o
o
o
o
o
o
o
o
Sympathetic Nervous System
Response
- Epi and noriepi
o Adrenergic receptors
 Alpha and beta
-
-
receptor sites
Alpha 1: postysynaptic
Alpha 2: presynaptic
Beta 1: in heart
Beta 2: smooth muscle of bronchioles,
arterioles and visceral organs
Sympathetic nervous system response
o Dilates pupil
o Accelerates HR
o Inhibits digestive activity
o Stimulates glucose release
o Stimulates secretion of epi and
noriepi
Adrenergic stimulating drugs=
exaggerated SNS response
o Help with asthma COPD, help
w/ bp
o Contraindication: rapid hr,
dysrhythmia , glaucoma
-
Adrenergic Agonist
Epinephrine
- MOA
o Stimulates alpha 1= increase BP
o Stim. Beta 1= increase HR
o Stim Beta 2= bronchodilation
- Indications
o Allergic rx
o Anaphylaxis
o Asthma
o Bronchospasm
o Severe hypotension
o Cardiac arrest
- Contraindications
o Allergy
o Narrow angle glaucoma
o Cardiac dysrhythmias
- Side effects
o Tremors
o Agitation
-
Insomnia
Decrease renal tissue perfusion
Urinary retention
Palpitations
Tachycardia
Hypertension
V-fib
IV infiltration= necrosis and
tissue sloughing
Toxicity and management
o Short duration, so stop drug to
fix
 20-30 min effect
o CNS and CV risk
 Seizures= tx w/
diazepam
 hypertension,
dysrhythmias= tx w/
esmolol (betaadrenergic blocker)
o Decrease bp rapidly
o Support respiratory and cardiac
systems
o Infiltration
 Inject Phentolamine
Mesylate into area of
extravasation w/in 12
hrs of infiltration
Interactions
o Beta blockers antagonize
(block) epi effects
o MAOIs cause hypertensive crisis
o Lab: increases blood sugar
 Look at creatinine levels
 If high= decrease renal
tissue perfusion
Adrenergic Antagonists
-
Drugs that block the SNS
Eyes: miosis
Lungs: bronchoconstriction
Heart: decreased Hr
Blood vessels: vasodilation, decreased
bp
GU: reduced smooth muscle tone in
bladder and prostate
o
Alpha-1 Blockers
Doxazosin, prazosin, terazosin,
tamsulosin
- MOA:
o Interrupt stimulation of SNS at
the alpha 1- adrenergic
receptors
o Doxazosin, prazosin, terazosin:
 Used to treat
hypertension b/c they
cause arterial and
venous dilation
o Tamsulosin:
 Treat benign prostatic
hyperplasia (BPH) b/c it
causes relaxation of
smooth muscle in
bladder neck and
prostatic portion of
urethra= empty bladder
o Phentolamine:
 Alpha blocker=
vasodilation
- Indications:
o Hypertension, benign prostatic
hyperplasia
- Contraindication;
o Allergy
o Hypotension
o Use caution in hepatic and renal
disease pts
- Side effects
o 1st dose phenomenon- severe
and sudden drop in bp
o Orthostatic hypotension,
dizziness, headache,
constipation, edema, nasal
congestion
- Toxicity and management of overdose
o Bp should be supported by IV
fluid administration,
administration of vasopressors
(dopamine or norepinephrine)
- Interactions
o Additive effects
 Beta-blockers, erectile
dysfunction drugs
 Generic= sildenafil
-
-
-
-
Antagonistic effects
 Epinephrine
Assessment
o Med hist
 Look for meds that
cause interaction betablockers and erectile
dysfunction drugs will
had add. Effect causing
bp to become very low
and epi would have an
antagonistic effect= bp
remains elevated
o Vitals= bp and hr
o Assess renal function= drug
toxicity w/ renal failures
 Creatinine level and
urinary output.
Creatinine level- less
than1.3 urinary output
= >30 ml per hr
o Assess urinary system status
(BPH) = is pt able to completely
empty bladder, experience,
urgency, or nocturia)
Diagnosis
o Deficient knowledge related to
drug therapy
Planning
o Pt will verbalize effects
associated w/ alpha-blockers
o Pt bp in good range
Implementation
o Monitor vital signs, effect may
take up to 4 weeks
o Weight daily for fluid retention
o Look for ankle edema
o 1st dose given at night
o Pt teaching
 Don’t stop abruptly =
rebound hypertension
 Rise slowly, in stages =
hypotension
 Weigh self daily. Report
if gain is >5 pounds in 2
days
 Avoid OTC cold
medications – contain

-
adrenergic stimulating
meds and will
counteract alphablockers effects
Tamsulosin in evening.
Helps w/ urinary freq
and urgency at night
Evaluation
o Bp in Desired range
o Pt reports taking meds as
prescribed
o Evaluate for any pot side effects
o Able to start and keep a stream
of urine
-
-
Beta- Blockers
-
-
-
-
-
Non-selective beta-blockers (Blocks
beta 1 /2)
o Carvedilol, labetalol,
propranolol
o Beta-1 = found in heart
o Beta-2 in lungs
o Slow Hr but can cause
bronchoconstriction (asthma/
COPD pts).
Cardio-selective beta-blockers (blocks
beta-1 selectively)
o Metoprolol, atenolol
MOA:
o Block SNS, stimulation of betaadrenergic receptors by
competing w/ norepinephrine
and epinephrine.
o Decreases O2 demand and
slows conduction system of
heart
Indications:
o Angina, MI, cardiac
dysrhythmias, hypertension,
heart failure
o Not for use alone in African
Americans for hypertension will
use diuretic with it
Contraindications:
o Heart block, bradycardia,
cardiogenic , shock,
uncompensated HF, severe
pulmonary disease (COPD)
-
-
-
Side effects;
o Bradycardia
o Depression
o Constipation
o Fatigue
o Impotence
o Masking hypoglycemia
symptoms (tachycardia)
o Orthostatic hypotension
Toxicity and management of overdose
o Signs of overdose severe
bradycardia, hypotension, heart
block
o Withhold dose of beta-blocker
o atropine for symptomatic
bradycardia, dialysis if severe
overdose (pale, diaphoretic,
lightheaded)
o Glucagon may be effective as
first-line antidote for betablocker overdose but has to
administered w/ insulin
Interactions:
o Decreased absorption w/
antacids
o Add. Effect w/ digoxin,
diuretics, neuromuscular
blocking drugs, other cardiac
drugs
o Antagonistic effects w/
anticholinergic drugs/ epi
Assessment
o Med hist: meds that cause
interaction w/ beta-blockers
(digoxin, diuretics, antacids,
atropine)
o Vital signs: bp and Hr( hold if bp
is lower than 60)
o Assess severe pulmonary
disease (especially nonselective beta-blockers)
o Assess for hist of diabetes
mellitus
Diagnosis
o Decreased cardiac output
Planning
o Pt bp and hr will be normal
Implementation
o
o
-
Monitor bp and hr
Diabetic, monitor pt closely for
signs of hypoglycemia
o Pt teaching
 Do not stop abruptly=
rebound hypertension
or MI
 Teach pt how to check
bp and hr
 Rise slowly
 Diabetic pt to monitor
symptoms and blood
sugar
 Take sip of water
morning of surgery
unless instructed
otherwise= helps
decrease cardiac stress
during surgery and help
prevent MI post-op
Evaluation
o Bp b/w desired range
o Pt taking meds as described
o Adverse reactions
Anti-hypertensive Drugs
Alpha-2 Agonists
- Clonidine
o SNS stimulating drug, but works
w/ alpha 2 receptors
o It is alpha 2 pre-synaptic.
Stimulating alpha-2 will block
sympathetic outflow of
neurotransmitters, epi, and
norepinephrine
o Decreases alpha 1, beta 1, beta
2 = reduction of bp, reduces
renin in kidneys, converts
angiotensinogen into
angiotensin 1 which is
precursor to angiotensin ll,
potent vasoconstrictor
- MOA
o Work w/ CNS
o Stimulates the alpha2
receptors, blocking sympathetic
-
-
-
outflow or neurotransmitters
reducing bp
o Affects kidneys, reducing the
activity of Renin, which
converts angiotensinogen into
angiotensin 1, which is
precursor to angiotensin ll,
which is potent vasoconstrictor
Side effects
o Drowsiness, hypotension,
withdrawal phenomenon
Can be taken orally or transdermal
patch left on for 7 days
o Patch on chest or upper arm
Do not stop abruptly= severe rebound
hypertension
Can treat ADHD and opioid withdraw
Useful in treating sleep disturbances in
pts w/ brain injuries
ACE Inhibitors
- Catopril, enalapril, lisinopril
- MOA:
o Prevents ACE enzyme from
converting angiotensin l to ll
 ll is a potent
vasoconstrictor= raises
bp – induces
aldosterone, causes
sodium and water
retention and excretion
of potassium by
inhibiting aldosterone=
fluid loss and sodium
loss= retention of
potassium
 ACE inhibits block both
parts of bp- cardiac
output and systemic
vascular resistance
- Indications:
o Anitihypertensive drug
o Adjunctive drug for heart failure
o Nephroprotection for diabetic
patients
- Contraindications
o
PARK; pregnancy,
allergy/angioedema, renal
failure, hyperkalemia
o Pregnancy causes renal damage
in neonate; lung and skeletal
malformations; increase fetal
morbidity and death
o Allergy, especially if pt hasn’t
experienced angioedema w/
ACE inhibitor before, renal
failure, and hyperkalemia ( pot
>5 mEq/L) normal is 3.5 to 5
mEQ/L
- Side Effects
o Fatigue, dizziness, orthostatic
hypotension, hyperkalemia,
angioedema, renal impairment,
dry non-prod cough
o Angioedema common in African
Americans swelling of lips,
throat, tongue
- Interactions
o NSAIDs = renal impairment and
have antagonistic effect and
can lessen anti hypertensives
effect of ACE inhibitor
o Other anti-hypertensives= add
effect
o Potassium supps and
potassium-sparing diuretics =
can increase risk of
hyperkalemia
 Monitor serum
potassium
Angiotensin ll Receptor Blockers
- Losartan, valsartan, candesartan,
olmesartan
- MOA:
o Blocks the binding of
angiotensin ll to the angiotensin
ll receptor sites
o ARBs block both parts of blood
pressure-cardiac output and
systemic vascular resistance
o Do not cause annoying cough
like ACE inhibitors
- Indications
o
-
-
-
-
Excellent anti hypertensive,
adjunctive drug for Hf
Contraindications:
o PARK
o Less likely to cause renal
impairment compared to ACE
Side Effects:
o Fatigue, dizziness,
hyperkalemia, hypotension,
renal impairment
Interactions
o NSAIDs = decrease anti
hypertensive effect= increase
chance of renal impairment
o Potassium supps and
potassium-sparing diuretics
 Normal potassium is
3.5-5
Pts will most likely be on baby aspirin
EC
Nursing indications for ACE and ARBs
- Assessment
o Bp and pulse
o Past hist look for angioedema
o Assess pot levels
o Assess prego
- Diagnosis
o Risk for injury related to
possibility of falling related to
hypostatic hypotension
- Planning
o Bp will be b/w 100/60 or
140/80
- Implementation
o Hold drugs if lower than 100
o Monitor pot levels
o Monitor s/s of angioedema of
angioedema- facial
swelling,swollen lips, even pt
complaining that their tongue
feels thick
o Monitor for dry, hacking cough
(ACE inhibitor). If this occurs,
switch to ARB (prescribed by
doctor). ARB’s are more
expensive
- Patient teaching
o
-
Avoid salt substitutes, b/c made
with pot chloride instead of
sodium chloride
o Rise slowly in stages= avoid
orthostatic hypotension
o Teach pt if they feel numbness
or swollen in face lips tongue
o Do not stop meds abruptly=
rebound hypertension
o Teach pt how to take bp at
home and record readings
Evaluation
o Asses bp again to ensure med is
effective in lowering bp
Calcium Channel Blockers
- Amlodipine, diltiazem, verapamil
- MOA:
o Prevents calcium from entering
calcium channels in vascular
smooth muscle, causing
vasodilation
o Diltiazem and verapamil
decrease heart rate
- Indications:
o Angina
o Hypertension
o SVT
o Migraine/ headaches
o Atrial fibrillation/flutter
- Contraindications
o Allergy
o Acute MI
o 2nd/3rd degree heart block
o Hypotension
- Side effects
o Hypotension
o Palpitations
o Tachycardia
o Bradycardia
o Constipation
 Due to calcium
channels in intestine
being blocked
o Peripheral edema
o Flushing
- Interactions
o
-
-
-
-
-
Additive effects w/ beta
blockers
o Interferes w/ elimination of
digoxin
o Decreased metabolism of
amiodarone
o Grapefruit juice inhibits
metabolism of CCB= toxicity
and severe hypotension
Memory
o They are Very Awesome Drugs
(verapamil, amlodipine,
diltiazem)
Assessment
o Bp and pulse
o Assess cardiac rhythm b/c CCB
contraindicated in 2nd/3rd
degree heart blocks
o Assess for food-drug
interactions look for grapefruit
juice and other
antihypertensives
Diagnosis
o Risk for injury= falling or
orthostatic hypotension
Planning
o BP in range 100/60-140/80
Implementation
o Hold CCB if bp is less than 100
o Monitor fluid retention: ankle
edema, weight gain (daily
weight check)
o Patient teaching
 Rise slowly
 Rebound hypotension,
don’t stop
 Take bp and record
 Weigh daily and report
weight gain of 5 lbs in 2
days
Evaluation
o Assess bp to make sure meds
are working
Diuretic Drugs
-
Potassium wasting and sparing
-
Work by excreting sodium from the
body
Sodium and water leave the body
Increase urinary output= treat fluid
retention = decrease blood volume=
lower bp
Loop Diuretics
- Furosemide, torsemide, bumetanide
- MOA:
o Prevents the resorption of
sodium and water in loop of
henle
- Indications:
o Edema associated w/ heart
failure
o Renal disease/ hepatic disease
o Hypertension
- Contraindications
o Allergy
o Hepatic coma
o Severe electrolyte loss
- Side effects
o Tinnitus
o Dizziness
o Hypokalemia
o Hyperglycemia
o Hyperuricemia (gout like
symptoms w/ furosemide)
o Increase chance of lithium
toxicity
- Interactions
o Additive effects:
 Aminoglycosides
 Vancomycin
 Both cause
nephrotoxicity
o Hypokalemia
 Corticosteroids
 Digoxin (low pot = risk
for toxicity)
o Antagonism
 Antidiabetic drugs
 Due to effects of
hyperglycemia
Osmotic Diuretics
- Mannitol
- MOA
o
-
-
-
Works along the entire
nephron, causes excretion of
mostly water, very little loss of
electrolytes
Indications
o Acute kidney injury
o Increased intracranial pressure
o Cerebral edema
Contraindications
o Allergy
o Renal disease
o Pulmonary edema
o Active intracranial bleeding
Side Effects
o Convulsions
o Thrombophlebitis
o Pulmonary congestion
Potassium-Sparing Diuretics
- Spironolactone
- MOA
o Work in collecting duct and
distal convoluted tubules.
Competitively binds to
aldosterone receptors,
therefore blocking the
resorption of sodium and water
that is induce by aldosterone
system
o Remember: aldosterone wastes
pot. By blocking aldosterone,
pot is retained w/ the pot
sparing diuretics.
o Pot loving drugs
- Indications
o Hypertension
o HF (blocks cardiac remodeling)
o Edema associated w/ liver
disorders
o Portal vein hypertension
- Contraindications
o Allergy
o Hyperkalemia
o Severe renal failure
- Side effects
o Dizziness
o Headache
o Urinary frequency
-
o Hyperkalemia
o Weakness
Interactions
o ACE inhibitors, ARBS or
potassium supplements
 Hyperkalemia
o Lithium
 Lithium toxicity
Thiazides and Thiazide- Like Diuretics
- first line drug for hypertension
- Hydrocholorothiazide
- MOA
o Prevent the resorption of
sodium, water, and pot in the
distal convoluted tubule
o Hates pot
- Indications
o Hypertension
o edema
- Contraindications
o Allergy
o Hepatic coma
o Anuria
o Severe renal failure
- Side effects
o Hypokalemia
o Hypotension
o Hyperglycemia
o Hyperuricemia
- Interactions
o Digoxin = low pot = digoxin
toxicity
o Antidiabetic drugs =
hyperglycemia effect
o Lithium= prevent resorption of
sodium = increase effects of
lithium toxicity
o Corticosteroids = hypokalemia
- Assessment
o Assess pot level ( if pot wasting
diuretic (loop or thiazide) look
for low pot; if pot sparing
diuretic look for high pot
o Assess for drug interactions
o Assess past medical history
o Assess weight for baseline
o Assess vital signs; bp
-
-
-
-
Diagnosis
o Decreased cardiac output
related to decreased volume
due to diuresis of fluid
Planning
o Pt will have balance intake and
output ratios
Implementation
o Monitor bp
o Monitor fluid retention-edema
and weight gain
o Monitor I&O
o Monitor potassium levels and
for signs of electrolyte
imbalances
o If giving furosemide IV, give at
rate no faster than 20 mg/min.
if given to fast= hearing loss
o Monitor for gout-like symptoms
w/ loop and thiazide diuretics
o Check blood sugar more freq in
diabetic pt’s prescribed loop or
thiazide diuretics
o Pt teaching:
 Rise slow
 Increase pot intake (pot
wasting) or decrease
pot intake (pot sparing)
 Weigh daily in same
clothes at same time.
Report if 5 lbs in 2 days
 Teach diabetic pts that
thiazide diuretics and
loop diuretics cause
hyperglycemia and may
decrease the
effectiveness of their
antidiabetic medication
Evaluation
o Pt has increased ouput. Daily
weight shows decrease in pt
weight
Potassium Replacement
- Oral
- With/after meals
- Pt remain upright 30 min
- Side effects
-
o
GI distress, ulceration, bleeding,
oral ulcers, esophageal ulcers
o
Only for severe hypokalemia or
pts who cannot tolerate PO pot
Dangerous and can cause fatal
cardiac dysrthmias
Ensure continuous cardiac
monitor
Do not administer undiluted
Do not administer by IV bolus
(rapid push)
Rate should not exceed 10
mEq/hr for Med/surg or 20
mEq/hr ICU
IV
o
o
o
o
o
Heart Failure Drugs
-
-
-
-
-
Cardiac output: amount of blood
ejected from the left ventricle
o HR x Stroke volume
Stroke volume: output of blood from
heart per contraction
Ejection fraction: measurement of %
blood leaving heart (ventricles) each
time it contracts
Contractility: performance of cardiac
muscle to contract
Frank Starling’s Mechanism: match the
output of heart to constant changes in
right and left cardiac output and to
adjust rapidly to sudden changes in
preload conditions
o Up preload= up contractility =
up SV
Preload: amount of blood in ventricle at
end of diastole
Afterload: peripheral vascular
resistance
Lab is B-type natriuretic peptide (BNP).
o 100 pg/mL
o >100 pg/mL = HF
o Slightly above 100 is normal in
older-adult client
Angiotensin converting enzyme
inhibitors: help reduce circulating
volume by blocking action of
aldosterone and decrease peripheral
vascular resistance by causing
vasodilation
- Angiotensin ll receptor blocker: similar
to ACE inhibitors in results but achieves
the desired effect by blocking the
receptor sites for angiotensin ll instead
of blocking the formation of angiotensin
ll
- Beta- Blockers: (metoprolol and
carbedilol) blocks adrenergic beta 1
receptors which decreases the
workload of the heart and decreases
oxygen demand and decreases
peripheral vascular resistance
- Diuretics: work by decreasing
circulating blood volume, which helps
reduce preload. Furosemide and
spironolactone are commonly used in
Tx of HF.
- Nonpharmacologial Tx:
o Limit salt intake
o Limit or avoid alcohol
o Stop smoking
o Decrease saturated fat intake
o Perform milk exercise as
possible
Cardiac Glycosides: digoxin
- Harder, stronger, slower
- MOA
o + inotropic
 Increases myocardial
contractility
 Affects SV
o + chronotropic
 Increase in HR
o - chronotropic
 Decreases HR
o + dromotropic
 Increase in conduction
of cardiac electrical
impulses
o – dromotropic
 Decreases conduction
o Increases SV
 Increases cardiac
output
o Others


-
-
-
-
Reduces heart size
during diastole,
decreases venous bp,
and vein engorgement,
increases coronary
circulation, promotes
tissue perfusion and
diuresis
These effects
strengthen cardiac,
peripheral, and kidney
function by enhancing
cardiac output,
decreasing preload,
improving blood flow to
the periphery and
kidneys, decreasing
edema, promoting fluid
excretion= fluid
retention decreasing in
lungs
Indication
o Tx of CHP
o Atrial fib
o Atrial flutter
Contraindications
o Allergy
o 2nd/3rd degree heart block
o Ventricular fib
Side Effects
o Bradycardia
o Hypotension
Toxicity and Management of Overdose
o Monitor digoxin level
o Therapeutic range: 0.5-2 ng/mL,
toxicity >2 ng/mL
o S/S of toxicity
 Anorexia, nausea,
vomiting, diarrhea,
bradycardia, cardiac
dysrhythmias, colored
vision changes (yellow,
green, or purple halo
vision) confusion,
delirium
 Severe toxicity = severe
cardiac effects:

-
-
-
-
dysrhythmias or neuro
effects
Antidote: digoxin
Immune Fab (digibind)
Interactions
o Pot wasting diuretics (low pot =
digoxin toxicity)
o Herbal supps
 St jons wart = reduce
digoxin levels
 Food interactions: high
fiber meals
 Digoxin should be
admin 1 hr before or 2
hrs after high fiber meal
to help prevent
decreased absorption
Assessment
o Past med hist: kidney diseases.
Impaired renal function can
decrease renal excretion of
digoxin= toxicity
o Current meds: drug
interactions. HF is commonly tx
w/ diuretics (loop). Pt may be
on furosemide, which is okay,
just monitor pot level more
closely, and will also be on pot
supplement
o Assess bp and pulse. If pulse
less than do not administer. If
apical pulse is greater than 120
= sign of toxicity and dose
should be withheld
o Assess for digoxin toxicity prior
to admin
o Assess digoxin level
o Assess pot level; if low = digoxin
tox
Diagnosis
o Decrease CO
o Ineffective cardiac and cerebral
perfusion
Planning
o HR 60-100 BPM
Implementation
o Monitor apical pulse before
admin
o
o
o
-
-
Monitor digoxin level
Weight pt daily
Monitor K level b/c
hypokalemia potentiates effects
of digoxin and can lead to
digoxin toxicity
o Check dose for safety
o Monitor signs of toxicity
Pt teaching
o Teach how to take pulse
o Teach importance of med
compliance and lifestyle mods
o Teach pt to weight themselves
daily and record
o Report 5 lbs in 2 days
o Teach S/S of digoxin toxicity
and report
o Teach pt to increase pot in diet
(fresh fruit, dried fruit, fruit
juices and veggies)
o Teach to avoid high fiber meals
when taking digoxin. Often
dose in morning
Evaluation
o Evaluate drug effectiveness
(decreased HR)
o Digoxin level w/in therapeutic
range
o Diuresis is increased and fluid
retention is decreased (weight
and I&O)
Treating CHF
UNLOAD FAST
U- upright position
N- nitrates
L- Lasix
O- oxygen
A- ACE inhibitors
D- digoxin
F- fluids (decrease)
A-Afterload (decrease)
S- Sodium restriction
T- test (dig level, ABG’s, Pot level)