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HYPERTENTION

For PHO students


Wolkite University
By Dr. Nitsuh

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INTRODUCTION
• Definition= at 2 separate occasions(6 hours).
Systolic BP > or = 140
Diastolic BP > or = 90

• Stages
Normal: S BP< 120, D BP< 80
Pre HTN: S BP- 120-139, D BP- 80-89
Stage-I : SBP- 140-159, D BP- 90-99
Stage II : SBP- > or= 160, D BP> or=100
Isolated SHTN: S BP>or=140, D BP<90
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New ACC classification
• Blood pressure categories in the new guideline are:
• Normal: Less than 120/80 mm Hg;
• Elevated: Systolic between 120-129 and diastolic
less than 80;
• Stage 1: Systolic between 130-139 or diastolic
between 80-89;
• Stage 2: Systolic at least 140 or diastolic at least 90
mm Hg;

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Isolated systolic hypertension
* is defined as systolic blood pressure
≥140 mm Hg with diastolic pressure <90 mm
Hg.
*mainly affects people older than 55 years.

Secondary causes include

1. Increased cardiac output (anemia,


thyrotoxicosis, arteriovenous fistula, Paget
disease of bone, and beriberi)

2. Increased cardiac stroke volume (aortic


insufficiency and complete heart block).

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• Exclude= recent physical exercise, use of tobacco
or caffeine, or a full urinary bladder.

•Office (white coat) hypertension: elevated BP in


the clinic environment.Diagnosis made by self-
measurement or average awake ambulatory level=
≥135/85 mm Hg.

• Pseudohypertension: inaccurately high cuff blood


pressure as a result of a stiff vascular tree in older
persons.

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Risk factor for HTN

1.Nonreversible risk : older age, being African


American, and having a family history of
hypertension.

2. Reversible : prehypertension, overweight,


sedentary lifestyle, high-sodium–low-potassium
diet, excessive alcohol intake and metabolic
syndrome.

3.Genetic factor: Polygenic= two or greater


factors plus environmental factor, Monogenic- on
study
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Summary of basic facts on HTN
*Treatment of reversible risk factors can prevent or
delay the development of hypertension and lower
the risk of cardiovascular disease.

• Treatment of metabolic syndrome can prevent


cardiovascular disease and the development of
hypertension.

• Diastolic blood pressure is the best predictor of


cardiovascular disease in young people.

• Systolic blood pressure is the dominant predictor


of risk of cardiovascular disease in older people.
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• Mechanism of HTN

Intra vascular volume elevation.
Autonomic Nervous system over activity.
Renin Angiotensin Aldosterone System over activity
Vascular factors:
*includes arterial stiffness, Increased vascular smooth
muscle tone and growth, Endothelial
damage( decreased NO & vasodilator peptide).

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Treatment of HTN
- Decreases: CHF by 50%, CHD by 12-16%, SCD by 21%, LVH
by 35%.
- Central Nervous System
• Stroke: Ischemic and Hemorrhagic.
• Treatment of HTN decreases stroke by 35-50%
• Decreased dementia risk

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Primary HTN
• Accounts for 85-95%, Familial, increases with age, in
twins concordance rate M=60%, W=35%.

• Majority due to increased PVR but COP normal, in the


young due to increased COP and normal PVR

• Peak age= 25-55

• Associated with metabolic syndrome.

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Secondary HTN

• Accounts for 5-15% of HTN and major cause is Renal


paranchymal, next is renovascular HTN.
• Indication of screening: age <25 and >55, poor drug
response; Hx, PE, Lab evidence of underlying cause

Presentation
• Majority asymptomatic found accidentally
• Target organ damage
• Hypertensive Emergency

Basic Lab tests


• CBC, RFT, UA, FBS, Lipid profile, Electrolyte, TSH, T3 &
T4, ECG, CXR
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HYPERTENSIVE CRISIS
Emergency Vs Urgency
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt
changes in medication if there are no other indications of problems, or immediate
hospitalization if there are signs of organ damage.

• Imminent / overt target organ damage in association with acute onset or worsening of HTN

• Needs urgent lowering BP with in two hrs for emergency ( S BP < 160, D BP b/n 100 and 110)
or decreasing MAP by 1/4th

• RAAS is activated

I- Encephalopathy

• If focal sign R/O stoke by CT


• Drug : Nitroprusside, Nicardipine, Labetolol

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Management

If no Encephalopathy or other catastrophic event


lower BP over several minutes (over hours) with PO
short acting drugs with frequent dosage
Captopril, Clonidine, Labetalol

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HTN-Encephalopathy
oPresence of cerebral edema characterized by non
localizing neurologic manifestations.

*Headache, nausea, vomiting, restlessness, confusion,


seizure, coma could occur

*CT- R/O ischemia or infarction

oPathophysiology: disrupted cerebral auto regulation


leading to vasodilatation of cerebral microvasculature

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Treatment
*Rapidly lowering BP may precipitate ischemia( brain, kidney,
heart)
*Goal: to reduce BP to 160/100-110, with in minute to 2hrs
with initial fall of MAP not exceeding 25% of the presenting
value
*Drugs: IV Nitroprusside, Labetalol, Nicardipine
*After the target level of BP is achieved oral agents should
be started to bring DBP b/n 85-90 over two to three months
*Prognosis: at continued risk for coronary, CV and renal
disease, survival improves with time (90% by the 4th yr Vs 52
% in the 1st yr)

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Treatment of stable hypertensive patient

*Risk assessment and stratification: stage of HTN,


comorbid conditions, CVD risk factors, beneficial effect
on CV risks, age, availability and cost of drugs
*Follow up: drug selection and acceptable combination,
base line clinical and Lab data should be taken.

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When to start and mode of treatment
Pre hypertension: those with risk factor for CVD close
follow up and risk reduction, treatment of related disease
conditions and life style modification
Sage I : With out risk factors follow up for 3-6 months
and if persistent HTN ,start drug therapy.
Stage I with risk and above: drug therapy from the
outset
Isolated systolic HTN with risk factor other than age
start drug treatment, if with out risk follow up and treat
accordingly
oGoal of Rx : BP < 140/80

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Single Vs Combination drug treatment


• Depending on organ related risk (CVD related risk
reduction)
• Patient related risk
• Comorbid conditions
• Stage of HTN>=II
• BP=> 160|95, needs at least 2 drugs.
• Degree of control of clinical conditions and BP level.

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Life style changes
*Cessation of smoking.
*Salt restriction.
*Reduction of saturated and total fat intake.
*High fiber diet, fruits and vegetable.
*Supplemental Ca, Mg and K .
*Alcohol: Men < 2 drink/d, women<1drink/d.
*Aerobic exercise: 30min daily or every other day
*Tea and coffee: limited amount.

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Specific clinical conditions and drug choices

• DM: ACEI, beta blocker, Loop diuretic, ASA, statin, CCB, Diltiazem
(Verapamil ), glycemic control. If no proteinuria =goal of BP < 130/80
-If PU BP < 125/75
• CKD: ACEI, BB, Loop diuretics, CCB, statin, Warfarin (if needed)
• CHF and CHD: ACEI, BB, diuretic
• Stroke: ACEI, BB, CCB, HCT, ASA, Statin.
• Pregnancy: Aldomate, CCB, Labetolol
• Post MI: BB, ACEI, statin, ASA
• Blacks: diuretic plus BB/ACEI or CCB plus BB/ACEI
• PAD: ASA plus CCB plus surgery if needed(70% had IHD=BB+CCB).
• Elderly: Thiazide, CCB, Labetolol
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Refractory HTN
• Persistent BP of > 140/90 using three drugs and
above with appropriate combination, indication
and good adherence
• Common in old age
• DDx: Pseudo hypertension, poor adherence, salt
intake, obesity, excess alcohol intake, 2ry HTN,
hyperaldosteronism

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Screening and prevention of HTN
• For non risk groups once every three to five years
and at any clinic visit.
• For risk groups every six to twelve months Bp
measurement
• In general when to start screening and it’s benefit
is not well established, but at age>=3 years.

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History
*Most pts are asymptomatic.
*Severe hypertension may lead to headache, epistaxis,or
blurred vision.
Clues to Specific Forms of Secondary Hypertension
*Use of OCP& glucocorticoids.
*paroxysms of headache, sweating, or tachycardia
(pheochromocytoma);
*history of renal disease or abdominal bruie (renal
hypertension).

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Physical Examination
*Measure bp in both arms as well as a leg (to evaluate
for coarctation).

•Clues to secondary forms of hypertension include


cushinoid appearance, thyromegaly, abdominal bruit
(renal artery stenosis), delayed femoral pulses
(coarctation of aorta).

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Drug induced HTN
• Oral contraceptives =age>35 years, by inducing
sodium retention, increasing renin substrate, and
facilitating the action of catecholamines.
*D|C of OCP recovery from HTN after 6 months.

• NSAIDS=by inducing sodium retention by blocking the


formation of renal vasodilating, natriuretic PG and also
interfere with the effectiveness of diuretics, β-blockers,
and ACEIs.

• TCA= inhibit the action of centrally acting agents


(methyldopa and clonidine).

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Drug Therapy of Essential Hypertension.
*Goal is to control hypertension with minimal side effects
using a single drug if possible.

*First-line agents include diuretics, beta blockers, ACE


inhibitors, angiotensin receptor antagonists, and calcium
antagonists.

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Diuretics
. 1.Thiazides =preferred over loop diuretics because of
longer duration of action; however, the latter are more
potent when GFR 25 mL/min.

Major side effects include


hypokalemia, hyperglycemia& ca, and hyper uricemia,
which can be minimized by using low dosage (e.g.,
hydrochlorothiazide 12.5–25 mg qd).

Diuretics are particularly effective in elderly and black


pts. Prevention of hypokalemia is especially important in
pts on digitalis glycosides.

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Beta Blockers

*Particularly effective in young pts with


“hyperkinetic” circulation.

*Begin with low dosage (e.g., atenolol 25 mg qd).

*Relative contraindications: bronchospasm, CHF, AV


block, bradycardia, and “brittle” insulin-dependent
diabetes.

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ACE Inhibitors

*Side effects are uncommon and include rash, angioedema,


proteinuria, or leukopenia, particularly in pts with elevated
serum creatinine.

*A nonproductive cough in up to 10% of patients,1.2-3%


angioedema requiring an alternative regimen.

•Renal function may deteriorate as a result of ACE inhibitors in


pts with bilateral renal artery stenosis.

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CCB.

1.Dihydropyridines
=amlodipine, felodipine, isradipine, nicardipine, nifedipine,
nisoldipine,and nitrendipine.

2. Dihydropyridines

*diltiazem and verapamin.


*Only long-acting forms are approved for
use in hypertension.
*The short-acting forms should not be used.

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Furosemide:
*Indication= hypertension associated with chronic
kidney disease and estimated GFR <30 mL/min.

• Metabolic effects: hypokalemia, hyperuricemia, fasting


hyperglycemia, hypochloremic alkalosis, and increased
urinary calcium excretion (hypocalcemia).

• Adverse effects: reversible deafness and postural


hypotension.

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Spironolactone
Important indications for : primary aldosteronism and
states of secondary aldosteronism, especially severe heart
failure.
• The diuretic effect is antagonized by the concomitant use
of salicylates.

• Adverse effects: hyperkalemia, gynecomastia,


mastodynia, menorrhagia,and skin rash.

Eplerenone
Eplerenone is a mineralocorticoid receptor antagonist
similar to spironolactone, and its indications for use are
generally the same as for spironolactone. May be better
tolerated than spironolactone, primarily because of less
risk of gynecomastia in men.
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THANK YOU

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