HTN DRUG THERAPY MONITORING Flashcards
Drug Therapy Monitoring:
What and When
Efficacy – BP effects – Need for up- and down-titration (deprescribing) • Toxicity (Per drug class) • Thiazide diuretics • ACEi/ARBs • Calcium Channel Blockers (DHP/Non-dihydropyridines) • Beta-blockers • Know baseline for efficacy/safety
Diuretic Therapy
• Electrolyte disturbances: decrease K+, ¯ Na+
, increase Ca++ (thiazides), decrease Ca++ (loop)
• Renal function: Scr
WHEN? Baseline, after initiation, with dose changes (2-4
weeks after change(s)
Other noted effects:
• Metabolic disturbances: glucose
• Electrolyte disturbances: uric acid, Ca++
• Photosensitivity: sunscreen use important
thiazides can precipitate gout
Some people are having prophylactic gout therapy with tzd
Mechanisms to Minimize Hypokalemia:
Thiazide-induced
• Combine with ACEi or spironolactone
• Add potassium-sparing diuretic – amiloride or triamterene
– Available as Dyazide® or Moduret® with hydrochlorothiazide
– Amiloride 5 mg = triamterene 50 mg = approximately 30-40 mEq K+ (in normal renal fn)
• Add potassium supplement (available as 8mEq or 20 mEq)
• Reduce dose of thiazide
Drug Therapy Monitoring:
ACEI or ARB Therapy
1 BP control/proteinuria reduction
2 dry cough in up to 5-15% of patients; ensure
this is not cardiac in nature or due to
underlying lung disease (ACE ONLY)
- This effect absent with ARB therapy
3 hyperkalemia – dose-related
– Baseline, 1-2 weeks after initiation and 1-4
weeks after final dose titration
4 renal dysfunction - important to monitor Scr
as dose titration occurs
5 angioedema - rare, but can be life-threatening
explain how ACEi or ARBs protect the kidney
normal kidney: afferent arteriole tone is mostly controlled by prostaglandin (vasodilator)
efferent arteriole tone controlled by ang II (vasoconstrictor)
progression of nephropathy: dilation by prosta in aff arteriole aand constriction of eff art by ang II leads to increased glom capillary pressure, microalbuminuria
Damage: Proteinuria, thickening of the basement membrane, fibrotic scaring
ACE-I or ARB increase prostaglandin and decrease ang II, leading to aff and eff dilation, decreased damgage
Restore and reduce thicking of glom cap
Greaeter vasodilation of efferent arteriole compared to afferent
There should be less stress to glom
Decrease microalbin
who is ACEi and ARB contraindicated for
Contra-indicated in patients who have bilateral renal artery stenosis – If Scr ↑ >35%, then this should be considered • Frequency of monitoring – Scr + lytes at baseline – with dose changes, within 10-14 days
ACEi or ARB - Hyperkalemia
• Risk Factors
– Chronic renal failure, esp GFR<30 mL/min
– DM
– Volume depletion
– Advanced age
– Potassium supplements
– Drugs including K+-sparing diuretics, NSAIDs, beta-blockers
and heparin
• At least 28% of patients with CKD and 38% of
patients with HF (heart failure) have at least 1
episode of hyperkalemia
ACEi or ARB – Hyperkalemia: Tips for Management
• Evaluate baseline Scr and K+
– After dose titration and at regular intervals thereafter based on individual patient’s risk
• Combine with loop or thiazide diuretic
• When GFR is low, add or switch to loop diuretic
• Avoid or use with caution when GFR<30 mL/min –
assess clinical situation
• If K+ consistently above 5.5, should stop drug or
refer to specialist to consider K+-binding drug.
Drug Therapy Monitoring
CCBs - Dihydropyridines
• Generally well tolerated
• Dose-related:
– Pedal edema, non-pitting (may be reduced if
combined with ACEi), stretched or tight skin
– Headache
• No lab monitoring required
NOTE: Avoid short-acting
nifedipine in all clinical situation (not avail, quick drop in BP leads to risk of stroke)
Drug Therapy Monitoring
CCBs – Non-Dihydropyridines
• Dose-dependent: – HR – Constipation • Use caution when combining with a betablocker or digoxin; cumulative negative inotropic effects. • Cause less pedal edema than DHP-CCBs.
Drug Therapy Monitoring
Beta-blockers
• HR; caution when used with non-dihydropyridine
CCBs
• Fatigue, vivid dreams/nightmares, erectile
dysfunction may be associated
• Can worsen plasma glucose levels (clinical
significance unknown)
• Absolute CI: asthma
• Not contra-indicated in COPD; if mixed disease, close
monitoring of breathing required
• Withdrawal effect – tapering required
Single Agent vs SPC?
• My approach is to start with one agent if within
10/10 above target.
• Otherwise, start with SPC (if agents you want to
use are available as a combo)
• ACEi or ARB
• Long-acting diuretic (in Canada, indapamide and
chlorthalidone)
• Long-acting CCB (typically DHP-CCB used)
2 options of combinations
1. ACEi/ARB + thiazide Preferred in past stroke or TIA Many combos exist, although few with chlorthalidone or indapamide. Most use hydrochlorothiazide.
1. ACEi/ARB + DHP-CCB Preferred in diabetes or CAD A few combos exist with amlodipine. For example: telmisartan or perindopril + amlopdpine. (Twynsta© or Viacoram©)
- DHP-CCB + thiazide
No combos exist. Each
available as generic – quite
inexpensive.
Triple Combination:
ACEi/ARB + DHP-CCB + Thiazide Typically will use one combination tablet + single for total of 2 pills daily.
Drug Combination Considerations
• Most patients will do well starting with a low dose single
pill combination which can be up-titrated to medium
doses if necessary
Think about:
• Baseline patient factors to tailor – monitoring impt!
• Cost effectiveness
• Preventing side effects / lab abnormalities
– Thiazides and risk of hypokalemia (combine ACE/ARB)
– Drugs with (-) chronotropic effects (NDHP-CCB + BB)
– ACEi (or ARB) + potassium-sparing diuretic – concern?
• Least synergistic combo: ACEi (or ARB) + BB
