemia
<140/90
Non selective BBlocker
Low Dose-Diuretics (B), ACEIs (B), βBs with Intrinsic Sympathomemtic
β-Bs without Intrinsic
Sympathomemtic
Activity (B), α-Bs (D), ARBs (D),
Dihydropyridine–CCBs (D).
Activity, High-dose
Diuretics.
Early Pregnancy
<140/90
α -methyl dopa
ARBS, ACEI
(throughout pregnancy)
Elderly
<150/90
Low Dose-Diuretics (A), Long-Acting
Dihydropyridine-CCBs (A), ACEIs (B),
ARBs (D).
High Dose-Diuretics.
Gout
<140/90
NSR.
Thiazide diuretics (D),
Loop diuretic.
Hyperthyroidism
<140/90
β-Bs.
NSR.
Liver Disease
<140/90
NSR.
Labetalol, Methyldopa.
LV Hypertrophy
<140/90
ACEIs, (Indapamide)
Hydralazine (C),
Minoxidil (C).
Metabolic
Syndrome
<140/90
ACE inhibitor; angiotensin receptor
blocker, long acting non-Dihydropyridine
group (2nd generation)
Diuretic; b-blocker
MI
<130/85
β-Bs without Intrinsic Sympathomemtic
Activity (A), ACEls (A), Amlodipine
Short Acting
Dihydropyridine-CCB
(C). verapamil and
Diltiagem in presence
of CCF
34
Migraine
<140/90
Non Cardioselective β-Bs, nonDihydropyridine-CCBs.
NSR.
NSAID Use
<140/90
Calcium blocker
ACEIs; ARBs
Osteoporosis
<140/90
Thiazide diuretics
NSR.
Premenopause,
Adequate
Contraception
<140/90
NSR.
NSR.
Premenopause,
Pregnancy risk
<140/90
α -methyl dopa, Labelatol,
ACEIs; ARBs
Preoperative
<140/90
β-Bs.
NSR.
Postmenopause
<140/90
NSR.
NSR.
ACEIs (A), lndepamide, Loop Diuretics,
non-Dihydropyridine-CCBs (B).
NSR.
CCBs (B), α-Bs (B).
β-Bs (B), ACEIs (B).
ACEIs (A), lndepamide, Loop Diuretics,
non-Dihydropyridine-CCBs (B). ARB
NSR.
Proteinuria >1gm/d
PVD
Renal Diseas+
Proteinuria
with urine albumin
levels of 30-300mg
per 24 hr or
>300mg per 24 hr
with urine albumin
levels of <30mg per
24 hr
<130/90
(47)
<140/90
<130/90
(47)
<130/80
KDIGO 2012
<140/90 JNC8 and
KDIGO 2012
Renal Diseas with
no Proteinuria
Smoking
<140/90
Thiazide diuretics, ACEIs.
β-Bs.
Stroke; Old
<140/90
ACEIs(A), Dihydropyridine-CCBs (A).
NSR.
Stroke; Recovery
<140/90
ACEIs, Calcium blocker
NSR.
Young Patient
<140/90
ACE inhibitor; b-blocker
NSR.
(A) Highly Recommended; (D) Least Recommended; NSR: No Specific Recommendations.
35
10. Subsequence Therapeutic Approaches to Achieve Control
a. Drugs Manipulation
There are three options when initial drug therapy stated (47)

Increase the dose

Add another Drug

Change drug
Every time one of the options is selected to achieve target BP (Figure 5-6). For the list
of available antihypertensive drugs, their doses and different characteristics refer to
Appendix 4, 5 and 6.
b. Recommended Duration and Criteria to Achieve Control
Duration of Titration of Antihypertensive Drug Therapy
Table 14: Recommended Duration for Follow-up of Patients on Antihypertensive
Drug Treatment to Achieve Control :
Monthly Interval If
2-3 Weeks Interval If
o BP: ≥160 or ≥100
o Diabetes / CRD
o Those with target-organ damage
(TOD)
o Those with Associated Clinical
Conditions (ACC)
o Symptomatic patients
o Intolerance of antihypertensive drugs
o Resistant HTN
o BP: <160 and <100
* The majority of drugs exert most of their effect within 2 weeks, and therapy can be titrated at 2–4 week intervals
depending on the severity of the hypertension. Hence , no point of daily or weekly measuring BP and such an attitude can
exacerbate the stress level associated with BP measurement and unnecessary increase it.
Criteria for Achievement of Control Stage if :

Two blood pressure readings

One month apart

Below their target BP
36
11. Resistant Hypertension (47)
a. Definition: Any Patients with failure to achieve target BP control despite life style
measures and drug regimen.

Drugs Number: Triple-drug or more anti hypertensive medications

Drugs Dosage: Near or at maximum doses

Drugs Type: One of these medications has to be a diuretic

Life style measures and drug regimen compliance: Good

Target BP: Cannot be reduced to target BP

Duration: ≥ 3 months
b. Evaluation for Resistant Hypertension and Secondary Hypertension (figure 8)
37
Figure 8: Considerations in the Evaluation of Resistant Hypertension and General Strategy
for Diagnosing a Secondary Cause of Hypertension (47)
Resistant Hypertension
Measurement
Lifestyle Factors
Treatment Factors
Cuff size
Excess sodium intake
Noncompliance
Technique
Obesity
Office (White Coat) HTN
Excess alcohol use
Pseudohypertension in the elderly
Cigarette smoking
Suboptimal therapy:
o Inadequate diuretic therapy
o Inadequate drug doses
o Selection of combination
Home or ambulatory measurements
Chronic pain and/or mental illness
therapy
Drug interactions
Intolerant adverse side effects of
drugs high doses
If BP remains resistant, consider secondary cause
o
o
o
o
o
o
o
o
Poor response to therapy
(Resistant HTN)
Worsening of control in
previously stable HTN patient
SBP > 180 or DBP >110
Onset of HTN in persons < 20
Significant TODs
Lack of family history of HTN
Initial clinical evaluation findings
that suggest a secondary cause
(Appendix 2)
Relative or absolute volume
expansion specially with
underlying lower insufficiency
Risk factors for secondary
hypertension present
(Table 7)?
No
Yes
Treat hypertension and
assess response
Screening results
suggest a specific
cause (Appendix 1,3)
Screening results do
not suggest a specific
cause.
Identify and treat
suspected cause and
assess response.
Consider
more
aggressive evaluation
for
secondary
hypertension
(Appendix 3)
 Adding potent vasodilator like
clonidine or hydralazine
 Increasing dose of d usually
loop diuretic
 Add spironalactore
38
Table 15: Strategies to Improve Patient Adherence
Assist your Patient to Adhere by:
o Tailoring pill taking to fit patients’ daily habits (Grade D);
o Simplifying medication regimens to once-daily dosing;
o Replacing two antihypertensive agents with a fixed-dose combination (when available and
appropriate), provided it is the same combination the patient is already taking (Grade D);
and
o Using unit-of-use packaging (of several medications to be taken together) (Grade D).
Assist Patients in Getting more Involved in their Treatment by:
o Encouraging greater patient responsibility and autonomy in monitoring their blood pressure
and adjusting their prescriptions (Grade C); and
o Educating patients and patients’ families about their disease or treatment regimens (Grade
C).
Improve your Management in the Office and Beyond by:
o Assessing adherence to pharmacological and nonpharmacological therapy at every visit
(Grade D);
o Encouraging adherence with therapy by out-of-office contact (either by telephone or mail),
particularly over the first three months of therapy (Grade D);
o Coordinating with work-site health care givers to improve monitoring of adherence with
pharmacological and lifestyle modification prescriptions (Grade D); and
o Using electronic medication compliance aids (Grade D).
Grading Scheme for Recommendations
Grade A: Recommendations are based on randomized trials (or systematic reviews of trials) with high levels of internal validity
and statistical precision, and for which the study results can be directly applied to patients because of similar clinical
characteristics and the clinical relevance of the study outcomes
Grade B: Recommendations are based on randomized trials, systematic reviews or prespecified subgroup analyses of randomized
trials that have lower precision, or there is a need to extrapolate from studies because of differing populations or
reporting of validated intermediate/surrogate outcomes rather than clinically important outcomes
Grade C: Recommendations from trials that have lower levels of internal validity and/or precision, or report unvalidated surrogate
outcomes, or results from nonrandomized observational studies
Grade D: Recommendations are based on expert opinion alone
39
12. Hypertension Consultation
Table 16: Suggested Indications for Specialist Referral (47)
Hypertension
Stage
Reasons
Urgent Treatment Needed:
 Accelerated (malignant) hypertension (severe hypertension with grade III–IV
retinopathy)
 Severe hypertension (e.g. ≥180/110 mm Hg)
 Impending complications (e.g., TIA, left ventricular failure)
Special Situations
 Unusual BP variability – Consider ABPM
 Possible isolated clinic hypertension – Consider ABPM
 Hypertension in pregnancy – Consider ABPM
 Evaluating hypertension with autonomic dysfunction – Consider ABPM
 Identifying nocturnal hypertension – Consider ABPM
Diagnostic
Stage
Possible Underlying Cause:
 Findings on history, physical examination, or laboratory testing that suggest a
secondary cause (Appendix 1-3).
 Poor response to therapy (resistant hypertension) repeated
 Worsening of control in previously stable hypertensive patient
 Rapid and severe course
 Sever hypertension (systolic blood pressure > 180 mm Hg or diastolic blood
pressure >110 mm Hg)
 Onset of hypertension in persons younger than age 20
Note: Renovascular HTN should be suspected in children or young women (fibromuscular dysplasia) or
old men (atherosclerotic disease).





Control
Stage
Significant hypertensive target organ damage
Lack of family history of hypertension
Hypokalemia/ increased plasma sodium and metabolic alkalosis (Conn’s
syndrome?)
Elevated serum creatinine
Proteinuria or hematuria
Therapeutic Problems:
 Treatment resistance (Resistant Hypertension) – Consider ABPM
 Multiple drug intolerance
 Multiple drug contraindications
 Persistent non-compliance – Consider ABPM
 Treatment declined (the reluctant hypertensive) – Consider ABPM
 Whose blood pressures are responding poorly to drug therapy – Consider ABPM
 Evaluation of symptomatic hypotension (with or without antihypertensive
medication) – Consider ABPM
 Informing equivocal treatment decisions – Consider ABPM
 Evaluation of efficacy of antihypertensive drugs in clinical research – Consider
ABPM
40
Part VI: Follow-up Stage (Hypertension Continuing Care)
13. Follow-up Criteria and Evaluation (47)
a. Duration: Once target blood pressure has been reached, patients should be seen at 3 to
6 month intervals (Appendix 7-8 )
b. Assessment: refer to Hypertension sheet (NCD form) (Appendix 8) for items to be
assessed at each visit. Serum potassium and creatinine should be monitored at least 1–
2 times/year
41
CHAPTER TWO
HYPERTENSION DURING RAMADAN AND HAJJ
1. Hypertension and Ramadan Fasting (1)
Some small-scale studies have looked at the effects of fasting on BP in hypertensive patients.
These studies observations and conclusions:

Beneficial effect of fasting on BP.

Statistically significant reduction differences in obese hypertensive women who fasted for
48 hours in both SBP and DBP.

Medically supervised, water-only fasting appears to be a safe and effective means of
normalizing BP.

(1)
(1)
Uncomplicated essential HTN patients, Ramadan fasting was well tolerated. The
variations of BP are minimal and are probably related to the changes in sleep, activity, and
eating patterns.

Treated hypertensive patients might be assured that, with continuation of prescribed
medications, fasting during Ramadan could be safely undertaken.
2. General Recommendations for Hypertensive Patients during Ramadan (1)
Based on the scarce available data, the following recommendations can be reasonably made
(expert opinion):

Physician's advice and management should be individualized.

Patient
education
should
emphasize
the need
to
maintain
compliance
with
nonpharmacological and pharmacological measures.

Diuretics are better avoided, especially in hot climates or to be administered in the early
evening.

Patients are encouraged to seek medical advice before fasting in order to adjust their
medications if needed.

A once daily dosage schedule with long acting preparations is recommended.

HTN patients should be advised to take a low salt, low fat diet.

Difficult to control HTN patients should be advised not to fast until their BP is reasonably
controlled.

Hypertensive emergencies should be treated appropriately regardless of fasting.
42
3. Hypertension and Hajj (Pilgrimage) (47)
Based on the scarce available data, the following recommendations can be reasonably made:

Hypertensive Pilgrims should have a medical check-up before they leave home for Hajj,
especially the elderly and those with other co-morbidities.

Severe HTN patients should be considered unfit for a long journey such as Hajj.

Once daily medication regimens are preferable.

Due to the hot climate in the Makkah region and the possibility of dehydration, diuretics
are better avoided (unless indicated for other reasons).

To keep the BP under control, patients should take their BP medications as directed.

Patients should check their BP regularly and try to reduce stress during the Hajj.
43
CHAPTER THREE
HYPERTENSION AND CO-MORBIDITIES
2. Hypertension and Chronic Renal Disease
7. Obese patients
Approximately 60% to 80% of diabetic patients will develop HTN. Strict control of BP in these
patients is as important as the control of blood sugar. Thiazide diuretics, ACEIs, ARBs, β-Bs
and CCBs have all been shown to be effective agents in diabetic patients to reduce
microvascular and macrovascular complications. ACEIs and ARBs are particularly effective
when there is diabetic nephropathy, as evidenced by microalbuminuria or proteinurea.

The goal BP is < 140/85 mm Hg in diabetic patients.

Start antihypertensive drug if SBP ≥ 140 mm Hg.

In a patient with no evidence of microvascular or macrovascular damage, there is no clear
benefit of one drug over the other.

In patients with microalbuminuria or proteinuria ACEIs or ARBs provide the best
renoprotection.
▪
It is recommended that individual drug choice take morbidities into account.
▪
Multiple drugs are often needed to achieve the target BP.
▪
Diabetes mellitus is an IHD equivalent & ASA should be added to all patients who are
above 50 years or who have additional risk factors (Family history of CVD,
Hypertension, smoking, dyslipidemia or albuminuria) NICE 2013
2. Hypertension and Chronic Renal Disease
44
Treatment of HTN can slow the progression of CRD.
In addition to sodium and fluid
restriction, all antihypertensive medications can be used to lower BP in CRD, and usually
multiple medications are required. Loop diuretics in an adequate dose help to control volume
overload. Some physicians are reluctant to administer ACEIs in spite of their proven efficacy in
preventing progression of CRD for the initial rise of serum creatinine. ACEIs are the preferred
medications, particularly with proteinuria, as they reduce proteinuria by 30 to 50%, prevent
progression of CRD, and reduce cardiovascular morbidity and mortality as evidenced by several
randomized controlled trials. But bilateral renal artery stenosis has to be ruled out.
Recommendations

A BP (< 140/90 mm Hg)
125/75 OR <130/80

(43)
(37, 43)
should be achieved in all patients with CRD and a BP <
and <130/90 mm Hg
(47)
in patients with proteinuria (> 1 gm/day).
Decrease proteinuria < 60% of the baseline with lowest achievable level is targeted,
preferably with ACEIs and/or ARBs.

Monitor renal function and potassium level within one week after initiation of therapy.

Titrate-up with small doses gradually to maximum dose level to achieve reduction in
proteinuria and control of BP.

If that is not achieved, additional therapy with diuretics or non-dihydropyridine CCBs
could be used.

Labetalol is the agent of choice for pregnant women with CRD.

Additionally, control of dyslipidemia, cessation of smoking, and moderate protein
restriction should be followed to decrease the rate of progression of CRD.
From 2012 KDIGO

(43)
Individualize BP targets and agents according to age, co-existent cardiovascular disease and
other co-morbidities, risk of progression of CKD, presence or absence of retinopathy (in
CKD patients with diabetes) and tolerance of treatment.(Not graded)

Inquire about postural dizziness and check for postural hypotension regularly when treating
CKD patients with BP-lowering drugs. (Not graded)

Encourage healthy lifestyle modification in patients with CKD to lower BP and improve
long-term cardiovascular and other outcomes:
Achieve or maintain a healthy weight (BMI 20 TO 25). (1D)
Lower salt intake to <90mmol (<2g) per day of sodium (corresponding to 5g of sodium
chloride), unless contraindicated. (1C)
45
Engage in a regular exercise program compatible with cardiovascular health and tolerance,
aiming for at least 30minutes 5 times per week. (1D)
Limit alcohol intake to no more than two standard drinks per day for men and no more than
one standard drink per day for women. (2D)

Non-diabetic adults with CKD ND and urine albumin excretion <30mg per 24 hours (or
equivalent*) whose office BP is consistently >140mmHg systolic or >90mmHg
diastolic be treated with BP-lowering drugs to maintain a BP that is consistently
≤140 mmHg systolic and ≤90 mmHg diastolic. (1B)

Non-diabetic adults with CKD ND and urine albumin excretion of 30 to 300mg per 24 hours
(or equivalent*) whose office BP is consistently >130mmHg systolic or >80mmHg
≤130 mmHg systolic and ≤80 mmHg diastolic. (2D)

Non-diabetic adults with CKD ND and urine albumin excretion of ≥ 300mg per 24 hours (or
≤130 mmHg systolic and ≤80 mmHg diastolic. (2C)

An ARB or ACE-I are to be used in non-diabetic adults with CKD ND and urine albumin
excretion of 30 to 300mg per 24 hours (or equivalent*) in whom treatment with BPlowering drugs is indicated. (2D)

An ARB or ACE-I are to be used in non-diabetic adults with CKD ND and urine albumin
excretion of > 300mg per 24 hours (or equivalent*) in whom treatment with BPlowering drugs is indicated. (1B)

Diabetic adults with CKD ND and urine albumin excretion <30mg per 24 hours (or
≤140 mmHg systolic and ≤90 mmHg diastolic. (1B)

Diabetic adults with CKD ND and urine albumin excretion >30mg per 24 hours (or
≤130 mmHg systolic and ≤80 mmHg diastolic. (2D)

An ARB or ACE-I are to be used in diabetic adults with CKD ND and urine albumin
excretion of 30 to 300mg per 24 hours (or equivalent*). (2D)

An ARB or ACE-I are to be used in diabetic adults with CKD ND and urine albumin
excretion of >300mg per 24 hours (or equivalent*). (1B)
46
Figure 9: Algorithm for Treating Patients with Diabetes or Kidney Disease to Goal BP(43 )
If BP >140/90 mmHg with albumin excr. Of <30mg in or in DM or ND with CKD
or if
BP>130/80mmHg with alb. Excr. 30-300mg in in DM or ND with CKD
Stage I
Stage
Start ARB or
ACE Inhibitor
titrate upwards
2
START with
ACEI or ARB/
thiazide diuretic*)
Recheck within 2–3 weeks
weeks
If BP Still Not at Goal
(140/90) or (130/80
mmHg)
Add CCB or b–
blocker** (titrate dose
upward)
Add Long Acting
Thiazide Diuretic*
Recheck within 2–3 weeks
weeks
If used CCB, Add Other Subgroup of
CCB
(i.e., amlodipine-like agent if verapamil
or diltiazem already being used and the
converse)
OR if β blocker used add CCB
Recheck within 4 weeks
weeks
Add Vasodilator (hydralazine,
minoxidil) OR Refer to a Clinical
Hypertension Specialist
†This figure represents an integration of the National Kidney Foundation-BP, JNC-8 and American Diabetes Association guidelines.
*Thiazide diuretic should only be used if eGFR < 50 mL/min otherwise loop diuretic should be substituted. Refers to thiazide-type
diuretics, specifically chlorthalidone as this is the agent used in the majority of outcome trials showing benefit of diuretics.
**The preferred b-blocker is carredilol since it has a neutral metabolic profile compared to other agents in the class.
47
Table 17 : NKF-K/DOQI* Guidelines on Blood Pressure Management and Use of Antihypertensive
Agents in Chronic Kidney Disease (43)
Type of Kidney Disease
Diabetic kidney disease
Non-diabetic kidney disease with
proteinuria (≥200 mg/g)
Non-diabetic kidney disease without
proteinuria (<200 mg/g)
Disease in the kidney transplant
Blood
Pressure
Target
(mmHg)
<140/90
<130/80
<140/90
<130/80
Recommended
Agents for CKD,
with or without
Hypertension
ACEIs or ARB
ACEI
No preference
No preference
Other Agents to Reduce CVD
Risk and Reach Blood
Pressure Target
Diuretics preferred, then BB or
CCB
Diuretics preferred, then BB or
CCB
Diuretics preferred, then ACEI,
ARB, BB, or CCB
CCB, Diuretic, BB, ACEI,
ARB
*NKF-K/DOQI: The National Kidney Foundation Kidney Disease Outcomes Quality Initiative
The risk of recurrent cardiovascular events in patients with CHD has a direct relationship to BP
level, but excessive and rapid lowering of BP should be avoided especially if associated with
reflex tachycardia.
a) Hypertension and Angina: Recommendations for Hypertensive Patients with Coronary
Artery Disease

First choice: β-Bs.

Second choice: Long-acting CCBs.
1. An ACE inhibitor is recommended for patients with hypertension and documented coronary
artery disease.
2. For patients with stable angina, beta-blockers are preferred as initial therapy. CCBs may
also be used.
3. Short-acting nifedipine should not be used.
4. For patients with coronary artery disease, but without coexisting systolic heart failure, the
combination of an ACE inhibitor and ARB is not recommended.
5. In high-risk patients, when combination therapy is being used, choices should be
individualized. The combination of an ACE inhibitor and a dihydropyridine CCB is
preferable to an ACE inhibitor and a thiazide/thiazide-like diuretic in selected patients.
48
6. When lowering SBP to target levels in patients with established CAD (especially if isolated
systolic hypertension is present), be cautious when the diastolic blood pressure is ≤60
mmHg because of concerns that myocardial ischemia may be exacerbated. (22)
c) HTN and Recent MI:
Recommendations for Patients with Hypertension Who Have Had a Recent STelevation Myocardial Infarction or Non-ST Segment Elevation Myocardial Infarction
o β-Bs preferably without intrinsic sympathomimetic activity and/or ACEIs.
o Diltiazem or Verapamil could be used if β-Bs are contraindicated especially in non
STEMI and normal LV systolic function.
o There is a trend towards using ACEIs or ARBs in all patients with CHD even
without HTN and normal LV systolic function.
o ACEI and ARB are strongly recommended in all patients wither acute myocardial
infarction unless contraindicated due to their great benefit on mortality.
o Extreme caution to be experienced while using non-Dihydropyridine group in the
setting of STEMI especially with evidence of heart failure.
o Initial therapy should include both a beta-blocker and an ACE inhibitor. An ARB can
be used if the patient is intolerant of an ACE inhibitor.
o CCBs (mainly Diltiazem or Verapamil) may be used in postmyocardial infarction
patients when beta-blockers are contraindicated or not effective. Nondihydropyridine
CCBs should not be used when there is heart failure. (22)
In hypertensive patients, elevated total cholesterol and LDL-C are major risk factors for
cardiovascular events. Lifestyle modification is the first approach for management of HTN and
dyslipidemia.
In hypertensive patients, the presence of any of the following factors is an indication for
lowering LDL-C

Men over 45 years

Women over 55 years

Positive family history of premature cardiovascular disease

Smoking

HDL-C < 40 mg/dl (<1 mmol/l)
Hypertensive patients with history of CHD or DM irrespective of the presence or absence of
other risk factors should have their LDL-C level reduced.
49
This last recommendation is based on the finding that these patients have a risk of MI 20 times
more than those without CHD.
Effect of antihypertensive medications on lipid profile:

Neutral effects: ACEIs, ARBs, CCBs and Central Adrenergic Agonists

Beneficial effects: α- Blockers.

Transient adverse effect: Hydrochlorothiazide or β-Bs especially in large doses.
The choice of antihypertensive therapy should not be significantly affected by consideration of
patient’s lipid profile as the beneficial effects of these drugs outweigh their minimal transient
adverse effects.
Hypertension and dyslipidemia
-
There is a beneficial effect from statin administration to hypertensive patients without previous
CV events (targeting a low-density lipoprotein cholesterol value <3.0mmol/L;(115mg/dL)
(JUPITER) study(47). This justifies use of statins in hypertensive patients who have a high CV
risk.
-
When overt CHD is present , there is clear evidence that statins should be administered to
achieve low-density lipoprotein cholesterol levels<1.8mmol/L (70mg/dL) (47).Beneficial effects
of statin therapy have also been shown in patients with a previous stroke, with low-density
lipoprotein targets definitely lower than 3.5mmol/L(135mg/dL) (47).
Congestive Heart Failure is five times more common in hypertensive patients as compared to
normotensive persons. LV dysfunction is related to the level of BP even in the normal range.
a) Treatment of Choice:

ACEIs and diuretics

Combined α- and β-Bs (Carvedilol), and β-Bs (Metoprolol or Bisoprolol) have been
proved to be useful in the whole spectrum of LV systolic dysfunction
b) Alternative Treatment:

Isosorbid dinitrate + Hydralzine: if ACEIs are contraindicated on top of a beta blocker
to avoid reflex tachycardia or (Emdure)

ARBs are alternatives to ACEIs if not tolerated especially in elderly

Aldosterone antagonists are useful in severe CHF
50

Long-acting dihydropyredin CCBs may be added to control hypertension
Reduction of BP in hypertensive patients is effective in primary and secondary prevention of
stroke.
Treatment of HTN in the acute stroke settings:
a) In Acute Ischemic Stroke:
There is a general agreement that these patients don’t need fast aggressive lowering of BP.
Reduction of the blood pressure by approximately 15 percent, and not more that 25%,
over the first 24h with gradual reduction thereafter (22)
Early use of antihypertensive medications is warranted when:
▪
DBP is more than 110 mm Hg
▪
SBP more than 180 mm Hg (22)
SBP should be < 180 and DBP should be < 100 if thrombolytic therapy is to be initiated.
The best agent to be used is labetalol starting with a bolus of 10 mg over 1-2 min.
followed by an infusion of 2-8 mg/min. till the desired BP is achieved.
▪
BP should be lowered if Hypertensive encephalopathy is suspected.
▪
The use of sublingual BP lowering agent nefidipine is contraindicated.

The results of a small trial called Controlling Hypertension and Hypertension
Immediately Post-Stroke (CHHIPS) suggested a beneficial impact in administering
lisinopril or atenolol in patients with acute stroke and a systolic BP >160 mmHg(47) .
The same was the case for the Acute Candesartan Cliexetil Therapy in Stroke
Survival (ACCESS) study
(47)
, which suggested benefits of Candesartan given for 7
days after acute stroke. There is a recent review that gives a useful update of this
area (47).
Blood Pressure Management after Acute Stroke
☒ Strong consideration should be given to the initiation of antihypertensive therapy after the
acute phase of a stroke or transient ischemic attack.
☒ Following the acute phase of a stroke, blood pressure lowering treatment is recommended to
a target of consistently lower than 140/90 mmHg.
☒ Treatment with an ACE inhibitor/diuretic combination is preferred.
51
☒ For patients with stroke, the combination of an ACE inhibitor and ARB is not
recommended (22).
7. Obese Patients
Obesity is a risk factor for HTN and other cardiovascular diseases. As Body Mass Index (BMI)
increases, so does the risk of HTN. It is important to assess BMI and waist circumference in
each individual. Using BMI, patients can be classified as normal weight (BMI 18.5-24.9 kg/m2),
overweight (25-29.9 kg/m2) or obese (≥ 30kg/m2). For those obese patients a weight
management plan should be constructed and discussed with the patient. Options available
include lifestyle modification (including behavior therapy), pharmacotherapy, and bariatric
surgery.
At a 5% weight loss, a weighted mean reduction in systolic and diastolic BP of approximately 3
and 2 mm Hg, respectively, is observed. At >5% weight loss, there are more modest and more
variable reductions in BP. (39)
Recommendation:

Lifestyle changes particularly weight loss and physical exercise is to be recommended to all
individuals with the metabolic syndrome (IB).

As metabolic syndrome can be considered a pre-diabetic state, antihypertensive agents
potentially improving or at least not worsening insulin sensitivity, such as RAS blockers and
CCB, should be considered as the preferred drugs (IIaC).
Table 18: Definitions of the Cardiometabolic Syndrome
WHO
NCEP
Hyperinsulinemia (upper quartile fasting INS of the nondiabetic
population) or FPG ≥110 mg/dL (6.1 mmol/L) or 2 h postglucose load
of >200 mg/dL (11.1 mmol/L) plus at least two of the following:
(1) Abdominal obesity: waist-to-hip ratio >0.9, BMI ≥30 kg/m 2, or a
waist girth ≥94 cm (37 in.)
(2) Dyslipidemia: serum TG ≥150 mg/dL (1.7 mmol/L) or HDL-C
<35 mg/dL (0.9 mmol/L)
(3) Hypertension: ≥140/90 mmHg or on medications
(4) Microalbuminuria: urinary albuminexcretion rate >20 mg/min or
albumin to creatinine ratio >30 mg/g
At least three of the following:
(1) FPG ≥110 mg/dL(6.1 mmol/L)
(2) Abdominal obesity: waist girth in men >102 cm and
in women >88 cm
(3) Serum TG >150 mg/dL (1.7 mmol/L)
(4) HDL-C: in men <40 m/dL (1 mmol/L) in women <50
mg/dL (1.3 mmol/L)
(5) Blood pressure ≥130/85 mmHg or on medications
52
The blood pressure frequently rises after kidney transplantation, as hypertension develops in up
to 60 to 80 percent of renal allograft recipients (although the incidence varies in different
populations).(43)
Elevated blood pressure and pulse pressure can result in decreased allograft survival and left
ventricular hypertrophy, with the latter being an independent risk factor for heart failure and
death in the general population and renal transplant recipients.

Risk Factors
The following risk factors have been associated with a higher incidence of post transplant
hypertension (43).
 Delayed and /or chronic allograft dysfunction
 Deceased donor allograft, especially from a donor with a family history of hypertension
 Presence of native kidneys
 Cyclosporine, tacrolimus, and /or corticosteroid therapy
 Increased body weight
 Renal artery stenosis

Treatment
Initially acute rejection has to be excluded as possible cause for the elevated blood pressure.
A potential casus is the remained functioning Arteriovenous shunts that were not closed post
transplant.
It also assumed that the corticosteroid dose is being reduced to a low
maintenance level both to reduce the blood pressure and to minimize other metabolic
complications which might have adverse cardiovascular effects, such as glucose intolerance
and hyperlipidemia.
 Patient is taking a calcineurin-inhibitor – an attempt should be made to reduce the
calcineurin inhibitor dose in hypertensive patients receiving one of those agents. If the
patient remains hypertensive, therapy with a calcium channel blocker (taking into
53
account the drug interactions noted above) or a diuretic (with concurrent salt restriction)
should be begun.
 Calcium channel blocker – Many physicians prefer a calcium channel blocker
(63)
because, in addition to proven antihypertensive efficacy, it minimize cyclosporineinduced renal vasoconstriction.
 Patient is not taking a calcineurin inhibitor – Hypertensive patients not taking
cyclosporine/tacrolimus should be started on antihypertensive medications. Calcium
channel blockers, ACE inhibitors, and beta-blockers all may be effective in this setting.
A diuretic may also be necessary in patients with allograft dysfunction in whom volume
expansion often contributes to the rise in blood pressure.
54
CHAPTER FOUR
HYPERTENSION IN SPECIAL POPULATIONS
1. Hypertension in Children
2. Hypertension in Women
3. Hypertension in the Elderly
4. Minority populations
1. Hypertension in Children (1)

Hypertension in children is defined: as average SBP and/or DBP that is greater than or
equal to the 95th percentile for sex, age, and height on three or more occasions.

Pre-hypertension in children is defined: as average SBP or DBP levels that are greater
than or equal to the 90th percentile, but less than the 95th percentile. As with adults,
adolescents with BP levels greater than or equal to 120/80 mmHg should be considered
pre-hypertensive.

Elevated BP must be confirmed on repeated visits before characterizing a child as
having hypertension.

BP increases gradually with age and height, therefore, standard nomograms are
necessary for interpretation of BP in children. Most children track in a constant
percentile around the mean. (See percentiles charts Appendix III not provided in this
document, should be added, I prefer the tables). Secondary HTN is more common in
younger children while essential HTN is more common in older children and
adolescents.
55
Table 19: classification of hypertension in children and adolescents
Most hypertensive patients are asymptomatic or have non-specific symptoms; measurement of
BP with appropriate cuff should be part of the routine pediatric clinical evaluation of children
over the age of 3 years. Children under age 3 should have their BP measured in special
circumstances.
The primary investigation for hypertensive children should include: CBC, urinalysis, urine
culture, blood urea nitrogen, creatinine, electrolytes, lipid profile, ECG, chest X-ray,
echocardiogram, as well as renal ultrasound and Doppler study.
Treatment should be guided by the following:

Transient or persistent HTN.

Cure of the secondary causes might cure or eliminate HTN.

Non-pharmacological measures should be tried.

Selection of the antihypertensive agent should take into consideration the possible
pathophysiology.
56

In children, dose adjustment of antihypertensive drugs is imperative.

Severe HTN (BP > 99th percentile for age, gender, and height) or malignant HTN
(marked HTN with retinal hemorrhage, exudate, papilledema, seizure with or without
renal involvement) should be treated immediately and the treatment should go hand in
hand with the investigations.
In general, hypertensive children should be referred to a specialized pediatrician.
57
58
Table 20: Blood pressure levels for boys by age and height percentile
59
60
Table 21: Blood pressure levels for girls by age and height percentile
61
2.Hypertension in Women
A subgroup analysis by sex of 31 RCTs found similar BP reductions for men and women
and no evidence that the two genders differ in their response to treatment. However, in
women with child-bearing potential, ACE inhibitors, angiotensin receptor blockers and
renin inhibitors should be avoided, due to possible teratogenic effects.(47)
a) Pregnancy: (please refer to the national guidelines)
There are four types of HTN in pregnancy:

Pre-existing HTN: Diagnosed before pregnancy or before the 20th week of gestation
and persists post-delivery.

Gestational HTN: HTN occurs for the first time in the second half of pregnancy
without proteinuria and normalizes by 12 weeks post-partum.

Pre-eclampsia:
the onset of hypertension and proteinuria after 20 weeks of
gestation in previously normotensive non-proteinuric pregnant women.

Eclampsia: is the occurrence of convulsion in a preeclapmptic patient

Pre-eclampsia superimposed on chronic HTN.
Management:
ACE inhibitors, ARBs, renin inhibitors should absolutely be avoided in pregnant
women.
Preexisting hypertension:
Refer within the same week to obstetric clinic after switching her medicine to
Aldomet.
Gestational hypertension: (high blood pressure and asymptomatic patient)
Refer patient to the admission room in the same day as a walk in patient.
Mild pre-eclampsia: refer to the admission room by ambulance.
Severe preeclampsia:
-
Stabilize the patient
-
Call 999
-
Start treatment as per antenatal guideline.
62
Eclampsia:
-
Stabilize the patient, check blood glucose level & administer oxygen.
-
Call 999
-
Start treatment as per antenatal guideline
b) Women using Hormone Replacement Therapy
Hormone replacement therapy has the potential to worsen BP in hypertensive women. It
should be withheld in women with resistant HTN in order to assess its contribution to the
increase in BP. It is advisable to monitor BP two to three times in the first six months after
starting hormone replacement therapy, then twice a year thereafter. Recent
recommendations advise against the use of hormone replacement therapy for
cardiovascular protection in menopausal females.
3. Hypertension in the Elderly
The definition of HTN in the general adult population applies to the elderly (Age > 65 years).
Among older persons, elevation in SBP or increase pulse-pressure is a better predictor of
cardiovascular morbidity and mortality than elevated DBP. Primary HTN is by far the most
common form of HTN in older persons. However, in the case of clinical suspicion (or when the
onset of HTN occurs at old age) a secondary cause should be sought. Renal parenchymal
disease is the most common secondary cause to be considered, followed by renal artery stenosis.
The later is suspected in any patient with resistant HTN and known atherosclerosis in other
arteries. Many randomized trials of antihypertensive treatment in the elderly (including one in
hypertensive patients aged 80 years or more) showed reduction in CV events through lowering
of BP (47).
The goal of treatment in older patients with no co-morbidity is 150/90 mmHg. However, at least
in elderly individuals younger than 80 years, antihypertensive treatment may be considered at
SBP values >140mmHg and aimed at values <140 mmHg, if the individuals are fit and
treatment is well tolerated.(47 )
RCTs that have shown beneficial effects of antihypertensive treatment in the elderly have used
different classes of compounds and so there is evidence in favour of diuretics, beta-blockers
calcium antagonists, ACE inhibitors, and angiotensin receptor blockers. The three trials on
isolated systolic hypertension used a diuretic or a calcium antagonist. A prospective metaanalysis compared the benefits of different antihypertensive regimens in patients younger or
63
older than 65 years and confirmed that there is no evidence that different classes are differently
effective in the younger vs. the older patient. (47)
Special notes:

Pseudo hypertension can be suspected if BP readily remains high despite absence of
target organ damage.

Pseudo-HTN, orthostatic hypotension even without treatment, or white coat HTN
especially among elderly women is more common than in the young patient.

Sodium reduction is especially effective in the elderly because of their greater sensitivity
to sodium intake.

The starting dose of medications in older patients should be about half of that used in
younger patients: “Start low and go slow”.

Medications with once daily dosage are preferred for better compliance and in order to
keep the drug regimen as simple as possible.

Low-dose thiazide therapy (12.5 - 25 mg of hydrochlorothiazide or equivalent) can be
prescribed as the first-line treatment of HTN.

Long acting CCBs are second choice

ß-Bs are less appropriate as first line therapy for HTN in the elderly.

Drugs that exaggerate postural hypotension (α-Bs, high dose diuretics) or drugs that can
cause cognitive dysfunction (central α -2 agonists) should be used with great caution.

Presence of other co-morbidities dictates the choice of the first line drugs.
4. Minority Populations
Socio-economic factors and lifestyle may influence BP control in some minority patients.
However, there are no studies published that address BP control in these populations in Bahrain
and Saudi Arabia. American studies have indicated that prevalence, severity, and impact of
HTN are increased in Blacks, who also demonstrate somewhat reduced BP responses to
monotherapy with β-Bs, ACEIs, or ARBs compared with diuretics or CCBs. Three major
clinical trials suggest that CCBs are most effective in Black people. South-East Asian patients
tend to consume large amount of sodium monoglutamate salt that may interfere with BP
control.
64
CHAPTER FIVE
HYPERTENSIVE CRISES
1. Hypertensive Urgencies
2. Hypertensive Emergencies

Definitions (Table 22)

End-Organ Damage Seen in Hypertensive Emergencies ( Table 23)

Recommended approach and treatment (Figure 10)

Acute reductions in BP duration and Target BP (Table22, Figure 10)
Table 22: Definition and Acute Reductions in BP Duration and Target BP for Hypertensive
Crises (53,47)
Hypertensive Urgencies
Hypertensive Emergencies
Critically elevated BP (SBP≥180, and/or DBP≥110 mm Hg) (47)
BP
Evidence of acute TOD or one of the
following conditions:
pheochromocytoma, vasculitis and
clonidine withdrawal, head trauma and
life threatening arterial bleeding, etc.
Definition
Acute
TOD
Acute Reductions
in BP Duration
and Target BP
Absent
Since lack of evidence of its
effectiveness (36-38):
It does not require:
 Immediate BP lowering
 Parenteral agents
Requires:
 Immediate hospitalization
 Acute reductions in BP
 Parenteral agents
If oral agents used (Table):
 Aim: Avoid overly
aggressive initial
reductions in blood
pressure
If parenteral agents used (Table):
 Aim: Lowered rapidly but in a
controlled fashion to avoid and limit
the risk of serious complications and
to avoid sudden drop of BP and
reduction of perfusion to vital
organs (brain, heart).

Duration: gradually
within 24 hours

Duration: Lowered rapidly within
15-30 minutes

Target BP: 160/100
mmHg

Target BP: Reduction of MBP by
25%, aim DBP 100-110, SBP 160
mm Hg
65

Follow-up within 48–72 h.
Table 23: End-Organ Damage Seen in Hypertensive Emergencies
Organ System
Pathophysiology
Neurologic


Hypertensive encephalopathy
Stroke/intracranial hemorrhage
Cardiac


Acute myocardial infarction
Acute left ventricular failure with pulmonary edema
Vascular


Acute aortic dissection
Other vascular dissection, arteritis / thrombosis
Endocrine/obstetrical

Eclampsia
Renal

Acute renal failure
66
Figure (10): Approach to Hypertensive Crises ( 53,47)
Hypertensive Crises
Hypertensive Emergencies
Hypertensive Urgencies
Uncomplicated Severe
Hypertension
Critically elevated BP (SBP ≥180
and/or DBP ≥110 mm Hg) + No
Acute TOD
Acute reductions in
BP


Complicated Severe
Hypertension
Critically elevated BP (SBP ≥180
and/or DBP ≥110 mm Hg) + Acute
TOD
Requires:
 Immediate hospitalization
 Acute reductions in BP
 Parenteral drug therapy
Long-term followup treatment


Not recommended:
Parenteral drug therapy
Oral drug therapy:
o No evidence of long term
benefit
o Unacceptably high failure rates
o High side effect
o Ultimately require close
monitoring for the rest of their
lives
o Monotherapy is not first line
treatment


67
Focus on long term tratment
Adjust oral treatment regime with
comination therapy that includes
diuretics
Carefully evaluated and monitored
for hypertension-induced heart and
kidney damage and for identifiable
causes of hypertension. (See
Appendix )
Folloup within 48-72 hours
Table 24: Preferred Agents Used for the Acute Treatment of Hypertensive Urgencies
Drug
Dose/Route
Onset of
Action
Angiotensin-Converting Enzyme Inhibitors
Starting dose 12.5–
15 min–1 h
Captopril
12.5 mg; 25 mg; 50
25 mg
mg; 100 mg
P.O., repeat as
tablets
needed; once
effect obtained
give three times
daily (may be
administered
sublingually; no
clear benefit
of this route)
Adrenergic Blockers
Initial 0.1–0.2 mg
30–60 min
Clonidine
0.1 mg; 0.2 mg
P.O., repeat
tablets
hourly, maximum
total dose
0.6 mg
Initial 200–400 mg
30–60 min
Labetalol
100 mg; 200 mg;
P.O.,
300 mg tablets
repeat 2–3 h
Duration of
Action
Side Effects
Cautions
Rash, hypotension,
dizziness,
hyperkalemia,
worsening
of renal function,
hypersensitivity
reaction,
cough
Case reports of Stevens–
Johnson’s
syndrome in association
with allopurinol
Use at lower dose and 12 h
intervals in patients with
renal impairment
Use with caution in patients
at risk for hyperkalemia or
in association with
potassium sparing diuretics
4–8 h
Dry mouth,
drowsiness,
rebound
hypertension
Clonidine should not be
abruptly discontinued as
significant rebound
hypertension may occur
2–12 h
Dizziness, nausea,
edema,
hypotension,
bradycardia,
fatigue,
paresthesias,
transaminitis,
mental
depression
Use with caution in patients
with asthma, bronchospastic
disease, or congestive heart
failure
6–8 h, but
dose-related
68
Table 25: Recommended Antihypertensive Drugs for Hypertensive Emergencies
Clinical Condition
Acute Pulmonary
Edema
Acute Myocardial
Ischemia
Hypertensive
Encephalopathy
Acute Aortic
Dissection
Eclampsia
Acute Renal Failure
Microangiopathic
Hemolytic Anemia
Pheochromocytoma
Clonidine
withdrawal
Preferred Initial
Treatment
Nitroglycerine
Furosemide 40 mg
I.V.
Dosages of I.V. Antihypertensive
Medications
Enalaprilat; I.V.; 1.25 mg over 5 min
every 6 h, titrated by increments of 1.25
mg at 12-24 h intervals to a maximum of 5
mg every 6 h.
Nitroglycerine 5 mg sublingual,
Labetalol or Esmolol
in combination with
Nitroglycerin. Nitroprusside
Nicardipine may be
added if pressure is
controlled poorly with
Labetalol/Esmolol alone.
Esmolol; Loading dose of 500 mg/kg over
1 min, followed by an infusion at 25 to 50
mg/kg/min, which may be increased by 25
mg/kg/min every 10 to 20 min until the
desired response to a maximum of 300
mg/kg/min.
Labetalol or
Nicardipine
Fenoldopam; initial dose of 0.1
mg/kg/min, titrated by increments of 0.05
to 0.1 mg/kg/min to a maximum of 1.6
mg/kg/min.
Labetalol or
combination of
Nitroprusside and
Esmolol.
Verapamil or diltiazem are
alternatives in patients who can
not tolerate beta blockers.
Hydralazine
(traditional). In the
ICU, Labetalol or
Nicardipine is preferred.
Hydralazine; may be administered in
doses of 10 to 20 mg.
Labetalol; Initial bolus 20 mg, followed by
boluses of 20 to 80 mg or an infusion
starting at 2 mg/min; maximum cumulative
dose of 300 mg over 24 h.
Nicardipine; 5 mg/h; titrate to effect by
increasing 2.5 mg/h every 5 min to a
maximum of 15 mg/h.
Nitroglycerin (up to 200 μg /min)
Nicardipine or
Fenoldopam
Nitroprusside; 0.5 mg/kg/min; titrate as
tolerated to maximum of 2 mg/kg/min.
Nicardipine or
Fenoldopam
Phentolamine; 1-5 mg blouses; maximum
dose, 15 mg.
Phentolamine I.V.
followed by oral
Phenoxybenzamine
Oral Cloindine (0.1
mg every 20 min)
IV slowly Clonidine 0.1 mg
69
Trimethaphan; 0.5 to 1 mg/min; titrate by
increasing by 0.5 mg/min as tolerated;
maximum dose, 15 mg/min.
CHAPTER SIX
THE ROLE OF NURSES AND NURSE PRACTITIONERS IN HYPERTENSION
MANAGEMENT(57)
1. Detection, referral, and follow-up
2. Medication management
3. Patient education, counseling, and skill building (Table 25)
a. Identify patient knowledge, attitudes, beliefs, and experiences
b. Educate the patient about conditions and treatment
c. Individualize the treatment regimen
d. Provider reinforcement
e. Promote social support
f. Collaborate with other professionals
4. Coordination of care
5. Management of clinic or office
Table 26: Strategies to Promote Blood Pressure Control (53)
Identify Knowledge, Attitudes, Beliefs, and
Experience
o Assess patient’s understanding and
acceptance of the diagnosis and
expectations of being in care
o Discuss patient’s concerns, and clarify
misunderstandings
Educate about Conditions and Treatment
o Inform patient of blood pressure level
o Agree with patients on a target blood
pressure
o Inform patient about recommended
treatment, providing specific oral and
written information
o Elicit concerns and questions and provide
opportunities for patient to state specific
behaviors to carry out treatment
recommendations
o Emphasize need to continue treatment,
that patient cannot tell if blood pressure is
elevated, and that control does not mean
cure
o Teach self-monitoring skills
70
Provide Reinforcement
o Provide feedback regarding blood
pressure level
o Ask about behaviors to achieve
blood pressure control
o Give positive feedback for
behavioral and blood pressure
improvement
o Hold exit interviews to clarify
regimen
o Make appointment for next visit
before patient leaves the office
o Use appointment reminders, and
contact patients to confirm
appointments
o Schedule more frequent visits to
counsel patients who do not
adhere to program
o Contact and follow-up patients
who missed appointments
o Consider clinician-patient
contracts
o Consider home visits
o
o
o
o
o
o
o
o
o
o
o
o
Individualize the Regimen
Include patient in decision-making
Simplify the regimen
Incorporate treatment into patient’s daily
lifestyle
Set (with the patient) realistic short-term
objectives for specific components of the
treatment plan
Encourage discussion of side effects and
concerns
Encourage self-monitoring of blood
pressure
Prioritize critical aspects of the regimen
Implement treatment plan in steps
Modify dosages or change medications to
reduce side effects
Minimize cost of therapy
Indicate that you will ask about adherence
at next visit
When weight loss is established as a
treatment goal, discourage quick weightloss regimens, fasting, or unscientific
methods because these methods are
associated with weight cycling, which
may increase cardiovascular morbidity
and mortality
71
Promote Social Support
o Educate family members to be
part of the blood pressure control
process and to provide daily
reinforcement
o Suggest small group activities to
enhance mutual support and
motivation
Collaborate with other Professionals
o Draw upon complementary skills
and knowledge of nurses,
pharmacists, dietitians,
optometrists, dentists, and
physician assistants
o Recognize shared practice goals
o Refer patients for more intensive
counseling
72
Appendix 1
Initial History, Physical Exam, and Basic Investigation (47)
History
Hypertension*
Physical Exam.
Basic Investigation
1. CHD Risk Factor
Patients hypertensive
BP measurement
Rx Hx: (Onset,
(establish or verify
Duration, Current Rx,
diagnosis) and repeat
controlled?, SE)
measurement to
confirm diagnosis)
Diabetes mellitus*
FBS
HbA1C ( if fasting
plasma glucose > 5.6
mmol/l , or previous
diagnosis of DM)**
Modifiable
(M)
Microalbuminuria or
estimated GFR
<60ml/m
Dyslipidemia*
Smoking
F.LIPIDS
+
Obesity* (body mass
index ≥30 kg/m2)
BMI
Non-Modifiable (NM)
(Waist
circumference)
measured in the
standing position, at a
level midway
between the lower
border of the costal
margin (the lowest
rib) and upper most
border of the iliac
crest.ESH/ESC
Absolute
Age
 Men >55
 Women >65
+
Sex
Men
Postmenopausal
women
+
Family history of
premature
cardiovascular disease/
death:
 Women < 65
 Men <55
+
HB (CBC), Uric acid


Relative (Contributory HTN Factors)
(M)
Sedentary lifestyle
(±Absolute Risk
+
73
Factor-JNC VII)
Diet
+
Alcohol (43 units/day)
+
High stress (type A)
+
High risk
socioeconomic group
+
High risk ethnic group
+
(NM)
High risk geographic
region
Psychosocial , environmental and
personal factors
+
+
2. TOD & ACC
+
CNS
Neurological deficits
on exam
Fundoscopy :
Arteriolar narrowing,
AV nicking,
papilloedema,
hemorrhages or
exudates in the fundi
+
EYE
+
Cardiomegaly,
Odema, JVP, Apex
beat, Basal
crepitation, Murmurs,
gallops or arrythmias
and auscultation of
carotid arteries
+
and auscultation of
renal arteries
Urine R/M ,U / E /Cr
+
All pulses , Carotid
bruits or diminished
upstroke,
Tachycardia
Duplex
4s
angiography
CVS
RENAL
PVD
3. Secondary Causes
Abdominal mass or
+
palpable kidney
Renal Disease
Endocrine
Pheochromocytoma
+
Conn’s syndrome
+
Cushing's
Ch. Steroid therapy
+
Sleep apnea
+
ECG
(Echo, holter
monitoring in case of
arrhythmias , carotid
US, peripheral
artery/abdominal US,
pulse wave velocity,
ankle brachial index)**
Urine R/M ,U/E/C
K+: Hypokalaemia
General appearance,
Skin (Cushingoid
appearance)
+
Thyroid or
parathyroid disease
Vascular
Coarctation of aorta
Visual acuity, IOP
Neck exam:
Thyromegaly or
thyroid nodules
 Abdominal or loin
bruit
 Radial/femoral
+
74
TSH
PTH, Ca++, Poa‫־־‬
 CT/MRI
 Renal angiograms
 Duplex 4s renal
pulse delay or
weak femoral
pulses
 Unequal blood
pressures in arms
(more than 10
mmHg)
Drugs
NSAID, Coccaine, decongestants
anorectic, oral, adrenal steroid,
cyclosporine, Erythropoietin,
licorice, chewing tobacco.
Dietary supplely e.g ephedrine,
bitter orang
Pregnancy
+
+
4- Other co-Morbid Disease (Drug Contraindications- Appendix 5)
Prostate
+
Impotence
+
Bronchial asthma ect…
+
P/R
* Components of the metabolic syndrome
75
artery
76
77
Appendix 2
Risk Stratification & Assessment
Major Risk Factors for CVD, TODs and ACCs
It is important to integration of BP, cardiovascular (CV) risk factors, asymptomatic organ damage
(OD) and clinical complications for total CV risk assessment.
Risk Factors For CVD
Major absolute risk factors used for
risk stratification:
 HTN
 Age > 60 yrs
 Sex
 Men
 Postmenopausal women
 Smoking
 Diabetes mellitus
 Dyslipidemia
 Family history of premature CVD
 Women younger < 65
 Men younger < 55
Target Organ Damage (TOD)
CVS:
 LVH
Renal:
 Proteinuria and/or slight
elevation of plasma Creatinine
:106 - 177 mmol/L
Peripheral vascular Disease:
 Ultrasound or radiological
evidence of atherosclerotic
plaque (carotid, iliac and
femoral arteries, aorta)
Eye:

Narrowing of the retinal
arteries
Risk stratification summery:
 Stage of BP:
 Number of risk factors:
 Presence or absent of TOD:
 Presence or absent of ACC:
 Presence or absent of DM:
Associated Clinical Conditions (ACC)
Cerebrovascular disease
 Ischemic stroke
 Cerebral hemorrhage
 Transient ischemic attack
Heart disease
 Myocardial infarction
 Angina pectoris
 Coronary revascularization
 Congestive heart failure
Renal disease
 Diabetic nephropathy
 Renal failure (plasma creatinine
:>177 mmol/L)
Vascular disease

Dissecting aneurysm
 Symptomatic arterial disease
Advanced hypertensive retinopathy
 Hemorrhages or exudates
 Papilloedema
2- (World Health Organization/International Society of hypertension)
risk prediction charts
Coronary risk prediction charts are for estimating coronary heart disease (CHD) risk (non-fatal MI,
coronary death and new angina pectoris) for individuals who have NOT already developed CHD or
other major atherosclerotic disease. They are an aid to making clinical decisions about how intensively
to intervene on lifestyle and whether to use antihypertensive and lipid lowering medication, but should
not replace clinical judgment.
A systematic strategy should be used to identify people aged 40-74 who are likely to be at high risk.
People should be prioritized on the basis of an estimate of their CVD risk before a full formal risk
assessment. Their CVD risk should be estimated using CVD risk factors already recorded in primary
care electronic medical records.
78
People older than 40 should have their estimate of CVD risk reviewed on an ongoing basis.
People should be prioritized for a full formal risk assessment if their estimated 10-year risk of CVD is
20% or more opportunistic assessment should not be the main strategy used in primary care to identify
CVD risk in unselected people.
When is grading cardiovascular risk using charts unnecessary for making
treatment decisions?
Some individuals are at high cardiovascular risk because they have established cardiovascular disease
or very high levels of individual risk factors. Risk stratification is not necessary for making treatment
decisions for these individuals as they belong to the high risk category; all of them need intensive
lifestyle interventions and appropriate drug therapy they include people:
-
With established cardiovascular disease
-
Without established CVD who have a total cholesterol ≥ 8 mmol/l (320 mg/dl) or lowdensity lipoprotein (LDL) cholesterol ≥ 6 mmol/l (240 mg/dl) or TC/HDL-C (total
cholesterol/high density lipoprotein cholesterol) ratio >8
-
Without established CVD who have persistent raised blood pressure (>160–170/100–
105 mmHg)
-
With type 1 or 2 diabetes, with overt nephropathy or other significant Renal disease
-
With renal failure or renal impairment.
How do you use the charts to assess cardiovascular risk?
-
First make sure that you select the appropriate charts .(East Mediterranean B, below )
-
If blood cholesterol cannot be measured due to resource limitations, use the charts that
do not have total cholesterol (below )
-
Before applying the chart to estimate the 10 year cardiovascular risk of an individual,
the following information is necessary:
-
Presence or absence of diabetes.
-
Gender.
-
Smoker or non-smoker.
-
Age.
-
Systolic blood pressure (SBP).
-
Total blood cholesterol4 (if in mg/dl divide by 38 to convert to mmol/l).
Once the above information is available proceed to estimate the 10-year cardiovascular risk as
follows:
-
Step 1 Select the appropriate chart depending on the presence or absence of diabetes.
79
-
Step 2 Select male or female tables
-
Step 3 Select smoker or nonsmoker boxes
-
Step 4 Select age group box (if age is 50-59 years select 50, if 60-69 years select 60 etc.)
-
Step 5 Within this box find the nearest cell where the individuals systolic blood pressure
(mm Hg) and total blood cholesterol level (mmol/l) cross. The color of this cell
determines the 10 year cardiovascular risk.
Practice points
-
Smoking status should reflect lifetime exposure and not simply relate to the time of
assessment. For example, if a patient gave up smoking within 5 years then they should
be regarded as current smoker for the purposes of the charts
-
The initial blood pressure and the first random (non-fasting) total cholesterol and HDL
cholesterol are used to estimate an individual's risk. However, the decision on using drug
therapy should generally be based on repeat risk factor measurements over a period of
time .
-
Please note that CVD risk may be higher than indicated by the charts in the presence of
the following:
-
Already on antihypertensive therapy
-
Premature menopause
-
Approaching the next age category or systolic blood pressure category
-
Obesity (including central obesity)
-
Sedentary lifestyle
-
Family history of premature CHD or stroke in first degree relative (male <
-
55 years, female < 65 years)
-
Raised triglyceride level (>2.0 mmol/l or 180 mg/dl)
-
Low HDL cholesterol level (< 1 mmol/l or 40mg/dl in males, < 1.3 mmol/l
-
or 50 mg/dl in females)
-
Raised levels of C-reactive protein, fibrinogen, homocysteine,
-
Apolipoprotein B or Lp(a), or fasting glycaemia, or impaired glucose tolerance
-
Micro albuminuria (increases the 5-year risk of diabetics by about 5%)
-
Raised pulse rate
-
Socioeconomic deprivation.
Risk levels
80
-
The color of the cell indicates the 10-year risk of combined myocardial infarction and
stroke risk (fatal and non-fatal) as shown below.
-
10-year combined myocardial infarction and stroke risk (fatal and non-fatal)
-
■ Green <10%
■ Yellow 10% to <20%
■ Orange 20% to <30%
■ Red 30% to <40%
81
82
83
The CV risk assessment and Organ Damage (OD) (47)
As only a small fraction of the hypertensive population has an elevation of BP alone, with the
majority exhibiting additional CV risk factors. Moreover, when concomitantly present, BP and
other CV risk factors may potentiate each other, leading to a total CV risk that is greater than the
sum of its individual components. Finally, in high risk individuals, antihypertensive treatment
strategies (initiation and intensity of treatment, use of drug combinations, etc), as well as other
treatments, may be different from those implemented in lower-risk individuals. The therapeutic
approach should consider total CV risk in addition to BP levels in order to maximize costeffectiveness of the management of hypertension.
CVD risk estimation becomes a composite of several risk factors such as age, sex, smoking status,
and TC: HDL ratio, and BP. In addition, overweight and central obesity, a sedentary lifestyle, a
family history of premature CVD, TG, and DM should be considered.
Total CV risk estimation is easy among high risk groups calling for intensive CV risk-reducing
measures. However, a large number of patients with hypertension do not belong to any of the high
risk group and the identification of those at low, moderate, high or very high risk requires the use of
models to estimate total CV risk, so as to be adjust the therapeutic approach accordingly.
Risk estimation is expressed as the chance of developing CVD over a defined period, and according
to the risk estimation system used (e.g. within the next 10-years). It is known as absolute
multifactorial risk.
Several computerized methods have been developed for estimating total CV risk. Their values and
limitations have been reviewed. In the 2013 ESC/ ESC HTN guidelines, the Systematic Coronary
Risk Evaluation (SCORE) model has been adopted .It is developed based on large European cohort
studies.
The risk is communicated by health profficienals as an absolute risk or relative risk. The relative
risk is defined as the ratio of absolute CVD risk for an individual with one or more risk factors to
that of an individual at a reference level of risk (either low risk, or average), and of the same age
and sex. The relative risk is important to young individuals who are always at low absolute risk.
The absolute CVD risk can be calculated and expressed as short term or as a cumulative CVD
risk during the reminder of an individual’s life (Lifetime Risk).Assessing patients’ CVD chance
helps in targeting prevention and treatment to though asymptomatic patients, but high risk for
developing CVD.
The developed risk estimation systems are evidence-based on many different CVD prevention
guidelines, several methods and logarithms and are variable regarding their ease of use and
84
communicating to the patients and their families. In order to reduce CVD prevalence, it is very
important to implement high -risk prevention approaches and population-based approaches.
High-risk patients include:
1. Patient with established atherosclerotic CVD, whether of the coronary, peripheral,
cerebral vessels, or of the aorta, even if asymptomatic.
2. Asymptomatic individuals who are at increased risk of CVD because of multiple risk factors
resulting in raised total CVD risk:
JES5: total CVD risk (SCORE) ≥ 5% 10-year risk of CVD death
JBS2 and JBS3: total CVD risk ≥20% over 10 years of developing atherosclerotic CVD
WHO-HIS: total CVD risk ≥ 20% over 10 years of developing atherosclerotic CVD
ASCVD: 10-yr ASCVD risk ≥7%
3. Diabetes type 2 and type 1.
4. Patients with markedly increased single risk factors, especially if associated with end-organ
damage:
I.
Blood pressure ≥180/110mmHg; total cholesterol ≥8mmol/l, LDL cholesterol ≥ 6mmol/l
according to JES5 or blood pressure ≥160/100mmHg; total cholesterol/HDL cholesterol
ratio ≥6 according JBS2,3.
II.
Close relatives of subjects with premature atherosclerotic CVD or of those at particularly
high risk.
III.
Familial dyslipidemia, such as familial hypercholesterolemia or familial combined
hyperlipidemia.
IV.
Elevated total cholesterol to high-density lipoprotein (HDL) cholesterol ratio ≥6 (38).
85
86
Appendix 3
Etiological Classification of Hypertension with Clinical Finding and
Recommended Evaluation
Findings That Suggest Secondary Hypertension
Findings
(28,58,59,47)
Disorder Suspected
Further Diagnostic Studies
I. Systolic and Diastolic Hypertension
A. Primary, Essential or Idiopathic (90%)
B. Secondary (10%)
1. Renal
Renal insufficiency, atherosclerotic
cardiovascular disease, edema, elevated
blood urea nitrogen and creatinine
levels, proteinuria, abnormal urinalysis
Renal parenchymal disease
Creatinine clearance, renal
ultrasonography
Renovascular disease*
Magnetic resonance angiography,
captopril (Capoten)-augmented
radioisotopic renography, renal
arteriography
Aldosteronism
Ratio of plasma aldosterone to
plasma renin activity, CT scan of
adrenal glands
Use of sympathomimetics,
perioperative setting, acute stress,
tachycardia
Excess catecholamines
Confirm patient is normotensive in
absence of high catecholamines.
Weight gain, fatigue, proximal muscle
weakness, hirsutism, amenorrhea,
Cushingoid moon facies, dorsal hump,
purple striae, central obesity,
ecchymoses, and hypokalemia.
May have a history of glucocorticoid
use
Cushing's syndrome
Dexamethasone-suppression test
Paroxysmal hypertension, Triad of
headache (usually pounding),
palpitations, and sweating
Pheochromocytoma
Fatigue, weight loss, hair loss, diastolic
hypertension, muscle weakness
Hypothyroidism
Urinary catecholamine metabolites
(vanillylmandelic acid (VMA),
metanephrines, normetanephrines)
Plasma free metanephrines
MIBh scan
TSH levels
Heat intolerance, weight loss,
palpitations, systolic hypertension,
exophthalmos tremor, tachycardia
Hyperthyroidism
TSH levels
Systolic/diastolic abdominal bruit
An acute elevation in serum creatinine
after administration of ACE inhibitor or
angiotensin II receptor blocker
Moderate to severe hypertension in a
patient with diffuse atherosclerosis or a
unilateral small kidney
2. Endocrine
Hypernatremia, hypokalemia
87
Kidney stones, osteoporosis,
depression, lethargy, muscle weakness
Hyperparathyroidism
Serum calcium, parathyroid hormone
levels
Headaches, fatigue, visual problems,
enlargement of hands, feet, tongue
Acromegaly
Growth hormone
S.IGF-I as screening test for,
confirmation GH suppression test
Coarctation of aorta
Doppler or CT imaging of aorta
Obstructive sleep apnea
Sleep study
3. Coarctation of the Aorta
Hypertension in the arms with
diminished or delayed femoral pulses,
and low or unobtainable blood
pressures in the legs , abnormal chest
radiograph
4. Pregnancy-Induced Hypertension
5. Obstructive Sleep Apnea (OSA)
Loud snoring, daytime somnolence and
fatigue and morning confusion, obesity,
gasping
6. Neurologic Disorders
Neurological deficit
7. Acute stress, Including Surgery
a) Psychogenic hyperventilation
b) Hypoglycemia
c) Burns
d) Pancreatitis
e) Alcohol withdrawal
f) Sickle cell crisis
g) Postresuscitation
h) Postoperative
Assess
8. Increased Intravascular Volume
9. Alcohol and Drug Use
II. Systolic Hypertension
A. Increased Cardiac Output
H/O Anxiety or Psychological Dis.
Fasting and DM on insulin with
hypoglycemic symptoms
H/O Burn
H/O Alcoholism and recurrent vomiting
and epigastric pain
H/O SCD with recurrent VOC
H/O CPR or Surgery
a)
b)
c)
d)
e)
f)
g)
h)
Psychogenic
hyperventilation
Hypoglycemia
Burns
Pancreatitis
Alcohol withdrawal
Sickle cell crisis
Postresuscitation
Postoperative
B. Rigidity of Aorta or Small Arteries
88
HB Electrophoresis
III. Iatrogenic Hypertension (Table 2)
Use of drug in (Table 2)
Drug side effect
Trial off drug, if possible
High salt intake, excessive alcohol
intake, obesity
Diet side effects
Trial of dietary modification
Persistent or severe elevation, excessive
alcohol intake, drug addict
Consider medications, illicit
drug use and excessive alcohol
use
Trial of dietary and drugs
modification and rehabilitation
Erythropoietin use in renal disease,
polycythemia in COPD
Erythropoietin side effect
Trial off drug, if possible
* Most common curable cause of secondary hypertension
Drugs and Other Substances That Can Raise Blood Pressure
o
o
o
1- Chemical elements and other industrial
chemicals
o
o
o
o
o
Lead
Mercury
Thallium and other heavy metals
Lithium salts, especially the chloride
Chloromethane
Carbon disulfide
Polychlorinated (and polybrominated) biphenyls
Parathion and other insecticides
o
Sodium chloride**
Licorice
o Caffeine
o Tyramine-containing foods (with MAO-I)
o Ethanol
o
2- Food substances
o
o
o
o
o
3- Street Drugs and other “Natural
Products”
o
o
o
o
o
o
o
Anabolic steroids
Cocaine (“?”) (and cocaine withdrawal)
Heroin withdrawal
Methylphenidate
Phencyclidine
g-hydroxybutyric acid (and withdrawal from it)
Ma Huang, “herbal ecstasy,” and other phenylpropanolamine**
analogsa
Nicotine (“?”) (and nicotine withdrawal)
Ketamine
Ergotamine and other ergot-containing herbal preparations
St. John’s Wort
o
4- Venoms and toxins
Spider bites (especially the brown recluse or
o “fiddleback” spider)
o Scorpion bites
o Snake bites
89
5- Prescription Drugs
Drug class
Drug examples
Immunosuppressive agents**
Cyclosporine (Sandimmune), tacrolimus (Prograf), corticosteroids
Nonsteroidal anti-inflammatory drugs**
Ibuprofen (Motrin), naproxen (Naprosyn), piroxicam (Feldene)
COX-2 inhibitors**
Celecoxib (Celebrex), rofecoxib (Vioxx), valdecoxib (Bextra)
Estrogens **
30- to 35-mcg estrogen oral contraceptives**
Weight-loss agents **
Sibutramine (Meridia), phentermine (Adipex), ma huang (ephedra)
Stimulants**
Nicotine, amphetamines
Mineralocorticoids
Fludrocortisone (Florinef)
Antiparkinsonian
Bromocriptine (Parlodel)
Monoamine oxidase inhibitors
Phenelzine (Nardil)
Anabolic steroids
Testosterone
Sympathomimetics
Pseudoephedrine (Novafed)
Others Drugs
o
o
o
o
o
o
o
o
o
o
o
Erythropoietin
Naloxone
Ketamine
Desflurane
Carbamazepine
Bromocryptine
Metoclopramide
Antidepressants (especially venlafaxine)
Buspirone
Disulfuram
Clonidine, b-blocker (and maybe calcium
antagonist) withdrawal
o
o
o
o
o
o
o
o
o
Pheochromocytoma: b-blocker without a-blocker first; glucagon
Pentagastrin
Digitalis
Thyrotropin-releasing hormone (Protirelin)
Synthetic ACTH (Corticotropin)
Sibutramine
Alkylating agents (typically used for cancer chemotherapy)
Clozapine
Orlistat?
**Substances of greatest current clinical importance.
90
Appendix 4
Antihypertensive Drugs (43)
Drug Class
Trade Name
Available Tablet Dose
Initial Dose/ Day
Maximum Dose/ Day
Frequency/Day*
Angiotensin - Converting Enzyme Inhibitors (ACEIs)
Captopril
Capoten
25 , 50 mg
12.5mg
100mg
BD-TDS
Enalapril
Renitec
5 , 10 , 20 mg
5mg
40mg
OD-BD
Ramipril
Tritace
2.5 , 5 mg
2.5mg
10mg
OD
Perindopil*
Coversyl
4 , 8 mg
4mg
8mg
OD
Cilazapril*
Inhibace
2.5 , 5 mg
2.5mg
5mg
OD
Calcium Channel Blockers (CCB)
A: Dihydropyridines:
Nifidipine*
Adalat
10 , R 20 mg
LA 30 LA 60
10 , 20 mg
120 mg
TDS - QID
OD (R)
Amlodipine*
Norvasc
Istin
5 mg
10 mg
5 mg
10 mg
OD
Plendil
2.5, 5, 10 mg
5 mg
20 mg
OD
•
Felodipine*
B: Non-Dihydropyridines:
Verapamil (immediate release)
Isoptin
40 , 80 mg
40 mg
480 mg
TDS
Dilzem (Extended release)
Diltiazem
60 mg
60 mg
480 mg
TDS - QID
Atenolol
Tenormine
50 , 100 mg
25-50mg
100mg
OD
Bisoprolol
Concor
2.5 , 5 mg
2.5mg
10mg
OD
Metoprolol
Lopressor
25 , 50 , 100mg
25 mg
200mg
BD
Dilatrend
25 mg
12.5 X 2days then
25mg BD
100mg in weight ≥ 85
kg
BD
Β ± α Blockers
Carvidolol (
α - b blocker )
Diuretics
1-Thiazide type:
Hydrochlorothiazide (HCT) *
Esidrix
25 mg
12.5
25mg
OD
Indapamide
Natrilex
2.5 , 1.5 mg R
1.25mg AM
2.5mg
OD
2- K sparing: Alone:
91
Spironolactone
Aldactone
25 mg
Lasix
40 mg
12.5mg
50mg
OD
3- Loop Type:
Furosamide
20mg
80mg
BD
1000mg
BD/TDS
Central Sympatholytics
Methyldpoa
250mg
Aldomet
Angiotensin II Receptor Blockers (ARBs)
•
Cozaar
Valsartan*
Diovan
Losartan
Telmisartan
•
•
Irbesartan*
25, 50 mg
25mg
100mg
OD - BD
80mg
320mg
OD - BD
Micardis
40 mg
20mg
80mg
OD
Aprovel
75, 150, 300 mg
150mg
300mg
OD
92
Combination Drugs for Hypertension
Combination
Type
Available Tablet
Dose
Initial
Dose/ Day
Maximum
Dose/ Day
(37.5/25, 75/50)
1 tablet
2 tablet
OD - BD
Preterax
(Coversyl+Natrlix)
(2/ .625)
1 tablet
2 tablet
OD
Perindopril+indapamide
Bipreterax
(Coversyl+Natrlix)
(4/1.25)
1 tablet
2 tablet
OD
ACEIs and
CCB
Perindopril+Amlodipine
Coveram
5/5 , 5/10 , 10/5 ,
10/10 mg
1 tablet
1 tablet
10/10mg
OD
ARBs and
Diuretics
Valsartan+HCT
Co-Diovan
(80/12.5, 160/12.5,
160/25)
1 tablet
2 tablet
OD/BD
Losartan+HCT
HYZAAR
(50/12.5)
1 tablet
2 tablet
OD
Irbesartan+HCT
Co-Aprovel
150/12.5,
300/12.5
1 tablet
1 tablet
300/12.5
OD
ARBs and
CCB
Valsartan+Amlodipine
EXFORGE
160/5, 160/10mg
1 tablet
1 tablet
160/10mg
OD
ARBs, CCB
and Diuretics
Valsartan+Amlodipine+
HCT
EXFORGE HCT
160/5/12.5,
160/5/25,
160/10/12.5,
160/10/25,
320/10/25
1 tablet
1 tablet
320/10/25
OD
Maximum Dose/ Day
Frequency/Day*
Diuretic and
Diuretic
Triamterene+HCT
Dyazide
ACEIs and
Diuretics
Perindopril+indapamide
*
Frequency/Day*
•
Long acting AHTDs - Available only in SMC
Note: In elderly & renal pt always start with half initial dose
Note: SR, sustained release; CD, controlled-diffusion; XR and ER, extended release; GITS, gastrointestinal therapeutic system; COER, controlled-onset extended
release.
*In some patients treated once daily, the antihypertensive effect may diminish toward the end of the dosing interval (trough effect). BP should be measured just prior to
dosing to determine if satisfactory BP control is obtained. Accordingly, an increase in dosage or frequency may need to be considered. These dosages may vary from
those listed in the “Physicians’ Desk Reference, 57th ed.”
93
Appendix 5
Antihypertensive Drugs Indications, Contraindications, Interactions and Potential Side Effects (43)
Drug
Thiazide Diuretics
 preferred initial therapy for most
patients with uncomplicated
hypertension
 especially effective in African
Americans
Associated
Conditions
Where Indicated




ISH in elderly
heart failure
diabetes
high coronary
risk
 previous MI
(non-ISA)**
 heart failure
 diabetes
 high coronary
risk
Beta-Blockers
Associated
Conditions
Where
Useful
 edema states
 Renal
insufficiency
(loop agents for
CR > 2.0 mg/dl)
 angina pectoris
 Supraventricular
arrythmias
 suppression of
PVCs
 prophylaxis for
migraines
 Hypertrophic
cardiomyopathy
 anxiety
 essential tremor
 glaucoma





Associated
Conditions
Requiring
Caution
cardiac arrythmias
glucose intolerance
Elevated
triglycerides
gout
Hypertrophic
cardiomyopathy
 COPD with mild
bronchospasm***
 rhinitis
 variant angina
 Raynaud's disease
 peripheral vascular
disease
 hyperlipidemia
 pheochromocytoma
depression
 mild asthma**
94
Contraindications
Drug
Interactions*
 sensitivity to
thiazides
 increase lithium
blood levels
 action blocked
by NSAIDs
 hypokalemia
enhances digoxin
toxicity
 ACE inhibitors
lessen
hypokalemia
 asthma (moderate
or severe)
 COPD with
significant
bronchospasm
 sinus bradycardia
(non-ISA)
 2nd or 3rd degree
heart block
 sensitivity to betablockers
 Hypoglycemiaprone
IDDM
 cimetidine and
nicotine reduce
bioavailability of
livermetabolized
drugs
 Livermetabolized
beta-blockers
may increase
warfarin activity
 additive negative
inotropic effect
with verapamil
 addition of
reserpine –
bradycardia and
syncope
 combined with
verapamil may
cause complete
heart block
Potential Side
Effects*


























hypokalemia
hyperuricemia
hyponatremia
hyperglycemia
dizziness
fatigue
Erectile dysfunction
dry mouth
nausea
constipation
Orthostatic hypotension
rash
erectile dysfunction
fatigue
lightheadedness
dizziness
dyspnea
wheezing
cold extremities
claudication
confusion
vivid dreams
insomnia
depression
diarrhea
bradycardia
ACE Inhibitors
Calcium Channel Blockers
 type 1 diabetes
with renal
disease
 congestive heart
failure
 previous MI
with impaired
LV function
 non-diabetic
renal diseases
associated with
proteinuria
 high coronary
risk
 ISH in elderly
patients 60
(long acting
dihydropyiridin
es)
 diabetes
 high coronary
risk
 nephritic
syndrome
 unilateral
renovascular
hypertension
 type 2 diabetes
with renal
disease
 renal insufficiency
(renal function and
hyperkalemia)
 bilateral renal
artery stenosis
 renal artery
stenosis in solitary
kidney
 hypertrophic
cardiomyopathy
 less effective for
monotherapy in
African Americans
 pregnancy†
 sensitivity to ACE
inhibitors
 angina pectoris
 variant angina
pectoris
 migraine
prophylaxis
(verapamil)
 Raynaud's
disease
(nifedipine)
 esophageal
spasm
 hypertrophic
cardiomyopathy
without
obstruction
(verapamil,
diltiazem)
 supraventricular
tachycardia
(verapamil)
 pulmonary
hypertension
(nifedipine)
 mild heart failure
(verapamil >
diltiazem >
dihydropyiridines)
 liver disease
 high risk for heart
failure
 severe heart failure
(verapamil)
 2nd or 3rd degree
heart block
 sick sinus syndrome
(verapamil,
diltiazem)
 Wolf-ParkinsonWhite syndrome
(verapamil)
 previous MI with
heart failure
(diltiazem)
 sensitivity to
calcium channel
blockers
95
 antihypertensive
effect blocked by
NSAIDs
 NSAIDs
(hyperkalemia)
 potassium
supplements
(hyperkalemia)
 potassium
sparing diuretics
(less
hypokalemia or
hyperkalemia)










angioedema
cough
Tachycardia
increase in serum
creatinine
increase in serum
potassium
nausea
hypotension
diarrhea
fatigue
taste disorders (rare)
agranulocytosis (rare)
 additive negative
inotropic effect
with betablockers
(verapamil)
 verapamil
increases digoxin
blood levels
 cimetidine
increases
nifedipine blood
levels









dizziness
peripheral edema
headache
flushing
constipation (verapamil)
heart block (verapamil)
rash
abnormal live enzymes
hypotension

Angiotensin Receptor Blockers
 type 2 diabetes
with renal
disease
 non-diabetic
renal disease
with proteinuria
 heart failure
 left ventricular
hypertrophy
 congestive heart
failure
 type 1 diabetes
with renal
involvement
 nephritic
syndrome
 unilateral
renovascular
hypertension
 renal insufficiency
(renal function and
hyperkalemia)
 bilateral renal
artery stenosis
 renal artery
stenosis in solitary
kidney
 hypertrophic
cardiomyopathy
 pregnancy
 sensitivity to
angiotensin receptor
blockers
* For a complete listing of side effects and drug interactions for any particular drug, consult the PDR or academic pharmacology texts.
** ISA = Intrinsic Sympathomimetic Activity (acebutolol, penbutolol, pindolol)
*** Use cardioselective agents
† Cooper, 2006
96
 antihypertensive
effect blocked by
NSAIDs
 NSAIDs
(hyperkalemia)
 potassium
supplements
(hyperkalemia)
 potassium
sparing diuretics
(less
hypokalemia or
hyperkalemia)
 angioedema
 tachycardia
 increase in serum
creatinine
 increase in serum
potassium
 hypotension
 fatigue
Appendix 6
Adverse Effects of Antihypertensive Drugs
Common Adverse effects
Thiazide Diuretics
B-B
ACEIs
CCBs
ARBs
Constipation
–
–
–
+
(especially verapamil)
–
Cough, angioedema
–
–
+
–
rare reports
Dyspnoea
–
+
–
–
–
Gout
+
–
–
–
–
Headache, flushing
–
–
–
+
–
Hyperglycaemia
+
–
–
–
–
Hyperkalaemia
–
–
+
–
+
Hypokalaemia
+
–
–
–
–
Impotence
+
+
–
–
–
Lethargy
–
+
–
–
–
Oedema
–
–
–
+
–
Postural hypotension
+
–
+
–
–
97
Appendix 7
Recommended Education Messages (53)
Purpose
The following educational messages will support the goals of patient education and selfinvolvement in ongoing hypertension management:
Health Care Provider Visits
a. Basic Information

Discuss:
* What is blood pressure?
* What do the numbers mean?
* Factors affecting blood pressure, e.g., OTC. meds.
* How HBP affects health.
b. Lifestyle Modification

Recommend appropriate lifestyle modification:
* Weight reduction and maintenance
* Moderation of dietary sodium
* Moderation of alcohol intake
* Adequate physical activity
* Incorporation of DASH diet

Recommend interventions for cardiovascular risk factors (e.g., smoking, hyperlipidemia,
diabetes).
c. Pharmacologic Therapy

Reinforce lifestyle modification and cardiovascular risk factor interventions.

Provide medication information (i.e., what, when, and why taking medication, possible
side effects).

Advise when to call with problems.
98
d. Ongoing Management

Advise on necessity for follow-up.

Set realistic goals in partnership with the patient.

Reinforce educational messages.

Adopt an attitude of concern along with hope and interest in the patient's future.

Provide positive feedback for BP and behavioral improvement.
99
Appendix 8
HTN Sheet
NCD clinic updated forms are in use in NCD in Primary
Health Care but the hypertension sheet is kept for the
guideline
100
Kingdom of Bahrain
Ministry of Health
Primary Health Care
HYPERTENSION ASSESSMENT SHEET
Date:
Health Center:
Health Center File:
First
Middle
Last
Name:
CPR NO:
DD
MM
YYYY
Date of Birth:
Sex:

Male

Female
Contact Number: _____________ / _____________ / _____________ / ______________
History of Present Illness
________________________________________________________________________________
________________________________________________________________________________
________________________________________________________________________________
________________________________________________________________________________
________________________________________________________________________________
________________________________________________________________________________
101
1. Screening
2. Standardization of BP Measurement (Table 1)


Yes
No
If no why?
_______________________________________________________________________
_______________________________________________________________________
Part II: Diagnosis Stage



3. Accurate Staging (Table 2)
4. Confirm Chronicity (Table 3-4)
First Visit
Basic
Readings
Sitting
Right
Left
Duration
Recommended to
Confirm Chronicity:
Standing*
Right
Diagnosis Confirmed by(tTable5):
Serial measurements in the office
Serial measurements at home
Ambulatory blood pressure monitoring
Second
Visit
Third
Visit
Left
Duration
Date
Average
Readings
(SBP/DBP)
Arm used for
follow-up
Accurate
Staging
* Standing BP if indicated
Indication for Prolongation of the Duration Recommended Confirming Chronicity
No. of
Readings
Fourth visit
Fifth visit
Sixth visit
Duration
Date
Average
Readings
102
Seventh visit
Eighth visit
Ninth visit
6. Complete Initial Clinical Evaluation
a. First Visit: History
History
Comment if Abnormal
I CHD Risk Factor
1. Absolute
Age:
Men >55
 Women >65
Non-Modifiable (NM)

Sex:
 Men
 Postmenopausal women
Family history of premature
cardiovascular disease/ death:
 Women < 65
 Men <55







Stroke
CVD
DM
Renal
Hypertension
Hyperlipidemia
Sudden Death
Modifiable
Hypertension*: Patients hypertensive Hx: Onset, Duration, Current Rx,
controlled?, SE†
Diabetes mellitus*
Dyslipidemia*
Smoking
Obesity* (body mass index ≥30 kg/m2)
2. Relative:
Sedentary lifestyle
Modifiable
Diet :salts
Alcohol (43 units/day) - units/day
High stress (type A)
High risk socioeconomic group
High risk ethnic group
Psychosocial , environmental and personal factors
II Target organ Damage & Associated Clinical Conditions:
1. CNS:
 Hypertensive encephalopathy
 Stroke/Intracranial hemorrhage
 TIA
 Sudden onset acute Headache with malignant
HTN
 Neurological deficit
 Loss of consciousness
 Retinopathy
 Visual symptoms
2. EYE:
103
3. CVS
 Myocardial infarction
(Acute/Past)
 Angina pectoris
 Coronary revascularization
 Congestive heart failure
(Acute/Chronic)




Chest pain
Dyspnea
PND/Orthopnea
Heart surgery
4. RENAL
 Acute Renal Failure
 Chronic Renal Disease
5. VASCULAR
 Acute aortic dissection
 Other vascular dissection,
arteritis / thrombosis
 Symptomatic arterial disease,
PVD


Sudden onset chest pain/ Abdominal pain
Leg claudication
6. Endocrine/ Obstetrical
 Eclampsia
III Secondary Causes
1. Renal
Renal parenchymal disease
 Acute glomerulonephritis
 Chronic nephritis
 Polycystic disease
 Diabetic nephropathy
 Hydronephrosis

Recurrent UTI,
particularly in
young patients,
(congenial
bladder
abnormalities or
reflux
nephropathy)
 Potential
nephrotoxin
drugs
 Previous renal failure
 Diabetic retinopathy,
which suggests a
diagnosis of diabetic
nephropathy
 Edema
2. Endocrine


Headaches
Fatigue


Visual problems
Enlargement of hands,
feet, tongue
b) Hypothyroidism



Fatigue
Weight loss
Hair loss


Diastolic hypertension
Muscle weakness
c) Hyperthyroidism



Heat intolerance
Weight loss
Palpitations



Systolic hypertension
Exophthalmos
Tremor
d) Hypercalcemia
(hyperparathyroidism)



Kidney stones
Osteoporosis
Depression


Lethargy
Muscle weakness



Use of sympathomimetics
Perioperative setting
Acute stress
a) Acromegaly
Excess
catecholamines
e) Adrenal

Cushing's syndrome 

Weight gain
Fatigue
Hirsutism


Amenorrhea
H/O glucocorticoid use
Triad of :
 Headache (usually pounding)
Pheochromocytoma  Palpitations
 Sweating
104
3. Vascular




Chest pain
Backache
Abdominal pain
Leg claudication


Loud snoring
Daytime sleepiness
4. Sleep Apnea


Obesity
Gasping

5. Pregnancy
6. Drugs












Immunosuppressive agents**
Nonsteroidal anti-inflammatory drugs**
COX-2 inhibitors**
Estrogens **
Weight-loss agents **
Stimulants**
Mineralocorticoids
Antiparkinsonian
Monoamine oxidase inhibitors
Anabolic steroids
Sympathomimetics
Others(specify)
7. Acute stress








Psychogenic hyperventilation
Hypoglycemia(Fasting. Insulin SE)
Burns
Pancreatitis
Alcohol withdrawal
Sickle cell crisis
Postresuscitation
Perioperative/Postoperative
IV Other Comorbid Disease (Drugs Contraindications )

Degenerative Joint Diseases

Prostate problems (BPH)

Sexual dysfunction / Impotence

Bronchial asthma

Psychiatric disorder
Enter (√) if present
Enter (*) to see medical notes
**Substances of greatest current clinical importance.
105
b. Second Visit
1. Physical Exam
Normal
Abnormal
Looking for
Comment if Abnormal
a. General
Height
________ cm
Ideal Body Weight:
Weight ________ Kg
Weight
I) Appearance and Skin
Cushingoid Moon
facies
Purple striae
BMI
- At 24BMI
_________ Kg
- At 22BMI
_________ Kg
________ Kg /m²




Hirsutism


Central obesity


Dorsal hump


Ecchymoses


Proximal muscle
weakness


Exophthalmos


Tremor


Leg BP*


Carotid bruits


Weight to lose to reach: - 24BMI
_________ Kg
- 22BMI
_________ Kg
Secondary Causes:
 Cushing's syndrome
Secondary Causes:
 Hyperthyroidism
II) BP and Pulse
Secondary Causes:
 Coarctation of aorta
TOD/ACC
Radio-Femoral
delay
 A sign of higher stroke
risk.
Secondary Causes:


Periorbital


Secondary Causes:
Ankle & feet


TOD/ACC
Secondary Causes
 Coarctation of aorta
III) Odema
 Renal
b. Neurologic Examination
Neurological deficit


TOD:
 CNS
c. Eye Examination
Funduscopic
examination
IOP




TOD/ACC
Other comorbid disease
(Drugs Contraindications )
 Glaucoma
106
Date of last eye examination:
d. Neck Examination

Thyroid gland

Secondary Causes:
 Thyroid disease
e. Heart examination
TOD/ACC
Murmur
Gallop


 Valvular Heart Disease
 Cardiomegaly
f. Lungs examination

Basal crepetation

TOD/ACC
g. Abdomen examination
Aortic pulsation


Mass


Abdominal bruits


Secondary Causes:
 Renovascular disease
h. Prostate examination

P/R

Other comorbid disease
(Drugs Contraindications )
 BPH
Enter (√) if present, and enter (X) if absent
2. Lab Investigations
MANDATORY
OPTIONAL *
Urine R&M
ACR:
Hb
PCR:
FBS
GFR:
Total
Cholesterol
HDL
LDL
Triglyceride
VMA:
X-ray Chest:
IVP:
Ultrasound:
Urea
Others:
Creatinine
TFT
Uric Acid
TSH
T4
Sodium
Calcium
Potassium
PTH
Chloride
Bicarbonate
ECG
* If secondary cause is suspected
107
c. Third Visit: Finalization
Date of
Established
Diagnosis
Initial Rx
Target BP
108
Date of Next Visit
Duration*
Weeks /
Month
Date
BP
Reading
Achieved
Target
BP
Rx Option:
Rx:
Compliance
Toleration
* Duration according to the control stage criteria
109
Life Style
Mod.
Drug Rx
Change
Drug
Add Another
Drug
Increase
the Dose
Part IV: Follow-up Stage (Hypertension Continuing Care)
Frequency
3/12
6/12
Date
History
Neurological
Symptoms
Angina
Impotence
Claudication
Physical Exam
Target BP
BP Reading
Weight /Kg
Odema
Basal crepitation
Fundoscopy
Investigation
Urine dipstick
(protein)
FBS
F.LIPIDS
Potassium
Creatinine
ECG
Management
Compliance
Toleration
Life style
modification
Drugs 1.
2.
3.
4.
5.
6.
110
9/12
Year
Indications for Specialist Referral
Date
Noticed
Indications
Urgent Treatment Needed
 Accelerated (malignant) hypertension (severe hypertension with


grade III–IV retinopathy)
Severe hypertension (eg, ≥220/120 mm hg)
Impending complications (eg, TIA, left ventricular failure)
Special Situations
 Unusual BP variability – Consider ABPM
 Possible isolated clinic hypertension (White coat hypertension) –
Consider ABPM
 Hypertension in pregnancy – Consider ABPM
 Evaluating hypertension with autonomic dysfunction – Consider

ABPM
Identifying nocturnal hypertension – Consider ABPM
Possible Underlying Cause
 Findings on history, physical examination, or laboratory testing that





suggest a secondary cause (Appendix 1-3).
Poor response to therapy (resistant hypertension) – Consider ABPM
Worsening of control in previously stable hypertensive patient
Rapid and severe course
Sever hypertension (systolic blood pressure > 180 mm Hg or
diastolic blood pressure >110 mm Hg)
Onset of hypertension in persons younger than age 20 or older than
age 50
Significant hypertensive target organ damage

 Lack of family history of hypertension
 Hypokalaemia/ increased plasma sodium and metabolic alkalosis





(Conn’s syndrome?)
Elevated serum creatinine
Proteinuria or haematuria
Sleep apnea
Neurologic disorders
Postoperative hypertension
Therapeutic Problems






Treatment resistance (Resistant Hypertension) – Consider ABPM
Multiple drug intolerance
Multiple drug contraindications
Persistent non-compliance – Consider ABPM
Treatment declined (the reluctant hypertensive) – Consider ABPM
Evaluation of symptomatic hypotension (with or without
antihypertensive medication) – Consider ABPM
Informing equivocal treatment decisions – Consider ABPM

 Evaluation of efficacy of antihypertensive drugs in clinical
research – Consider ABPM
111
Yes (If Yes:
Action Taken)
No
REFERENCES
(1) Saudi Hypertension Management Guidelines. 2011.
(2) Rules of halves: implications of increasing diagnosis and reducing dropout for future workload and
prescribing costs in primary care. Br J Gen Pract. 1992 March;42(356):116-119.
(3) The National Non-Communicable Diseases Survey 2007.
(4) Agyemang C, Bindraban N, Mairuhu G, van Montfrans G, Koopmans R, Stronks K. Prevalence,
awareness, treatment, and control of hypertension among Black Surinamese, South Asian Surinamese
and White Dutch in Amsterdam, The Netherlands: the SUNSET study. J Hypertens 2005;23(11):19711977.
(5) Agyemang C, Ujcic-Voortman J, Uitenbroek D, Foets M, Droomers M. Prevalence and management of
hypertension among Turkish, Moroccan and native Dutch ethnic groups in Amsterdam, the Netherlands:
The Amsterdam Health Monitor Survey. J Hypertens 2006 Nov;24(11):2169-2176.
(6) Altun B, Arici M, Nergizoglu G, Derici Ü, Karatan O, Turgan Ç, et al. Prevalence, awareness, treatment
and control of hypertension in Turkey (the PatenT study) in 2003. J Hypertens 2005;23(10):1817-1823.
(7) Amarenco P, Benavente O, Goldstein LB, Callahan A,3rd, Sillesen H, Hennerici MG, et al. Results of
the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial by stroke subtypes.
Stroke 2009 Apr;40(4):1405-1409.
(8) Amarenco P, Goldstein LB, Callahan III A, Sillesen H, Hennerici MG, O’Neill BJ, et al. Baseline blood
pressure, low- and high-density lipoproteins, and triglycerides and the risk of vascular events in the
Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial. Atherosclerosis 2009
6;204(2):515-520.
(9) Beevers G, Lip GY, O'Brien E. ABC of hypertension: Blood pressure measurement. Part IIconventional sphygmomanometry: technique of auscultatory blood pressure measurement. BMJ 2001 Apr
28;322(7293):1043-1047.
(10) Bender SR, Filippone JD, Heitz S, Bisognano JD. A systematic approach to hypertensive urgencies
and emergencies. Current Hypertension Reviews 2005;1(3):275-281.
(11) Boggia J, Li Y, Thijs L, Hansen TW, Kikuya M, Björklund-Bodegård K, et al. Prognostic accuracy of
day versus night ambulatory blood pressure: a cohort study. The Lancet 2007;370(9594):1219-1229.
(12) Cherney D, Straus S. Management of patients with hypertensive urgencies and emergencies. Journal
of general internal medicine 2002;17(12):937-945.
(13) Cífková R, Škodová Z, Lánská V, Adámková V, Novozámská E, Petržílková Z, et al. Trends in blood
pressure levels, prevalence, awareness, treatment, and control of hypertension in the Czech population
from 1985 to 2000/01. J Hypertens 2004;22(8):1479-1485.
(14) Collaboration PS, Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, et al. Blood
cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data
from 61 prospective studies with 55,000 vascular deaths. Lancet 2007;370(1829):1839.
(15) Collins R, Peto R, MacMahon S, Godwin J, Qizilbash N, Collins R, et al. Blood pressure, stroke, and
coronary heart disease: Part 2, short-term reductions in blood pressure: overview of randomised drug
trials in their epidemiological context. The Lancet 1990 4/7;335(8693):827-838.
(16) Conen D, Bamberg F. Noninvasive 24-h ambulatory blood pressure and cardiovascular disease: a
systematic review and meta-analysis. J Hypertens 2008 Jul;26(7):1290-1299.
112
(17) Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK, et al. Long term effects of
dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of
hypertension prevention (TOHP). BMJ 2007 Apr 28;334(7599):885-888.
(18) Cornelissen VA, Fagard RH. Effects of endurance training on blood pressure, blood pressureregulating mechanisms, and cardiovascular risk factors. Hypertension 2005 Oct;46(4):667-675.
(19) Costanzo S, Di Castelnuovo A, Zito F, Krogh V, Siani A, Arnout J, et al. Prevalence, awareness,
treatment and control of hypertension in healthy unrelated male-female pairs of European regions: the
dietary habit profile in European communities with different risk of myocardial infarction--the impact of
migration as a model of gene-environment interaction project. J Hypertens 2008 Dec;26(12):2303-2311.
(20) Cushman WC, Cutler JA, Hanna E, Bingham SF, Follmann D, Harford T, et al. Prevention and
Treatment of Hypertension Study (PATHS): effects of an alcohol treatment program on blood pressure.
Arch Intern Med 1998;158(11):1197-1207.
(21) Danon-Hersch N, Marques-Vidal P, Bovet P, Chiolero A, Paccaud F, Pecoud A, et al. Prevalence,
awareness, treatment and control of high blood pressure in a Swiss city general population: the CoLaus
study. Eur J Cardiovasc Prev Rehabil 2009 Feb;16(1):66-72.
(22) Dasgupta K, Quinn RR, Zarnke KB, Rabi DM, Ravani P, Daskalopoulou SS, et al. The 2014 Canadian
Hypertension Education Program (CHEP) Recommendations for blood pressure measurement, diagnosis,
assessment of risk, prevention and treatment of hypertension. Can J Cardiol 2014;10.
(23) de Lemos J, Braunwald E, Blazing M, Murphy S, Downs J, Gotto A, et al. Efficacy and safety of more
intensive lowering of LDL cholesterol: a meta-‐analysis of data from 170,000 participants in 26
randomised trials. Lancet 2010;376(9753):1670-1681.
(24) Devereux RB, Wachtell K, Gerdts E, Boman K, Nieminen MS, Papademetriou V, et al. Prognostic
significance of left ventricular mass change during treatment of hypertension. JAMA 2004;292(19):23502356.
(25) Dickinson HO, Mason JM, Nicolson DJ, Campbell F, Beyer FR, Cook JV, et al. Lifestyle interventions
to reduce raised blood pressure: a systematic review of randomized controlled trials. J Hypertens
2006;24(2):215-233.
(26) Doll R, Peto R, Wheatley K, Gray R, Sutherland I. Mortality in relation to smoking: 40 years'
observations on male British doctors. BMJ 1994 Oct 8;309(6959):901-911.
(27) Efstratopoulos AD, Voyaki SM, Baltas AA, Vratsistas FA, Kirlas DP, Kontoyannis JT, et al. Prevalence,
awareness, treatment and control of hypertension in Hellas, Greece: the Hypertension Study in General
Practice in Hellas (HYPERTENSHELL) national study. American journal of Hypertension 2006;19(1):53-60.
(28) Erem C, Hacihasanoglu A, Kocak M, Deger O, Topbas M. Prevalence of prehypertension and
hypertension and associated risk factors among Turkish adults: Trabzon Hypertension Study. J Public
Health (Oxf) 2009 Mar;31(1):47-58.
(29) Estruch R, Ros E, Salas-Salvadó J, Covas M, Corella D, Arós F, et al. Primary prevention of
cardiovascular disease with a Mediterranean diet. N Engl J Med 2013;368(14):1279-1290.
(30) Fagard RH, Celis H, Thijs L, Staessen JA, Clement DL, De Buyzere ML, et al. Daytime and nighttime
blood pressure as predictors of death and cause-specific cardiovascular events in hypertension.
Hypertension 2008 Jan;51(1):55-61.
(31) Falaschetti E, Chaudhury M, Mindell J, Poulter N. Continued improvement in hypertension
management in England: results from the Health Survey for England 2006. Hypertension 2009
Mar;53(3):480-486.
(32) Fuentes Patarroyo S, Anderson C. Blood Pressure Lowering in Acute Phase of Stroke, Latest
Evidence and Clinical Implication. Ther Adv Chronic Dis 2012;3:163-171.
113
(33) Goldstein LB, Adams R, Alberts MJ, Bushnell CD, Culebras A, DeGraba TJ, et al. AHA/ASA Guideline.
2006.
(34) Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low-sodium diet vs. high-sodium diet on blood
pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review). Am J
Hypertens 2012 Jan;25(1):1-15.
(35) Grégoire J, Moisan J, Guibert R, Ciampi A, Milot A, Côté I, et al. Tolerability of antihypertensive
drugs in a community-based setting. Clin Ther 2001;23(5):715-726.
(36) Hajjar I, Kotchen JM, Kotchen TA. Hypertension: trends in prevalence, incidence, and control. Annu
Rev Public Health 2006;27:465-490.
(37) James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. 2014
evidence-based guideline for the management of high blood pressure in adults: report from the panel
members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311(5):507-520.
(38) JBS3 Board. Joint British Societies' consensus recommendations for the prevention of cardiovascular
disease (JBS3). Heart 2014 Apr;100 Suppl 2:ii1-ii67.
(39) Jensen MD, Ryan DH, Hu FB, Stevens FJ, Hubbard VS, Stevens VJ, et al. 2013 AHA/ACC/TOS
Guideline for the Management of Overweight and Obesity in Adults. J Am Coll Cardiol 2013.
(40) Kannel WB. Risk stratification in hypertension: new insights from the Framingham Study. American
Journal of Hypertension 2000;13(S1):3S-10S.
(41) Kannel WB, Vasan RS, Levy D. Is the relation of systolic blood pressure to risk of cardiovascular
disease continuous and graded, or are there critical values? Hypertension 2003 Oct;42(4):453-456.
(42) Kastarinen M, Antikainen R, Peltonen M, Laatikainen T, Barengo NC, Jula A, et al. Prevalence,
awareness and treatment of hypertension in Finland during 1982-2007. J Hypertens 2009
Aug;27(8):1552-1559.
(43) Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical
practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney DiseaseMineral and Bone Disorder (CKD-MBD). Kidney Int Suppl 2009 Aug;(113):S1-130. doi(113):S1-130.
(44) Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in the prevention of
cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from
prospective epidemiological studies. BMJ 2009 May 19;338:b1665.
(45) Little P, Barnett J, Barnsley L, Marjoram J, Fitzgerald-Barron A, Mant D. Comparison of acceptability
of and preferences for different methods of measuring blood pressure in primary care. BMJ 2002 Aug
3;325(7358):258-259.
(46) Macedo ME, Lima MJ, Silva AO, Alcantara P, Ramalhinho V, Carmona J. Prevalence, awareness,
treatment and control of hypertension in Portugal: the PAP study. J Hypertens 2005;23(9):1661-1666.
(47) Mancia G, Fagard R, Narkiewicz K, Redán J, Zanchetti A, Böhm M, et al. 2013 Practice guidelines for
the management of arterial hypertension of the European Society of Hypertension (ESH) and the
European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension.
J Hypertens 2013;31(10):1925-1938.
(48) Manson JE, Tosteson H, Ridker PM, Satterfield S, Hebert P, O'Connor GT, et al. The primary
prevention of myocardial infarction. N Engl J Med 1992;326(21):1406-1416.
(49) McAlister FA, Straus SE. Measurement of blood presssure: an evidence based review. BMJ
2001;322(7291):908-911.
(50) McManus RJ, Caulfield M, Williams B, National Institute for Health and Clinical Excellence. NICE
hypertension guideline 2011: evidence based evolution. BMJ 2012 Jan 13;344:e181.
114
(51) Meisinger C, Heier M, Völzke H, Löwel H, Mitusch R, Hense H, et al. Regional disparities of
hypertension prevalence and management within Germany. J Hypertens 2006;24(2):293-299.
(52) Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a
causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169(7):659-669.
(53) Miller N, Hill M. Nursing clinics in the management of hypertension. Hypertension 2004(2nd).
(54) Mohan V. Effects of a polypill (Polycap) on risk factors in middle-aged individuals without
cardiovascular disease (TIPS): a phase II, double-blind, randomised trial. The Lancet
2009;373(9672):1341-1351.
(55) National High Blood Pressure Education Program. The fourth report on the diagnosis, evaluation, and
treatment of high blood pressure in children and adolescents. : US Department of Health and Human
Services, National Institutes of Health, National Heart, Lung, and Blood Institute, National Hight Blood
Pressure Education Program; 2005.
(56) Nelson D, Kennedy B, Regnerus C, Schweinle A. Accuracy of automated blood pressure monitors.
American Dental Hygienists Association 2008;82(4):35-35.
(57) O'Brien E, Asmar R, Beilin L, Imai Y, Mancia G, Mengden T, et al. Practice guidelines of the European
Society of Hypertension for clinic, ambulatory and self blood pressure measurement. J Hypertens
2005;23(4):697-701.
(58) O'Brien E, Waeber B, Parati G, Staessen J, Myers MG. Blood pressure measuring devices:
recommendations of the European Society of Hypertension. BMJ 2001 Mar 3;322(7285):531-536.
(59) Panagiotakos DB, Pitsavos CH, Chrysohoou C, Skoumas J, Papadimitriou L, Stefanadis C, et al.
Status and management of hypertension in Greece: role of the adoption of a Mediterranean diet: the
Attica study. J Hypertens 2003;21(8):1483-1489.
(60) Parving H, Brenner BM, McMurray JJ, de Zeeuw D, Haffner SM, Solomon SD, et al. Cardiorenal end
points in a trial of aliskiren for type 2 diabetes. N Engl J Med 2012;367(23):2204-2213.
(61) Parving HH, Brenner BM, McMurray JJ, de Zeeuw D, Haffner SM, Solomon SD, et al. Aliskiren Trial in
Type 2 Diabetes Using Cardio-Renal Endpoints (ALTITUDE): rationale and study design. Nephrol Dial
Transplant 2009 May;24(5):1663-1671.
(62) Patarroyo SXF, Anderson C. Blood pressure lowering in acute phase of stroke: latest evidence and
clinical implications. Therapeutic advances in chronic disease 2012;3(4):163-171.
(63) Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, et al. Recommendations for blood
pressure measurement in humans and experimental animals: Part 1: blood pressure measurement in
humans: a statement for professionals from the Subcommittee of Professional and Public Education of
the American Heart Association Council on High Blood Pressure Research. Hypertension 2005
Jan;45(1):142-161.
(64) Pignone M, Mulrow CD. Evidence based management of hypertension: Using cardiovascular risk
profiles to individualise hypertensive treatment. BMJ 2001 May 12;322(7295):1164-1166.
(65) Pimenta E, Gaddam KK, Oparil S, Aban I, Husain S, Dell'Italia LJ, et al. Effects of dietary sodium
reduction on blood pressure in subjects with resistant hypertension: results from a randomized trial.
Hypertension 2009 Sep;54(3):475-481.
(66) Potter JF, Robinson TG, Ford GA, Mistri A, James M, Chernova J, et al. Controlling hypertension and
hypotension immediately post-stroke (CHHIPS): a randomised, placebo-controlled, double-blind pilot
trial. The Lancet Neurology 2009;8(1):48-56.
(67) Primatesta P, Brookes M, Poulter NR. Improved hypertension management and control: results from
the health survey for England 1998. Hypertension 2001 Oct;38(4):827-832.
115
(68) Psaltopoulou T, Orfanos P, Naska A, Lenas D, Trichopoulos D, Trichopoulou A. Prevalence,
awareness, treatment and control of hypertension in a general population sample of 26,913 adults in the
Greek EPIC study. Int J Epidemiol 2004 Dec;33(6):1345-1352.
(69) Puddey I, Beilin L, Vandongen R. Regular alcohol use raises blood pressure in treated hypertensive
subjects: a randomised controlled trial. The Lancet 1987;329(8534):647-651.
(70) Quinn M. Blood pressure measurement. ABC shows absence of evidence in measuring blood
pressure during pregnancy. BMJ 2001 Oct 6;323(7316):805; author reply 806.
(71) Redon J, Olsen MH, Cooper RS, Zurriaga O, Martinez-Beneito MA, Laurent S, et al. Stroke mortality
and trends from 1990 to 2006 in 39 countries from Europe and Central Asia: implications for control of
high blood pressure. Eur Heart J 2011 Jun;32(11):1424-1431.
(72) Ridker PM, Danielson E, Fonseca F, Genest J, Gotto Jr AM, Kastelein J, et al. JUPITER Trial Study
Group: Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation
of rosuvastatin: a prospective study of the JUPITER trial. Lancet 2009;373(9670):1175-1182.
(73) Rodríguez-Artalejo F, Graciani A, Guallar-Castillón P, León-Muñoz LM, Zuluaga MC, López-García E,
et al. Rationale and methods of the study on nutrition and cardiovascular risk in Spain (ENRICA). Revista
Española de Cardiología (English Edition) 2011;64(10):876-882.
(74) Sarafidis P, Lasaridis A, Gousopoulos S, Zebekakis P, Nikolaidis P, Tziolas I, et al. Prevalence,
awareness, treatment and control of hypertension in employees of factories of Northern Greece: the
Naoussa study. J Hum Hypertens 2004;18(9):623-629.
(75) Scheltens T, Bots M, Numans M, Grobbee D, Hoes A. Awareness, treatment and control of
hypertension: the ‘rule of halves’ in an era of risk-based treatment of hypertension. J Hum Hypertens
2006;21(2):99-106.
(76) Schmieder RE, Hilgers KF, Schlaich MP, Schmidt BM. Renin-angiotensin system and cardiovascular
risk. The Lancet 2007;369(9568):1208-1219.
(77) Schrader J, Luders S, Kulschewski A, Berger J, Zidek W, Treib J, et al. The ACCESS Study:
evaluation of Acute Candesartan Cilexetil Therapy in Stroke Survivors. Stroke 2003 Jul;34(7):1699-1703.
(78) Scuteri A, Najjar SS, Orru M, Albai G, Strait J, Tarasov K, et al. Age-and gender-specific awareness,
treatment, and control of cardiovascular risk factors and subclinical vascular lesions in a founder
population: the SardiNIA Study. Nutrition, Metabolism and Cardiovascular Diseases 2009;19(8):532-541.
(79) Smith WC, Lee AJ, Crombie IK, Tunstall-Pedoe H. Control of blood pressure in Scotland: the rule of
halves. BMJ 1990 Apr 14;300(6730):981-983.
(80) Staessen JA, Fagard R, Thijs L, Celis H, Arabidze GG, Birkenhäger WH, et al. Randomised doubleblind comparison of placebo and active treatment for older patients with isolated systolic hypertension.
The Lancet 1997 9/13;350(9080):757-764.
(81) Stone NJ, Merz CNB, ScM F, Blum FCB, McBride FP, Eckel FRH, et al. 2013 ACC/AHA Guideline on
the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. J Am Coll
Cardiol 2013.
(82) Thomas F, Rudnichi A, Bacri AM, Bean K, Guize L, Benetos A. Cardiovascular mortality in
hypertensive men according to presence of associated risk factors. Hypertension 2001 May;37(5):12561261.
(83) Thomas F, Rudnichi A, Bacri AM, Bean K, Guize L, Benetos A. Cardiovascular mortality in
hypertensive men according to presence of associated risk factors. Hypertension 2001 May;37(5):12561261.
(84) Trilling JS, Froom J. The urgent need to improve hypertension care. Arch Fam Med 2000 SepOct;9(9):794-801.
116
(85) Tugay Aytekin N, Pala K, Irgil E, Akis N, Aytekin H. Distribution of blood pressures in Gemlik District,
north‐west Turkey. Health & social care in the community 2002;10(5):394-401.
(86) Verro P, Gorelick PB, Nguyen D. Aspirin plus dipyridamole versus aspirin for prevention of vascular
events after stroke or TIA: a meta-analysis. Stroke 2008 Apr;39(4):1358-1363.
(87) Vidt DG. Telmisartan, ramipril, or both in patients at high risk for vascular events. Curr Hypertens
Rep 2008;10(5):343-344.
(88) Wachtell K, Ibsen H, Olsen MH, Borch-Johnsen K, Lindholm LH, Mogensen CE, et al. Albuminuria and
cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE study. Ann Intern
Med 2003;139(11):901-906.
(89) Williams B, Poulter NR, Brown MJ, Davis M, McInnes GT, Potter JF, et al. British Hypertension
Society guidelines for hypertension management 2004 (BHS-IV): summary. BMJ 2004 Mar
13;328(7440):634-640.
(90) Wilson P. Established risk factors and coronary artery disease: The Framingham study. Am J
hypertens 1994;7(7 S).
(91) Woodwell DA. National ambulatory medical care survey: 1998 summery. Adv Data 2000;1:315.
(92) World Health Organization. Diet, nutrition and the prevention of chronic diseases: report of a joint
WHO/FAO expert consultation. : Diamond Pocket Books (P) Ltd.; 2003.
(93) Yano Y, Fujimoto S, Sato Y, Konta T, Iseki K, Moriyama T, et al. Association between
prehypertension and chronic kidney disease in the Japanese general population. Kidney Int
2011;81(3):293-299.
(94) Zdrojewski T, Szpakowski P, Bandosz P, Pająk A, Więcek A, Krupa-Wojciechowska B, et al. Arterial
hypertension in Poland in 2002. J Hum Hypertens 2004;18(8):557-562.
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Guidline for managment of Hyperyension in Primary care

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