3.

04 Approach to Hypertension
DR. MARIEL BAGO-AZARES | 11/22/2018
LE 3
OUTLINE • PHILIPPINES
VI. Approach to Patient with → PRESYON 3 presented in 2013 (Figure 1). Increasing
I. Blood Pressure and Elevated Blood Pressure prevalence until it reached 28% prevalence.
Cardiovascular Risk A. Historical features → No data yet on the latest prevalence; they are yet to
II. Epidemiology favoring come out with another study.
III. Mechanisms Regulating hypertension cause
Blood Pressure B. Patient's relevant
A. Intravascular history
Volume C. Physical
B. Autonomic Nervous Examination
System D. Laboratory testing
C. Renin-Angiotensin- VII. Management of
Aldosterone System Hypertension
(RAAS) A. Non-
IV. Etiology pharmacological
V. Classification of Blood interventions
Pressure B. First line agents
A. Primary (Essential) C. Second line agents Figure 1. PRESYON 3: Report of the Council on Hypertension (COH).
Hypertension D. How to treat and In the Philippines the prevalence of hypertension has been determined by
B. Secondary follow-up several studies conducted throughout the years. Starting in 1992 by the
Nationwide Hypertension Registry and through the years by Council of
Hypertension VIII. Hypertensive Crisis Hypertension of the Philippine Heart Association. The studies have shown
a trend of increasing prevalence of hypertension among the Filipino
population. The study PRESYON 3 by the COH was presented in 2013
and showed the prevalence of Hypertension in Adults was 28%. PRESYON
LEGEND 3 is a prospective multi-staged stratified nationwide survey on hypertension
Remember Lecturer Book Previous Presentation which reported a high prevalence of hypertension in adults (>18 years old)
Trans at 28%.

III. MECHANISMS REGULATING BLOOD PRESSURE

Learning Objectives:
• To understand the mechanisms of blood pressure regulation
• To interpret blood pressure measurements to confirm and
diagnose hypertension
• To determine proper history and PE for assessing patients with
elevated BP
• To know the appropriate management for elevated blood
pressure Figure 2. Determinants of Arterial Pressure. Cardiac Output and
Peripheral Resistance.
I. BLOOD PRESSURE AND CARDIOVASCULAR RISK
• For adults >30 years old – a higher systolic BP (SBP) and • To provide a framework for understanding pathogenesis
diastolic BP (DPB) is associated with increased risk of CV of and treatment options for hypertensive disorders, it is
incidence, angina, MI, heart failure, stroke, Peripheral useful to understand the factors involved in the regulation
Artery Disease (PAD) and abdominal aortic aneurysm of arterial pressure.
• When the BP components are considered separately, a • The two determinants of arterial pressure are:
higher SBP has been CONSISTENTLY associated with → CARDIAC OUTPUT = SV x HR
increased CV risk while DBP has NOT BEEN ▪ the amount of blood pumped by the heart
CONSISTENTLY associated with CVD risk each minute
• SBP more important ▪ determined by Stroke Volume (SV) and
Heart Rate (HR)
II. EPIDEMIOLOGY ▪ SV - the volume of blood pumped from the
heart per beat; related to myocardial
• Age 60 and older, SBP of women are higher than men
contractility
• Among adults – DBP increases progressively with age until ▪ HR - the number of heart beats per minute
~55 years old after which it tends to decrease. This results ▪ Increase in SV or HR will decrease Cardiac
in a widening pulse pressure beyond age 60 Output which will increase the arterial
• PULSE PRESSURE = SBP - DBP pressure (verbatim)
• USA o Note: It should be INCREASE in HR
→ 2012 – Hypertension was the second leading cause of or SV INCREASES CO which will
End Stage Renal Disease (ESRD) behind Diabetes INCREASE arterial pressure
Mellitus (Example: in exercise where other
→ > 50% of deaths from coronary heart disease and mechanisms are activated)
stroke occurred among patients with hypertension o Increase in HR alone can negatively
based on US NHANES (national health and nutrition affect SV (decreased filling time →
examination survey) decreased CO)
→ ~30% of adults of 65 million people have hypertension → PERIPHERAL RESISTANCE
▪ determined by the functional and anatomic
changes in the small arteries and arterioles
Trans Group 25: Amatorio, Andres, Ereño, Escovidal, Espeleta EDITOR: Alcos (09158255900) 1 of 11
3.04 Approach to Hypertension
▪ increase in peripheral resistance will increase Table 1. Adrenergic Receptors and their locations and actions.
the arterial pressure RECEPTOR LOCATION ACTION
• An increase in cardiac output and peripheral resistance Alpha 1 Post synaptic cells in Vasoconstriction
will increase BP Smooth muscle
Kidneys Increase in renal
A. INTRAVASCULAR VOLUME tubular absorption of
sodium
• SODIUM Alpha 2 Presynaptic Negative feedback
→ The predominant extracellular ion which primarily membranes of controllers inhibiting
determinines the extracellular fluid (ECF) volume postganglionic nerve further NE release
→ Increase in NaCl intake more than the capacity of the terminal that
kidneys to excrete will result in expansion of the synthesize NE
vascular volume which can increase Cardiac Output Beta 1 Myocardium Increase rate and
resulting in increase in Blood Pressure contractility of the
heart
• ↑NaCl : ↑ vascular volume: ↑ CO : ↑ BP
→ Salt in the chloride form (NaCl) has effects on blood
pressure Kidney Renin release
- activation of RAAS
• The effect of sodium on blood pressure is related
system
to the provision of sodium with CHLORIDE.
Beta 2 Vascular smooth Vasodilation
• NONCHLORIDE salts have LITTLE TO NO effect
muscles
on BP (Ex,. Pressor effect NaCl >>> NaHCO3)
o Implies that Cl- has a role in BP
regulation C. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
(RAAS)
B. AUTONOMIC NERVOUS SYSTEM • Contribute to the regulation of arterial pressure via
• Baroreflex vasoconstrictor properties of Angiotensin II and
• Adrenergic Function Aldosterone (Figure 3)
• RENIN
Baroreflex → RAAS starts from its release
• Short-term regulation → Synthesized in the renal afferent arteriole
• Primary mechanism for rapid buffering of acute → Secretion due to:
fluctuations of arterial pressure that may occur during 1. Decrease in NaCl transport in thick ascending loop
postural changes, behavioral or physiologic stress and of Henle (TALH)
changes in blood volume. This reflex modulates blood 2. Decrease in pressure or stretch of renal afferent
pressure on a minute to minute basis. arteriole
o It continuously monitors arterial pressure 3. Sympathetic nervous system stimulation via Beta 1
changes and responds rapidly to those receptors in the kidneys
changes, • Renin will cleave angiotensinogen to angiotensin I
• Mediated by stretch-sensitive sensors (inactive form) and upon action of angiotensin
(BARORECEPTORS) located in the Carotid Sinus and converting enzyme (ACE; mainly located in the lungs) it
Aortic Arch becomes angiotensin II (active form)
• Stretch of blood vessel due to increase in pressure o Effects:
results to firing of signals of baroreceptors to the CNS o Activation of sympathetic system
which will influence sympathetic outflow causing: o Aldosterone production
→ Vasodilation → ↓Peripheral resistance o Arteriolar vasoconstriction
→ Decrease heart rate and cardiac contractility o Increase reabsorption of NaCl
o Increased ADH leading to water retention
▪ ↑BP → negative feedback → renin
Adrenergic Function
inhibition
• Adrenergic function together with hormonal and • ANGIOTENSIN II
volume-related factors contribute to the long-term → potent pressor substance
regulation of the arterial pressure → Acts on angiotensin II type 1 receptor (AT1) on cell
• Mediated by endogenous catecholamines: membranes
→ Norephinephrine (NE), Epinephrine (E), and Dopamine → Primary tropic factor for secretion of aldosterone by
→ Role in the tonic and phasic cardiovascular regulation adrenal zona glomerulosa
→ Acting on adrenergic receptors (alpha and beta → Potent mitogen = vascular smooth muscle cell and
receptors) myocyte growth
▪ Alpha Receptors 1 and 2 – occupied and → Angiotensin II type 2 receptor have the opposite
activated by NE more than E functional effects of AT1 = vasodilation, sodium
▪ Beta Receptors 1 and 2 – occupied and excretion and inhibits cell growth and matrix formation
activated by E more than NE • ALDOSTERONE
• Antihypertensive medications can be → Synthesis also dependent on potassium levels
o Alpha 2 agonist resulting in reduced → Increases sodium reabsorption
sympathetic outflow, hence less NE release
o Beta blockers (inhibit B1 receptors) resulting in
decrease in HR

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3.04 Approach to Hypertension
• Atherosclerosis is the most common cause of renovascular
disease
Table 3. Uncommon causes of secondary hypertension
Common causes Prevalence
Pheochromocytoma 0.1-0.5%
Cushing’s syndrome <0.1%
Hypothyroidism/Hyperthyroidism 1%
Coarctation of the aorta 0.1%
Congenital adrenal hyperplasia Rare

Renal Parenchymal Disease

• Virtually all disorders of the kidney may cause
hypertension
• Hypertension is more severe in glomerular disease
than in interstitial kidney disease
• Hypertension is seen in >80% of patients with chronic
renal failure
• Renal failure can be the cause of hypertension or vice
versa
Figure 3. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS) o That is why it is sometimes difficult to determine
which came first in a patient with renal disease
and a hypertension
IV.ETIOLOGY
• The causes in the elevation of blood pressure can be due Renovascular Disease
to: • Due to an occlusive lesion of the renal artery (renal artery
• Genetic Predisposition stenosis)
→ Hypertension is a complex POLYGENIC disorder and • 2 groups of patients at risk for this disorder:
many genes/gene combinations that influence BP o Older atherosclerotic patients
• Environmental Risk Factors/Exposures o Fibromuscular dysplasia – strong predilection
→ Diet-related factors for young white female
• Excessive NaCl intake (positive association • Atherosclerotic disease (90%) is by far the most common
between intake and BP) cause of renal artery stenosis
• Being overweight/Obesity (direct relationship • Clues in the history and PE for the diagnosis of renal
between BMI and BP that is continuous and linear; artery stenosis
higher BMI correlates with having elevated BP) o Severe or refractory hypertension, unexplained
→ Physical Fitness deterioration of renal function or deterioration of
renal function with an ACEI
• There is an inverse relationship between physical
o Presence of an abdominal or flank bruit –
activity and level of BP. No/absent physical activity
bruit is hemo-dynamically significant if it
likely to elevate BP.
lateralizes or extends throughout systole into
• Studies have shown that even modest levels of
diastole
activity are associated with decrease in risk of
• Treatment
hypertension.
o Medical therapy for adults with atherosclerotic
→ Alcohol consumption
renal artery stenosis – antihypertensive
• Direct relationship between alcohol consumption medications, high intensity statins
and BP. o Revascularization by percutaneous
A. PRIMARY “ESSENTIAL” HYPERTENSION transluminal angioplasty (PTA) - for those not
• 80-95% of patients responding to medications or those diagnosed
• NO IDENTIFIABLE cause with fibromuscular dysplasia
• Familial
• Consequence of interaction between environmental and Primary Alderosteronism
genetic factors • Disorder of excess aldosterone production
• Aldosterone production is inappropriately high and
B. SECONDARY HYPERTENSION independent to its major regulators of secretion
• 5-20% of patients (angiotensin II and potassium)
• A specific underlying disorder causing the elevation of BP • Induces hypertension, sodium retention, increased
can be identified potassium excretion and suppressed plasma renin
• According to the 2017 High Blood Pressure Clinical activity (PRA)
Practice Guideline, there are common and uncommon • 2 most common cause:
causes of hypertension o Aldosterone producing adenoma
▪ Unilateral
Table 2. Common causes of secondary hypertension ▪ Responsive to surgery
Common causes Prevalence o Bilateral adrenal hyperplasia
Renal Parenchymal Disease 1-2 % ▪ Treated medically with aldosterone
Renovascular Disease 5-34% antagonist
Primary Aldosteronism 8-20% • History
Obstructive Sleep Apnea 25-50% o Consider in patients with refractory
Drug or Alcohol Induced 2-4% hypertension. However, most patients are
asymptomatic. If suspected, do screening.
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3.04 Approach to Hypertension
• Screening Test o Recreational drugs (e.g. cocaine,
o Ratio of aldosterone to plasma renin activity methamphetamine)
(PRA) o Systemic Corticosteroids given via IV (e.g.
o If ratio of 30:1, do confirmatory test. dexamethasone, prednisone, prednisolone)
▪ Aldosterone:PRA is currently the o Angiogenesis Inhibitors (e.g. bevacizumab) and
most accurate and reliable means of tyrosine kinase inhibitors (e.g. sunitinib)
screening for primary aldosteronism.
▪ Cutoff value is 30:1 where plasma V. CLASSIFICATION OF BLOOD PRESSURE
aldosterone conc is in ng/dL and PRA
• It is useful to categorize bp levels for clinical and public
is in ng/ml.h
health decision making.
• Confirmatory Test - demonstrates failure to suppress
aldosterone production upon administration
Table 4. BP Categories based on Harrisons 2003.
o Intravenous saline suppression test
BP Category SBP (mmHg) DBP (mmHg)
▪ 2L of isotonic slaine over 4 hours
Normal < 120 and < 80
o Oral salt load, captopril or fludrocortisone
administration Prehypertension 120 – 139 or 80-89
Stage 1 HTN 140 – 159 or 90 – 99
Obstructive Sleep Apnea (OSA) Stage 2 HTN ≥160 or ≥100
Isolated systolic ≥140 and <90
• Chronic condition characterized by recurrent collapse of
hypertension
upper airway during sleep, inducing intermittent episodes
of apnea/hypopnea, hypoxemia and sleep disturbance
• Associated with increased risk of hypertension • Based in Harrison, which was taken from a journal back in
2003
• Hypertension related to OSA should be considered in
patients with drug resistant hypertension and patients • Normal BP is at 120/80
with history of snoring (and daytime somnolence ) • Prehypertension is at 120-139/80-89
• Confirmed by polysomnography • Stage 1 hypertension is at a SBP level of 140-159/90-99
• Treatment: CPAP or Bi PAP during sleep • THIS CLASSIFICATION IS NOW OUTDATED as newer
o CPAP - continuous positive airway pressure guidelines have been published over the years.(JNC 8 for
HTN)
o BiPAP - bilevel positive airway pressures

Pheochromocytoma Guideline for the Prevention, Detection, Evaluation, and

• Catecholamine secreting tumors located in the adrenal Management of High Blood Pressure in Adults
medulla • This guideline categorizes BP into 4 levels on the basis of
• Increased levels of catecholamines will result in average BP measured in the healthcare setting (office/clinic BP
hypertension (can be continuous or episodic HTN) readings)
• Symptoms include headache, palpitations and sweating
during episodes of elevated BP Table 5. BP Categories based on new guidelines in 2017.
• Lab testing – measuring catecholamines in urine or BP Category SBP (mmHg) DBP (mmHg)
plasma (e.g 24 hour urine metanephrine excretion or Normal < 120 and < 80
fractionated plasma free metanephrines) Elevated 120 – 129 and < 80
• Imaging is done to confirm tumor Stage 1 HTN 130 – 139 or 80 – 89
• TREATMENT : Surgery Stage 2 HTN ≥140 or ≥90

Coarctation of the aorta In BP categories, do not forget to take note of the logical operators
• Most common congenital cardiovascular cause of AND & OR.
hypertension Exam tip! Doc will give BP measurements so know the categories!
• PE findings:
o Diminished and delayed femoral pulses • Recommends the following BP criteria for defining NORMAL
o Systolic pressure gradient between the right BP, elevated BP and Staging of Hypertension levels.
arm and legs • Take note that the normal BP level should still be <120/80.
o Blowing systolic murmur in the posterior left • Elevated BP is considered at 120-129/80
interscapular area • STAGE 1 HTN is now at level of 130-139/80-89mmHg.
• Treatment: surgical repair and balloon angioplasty with or • The rational for this categorization is based on observational
without intravascular stent data (Randomized controlled trials of treatment with
hypertensive medications to prevent CVD) related to the
Frequently used medications and other substances that association between SBP, DBP, and CVD risk.
may cause elevated BP • The prevalence of hypertension among US adults is
• Some medications and substances that the patient takes substantially higher when the definition in this present guideline
may cause elevated BP. is used as compared to previous guidelines. (prevalence
• It is important to ask in the history of consumption/use of increased to 46% vs. 32%)
these substances.
o ALCOHOL
o AMPHETAMINES
o ANTIDEPRESSANTS ( e.g. MAOI,SNRI)
o Atypical antipsychotics (e.g. Clonazipine)
o Caffeine
o Decongestants (e.g. Phenylephrine)
o Oral contraceptives
o NSAIDs
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VI. APPROACH TO PATIENT WITH ELEVATED BLOOD → smoking
PRESSURE → diabetes
→ physical inactivity
• The evaluation of patients with elevated BP is to
• Evidence of secondary hypertension
→ identify if they have target organ damage related to the high → history of renal disease
BP
→ change in appearance
→ determine if there are secondary causes for the hypertension
→ muscle weakness
→ assist in effective planning and treatment regimen of the
→ spells of sweating
patient
→ palpitation
→ tremor
• Certain features in your history should include the pattern or
change in blood pressure → erratic sleep
→ Did it start increasing slowly over the years or is it fluctuating → snoring
▪ Primary hypertension usually a gradual increase over the → daytime somnolence
years → symptoms of hypo- or hyperthyroidism
▪ Secondary hypertension usually refractory, or sudden → use of agents that may increase blood pressure
elevation in BP (of previously controlled BP) • Evidence of target organ damage
→ History of transient ischemic attack (TIA)
→ Stroke
A. HISTORICAL FEATURES FAVORING
→ Transient blindness
HYPERTENSION CAUSE * → Angina
*from the 2017 HBP guideline (was emphasized) → Myocardial infarction
• Historical features are relevant to the evaluation of the → Congestive heart failure
patient as this may help identify cause of the hypertension → Sexual function
• Ask regarding the pattern of BP measurement and changes • Other co-morbidities
overtime as this may help to differentiate a primary from • In general, there are no specific symptoms referable to BP
secondary cause of HTN elevations
• History taking should also include the occurrences of → Patients may complain about getting a headache or nape
symptoms that indicate a possible secondary cause of HTN pain and think they have hypertension
• For example: symptoms suggestive of thyroid disease (hyper ▪ But majority of patients are asymptomatic
or hypothyrodism), symptoms suggestive of → Headache generally occurs with severe hypertension
pheochromocytoma (repetitive episodes of sweating → Hypertensive headache occurs in the morning localized on
headache palpitations with elevated BP) the occipital region
→ Px can also complain of non-specific symptoms such as
Primary Hypertension dizziness, palpitations, and easy fatiguability
• Gradual increase in BP, with slow rate of rise in BP
• Lifestyle factors that favor higher B (e.g., weight gain, high- C. PHYSICAL EXAMINATION
sodium diet, decreased physical activity, job change entailing
increased travel, excessive consumption of alcohol) • Assess for physical features that may suggest secondary
hypertension
• Family history of hypertension
• Assessment of hypertension related target organ damage
• Accurate blood pressure measurement
Secondary Hypertension
• Body habitus including weight and height
• BP lability, episodic pallor and dizziness (pheochromocytoma) → Compute for BMI
• Snoring, hyper somnolence (obstructive sleep apnea) • Pulses
• Prostatism (chronic kidney disease due to post-renal urinary → Various pulses should be palpated
tract obstruction) → Comparison of radial and femoral pulses to detect radial
• Muscle cramps, weakness (hypokalemia from primary femoral delay
aldosteronism or secondary aldosteronism due to renovascular ▪ Indicates coarctation of the aorta
disease) • Neck
• Weight loss, palpitations, heat intolerance (hyperthyroidism) → Palpate for enlarged thyroid gland; check for thyroid
• Edema, fatigue, frequent urination (kidney disease or failure) problems
• History of coarctation repair (residual hypertension associated • Examination of blood vessels
with coarctation) → Examinations may provide clues about underlying vascular
• Central obesity, facial rounding, easy bruisability (Cushing’s disease
syndrome) → Fundoscopy of retina – only tissue where arteries and
• Medication or substance use (e.g., alcohol, NSAIDS, cocaine, arterioles can be examined directly
amphetamines) → Fundoscopic changes with increasing severity of HTN (figure
• Absence of family history of hypertension 4 & Table 6)

B. PATIENT’S RELEVANT HISTORY

• Duration of hypertension
• Previous therapies
→ responses and side effects
• Family history of hypertension and cardiovascular disease
• Dietary and psychosocial history
• Other risk factors
→ weight change
→ dyslipidemia
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• Use correct cuff size, bladder encircles 80% of the arm

STEP 3: Take the proper measurements needed for diagnosis

and treatment of elevated BP/hypertension
•

• First visit record BP in both arms. Use the arm that gives
the higher reading for subsequent readings.
• For auscultatory readings, deflate the cuff pressure 2mmHg
per second, and listen for Korotkoff sounds

STEP 4: Properly document accurate BP readings

•

• Record SBP and DBP

STEP 5: Average the readings

•

• Use an average of ≥2 readings obtained on ≥2 occasions

to estimate the individual’s level of BP
• Because individual BP measurements tend to vary in an
unpredictable manner or random fashion, a single reading is
Figure 4. Different stages of hypertensive retinopathy. Grade 1- tortuous inadequate for clinical decision making. An average of 2 to 3
retinal arteries, silver wiring Grade 2 - AV nicking Grade 3- flame-shaped BP measurements obtained on separate occasions will
hemorrhages, cotton wool patches Grade 4 – papilledema. (I suggest you minimize random errors and provide a more accurate basis
guys check this in Google for a clearer picture with labels 😊) for estimation of BP.
• On the first BP, you do not label then as hypertensive right
Table 6. Hypertensive retinopathy grading. away

STEP 6: Provide BP readings to patient

• Provide patient’s the SBP/DBP readings both verbally and in
writing

Hypertension is based on the average of 2 or more BP readings

during two or more outpatient visits

Out-of-Office Blood Pressure Measurements

• Refers to the use of Ambulatory BP monitoring (ABPM) or
Home BP monitoring (HBPM)
• Heart • OOBP measurements are recommended to confirm the
diagnosis of hypertension and for titration of BP lowering
→ Enlarged sustained laterally displaced apical impulse = LVH
medications.
→ Check for murmurs that may indicate presence of coarctation
• Provides a larger number of BP measurements than
of the aorta
conventional office/clinic BP.
• Abdomen
→ Check for abdominal bruit
→ Bruit that lateralizes and extends throughout systole into
ABPM HBPM
diastole caused by renal artery stenosis = renovascular • Obtains out of office BP • Out-of-office BP readings
hypertension readings at set intervals, taken by a patient
usually over 24 hours • They [patients] record,
Key Steps for Proper BP Measurement • Conducted while come back, and show their
from 2017 guidelines individuals go about their BP readings
daily activity • A more practical approach
• The physical exam should include accurate measurement of
• Estimates mean BP over (Compared to ABPM
BP.
the entire day, and wherein the patient needs
• Although measurement of BP in the clinic setting is relatively separately during daytime to be scheduled, and limited
easy, errors are common and can result in a misleading and nighttime availability of ABPM
estimation of an individual’s true level of BP
• Provides a better method apparatus )
• Errors can be avoided by paying attention to proper technique to predict long-term CVD
STEP 1: Properly prepare the patient outcomes than office/clinic
• Patient should be relaxed, sitting in a chair (feet on floor, BPs
back supported) for >5 minutes • The apparatus is a cuff that
• Remove all clothing covering location of cuff placement the patient puts on and
• Avoid caffeine, exercise and smoking at least 30 mins before automatically takes BP
measurement readings at certain
intervals throughout the
STEP 2: Use the proper technique for BP measurements day. They cannot take the
• cuff off until the end of 24
• Use a BP device that has been validated and ensure the hrs.
device is calibrated periodically
• Support the patient’s arm (eg resting on a desk)
• Position middle of the cuff on patient’s upper arm at the level
of the right atrium (midpoint of the sternum)

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Table 7. Corresponding values of SBP/DBP for clinic, HBPM, → It will depend on how you look at the patient's clinical profile
Daytime, Nighttime, and 24-hour ABPM Measurements. if you will give them antihypertensive medications.
Daytime Nighttime 24-Hour
Clinic HBPM
ABPM ABPM ABPM D. LABORATORY TESTING
120/80 120/80 120/80 100/65 115/75 Table 9. Basic Laboratory Tests for Initial Evaluation from
Harrison’s.
130/80 130/80 130/80 110/65 125/75 System Test
Renal Microscopic urinalysis, albumin excretion,
140/90 135/85 135/85 120/70 130/80 serum BUN and/or creatinine
Endocrine Serum sodium, potassium, calcium, TSH
160/100 145/90 145/90 140/85 145/90
Metabolic Fasting blood glucose, total cholesterol, HDL
Table interpretation: Values at the same row level are equivalent and LDL (often computed) cholesterol,
pressure readings across the different modes of BP measurement. triglycerides
*highlighted in red is elevated/abnormal threshold. Other Hematocrit, electrocardiogram
• Threshold for an elevated BP will differ for HBPM and for ABPM
as compared to clinic BP • Laboratory measurements should be obtained for all patients
• Significant BP in the clinic is 140/90 with a new diagnosis of elevated BP
• When a patient comes back to you and says, ‘Doc, my (H)BP → to facilitate CVD risk factor profiling
for the past days/week has been at 135/85’ this is equivalent to → to establish a baseline for medication use
a clinic BP of 140/90 = considered abnormal or elevated → to screen for secondary causes of hypertension.
• For ABPM, it has 3 results: average BP in the daytime, • Optional tests may provide information on target organ damage:
nighttime and 24-hour echocardiogram
→ These three values [135/85, 120/70, 130/80; respectively]
are equivalent to a clinic BP of 140/90 VII. MANAGEMENT OF HYPERTENSION
→ When the patient brings back the ABPM, there is a print out • Prevention of HTN and treatment of established HTN are
of all the BPs in 24 hours and then it also averages complementary approaches to reducing CVD risk.
→ Higher daytime ABPM – associated with increase risk of
CVD A. NON-PHARMACOLOGICAL INTERVENTIONS
→ An abnormal nighttime BP – stronger risk factor for coronary • Health-promoting lifestyle modifications are recommended for
heart disease and stroke than either daytime SBP or a individuals with pre-hypertension and as an adjunct to drug
clinic/office BP therapy in hypertensive patients.
▪ Why? At night, BP should be lower • Non-pharmacologic interventions are effective in lowering BP
and the most important of these non-pharmacologic
• The availability of out of office BP measurements have resulted interventions are as follows: (Summary Table: Appendix 1)
in differentiation of hypertension in several clinically useful → Weight loss: Core recommendation; achieved through
categories that are based on the place of BP measurement combinations of reduced caloric intake and increased
(Table 8) physical activity. Effect has a dose-response relationship: 1
mmHg lowering effect per kg of weight loss
Table 8. BP Patterns Based on Office and Out-of-Office → DASH Diet: Diet best demonstrated to be effective for
Measurements lowering BP. DASH diet consists of high vegetables, fruits,
Home/Non whole grain, and low-fat dairy products with reduced
Office/Clinic/Health
HealthCare/ content of saturated and total fat. Overall SBP reduction of
Care Setting
ABPM Setting 11 mmHg in hypertensive patient
→ Na Reduction: reduction in Na intake to 1000 mg/day
Normotensive No hypertension No hypertension
decreases SBP by 5-6 mmHg in hypertensive patients.
Sustained → Dietary K intake: WHO recommends a K intake of 3500
Hypertension Hypertension
hypertension mg/day for adults and good sources of dietary K are in fruits
Masked and vegetables. 4 to 5 servings of fruits and vegetables
No hypertension Hypertension
Hypertension per day will provide 1500 – 3000 mg of K. A potassium rich
White coat diet will decrease SBP by 4-5 mmHg in hypertensive
Hypertension No hypertension patients.
hypertension
→ Increased Physical Activity: shows a BP lowering effect
• MASKED HYPERTENSION → Reduce Alcohol Consumption: safe level of regular alcohol
→ Office BP readings are normal but out of office BP consumption with regards to hypertension is 2 drinks/day in
(ABPM/HBPM) are consistently above normal. men and 1 day/day in women.
→ Associated with an increased prevalence of target organ ▪ One standard drink approx. 14 grams of pure alcohol
damage and risk of CVD, stroke and mortality than found in 12 oz of regular beer (5% alcohol), 5 oz of wine
normotensive patients and those with white coat (12% alcohol) and 1.5 oz distilled spirits (40% alcohol)
hypertension

• WHITE COAT HYPERTENSION

→ Elevated office BP but normal readings when measured
out the clinic using HBPM/ABPM
→ Clinical relevance- associated with MINIMAL to only slight
increase in risk of CVD and all cause mortality
→ No data on the risk and benefits of treating this type of
hypertension
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Table 10. Lifestyle modifications to manage hypertension Angiotensin Receptor Blockers (ARBs)
Factor Action
• MOA: RAAS antagonist; selective blockade of Angiotensin I
Weight Attain and maintain BMI<25kg/m2 receptors
Reduction • Result: decreases peripheral vascular resistance
Dietary salt <6 g NaCl/d • Side effects: hyperkalemia (same as ACEI)
reduction → Ex: Losartan, Valsartan
Adapt DASH- Diet rich in fruits, vegetable, and low-fat
type dietary dairy products with reduced content of
plan saturated and total fat NOTE: &
Moderation For those who drink alcohol, consume ≤ 2 • ACEI and ARBs can cause hyperkalemia due to hypoaldosteronism
of alcohol drinks/day in men and ≤ 1 drink/day in • ACEI / ARB combinations are less effective in lowering BP than is the
consumption women case when either class of agents is used in combination with other
Physical Regular aerobic activity, e.g. brisk walking classes of agents
Activity for 30 min/d

B. FIRST LINE AGENTS

C. SECOND LINE AGENTS
• Pharmacologic agents in addition to lifestyle modifications are
the primary basis for treatment of high BP. Antihypertensive • These are other drug classes that can be used to treat elevated
medications not only lowers BP but reduces the risk of CVD and BP but studies needed to show that these agents decrease
death. clinical outcomes similar to the 4 primary agents mentioned
• The recommended primary agents used in treatment of HTN earlier is lacking, or the safety and tolerability may regulate their
are thiazide diuretics, calcium channel blockers (CCBs), role. Hence, they are to be used as second line agents.
angiotensin converting enzyme inhibitors (ACEI) or Beta Blockers
angiotensin receptor blockers (ARBs). These agents have
• MOA: decrease cardiac output (by decreasing heart rate), CNS
been proven to reduce clinical events and should be used
effect, inhibit renin release
preferentially as the first line agents.
• Result: decreases heart rate and contractility, decrease renin
• Drug therapy is recommended for individuals with BP ≥
release
140/90mmHg
→ Non-Cardioselective (ex: propranolol)
→ Cardioselective (ex: atenolol, metoprolol)
Diuretics (Thiazides or Thiazide-like Agents) → Combined Alpha & Beta blocker (ex: carvedilol)
• MOA: inhibits Na+/Cl- pump in the distal convoluting tubules and • There is inadequate evidence to support the initial use of BB for
increases Na+ excretion HTN in the absence of specific CV co-morbidities
• Result: decreases circulating volume • Low doses exert greater inhibitory effect on B1 receptors than
• Side effects: increased cholesterol, insulin resistance, B2 receptors on bronchial and vascular smooth muscle cell, but
hypokalemia (higher doses are not recommended ) selectivity is lost at high doses.
→ Ex: Hydrochlorothiazide, Indapamine
• Maybe used alone or in combination with other antihypertensive Alpha Adrenergic Blockers
drugs • MOA: post-synaptic alpha adrenoreceptor antagonist
• Provide an additive BP lowering effect when combined with • Result: decrease peripheral vascular resistance
ACEI/ARBS. → Ex: Prazosin, Phenoxybenxamine
• Block the interaction of NE on vascular alpha receptors that can
Calcium Channel Blockers (CCBs) lead to vasoconstriction (causing peripheral dilation)
• MOA: reduces intracellular Ca2+ by blocking L channels which
NOTE: &
reduces vascular resistance
• Alpha and Beta blockers block both beta receptors and peripheral
• Result: decreases peripheral resistance
adrenergic receptors
• Side effects: flushing headache, edema with dihyropyridine use
which is related to arteriolar dilation
• The edema is due to an increase in transcapillary pressure Sympatholytics
gradient NOT to net salt and water retention • MOA: centrally acting alpha 2 sympathetic agonist decrease
→ Ex: Amlodipine, Nifedipine (Dihydropyridine), peripheral resistance by inhibiting sympathetic outflow
Verapamil/Diltiazem (Non-Dihydropyridine) • Result: decreases peripheral resistance and venous
• Used alone or with other antihypertensive agents constriction by depleting nerve terminal NE.
• Side effects: somnolence, dry mouth, sexual dysfunction,
Angiotensin Converting Enzyme Inhibitors (ACEI) rebound hypertension on withdrawal (abrupt cessation of drugs
with a short half-life); Usefulness is limited by their side effects
• MOA: RAAS antagonist; inhibits ACE from converting
→ Ex: Clonidine, Methyldopa
Angiotensin I to the active form of Angiotensin II; decreases
Angiotensin II production
• Result: decreases peripheral vascular resistance Direct Vasodilators
• Side effects: dry cough, angioedema, hyperkalemia • MOA: Vasodilators; Hydralazine has nitric oxide enhancing
→ Ex: Captopril, Ramipril actions (direct action)
• Dry cough occurs in 15 % of patients. • Result: decrease peripheral resistance
→ ACEI also inhibits the degradation of bradykinin. Increased • Side effects: lupus-like syndrome (hydralazine), hypertrichosis
levels in bradykinin can activate nociceptive sensory and pericardial effusion (minoxidil)
receptors in the lungs triggering cough. → Ex: hydralazine, minoxidil
• Angioedema – occurs in <1% of patients • Most effective when added to a combination that includes a
diuretic and a beta blocker.
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Table 11. Drugs and their contraindications Table 13. Preferred parenteral drugs for selected hypertensive emergencies
Drug Class Contraindication / Caution
Diuretics Diabetes, gout
Beta blockers Asthma, COPD, 2nd or 3rd degree
heart block, sick sinus syndrome
ACEI and ARBs Acute renal failure, bilateral renal
artery stenosis, hyperkalemia,
pregnancy
CCBs (non-dihydropyridines) 2nd and 3rd degree heart block
Direct Vasodilators Severe coronary artery disease

D. HOW TO TREAT AND FOLLOW-UP

• You now know the patient’s BP, HTN classification. Now what?
• See Appendix 2 flowchart. (Don’t skip!)
→ Clinical CVD is defined as CHD, congestive HF and stroke.
→ Green: Class 1 recommendation in the guidelines.

VIII. HYPERTENSIVE CRISIS

Table 12. Hypertensive Emergency vs. Hypertensive Urgency
Hypertensive Emergency Hypertensive Urgency
• Severe elevation in BP • Severe BP elevations in a
>180/120mmHg associated stable patient without
with evidence of new or acute or impending Table 14. Usual Intravenous Doses of Anti-Hypertensive Agents used in
worsening target organ change in target organ Hypertensive Emergencies
damage (TOD) damage or dysfunction
• TOD - presence of • No indication for referral to
hypertensive the ER or immediate
encephalopathy, ICH, acute reduction of BP in the ER or
MI, acute LV failure with hospitalization
pulmonary edema, unstable • Patients who withdrawn from
angina pectoris, acute renal or non-compliant to
failure antihypertensive therapy
• Immediate reduction of BP • Reinstitute or intensify
(not necessarily to normal) antihypertensive drug
• Intravenous administration of therapy
appropriate BP lowering
agent. ORAL agents are
discouraged

• Malignant hypertension
→ Syndrome associated with an abrupt increase on BP in a
patient with underlying hypertension or related to the
sudden onset of hypertension in a previously
normotensive individual.

A. DRUGS USED IN HYPERTENSIVE EMERGENCIES

• No high-quality randomized control trial (RCT) evidence to
inform which first line antihypertensive class provides more
benefit than harm in hypertensive emergencies. REFERENCES
• Treatment goal in hypertensive emergencies- minimize TOD Harrison’s Principles of Internal Medicine 19th Ed.
safely by rapid recognition of the problem and early initiation of Dr. Bago-Azares’ Powerpoint.
appropriate therapy. Lecture Recording
• (Ermmm tiwalang hindi ito itatanong. OTL)

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APPENDIX
Appendix 1. Summary of the Non-pharmacologic interventions for prevention and treatment of hypertension.
Non-pharmacological
Dose
Intervention Hypertension Normotension

Best goal is ideal body weight, but aim for at least

a 1-kg reduction in body weight for most adults who
Weight loss Weight/body fat -5 mm Hg -2/3 mm Hg
are overweight. Expect about 1 mm Hg for every
1-kg reduction in body weight.

DASH dietary pattern

Consume a diet rich in fruits, vegetables, whole
Healthy diet grains, and low-fat dairy products, with reduced -11 mm Hg -3 mm Hg
(DIETARY APPROACH content of saturated and total fat.
TO STOP
HYPERTENSION)

Reduced
intake of Optimal goal is <1500 mg/d, but aim for at least a
Dietary sodium -5/6 mm Hg -2/3 mm Hg
dietary 1000-mg/d reduction in most adults.
sodium

Enhanced
intake of Aim for 3500–5000 mg/d, preferably by
Dietary potassium -4/5 mm Hg -2 mm Hg
dietary consumption of a diet rich in potassium.
potassium

● 90–150 min/wk
Aerobic -5/8 mm Hg -2/4 mm Hg
● 65%–75% heart rate reserve

● 90–150 min/wk

● 50%–80% 1 rep maximum

Dynamic resistance -4 mm Hg -2 mm Hg

● 6 exercises, 3 sets/exercise, 10 repetitions/set

Physical
activity

● 4 × 2 min (hand grip), 1 min rest between

exercises, 30%–40% maximum voluntary
Isometric resistance -5 mm Hg -4 mm Hg
contraction, 3 sessions/wk

● 8–10 wk

In individuals who drink alcohol, reduce alcohol† to:

Moderation in
Alcohol consumption -4 mm Hg -3 mm
alcohol intake
● Men: ≤2 drinks daily

● Women: ≤1 drink daily

Appendix 2. Blood Pressure thresholds and recommendation for treatment and follow-up
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