ANTI-HYPERTENSIVES
Krisi Amsden, DNP, RN
ATI: Chapter 20
Frandsen: Chapter 26
HTN Overview
• Common, chronic disorder affecting more
than 100 million adults in the United States
• Hypertension  the risk of
– MI, HF
– Cerebral infarction and hemorrhage
– Renal disease
BP Regulation Mechanisms
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Pages 509 – 511 Box 26.1
Neural
Hormonal
Vascular
Vascular Remodeling
BP Regulation: Neural
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SNS stimulation
– Chronotropy
– Inotropy
Activated by vasomotor
center in the brain
– Baroreceptors
– Chemoreceptors
Blunted response with antihypertensives = orthostatic
hypotension
Hypotension
SNS activation – Production
Epinephrine/Norepinephrine
Vasoconstriction
Stimulation of beta-adrenergic
receptors in the heart
Increased BP, CO, tissue
perfusion
BP Regulation: Hormonal (RAAS)
BP LOW
Renin secreted from
kidneys
Renin stimulates
increased conversion of
angiotensinogen to
angiotensin I 
Angiotensin I converted
to angiotensin II by
angiotensin-converting
enzyme (ACE)
Angio II causes
vasoconstriction &
stimulates release of
aldosterone
Aldosterone causes Na
and H2O retention
B/P rises
Renin release is
inhibited
BP Regulation: Vascular
• Vasoconstrictors:
– Angiotensin II
– Endothelin 1
– Platelet-derived
growth factor
– Thromboxane A2
• Vasodilators:
– Nitric oxide (NO)
– Prostacyclin
BP Regulation: Vascular Remodeling
• Thickening of the blood vessel wall =
narrowing of the blood vessel lumen.
• Less flexible – Unable to respond as well
to vasodilating substances.
Hypertension
• Persistently high blood pressure that results from
abnormalities in regulatory mechanisms
– Systolic pressure greater than 140 mm Hg
– Diastolic pressure greater than 90 mm Hg
• Primary: 90% to 95% of known cases
• Secondary: may result from renal, endocrine, or CNS
disorders or from medications
HTN Pharm Therapy
• Keep B/P less than 140/90
• Two main actions:
– Decrease volume of circulating blood
– Reduce systemic vascular resistance (SVR)
• Remember…B/P = CO x SVR
(CO = HR x SV)
Principles of Therapy
• JNC 8
– Patients ≥ 60,
otherwise healthy –
GOAL ˂ 150/90
– Patients 30-59,
otherwise healthy –
GOAL ˂ 140/90
– Lifestyle modifications
• JNC 10
– Patients ≥ 65,
otherwise healthy –
GOAL ˂ 140/90
– Patients ˂ 65,
otherwise healthy –
GOAL ˂ 130/80
– Lifestyle modifications
Drug Selection
• First line agents:
– Thiazide diuretics
– ACE/ARBs
– CCBs
• Choice dependent on numerous factors,
including age, ethnicity, concomitant
CV/kidney disorders.
HTN Management Guidelines
• Factors to be considered: age, ethnicity, concomitant CV
disorders.
• Start medications in lowest available dose.
• Change medication groups instead of increasing the dose if
1st medication is ineffective.
• Many patients require 2+ medications for adequate BP
control.
• Medications are titrated and dispensed according to individual
response.
• Patient Teaching Box: 26.4 (Page 521)
Antihypertensive Medications
(Table 26.1, Page 515)
Angiotensinconverting
enzyme (ACE)
inhibitors
Angiotensin II
receptor
blockers (ARBs)
Antiadrenergics
Calcium
channel
blockers
Diuretics
Direct
vasodilators
ACE Inhibitors
ACE Inhibitors (-prils)
• Angiotensin-Converting Enzyme Inhibitors
• MOA: Block the conversion of angiotensin I to angiotensin II
(potent vasoconstrictor)
– Decreased aldosterone production = reduced retention of
Na and H2O
• Metabolism highly dependent on genetics and ethnicity
• Current guidelines: ALL nonblack individuals, including
those with DM or CKD, should receive ACEI as part of their
drug therapy.
• Not as effective in African American populations
ACE Inhibitors (-prils)
captopril
(Capoten)*
benazepril
(Lotensin)
enalapril
(Vasotec)
fosinopril
(Monpril)
ramipril
(Altace)
Lisinopril
(Zestril)
ACE Inhibitor MOA on RAAS
BP LOW
Renin secreted from
kidneys
Renin stimulates
increased conversion of
angiotensinogen to
angiotensin I 
Angiotensin I converted
to angiotensin II by
angiotensin-converting
enzyme (ACE)
Angio II causes
vasoconstriction &
stimulates release of
aldosterone
Aldosterone causes Na
and H2O retention
B/P rises
Renin release is
inhibited
Side/Adverse Effects
• Dry, persistent cough –
May warrant D/C
• First dose orthostatic
hypotension
• ANGIOEDEMA
• Hyperkalemia
• Worsening renal
function…check
BUN/Cr frequently
A: Angioedema
C: Cough
E: Electrolytes
Nursing Implications
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BBW: Not to be used during pregnancy – TERATOGENIC
– Cautious use in women of childbearing age
QSEN Safety (p. 519): ACE + K sparing diuretics or foods high in K increases risk for
hyperkalemia
– Foods high in K: bananas, oranges, salt-substitutes, potatoes, almonds
BP checks – orthostatic hypotension (worsened with 1st dose)
– Check BP for 2 hours after 1st dose
– Take first dose at bedtime
– Change positions slowly
– Avoid hot showers/saunas
Monitor BUN/Cr baseline and routinely
Do not take captopril with meals, if possible
– 1 hr before or 2 hrs. after meals
ARBs
ARBs (-tans)
• Angiotensin II Receptor Blockers
• MOA: Blocks vasoconstricting and aldosterone secreting effects of
angiotensin II at various receptor sites.
– Increases renal flow and enhances excretion of chloride,
calcium, magnesium, and phosphate.
• Well-tolerated with less AE than ACEI
– Less profound effect on K
– No dry cough
– Can take with/without meals
• AE: Angioedema, impaired renal function (BUN/Cr)
• BBW: Women of childbearing age/Pregnancy - TERATOGENIC
ARBs (-tans)
losartan
(Cozaar)
irbesartan
(Avapro)
valsartan
(Diovan)
olmesartan
(Benicar)
ARB MOA on RAAS
BP LOW
Renin secreted from
kidneys
Renin stimulates
increased conversion of
angiotensinogen to
angiotensin I 
Angiotensin I converted
to angiotensin II by
angiotensin-converting
enzyme (ACE)
Angio II causes
vasoconstriction &
stimulates release of
aldosterone
Aldosterone causes Na
and H2O retention
B/P rises
Renin release is
inhibited
Calcium channel blockers
CCBs (-pines)
• Calcium Channel Blockers
• MOA: Inhibit the influx of calcium ions
across cardiac and smooth muscle cells,
resulting in relaxation and vasodilation.
• Negative inotrope
• Also used in treatment of CAD/angina
– Prinzmetal angina
CCBs (-pines)
amlodipine
(Norvasc)
nicardipine
(Cardene)
felodipine
(Plendil)
diltiazem
(Cardizem)
verapamil
(Calan)
nifedipine
(Procardia)
Indications for Use
• HTN, Angina, CAD
• SVT Dysrhythmias (diltiazem)
• Subarachnoid hemorrhage/cerebral
aneurysm…..Nimotop (nimodipine)
• Raynaud’s phenomenon
• Hypertrophic cardiomyopathy
Side/Adverse Effects
• Generally well-tolerated
• CV effects:
– Slowed HR/contractility
– Hypotension
– Peripheral edema of hands, ankles, feet
– Pulmonary edema
– Worsened in patients with HF
– QSEN Safety: Anginal exacerbation (abrupt withdrawal)
• Other: H/A, drowsiness, fatigue, dizziness, flushing,
palpitations, nausea, abdominal pain.
Drug/Food Interactions
• Do not give with grapefruit juice…inhibits first pass
liver metabolism…will have higher serum levels and
lead to toxicity
• Increased serum levels of (-statin) drugs
• Don’t give in IV form with beta blockers at the same
time
• Can increase serum digoxin levels
– Digoxin + CCB =  risk of heart blocks
Beta blockers
Beta Blockers (-lols)
• MOA: Inhibits Beta1 and/or Beta2 receptors
• Work on the SNS (sympathetic nervous
system)
– Decreasing overall stimulation
– Negative inotrope and chronotrope effect
– Decreased renin release from kidneys
• Decreases the 3 Cs!! + 1 more…. And
maybe +1 more
Beta Blockers (-lols)
• Types:
– Selective – drugs that
inhibit only one type of
beta receptor
• Beta1 only:
cardioselective
• Beta2 only: block lung
receptors
– Nonselective: Block
both
– Alpha AND BetaBlockers
Beta Blockers (-lols)
atenolol
(Tenormin)
bisoprolol
(ApoBisoprolol)
metoprolol
(Lopressor)
carvedilol
(Coreg)
propanolol
(Inderal)
Indications for Beta Blocker Use
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Hypertension
Angina
Dysrhythmias
Hypertrophic
Cardiomyopathy
• Glaucoma (topical)
• Tremors & Anxiety
• Vascular Headaches
(migraines)
• Adjunct use in:
– Thyrotoxicosis
– Pheochromocytoma
Side/Adverse Effects
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Primarily extensions of their pharmacologic activity
CV effects:
– Negative chronotropy (Bradycardia!)
– Hypotension
– Heart failure exacerbation
– BBW: Anginal exacerbation (with abrupt withdrawal)
Non-CV effects:
– Bronchospasm
– Depression exacerbation
– Decline in sexual function
– Weakness/Fatigue (why??)
– Masking of hypoglycemia
Remember these are all “high alert” drugs!
– Second nurse should check calculations for correct dosing when giving IV
Contraindications/Cautious Use
• AV Block
• Bradycardia
• Uncompensated Heart Failure…and use
cautiously with all HF
• Asthma, COPD – use cardio-selective
drugs only
• Cautious use with DM, MG, depression
Nursing Implications
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Check HR!!!
– Hold and notify HCP for a HR ˂ 60 bpm
– Apical pulse x 1 FULL minute
– Teach patient how to check their pulse
daily
Check B/P!!!
– Hold and notify HCP for SBP < 90 mmHg
IVP given over 2.5 minutes.
– Continuous telemetry
– 2nd RN verification
– BP monitoring every 5 minutes
– Supine/HOB flat
Daily weights, check for edema
Wean drugs off over 1-2 weeks
Drug – Drug Interactions
• Careful with CCBs….added bradycardic effect!
• Anti-diabetic agents: mask s/sx of hypo- and
hyperglycemia
• Cocaine: reduce or cancel effects of beta blockers
• MAOIs (monoamine oxidase inhibitors): can cause
hypertensive crisis
• OTC drugs
Combined alpha and beta blockers
• carvedilol (Coreg) and labetalol (Normodyne)
• MOA: Same as nonselective beta blockers, but work
on alpha-receptors too = increased vasodilation
• May have more orthostatic hypotension
– Supine/HOB flat with IVP administration!
• carvedilol (Coreg) is used primarily for CHF, but works
for HTN as well
• carvedilol (Coreg) can increase Digoxin levels
• carvedilol (Coreg) may also cause drug-induced SLE
Anti-adrenergics
Centrally-acting Alpha Agonists
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Alpha2 Receptor Agonists
MOA: Stimulates alpha2 receptors in the brain, which blocks SNS activity
and leads to the release of less norepinephrine and a reduction of
sympathetic outflow from the vasomotor center.
– Decreases BP
Other indications for use: chronic pain treatment.
clonidine (Catapres)
– Can be PO or a weekly TTS patch
– May slow HR
Adverse effects: orthostatic hypotension, bradycardia, decreased
sexual function, drowsiness, rebound HTN (taper off slowly)
Since these work on decreasing activity in the CNS, watch out for other
CNS depressants!
Peripherally-acting Alpha-Adrenergic Blockers
• Alpha1-Adrenergic Blockers
• MOA: Block peripheral
alpha1-adrenergic receptors,
resulting in blood vessel
dilation and decreased PVR.
• Peripheral acting – AE firstdose phenomenon
– Orthostatic hypotension
– 1-3 hours after 1st dose
– Give first dose at bedtime to
prevent.
doxazosin
prazosin
terazosin
Direct Renin Inhibitors
• aliskiren (Tekturna)
• MOA: Decreased plasma renin activity and inhibits
conversion of antiotensinogen to angiotensin I.
• Contraindicated with ACE/ARB and CKD
• Not to be taken with high-fat meal – absorption of drug
effected 75%
• AE: Angioedema/Hyperkalemia
Diuretics
• Thiazide: 1st line drug
class for HTN.
• All decrease plasma and
extracellular fluid
volumes causing
decreased
preload…which causes
decreased CO and
decreased SVR
Thiazides:
(hydrochlorothiazide)
Loop:
(furosemide)
K-sparing:
(spironolactone)
K-sparing Diuretics
• MOA: Block aldosterone
(thereby sparing
potassium!)
• Examples:
– spironolactone
(Aldactone)
– eplerenone (Inspra)
• Nursing Implications:
Electrolytes! I&O
Direct Vasodilators
• MOA: Directly relax smooth muscle in the
blood vessels, resulting in dilation and
decreased PVR.
• Effective in HTN emergencies and
management of HF.
• BBW: minoxidil – anginal exacerbation –
preceipitated pericardial effusion
• Watch for drug-induced Lupus
Erythematosus, Na retention (edema),
tachycardia
nitroprusside
hyralazine
minoxidil
dopamine (Intropin)
• Opposite of previous drugs
• vasopressor…makes B/P and CO rise
• Can also be given at a low “renal” dose to improve
renal and mesenteric blood flow…to improve kidney
perfusion (1-2mcg/kg)
• Given in ICU
• SE: HA, nausea, angina, HTN, Tachycardia
Final Tid-Bits…..
• Patients may be on several classes of drugs to
achieve a therapeutic B/P
• More classes = more difficulty controlling B/P
• Never give 2 of the same class without clarifying
order!!!
• Patient Teaching – What do your patients need to
know to take their medications safely??
What if…
• The antihypertensive drugs your patient
received have bottomed out his B/P to
70/40. What would you do?