Treatment of HTN 2 Flashcards
ACEI can cause what when initiated?
Elevated SCr but this is normal
ACEI indication
DM, CKD, HF, Stroke, CHD
ACEI Adverse Effects
Dry cough Angioedema (blacks and smokers) HYPOtension Renal dysfunction HYPERkalemia
Management of Dry Cough
Continue if it isn’t annoying
Switch to a different ACEI
Switch to an ARB
What causes the Cough?
Increase in bradykinin
ACEI Contraindications
Pregnancy
Bilateral Renal artery stenosis
Concurrent NSAID use
Why NSAIDs?
Decrease the GFR bc they inhibit PG synthesis which dilates the afferent arteries –> block that then you will have constriction at the afferent
Overall vasoconstriction occurs
ACEI Clinical Pearls
Decrease or stabilize albumiuria
Chronic renal insuf: start low and go slow
Monitor renal function and potassium
Limit salt intake
ARB Adverse Effects
Angioedema (blacks and smokers)
HYPOtension
Renal dysfunction
HYPERkalemia
ARB Containdications
Pregnancy
Bilateral Renal artery stenosis
Concurrent NSAID use
ARB Clinical Pearls
No cough and dreased risk for angioedema Similar outcomes as ACEI Renal data available in DM and CKD More expensive Not to be in combo with another RAAS inhibitor
Dihydropyridines
Potent peripheral vasodilatory effects
Weak Negative inotropic effects (NOT amlodipine)
No effect on conduction (dromotropic)
Dihydropyridines adverse effects
Baroreceptor-mediated reflex tachycardia
Pedal edema
Non-Dihydropyridines
Verapamil
Diltiazem
Non-Dihydropyridines MOA
Decrease chronotropic Slow AV conduction (negative dromotropic effects) Decreased inotropic effects (esp verap) Weak peripheral vasodilatory effect Coronary vasodilators
Non-Dihydropyridines Useful for?
Supreventrivcular tachyarrhythmias
Afib
Non-Dihydropyridines Adverse Effects
Bradycardia
Heart block
CCB Clinical Pearls
May use DHP + Non-DHP together
Constipation (verap)
Caution in combo with beta-blocker + Non-DHP (cause bradycardia)
Avoid short-acting DHP –> potent vasodilators –> lower BP really quickly
Watch for drug interactions (esp Non-DHP)
Beta Blockers place in therapy
1st line along with thiazides with MI, HF, angina High renin-hypertensives Arrhthmias Migraine headaches Tremors Anxiety Thyrotoxicosis
Beta blockers are less effective?
In black pts
Beta blockers MOA
block B1 receptors in the heart and decrease inotropic and chronotropic in the heart
Also block beta receptors in the kidney and decrease renin release
Beta Blocker Adverse Effects
B1 blockade: bradycardia, 2nd or 3rd degree heart block, acute HF
B2 blockade: bronchospasm, cold extremities, Raynaud’s, Increased blood glucose and lipids, Mask hypoglycemia
Fatigue, depression and sexual dysfunction
Beta-Blocker Clinical Pearls
All lower BP to a similar extent
Cardio selective is dose dependent and varies
Use selective agents in those with COPD or asthma
Do not abruptly withdraw
Use with extreme caution if also on non-DHP
Direct Renin Inhibitor
Aliskiren (Tekturna)
Aliskiren MOA
RAAS Inhibitor: inhibits the release of renin so there is no Ang II made
Renin normally does what?
Elevates BP via angiotensinogen to Ang I and Ang I to Ang II via ACE
Aliskiren Clinical Pearls
Equally as effective as ACEI or ARB
Do not use with another RAS inhibitor
No hard data
Alpha 2 Blockers MOA
Block receptors on blood vessels which causes vasodilation in the periphery
Alpha 2 Blockers drugs
Doxazosin (Cardura)
Prazosin (Minipress)
Terazosin (Hytrin)
Alpha 2 Blocker Clinical Pearls
Useful in men with benign prostate hyperplasia
Take 1st dose at bedtime
May cause Na and H20 retention
How do Alpha 2 Blockers cause Na and H20 retention?
Body wants to stay at homeostasis and you are causing vasodilation so the kidney would increase RAAS and cause the body to keep Na and H20