treatment of hypertension by dr sarma

8/13/2019 Treatment of Hypertension by Dr Sarma

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The Almighty

Pardons and Grants me heaven

Even if I don't know a single letter about

Crutz Feld Jacobs Disease

Tsutsugamushi Fever

Criggler Nazzar Syndrome

South American equine encephalitis and

Many and much more rarer topics

BUT .


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The Almighty

Will drag me to hell and will not pardon

My ignorance of even the minute details of HT

My indifference to apply the current knowledge

My negligence in screening for HT, TOD

My despondency about preventing TOD

My inadequacy in maintaining my patients

as normo-tensive as possible

(This is applicable to all common diseases)


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Dr.Sarma RVSN, M.D., M.Sc (Canada)

Consultant Physician and Chest Specialist,

# 5, Jayanagar, Tiruvallur 602 001

93805 21221, (044) 27660593

Treatment of Hypertension

A CLINICAL APPROACH


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Management of Hypertension

Based on the latest recommendations of

JNC VII, ISH, ESH, WHO

Treatment of Hypertension

A CLINICAL APPROACH


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Globally Renowned HT Societies

1. JNC VIIJoint National Committee on HT, USA

2. ISHWHO International Society on HT

3. AHAAmerican Heart Association, USA

4. ACCAmerican College of Cardiologist

5. BHSBritish Hypertension Society

6. NIHLBNational Inst. Heart Lung & Blood vessels

7. EHSEuropean Hypertension Society

8. CHSCanadian Hypertension Society

9. NKFNational Kidney Foundation, USA

10.AKAAmerican Kidney Association, USA


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WHAT IS NEW IN HYPERTENSION?

7


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HYPERTENSION

The Truth is

It is only a marker of the bigger problem

Hypertension is a multi-organ systemic disease

What we record as B.P.

The Problem is

Hypertension is asymptomatic in 85% of cases


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How to be wise in HT?

The Truth is

To consider Hypertension as an isolated disease

Hypertension, DM, Dyslipidemia, Obesity often coexist

They are the 4 pallbearers to the grave of CHD, CVD

For all of themPrimary and secondary prevention by TLC is the answer

Afflicted with one, must be screened for all other thieves

It is wrong


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Treatment Goal

The Truth is

Keep B.P. < 140/90 mm Hg in each patient

This may be revised to 120/80 may be ? 110/70MRFITs cut off values are 115/75 mm Hg

It is essential to keep the B.P at or below the goal

But, It also matters how the goal B.P. is achieved !

Goal BP


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Definitions

As per JNC VII and ISH (WHO) 2004

1. What is normal B.P ?

2. What is pre hypertension ?

As per JNC VII and ISH (WHO) 2004

Normal SBP < 120 and DBP < 80

Pre HT SBP 120 to 139 mm Hg

DBP 80 to 99 mm Hg


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Definitions

1. What is stage 1 HT ?

2. What is stage 2 HT ?

Stage 1 SBP 140 to 159

DBP 90 to 99

Stage 2 SBP 160 and moreDBP 100 and more


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13

JNC VII Classification

Category SBP (mm Hg) DBP (mm Hg)

Normal < 120 < 80

Prehypertension 120-139 80-90

Hypertension

Stage 1 140159 9099

Stage 2 160 and above 100 and above


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Definitions

Are the values same for Diabetics , CKD?

No, for DM, IHD and CKD the criteria

are more stringentThe cut off values are 10 mm lower

Stage 1 SBP 130 to 149

DBP 80 to 89Stage 2 SBP 150 and more

DBP 90 and more


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Hypertension Optimal Treatment (HOT) Study

Lancet 1998; 351: 175562

p=0.005 (DM)

0

5

10

15

20

25

Events/1000pt-years


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Rule of Halves

What is this rule of halves in HT ? For every 800 adults in the community

400are HT (either SBP or DBP or both)

Of them only 200 are diagnosed HT

Of them only 100 are started on treatment

Of them only 50 are on correct drug

Of them in only 25the goal B.P. is attained

Means 25 400 = 6%only have goal BP


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Normotensives (78%)

Hypertensives

(22%)

Under control (40%)

(7.5% of the total

hypertensives)

Uncontrolled

hypertension (60%)

Diagnosed

HT Under

treatment

(50%)

Undiagnosed

HT

How many are really Dx. and Rx.ed ??

37%

63%

Un Rx.

HT

A study from Europe on 23,339 patients


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USA

27

Canada

13

England

6

France

24

Adapted from G. Mancia / L.Adapted from G. Mancia / L.

RuilopeRuilope

< 140/90 mmHg

MarquesMarques--Vidal P et al. JVidal P et al. J Hum HypertensHum Hypertens 19971997

Finland Spain

20

Germany Scotland

< 160/95 mmHg

Australia

19

India

9

20.5

17.522.5

> 65 years

USA:USA: JNC VI.JNC VI. Arch Intern MedArch Intern Med 19971997

Canada:Canada: JoffresJoffres et al.et al. AmAm JJ HypertensHypertens 20012001

England:England: Colhoun et al. J Hypertens 1998Colhoun et al. J Hypertens 1998

France:France: Chamontin etChamontin et al.al. AmAm JJ HypertensHypertens19981998

Global Hypertension Control


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Isolated Systolic Hypertension

1. What is ISH ?

2. What percentage of 65+ aged have ISH ?

3. Which is more harmful SBP or DBP ?

4. Why is ISH important ?


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Relative prevalence of SBP and DBP

Normal

ISH

DHT

S&DHT

40 + yrs


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ISH is universal after 65+

Persons who are normo-tensive at age 55

have a 90% lifetime risk for developing HTN.


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0

5

10

15

20

0 100 200 300

5YearRisk(%)

Stroke

Myocardial

Infarction

Systolic Blood Pressure (mmHg)

HT- RR of stroke and MI

Brown, M.J.Lancet2000; 355:659 - 660

20 40 60 80 120 140 160 180 220 240 260 280

Normotensives Hypertensives


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Is SBP more dangerous or DBP ?


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Isolated Systolic Hypertension

1. What is ISH ?SBP 140+ , DBP < 90

2. What percentage of 65+ aged have ISH ?

More than 90%

3. Which is more harmful SBP or DBP ?

Of course SBP

4. Why is ISH important ?Because of CVA and CHD mortality


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For adequate control of B.P.

Do you think we can control most of thepatients of hypertension with

One drug

Two drugsThree drugs

Cant control

In most of the patients of hypertensionTwo drugs are required for adequate control

More so if the initial BP is 20/10 above the goal


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TODAYS PARADIGM

Gone are the days of monotherapy

It is the era of combination therapy

Why is it so?

27


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What are the so called CHD risk factors ?

What are known as CHD risk equivalents ?

What is Framingham risk score ?

CVD Risk Factors


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Global Risk Profile and HT

25)


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HT combined with other CHD RF

Framingham offspring study, subjects aged 1784


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What are the so called CHD risk factors ?List discussed in previous slide

What are known as CHD risk equivalents ?

DM, PVD, CVA, Nephropathy, Retinopathy

What is Framingham 10 CHD risk estimate ?

10 yearCHD risk estimate based on age,sex, smoking, TC, HDL, SBP, Rx. for HT

see the program

CVD Risk Factors


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Why is there TOD in HT ?

What are the organs targeted for damage ?

What is the basis of TOD ?

What tests we need to do to assess HT ?

Target Organ Damage


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Diseases Attributable to Hypertension

Hypertension

Heart failure

StrokeCoronary heart disease

Myocardial infarction

Left ventricular

hypertrophy

Aortic aneurysm

Retinopathy

Peripheral vascular disease

Hypertensive

encephalopathy

Chronic kidney failure

Cerebral hemorrhage

Adapted from:Arch Intern Med1996; 156:1926-1935.

All

Vascular


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Target Organ Damage (TOD)

HeartLeft ventricular hypertrophy (LVH)

Angina or prior myocardial infarction (CHD)

Prior Coronary revascularization PTCA or CABG

Heart failure (Systolic / Diastolic dysfunction)

Brain

CVA Stroke or Transient Ischemic Attack (TIA)

Kidney: Chronic kidney disease and CRF Vessels: Peripheral arterial disease PVD

Eyes: Hypertensive Retinopathy


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AtherosclerosisTime line


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Endothelial NO Balance

NO

T O D A


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Target Organ Damage - Assessment

Routine Tests Electrocardiogram, Echocardiography (desirable)

Urinalysis for proteinuria, Microalbuminuria

Blood glucose (F and PP), and Hematocrit

Serum Na and K, Creatinine or GFR, Calcium

Lipid Profile complete, Eye examination, ABI

Optional tests

X-Ray Chest PA

24 hr. urine albumin excretion or ACR

More extensive testing is not generally indicated

T t O D


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Why is there TOD in HT ?It is a disease of blood vessels.

What are the organs targeted for damage ?

Heart, brain, kidney, eye, peripheral vessel

What is the basis of TOD ?

ED, Arterial stiffness and Atherosclerosis

What tests we need to do to assess TOD ?

List discussed

Target Organ Damage

P di Shift i HT Th


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It is not just B.P.

Paradigm Shift in HT Therapy

1. Alter the modifiable risk factors

2. Keep the SBP < 140 and DBP < 90

3. Prevent or halt or reduce TOD LVH, CHD, CHF, CVA, CRF, PVD & Retino.

4. Prevent or control DM (as HT + DM is hazardous)

5. Prevent or control Dyslipidemia (Endothelial Dysf.)6. Reduce morbidity and mortality

7. Improve QUALYQuality Adjusted Life Years

TODAY we must strive to

T t O D


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What is single most imp. predictor of CHD, HF, Death ?

What time course of HT to LVH to LVF to death ?

Can LVH be regressed at all ?

Will drugs help to regress LVH andTOD ?

How important is Micro-albuminuria ?

Target Organ Damage


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Normal weight 350 to 450 g

T S ti f HEART LVH


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Transverse Section of HEART - LVH

10 mm 25 mm

Echocardiograph of Heart LVH


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Echocardiography of Heart - LVH


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ECG and Left Ventricular Hypertrophy


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Chest PA view of Heart - LVH

C/T ratio > 50%

Progression of HT to LVH to HF


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Progression of HT to LVH to HF

Survival Rate HT + LVH v/s NT + LVH


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Survival Rate HT + LVH v/s NT + LVH

1.00

0.99

0.98

0.97

0.96

0.95

0.94

0.93

20 4 6 8 10 12 14 16 18

Survival Time (Years)

Hypertensive-LVH

Normotensive-LVH

Hypertensive-No LVH

Nomotensive-No LVH

Portion

Sur

viving

Source : Am Hear J, 2000; 140 (6) : 848-856.

Can LVH be reduced at all ??


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LVHis the Single Mostimportant predictor

-90

-80

-70

-60

-50

-40

-30

-20

-10

0

D A B C A + D

Can LVH be reduced at all ??

Will Treatment Help ??


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-60

-50

-40

-30

-20

-10

0

CHF CVA LVH CVD CHD

Combined results of 17 RCTs ( n = 48,000)

Hebert 1993, Moser 1996

Will Treatment Help ??

V l f ll t d bl d t l i NIDDM


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Value of excellent vs. good blood pressure control in NIDDM(144/82 vs. 154/87mmHg)

0

10

20

30

40

0 1 2 3 4 5 6 7 89

PatientsWith

Events(%) Less tight control

Tight control

Years From Randomisation

UKPDS, BMJ1998;317:703-713.

Reduction in risk with tight control 32% (95% CI 6% to 51%) (P=0.019)

MAU as a Predictor of Morbidity and Mortality


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MAU as a Predictor of Morbidity and Mortality

Retinopathy

Diabetes

+MAU

LVH

Non-fatalcardiovascular

diseaseAll-causemortality

Nephropathy

Peripheral/autonom

ic neuropathy

Parving HH. J Hypertens1996;14 Suppl 2:S89-S94.

Definitions of abnormalities in albuminuria


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Definitions of abnormalities in albuminuria

Category

24 hour

collection(mg/24h)

Timed collection(g/min) Spot collection(g/mg Cr)

Normal < 30 < 20 < 30

Microalbuminuria 30-299 20-199 30-299

Clinical (macro)

albuminuria300 200 300

Because of variability in urinary albumin excretion, 2 of 3 specimens over

3-6 mon should be abnormal before considering diagnostic threshold positive

False positive:exercise < 24 hours, fever, CHF, marked hyperglycemia,

marked HTN, pyuria and hematuria.

Relative Importance of MAU


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Eastman RC, Keen H. Lancet 1997;350 Suppl 1:29-32.

Microalbuminuria

10

8

6

4

2

0

10.02

Smoking Hypertension

CHD Odds

Ratio

6.52

Cholesterol

2.32

3.20

Relative Importance of MAU

Target Organ Damage


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What is single most imp. predictor of CHD, HF, Death ?LVHLV mass index

What is the time course of HT to LVH to LVF to death ?

The chart is explained

Can LVH be regressed at all ?

Very much Yes. Diuretics and ACEi are the best

Will drugs help to regressTOD ?

Yes. All TOD regresses; LVF and CVA most

How important is Micro-albuminuria ?

The most important prognostic indicator of TOD

Target Organ Damage

Clinical Signs of LV Dysfunction


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Clinical Signs of LV Dysfunction

Hypotension

Pulsus alternans

Trigeminy, Bigeminy

Reduced volume of carotidLV apical

Enlargement/displacement

Sustained heave of apexChange in heart sounds

Soft S1Paradoxically split S2S3gallop

S4impaired LV compliance)

Mitral regurgitation

Pulmonary congestion rales

Ankle-Brachial Index


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Ankle-Brachial Index

Resting and post exercise SBP in ankle and arm.

1. Normal ABI > 1 (Ankle BP more than the arm BP)

2. ABI < 0.9 has 95% sensitivity for angiographic PVD3. ABI of 0.5- 0.84 correlates with claudication

4. ABI < 0.5 indicates advanced ischemia

Dippers & Non Dippers


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What is this pattern in HTDippers and Non-dippers ?

What is its significance and clinical relevance ?




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Yonsei, Med J, Vol 43, No 3: 2002


Non - dippers

Dippers

24 hours clock time

Syst

olicBloodPres

sure(mmH

g)

110

120

130

140

150

160

6 8 10 12 14 16 18 20 22 24 2 4

Systolic Blood Pressure



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Yonsei, Med J, Vol 43, No 3: 2002


Non - dippers

Dippers

24 hours clock time

Dias

tolicBloodPre

ssure(mmH

g)

70

80

90

100

6 8 10 12 14 16 18 20 22 24 2 4

Diastolic Blood Pressure



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1. Less than 10% circadian variation in SBP and DBP

2. Essential hypertension patients areusually Dippers

3. Non dippers are Dx. by ABPMThey are usually

1. Secondary HT cases

2. More end organ damage

3. More LVH

4. More responsive to salt restriction5. Diabetics are non dippers

6. Diuretics convert a non dipper to dipper


Ambulatory Blood Pressure Monitoring ABPM


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Ambulatory Blood Pressure Monitoring - ABPM

61

1. 24 hour B.P monitoring (every 15 minutes)

2. Today - 24 hour B.P. control is essential3. Identifies dippers and non-dippers

4. Excludes white coat hypertension

Pulse wave velocity Arterial Stiffness


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Pulse wave velocityArterial Stiffness

Systole Diastole

Sphygmocor

PulseTrace PCA

What is MOST essential ??


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What is MOST essential ??

Not that my drug is superior to yours

Not that this trial is better than that

Nor this combination is better than that

But to getAS MANY PEOPLEas we

can togoalSBP < 140 & DBP < 90

And prevent or halt TOD.

Of course, tailor the treatment as per

individual patients co-morbidities.

Morbidity and Mortality in HT


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Morbidity and Mortality in HT

Most of the morbidity and mortality of HT is due to

LVHLV diastolic and systolic dysfunction

Increased risk of Coronary Artery Disease

Increased risk of Cerebral Vascular Disease

Hypertensive heart failure

Chronic Renal Disease of hypertension

Hypertensive vascular damage

The correct Approach to HT


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The correct Approach to HT

Step1

Are all patients screened for hypertension?

Are all hypertensives correctly identified?

Step2

Are they evaluated for co-morbidities/TOD?

Are they assessed for CHD risk factors?

Step3

Are the correct drug combinations prescribed?

What is the compliance for medicines & f/u?

Step4

Is the goal B.P. achieved and maintained?

Are there any complications/ side effects?

65

So What is new in Hypertension ?


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So, What is new in Hypertension ?

1. High B.P recorded is only a clinical marker disease

2. HT is a multi-organ disease, often asymptomatic

3. Not to consider in isolation- Must look for Co-Thieves

4. Todays goal BP is 140/90 It will sure be less tomorrow

5. It matters to attain goal; matters more how it is attained

6. In DM, CKD, IHD the cut off values are 10 mm less

7. Remember rule of in HT Adequate control only in 7%

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What is new in Hypertension - continued


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What is new in Hypertension - continued

8. SBP is more important than DBP; Often ignored it is !9. Wide pulse pressure (SBP-DBP) signifies arterial damage

10. Days of monotherapy have gone; Combined Rx replaces

11. All HT must be screened for CHD risk factors & addressed

12. Target organ damage (TOD) must be investigated and Rx.

13. LVH is the single most predictor of mortality and morbidity

14. ABI, MAU, ABPM, PWV etc., identify high risk cases early

67


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Lifestyle Modification


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y

1. Life style modification is the sheet anchor

in the management Hypertension.

2. This surely reduces the number of drugsused and their dosage in controlling HT.

3. Any drug treatment has value only when

coupled with Life style modification.


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Lifestyle Modification


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y

Modification Approximate BP reduction(range)

Weight reduction 520mm/10 kg wt loss

Adopt DASH eating plan 814 mmHg

Dietary sodium reduction 28 mmHg

Physical activity 49 mmHg

Abstinence from alcohol 24 mmHg

All put together reduce BP by 20 to 55 mmHg

What to choose from the ocean


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16 different classes of drugs

117 approved molecules as on date

Innumerable drug combinations

Over 1800 clinical trials of repute

Five international societies on HT

Seven JNC guidelines so far

Multiple target organs damage

Many co-morbidities

Varied outcomes of interest

Cost constraints

No significant change in the

proportion of HT under control

Many avoidable HT deaths !


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On April 12, 1945, US President Franklin D. Rooseveltdied of cerebral hemorrhage, a consequence of HT. It

was a devastating illness for him.

By current standards, President Rooseveltsdeath was

unnecessary. President Roosevelt was never treated

with Anti-hypertensive drugs.

Modern treatment would have controlled his BP and

prolonged his life.

Arch Int Med, Sept, 23,1996

. . . so also of many others!

y

The Many Faces of HT Therapy Today


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y py y

Enalapril

Lisinopril

Ramipril

Quinapril

Perindopril

Hypertension

Which drug should we prescribe ?


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g p

Choice must be tailored to individual

patient

Should be rational and as per approved

guidelines Only class1 evidencebased medications

to be used

Suitable to patientspurse

Can neverbe arbitrary

Physicians Bias in HT


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Isolated SHT is often dubbed as aging factor

To consider HT is only in the ARM and not in the body

No concept of pulse pressure Not seeing the whole

Worry about side effectsNeed to watch, not to worry

OK, some control is achievedwhy attain goal BP ?

Not insisting on compliance with drugs and assessments

Pressure from patientsB.P. How much ? How much ?

Concentrating on the pill and not on the illTLC forgotten

Anti Hypertensive drug classes


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The

A, B, C, Dapproach

Anti Hypertensive drug classes


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ACEiAngiotensin converting enzyme

inhibitorsEnalapril- let us call them A

ARBAngiotensin Receptor Blockers

Losartan- Let us call them also as A

BBBeta Receptor Blockers Metoprolol,

Carveidilol, Atenelol - let us call them B

CCBCalcium channel blockers Amlodepine

Verapamil, Diltiazem - let us call them C

DiureticsHydrochlor Thiaz.- Furosemide,

Spiranolactone - let us call them D

AB/CD RuleHT Treatment


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AGE

Younger (< 55)

High Renin HT

Renin

ACEi, Beta-blocker Ca++-blocker, Diuretic)(AB/CD =

Dickerson et al. Lancet 353:2008-11;1999

Resistant HT /

Intolerance

Add / substitute alpha blocker

Re-consider 20causes trial of spironolactone

IV:

V:

Older (> 55)

Low Renin HT

ACEi BB

A + B A + B + D

DiureticCCB

D + C + A D + C

I

II

III III

II

I

The A B C D classes


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DIURETICS

First and Best Choice

Can be combined with A, B, C

Blockers

Good thirdChoice

Can be combined with A, D

Ca channelBlockers

FourthChoice, UsefulCan be combined with D, A

ACEI and ARB

Second Best Choice

Can be combined with D, B, C

D

Diuretics

A

ACEI, ARB

B

-Blockers

C

Ca-Blockers

D A

B C

A B C Dsome brand names


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Thiazide diuretics

Hydrochlorothiazide- Aquazide, Hydride, XeniaChlorthalidoneHythalton, Loop diureticFrusemide

Potassium sparing

Triamterene,Amiloride, Spironalactone (Aldo anta)

Beta blockers

SelectiveMetoprolol, Metoprolol XL, Atenelol

Combined alpha and beta blockersCarveidilol, Labetolol

ACEIEnalapril, Ramipril, Lisinopril, Quinapril, Perindopril

ARBLosartan,Valsratan, Candesartan, Irbesartan

CCBNefedipine,Amlodipine,Varapamil, Diltiazem

Alpha BlokersPrazocin, Doxizocin, Terazocin, Tamsulocin

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HypertensionWhy Combinations ?


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If goal BP is not achieved by a single drug in full dose

Then adding another agent will help achieve the goal BP

Two agents sometimes nullify each others side effects

Fixed dose combinations will reduce the no. of tablets

Once daily formulations are good for compliance

Sustained release or LA formulations for 24 h BP control

If three drugs cant achieve goal BPResistant HT

www.drsarma.in

Drug Combinations


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HypertensionRational Drug Combinations


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ACEI and ARB = ABeta Blockers = B

Calcium Channel (CCB) = C

Diuretics Drugs= D

D and A combination is excellent - Ramace H, Losar H, Enace D

D and B combination next - Betaloc H, Atecard D, Tenoric

D and C combination sixth - Amlogaurd H, Stamlo D

A and B combination Third - Losar A, Cardif Beta

A and C combination fourth - Amlopres L, Hipril A, Amlo LS

B and C combination fifth - Amlo AT, Amlobet, Beta Nicardia

Diuretics = DRank 1ACEI and ARB = ARank 2

Beta Blockers = B Rank 3

CCB = CRank 4

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Some Irrational Combinations


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Beta blockers + Beta1stimulants - Rebound HT, Paradoxical BP

Beta blockers + Vepapamil - Extreme bradycardia, HB, CHF

Thiazide + Furesemide - Potential volume and K

CCB + Thiazide - No RCTs to support the additive

Prazocin + Beta blocker - They nullify the effects of each other

Verapamil / Dilzem + Nefidepine - No rationale (cardiac actions contridic)

Beta blocker + ACEI Not for HT alone, Good for CHF, MI, IHD

Sub clinical doses of two drugs Try one drug in good dosage, then add

Two drugs of same class - No rationale (like Enalapril + Ramipril)

(Atenelol + Metoprolol, Nefidepine + Amlo)

KNOW ME WELLI am D for DIURETICDIURETIC


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My Good aspectsFluid depletion, Na washout, Low cost

Improve CHF, Systolic function, Ca saving

Reduce LVH, Morbidity & Mortality

My Bad aspects

Potassium washout, in Uric acid, Ca

Adverse on Lipids, Glucose control

Dont use me inGout, Hypokalaemia

Dyslipedemia, Uncontrolled DM

www.drsarma.in

KNOW ME WELLI am A for ACEI and ARBACEI, ARB


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My Good aspects

Improve Diastolic function, Systolic function

Control Proteinuria, Very favourable in DM

Improve Coronary Ischemia, Good on Lipids

Reduce LVH, Morbidity & Mortality My Bad aspects

Bradykinin accumulation, Angio-edema

Serum K , GFR

Dont use me in

Pregnancy, Creatinine is > 3 mg%, K 5.0 meq

Bilateral Renal Artery Stenosis, Angio-edemawww.drsarma.in

I am B for BlockerBlocker KNOW ME WELL


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My Good aspects

Heart rate, Forceof contraction, Conduction

Myocardial O2demand, Improve Ischemia

Improve QUALY in CHD, Useful in CHF, Migraine

My Bad aspectsConstrict peripheral vessels, Bradycardia

Unfavourable on Lipids, Glucose

Dont use me in

Bradycardia, Conduction defects, Caution in CHF

Prinzmetal Angina, MSD, PVD, BA, COPD, Dys lipid

Pheochromocytoma, Chronic smokerswww.drsarma.in

KNOW ME WELLI am C for Ca channel BlockerCa+ Blockers


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My Good aspectsVasodilatory, Suitable in elderly, Low cost

Anti arrhythmic (Verapamil), Coronary BF (Diltz)

Neutral on lipidemia, Vasospastic Angina

My Bad aspects

Fluid retention, Impair failing heart

Adverse on Glucose control , Pedal edema ? Rx.

Dont use me inTachycardia, arrhythmias, CHF,

Uncontrolled DM, Volume overload

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ABCD Compare & Contrast


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Parameter Diuretic ACEi, ARB blocker Ca+Blocker

Ischemia No effect Improves Improves Negative

LVH, LVF Improves Improves Improves* Negative

CV Mortality Improves Improves Improves Increases

Heart rate No effect No effect Bradycardia Tachycardia

Use in DM Negative Excellent Negative Negative

Lipid effects Negative Excellent Negative Neutral

Fluid & Na Enhances No effect Vasoconstr. VasodilatoryK ex / bronchi Enhances No effect Bronchospa No effect

UA / Conduct. Uric acid No effect conduction No effect

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Which drug in each class


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DIU

HCZ

Chlortha

Indapami Furosemi

Torsemid

Spirono

Triamter

ACEi

Enalapril

Ramipril

Lisinopril Perindopr

Quinapril

Captopril

Benazopr

ARB

Losartan

Telmisart

Valsartan Irbesartan

Candesart

BB

Metoprol

Carvedio

Atenelol Labetolol

Nebivol

Bisiprol

Pindolol

Proprano

CCB

Amlodep

Nefidepin

Felodepin Nitrendep

Verapami

Diltiazem

Persistence with hypertensive therapy


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Hypertension

Case specific approach

some selected case scenarios

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p pp

Case 1 Pre Hypertension TLC, No Drug Yearly F/u

Case 2 Stage 1 HT Single Drug D or D + A

Case 3 Stage 2 HT Two Drugs D + A, D + B

Case 4 HT + Tachycardia Beta blockers Not CCB

Case 5HT + Bradycardia

Heart Blocks BBBCCB, ACEi Not BB

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p pp







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Case 6 HT + CHD Risk F ACEi (Perindo) BB (Meto)

Case 7 HT + IHD (No MI) BB + ACEi B + A + D

Case 8 HT + MI or (RVP)BB (Car) +

ACEi, ARB

Aldactone

Diltiazem

Case 9 HT + PZM Angina CCB, bloc Not BB

Case 10 HT + Diast. Dys ARB LosartanACE Ramipril

BB - Meto

Case 11 HT + Sys Dys ACEi + D A + D + B

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ACEi, ARB

Aldactone

Diltiazem


Case 10 HT + Diast. Dys ARB LosartanACE Ramipril

BB - Meto


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ACEi, ARB

Aldactone

Diltiazem


Case 10 HT + Diast. Dys ARB LosartanACE Ramipril BB - Meto


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Case 6 HT + CHD Risk f ACEi (Perindo) BB (Meto)



ACEi, ARB

Aldactone

Diltiazem




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ACEi, ARB

Aldactone

Diltiazem




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ACEi, ARB

Aldactone

Diltiazem




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ACEi, ARB

Aldactone

Diltiazem




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Case 12 HT + CHFDiu - Fru. Sp.

+ ARB / ACEi

Not CCB,

bloc

Case 13 HT + DM (No DK) ARB, ACEi Not D, C

Case 14 HT + DM+ DKD MD, HYZ, D

Not CCB,

ACEi, ARB

Case 15 HT + Dys lipidem. ACEi, CCB Not BB, D

Case 16 HT + BA / COPD ACEi / ARB Not BB

Case 17 HT + PVD / smoker CCB, ACEi, HZ Not BB

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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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+ ARB / ACEi

Not CCB,

bloc



Not CCB,

ACEi, ARB




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Case 18 HT + BPH bloc, Tamsu Not BB

Case 19 HT + EDbloc, HZ,

ACEi /CCBNot BB

Case 20 HT + Pregnancy MD, HYZ, CCB

Not ACEi,

or ARB

Case 21 HT + Gout, UA ACEi, CCB Not DCase 22 ISH Indap, Amlo,Enalapril Not BB

Case 23 HT + Cough ACEi coughCough

remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB

Case 21 HT + Gout, UA ACEi, CCB Not DCase 22 ISH Indap, Amlo,Enalapril Not BB


remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB

Case 21 HT + Gout, UA ACEi, CCB Not DCase 22 ISH

Indap, Amlo,

Enalapril Not BB


remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB


Indap, Amlo,

Enalapril Not BB


remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB

Case 21 HT + Gout, UA ACEi, CCB Not DCase 22 ISH - SBP > 140

Indap, Amlo,

Enalapril Not BB


remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB


Indap, Amlo,

Enalapril Not BB


remedy

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ACEi /CCBNot BB


Not ACEi,

or ARB


Indap, Amlo,

Enalapril Not BB


remedy

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Case 24 Hypertension and cough


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Hypertensives may present with coughwatch out

1. Consider LVF as the cause of cough

2. Consider ACEI induced dry cough

3. Stop ACEI and give ARB or other agents

4. Check the composition of the cough remedy you give

5. Ephedrine, Pseudephedrine, should be avoided

6. Oral Beta agonists like Orciprenaline, Salbutamol,

Terbutaline the less used, the better.

7. Inhaled beta agonists, ICS are safe

8. Decongestants like phenyl propanolamine to be avoided

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Case 25 Secondary Hypertensionvarious causes


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Secondary HT Usually Stage 2 - HT

Secondary causes will be present

May present in young individuals

Treatment Look for secondary cause and treat

Life style interventions must

Vigorous efforts required to control HT

Often two or even 3 drugs may be required

Resistant HT may be encountered

Anti HT drugs as per secondary cause

Absolute contra ACEI or ARB in bilateral renal artery stenosis

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Case 26 Secondary Hypertension in Pheochromocytoma


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Pheochromocytoma Usually Stage 2 HT, Episodic or Labile

Secondary adrenal medullay tumor

May present in young individuals

Treatment Surgical Ablation of the chromaffin tissue

HT needs to be controlled before surgery

Alpha blockersare the drugs of choicePhentolamine, Phenoxybenzamine, Prazocin

Vigorous efforts required to control HT

Often two or even 3 drugs may be required

Resistant HT may be encountered

Surgery First reduce HT, then surgery

Do not use Beta blockers

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Case 27 Resistant Hypertension


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Resistant HT Usually Stage 2 HTMay present in young individuals

May have secondary causes

Reasons Not taking medication (liers)

Improper BP measurement

Excessive Na intake, Inadequate diuretic Rx.

Full doses of drugs not employed

Drug interactionsNSAIDs, SMA, OCP, OTC

Herbal remedies, Excessive alcohol use

Rationale Identify the above and correct

Secondary causes to be searched for

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Case 29 Hypertensive emergencies


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HT emergency Marked DBP elevation

Acute TOD present

TOD Presentation Encephalopathy, MI, ACS, Pul Edema,

Eclampsia, stroke, head trauma, life-

threatening arterial bleeding, or aortic

dissection Treatment With TOD immediate admission to ICU

IV Nitroprusside, Diazoxide, Labetolol

Without TOD Combination of 2 or 3 drugs

Close monitoringLife style modification not nowno time

Do not use No sublingual nefedipine,

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Case 30 Hypertensive with Acute CVA (Stoke)


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HT + CVA (Stroke) Marked DBP elevation

May be SAH, ICH, Acute Brain Infarction

Rationale In acute setting, no consensus on

treatment of elevated BP

HT at time of an acute stroke associated

with increased risk of cerebral hemorrhageand edema, increased mortality

After acute ischemic stroke, cerebral

auto regulation affected

Active treatment of BP in the first 7 days

could worsen symptoms Treatment Recommendation not to start HT Rx.

before 7 to 10 days after ischemic stroke

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Learning is a cyclical process


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Each of these presentations

is a valuable learningexperience for meThank You all

treatment of hypertension by dr sarma

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