Transcript Hypertension update

Hypertension & Guidelines
Update
By : Dr. Hala M. Al- Khalidi, Pharm.D.
Faculty of Pharmacy,
King Abdulaziz University
26th , Oct., 2008.
Introduction
JNC 7 key messages
Classification of BP
Diagnostic tool
Causes of HTN/ Etiology
CV risk factors
Pathophysiology
Principles of HTN treatment
Nifedipine warning
BP measurement techniques
Life style modification
Pharmacologic therapy
Compelling indication
Causes of resistance HTN
TOD
HTN in ESRD
Improving patient compliance
JNC7 Key messages
Subjects > then 50 yo, systolic BP > 140 mmHg is more of a
risk factor the diastolic BP.
CVD risk begins at 115/75 mmHg doubles with increments
of 20/10 mmHg; normotensive individuals at age 55 have a
90% risk for developing HTN.
Prehypertensives with SBP of 120-139mmHg or a DBP 8089mmHg, need to stress on lifestyle modification to prevent
CVD.
JNC7 Key messages
Uncomplicated HTN treatment for most patients are
Thiazide-type diuretics, either alone or in combination
with other classes. With high risk conditions that require
use other antihypertensive drug classes (ACEI, ARB’s, BB, and CCB).
Tow or more classes of Anti-HTN’s are required to achieve
goal BP (< 140/90 mmHg, or < 130/80 mmHg for
diabetics or chronic kidney disease).
JNC7 Key messages
Two agents should be initiated If BP is >20/10 mmHg
above goal BP , one of which should be a thiazide-type
diuretic.
Motivation is a key aspect in BP control, and it is
maintained with BP control, (+ve) experience & trust in
clinicians is built (empathy build trust).
In providing these guidelines, physicians judgment remains
paramount.
Taking BP

Classification of HTN
Category
Normal
SBP mmHg
< 120
DBP mmHg
&
< 80
Prehypertension
120 - 139
Or
80-89
Hypertension, stage 1
140 - 159
Or
90-99
Hypertension, stage 2
≥ 160
Or
≥ 100
Isolated Systolic Hypertension
Definition
A systolic BP of ≥ 140mmHg and diastolic BP
< 90 mmHg, and staged @ BP 170/82mmHg is stage 2
isolated systolic HTN .
Treatment used in the study is chlorthalidone
(SHEP trial 1999).
Causes of Secondary HTN
Renovscular disease (abdomanal
bruits, recent onset, & accelerated
HTN = renal artery stenosis
Drug induced
- OC (develop over 1-2 years)
RF = age>35/ smoking/ obesity/ FH
-HTN
- PPA, NSAIDs, nasal
decongestants, Cyclosporine,
Erythropoietin, MAO+ tyramin.
1ry aldosteronism ( ↓K, weakness,
↑urination, muscle cramps)
Coarctation of aorta, Sleep
apnea, Thyroid, &
parathyroid disease (JNC-7)
Pheochromocytoma
Wt. loss/ HA/ diaphoresis/
flushing
Cushing’s syndrom
Cardiovascular Risk Factors
Hypertension
Cigarette smoking
Obesity (BMI ≥ 30 kg/m2)
Physical inactivity
Microalbuminuria or ~
GFR < 60ml /min
Age older then 55 men,
65 women
Dyslipidemia
FH of premature CVD
Men < 55, woman < 65 yr
old
Target Organ Damage
Heart
- LVH
- Angina or Hx . MI
- Hx . coronary
revascularization
- HF
Brain
- Stroke or TIA
- Peripheral arterial disease
- Retinopathy
Kidney
- Glomerular filtration rate
- Components of the
metabolic syndrome
- Chronic kidney disease
Diagnostic Tools
Assess RF and
comorbidities
Causes of HTN
Detection of TOD
Conduct hx and physical
examination
Obtain laboratory tests:
UA, SCr, FBS, H+/H+, FLP,
serum K,+ and Ca+
Optional:
urinary albumin/creatinine
ratio
EKG
BP Measurement Techniques
Method
Notes
IN-office
Two readings, 5 minutes apart, sitting
in a chair . Confirm BP reading in
contra lateral arm
Ambulatory BP
monitoring
White Coat HTN , absence of 10-20%
BP ↓ during sleep may ↑ CVD risk
Assess in response to Tx
Improve adherence to therapy
Patient self-check
Useful for evaluating white coat
HTN
Lifestyle Modification
Recommendation
Avg. BP
Reduction range
Weight
Reduction
Maintain normal body weight (BMI
18.5-24.9kg/m2)
5-20
mmHg/10kg
DASH DIET
A Diet rich in fruits, vegetables, &
low fat dairy product, low saturated
& fat
8-14 mmHg
Na+ restriction
Reduce Na+ in diet 2.4-6 G/day
Modification
Physical
activity
Aerobics e.g. Brisk walking (at least
Alcohol Mod.
Male vs. Female & light weight
2-8 mmHg
30mints/day most days of the week
4-9 mmHg
2-4 mmHg
Treatment Recommendations
 Thiazide diuretics are first-line agents for the management
of hypertension in most patients. supported by clinical trials
showing reduced morbidity & mortality with these agents.
Comparative data from the landmark clinical trial, the
ALLHAT, confirm the first-line role of thiazide diuretics.
 Older patients with isolated systolic hypertension are often
at risk for orthostatic hypotension when drug therapy is
started.
 Particularly prevalent with diuretics, ACE inhibitors, and
ARBs.
 Although overall treatment should be the same, initial doses
should be very low and dose titrations gradual to minimize
risk of orthostatic hypotension.
Primary Antihypertensive Agents
Furosemide (Lasix) Dose 20–80mg bid
 Dose in the morning & afternoon to avoid nocturnal diuresis
higher doses may be needed for patients with
 severely decreased glomerular filtration rate or heart failure
Spironolactone Dose 25–50 qd/ bid
 Dose morning or afternoon to avoid nocturnal diuresis
 Eplerenone CI in patients with Cr Cl< 50 mL/min, elevated
serum creatinine (> 1.8 mg/dL in women,> 2 mg/dL in men),
and type 2 diabetes with microalbuminuria
 Avoid spironolactone in chronic kidney disease CrCl< 30
mL/min); may cause hyperkalemia, especially in combination
with an ACEI, ARB or potassium supplements
B-Adrenergic blockers
Three pharmacodynamic diffrences;
1- Cadioselectivity = > affinity for B1-R then B2-R
(Atenolol, metoprolol, bisoprolol, & acebutolol) dose
dependent phenomenon , effect is lost at higher
doses.
2- Intrinsic sympathomimetic activity (ISA) = these
agents can release catecholamines to maintains
normal basal sympathetic tone while blocking access
adrenergic stimulation, this is manifested at all dosage
levels, so theoretically wouldn’t be safer to use in HF,
sinus bradycardia, PVD, but no confirmed studies,
(e.g. acebutolol, carteolol, penbutolol, pindolol) .
Cont. B-Adrenergic blockers
3- Membrane-stablilizing action (MSA) =(or
quinidine-like effect) on cardiac cells if large enough
doses are given (antidysrhythmic effect), the dose
exceeds that used in tx HTN, or cardiac arrhythmias,
all B-B share this property.
only (e.g. propranolol, sotolol, acebutolol) indicated
for arrythmias.
Primary Antihypertensive Agents
Atenolol (Tenormin) Dose 25–100mg qd
Metoprolol (Lopressor) Dose 50–200mg bid
Propranolol (Inderal)
Dose 160–480mg bid
 Abrupt discontinuation may cause, rebound HTN inhibit β1
and β2 receptors at all doses; can exacerbate asthma; have
additional benefits in patients with essential tremor, migraine
headache, thyrotoxicosis
Carvedilol (Coreg)
Dose 12.5–50 bid
 Abrupt discontinuation may cause rebound hypertension;
additional α blockade produces more orthostatic
hypotension
Primary Antihypertensive Agents
 Dihydropyridines are more potent peripheral vasodilators
than nondihydropyridines and may cause more reflex
sympathetic discharge (tachycardia), dizziness, headache,
flushing, and peripheral edema
 additional benefits in Raynaud’s syndrome
 Extended-release products are preferred for hypertension;
these agents block slow channels in the heart and reduce
heart rate; may produce heart block
 these products are not AB rated as interchangeable on a
equipotent mg-per-mg basis due to different release
mechanisms and different bioavailability parameters
Alternative Antihypertensive Agents
Clonidine (Catapres) Dose 0.1–0.8mg bid
Methyldopa (Aldomet) Dose 250–1000 bid
 Central α2-agonists -most effective if used with
adiuretic to diminish fluid retention; clonidine
 Patch is replaced once per week
Warning Associated with Nifedipine (Procardia®)
Not enough studies dun or sufficient numbers of subjects with
patients > 65 yo
occasional y patient had excessive & poorly tolerated
hypotension
Procardia & immedate-release forms should not be used for the
acute reduction of BP, several well-documented reports describe
cases of profound hypotension, MI, & death
Randomized trials studied the use of immediate-release
nifedipine in patients that just had an MI, showed no
benefit & in some showed significantly worse outcome then
placebo patients, so it was concluded that within the 1st
week or two after an MI procardia should be avoided.
Alternative Antihypertensive Agents
Minoxidil (Loniten) 10–40mg qd/bid
Hydralazine (Apresoline) 20–100 bid/qid
 Direct arterial vasodilators; should be used with diuretic
and β-blocker to diminish fluid retention and reflex
tachycardia
Compelling Indications for Individual
Drug Classes
Compelling Indication
Initial Therapy Options
Heart Failure
THIAZ, BB, ARB, ALDO ANT
POST MI
BB, ACEI, ALDO ANT
High CVD risk
THIAZ, BB, ACEI, CCB
Diabetes
THIAZ, BB, ACEI, ARB, CCB
Chronic kidney disease
ACEI, ARB
Recurrent stroke prevention
THIAZ, ACEI
Recommendations in CKD
Chronic kidney disease (CKD) with an estimated
GFR < 60ml/min ~ 1.5mg/dl in men & 1.3mg/dl in
women, albuminuria > 300mg/day, or 200mg
albumin /g creatinine.
Goal is to slow deterroration of renal function and
prevent CVD.
Aggressive BP management with three or more
drugs to a goal BP < 130/80mmHg.
Recommendations in CKD
ACEI’s or ARB’s show favorable effects with DM,
and renal patients, and up to > 35% inc. in SCr ,
therefore with holding Tx would be due to
hyperkelimia.
GFR < 30ml/min, corresponding to SCr = 2.5-3
mg/dl, inc. ↑ dose of loop diuretics are usually
needed in combination with other drug classes.
Thiazides efficacy is ↓, or ineffective to lower BP
in renal function/CrCl < 30ml/min , therefore high
dose loops is recommended , see JNC 6.
HTN in ESRD
BP should be controlled prior starting epoetin
Bone marrow depression up to 10% in renal failure
patients on captopril (sulfhydryl gp.) especially
autoimmune disease, therefore close monitor of WBC,
and low dose captopril.
Central alpha-2 agonists as clonidine appear to be the
safest in the dialysis population.
Trans dermal clonidine up to 1.2mg/day as monotherapy
in one short-term study was successful.
Hypertension in Older Persons
More than two-thirds of people over 65 have HTN.
This population has the lowest rates of BP control.
Treatment, including those who with isolated systolic
HTN, should follow same principles outlined for general
care of HTN.
Lower initial drug doses may be indicated to avoid
symptoms; standard doses and multiple drugs will be
needed to reach BP targets.
Followup and Monitoring
Patients should follow-up & adjust medications on a
monthly basis until BP control is achieved, then f/u can
be every 3-6 month intervals.
Stage 2 HTN & comorbid conditions well need more
frequent visits .
Serum K and SCr should be monitored 1-2 times/year.
Tobacco abuse should be addressed vigorously.
Low dose ASA is only considered when BP control is
achieved , due to the increased risk of hemorrhagic
stroke in this population .
Improving Patient Compliance
I. Convince your patients that the treatment plan is
necessary and efficacious.
II. Explain exactly what your patients should expect
- What the drug does
- How it should be taken
- What are the major side effects
- What patients should do if they experience SE
- How the drug’s effect will be monitored.
Causes of Resistant HTN
Improper BP measurement
Excess Na+ intake
Inadequate diuretic therapy
Medication
- Inadequate doses
- Drug action & interaction (e.g. NSAIDs) , sympathomimetics, OC
- OTC drugs & herbal supplements
Excess alcohol intake
Improving Patient Compliance
III. Listen carefully
IV. Assess your patient’s mental state
V. Encourage the help of family and friends
VI. Keep medication regimens as simple as possible
VII. Troubleshoot potential obstacles
VIII. Build reminders into the treatment plan
IX. Include a plan to monitor compliance
X. Ask your patients how they are doing