INTERNAL MEDICINE - CARDIOLOGY

HYPERTENSION Dr. Bartolome

GLOBAL BURDEN BLOOD PRESSURE REGULATION

Blood pressure is equal to Cardiac output x Peripheral resistance;

and as you increase your cardiac output, you also increase your blood
pressure. As you increase your total peripheral resistance, you also
increase your blood pressure. so ito yung minamanipulate natin class.
Determinants of cardiac output:
- stroke volume
- heart rate
- only 25% of people with hypertension know that they have Stroke volume amount of blood going outof the left ventricle,
hypertension mas maraming volume mas maraming cardiac output, on the other hand,
- it’s quite common among blacks as compared to white as you increase your Heart rate, you also increase your cardiac output to
americans; and a certain point lang ~ because a heart rate of more than 160 beats/min is
- if you are greater than 60 years old, most probably you have already detrimental, there’s no more filling time, less blood volume goes to
hpn ~ incidence: 65 years old the left ventricle so eventually, cardiac output goes down
Contractility. the more contractility, you’d end up with more
FACTORS THAT CAN CONTRIBUTE TO THE DEVELOPMENT OF HPN cardiac output
- obesity and weight gain
- increase dietary intake of sodium Total Peripheral Resistance
- decrease dietary intake of calcium and potassium - decrease in BP: we give vasoconstrictors (stimulate alpha rec)
- alcohol consumption - increase in BP: we give vasodilators (stimulate beta receptors)
- psychosocial stress *take note of the actions of your alpha and beta receptors
- low levels of physical activity
Local Factors
GENETIC FACTORS ● autoregulation
1. 4 times more likely you would end up having hpn if you have a ● ph - pag acidic ang dugo niyo, it will cause vasodilation
relative with hypertension ● hypoxia - causes vasodilatation in the arterial circuit,
2. polygenic disorder ~ multiple genes identified that contributes to vasoconstriction in pulmonary vessels
the development of hpn
3. others:
● genes encoding angiotensin II type 1 receptor (AT1
receptor), aldosterone synthase, atrial natriuretic
peptide, and B2 adrenoceptor

HPN doube the risk of cardiovascular diseases including coronary heart

disease, congestive heart dse, ischemic and hemorrhagic stroke, rewnal
failure and peripheral arterial disease
- ito yung pinpiprevent natin kay natin inaidentified
yung high blood at para maprevebt complications

● Starting at BP of 115/75, every increase of 20mmHg in SBP

and/or increase of 10mmHg in DBP is associated with a
doubling of the risk of death from stroke, heart disease and
other vascular diseases
● Isolated systolic HTN is associated with increase in CV disease
RAAS mechanism
● 30% of adults have HTN
when you activate your RAAS, you increase your blood pressure, and too
● Likelihood of HTN increases with age (at age 55, 90% lifetime
much blood pressure will decrease the secretion of these substance
risk of HTN)

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 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
Angiotensin II is one of the most potent vasoconstricting agent, that’s BP Classification for Adult Filipinos (2020 Clinical Practice
why this is one of the substances that is being manipulated in the Guidelines)
treatment of hypertension (ARBs, ACE inhibitors)

DEFINITION OF HYPERTENSION
● Consistent constant elevation of systolic or diastolic pressure
above 140/90 mmHg
● Clinical criteria generally based on the average of 2 or more
seated BP readings during each of 2 or more OPD visits of ≥
140 and/or 90 mmHg
● 24-hour BP monitoring CPG simplified it already but again, don’t forget about the Hypertensive
○ average awake BP ≥ 135/85 mmHg emergency in the previous table
○ Asleep BP ≥ 120/75 mmHg
OTHER TERMINOLOGIES
BP CLASSIFICATION White Coat Hypertension
JNC8 classification ● increased BP at clinic, normal at home
● studies have shown that there is an increased in target organ
damage in people with white coat hypertension
● increased risk for developing sustained hypertension
● management: lifestyle modification

Masked Hypertension
-previous classification followed in the Philippines ● normal BP in the clinic, elevated at home
● increased target organ damage; increased adverse prognosis ~
From Medscape/AHA kasi hindi nagagamot since normal pag dating sa clinic
● associated with relatively young age, male, stress or increased
physical activity during daytime, smoking and alcohol intake

24 hour BP monitoring
- to diagnose White coat hypertension and masked hypertension

Hypertensive crisis (Urgency or Emergency)

● Hypertensive Urgency
○ severe elevations in BP WITHOUT progressive target
end organ dysfunction
*take note of the Hypertensive Emergency ● Hypertensive Emergency
○ severe elevations in BP (>180/120 mmHg)
Comparison of American and European complicated by evidence of impending progressive
target end organ dysfunction (ex. in pregnancy)
○ previously called Malignant Hypertension
■ severely elevated BP with retinal
hemorrhages or papilledema vs.
encephalopathy or acute nephropathy

Resistant Hypertension
● patients with BP >140/90mmHg despite taking 3 or more
anti-hypertensive agents, including a diuretic
● difficult to control
● common in patients >60 y/o
● may be related to pseudo resistance, non-adherence to therapy,
identifiable causes of HTN (obesity, excessive alcohol), use of
medications (decongestants, etc)
○ decongestants are sympathomimetic agents ->
activates alpha receptors -> vasoconstriction (refer sa
mechanism sa taas)

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 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
PRIMARY HYPERTENSION ● Insulin resistance is associated with unfavorable imbalance in
● no specific mechanism causing the elevated BP; likely caused endothelial production of mediators regulating platelet
by interaction between environmental and genetic factors aggregation, coagulation, fibrinolysis & vessel tone
● also called “Essential hypertension”; 80-95% of hypertensive ○ increased risk for CHD, stroke, diabetes, & CV
patients mortality
● tend to be familial; prevalence increases with age ○ 25-50% of non-obese, non-diabetic hypertensive
persons are insulin resistant
Pathophysiology ● basically mas vasoconstricted sila and hypercoagulable sila, so
ito yung ginagamot
● the expression of the metabolic syndrome is modified by
environmental factors, such as degree of physical activity and
diet

SECONDARY HYPERTENSION
● with specific underlying disorder causing the BP elevation
● 5-20% of hypertensive patients
● specific mechanism for BP elevation is often more apparent
● basically we cannot cure Primary HTN, only control, whereas sa
Secondary HTN, pag na-identify yung primary cause pwede pa
gumaling

Causes of Secondary Hypertension

-the pathophysiology of primary hypertension is multifactorial, so what

we can just really do is to treat the hypertension by giving anti
hypertensive drugs

In majority of patients, peripheral resistance is increased, and cardiac

output is normal or decrease ~ vasodilator therapy

In younger patients with mild or labile hypertension, cardiac output may

be increased, and peripheral resistance may be normal

When plasma renin activity (PRA) is plotted against 24-hr sodium

excretion:
● 10-15% of hypertensive patients have high PRA
● 25% of hypertensive patients with low PRA
Patients with high renin have a vasoconstrictor form of hypertension ~
so give beta blockers
Patients with low renin have volume-dependent hypertension ~ give
diuretics
Renal Parenchymal Diseases
- virtually all disorders of the kidney may cause hypertension
- renal disease is the most common cause of secondary
hypertension
- > 80% of patients with chronic renal failure have hypertension
- HTN more severe in glomerular diseases
- Mechanism for Hypertension:

Role of Obesity
● direct linear correlation between body weight (or BMI >30
kg/m2) and BP
● 60% of hypertensive adults are more than 20% overweight
● centrally located body fat is a more important determinant of
BP than is peripheral body fat

Role of Metabolic Syndrome

● metabolic syndrome: insulin resistance, abdominal obesity, -
hypertension & dyslipidemia

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 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
Renovascular Hypertension Management algorithm in patients with hypertension and renal artery
- hypertension due to an occlusive lesion of a renal artery; stenosis
potentially curable
- 2 groups of patients at risk:
1. older patients with arterosclerotic plaque obstructing
renal artery (usually at origin); majority with
atherosclerosis
2. patients with fibromuscular dysplasia - young white
women; medial fibroplasia most common variant (⅔
of patients); affect more distal portions of renal artery

- Clinical features:
1. a sudden onset of hypertension/development of
hypertension before the age of 30 years
2. development of severe hypertension after the age of
50 years
3. treatment-resistant or malignant hypertension
4. deterioration of renal funcion (eg. >30%) after
administration of an angiotensin- converting enzyme
inhibitor (ACEI) or an angiotensin receptor blocker
(ARB)
5. unexplained renal atrophy or a difference >1.5 cm in
the kidney size
6. unexplained progressive deterioration in the kidney
function
7. unexplained flash pulmonary edema Primary Aldosteronism
8. fibromuscular dysplasia of other vascular beds - increased aldosterone production is independent of RAAS
9. an epigastric or abdominal bruit that lateralizes or leading to sodium retention, hypertension, hypokalemia,
extends throughout systole into diastole and low plasma renin activity (PRA)
- age at onset 3rd-5th decade
- mild to moderate hypertension but occasionally severe
- consider in all patients with refractory hypertension
- may be associated with glucose intolerance; may present with
polyuria and polydipsia
- most patients are asymptomatic
- some may present with consequences of
hypokalemic alkalosis (paresthesia or muscle
weakness)
- edema is rare
- increased incidence of renal dysfunction and CV disease
- suspected in patients with unprovoked hypokalemia (unrelated
to diuretics, vomiting or diarrhea)
- in patients on diuretics, suspect if serum potassium is
<3.1 mmol/L (<3.1 meq/L)
- 25% of patients with normal serum potassium

*pag na modify yung A-II secretion, marami naiimprove sa patient WORK-UP

For Screening
● ratio of plasma aldosterone to plasma renin activity (PA/PRA)
useful
○ preferably obtained in ambulatory patients in the
morning
○ Ratio >30:1 + plasma aldosterone concentration >20
ng/dL highly suggestive of aldosterone-producing
adenoma
Confirmatory
● In patients with elevated PA/PRA ratio, diagnosis of primary
aldosteronism can be confirmed by demonstrating failure to
suppress plasma aldosterone to <10ng/dL after IV infusion
of 2L isotonic saline over 4 hours

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 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
● alternative confirmatory tests: failure to suppress aldosterone
in response to oral NaCl load, fludrocortisone or captopril
● Adenoma CT should be done in all patients diagnosed with
primary aldosteronism to rule out the 2 most common cause of
sporadic primary aldosteronism (aldosterone-producing
adenoma and bilateral adrenal hyperplasia)
Cushing’s Syndrome
- excess cortisol production due to either:
1. excess ACTH secretion from a pituitary or ectopic
tumor, or
2. ACTH-independent adrenal production or cortisol
- 75-80% of patients with hypertension
- Mechanism: stimulation of mineralocorticoid receptors by
cortisol and increased secretion of other adrenal steroids
Laboratory screening:
1. measurement of 24-hour excretion rates of urine free cortisol
2. overnight dexamethasone suppression test
3. late night salivary cortisol measurement
4. identification of cause of Cushing’s syndrome
Pheochromocytoma
- catecholamine-secreting tumor
- location: adrenal medulla or extra-adrenal
paraganglion tissue (paraganglioma)
- Clinical manifestations primarily relates to increased circulating
catecholamines
- in some patients, epinephrine is the predominant
catecholamine secreted —> present with hypotension
rather than hypertension
- 20% familial with autosomal dominant inheritance
- may be part of MEN type 2A & 2B, von Hippel-Lindau
disease and neurofibromatosis
Laboratory work-up
● measurement of either urine or plasma catecholamine (e.g.
24-h urine metanephrine)
● urine is less sensitive but more specific
Management: Surgical excision definitive
COMPLICATIONS OF HYPERTENSION
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HEART
● heart disease is the most common cause of death in
hypertensive patients
● hypertension decreases structural & functional adaptations and
decreases LVH
○ increased risk for CHD, stroke, CHF, and sudden
death
BRAIN
● Stroke - 2nd most frequent cause of death in the world
○ 85% due to infarction
○ 15% due to either to intracerebral or subarachnoid
bleed
● Elevated BP is the strongest risk factor for stroke
○ incidence of stroke rises progressively with incresing
BP levels, particularly systolic BP in persons >65
years
● patients with malignant hypertension with failure of
autoregulation of cerebral blood flow at upper pressure limit (+
Hypertensive Encelopathy)
○ Manifestations:
■ Severe headache
■ Focal neurologic sign
■ nausea & vomiting
■ altered mental status
○ if untreated, may progress to stupor, coma, seizures,
and death within hours
KIDNEY
● the kidney is both target and cause of hypertension
○ Primary kidney disease is the most common etiology
of severe hypertension
■ Mechanism
1. Decrease capacity to excrete sodium
2. Excessive renin secretion in relation to
volume status
3. Sympathetic nervous system overactivity
● Hypertension is a risk factor for renal injury and ESRD
○ Renal risk more closely related to systolic than to
diastolic BP
○ Primarily affects glomerular arterioles leading to
ischemic changes in the glomeruli and
post-glomerular structures
○ Glomerular injury may also be due to direct damage
to the glomerular capillaries dueto glomerular
hyperperfusion
● Loss of autoregulation of renal blood flowat afferent areteioles
—> elevated pressure transmitted to glomeruls —> (+)
hyperfiltration, hypertrophy & focal segmental
glomerulosclerosis
● Glomerulosclerosis eventually progresses leading to ischemia
and atrophy of tubules
● In Malignant hypertension, renal lesion consists of fibrinoid
necrosis of afferent arterioles resulting in focal necrosis of
glomerular tufts
● Early markers of renal injury/risk factors for renal disease
progression & CV disease
○ Macroalbuminuria (random urine albumin/creatinine
ratio > 300mg/g), OR
 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
○ Microalbuminuria (random urine albumin/creatinine *basically, the approach to patient with hypertension is try to identify if
ratio > 30-300 mg/g) there is a secondary cause for the hypertension, do lab tests to confirm
the secondary cause. Otherwise, if after the Hx and PE, and laboratory
EYES appears normal, it is more likely Primary hypertension.

Elements of the Personal Hx for HTN:

APPROACH TO PATIENT WITH HYPERTENSION
● dietary intake of salt, processed foods, and fruits and
vegetables
● Smoking history
● Alcohol consumption (specific amounts and type)
● Caffeine intake (coffee, tea, cola, beverages, pills)
● use of pressor agents (nasal sprays, cold remedies)
● Licorice intake, with a focus on licorice of British, French, or
Belgian origin; certain laxative abuse and chewing tobacco
(rare)
● use or abuse or organic, herbal, and health food remedies
● use of nonsteroidal anti-inflammatory drugs
● exercise type, frequency, and duration
● occupational history; note stress levels
● Marital history
● Educational history if not defined by occupation

Physical Examination
● body habistus, including weight and height
● meaurement of arterial pressure
○ femoral and pedal pusle palpation
○ measure at least once in the lower extremity in
patients in whom HTN is dicovered before age 30
● heart rate; quality of S2 heart sound; prresence of S4 gallop
● palpation of neck for enlarged thyroid
● Fundoscopic exam of retina
● auscultation of bruits over the bdomen and carotid arteries

24 HOUR AMBULATORY BP
- average awake BP >135/85 mmHg
- average asleep BP >125/85 mmHg
- reliably predicts CV risk
- Indications:
1. for white coat hypertension
2. treatment resistance
3. symptomatic hypotension
4. autonomic failure
5. episodic hypertension

Recommendation for Office Blood pressure measuremant

AVIS
 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome

Weight reduction - can reduce BP as high as 10-20 points systolic BP

Dietary salt reduction - reduce BP by 4-8 points
DASH - reduce BP by 8-12 points
Mod. alcohol consumption - reduce BP by 2-4 points
Physical activity - reduce BP by 4-8 points
CORRECT WAY TO MEASURE BLOOD PRESSURE
1. Calibrated manometer
- pano niyo chinecheck kung tama manometer niyo?
yung 0 dapat nasa 0, kapag compress niyo dapat
aabot sa 300. pero meron mga accredited technician
na nagchecheck sa mga apparatus
2. Seated quietly on a chair with feet on the floor for 5 minutes in a
quiet & comfortable room
3. At least 2 measurements should be made; supine, sitting and
standing positions
4. Center of the cuff should be at the heart level & the width of the
bladder cuff should be equal to at least 40% of the arm
circumference. The length of the cuff bladder should encircle at
least 80% of the arm circumference
5. Pay attention to cuff placement, stethoscope placement and
rate of deflation (2mmHg)

LABORATORY TESTING
Basic Laboratory Tests for Initial Evaluation

*remember the target therapeutic BP of below 130/80 mmHg

TREATMENT ALGORITHM

MANAGEMENT OF HYPERTENSION
● lowering systolic BP by 10-12 mmHg and diastolic by 5-6mmHg
confers relative risk reductions of 35-40% for stroke and
12-16% for CHD within 5 years of initiation of treatment
● The risk of heart failure is reduced by >50%
● Hypertension control is the single most effective intervention for ● the standard therapy recommend is the use of ACEi, ARBs,
slowing the rate of progression of HTN-related kidney disease Ca-blockers, and thiazides like diuretics

AVIS
 INTERNAL MEDICINE - CARDIOLOGY
HYPERTENSION Dr. Bartolome
● Beta blockers recommended nalang if there is coronary artery
disease,

● pag Urgency, di agad pinapababa ang BP, you have 24 hours

to lower down the BP
● pag Emergency, give IV drugs ~ commonly use Nicardipine (in
the Ph). Nitroglycerin maganda pag HTN with chest pain
○ MI,CHF - Nitroglycerin drip
○ Eclampsia - Nicardipine drip or hydralazine drip
○ Thyrotoxicosis - Esmolol
○ Vasculitis - depends, if constricted ang vessels,
Nicardipine
○ Intracranial hemorrhage - Nicardipine
○ Encephalopathy - Nicardipine and diuretics
○ Acute Aortic Dissection - Beta blockers and
Nicardipine
● Know the peak effect of drugs and duration

Additional reading: Executive Summary of the 2020 Clinical Practice

Guidelines Management of Hypertension in the Philippines

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