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Hypertension
M. Deepalakshmi
Lecturer
Department of Pharmacy Practice
JSS College of Pharmacy, Ooty
(A Constituent College of JSS University, Mysore)
Blood Pressure:
The force exerted by the blood against
the walls of the blood vessels
Factors Influencing
Blood Pressure (BP)
Cardiac output is total blood flow through systemic or pulmonary
circulation per min. CO =stroke volume (amt pumped out of
L ventricle per beat [70 ml]) times the HR for 1 min.
SVR + force opposing movement of blood in vessels;
determined primarily by radius of small arteries & arterioles
Blood
Pressure
Cardiac
Output
Systemic
Vascular
Resistance
= x
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Introduction….
• Hypertension is known as the "silent killer" since it has no initial
symptoms but can lead to long-term disease and complications..
• Many people have high blood pressure and don't know it.
• Important complications of uncontrolled or poorly treated high blood
pressure include heart attack, congestive heart failure, stroke, kidney
failure, peripheral artery disease, and aortic aneurysms (weakening
of the wall of the aorta, leading to widening or ballooning of the
aorta).
• Public awareness of these dangers has increased. High blood
pressure has become the second most common reason for medical
office visits in the United States.
• Hypertension is defined by persistent elevation of arterial blood
pressure.
• Patients with diastolic blood pressure (DBP) values <90 mm Hg and
systolic blood pressure (SBP) values≥140 mm Hg have isolated systolic
hypertension.
• A hypertensive crisis (BP >180/120 mm Hg) may be categorized as
either
– a hypertensive emergency (extreme BP elevation with acute or progressing
target organ damage) or
– a hypertensive urgency (severe BP elevation without acute or progressing
target organ injury).
JNC-7 CLASSIFICATION
Class Systolic(mm of Hg) Diastolic(mm of Hg)
Normal 120 80
Prehypertension 120-139 80-89
Stage-1 hypertension 140-159 90-99
Stage-2 hypertension 160-179 100-109
Stage-3 hypertension ≥180 ≥110
Etiology
Primary hypertension:
 Also known as Essential hypertension (or) Idiopathic hypertension
 Result of unknown etiology (cause)
 Symptomatic treatment given
 Almost 90 – 95 % patients showing this type
Secondary hypertension:
 Result of some known Pathology (Chronic renal disease, Endocrine
disease, etc,.)
 Occurs in about 5 – 10 % of patients
Other types of hypertensions:
 Isolated systolic hypertension: (SBP>140mmHg)
 Malignant hypertension: (diastolic >140mmHg)
 White coat hypertension: BP Elevated only when examined by a
health care professional
• Socioeconomic status: High blood pressure is found more commonly
among the less educated and lower socioeconomic groups. Residents
of the southeastern United States, both Caucasian and African
American, are more likely to have high blood pressure than residents
of other regions.
• Family history (heredity): The tendency to have high blood pressure
appears to run in families.
• Gender: Generally men have a greater likelihood of developing high
blood pressure than women. This likelihood varies according to age
and among various ethnic groups.
Primary hypertension
Genetic Factors
Racial & Environmental Factors
Humoral abnormalities
Pathologic disturbances in autonomic nerve fibers,
adrenergic and baro receptors.
Abnormalities in either the renal or tissue auto regulatory
processes.
Secondary hypertension
Renal diseases :
 Stenosis of renal arteries
 Tumor of justaglomerular cells →Angiotensin II
Endocrine disorders :
Adrenal Gland
 Pheo chromocytoma
 Cushing´s syndrome
Coarctation of aorta
Other factors
 Drugs Induced : e.g. oral contraceptives
 Pregnancy Induced
 Deficiency of vaso dilating substance
(prostacyclin,bradykinin)
 Increase production of vasoconstructing
substance(Angiotensin II, Endothelin I)
Pathophysiology
Humoral abnormalities involving
 Renin – Angiotensin,Aldosterone system
 Natriuritic hormone
 Hyperinsulinemia (side effect of insulin therapy)
Renin – Angiotensin System:
• ‘Angiotensinogen’ is a δ – globulin type of protein secreted in
the liver
• Another substance ‘renin’ secreted by juxtaglomerular cells
• Renin acts on angiotensinogen and converts it to Angiotensin – I
• Angiotensin converting enzyme (ACE) along with Aldosterone,
converts
Angiotensin – I → Angiotensin – II (this is a powerful
vasoconstrictor)
Regulation of aldosterone secretion by the renin–
angiotensin–aldosterone (RAA) pathway
Regulation of secretion and actions of antidiuretic
hormone (ADH).
Blood Pressure Regulation by Hormones
ANS innervation of the heart and the baroreceptor reflexes that help
regulate blood pressure.
ROLE OF NATRIURETIC HORMONE
Concentration of
Natriuretic Harmone
Inhibits Na +K +ATPse
Pump
Inhibition of sodium
transport across the cell
membrane
BP
Sympathetic
neuronal fibers on
the surface of the
effector cells
α 1
receptors
β
receptors
Postsynaptic
stimulation on
arterioles & venules
Vasoconstriction
β1 β2
Postsynaptic
stimulation in Heart
Heart rate & Contractility
Postsynaptic
stimulation on
arterioles &
Venules
Vasodilatation
Neuronal Mechanisms
In vascular endothelium (innermost layer)
1.
↓ Synthesis of vasodilating ↑ Synthesis of vaso-
substances (Prostacycline, constricting substances
bradikinin, NO2) OR (Angiotensin – II,
Prostaglandin in muscle cells endothelin – I, etc,.)
2.↑ Na+ intake + ↓ excretion of Na+ →↑ Natriuritic
hormone
inhibit
↑vascular activity intra cellular Na+ uptake
(constriction of vessels)
this may also cause oedema
3.Release of Ca + stored in sarcoplasmic reticulum
cause
↑intracellular coation of calcium
cause
Altered vascular smooth muscle function (↑tone)
↑PVR
4. Hyperinsulinemia:
• Constriction of blood vessels
• Deposition of cholesterol in blood vessel (atherosclerosis)
Clinical presentation
 Patients with uncomplicated primary hypertension are usually
asymptomatic initially.
 Patients with secondary hypertension may complain of symptoms
suggestive of the underlying disorder.
 Patients with pheochromocytoma may have a history of paroxysmal
headaches, sweating, tachycardia, palpitations
 In primary aldosteronism, hypokalemic symptoms of muscle cramps
and weakness may be present.
 Patients with hypertension secondary to Cushing’s syndrome may
complain of weight gain, polyuria, edema, menstrual irregularities,
recurrent acne,muscular weakness.
TIA = transient ischemic attack; LVH = left ventricular hypertrophy; CHD = coronary heart disease
HF = heart failure.
Cushman WC. J Clin Hypertens. 2003;5(Suppl):14-22.
Renal failure
Peripheral vascular
disease
Complications of Hypertension:
LVH,
HF,CHD,
TIA, stroke
Hypertension
is a risk factor
Diagnostic Studies
 Use auscultatory method with a properly calibrated instrument
 Patient seated quietly for 5 min in a chair, feet on the floor, and arm
supported at heart level
 Appropriate-sized cuff is necessary to ensure accurate reading
 At least two measurements should be obtained
 Allow at least 1 minute between readings. If one arm higher than
other; take BP in higher arm for subsequent measurements
Diagnostic studies
 Basic laboratory studies are performed to (1) identify or rule out
causes of secondary hypertension, (2) evaluate target organ disease,
(3) determine overall cardiovascular risk, or (4) establish baseline
levels before initiating therapy.
 Routine urinalysis, BUN, serum creatinine, and creatinine clearance
levels are used to screen for renal involvement and to provide
baseline information about kidney function.
 Measurement of serum electrolytes, especially potassium levels, is
done to detect hyperaldosteronism, a cause of secondary
hypertension.
Diagnostic studies….
 Blood glucose levels assist in the diagnosis of diabetes
mellitus.
 Lipid profile provides information about additional risk
factors that predispose to atherosclerosis and
cardiovascular disease.
 ECG and echocardiography provide information about the
cardiac status.
Management
 Treatment goals are to lower BP to less than 140 mm Hg systolic and
less than 90 mm Hg diastolic for most persons with hypertension (less
than 130 mm Hg systolic and less than 80 mm Hg diastolic for those
with diabetes mellitus and chronic kidney disease).
 Lifestyle modifications are indicated for all patients with pre
hypertension and hypertension and include the following:
 Weight reduction. A weight loss of 10 kg may decrease SBP by
approximately 5 to 20 mm Hg.
 Dietary Approaches to Stop Hypertension (DASH) eating plan.
Involves eating several servings of fish each week, eating plenty
of fruits and vegetables, increasing fiber intake, and drinking a
lot of water. The DASH diet significantly lowers BP.
 Restriction of dietary sodium to less than 6 g of salt (NaCl) or less
than 2.4 g of sodium per day.
 This involves avoiding foods known to be high in sodium (e.g.,
canned soups) and not adding salt in the preparation of foods or
at meals.
 Restriction of alcohol
 Regular aerobic physical activity (e.g., brisk walking) at least 30
minutes a day most days of the week. Moderately intense
activity such as brisk walking, jogging, and swimming can lower
BP, promote relaxation, and decrease or control body weight.
 It is strongly recommended that tobacco use be avoided.
 Stress can raise BP on a short-term basis and has been implicated
in the development of hypertension. Relaxation therapy may be
useful in helping patients manage stress, thus decreasing BP.
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
Drug Therapy
 Drug therapy is not recommended for those persons with
prehypertension unless it is required by another condition, such as
diabetes mellitus or chronic kidney disease.
 The overall goals for the patient with hypertension include
 achievement and maintenance of the goal BP
 reduce mortality due to hypertension-induced disease
 acceptance and implementation of the therapeutic plan
 minimal or no unpleasant side effects of therapy
 ability to manage and cope with illness.
Ways of lowering BP
Reduce cardiac output
 Beta blockers
 Ca2+ channel antagonists
Reduce plasma volume
 Diuretics
Reduce Total Peripheral Resistance
 vasodilators
 alpha1-adrenergic receptor antagonists
 ACE inhibitors
Summary of Drug Targets
32
The Many Faces of HT Therapy Today
Enalapril
Lisinopril
Ramipril
Quinapril
Perindopril
Hypertension
Drug use in Hypertension
Class Drugs / Trade name
DIURETICS
A. Thiazide diuretics a. Bendro fluazide
b. Cyclopenthiazide
c. Hydrochlorothiazide
B. Loop diuretics a. Bumetanide
b. Frusemide
C. Potassium-sparing a. Spironolactone
b. Amiloride
c. Triamterene
Class Drugs / Trade name Drugs / Trade name
Anti-adrenergic agents
A. β-adreno receptor
antagonist (BBs)
Cardio selective
• Atenolol
• Metaprolol
• Acebutolol
• Betaxolol
• Bisoprolol
Non selective
• Propranolol
• Oxprenolol
• Alprenolol
• Timolol
• Pindolol
B. α- adreno receptor
antagonist
a. Prazosin
b. Doxazonic
c. Indoramin
C. Non selective
adrenergic receptor
blocker
a. Phantolamine
b. Phenoxy benzamine
Central acting
a. Methyldopa
b. Clonidine
α/β receptor blocker
a. Lebetolol
Calcium channel blocker
Dihydropyridine Phenyl alkylamine
• Nifidipine
• Amlodipine
• Nicardipine
• Isradipine
• Felodipine
• Varapamil
• Diltiazem
ACE inhibitor
• Captopril
• Enalopril
• Lisinopril
• Ramipril
• Benapril
• Fosinopril
Thiazide Diuretics
Mechanism: inhibit Na/K pumps in the distal tubule
Examples:
 Hydrocholorthiazide 12.5-25 mg daily
 Chlorthalidone 12.5-50 mg daily
Effective first line agent and provides synergistic benefit
Compelling indications: HF, High CAD risk, Diabetes, Stroke, ISH
Loop Diuretics
•Mechanism: Inhibit Na/K/Cl ATPase in ascending loop of henle
•Examples:
• Furosemide 20 mg BID
•Typically only beneficial in patients with resistant HTN and evidence of fluid;
•MUST be dosed at least twice daily (Lasix = Lasts six hours)
•Administer AM and lunch time to avoid nocturia
Aldosterone Receptor Antagonists
Mechanism: inhibit aldosterone’s effect at the receptor, reducing Na and
water retention
Examples:
Spironolactone 25 mg daily
Can provide as much as 25 mmHg BP reduction on top of 4 drug
regimen in resistant hypertension
Monitor SCr and K
Compelling indications: HF
Nitrates
 Mechanism: Direct venodilation by release of nitric oxide
 Examples:
Isosorbide dinitrate 10 mg TID
 IMDUR 30 mg daily
 In renal patients with resistant hypertension addition to 3-4 drug
regimen may help get patient to goal
 Provide 8h nitrate free interval daily
 Compelling indications: Angina
ACEI & ARB’s
• Block the conversion of angiotensin I to II through
ACE pathway
• Does not block chymase pathway
• Blocks the degradation of bradykinin
Examples:
 Enalapril 2.5-40 mg daily –BID
 Lisinopril 5 – 40 mg daily
 Irbesartan 150-300 mg daily
 Losartan 25-100 mg Daily - BID
Monitor: SCr, K
Compelling indications: HF, post-MI, High CAD risk,
Diabetes, CKD, Stroke
Drugs interacting with Renin-Angiotensin system
ACE inhibitors: inhibit Angiotensin II formation
Angiotension receptor antagonists: block Angiotensin receptor
activation
Diltiazem and Verapamil
 Mechanism: Decrease calcium influx into cells of vascular
smooth muscle and myocardium
 Examples:
 Diltiazem 60-480mg q6h to daily
 Verapamil 60-480 q8h to daily
 Monitor: HR
 Verapamil causes constipation
 Relatively contraindicated in heart failure
 Compelling indications: Diabetes, High CAD risk
Beta Blockers
 Mechanism: Competitively inhibit the binding of catecholamines to
beta-adrenergic receptors
 Examples:
 Atenolol 25-100 mg PO daily
 Metoprolol 25 -100 mg PO daily or BID
 Carvedilol 6.25-25 mg PO BID
 Monitor: HR, Blood Glucose in DM
 Not contraindicated in asthma or COPD but use caution
 Compelling indications: HF, post-MI, High CAD risk, Diabetes
Alpha2 Agonists: Central Acting Agents
 Mechanism: false neurotransmitters reduce sympathetic
outflow reducing sympathetic tone
 Examples:
 Clonidine 0.1-0.6 mg PO BID-TID; patch
 Methyldopa, Guanabenz, Guanfacine
 Monitor: HR
 Side effects often limiting: Dry mouth, orthostasis, sedation
 Clonidine patch can be useful in elderly patients with labile
blood pressure
 Withdrawal: real at doses > 0.3 mg
Dihydropyridine Calcium Channel Blockers
 Mechanism: Decrease calcium influx into cells of vascular
smooth muscle
 Examples:
 Amlodipine 2.5-10 mg PO daily
 Felodipine2.5-10 mg PO daily
 Do not use immediate release nifedipine
 Monitor: Peripheral edema, HR (can cause reflex tachycardia)
 Good add on agent if cost is not an issue
Vasodilators
 Mechanism: Direct vasodilation of arterioles via increased
intracellular cAMP
 Examples:
 Hydralazine 20-400 mg BID-QID
 Minoxidil 2.5-40 mg PO daily-BID
 Monitor: HR (can cause reflex tachycardia), Na/Water
retention
 Hydralazine is an alternative in HF if ACEI contraindicated
 Consider minoxidil in refractory patients on multi-drug
regimens
Alpha1 Blockers
Mechanism: Inhibit peripheral post-synaptic alpha1
receptors causing vasodilation
Examples:
 Terazosin 1 – 20 mg daily
 Doxazosin 1 – 16 mg daily
Cause marked orthostatic hypotension, give dose at
bedtime
Consider only as add on therapy
Can be beneficial in patients with BPH
ACEI & ARB’s
Mechanism: Inhibit vasoconstriction by inhibiting synthesis or blocking
action of angiotensin II; provides balanced vasdilation
Examples:
 Enalapril 2.5-40 mg daily –BID
 Lisinopril 5 – 40 mg daily
 Irbesartan 150-300 mg daily
 Losartan 25-100 mg Daily - BID
Monitor: SCr, K
Compelling indications: HF, post-MI, High CAD risk, Diabetes, CKD,
Stroke
Hypertension
Antihypertensive Drug Therapy
Algorithm for Treatment of Hypertension
Not at Goal Blood Pressure (<140/90 mmHg)
(<130/80 mmHg for those with diabetes or chronic kidney disease)
Initial Drug Choices
Drug(s) for the compelling
indications
Other antihypertensive drugs
(diuretics, ACEI, ARB, BB, CCB)
as needed.
With Compelling
Indications
Lifestyle Modifications
Stage 2 HTN (SBP >160 or DBP
>100 mmHg)
2-drug combination for most
(usually thiazide-type diuretic
and
ACEI, or ARB, or BB, or CCB)
Stage 1 HTN (SBP 140–159 or
DBP 90–99 mmHg)
Thiazide-type diuretics for
most.
May consider ACEI, ARB, BB,
CCB, or combination.
Without Compelling
Indications
Not at Goal
Blood Pressure
Optimize dosages or add additional drugs
until goal blood pressure is achieved.
Consider consultation with hypertension
specialist.
Follow-up and Monitoring
Patients should return for follow-up and adjustment of
medications every 1-2 months until the BP goal is
reached
After BP at goal and stable, follow-up visits at 3- to 6-
month intervals
 More frequent visits for stage 2 HTN or with
complicating comorbid conditions
 Continue to encourage self BP monitoring
Serum potassium and creatinine monitored 1–2 times
per year
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
Drug Combinations
52 Dr.Sarma@works
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
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
D and C combination sixth - Amlogaurd H, Stamlo D
Diuretics = D – Rank 1
ACEI and ARB = A – Rank 2
Beta Blockers = B – Rank 3
CCB = C – Rank 4
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)
55
Hypertension
Case specific approach
some selected case scenarios
www.drsarma.in
Case 1: Diagnosis
AB is a 56 yo female with no significant PMH.
Her BMI is 26 kg/m2 and she has a family history
positive for Type 2 Diabetes. Her BP measured
on two consecutive clinic visits is 132/84. What
is AB’s BP classification?
1. Normal
2. Prehypertensive
3. Stage 1 Hypertension
4. Stage 2 Hypertension
Case 1: Therapy
What therapy should be initiated for AB?
1. Enalapril 5 mg PO daily
2. Hydrochlorothiazide 25 mg PO daily
3. No therapy is indicated
4. Lifestyle modifications including weight loss and
DASH eating plan should be encouraged
Case 1: Goal of Therapy
What is the goal of lifestyle modification in AB?
1. Goal BP < 140/90, the goal is to get to goal
2. Goal BP < 130/80, the goal is to get to goal
3. Improve patients quality of life
4. Prevent onset of hypertension
Case 1: 5 years later
AB, now 59, returns to clinic with marginal
success at lifestyle changes. Her BP has
repeatedly measured around 146/92. What is
AB’s BP classification?
1. Normal
2. Prehypertensive
3. Stage 1 Hypertension
4. Stage 2 Hypertension
Case 1: 5 years later
AB, now 59, returns to clinic with marginal
success at lifestyle changes. Her BP has
repeatedly measured around 146/92. What
should be done?
1. Enalapril 5 mg PO daily
2. Hydrochlorothiazide 25 mg PO daily
3. No therapy is indicated
4. Reinforce lifestyle modifications including
weight loss and the DASH eating plan.
Case 2: Therapy
What therapy should be initiated for CD?
1. A 6 month trial of lifestyle changes should be
initiated immediately
2. Hydrochlorothiazide 25 mg PO daily
3. Enalapril 10 mg PO daily
4. Enalapril / Hydrochlorothiazide 5/12.5 mg PO
daily
Case 2: Goal of Therapy
CD is a 50 yo black male with diet controlled type 2
diabetes. Consecutive BP measurements during recent
clinic visits are 162/98 and 158/96. He is diagnosed with
Stage 2 Hypertension. What is the goal of therapy for
CD?
1. Goal BP <140/90
2. Goal BP <130/80
3. Slow the progression of diabetic renal disease by
reducing BP to <125/80
4. Improve patients quality of life
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 5
HT + Bradycardia
Heart Blocks BBB
CCB, ACEi Not BB
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. Dys
ARB Losartan
ACE Ramipril
BB - Meto
Case 11 HT + Sys Dys ACEi + D A + D + B
Case specific approach
Case 12 HT + CHF
Diu - 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, 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
Case specific approach
Case 18 HT + BPH α bloc, Tamsu Not BB
Case 19 HT + ED
α bloc, HZ,
ACEi /CCB
Not BB
Case 20 HT + Pregnancy MD, HYZ, CCB
Not ACEi,
or ARB
Case 21 HT + Gout, ↑ UA ACEi, CCB Not D
Case 22 ISH
Indap, Amlo,
Enalapril
Not BB
Case 23 HT + Cough ACEi cough
Cough
remedy
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
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
Case 26 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, OTC
Herbal remedies, Excessive alcohol use
 Rationale Identify the above and correct
70
Case 27 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
 Do not use No sublingual nifedipine,

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hypertension-definition,causes,diagnosis.pptx

  • 1. Hypertension M. Deepalakshmi Lecturer Department of Pharmacy Practice JSS College of Pharmacy, Ooty (A Constituent College of JSS University, Mysore)
  • 2. Blood Pressure: The force exerted by the blood against the walls of the blood vessels
  • 3. Factors Influencing Blood Pressure (BP) Cardiac output is total blood flow through systemic or pulmonary circulation per min. CO =stroke volume (amt pumped out of L ventricle per beat [70 ml]) times the HR for 1 min. SVR + force opposing movement of blood in vessels; determined primarily by radius of small arteries & arterioles Blood Pressure Cardiac Output Systemic Vascular Resistance = x Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
  • 4. Introduction…. • Hypertension is known as the "silent killer" since it has no initial symptoms but can lead to long-term disease and complications.. • Many people have high blood pressure and don't know it. • Important complications of uncontrolled or poorly treated high blood pressure include heart attack, congestive heart failure, stroke, kidney failure, peripheral artery disease, and aortic aneurysms (weakening of the wall of the aorta, leading to widening or ballooning of the aorta). • Public awareness of these dangers has increased. High blood pressure has become the second most common reason for medical office visits in the United States.
  • 5. • Hypertension is defined by persistent elevation of arterial blood pressure. • Patients with diastolic blood pressure (DBP) values <90 mm Hg and systolic blood pressure (SBP) values≥140 mm Hg have isolated systolic hypertension. • A hypertensive crisis (BP >180/120 mm Hg) may be categorized as either – a hypertensive emergency (extreme BP elevation with acute or progressing target organ damage) or – a hypertensive urgency (severe BP elevation without acute or progressing target organ injury).
  • 6. JNC-7 CLASSIFICATION Class Systolic(mm of Hg) Diastolic(mm of Hg) Normal 120 80 Prehypertension 120-139 80-89 Stage-1 hypertension 140-159 90-99 Stage-2 hypertension 160-179 100-109 Stage-3 hypertension ≥180 ≥110
  • 7. Etiology Primary hypertension:  Also known as Essential hypertension (or) Idiopathic hypertension  Result of unknown etiology (cause)  Symptomatic treatment given  Almost 90 – 95 % patients showing this type Secondary hypertension:  Result of some known Pathology (Chronic renal disease, Endocrine disease, etc,.)  Occurs in about 5 – 10 % of patients Other types of hypertensions:  Isolated systolic hypertension: (SBP>140mmHg)  Malignant hypertension: (diastolic >140mmHg)  White coat hypertension: BP Elevated only when examined by a health care professional
  • 8. • Socioeconomic status: High blood pressure is found more commonly among the less educated and lower socioeconomic groups. Residents of the southeastern United States, both Caucasian and African American, are more likely to have high blood pressure than residents of other regions. • Family history (heredity): The tendency to have high blood pressure appears to run in families. • Gender: Generally men have a greater likelihood of developing high blood pressure than women. This likelihood varies according to age and among various ethnic groups.
  • 9. Primary hypertension Genetic Factors Racial & Environmental Factors Humoral abnormalities Pathologic disturbances in autonomic nerve fibers, adrenergic and baro receptors. Abnormalities in either the renal or tissue auto regulatory processes.
  • 10. Secondary hypertension Renal diseases :  Stenosis of renal arteries  Tumor of justaglomerular cells →Angiotensin II Endocrine disorders : Adrenal Gland  Pheo chromocytoma  Cushing´s syndrome Coarctation of aorta
  • 11. Other factors  Drugs Induced : e.g. oral contraceptives  Pregnancy Induced  Deficiency of vaso dilating substance (prostacyclin,bradykinin)  Increase production of vasoconstructing substance(Angiotensin II, Endothelin I)
  • 12. Pathophysiology Humoral abnormalities involving  Renin – Angiotensin,Aldosterone system  Natriuritic hormone  Hyperinsulinemia (side effect of insulin therapy) Renin – Angiotensin System: • ‘Angiotensinogen’ is a δ – globulin type of protein secreted in the liver • Another substance ‘renin’ secreted by juxtaglomerular cells • Renin acts on angiotensinogen and converts it to Angiotensin – I • Angiotensin converting enzyme (ACE) along with Aldosterone, converts Angiotensin – I → Angiotensin – II (this is a powerful vasoconstrictor)
  • 13. Regulation of aldosterone secretion by the renin– angiotensin–aldosterone (RAA) pathway
  • 14. Regulation of secretion and actions of antidiuretic hormone (ADH).
  • 16. ANS innervation of the heart and the baroreceptor reflexes that help regulate blood pressure.
  • 17. ROLE OF NATRIURETIC HORMONE Concentration of Natriuretic Harmone Inhibits Na +K +ATPse Pump Inhibition of sodium transport across the cell membrane BP
  • 18. Sympathetic neuronal fibers on the surface of the effector cells α 1 receptors β receptors Postsynaptic stimulation on arterioles & venules Vasoconstriction β1 β2 Postsynaptic stimulation in Heart Heart rate & Contractility Postsynaptic stimulation on arterioles & Venules Vasodilatation Neuronal Mechanisms
  • 19. In vascular endothelium (innermost layer) 1. ↓ Synthesis of vasodilating ↑ Synthesis of vaso- substances (Prostacycline, constricting substances bradikinin, NO2) OR (Angiotensin – II, Prostaglandin in muscle cells endothelin – I, etc,.) 2.↑ Na+ intake + ↓ excretion of Na+ →↑ Natriuritic hormone inhibit ↑vascular activity intra cellular Na+ uptake (constriction of vessels) this may also cause oedema
  • 20. 3.Release of Ca + stored in sarcoplasmic reticulum cause ↑intracellular coation of calcium cause Altered vascular smooth muscle function (↑tone) ↑PVR 4. Hyperinsulinemia: • Constriction of blood vessels • Deposition of cholesterol in blood vessel (atherosclerosis)
  • 21. Clinical presentation  Patients with uncomplicated primary hypertension are usually asymptomatic initially.  Patients with secondary hypertension may complain of symptoms suggestive of the underlying disorder.  Patients with pheochromocytoma may have a history of paroxysmal headaches, sweating, tachycardia, palpitations  In primary aldosteronism, hypokalemic symptoms of muscle cramps and weakness may be present.  Patients with hypertension secondary to Cushing’s syndrome may complain of weight gain, polyuria, edema, menstrual irregularities, recurrent acne,muscular weakness.
  • 22. TIA = transient ischemic attack; LVH = left ventricular hypertrophy; CHD = coronary heart disease HF = heart failure. Cushman WC. J Clin Hypertens. 2003;5(Suppl):14-22. Renal failure Peripheral vascular disease Complications of Hypertension: LVH, HF,CHD, TIA, stroke Hypertension is a risk factor
  • 23. Diagnostic Studies  Use auscultatory method with a properly calibrated instrument  Patient seated quietly for 5 min in a chair, feet on the floor, and arm supported at heart level  Appropriate-sized cuff is necessary to ensure accurate reading  At least two measurements should be obtained  Allow at least 1 minute between readings. If one arm higher than other; take BP in higher arm for subsequent measurements
  • 24. Diagnostic studies  Basic laboratory studies are performed to (1) identify or rule out causes of secondary hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular risk, or (4) establish baseline levels before initiating therapy.  Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to screen for renal involvement and to provide baseline information about kidney function.  Measurement of serum electrolytes, especially potassium levels, is done to detect hyperaldosteronism, a cause of secondary hypertension.
  • 25. Diagnostic studies….  Blood glucose levels assist in the diagnosis of diabetes mellitus.  Lipid profile provides information about additional risk factors that predispose to atherosclerosis and cardiovascular disease.  ECG and echocardiography provide information about the cardiac status.
  • 26. Management  Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney disease).  Lifestyle modifications are indicated for all patients with pre hypertension and hypertension and include the following:  Weight reduction. A weight loss of 10 kg may decrease SBP by approximately 5 to 20 mm Hg.  Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves eating several servings of fish each week, eating plenty of fruits and vegetables, increasing fiber intake, and drinking a lot of water. The DASH diet significantly lowers BP.
  • 27.  Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g of sodium per day.  This involves avoiding foods known to be high in sodium (e.g., canned soups) and not adding salt in the preparation of foods or at meals.  Restriction of alcohol  Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a day most days of the week. Moderately intense activity such as brisk walking, jogging, and swimming can lower BP, promote relaxation, and decrease or control body weight.  It is strongly recommended that tobacco use be avoided.  Stress can raise BP on a short-term basis and has been implicated in the development of hypertension. Relaxation therapy may be useful in helping patients manage stress, thus decreasing BP.
  • 28. 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
  • 29. Drug Therapy  Drug therapy is not recommended for those persons with prehypertension unless it is required by another condition, such as diabetes mellitus or chronic kidney disease.  The overall goals for the patient with hypertension include  achievement and maintenance of the goal BP  reduce mortality due to hypertension-induced disease  acceptance and implementation of the therapeutic plan  minimal or no unpleasant side effects of therapy  ability to manage and cope with illness.
  • 30. Ways of lowering BP Reduce cardiac output  Beta blockers  Ca2+ channel antagonists Reduce plasma volume  Diuretics Reduce Total Peripheral Resistance  vasodilators  alpha1-adrenergic receptor antagonists  ACE inhibitors
  • 31. Summary of Drug Targets
  • 32. 32 The Many Faces of HT Therapy Today Enalapril Lisinopril Ramipril Quinapril Perindopril Hypertension
  • 33. Drug use in Hypertension Class Drugs / Trade name DIURETICS A. Thiazide diuretics a. Bendro fluazide b. Cyclopenthiazide c. Hydrochlorothiazide B. Loop diuretics a. Bumetanide b. Frusemide C. Potassium-sparing a. Spironolactone b. Amiloride c. Triamterene
  • 34. Class Drugs / Trade name Drugs / Trade name Anti-adrenergic agents A. β-adreno receptor antagonist (BBs) Cardio selective • Atenolol • Metaprolol • Acebutolol • Betaxolol • Bisoprolol Non selective • Propranolol • Oxprenolol • Alprenolol • Timolol • Pindolol B. α- adreno receptor antagonist a. Prazosin b. Doxazonic c. Indoramin C. Non selective adrenergic receptor blocker a. Phantolamine b. Phenoxy benzamine Central acting a. Methyldopa b. Clonidine α/β receptor blocker a. Lebetolol
  • 35. Calcium channel blocker Dihydropyridine Phenyl alkylamine • Nifidipine • Amlodipine • Nicardipine • Isradipine • Felodipine • Varapamil • Diltiazem ACE inhibitor • Captopril • Enalopril • Lisinopril • Ramipril • Benapril • Fosinopril
  • 36. Thiazide Diuretics Mechanism: inhibit Na/K pumps in the distal tubule Examples:  Hydrocholorthiazide 12.5-25 mg daily  Chlorthalidone 12.5-50 mg daily Effective first line agent and provides synergistic benefit Compelling indications: HF, High CAD risk, Diabetes, Stroke, ISH Loop Diuretics •Mechanism: Inhibit Na/K/Cl ATPase in ascending loop of henle •Examples: • Furosemide 20 mg BID •Typically only beneficial in patients with resistant HTN and evidence of fluid; •MUST be dosed at least twice daily (Lasix = Lasts six hours) •Administer AM and lunch time to avoid nocturia
  • 37. Aldosterone Receptor Antagonists Mechanism: inhibit aldosterone’s effect at the receptor, reducing Na and water retention Examples: Spironolactone 25 mg daily Can provide as much as 25 mmHg BP reduction on top of 4 drug regimen in resistant hypertension Monitor SCr and K Compelling indications: HF
  • 38. Nitrates  Mechanism: Direct venodilation by release of nitric oxide  Examples: Isosorbide dinitrate 10 mg TID  IMDUR 30 mg daily  In renal patients with resistant hypertension addition to 3-4 drug regimen may help get patient to goal  Provide 8h nitrate free interval daily  Compelling indications: Angina
  • 39. ACEI & ARB’s • Block the conversion of angiotensin I to II through ACE pathway • Does not block chymase pathway • Blocks the degradation of bradykinin Examples:  Enalapril 2.5-40 mg daily –BID  Lisinopril 5 – 40 mg daily  Irbesartan 150-300 mg daily  Losartan 25-100 mg Daily - BID Monitor: SCr, K Compelling indications: HF, post-MI, High CAD risk, Diabetes, CKD, Stroke
  • 40. Drugs interacting with Renin-Angiotensin system ACE inhibitors: inhibit Angiotensin II formation Angiotension receptor antagonists: block Angiotensin receptor activation
  • 41. Diltiazem and Verapamil  Mechanism: Decrease calcium influx into cells of vascular smooth muscle and myocardium  Examples:  Diltiazem 60-480mg q6h to daily  Verapamil 60-480 q8h to daily  Monitor: HR  Verapamil causes constipation  Relatively contraindicated in heart failure  Compelling indications: Diabetes, High CAD risk
  • 42. Beta Blockers  Mechanism: Competitively inhibit the binding of catecholamines to beta-adrenergic receptors  Examples:  Atenolol 25-100 mg PO daily  Metoprolol 25 -100 mg PO daily or BID  Carvedilol 6.25-25 mg PO BID  Monitor: HR, Blood Glucose in DM  Not contraindicated in asthma or COPD but use caution  Compelling indications: HF, post-MI, High CAD risk, Diabetes
  • 43. Alpha2 Agonists: Central Acting Agents  Mechanism: false neurotransmitters reduce sympathetic outflow reducing sympathetic tone  Examples:  Clonidine 0.1-0.6 mg PO BID-TID; patch  Methyldopa, Guanabenz, Guanfacine  Monitor: HR  Side effects often limiting: Dry mouth, orthostasis, sedation  Clonidine patch can be useful in elderly patients with labile blood pressure  Withdrawal: real at doses > 0.3 mg
  • 44. Dihydropyridine Calcium Channel Blockers  Mechanism: Decrease calcium influx into cells of vascular smooth muscle  Examples:  Amlodipine 2.5-10 mg PO daily  Felodipine2.5-10 mg PO daily  Do not use immediate release nifedipine  Monitor: Peripheral edema, HR (can cause reflex tachycardia)  Good add on agent if cost is not an issue
  • 45. Vasodilators  Mechanism: Direct vasodilation of arterioles via increased intracellular cAMP  Examples:  Hydralazine 20-400 mg BID-QID  Minoxidil 2.5-40 mg PO daily-BID  Monitor: HR (can cause reflex tachycardia), Na/Water retention  Hydralazine is an alternative in HF if ACEI contraindicated  Consider minoxidil in refractory patients on multi-drug regimens
  • 46. Alpha1 Blockers Mechanism: Inhibit peripheral post-synaptic alpha1 receptors causing vasodilation Examples:  Terazosin 1 – 20 mg daily  Doxazosin 1 – 16 mg daily Cause marked orthostatic hypotension, give dose at bedtime Consider only as add on therapy Can be beneficial in patients with BPH
  • 47. ACEI & ARB’s Mechanism: Inhibit vasoconstriction by inhibiting synthesis or blocking action of angiotensin II; provides balanced vasdilation Examples:  Enalapril 2.5-40 mg daily –BID  Lisinopril 5 – 40 mg daily  Irbesartan 150-300 mg daily  Losartan 25-100 mg Daily - BID Monitor: SCr, K Compelling indications: HF, post-MI, High CAD risk, Diabetes, CKD, Stroke
  • 49. Algorithm for Treatment of Hypertension Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease) Initial Drug Choices Drug(s) for the compelling indications Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. With Compelling Indications Lifestyle Modifications Stage 2 HTN (SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB) Stage 1 HTN (SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Without Compelling Indications Not at Goal Blood Pressure Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension specialist.
  • 50. Follow-up and Monitoring Patients should return for follow-up and adjustment of medications every 1-2 months until the BP goal is reached After BP at goal and stable, follow-up visits at 3- to 6- month intervals  More frequent visits for stage 2 HTN or with complicating comorbid conditions  Continue to encourage self BP monitoring Serum potassium and creatinine monitored 1–2 times per year
  • 51. 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
  • 53. 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 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 D and C combination sixth - Amlogaurd H, Stamlo D Diuretics = D – Rank 1 ACEI and ARB = A – Rank 2 Beta Blockers = B – Rank 3 CCB = C – Rank 4
  • 54. 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)
  • 55. 55 Hypertension Case specific approach some selected case scenarios www.drsarma.in
  • 56. Case 1: Diagnosis AB is a 56 yo female with no significant PMH. Her BMI is 26 kg/m2 and she has a family history positive for Type 2 Diabetes. Her BP measured on two consecutive clinic visits is 132/84. What is AB’s BP classification? 1. Normal 2. Prehypertensive 3. Stage 1 Hypertension 4. Stage 2 Hypertension
  • 57. Case 1: Therapy What therapy should be initiated for AB? 1. Enalapril 5 mg PO daily 2. Hydrochlorothiazide 25 mg PO daily 3. No therapy is indicated 4. Lifestyle modifications including weight loss and DASH eating plan should be encouraged
  • 58. Case 1: Goal of Therapy What is the goal of lifestyle modification in AB? 1. Goal BP < 140/90, the goal is to get to goal 2. Goal BP < 130/80, the goal is to get to goal 3. Improve patients quality of life 4. Prevent onset of hypertension
  • 59. Case 1: 5 years later AB, now 59, returns to clinic with marginal success at lifestyle changes. Her BP has repeatedly measured around 146/92. What is AB’s BP classification? 1. Normal 2. Prehypertensive 3. Stage 1 Hypertension 4. Stage 2 Hypertension
  • 60. Case 1: 5 years later AB, now 59, returns to clinic with marginal success at lifestyle changes. Her BP has repeatedly measured around 146/92. What should be done? 1. Enalapril 5 mg PO daily 2. Hydrochlorothiazide 25 mg PO daily 3. No therapy is indicated 4. Reinforce lifestyle modifications including weight loss and the DASH eating plan.
  • 61. Case 2: Therapy What therapy should be initiated for CD? 1. A 6 month trial of lifestyle changes should be initiated immediately 2. Hydrochlorothiazide 25 mg PO daily 3. Enalapril 10 mg PO daily 4. Enalapril / Hydrochlorothiazide 5/12.5 mg PO daily
  • 62. Case 2: Goal of Therapy CD is a 50 yo black male with diet controlled type 2 diabetes. Consecutive BP measurements during recent clinic visits are 162/98 and 158/96. He is diagnosed with Stage 2 Hypertension. What is the goal of therapy for CD? 1. Goal BP <140/90 2. Goal BP <130/80 3. Slow the progression of diabetic renal disease by reducing BP to <125/80 4. Improve patients quality of life
  • 63. 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 5 HT + Bradycardia Heart Blocks BBB CCB, ACEi Not BB
  • 64. 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. Dys ARB Losartan ACE Ramipril BB - Meto Case 11 HT + Sys Dys ACEi + D A + D + B
  • 65. Case specific approach Case 12 HT + CHF Diu - 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, 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
  • 66. Case specific approach Case 18 HT + BPH α bloc, Tamsu Not BB Case 19 HT + ED α bloc, HZ, ACEi /CCB Not BB Case 20 HT + Pregnancy MD, HYZ, CCB Not ACEi, or ARB Case 21 HT + Gout, ↑ UA ACEi, CCB Not D Case 22 ISH Indap, Amlo, Enalapril Not BB Case 23 HT + Cough ACEi cough Cough remedy
  • 67. 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
  • 68. 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
  • 69. Case 26 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, OTC Herbal remedies, Excessive alcohol use  Rationale Identify the above and correct
  • 70. 70 Case 27 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  Do not use No sublingual nifedipine,