Hypertension Meds

4 external factors that could elevate BP

exercise

caffeine

smoking

pain

medications that raise BP (12)

amphetamines

estrogen

steroids

triptans

SNRIs

decongestants

atypical antipsychotics

anabolic steroids

erythropoietin

cyclosporin

NSAIDs

cocaine

diagnosis of hypertension requirements

2 or more readings on 2 or more occassions

6 conditions to screen for primary aldosteronism

adrenal mass

family history of stroke less than 40 yo

FH of early onset HTN

OSA

hypokalemia

resistant HTN

who is the PREVENT risk estimator validated in

adults 30-79 without known CVD

4 categories of cardiovascular disease

atherosclerotic

heart failure

valvular diseases

arrhythmias

3 indications for initiating HTN treatment

BP >140/90

BP >130/80 + CVD/DM/CKD/7.5% + risk

10 year CVD risk >7.5 if BP greater than 130/80

additional criteria for initiating treatment in BP >130/80

CVD

diabetes

CKD

>7.5% risk score

if a patient has a risk score >7.5%, what additional criteria is needed to initiate treatment?

BP >130/80 after 3-6 mo of lifestyle change

workflow if patient has ELEVATED BP

initiate lifestyle therapy

reassess in 3-6 mo

stage I HTN algorithim for treatment

1. lifestyle therapy

2. reassess in 3-6 mo

3. start medication if BP still elevated / reassess in another 3-6 mo if not

if a patient has stage I HTN and has _, then medications should be initiated immediately

DM

CKD

risk >7.5%

stage 2 HTN initiating therapy algorithim

lifestyle therapy + start medication

reasess in 1 mo

weight loss goal

sustained >5% reduction in body weight OR >3 pt reduction in BMI

heart healthy diet recs

rich in fruits, veggies, whole grains, and low-fat dairy

reduce saturated and total fat

optimal dietary sodium intake goal

<2300 but IDEALLY <1500

dietary K+ goal

3500-5000 mg/d

alcohol intake recommendations as lifestyle intervention

abstinence is best

aim for >50% reduction in daily intake

no more than 2 daily drinks for men

no more than 1 daily drink for women

alcohol rec in drinks/day for men and women

men: no more than 2/day

women: no more than 1/day

aerobic exercise weekly rec

90-150 min

dynamic exercise weekly rec

90-150

isometric resistance weekly rec

3 times per week

4 first line agents for HTN

1. thiazides

2. ACEi

3. ARB

4. CCB

7 additional HTN agents outside of the first-lines

loop diuretic

beta blocker

MRA

central alpha agonist

alpha-1 antagonist

direct renin inhibitors

direct vasodilators

which drug classes are RAAS inhibitors

ACEi

ARBs

ACEi MOA

competitive inhibition of ACE

prevents formation of angII

indirectly inhibits increased fluid volume due to inhibition of angII release of aldosterone

what is the physiological explanation for dry cough from ACEi

a buildup of bradykinin in the respiratory tract due to the inhibition of ACE (which normally breaks it down)

3 results from ACEi MOA

reduced sympathetic stimulation

increased Na/water loss

vasodilation

4 indications for ACEi

HTN

HF

post-MI

nephro-protection for those with DM

contrainidcations of ACEi

2nd/3rd trimester of pregnancy

history of angioedema

bilateral renal artery stenosis

SE’s of ACEi

• dry cough

• hyperkalemia

• angioedema

• acute renal failure

ACEi dry cough usually resolves in what timeframe?

1-4 wks AFTER discontinuation

why do ACEi’s have angioedema as a risk factor

increased bradykinin that causes vasodilation and fluid buildup

how do ACEi’s affect renal function

transient increase in Scr within the 1st week of initiation but it should resolve to baseline

ACEi’s are preferred in what patients (4)

CKD

diabetes with albuminuria

HF

stable ischemic heart disease

who are lower response rates for ACEi monotherapy seen in

people who are salt sensitive

people with low renin

how long does it take for ACEi full effect

several weeks

ARB MOA

selective binding to AT1 receptor → blocks actions of ang II

stimulate AT2 receptor to mediate vasodilation → activates NO

results of ARB action

less ang II → less sympathetic

less aldosterone → Na/water loss

indications of losartan

HTN + LVH

HF

nephro-protection with diabetes

which ARBs are indicated for HF

losartan

valsartan

candesartan

substitute for ACEi when dry cough is produced

ARB

contraindications of ARBs

2nd/3rd trimesters of pregnancy

bilateral renal artery stenosis

ARBs side effects

hyperkalemia

angioedma

acute renal failure

are ACEi or ARBs more likely to cause angioedema?

ACEi

do not use _ with any ACEi or ARB induced angioedema

sacubitril-valsartan

if angioedema occurs with ACE-i when can they start an ARB?

6 weeks

ARBs are preferred in those with _

CKD

DM w albumninura

HF

stable ischemic heart disease

who to reduce the started dose of ARBs in

elderly

volume depleted

ACE and ARBs drug interactions

avoid taking them together

avoid direct renin inhibtors with etiher

drugs that can increase K+

NSAIDs

ACE-I drug interaction

an ARB

sacubitril/valsartan (Entresto)

what can taking sacubitril/valsartan with ACEi cause

angioedema

guideline for switching from sacubitril/valsartan to ACEi

36 hours washout

examples of drugs that can increase K+

K+ sparing diuretics

K+ supplements

trimethoprim

what effect do NSAIDs have on the kindey physiology

vasoconstriction of afferent arteriole

how often to follow up for ACEi and ARBs

2 weeks, then 4 weeks, every 3-6 mo until stable

labs to monitor with RAAS drugs

BMP (K+, BUN, SCr)

CCB MOA

L-type Ca+ channel blockade → decreased Ca+ current → smooth muscle relaxation and reduced contractility/O2 demand/PVR/HR

effects of CCBs

smooth muscle relaxation

reduced contractility

reduced O2 demand

reduced PVR

reduced HR

non-dihydropyridines affect _ to a greater extent

AV nodal conduction

dihydropyridines affect _ to a greater extent

vascular smooth muscle

non-DHP CCBs examples

diltiazem

verapamil

diltiazem indications

angina

HTN

Afib

verapamil indications

angina

HTN

afib

arrythmias

non-DHP CCB side effects

1st degree heart block

constipation

which non-DHP CCB causes more constipation

verpamil > diltiazem

DHP CCB side effects

PERIPHERAL EDEMA

headache

dizziness

flushing

nausea

reflex tachy

CCB drug interactions

simvastatin

phenytoin

carbamezepine

4 things to monitor with CCBs

BP

HR

peripheral edema

constipation

what kind of CCB’s are NOT recommended for HTN

short acting DHPs

why are short acting DHP CCB’s not recommended for HTN

risk of adverse cardiovascular events

when to avoid nonDHP CCB’s

left ventricular dysfunction

HFrEF

with beta blockers

FDA Medwatch for CCBs

concurrent use of CCBs + simvastatin

how much simvastatin can be taken with verapmil or diltiazem

no more than 10 mg daily

how much simvastatin can be taken with amlodipine

no more than 20 mg daily

diuretic MOA

inhibits reabsorption of sodium and water in the renal tubules

physiological effect of diuretics

decreased blood volume and SV

decreased CO

increased TPR due to reflex sympathetic activity (initially)

what happens after 6-8 weeks of diuretic therapy

CO normalizes and TPR declines

4 types of diuretics

loop

thiazide

carbonic anhydrase inhibitors

MRAs

loop diuretic site of action

loop of henle (thick ascending limb)

thiazide diuretic site of action

distal convoluted tubule (proximal portion)

carbonic anhydrase inhibitors site of action

proximal convoluted tubule

mineralocorticoid receptor antagonist site of action

distal convoluted tubule (distal portion)

thiazide diuretic MOA

inhibits NaCl reabsoprtion by blocking Na/Cl transporter

excertion of Na/K/Cl/H/water

LESS excretion of Ca

4 thiazide diuretic examples

Hydrochlorothiazide

chlorthalidone

metolazone

indapamide

which thiazide diuretic can be PRN

metolazone

preferred thiazide diuretic

chlorthalidonew

why is chlorthalidone the preferred thiazide

prolonged half-life

proven reduciton of CVD

electrolyte imbalances of thiazide diuretics

HYPO: K, Na, Mg

HYPER: Ca

adverse effects of thiazide diuretics

electrolyte imbalances

hyperuricemia (caution with gout)

hypersensitivity

hyperglycemia

HLD

metabolic alkalosis

adverse effects of thiazide diuretics have been shown to be _

dose related

allergy associated with thiazide diuretics

sulfa

how do the effect of thiazide diuretics compare to loop diuretics

GREATER BP lowering response

LESS diuresis

how long does it take for response to be seen with thiazide diuretics

3-4 weeks

Max BP lowering effect of HCTZ is at what dose?

25 mg/day

if thiazides are taken with loop diuretics, what is the timing of taking them?

take thiazides 30 min before loop diuretic

when are thiazide diuretics not effective

when CrCl < 30 (metolazone is the exception)

time of day to take thiazides

MORNING (prevents nocturia)

which thiazide can be taken with reduced CrCl

metolazone

loop diuretic MOA

inhibits active chloride binding transport

excretion of electrolytes

COX-2 induciton → increased renal blood flow