CH 26: Hypertension Flashcards
homeostasis resulting from increased blood pressure in the cardiovascular system
vasodilation
decreased stroke volume
decreased HR
decreased CO
blood pressure back to normal
homeostasis resulting from increased blood pressure in the kidneys
increased urine output
decreased blood volume
blood pressure returns to normal
primary HTN
no identifiable cause
secondary HTN caused by:
Diseases: for example, Cushing’s, hyperthyroid, CKD
Drugs: corticosteroids, contraceptives, alcohol, amphetamines,
caffeine, decongestants,
Many times there are no symptoms
4 organs most affected by prolonged HTN or uncontrolled HTN
Heart
Brain
Kidneys
Retina
consequences of HTN
Heart must work harder
o Excessive workload can ultimately cause heart to fail = heart
failure (HF)
Damage to the blood vessels
o Can result in transient ischemic attacks and strokes
Damage to the arteries of the kidneys
o Can result in CKD
Damage to the vessels in the retina
o Can result in rupture or occlusion = visual impairment and
blindness
If HTN continues, damage to the organs and tissues can be irreversible
lifestyle recommendations for HTN
Limit intake of alcohol.
Restrict sodium consumption and increase potassium intake.
Reduce intake of saturated fat and cholesterol and increase
consumption of fresh fruits and vegetables.
Increase physical activity.
Discontinue use of tobacco products.
Reduce sources of stress and learn to implement coping strategies.
Maintain optimal weight.
goal of pharmacotherapy for HTN
reduce morbidity and mortality
Alpha2 Agonists action
Decrease SNS impulses to heart and arterioles = vasodilation
Alpha 1 Blockers action
inhibit SNS action on arterioles = vasodilation
direct vasodilators
Act on smooth muscle of arterioles = vasodilation
calcium channel blockers
Block calcium ion channels in arteries causing vasodilation
Angiotensin receptor blockers
Prevent angiotensin II from reaching the receptors = vasodilation
ACE inhibitors (angiotensin-converting enzyme)
Block formation of angiotensin II = vasodilation AND block aldosterone secretion = decrease fluid volume
diuretics
Increase urine output = decrease fluid volume
Beta blockers
Decrease heart rate and myocardial contractility = reduce CO
treatment begins at systolic greater than 120 with:
non-pharmacologic changes
drug treatment starts with systolic greater than
130
therapeutic effects of lisinopril (ACE inhibitors)
Block formation of angiotensin II = vasodilation AND block
aldosterone secretion = decrease fluid volume
adverse effects of lisinopril (ACE inhibitors)
Headache,
dizziness,
orthostatic hypotension,
rash,
cough
Angioedema,
acute renal failure,
first-dose phenomenon,
fetal toxicity,
hyperkalemia
monitoring for lisinopril (ACE INHIBITORS)
Persistant cough
Postural hypotension– first dose phenomenon
Hyperkalemia with potassium sparing diurectics
Monitor labs for glucose,
eletrolytes, AST, ALT, BUN, creatinine
Potassium!
safety for lisinopril (ACE inhibitors)
angioedema - emergency!
No use during pregnancy
NSAIDs can reduce the effect
Alcohol may increase hypotension
Can lead to lithium toxicity
adverse effects of losartan (ARBs)
Headache,
dizziness,
orthostatic
hypotension,
diarrhea,
fatigue,
upper respiratory tract infection
Angioedema,
acute renal
failure,
first-dose phenomenon,
fetal toxicity,
hyperkalemia,
nephrotoxicity
(aliskiren)
safety and monitoring for losartan (ARBs)
Hypoglycemia
UTIs
anemia
Dizziness and fainting after first couple of doses
Fetal injury and death when taken with pregnancy
therapeutic effects of nifedipine (selective CCB) and diltiazem (non-selective CCB)
Block calcium ion channels in arteries causing vasodilation
Nifedipine: decrease HTN and angina
adverse effects of nifedipine (selective CCB) and diltiazem (non-selective CCB)
Flushed skin,
headache,
dizziness,
peripheral edema,
lightheadedness,
nausea,
constipation,
fatigue,
sexual dysfunction
Hepatotoxicity,
MI, HF,
confusion,
mood changes,
angioedema
safety and monitoring of nifedipine (selective CCB) and diltiazem (non-selective CCB)
monitor for digoxin toxicity
do not crush or divide
alcohol increases vasodilation and can lead to syncope
therapeutic effects of atenolol (beta blocker)
Decrease heart rate and myocardial contractility = reduce cardiac output
Reduced blood pressure
Reduce angina
Heart failure,
MI
Migraines
adverse effects of atenolol (beta blocker)
Fatigue,
insomnia,
drowsiness,
impotence or decreased libido,
bradycardia,
confusion
Agranulocytosis,
laryngospasm,
Stevens-Johnson syndrome,
anaphylaxis; if the drug is abruptly withdrawn,
palpitations,
rebound HTN,
dysrhythmias,
MI
safety and monitoring for atenolol (beta blocker)
Broncho-constriction
Fatigue and intolerance
Caution in patients with asthma or HF
Do not stop abruptly!
Can result in rebound hypertension and MI
therapeutic effects of doxazosin (alpha 1 - alpha blockers)
Inhibit SNS activation in arterioles = vasodilation
Lower blood pressure
Bph symptoms
adverse effects of doxazosin (alpha 1 - alpha blockers)
Orthostatic
hypotension,
dizziness,
headache,
fatigue
First-dose phenomenon,
tachycardia,
dyspnea
safety and monitoring of doxazosin (alpha 1 - alpha blockers)
Orthostatic hypotension
HYPOTENSION
Sedation and dizziness
Hemolytic
anemia,
leukopenia,
thrombo-
cytopenia,
lupus.
Caution with erectile dysfunction drug = low bp
NSAIDs can decrease effect
therapeutic effects of clonidine (alpha 2 adrenergic blockers)
Decrease SNS impulses
to heart and arterioles
= vasodilation
adverse effects of clonidine (alpha 2 adrenergic blockers)
Peripheral edema,
sedation,
depression,
headache,
dry mouth,
decreased
libido
Hepatotoxicity,
hemolytic anemia,
granulocytopenia
therapeutic effects of hydralazine (direct acting vasodilators)
Act on the smooth muscle of arterioles = vasodilation
Not first choice due
to side effects
adverse effects of hydralazine (direct acting vasodilators)
Orthostatic hypotension, fluid retention,
headache,
palpitations
Lupus-like reaction
(hydralazine),
severe hypotension,
MI,
dysrhythmias,
shock
safety and monitoring of hydralazine (direct acting vasodilators)
Reflex tachycardia**
Sodium and water retention
Can develop tolerance
over time
DO NOT STOP ABRUPTLY
Severe hypotension with other anti-hypertensives
swelling around the lips, eyes, throat, and other body regions.
angioedema
compensatory response to the sudden decrease in blood pressure caused by the
drug.
reflex tachycardia
