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www.drsarma.in1 Dr.Sarma@works
www.drsarma.inDr.Sarma@works 2
Welcome, Dear Friends
www.drsarma.inDr.Sarma@works 3
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 …….
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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 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
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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. 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
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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 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
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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, 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
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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
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
Dippers & Non Dippers
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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Dippers & Non Dippers
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
Dippers & Non Dippers
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
67
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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
83
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
85Dr.Sarma@works
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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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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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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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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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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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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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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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Case specific approach
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 ISH - SBP > 140Indap, Amlo,
EnalaprilNot BB
Case 23 HT + Cough ACEi coughCough remedy
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Case specific approach
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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Case specific approach
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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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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