HTN – 12. 8.09
Raja – F&E
1
HTN is a risk factor for :
-Coronary artery disease
-Stroke
-End-stage renal disease
-Cause and consequent of HTN, damage to arterioles.
-Congestive heart failure
-HTN causes heart to work harder  hypertrophy. Ability of heart to relax dec 
CHF
Early detection and Tx is key!
What is HTN?
Classifications of BP:
-Normal BP: systolic < 120 and diastolic <80
-Pre-hypertension: systolic 120-139 or diastolic 80-89
-Stage 1: systolic 140-159 or diastolic 90-99
-Stage 2: systolic > 160 or diastolic > 100
Lower Blood Pressure is Better
-Should be enough so that you are not symptomatically hypotensive, anything other than
that is normal
-Treated Blood Pressure must take into account the risk of medications
-Low diastolic pressures are probably a marker for decreased arterial compliance in patients
over age 65 years (Hardening of the arteries)
-60-65 diastolic, as they harden they don’t transmit the aortic sensation. Isolated
systolic HTN is more common
Initial evaluation (see below History & evaluation)
-BP should be elevated on 2 separate occasions: office, home, ambulatory monitor
-Rule out secondary causes (correctable) of hypertension
-Evaluate for end-organ damage
-Evaluate the patient’s overall cardiovascular risk status – athlete? Obese? Smoker?
Clues to Secondary HTN:
-Young age of onset
-Sudden onset of HTN
-Uncontrolled/Refractory HTN
-Phenochromocytoma HTN hard to Tx
-Malignant HTN (End organ damage)
-Features of a recognized underlying cause
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HTN – 12. 8.09
Raja – F&E
Secondary HTN
Renovascular
hypertension
(secondary
hyperaldosteronism)
Mech
-
S/S
ischemic loss
of renal func,
unexplained
sudden onset
pulmonary
edema, flank
pain
Primary
hyperaldosteronism
Excess Aldo  Na Retention
 vol expansion HTN
Hypertension,
hypokalemia
 Muscle
weakness
Primary
hyperparathyroidism
Cushing’s disease
excessive Ca in bld 
vasoconstriction  high bp
HTN from mineralocorticoid
effect of the excess
glucocorticoids
pheochromocytoma
epi secreting, episodic
tachycardia, high BP, tumor
Cause
Atherosclerotic
Disease 
stenosis
Fibromuscular
dysplasia 
BOARDS
“string of beads
leading to
kidney in renal
artery”
-Adrenal
adenoma, -bilat adrenal
hyperplasia
Dx
angiogram
Notes
Most common
secondary HTN
-Serum renin
and
aldosterone
-Serum calcium
Thinning of
the skin
Episodic
headache,
tremor,
sweating &
inc HR,
-50% have
paroxysmal
HTN, the rest
apparently
have
“essential”
HTN
Excess
glucorticoid –
exogenous or
endogenous
Dexamethasone
suppression
test
-24 hour urine
collection for
metanephrines
Other causes of secondary HTN:
-Primary renal disease
-Hypothyroidism – unknown mechanism
-Oral contraceptives -Sleep apnea – snoring, thought that while you are asleep there is a shut down of the stress
horm (corticosteroids etc) as you wake up they inc. If you wake up the signals get mixed up.
-Coarctation of the aorta – constriction above the renal artery peds  dec bld flow to the
kidneys.
HTN – 12. 8.09
Raja – F&E
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Know the RAAS
system well!
History & Evaluation:
-Features of Essential Hypertension without End organ damage? NONE! Need to check BP
-Cardiovascular Risk Factors: Smoking, Diabetes mellitus, Dyslipidemia, Physical inactivity, Chronic
kidney disease
-Symptoms of target organ damage
-Headache – inc intracranial pressure form inc HTN
-Transient weakness or blindness
-Loss of visual acuity
-Chest pain
-Dyspnea
-Claudication – muscle pain in calves after walking a certain distance.
-Aggravating factors:
-Drugs: estrogens, adrenal steroids, sympathomimetics, and NSAIDS (Na rention)
-Diet: salt, alcohol, caffeine, and weight
-Family history – some correlation
-Race
-Sleep apnea
Physical Exam:
-Is there evidence for end-organ damage?
-Retinopathy (Flame Hemorrhage, hard exudates, cotton wool spot, papilloedema)
-Heart rhythm, extra sounds
–S4 (if you have a thick ventricle)
-Bruits (renal artery variety may suggest a secondary cause)
-Pulses
-Edema – Na retention
-Rales – lung crackles
Labs:
-Electrolytes (Na+, K+, Cl-, CO2-)
-Creatinine – marker for kidney func
-Urinalysis – protein or cells in the urine  kidney disease
-Lipid profile
-EKG – L vent hypertrophy (L axis deviation) tall
QRS complexes, deep T waves
-Echocardiogram
Treatment:
Lifestyle Modifications: (test Q)
-Weight loss for the overweight
-Increased aerobic physical activity
-Moderate sodium restriction
-Moderate alcohol consumption
HTN – 12. 8.09
Raja – F&E
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-Minimize caffeine consumption
PharmTx: (see HTN table above)
-First choice is ALWAYS a thiazide diuretic!!!
-In stage 2, you need to add a second, ACEi or ARB, then a B-blker
-In Stage 2, thiazide + ACEi
-other meds:
-Alpha 2 central blockers
-Clonidine – dec in sympt activity
-Direct vasodilators
-Nitro, hydralazine
-Sympathetic blockers
-Beta & Alpha blockers
-Direct renin inhibitors
-Thiazide diuretics:
-Mechanism of action is unclear but probably is a combination of mild plasma volume
decrease plus decreased intracellular calcium concentration leading to vasodilation
-Cheap, Effective, Very low incidence of side effects at low doses
-provide cardioprotection in: Left vent hypertrophy, Type 2 diabetes mellitus, previous MI,
stroke, current cigarette smoking, hyperlipidemia, atherosclerotic CV disease
Angiotensin converting enzyme inhibitors: agents of choice in hypertension and ….
-Congestive heart failure
-ST elevation myocardial infarction
-Non-ST elevation anterior myocardial infarction
-Diabetes mellitus
-Proteinuric chronic renal failure
-Angiotensin converting enzyme inhibitors and angiotensin receptor blockers used together are
indicated in: Congestive heart failure & Proteinuric chronic renal failure
-ACEi work by: Decreasing angiotensin II Increasing kinin levels (block kininase activity)
secretion of NO from endothelial surface. They also cause the cough side effect.
-Decrease aldosterone
-Increase insulin sensitivity
-Ang II recp antagonist:
-Impair binding of angiotensin II to AT1 receptors
-No cough (no increased kinin levels)
-No reduction in AT2 receptor activity (key in keeping other systems going, less arterial
hypertrophy, improved left ventricular activity after ischemia)
-Production of angiotensin II in the heart may be through another enzyme (chymase),
therefore AII receptor antagonists may be more effective than ACE inhibitors locally
-No change in insulin sensitivity (kinin mediated)
-Indications for and efficacy of ARB’s are not different from ACE inhibitors
-Direct Renin Inhibitors: Aliskiren, recently approved by FDA
-Beta blockers (without intrinsic sympathomimetic activity) are indicated in:
-Post myocardial infarction!! Sued if you don’t give them to pt!
-Stable patients with congestive heart failure
-Rate control in atrial fibrillation
-Control of angina pectoris
-Calcium channel blockers
- Dihydropyridines, Verapamil, Diltiazem
-no absolute indication for Tx in HTN but helpful in: Rate control in atrial fibrillation, Control
of angina pectoris, May be preferred in obstructive airway disease
-dihydropyridines side effects: Headache, Dizziness, Flushing, Edema (due to a redistribution
of fluid from vascular to interstitial space
Pregnancy:
-Difficult to Tx –essential HTN or preeclampsia
-Maintstay: Alpha Methyl Dopa
-Ok: Labetalol
-CCB
-Diuretics +/-
HTN – 12. 8.09
Raja – F&E
-No ACE-I or ARB!! Neural tube defects! Stop immediately and switch to dif drugs.
Practice Questions:
1. Normal BP: systolic < ? and diastolic < ?
2. Pre-hypertension: systolic 120-? or diastolic 80-?
3. Which of the following may cause neural tube defects if used during pregnancy? (2)
A. ACEi
B. ARB
C. Alpha methyl dopa
D. labetaol
4. Which of the following is first line drug treatment in HTN?
A. Calcium channel blockers
B. Thiazide diuretic
C. Beta Blocker
D. Alpha blocker
5. Which drug must you give post-MI or you may get sued?
A. Calcium channel blockers
B. Thiazide diuretic
C. Beta Blocker
D. Alpha blocker
6. When evaluating blood pressure it should be elevated on _____ occasions, both in the office and
outside the office.
A. 1
B. 2
C. 3
D. 4
Answers:
1. Normal BP: systolic < 120 and diastolic <80
2. Pre-hypertension: systolic 120-139 or diastolic 80-89
3. A & B
4. B
5. C
6. B
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