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Understanding Hypertension: Causes and Risks

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0% found this document useful (0 votes)
14 views68 pages

Understanding Hypertension: Causes and Risks

Uploaded by

tcj4bpj2pn
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

HYPERTENSION-

CHRONIC LONG STANDING


Abnormally Elevated- BP.
Means high Pressure Force exerted by
that
~
is the cause
why elderly Circulating intra- vascular blood flow
have

systolic Bp not diastolic


M
,

laterally on blood vessels wall both in systole and diastole.


Systolic BP- measure MAX.. BP- against
function of the left
ventricle
blood vessel wall during LV- contraction- systole.
It is a function of Cardiac out-put in systole.
Diastolic BP- measure the LOWEST BP- in
function of the L

blood vessels
- diastole during LV- filling before the next systole.
BP- is maintained by blood vessel wall elasticity
and compliance - peripheral vascular resistance .
Any decrease
<
in elasticity means
rigidity
& diastolic Bp .
HPN
HTN
• HTN- Extremely common clinical problem WORLD WIDE
• Affecting 20-30% of general adult population.
• 40 - 60% and more sever BLACK- AFRICAN
Age related disease 50% after age of 60Y.

>1.3 billon pat. have HTN an > 4-5 millon/ year died from HTN

Both Systolic- Diastolic- HTN-


Carry high risk of Cardiovascular Morbidity and Mortality.

ATHEROSCLEROSIS IHD- MI- LVH- HF-


ARRHYTHMIA - CVA –
PERIPHERAL VASCULAR DISEASE – CKD - BLINDNESS.


BRITISH HYPERTENSION SOCIETY
DEFINITION OF HPN-

Category Systolic BP Diastolic BP


(mmHg) (mmHg)
BP
Optimal < 120 < 80
Normal < 130 85
High normal&
Life style
130 – 139 85 – 89

Hypertension start medication .

Grade 1 (mild) 140 – 159 90 – 99


progressive .

Grade 2 (moderate) 160 – 179 100 – 109


V
Grade 3 (severe) > 180 > 110

Isolated systolic hypertension "Atheroscalarosis"


Grade 1 140 – 159 < 90
Grade 2 > 160 < 90
JNC-7 –DEFINITION-HTN
• NORMAL SYS. BP mmHg DIASTOLIC-BP
• <120 <80

• HIGH-NORMAL- 120-139 80-89


• PRE-HTN

• STAGE-1- 140-149 90-99

• STAGE-2- >160 >100

• ISOLATED-SYSTOLIC >140 <90


• HTN
JNC-8-2014
• 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)
• Normal-BP-<120/80
• Pre-HTN-BP-120-139/80-89
• HTN- stage-I-140-159/90-99
• HTN-stage-II->160/100
The National Institute for Health and
Care Excellence- NICE during Bp sleep .

>
Night dipper
(decrease BP) .

Non-dipping

>

NICE- 3- Recommended ABPM- Ambulatory ( still


high

• HBPM- Home
• BP Mointering for diagnosis of HTN.
• STAGE 1 HTN Clinic BP- 140/90 or
• Ambulatory
&
.

130/80
.
ABPM- HBPM

135/85 or higher
< Home


.

STAGE 2 HTN Clinic BP- 160/100 or


• ABPM- HBPM 150/95 or higher
• SEVER 3 HTN Clinic systolic >180 or more
• diastolic >100 or more
How to measure blood pressure
1- Use a machine that has been well maintained
and properly calibrated.
2- Remove tight clothing from the arm.
• Pt. should be relaxed for 5 min.
• To avoid stress and white-coat- HTN.
3- Support the arm of pt. at the level of the heart.
4- Measure both sitting and standing BP
Especially in Elderly – Diabetic- Dehydrated –
phaeochromocytoma- patients to exclude
postural hypotension >20mm Hg drop in BP-
after 1-2 min. standing.
How to measure blood pressure
HTW in children > Coartication of aorta , Nephritic Syndrome , Gomunephritis &
. CKD.

How to measure blood pressure


5- Use a cuff of appropriate size
(the bladder must encircle > 2/3 rd of the arm).
6- Lower the pressure slowly (2mmHg per second).
7- Read the BP to the nearest 2mmHg.
8- Use phase V (disappearance of sounds)
to measure diastolic BP.
9- Take two measurements at each visit.
10- 24 HOUR -Ambulatory - ABPM- Mointer .
HOME - HBPM- Machine.
Labile or White Coat- HTN - MASKED-HTN.
COMMON PROBLEMS IN BP EXAM.
1. Wrong cuff size.
• Obese pt. larger cuff must be used because
• Normal size cuff will give FALSE high BP- reading.
• Very thin pt. pediatric cuff must be used.
2- Excess pressure of stethoscope on brachial artery
wrongly gives lower10mmHg reading of diastolic BP.
3- Wrong level of pt. arm- elbow to the heart.
• Higher level than the heart level will give lower
5mmHgBP. Lower level will give higher 6mmHgBP.
COMMON PROBLEMS IN BP EXAM.
4. If BP- difference in both arms >10mmHg. a condition that sends blood to your arm
instead of your brain because of


narrowing in your subclavian artery
Exam. for peripheral vascular disease
Subclavian steal syndrome
• exclude - Subclavian artery stenosis.
• Record the highest reading. vertebral a

6- Auscultatory gap- 20% of elderly HTN-


• After systolic pressure reading
• Sound disappears then reappears before
• reading of diastolic pressure.
• If the first systolic sound missed.
• Sys. BP will be recorded wrongly low.
• To avoid this problem palpate radial pulse .
AUSCULTATORY GAP
AETIOLOGY-
MULTI-FACTORIAL
• HTN- a complex interaction between
• Genetics and Enviroment –life style factors.
• 95% pt. Idiopathic HTN
• 5% pt. Secondary HTN
• Essential - Idiopathic- HTN-
• No specific underlying cause can be identified
• which may be related to following CAUSES.
• I- GENETIC FACTORS
• HTN- has complex genetic disorders
• large number of Genes may be involved in HTN.
AETIOLOGY-
1- RENIN- ANGIOTENSIN - ALDOSETERON -SYSTEM- GENE
Affected
by ,
HIGH-RENIN- HTN– YOUNG.
stress smoking - C
best drug
> ACEI or ARBs (work on
renin-angiol.
activity obesity
,

LOW RENIN- HTN- ELDERLY- BLACK > Calcium channel blockers or diuretics-

2- ADRENERGIC RECEPTORS- GENE-


• Peripheral vascular resistance and vascular tone
3- VASCULAR ENDOTHELIAL FUNCTIONS –GENE-
• Vasoconstrictors Cytokines
• Agiotensin-II- Endothelin- Thrombaxin A2.
• Vasodilators – Cytokines
Prostaglandin- NO- Prostacyclin.
AETIOLOGY-

4- Na- and salt Sensitivity –GENE - Salt Sensitive HTN


5- Metabolic GENES-
• Regulator of insulin receptors .
• Hyperinsulinemia and insulin Resistance.
• SYNDROME-X- Metabolic syn. Secondary pulmonary hypertension & cause of HTN

• Marked central Obesity- Dyslipidemia- DMT2- HTN


II- FAMILIAL FACTORS-HTN- cause obstructive sleep appea
syndrome (pickwickian syndrome)
obese
daytime
patient , sleep disturbances (sleep
night) at I couldn't sleep at the ,

Children of hypertensive parents tend to have hypercapa with

Causel.
(without

my

Higher BP- Compared with Children treatment C-pap

of Normotensive parents.
AETIOLOGY-
III- RACIAL- FACTORS - ETHNIC GROUPS-
HTN more common and MORE sever in
BLACK- AFRICAN with higher incidence up to - 40-60%
IV- FETAL FACTORS –
Low birth wt. babies Impaired intra-uterine growth
• Reduced Small kidneys volume and size
Lower Nephrones number.
Glomerular Hyper-filteration -
Hypertrophy of the remaining Glomeruli.
RENAL- GLOMERULOSCLEROSIS
Higher chance to develope HTN during their adult life.
AETIOLOGY-
V- ENVIROMENTAL FACTORES-
• Obesity- Lack of exercise- Alcohol intake- Smoking
• Sleep- Apnea- syn. - Hypoxia
• High Na -ingestion-
• STRESS- SYMPATHETIC OVER DRIVE-HTN
• DRUGS - STEROID – NSAIDS- LICURICE- PILLS.
• All can cause HTN
On other hand another factors can decrease BP-
high -K- Ca- and Mg -intake - wt. loss-
Fresh fruits-Vegetables – Regular Aerobic Exercise
No alcohol drinking or Smoking – good sleep .
PATHO-GENESIS OF ESSENCIAL HPN-
PATHO-GENESIS OF ESSENCIAL HPN-
• Resistance small arteriols <1mm diameter.
• Vascular Intimal layer proliferation
• Muscular layer wall Thickening.
• Reduced vascular lumen diameter.
• Secondary Calcium and Hyaline deposition .
• Ending in vascular- ATHEROMA- atherosclerosis.
Increased peripheral vascular resistance
Tissues hypo-perfusion and tissues ischemia.
Arteriolar wall micro- aneurysm formation.
PATHO-GENESIS OF ESSENCIAL HTN-

• Larger arteriols >1mm diameter-


Thickened internal elastic lamina.
• Smooth muscles wall hypertrophy .
• Collagen- fibrous tissues formation- Fibrosis.
• Arterial wall calcification.
ONION - SKIN appearance.
Blood vessels becomes dilated tortuous
With loss of wall compliance.
ATHEROSCLEROSIS - IHD - MI - LVH- HF- CVD-PVD- CKD.
HTN more and more sever.
SECONDARY HTN-
• 5% of HTN- UNDERLYING secondary Aetiology
1- High Alcohol intake-
Obesity- DM- SLEEP APNEA SYN.
• Pregnancy- Pre-eclampsia- Eclampsia.
• DRUGS-
• ORAL CONTRA- CEPTIVE PILLS-
• CORTICOSTEROIDS - NSAIDS- CICLOSPORINE
• CABINOXOLONE - LICURICE INTAKE.
2- RENAL DISEASE. Congenital fibromascular dysplasia "in
young women 30s-40s"

• A- RENAL-VASCLAR DISEASES Aquired · > Atheroscabrosis


.

• RENAL ARTERY STENOSIS - UNI- BILATERAL


SECONDARY HTN-
Most of end causes of HTN are because of
hypokalemia
.

• B- RENAL PARENCHYMAL DISEASE-


• Chronic –GN – Small size shrinked kidneys
• Chronic -TIN- Reflux Nephropathy
• POLYCYSTIC KIDNEYS DISEASES
• DIABETIC NEPHROPATHY-
• LIDDLES SYN.
3- ENDOCRINE DISEASES.
• CUSHING SY. ACROMEGALY-
• HYPER- PARATHYOIDISM-
• HYPER- and HYPOTHYROIDISM.
s

Hypocolestemia .
SECONDARY HPN-

4- ADRENAL CAUSES
• CONNS SYN.- HYPERALDOSTERONISM
• CONGENITAL ADRENAL HYPERPLASIA
PHAEOCHROMOCYTOMA

5- CO-ARCTATION OF AORTA
6- VASCULITIS-
GN- RENO-VASCULAR-
TAKAYASU ARTERITIS- SCLERODERMA
Polycystic -kidney
PHAEOCHROMOCYTOMA
CONN S SYNDROME

hypokalemia + HTN .
CO-ARCTATION-OF -AORTA important signi
radial femoral
delay .
CO-ARCTATION-OF -AORTA
KIDNEY AND HTN-
• HTN-
may be the cause or the result of renal diseases.
• Difficult to differntiate between them .
• Renal mechanisms causing HTN-
1- Activation of Renin- Angiotensin- Aldosterone- sys.
2- Inability of the kidneys to excrete the Excess
Of Na from the body.
to maintain normal Na- balance
and intravascular volume.
KIDNEY AND HPN-

3- Reno- Vascular disease- ISCHAEMIA


• UNI- LATERAL
• BILATERAL Renal Artery diseases.
A- Fibro-Muscular dysplasia
Renal Artery Stenosis- CONGENITAL
More common in young female< 40years old.
• RENAL - DUPLEX DOPPLER- U/S
- MRA- CTA- shows - STRING OF BEADS- like
with multiple little aneurysmal dilations .
KIDNEY AND HTN-

B- Atherosclerotic – BI-LAT. RENAL ARTERY STENOSIS


• Age related disease affecting men
• > 50years old associated with
• Wide-spread- Atherosclerosis-
• Incidence- rises from 5% < 60years
- >16% > 60years old.
• Ostial lesion within 1 cm of renal artery origin.
• Reduced kidney size > 1 cm difference
• in kidney size unilateral or bilateral
• Asymmetrical kidney size
• C- VASCULITIS -SCLERODERMA- TAKAYASU ARTERITIS.

RENAL-ARTERY-STENOSIS

ischemia
KIDNEY AND HTN-
RENAL ARTERY-STENOSIS
RENAL ARTERY-STENOSIS
RENAL ARTERY DISEASE –should be
suspected in the following conditions-
1- Sever uncontrolled HTN.
2- Asymmetrical kidney size by U/S > 1cm difference.
3- Recurrent attacks of acute pulmonary edema .
4- Deterioration of renal function after ACEI or ARBS.
>
lead to loss work
5- Peripheral vascular disease- PVD. Angio
leading
on efferent to
so as

stop filtration
vasoconstrator

diffuse atherosclerosis - Carotid artery bruits.


• Abdominal bruits or aortic aneurysm.
6- Progressive CKD.
7- Hypokalemia.
RISK-FACTORS for an adverse
prognosis in HTN-
• 1- BLACK- AFRICAN
• 2- Male sex.
• 3- Persistent high diastolic BP>115mmHg.
• 4- Smoking- high alcohol- and sodium intake.
• 5- DM and Dyslipidemia.
• 6- Evidence of end organ damage-
• LVH- IHD -CHF- CVA- Retinopathy
• Renal function impairment - CKD.
REFRACTORY- RESISTANT-HTN
1- Failure of medical treatment
RESISTANT HTN
Patients on 3 antihypertensive medication
including diuretic still his BP- >130/85
or on 4 antihypertensive drugs and his BP- < 130/85
PSEUDO-RESISTANT- HTN – uncooperative pat.
REFRACTORY HTN-all medications and still high BP.
Failure to diagnose SECONDARY underlying causes-
• Renal artery stenosis
• Pheochromocytoma – CONNS SYN.
• SLEEP APNEA SYN.

HTN- ELDERLY-
• More than 50% of people > 60y. are HTN
• HPT- Age related disease. LOW RENIN HTN
Isolated Systolic HPN is common- Atherosclerosis.
• They are high risk group patients for
• Stroke - IHD- MI- HF-CKD- Peripheral vascular disease.
• DRUG of choice
• Hydrochlorthiazide diuretics + Calcium channel blockers
• AGE > 80 years- BP- TARGET -140/90 - Consider CO- Morbidity.
SYMPATHETIC OVER DRIVE-HTN-
SMOKER—OBESE-YOUNG-<50Y SYMPATHETIC STIMULATION -
VASOCONSTRICTION- HIGH RENIN-
• TACHYCARDIA- resting HR>80 -p/min. diastolic HTN-
• TREATMENT- B- BLOCKER- CENTRALLY ACTING DRUGS-MOXOIDINE.
HYPERTENSION IN PREGNANCY
Normal protienuria -30
:
mg/24 hours
.

Microprotienuria : -30-300
mg/24h > ACR test high risk for ischemic heart disease
.

HYPERTENSION IN PREGNANCY
BP-<120/80
1- Chronic -HTN- pre- existing before 20 weeks of gestation.
2- Gestational HTN-is BP >140/90 in 2nd trimester
in previously Normotensive women NO proteinuria.
3- Pre-Eclampsia -HTN-after 20 weeks of gestation+ proteinuria.
4- Eclampsia- HTN + grand mal seizures
leg edema- proteinuria >300mg/24hours .
5- HELLP syndrome – sever pre-eclampsia +
Hemolytic anemia - Elevated liver enzymes- Low plat.
ACEI- ARABs – TERATOGENIC- CONTRA-INDICATED.
First line Methyldopa.
Second line- Nifedipine - Labetalol- metoprolol-THIAZIDE.
Target organ damage in hypertension
Target organ damage in hypertension
LVH-HTN
LVH-HTN
LVH-HTN
IHD-ACUTE-MI-HTN
MALIGNENT- HTN
EMERGENCY-MALIGNENT- HTN
AORTIC-DISSECTING ANEURYSM
Hypertensive retinopathy
Grade 1 Arteriolar thickening, tortuosity and
increased reflectiveness (“silver wiring”).
Grade 2 Grade 1 plus constriction of veins at arterial
crossings (“arteriovenous nipping”).
Grade 3 Grade 2 plus evidence of retinal ischaemia
(flame – shapped or bolt haemorrhages and
“cotton wool “ exudates).
Grade 4 Grade 3 plus papilloedema.
HTN-RETINOPATHY
HTN-RETINOPATHY
HTN-RETINOPATHY
PAPILLOEDEMA
EMERGENCY-MALIGNENT- HTN

- Constitutes >1% of HTN-


• ACUTE RAPID RISE BP-
• Accelerated Micro-vascular damage and occlusion.
MULTI organs ISCHAEMIA - Heart- Kidney-Brain-Eyes.
• Splits in the intima of small blood vessles wall.
• Vascular wall Fibrinoid Necrosis.
Intra-vascular fibrin deposition and thrombosis.
Micro- Angiopathic Haemolytic Anaemia- fragmented thrombocyte
>

without
puttlet
THROMBOTIC MICRO-ANGIOPATHY
RBC- fragmentation- Thrombocytopenia.
EMERGENCY-MALIGNENT- HTN
EMERGENCY-MALIGNENT- HTN

• Clinically presented
• ACUTE-SEVER- HTN- diastolic BP>120-140mmHg,
• Progressive renal failure- AKI
• ACUTE Aortic- dissecting aneurysm-
Acute pulmonary odema.
• Encephalopathy- SEVER HTN- Cerebral odema
• brain hemorrhage -convulsion.
• PAPILLEDEMA- almost always present.
• COMA- Death.
EMERGENCY-MALIGNENT- HTN

• MANAGEMENT-
1- HOSP. ADMISSION- ICU
2- Slowly reduce BP-
To avoid cerebral – renal- and cardiac
ischemia because loss of autoregulation.
• TARGET- BP
• diastolic BP-100-110mmHg -Over 24- 48 h.
• Then control and normalize BP Over next 2-3days
3- IV- Na - Nitroprusside-
Labetolol-
Glycerin trinitrate - Hydralazine
CLINICAL [Link]
• DIGNOSIS-PTN-
1- Medical-History-
COMMONLY Asymptomatic- discovered by routine exam.
SYMPTOMES-
occiptal headache - dizzness - vertigo- tinnitus-
TARGET ORGAN DAMADE -IHD-MI-ARRHYTHMIA-HF-CVA-PVD-CKD.
• Drug history- NSAID- Alcohol -STEROID-PILLS –LICURICE-DIET.
• Family history- RENAL DISEASES-HTN-DM-LIPIDS PROBLEM.
2- Clinical physical examination-
GENERAL exam. VITAL SIGNS-
CARDIOVASCULAR system
• Looking for SECONDARY underling causes.
Target end organs damage-CNS -EYES-RENAL.
CLINICAL [Link]

fro Hf or take CCB


MANAGEMENT -THRESHOLDS OF HTN
CLINICAL –APPROCH

• 1- BP -110/75-100/70- NO COMPLICATIONS-
• BP-130/85- RE-ASSESS IN 2-3- YEARS.
• 2- BP 130-139/85-89- RE-ASSESS – YEARLY-life style
• 3- BP 140-159/90-99-
• A- TARGET ORGAN DAMAGE OR
• CARDIOVASCULAR COMPLICATIONS - OR DM
• Confirm high BP- Then treat - 2-3-weeks.
• B- IF NOT MONTHLY BP-
• OBSERVE AND CHECK CARDIOVASCULAR SYS.
• –LIFE STYLE CHANGE -
• TREAT- IF BP- LEVEL ARE MAINTAINED HIGH.
MANAGEMENT -THRESHOLDS OF HTN
CLINICAL -APPROCH
• 4- BP-160/100-
• CONFIRM AND TREATE-
• WITH OR WITHOUT
• DM- CARDIOVASCLAR COMPLICATION
• OR END ORGAN DAMAGE-
• TREATE WITHIN 1-2 WEEKS

• 5- BP-180/110
• WORK UP IMMEDIATLY
Lifestyle Modification

PREVENTION OF HPN-

1- Body weight Maintain normal body weight (BMI


20-25kg/m)

2-Aerobic exercise >30 min brisk walk most days/week

3- Diet Reduce intake of fat and saturated fat


Reduce salt intake
<6 g NaCI /day ,increase fish oil

4- Cardiovascular Avoid cigarette smoking –high alcohol


risk reduction
MANGMENT-HTN
first hydrochlorthiazide
ANTI-HYPERTENSIVE DRUGS
line
Like + ACEl ,
CCB

from
*
Any complication the
drug(stop it .

* Role ofJen Start 10 then 20 the 30 ·

• Reduce cardiovascular events


• 30% reduction - stroke- 20% IHD-
• ROLE OF TEN- MULTIPHARMACY
multiple drugs
>
of
1- AECI- GROUP- Give in case
unresponse rather than increase the dose.

• ENALOPRIL- LISINOPRIL- RAMIPRIL- PERINDOPRIL


• INDICATED – AFTER- ACUTE-MI- YOUNG -HF –
• DMT2- NEPHROPATHY-CKD- GFR>30 - STROKE.
2- ARBs- GROUP-
FOR - ACEI-INTOLERANCE
• LOSARTAN- CANDESARTAN- VALSARTAN
• OLMISARTAN- TELMISARTAN-
• INDICATED-
- -LVH- IHD- HF- DMT2- NEPHROPATHY-CKD- GRR>30.
ANTI-HYPERTENSIVE DRUGS
3- THIAZIDES- HYDROCLORTHIAZIDE LIKE-
INDAPMIDE-CHLORTHALIDONE- ~ Action duration .

OLD PT. SYSTOLIC HTN- HF- STROKE.


4- CALCIUM CHANNEL BLOCKERS GROUP- BEST
COMBINATION WITH ARBS- TO AVOID LEG ODEMA
• DIHYDROPYRIDE-GROUP Action duration
New ,
than more 24 h

• AMLODPINE-NIFEDIPINE-lercanidpine-3th gen
• NON-DIHYDROPYRIDINE-GROUP work on AU node.

• - DILTAIZEM - VERAPAMIL-
• Old pt. SYSTOLIC- HTN- ANGINA- ARRHYTHMIA
Long Survival .

&

5- B-BLOCKERS GROUP –NOT REDUCING CENTRALBy–BP-


• By decreasing ATENOLOL- BISOPROLOL-NEBIVOLOL
HR .

• CARVIDOLOL METOPROLOL
• HTN- HF- ANGINA- ARRHYTHMIA- AF
ANTI-HYPERTENSIVE DRUGS
6- ALPHA-BLOCKER GROUP prostate hypertrophy
· In .

• - PHENTOLAMINE-PHENOXYBENZAMINE
• DOXAZOSIN- HTN- BPH
7- ALPHA- B- BLOKERS-

Non-selective .
LABETOLOL- Pregnancy-Emergancy-IV.
<
Cavidabol .

8- VASODILATORS- GROUP-
Hydralazine- Na- nitroprusside- GTN.
9- Centrally acting—MOXOIDINE-methyldopa
• Pregnancy – lactating-
10- STENT- RENAL ARTERY STENOSIS
11-SURGERY-ADRENAL MASS- CO-ARCTATION OF
AORTA- RENAL DENERVATION.
• Key points
• Well CALBRATED -BP- MACHINE-measurement-BP- is important for
diagnosing and managing hypertension.
• Management of hypertension begins with an accurate assessment
of total risk of cardiovascular disease before complication.
• It is important to consider secondary hypertension.
• Changes in lifestyle may delay or avoid the need for drug treatment.
• You should offer patients in whom the clinic blood pressure is
greater than 140/90mm Hg-
• to confirm the diagnosis - (HBPM)BP<5mmHG and
• ABPM-another <5mmHG .
– You should start antihypertensive drug treatment in patients
after confirmation and life style change.
– BP>140-159/90-95 mm Hg WIH DM- OR HIGH RISK-
– WITHOUT WAIT FEW MONTHS.
– BP- >160/100 mmHg
– WITH OR WITHOUT CARDIOVASCULAR COMPLICATIONS .
– or the 10-year cardiovascular risk > 20%.

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