Treatment of Hypertension by DR Sarma

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 .
Dr.Sarma@works
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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)
Dr.Sarma@works
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Treatment of Hypertension
A CLINICAL APPROACH
Dr.Sarma RVSN, M.D., M.Sc (Canada)
Consultant Physician and Chest Specialist, # 5, Jayanagar, Tiruvallur 602 001 93805 21221, (044) 27660593
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Treatment of Hypertension
A CLINICAL APPROACH
Management of Hypertension
Based on the latest recommendations of
JNC VII, ISH, ESH, WHO
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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?
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HYPERTENSION
What we record as B.P. It is only a marker of the bigger problem

The Truth is Hypertension is a multi-organ systemic disease
The Problem is
Hypertension is asymptomatic in 85% of cases
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How to be wise in HT?
It is wrong To consider Hypertension as an isolated disease The Truth is Hypertension, DM, Dyslipidemia, Obesity often coexist They are the 4 pallbearers to the grave of CHD, CVD For all of them Primary and secondary prevention by TLC is the answer Afflicted with one, must be screened for all other thieves
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Treatment Goal
Goal BP Keep B.P. < 140/90 mm Hg in each patient This may be revised to 120/80 may be ? 110/70 MRFITs cut off values are 115/75 mm Hg
The Truth is It is essential to keep the B.P at or below the goal But, It also matters how the goal B.P. is achieved !
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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

Stage 2
SBP 140 to 159 DBP 90 to 99

SBP 160 and more DBP 100 and more
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JNC VII Classification

Category Normal
SBP (mm Hg)

< 120
DBP (mm Hg)

< 80
Pre hypertension
Hypertension Stage 1 Stage 2
120-139
80-90
140 159 160 and above
90 99 100 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 Stage 2
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SBP 130 to 149 DBP 80 to 89 SBP 150 and more DBP 90 and more
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Hypertension Optimal Treatment (HOT) Study

Reduction in CV events
25
p=0.005 (DM)
DM non-DM
20
Events/1000 pt-years
15
10
0 <90 <85 <80
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Target diastolic BP
Lancet 1998; 351: 175562
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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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How many are really Dx. and Rx.ed ??
Under control (40%) Diagnosed HT 37% Under Un Rx. treatment HT (50%) (7.5% of the total hypertensives)
Hypertensives (22%) Normotensives (78%)
63%
Uncontrolled hypertension (60%)
Undiagnosed HT
A study from Europe on 23,339 patients

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Global Hypertension Control Percentages of Patients whose Hypertension is Controlled

< 140/90 mmHg USA Canada
27 13
< 160/95 mmHg Finland Spain Australia

20.5
20 19
England
6
France
24
Germany Scotland
22.5
> 65 years
India
9
17.5
USA: JNC VI. Arch Intern Med 1997 Canada: Joffres et al. Am J Hypertens 2001
MarquesMarques-Vidal P et al. J Hum Hypertens 1997
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1998
www.drsarma.in France: Chamontin et al. Am J Hypertens
England: Colhoun et al. J Hypertens 1998
Adapted from G. Mancia / L. Ruilope 18
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
40 + yrs
ISH
S&DHT
DHT Normal
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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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HT- RR of stroke and MI
20
Normotensives
5 Year Risk (%)
15
Hypertensives
10
Stroke
5
Myocardial Infarction
0 0 www.drsarma.in
20 40 60 80
100
120
140
160
180
200
220
240
260
280
300
Systolic Blood Pressure (mmHg)
Brown, M.J. Lancet 2000; 355: 659 - 660
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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 the patients of hypertension with

One drug Two drugs Three drugs Cant control
In most of the patients of hypertension

Two 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?
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CVD Risk Factors
What are the so called CHD risk factors ?
What are known as CHD risk equivalents ?

What is Framingham risk score ?
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Global Risk Profile and HT
25)
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HT combined with other CHD RF
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Framingham offspring study, subjects aged 17 84

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CVD Risk Factors
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
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Target Organ Damage
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 ?

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Diseases Attributable to Hypertension
Coronary heart disease Myocardial infarction Left ventricular hypertrophy
Stroke
Heart failure
Cerebral hemorrhage
Hypertension
Chronic kidney failure Hypertensive encephalopathy
Aortic aneurysm Retinopathy Peripheral vascular disease

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Adapted from: Arch Intern Med 1996; 156:1926-1935.
All Vascular
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Target Organ Damage (TOD)

Heart Left 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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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, ABI Optional tests X-Ray Chest PA 24 hr. urine albumin excretion or ACR More extensive testing is not generally indicated
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Target Organ Damage
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
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Paradigm Shift in HT Therapy It is not just B.P. TODAY we must strive to
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
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Target Organ Damage
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 ?
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Normal weight 350 to 450 g

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Transverse Section of HEART - LVH
10 mm
25 mm
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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%

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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
Source : Am Hear J, 2000; 140 (6) : 848-856.
0.99
0.98
Nomotensive-No LVH Hypertensive-No LVH Normotensive-LVH
Portion Surviving
0.97
0.96
0.95
0.94
Hypertensive-LVH
0.93
0 2 4 6 8 10 12 14 16 18
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Survival Time (Years)
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Can LVH be reduced at all ??

0 -10 -20 -30 -40 -50 -60 -70 -80 -90 D A B C A+D
LVH is the Single Most important predictor

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Will Treatment Help ??

0 -10 -20 -30 -40 -50 -60 CHF CVA LVH CVD CHD
Combined results of 17 RCTs ( n = 48,000)
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Hebert 1993, Moser 1996
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Value of excellent vs. good blood pressure control in NIDDM

(144/82 vs. 154/87mmHg)
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Patients With Events (%)
Less tight control Tight control
30 20
10 0 0 9 1 2 3 4 5 6 Years From Randomisation 7 8
Reduction in risk with tight control 32% (95% CI 6% to 51%) (P=0.019)
UKPDS, BMJ 1998;317:703-713.
MAU as a Predictor of Morbidity and Mortality
Retinopathy
LVH
All-cause mortality
Diabetes + MAU
Peripheral/autonom ic neuropathy
Nephropathy
Non-fatal cardiovascular disease
Parving HH. J Hypertens 1996;14 Suppl 2:S89-S94. www.drsarma.in

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Definitions of abnormalities in albuminuria

24 hour collection (mg/24h) < 30 30-299 300 Timed collection (g/min) < 20 20-199 200 Spot collection (g/mg Cr) < 30 30-299 300
Category Normal Microalbuminuria Clinical (macro) albuminuria
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.
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Relative Importance of MAU
10.02
10
6.52
6
CHD Odds Ratio
3.20 2.32
Microalbuminuria
Smoking
Hypertension
Cholesterol
Eastman RC, Keen H. Lancet 1997;350 Suppl 1:29-32.
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Target Organ Damage 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
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Clinical Signs of LV Dysfunction
Hypotension Pulsus alternans Trigeminy, Bigeminy Reduced volume of carotid LV apical Enlargement/displacement Sustained heave of apex Change in heart sounds
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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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Dippers & Non Dippers
What is this pattern in HT Dippers and Non-dippers ? What is its significance and clinical relevance ?
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Systolic Blood Pressure
160
Systolic Blood Pressure (mm Hg)
150
140
Non - dippers
130
Dippers
120
110
6 8 10 12 14 16 18 20 22 24 2 4
24 hours clock time

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Yonsei, Med J, Vol 43, No 3: 2002 58

Diastolic Blood Pressure
Diastolic Blood Pressure (mm Hg)
100
90
Non - dippers
80
Dippers
70
6 8 10 12 14 16 18 20 22 24 2 4
24 hours clock time

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Yonsei, Med J, Vol 43, No 3: 2002 59
1. Less than 10% circadian variation in SBP and DBP 2. Essential hypertension patients are usually Dippers 3. Non dippers are Dx. by ABPM They are usually
1. Secondary HT cases 2. More end organ damage 3. More LVH 4. More responsive to salt restriction 5. Diabetics are non dippers 6. Diuretics convert a non dipper to dipper
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Ambulatory Blood Pressure Monitoring - ABPM

1. 2. 3. 4. 24 hour B.P monitoring (every 15 minutes) Today - 24 hour B.P. control is essential Identifies dippers and non-dippers Excludes white coat hypertension
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Pulse wave velocity Arterial Stiffness
Systole
Diastole
PulseTrace PCA
Sphygmocor
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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 patients 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 Are all patients screened for hypertension? Step1 Are all hypertensives correctly identified? Are they evaluated for co-morbidities/TOD? Step 2 Are they assessed for CHD risk factors? Are the correct drug combinations prescribed? Step 3 What is the compliance for medicines & f/u? Is the goal B.P. achieved and maintained? Step 4 Are there any complications/ side effects?
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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
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
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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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Dr.Sarma@works
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Lifestyle Modification
Modification
Approximate BP reduction (range) 520 mm/10 kg wt loss 814 mmHg 28 mmHg 49 mmHg
Weight reduction Adopt DASH eating plan Dietary sodium reduction Physical activity
Abstinence from alcohol

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24 mmHg
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All put together reduce BP by 20 to 55 mmHg
What to choose from the ocean

16 different classes of drugs 117 approved molecules as on date
Innumerable drug combinations

significant Over 1800 clinical trials of repute No change in the Five international societies on HT proportion of HT under control Seven JNC guidelines so far Multiple target organs damage Many co-morbidities Varied outcomes of interest
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Cost constraints
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Many avoidable HT deaths !
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 Roosevelts 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!

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The Many Faces of HT Therapy Today
Enalapril Lisinopril Ramipril Quinapril Perindopril Hypertension
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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
The A, 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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AB/CD Rule HT Treatment

(AB/CD = ACEi, Beta-blocker AGE Younger (< 55) High Renin HT
I ACEi BB A+B III A+B+D
Ca++-blocker, Diuretic)
Renin
Older (> 55) Low Renin HT

III CCB Diuretic I
II
D+C+A
D + C II
Resistant HT / Intolerance
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IV: Add / substitute alpha blocker V: Re-consider 20 causes trial of spironolactone Dickerson et al. Lancet 353:2008-11;1999
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The A B C D classes
D Diuretics A ACEI, ARB
Ca channelBlockers ACEI DIURETICS and ARB Blockers

Fourth Choice, Useful Second First and Best Best Choice Choice Good third Choice Can be combined with D,B, AC B C with Can Can becombined combined withD, A, B, C Canbe be combined with A, D
D A
B -Blockers
C Ca-Blockers
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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, Tamsulocin
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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 cant 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 D and B combination next D and C combination sixth A and B combination Third A and C combination fourth B and C combination fifth www.drsarma.in
Diuretics = D Rank 1 ACEI and ARB = A Rank 2 Beta Blockers = B Rank 3 CCB = C Rank 4 Ramace H, Losar H, Enace D Betaloc H, Atecard D, Tenoric Amlogaurd H, Stamlo D Losar A, Cardif Beta Amlopres L, Hipril A, Amlo LS Amlo AT, Amlobet, Beta Nicardia
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Some Irrational Combinations
Beta blockers + Beta1 stimulants - Rebound HT, Paradoxical BP Beta blockers + Vepapamil Thiazide + Furesemide CCB + Thiazide Extreme bradycardia, HB, CHF Potential volume and K No RCTs to support the additive They nullify the effects of each other
Prazocin + Beta blocker -
Verapamil / Dilzem + Nefidepine Beta blocker + ACEI Sub clinical doses of two drugs Two drugs of same class -
No rationale (cardiac actions contridic)

Not for HT alone, Good for CHF, MI, IHD Try one drug in good dosage, then add No rationale (like Enalapril + Ramipril) (Atenelol + Metoprolol, Nefidepine + Amlo)
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DIURETIC
I am KNOW D for ME DIURETIC WELL
My Good aspects Fluid 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 in Gout, Hypokalaemia Dyslipedemia, Uncontrolled DM
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ACEI, ARB
I am A KNOW for ME ACEI WELL and ARB
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-edema
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Blocker
KNOW ME WELL I am B for Blocker
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, 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 smokers
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Ca+ Blockers I am C KNOW for Ca ME channel WELLBlocker
My Good aspects Vasodilatory, 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 in Tachycardia, arrhythmias, CHF, Uncontrolled DM, Volume overload
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ABCD Compare & Contrast

Parameter Ischemia LVH, LVF Diuretic No effect Improves ACEi, ARB Improves Improves blocker Improves Improves* Ca+ Blocker Negative Negative
CV Mortality
Heart rate Use in DM Lipid effects Fluid & Na
Improves
No effect Negative Negative Enhances
Improves
No effect Excellent Excellent No effect No effect No effect
Improves
Bradycardia Negative Negative Vasoconstr. Bronchospa conduction
Increases
Tachycardia Negative Neutral Vasodilatory No effect No effect
90
K ex / bronchi Enhances UA / Conduct. Uric acid

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Which drug in each class
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
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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 Case 2 Case 3 Case 4 Pre Hypertension Stage 1 HT Stage 2 HT HT + Tachycardia TLC, No Drug Single Drug Two Drugs Beta blockers Yearly F/u D or D + A D + A, D + B Not CCB
Case 5
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HT + Bradycardia Heart Blocks BBB
CCB, ACEi
Not BB
94

Case 5
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CCB, ACEi
Not BB
95

Case 5
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CCB, ACEi
Not BB
96

Case 5
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CCB, ACEi
Not BB
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Case 5
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CCB, ACEi
Not BB
98

Case 1 Pre Hypertension TLC, No Drug Yearly F/u
Case 2
Case 3 Case 4 Case 5
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Stage 1 HT
Stage 2 HT HT + Tachycardia HT + Bradycardia Heart Blocks BBB
Single Drug
Two Drugs Beta blockers CCB, ACEi
D or D + A
D + A, D + B Not CCB Not BB
99

Case 6 Case 7 Case 8 Case 9 HT + CHD Risk F HT + IHD (No MI) HT + MI or (RVP) HT + PZM Angina ACEi (Perindo) BB + ACEi BB (Car) + ACEi, ARB CCB, bloc ARB Losartan ACE Ramipril ACEi + D BB (Meto) B+A+D Aldactone Diltiazem Not BB BB - Meto A+D+B
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Case 10 HT + Diast. Dys Case 11 HT + Sys Dys

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Case 6 Case 7 Case 8 Case 9 HT + CHD Risk f HT + IHD (No MI) HT + MI or (RVP) HT + PZM Angina ACEi (Perindo) BB + ACEi BB (Car) + ACEi, ARB CCB, bloc ARB Losartan ACE Ramipril ACEi + D BB (Meto) B+A+D Aldactone Diltiazem Not BB BB - Meto A+D+B
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Case 12 HT + CHF Case 13 HT + DM (No DK) Case 14 HT + DM+ DKD Case 15 HT + Dys lipidem. Case 16 HT + BA / COPD Diu - Fru. Sp. + ARB / ACEi ARB, ACEi MD, HYZ, D ACEi, CCB ACEi / ARB Not CCB, bloc Not D, C Not CCB, ACEi, ARB Not BB, D Not BB Not BB
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Case 17 HT + PVD / smoker CCB, ACEi, HZ

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Case 18 HT + BPH Case 19 HT + ED Case 20 HT + Pregnancy Case 21 HT + Gout, UA Case 22 ISH Case 23 HT + Cough
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bloc, Tamsu bloc, HZ, ACEi /CCB MD, HYZ, CCB ACEi, CCB Indap, Amlo, Enalapril ACEi cough
Not BB Not BB Not ACEi, or ARB Not D Not BB Cough remedy

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Case 18 HT + BPH Case 19 HT + ED Case 20 HT + Pregnancy Case 21 HT + Gout, UA Case 22 ISH - SBP > 140 Case 23 HT + Cough
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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
Treatment
Usually Stage 2 - HT Secondary causes will be present May present in young individuals 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 ACEI or ARB in bilateral renal artery stenosis
Absolute contra
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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
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Beta blockers
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Case 27
Resistant Hypertension
Resistant HT
Reasons
Rationale
Usually Stage 2 HT May present in young individuals May have secondary causes 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 Identify the above and correct Secondary causes to be searched for
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Case 29
Hypertensive emergencies
HT emergency TOD Presentation
Treatment
Do not use
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Marked DBP elevation Acute TOD present Encephalopathy, MI, ACS, Pul Edema, Eclampsia, stroke, head trauma, lifethreatening arterial bleeding, or aortic dissection 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 No sublingual nefedipine,
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Case 30
Hypertensive with Acute CVA (Stoke)
HT + CVA (Stroke) Rationale
Treatment
Marked DBP elevation May be SAH, ICH, Acute Brain Infarction 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 Recommendation not to start HT Rx. before 7 to 10 days after ischemic stroke
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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. Raynauds 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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Learning is a cyclical process
Thank You all
Each of these presentations is a valuable learning experience for me
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Treatment of Hypertension by DR Sarma

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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

The Almighty Will drag me to hell and will not pardon

My ignorance of even the minute details of HT

My despondency about preventing TOD

JNC VII, ISH, ESH, WHO

Globally Renowned HT Societies

6. NIHLB National Inst. Heart Lung & Blood vessels

9. NKF National Kidney Foundation, USA

WHAT IS NEW IN HYPERTENSION?

What we record as B.P. It is only a marker of the bigger problem

How to be wise in HT?

As per JNC VII and ISH (WHO) 2004

1. What is normal B.P ?

2. What is stage 2 HT ? Stage 1

SBP 140 to 159 DBP 90 to 99

JNC VII Classification

SBP (mm Hg)

DBP (mm Hg)

140 159 160 and above

90 99 100 and above

Hypertension Optimal Treatment (HOT) Study

0 <90 <85 <80

Lancet 1998; 351: 175562

What is this rule of halves in HT ?

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

Hypertensives (22%) Normotensives (78%)

Uncontrolled hypertension (60%)

A study from Europe on 23,339 patients

Global Hypertension Control Percentages of Patients whose Hypertension is Controlled

< 160/95 mmHg Finland Spain Australia

MarquesMarques-Vidal P et al. J Hum Hypertens 1997

www.drsarma.in France: Chamontin et al. Am J Hypertens

England: Colhoun et al. J Hypertens 1998

Adapted from G. Mancia / L. Ruilope 18

Isolated Systolic Hypertension

Relative prevalence of SBP and DBP

R R for CVD - SBP and DBP

ISH is universal after 65+

HT- RR of stroke and MI

Systolic Blood Pressure (mmHg)

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

Is SBP more dangerous or DBP ?

Isolated Systolic Hypertension

2. What percentage of 65+ aged have ISH ?

3. Which is more harmful SBP or DBP ?

4. Why is ISH important ?

For adequate control of B.P.

Do you think we can control most of the patients of hypertension with

In most of the patients of hypertension

Gone are the days of monotherapy

CVD Risk Factors

What are the so called CHD risk factors ?

What are known as CHD risk equivalents ?

Global Risk Profile and HT

HT combined with other CHD RF

Framingham offspring study, subjects aged 17 84

CVD Risk Factors

Target Organ Damage

What tests we need to do to assess HT ?

Diseases Attributable to Hypertension

Coronary heart disease Myocardial infarction Left ventricular hypertrophy

Chronic kidney failure Hypertensive encephalopathy