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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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 ?
Dippers & Non Dippers
Dippers & Non Dippers
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Yonsei, Med J, Vol 43, No 3: 2002
Dippers & Non Dippers
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
Dippers & Non Dippers
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Yonsei, Med J, Vol 43, No 3: 2002
Dippers & Non Dippers
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
Dippers & Non Dippers
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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
Dippers & Non Dippers
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?
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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
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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
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Drug Combinations
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83Dr.Sarma@works
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
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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
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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 - SBP > 140
Indap, Amlo,
Enalapril Not BB
Case 23 HT + Cough ACEi coughCough
remedy
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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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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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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