Www.drsarma.in 1 Dr.Sarma@works. Dr.Sarma@works 2 Welcome, Dear Friends

www.drsarma.in1 Dr.Sarma@works

www.drsarma.inDr.Sarma@works 2

Welcome, Dear Friends


The Almighty

Pardons and Grants me heaven

Even if I don't know a single letter about

Crutz Feld Jacob’s Disease

Tsutsugamushi Fever

Criggler Nazzar Syndrome

South American equine encephalitis and

Many and much more rarer topics

BUT …….


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)

www.drsarma.in 5

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 VII – Joint National Committee on HT, USA

2. ISH – WHO International Society on HT

3. AHA – American Heart Association, USA

4. ACC – American College of Cardiologist

5. BHS – British Hypertension Society

6. NIHLB – National Inst. Heart Lung & Blood vessels

7. EHS – European Hypertension Society

8. CHS – Canadian Hypertension Society

9. NKF – National Kidney Foundation, USA

10.AKA – American Kidney Association, USA

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WHAT IS NEW IN HYPERTENSION?

9

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

For all of them

Primary and secondary prevention by TLC is the answerAfflicted 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 patientThis may be revised to 120/80 may be ? 110/70 MRFIT’s cut off values are 115/75 mm Hg

It is essential to keep the B.P at or below the goalBut, 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) 2004Normal 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

15

JNC VII Classification

CategoryCategory SBP (mm Hg)SBP (mm Hg) DBP (mm Hg)DBP (mm Hg)

Normal < 120 < 80

Pre – hypertension 120-139 80-90

Hypertension

Stage 1 140 – 159 90 – 99

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 stringent

The cut off values are 10 mm lower

Stage 1 SBP 130 to 149 DBP 80 to 89

Stage 2 SBP 150 and moreDBP 90 and more

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Hypertension Optimal Treatment (HOT) Study

Lancet 1998; 351: 1755–62

p=0.005 (DM)

0

5

10

15

20

25

Ev

ents

/10

00 p

t-y

ears

<90 <85 <80

Target diastolic BP

DM

non-DM

Reduction in CV events

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Rule of Halves

What is this rule of halves in HT ?

• For every 800 adults in the community• 400 are 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 25 the goal B.P. is attained• Means 25 ÷ 400 = 6% only have goal BP

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Normotensives (78%)Normotensives (78%)

Hypertensives (22%)

Under control (40%)

(7.5% of the total hypertensives)

Uncontrolled hypertension

(60%)

Diagnosed HT

Diagnosed HT Under

treatment (50%)

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


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. J Vidal P et al. J Hum HypertensHum Hypertens19971997

Percentages of Patients whose Hypertension is Controlled

Percentages of Patients whose Percentages of Patients whose Hypertension is ControlledHypertension is Controlled

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 Med19971997Canada:Canada: Joffres Joffres et al. et al. AmAmJ J HypertensHypertens2001 2001

England:England: Colhoun et al. J Hypertens 1998Colhoun et al. J Hypertens 1998France:France: Chamontin et Chamontin et al. al. AmAmJ J 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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R R for CVD - SBP and DBP

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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

00 100100 200200 300300

5 Y

ea

r R

isk

(%

)

Stroke

Myocardial Infarction

Systolic Blood Pressure (mmHg)

HT- RR of stroke and MI

Brown, M.J. Lancet 2000; 355: 659 - 660

20 40 60 80 120 140140 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 drugTwo drugsThree drugsCan’t control

In most of the patients of hypertension Two drugs are required for adequate controlMore so if the initial BP is 20/10 above the goal

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TODAY’S PARADIGM

Gone are the days of monotherapy

It is the era of combination therapy

Why is it so?

29

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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


Global Risk Profile and HT

25)

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HT combined with other CHD RF

Framingham offspring study, subjects aged 17 – 84

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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 year CHD 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 failureStroke

Coronary heart disease

Myocardial infarction

Left ventricular hypertrophy

Aortic aneurysm

Retinopathy

Peripheral vascular disease

Hypertensive encephalopathy

Chronic kidney failure

Cerebral hemorrhage

Adapted from: Arch Intern Med 1996; 156:1926-1935.

AllVascular

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Target Organ Damage (TOD)

• Heart Left ventricular hypertrophy (LVH)Angina or prior myocardial infarction (CHD)Prior Coronary revascularization PTCA or

CABGHeart 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


Atherosclerosis – Time line

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Endothelial NO Balance

NO

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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, ABIOptional tests • X-Ray Chest PA• 24 hr. urine albumin excretion or ACR• More extensive testing is not generally indicated

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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

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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 QUALY – Quality Adjusted Life Years

TODAY we must strive to

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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 and ↓TOD ?

How important is Micro-albuminuria ?

Target Organ Damage

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Normal weight 350 to 450 g


Transverse Section of HEART - LVH

10 mm 25 mm


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%

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Progression of HT to LVH to HF

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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

0.9320 4 6 8 10 12 14 16 18

Survival Time (Years)

Hypertensive-LVH

Normotensive-LVH

Hypertensive-No LVH

Nomotensive-No LVH

Port

ion

Surv

ivin

g

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

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LVH is the Single Most important predictor

-90

-80

-70

-60

-50

-40

-30

-20

-10

0

D A B C A + D

Can LVH be reduced at all ??

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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 ??

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

Pat

ient

s W

ith E

vent

s (%

) Less tight controlTight control

Years From Randomisation

UKPDS, BMJ 1998;317:703-713.

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

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MAU as a Predictor of Morbidity and Mortality

Retinopathy

Diabetes+

MAU

LVH

Non-fatal cardiovascular

diseaseAll-cause mortality

Nephropathy

Peripheral/autonomic neuropathy

Parving HH. J Hypertens 1996;14 Suppl 2:S89-S94.

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Definitions of abnormalities in albuminuria

Category24 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) albuminuria

300 200 300

Because of variability in urinary albumin excretion, 2 of 3 specimens over3-6 mon should be abnormal before considering diagnostic threshold positive

False positive: exercise < 24 hours, fever, CHF, marked hyperglycemia, marked HTN, pyuria and hematuria.

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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

2.323.20

Relative Importance of MAU

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What is single most imp. predictor of CHD, HF, Death ?LVH – LV 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 regress ↓TOD ?Yes. All TOD regresses; LVF and CVA most

How important is Micro-albuminuria ?The most important prognostic indicator of TOD

Target Organ Damage

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Clinical Signs of LV Dysfunction

HypotensionPulsus alternansTrigeminy, BigeminyReduced volume of carotidLV apicalEnlargement/displacementSustained heave of apex – Change in heart sounds

Soft S1

Paradoxically split S2

S3 gallop

S4 impaired LV compliance)

Mitral regurgitation

Pulmonary congestion rales

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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 PVD

3. ABI of 0.5- 0.84 correlates with claudication

4. ABI < 0.5 indicates advanced ischemia

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What is this pattern in HT – Dippers and Non-dippers ?

What is its significance and clinical relevance ?

Dippers & Non Dippers

www.drsarma.in 60Yonsei, Med J, Vol 43, No 3: 2002


Non - dippers

Dippers

24 hours clock time

Sys

toli

c B

loo

d P

ress

ure

(m

m H

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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Non - dippers

Dippers

24 hours clock time

Dia

sto

lic

Blo

od

Pre

ssu

re (

mm

Hg

)

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 DBP2. Essential hypertension patients are – usually ‘Dippers’3. Non dippers are Dx. by ABPM – They are usually

1. Secondary HT cases2. More end organ damage3. More LVH4. More responsive to salt restriction5. Diabetics are non dippers6. Diuretics convert a non dipper to dipper


Ambulatory Blood Pressure Monitoring - ABPM

63

1. 24 hour B.P monitoring (every 15 minutes)2. Today - 24 hour B.P. control is essential3. Identifies dippers and non-dippers4. Excludes white coat hypertension

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Pulse wave velocity – Arterial Stiffness

Systole Diastole

Sphygmocor

PulseTrace PCA

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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 get AS MANY PEOPLE as we can to goal SBP < 140 & DBP < 90

And prevent or halt TOD. Of course, tailor the treatment as per

individual patient’s co-morbidities.

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Morbidity and Mortality in HT

Most of the morbidity and mortality of HT is due to

LVH – LV 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

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The correct Approach to HT

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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. Today’s 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 ½ in HT– Adequate control only in 7%68

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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. Day’s 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 early69

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Lifestyle Modification

1. Life style modification is the sheet anchor in the management Hypertension.

2. This surely reduces the number of drugs used 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

Modification Approximate BP reduction(range)

Weight reduction 5–20 mm/10 kg wt loss

Adopt DASH eating plan 8–14 mmHg

Dietary sodium reduction 2–8 mmHg

Physical activity 4–9 mmHg

Abstinence from alcohol 2–4 mmHg

All put together reduce BP by 20 to 55 mmHg

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What to choose from the ocean

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

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On April 12, 1945, US President Franklin D. Roosevelt died of cerebral hemorrhage, a consequence of HT. It was a devastating illness for him.

By current standards, President Roosevelt’s death 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!

Many avoidable HT deaths !

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The Many Faces of HT Therapy Today

Centrally acting agentsCentrally acting agents

DiureticsDiuretics

Beta blockers

Beta blockers

CCBsCCBs

ARBsARBs

ACE – inhibitorsACE – inhibitors

EnalaprilEnalapril

LisinoprilLisinopril

RamiprilRamipril

QuinaprilQuinapril

PerindoprilPerindopril

HypertensionHypertension

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Which drug should we prescribe ?

Choice must be tailored to individual patient

Should be rational and as per approved guidelines

Only class1 evidence based medications to be used

Suitable to patients’ purse

Can never be arbitrary

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Physicians’ Bias in HT

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 effects – Need to watch, not to worry

OK, some control is achieved – why attain goal BP ?

Not insisting on compliance with drugs and assessments

Pressure from patients – B.P. How much ? How much ?

Concentrating on the pill and not on the ill – TLC forgotten

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Anti Hypertensive drug classes

TheA, B, C, D approach

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Anti Hypertensive drug classes

ACEi – Angiotensin converting enzyme

inhibitors – Enalapril- let us call them ‘A’

ARB – Angiotensin Receptor Blockers –

Losartan - Let us call them also as ‘A’

BB – Beta Receptor Blockers – Metoprolol,

Carveidilol, Atenelol - let us call them ‘B’

CCB – Calcium channel blockers – Amlodepine

Verapamil, Diltiazem - let us call them ‘C’

Diuretics – Hydrochlor Thiaz.- Furosemide,

Spiranolactone - let us call them ‘ D ’

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AGEAGE

Younger (< 55)Younger (< 55)High Renin HTHigh Renin HT

Renin

AB/CD Rule – HT Treatment

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

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

Resistant HT /Intolerance

Add / substitute alpha blockerRe-consider 20 causes trial of spironolactone

IV:IV:V:V:

Older (> 55)Older (> 55)Low Renin HTLow Renin HT

ACEi BB

A + B A + B + D

DiureticCCB

D + C + A D + C

I

II

III III

II

I

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DIURETICS

First and Best Choice

Can be combined with A, B, C

βBlockers

Good third Choice

Can be combined with A, D

Ca channelBlockers

Fourth Choice, Useful

Can be combined with D, A

ACEI and ARB

Second Best Choice

Can be combined with D, B, C

D

Diuretics

A

ACEI, ARB

B

β-Blockers

C

Ca-Blockers

D A

B C

The A B C D classes

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A B C D – some brand names

Thiazide diuretics –

Hydrochlorothiazide - Aquazide, Hydride, Xenia

Chlorthalidone – Hythalton, Loop diuretic – Frusemide Potassium sparing

Triamterene, Amiloride, Spironalactone (Aldo anta)

Beta blockers

Selective – Metoprolol, Metoprolol XL, Atenelol

Combined alpha and beta blockers – Carveidilol, Labetolol

ACEI – Enalapril, Ramipril, Lisinopril, Quinapril, Perindopril

ARB – Losartan, Valsratan, Candesartan, Irbesartan

CCB – Nefedipine, Amlodipine, Varapamil, Diltiazem

Alpha Blokers – Prazocin, Doxizocin, Terazocin, Tamsulocinwww.drsarma.in

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Hypertension – Why Combinations ?

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 can’t achieve goal BP – Resistant HT

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Drug Combinations

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Hypertension – Rational Drug Combinations

ACEI and ARB = A

Beta 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 = D – Rank 1

ACEI and ARB = A – Rank 2

Beta Blockers = B – Rank 3

CCB = C – Rank 4

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Some Irrational Combinations

Beta blockers + Beta1 stimulants - 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)

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KNOW ME WELLI am ‘D’ for DIURETIC

My Good aspectsFluid depletion, Na washout, Low costImprove CHF, Systolic function, Ca savingReduce LVH, Morbidity & Mortality

My Bad aspectsPotassium washout, ↑ in Uric acid, ↑ CaAdverse on Lipids, Glucose control

Don’t use me inGout, HypokalaemiaDyslipedemia, Uncontrolled DM

DIURETIC

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KNOW ME WELLI am ‘A’ for ACEI and ARB

My Good aspectsImprove Diastolic function, Systolic functionControl Proteinuria, Very favourable in DMImprove Coronary Ischemia, Good on Lipids Reduce LVH, Morbidity & Mortality

My Bad aspectsBradykinin accumulation, Angio-edema↑ Serum K , ↓ GFR

Don’t use me inPregnancy, Creatinine is > 3 mg%, ↑ K 5.0 meqBilateral Renal Artery Stenosis, Angio-edema

ACEI, ARB

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I am ‘B’ for βBlocker

My Good aspects ↓Heart rate, ↓Forceof contraction, ↓Conduction ↓Myocardial O2 demand, Improve Ischemia

Improve QUALY in CHD, Useful in CHF, Migraine My Bad aspects

Constrict peripheral vessels, BradycardiaUnfavourable on Lipids, Glucose

Don’t use me inBradycardia, Conduction defects, Caution in CHFPrinzmetal Angina, MSD, PVD, BA, COPD, Dys lipidPheochromocytoma, Chronic smokers

β Blocker KNOW ME WELL

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KNOW ME WELLI am ‘C’ for Ca channel Blocker

My Good aspectsVasodilatory, Suitable in elderly, Low costAnti arrhythmic (Verapamil), ↑Coronary BF (Diltz)Neutral on lipidemia, Vasospastic Angina

My Bad aspectsFluid retention, Impair failing heartAdverse on Glucose control , Pedal edema ? Rx.

Don’t use me inTachycardia, arrhythmias, CHF, Uncontrolled DM, Volume overload

Ca+ Blockers

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ABCD Compare & Contrast

Parameter Diuretic ACEi, ARB βblocker 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. Vasodilatory

K ex / bronchi Enhances No effect Bronchospa No effect

UA / Conduct. ↑ Uric acid No effect ↓conduction No effectwww.drsarma.in

Which drug in each class

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Persistence with hypertensive therapy

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Hypertension Case specific approach

some selected case scenarios

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Case specific approach

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 BBB

CCB, ACEi Not BB

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CCB, ACEi Not BB

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CCB, ACEi Not BB

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CCB, ACEi Not BB

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CCB, ACEi Not BB

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CCB, ACEi Not BB

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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, α bloc Not BB

Case 10 HT + Diast. DysARB Losartan ACE Ramipril

BB - Meto

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

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Aldactone

Diltiazem



BB - Meto


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Aldactone

Diltiazem



BB - Meto


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



Aldactone

Diltiazem



BB - Meto


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Aldactone

Diltiazem



BB - Meto


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Aldactone

Diltiazem



BB - Meto


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Aldactone

Diltiazem



BB - Meto


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Case 12 HT + CHFDiu - Fru. Sp. + ARB / ACEi

Not CCB, α bloc

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

Case 14 HT + DM+ DKD MD, HYZ, DNot 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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Not CCB, α bloc



ACEi, ARB




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Not CCB, α bloc



ACEi, ARB




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Not CCB, α bloc



ACEi, ARB




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Not CCB, α bloc



ACEi, ARB




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Not CCB, α bloc



ACEi, ARB




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Not CCB, α bloc



ACEi, ARB




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Case 18 HT + BPH α bloc, Tamsu Not BB

Case 19 HT + EDα bloc, HZ, ACEi /CCB

Not BB

Case 20 HT + Pregnancy MD, HYZ, CCBNot ACEi,

or ARB

Case 21 HT + Gout, ￪ UA ACEi, CCB Not D

Case 22 ISHIndap, Amlo,

EnalaprilNot BB

Case 23 HT + Cough ACEi coughCough remedy

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Not BB


or ARB



EnalaprilNot BB


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Not BB


or ARB



EnalaprilNot BB


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Not BB


or ARB



EnalaprilNot BB


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Not BB


or ARB


Case 22 ISH - SBP > 140Indap, Amlo,

EnalaprilNot BB


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Not BB


or ARB



EnalaprilNot BB


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Not BB


or ARB



EnalaprilNot BB


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Case 24 Hypertension and cough

Hypertensives may present with cough – watch 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 Hypertension – various causes

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

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 blockers are the drugs of choice

Phentolamine, 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 blockerswww.drsarma.in

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Case 27 Resistant Hypertension

Resistant HT Usually Stage 2 HT

May 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 interactions – NSAIDs, SMA, OCP, OTC

Herbal remedies, Excessive alcohol use Rationale Identify the above and correct

Secondary causes to be searched forwww.drsarma.in

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Case 29 Hypertensive emergencies

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 monitoring

Life style modification not now – no time

Do not use No sublingual nefedipine,

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Case 30 Hypertensive with Acute CVA (Stoke)

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 hemorrhage and 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 strokewww.drsarma.in

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Current Indications for Alpha Blockers

1. Hypertension with BPH

2. In Pheochromoytoma before surgery

3. In the treatment of Ergot over dose

4. Raynaud’s syndrome and PVD, TAO

5. Vasospastic (prinzemetal Angina)

6. Diabetic neuropathy

7. Hypertensive smokers

8. Hypertension with Dyslipidemia

First dose syncope and Postural Hypotension

How to avoid ?

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Each of these presentations is a valuable learning experience for me

Learning is a cyclical process

Thank You all

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