Cardiac Medications
Chapter 15: Adrenergic Agonists and Adrenergic Blockers
Nervous System 101:
Autonomic Nervous System
Sympathetic
Parasympathetic
Fight or
Flight
Rest and
Digest
Epinephrine,
Dopamine,
Norepinephrine
Alpha 1, Alpha 2, Beta
1, Beta 2
Acetylcholinesterase
Muscarinic and nicotinic
Sympathetic Receptors



Alpha Receptors:
o Alpha 1:
 Blood vessels: vasoconstriction (raise our BP), increased BP increased contractibility of
the heart
 Eyes: mydriasis (pupil dilation)
 We need to see better in the fight-or-flight response
 Bladder: relaxation
 Bladder is pretty much shut down
 Prostate: contraction
 At this time, it is not time for the prostate to be active
o Alpha 2: more narrowly focused; inhibits norepinephrine release
 Blood vessels: decreased blood pressure
 Smooth muscle (GI tract): decreased GI motility and tone
Beta Receptors:
o Beta 1: located within the kidneys, but predominately in the heart itself
 Heart: increased heart contraction, increased HR, increase blood pressure
 Kidney: increased renin secretion, increased angiotensin, increased blood pressure
 RAAS System
o Beta 2:
 Smooth muscle (GI tract): decreased GI motility and tone
 Lungs: bronchodilation
 Uterus: relaxation of uterine smooth muscle
 Liver: activation of glycogenolysis, increased blood sugar
 Breakdown of glycogen use carefully with diabetic patients
Dopaminergic Receptors
o Located in the renal. mesenteric, coronary, and cerebral arteries
o Causes vasodilation  increased blood flow
o Dopamine is the only neurotransmitter/medication that can activate this receptor
 Dopamine is a normal neurotransmitter found in the body, but there is also synthetic
dopamine that is made in a lab that can activate the receptor sites when concentrations of
dopamine in the body
o Given when patients are septic because they are hypotensive increases blood flow increase
in blood pressure
Classification of Adrenergic Agonists/Sympathomimetics



Direct acting
o Epinephrine (Epi) and norepinephrine (NE)
o Directly stimulates adrenergic receptor
 Mimic normal neurotransmitters
o Stimulates normal neurotransmitters
o Main focus
Indirect Acting
o Amphetamine
o Stimulates the release of norepinephrine from terminal nerve endings
o The “middleman”
Mixed Acting
o Ephedrine
o Stimulates adrenergic receptor sites and stimulates the release of NE from terminal nerve
endings
o Lazier has people do work for them then decides to do work themselves
Catecholamines


Catecholamines
o Chemical structures of a substance
o Produce a sympathetic response
 Structures we have produced in a lab to mimic the synthetic receptors
o Endogenous or sympathetic
 Endogenous: epinephrine, norepinephrine, dopamine
 Can be produced in the body, but can also be created in the lab
 Sympathetic: isoproterenol and dobutamine (synthetic version of dopamine)
 Cannot be found in the body, so they have to be created in a lab
Noncatecholamines
o Stimulate adrenergic receptors
 Act on the receptor sites themselves
 Work like catecholamines, but work on the receptor sites
o Most often have a longer duration than endogenous and synthetic versions
o Examples:
 Phenylephrine
 Can be found in Sudafed
 Metaproterenol
 Albuterol
 Inhaler
Epinephrine (Medication)







Non-Selective
o Excites 3 different receptor sites equally
 Alpha 1, Beta 1, Beta 2
o Gets into the body quickly
Action
o Increase blood pressure (Alpha 1)
 Given during CPR (cardiac rescue medication)
o Increase heart rate (Beta 1)
o Bronchodilation (Beta 2)
 This is why we give medication in respiratory emergencies and anaphylactic reactions 
helps open up airways
Contraindications/caution
o Dysrhythmias, HTN
 Due to increase in heart rate and blood pressure
 Can put people into a lethal arrhythmia
 Could induce stroke-like symptoms
 If patient already has high blood pressure
o Hyperthyroidism (thyroid storm), DM
 Excites Beta 2 receptorsglycogenolysis which causes an increase in blood sugar
(closely monitor blood sugar)
o Pregnancy
 When they are pregnant, mom shares circulatory system with babies
 When the mothers heart rate and blood pressure are increased, the baby’s is as well
 Only given when absolutely critical  cardiac arrest or anaphylactic reactions
Action:
o Inotropic
 Positive inotropic effect  strengthen the force of the heartbeat
o Vasoconstrictor
o Bronchodilator
o Oral or lip swelling could also indicate airway constriction
Uses:
o Anaphylaxis/anaphylactic shock
o Bronchospasms
 Bad asthmatic attacks
o Cardiogenic shock/cardiac arrest (CPR)
Side effects:
o Cardiac
o Decreased renal perfusion
 Due to increase in blood pressure and heart rate
 The faster the heart pumps, the less blood coming out with each pump, thus reducing the
amount of blood perfusing the kidneys
Interactions:
o Beta-blockers
 Beta-blockers block the receptor sites; therefore, Epi cannot reach its target site; they
work against each other
o Digoxin


 Antiarrhythmic  will interact with Epi
Chart 15.1 on page 202
Nursing interventions:
o Monitor BP, HR, and urine output
 Monitoring urine output due to decrease in renal perfusion
o Report rhythm changes, tremors, dizziness, HTN, and palpations
 Sinus tachycardia  want to be cautious about and notify HCP
 Teach that they may feel tremor or shakes  heart will be pumping and they will not
know why
 Dizziness due to increase in heart rate
o Monitor IV site for infiltration
 Especially if giving an Epi drip
 Antidote: phentolamine mesylate
 Will do the opposite of epinephrine
 If reaching subcutaneous tissue
o Avoid cold medications/diet pills
 CONTAIN CAFFEINE will go into tachycardia
 Recommended for elderly patients  OTC cold medications; safe if taking any heart
medications (if they have a heart on the label)
o Avoid when breastfeeding
 Pump and dump
 Pumping breast milk and dumping it out
 Will reach the baby’s bloodstream and cause increase in blood mediations
o Avoid continuous use of adrenergic nasal sprays
 Adrenergic: does the same thing as epinephrine
Other Cardiac Adrenergic Agonists



Dobutamine
o Synthetic catecholamine
o Increases myocardial force and cardiac output
 Increases contractions and strength of contractions  providing more blood to the rest of
the body
o Used with heart failure and bypass surgery
o Not normally produced in the body  synthetic catecholamine
Dopamine
o The SYNTHETIC dopamine
o Increases BP and cardiac output (CO), and increases renal blood flow
o Used to treat mild kidney failure due to low CO
 Stage 1 renal disease
Norepinephrine
o Not given as often as epinephrine  given if Epi doesn’t seem to be working
o Stimulates the heart in cardiac arrest
o Vasoconstricts and increases blood pressure in hypotension and shock (septic shock, cardiac
shock, etc.)
Albuterol

Selective





o Acts on Beta 2 receptors
o Bronchodilation
 Used for respiratory distress and asthma
o Glycogenolysis (liver)
 NEED TO MONITOR BLOOD SUGAR
Uses
o Asthma, COPD, bronchospasm, chronic bronchitis
Side effects/adverse reactions
o Restlessness (agitated), nervousness, restless
o Tachycardia, dizziness, hallucinations (in severe cases; can see auras or different colors)
Drug interactions
o May increase other sympathomimetics and tricyclic antidepressants
 Want to be VERY cautious when given with tricyclic antidepressants
o Beta blockers  due to the blockage of beta receptors
Chart 15.2 (p. 204)
WE USE ALBUTEROL BECAUSE IT WORKS ON THE BETA 2 RECEPTORS
Central Acting Alpha Adrenergic Agonists


Alpha receptor; adrenergic agonist  WORKS WITH THE SYMPATHETIC NERVOUS SYSTEM
Clonidine
o Primarily used to treat hypertension
o Selective Alpha 2 agonist
 Only will work on Alpha 2 receptor sites
o Contraindication in liver disease
 Works on liver and causes glycogenolysis
 Make the liver pick up in production
o Side effects
 Edema, bradycardia
 Drowsiness/dizziness
 Dry mouth
 Number one complaint
 Stimulates alpha receptors  dries up secretions
 Suck on ice chips, chew on sugar-free gum or candy, or spongy oral swabs if
NPO
 Educate that this is a side effect, not a reason to stop taking the medication
o Nursing interventions
 Monitor BMP and I&Os
 Clonidine will retain sodium and water
 Assess and monitor VS
 Used to treat hypertension
 Blood pressure and heart rate before and after administration
 Treat c/o dry mouth
 Heavy machinery  educate!
 Due to drowsiness effect
 Know how medication affects them before driving or operating machinery
Adrenergic Antagonists




Works against or neutralizes effects of sympathetic nervous system
Blocks the effect of the adrenergic neurotransmitter
o Blocks the receptor site or inhibits the release of epinephrine and norepinephrine
Works on both alpha and beta receptor sites
o Normally on one or the other, but does not rule out that it will not work on both
o Classified based on their target receptor site
o Alpha 1 antagonist: vasodilation, decreased BP, pupil constriction, and reflex tachycardia
 For male patients, prostate will relax which will suppress ejaculation  will be more
difficult or inhibited entirely; EDUCATE
o Beta 1 antagonist: reduces cardiac contractility, decreases pulse
o Beta 2 antagonist: bronchoconstriction, contracts uterus, inhibits glycogenolysis
Medications
o TABLE 15.4
Alpha Blockers (-zosin)





Selective
o Blocks alpha 1 receptors
Non-selective
o Blocks both alpha receptor sites
Action
o Promotes vasodilation  want more blood flow
Use
o Decreases symptoms of benign prostatic hyperplasia (BPH) and peripheral vascular disease
(PVD)
Medications
o Prazosin and Terazosin
o These drugs are contraindicated or used with caution in cases of asthma, bradycardia, HF, severe
renal or hepatic disease, hypothyroidism, or if the patient has had a previous stroke
Beta Blockers (-lol)






Selective
o Blocks beta 1: decreased BP and HR
o Blocks beta 2: bronchoconstriction
Non-selective
o Blocks both beta receptor sites
Action
o Decreases CO and blocks the release of Epinephrine and Norepinephrine
Use
o Mild to moderate hypertension, angina, migraines, mild dysrhythmias, and heart failure
 Used in conjunction with other heart medications when used to treat heart failure
Contraindications/caution
o Patients with COPD/asthma
 Because of bronchoconstriction  may make it harder for these patients to breathe
Nursing considerations:
o Because beta blockers decrease heart rate  HAVE TO HAVE A HEART RATE BEFORE
ADMINISTERING BETA BLOCKERS
 IF HEART RATE IS LESS THAN 50, DO NOT GIVE THIS MEDICATION
o Always monitor vital signs (BP) and lung sounds
o Teach our patients to NEVER discontinue medication abruptly
 Can cause tachycardia, rebound blood pressure higher than before, can cause a stroke or
dysrhythmias
 If not tolerating, taper off over a 1-2 week period
o Avoid postural hypotension
 Have patients rise or stand up slowly
 Dangle feet on edge of bed for 20-30 seconds
o Make sure patients don’t operate vehicles or heavy machinery until they know how it affects
them because it can cause dizziness
Propranolol




Uses
o Angina, dysrhythmias, hypertension, heart failure
Contraindications
o Asthma and COPD patients
Side effects/adverse reactions
o Dizziness, low blood pressure, low heart rate
o Male patients: will cause impatience, decrease libido and alopecia (reversible)
 Can cause them to be noncompliant or stop medication  MUST EDUCATE
Drug interactions
o Decreased effect of phenytoin, NSAIDs, caffeine, and theophylline
o Heart block may occur when used with CCB and Digoxin
Atenolol




Selective
o Blocks beta 1 only, decreases blood pressure and heart rate with fewer side effects
Uses
o High blood pressure and angina
Side effects/adverse reactions
o HA, dizziness, hypoglycemia, fatigue, depression, and blood dyscrasias
Drug interactions
o Decreased effects with NSAIDs
o Decreased effects with alpha blockers, atropine, and anticholinergics
 Anticholinergics block the cholinergic/parasympathetic nervous system
o Increased risk of hypoglycemia with insulin and sulfonylureas
 Monitor blood sugar levels
Chapter 16: Cholinergic Agonists and Antagonists
Cholinergic Agonists

Stimulates the PNS



o Rest and digest
o Muscarinic and nicotinic receptor sites
o Mimics the PNS neurotransmitter acetylcholine/acetylcholinesterase
Cholinergic Receptors
o Muscarinic receptors
 Affects smooth muscles
o Nicotinic Receptors
 Affects skeletal muscles
Works in the eye, lungs, heart, blood vessels, GI, bladder, and salivary glands
Also known as parasympathomimetics, muscarinic agonists, or cholinesterase inhibitors
Effects of Cholinergic Agonists






Heart
o Decreases heart rate and blood pressure, vasodilation, slows AV conduction
 Rest and digest state
Eyes
o Constricts pupils, increases accommodation, increases lacrimation
 We no longer need more light let in to see better
Lungs
o Bronchial constriction, increases secretions
Urinary
o Stimulates urination by allowing bladder to relax
GI
o Increases gastric secretions/emptying
Muscles
o Maintains muscle strength and tone
 Will not contract like we need in fight or flight, but will maintain tone and strength
Direct Acting Cholinergic Agonists




Selective to muscarinic receptors
o Smooth muscle receptor sites
Located in the smooth muscles
o Heart, GI, GU, glands
Medications
o Metoclopramide
 Increases gastric emptying
 Used a lot in GI disorders
o Pilocarpine
 Constricts pupils
o Bethanechol
 Increases urination
 Used in patients that have issues emptying the bladder
Side Effects/Adverse Reactions
o Blurred vision, miosis
o Hypotension, bradycardia
o Increased secretions, GI distress (stomach is ramping up)
o Bronchoconstriction

Contraindications
o Bradycardia, hypotension, COPD, peptic ulcer, Parkinsonism, hyperthyroidism
 Not used to cure, but used to help in Parkinsonism and hyperthyroidism
Bethanechol




Cholinergic agonist  will lower blood pressure and heart rate
o Due to decrease in blood pressure, bethanechol can cause postural hypotension
Interventions
o Monitor heart rate and blood pressure
o Teach patient to rise slowly (to prevent orthostatic hypotension)
o Record/monitor I&Os
o Assess and monitor lung sounds  bronchoconstriction
o Give 1 hour before meals (ac) or 2 hours after meals (pc)
o Assess/monitor bowel sounds  to make sure the GI tract is not over doing it
Uses
o Used to increase urination
o Only to be used for urinary retention (not caused by an obstruction)
 From injury, will only increase bladder contraction to get urine out
 More of a muscle issue
Antidote
o Atropine
Indirect-Acting Cholinergic Agonists





Work with the parasympathetic  do not work directly, but rather work around it
Functions
o Breaks down AChE into choline and acetic acid
o Allows Ach to activate muscarinic and nicotinic (cholinergic) receptors
Effects
o Stimulates skeletal muscle; increases tone
o Greater GI motility, but can cause bradycardia, miosis
o Bronchial constriction, promotes urination
Contraindications/caution
o Intestinal and urinary obstruction; asthma/COPD
Classifications
o Reversible (Neostigmine, Physostigmine, and Donepezil)
 Medications can be counteracted if there is too much
 Used to treat glaucoma and used to improve muscle strength in myasthenia gravis
patients
o Irreversible (Echothiophate)
 Very hard to reverse
 Used to treat glaucoma, but can be seen in nerve agents and insecticides
SLUDGE



Too much of a cholinergic agonist  cholinergic crisis
Parasympathetic system is working in overdrive
S: salivation







L: lacrimation (crying)
U: urination
D: diarrhea
G: gastric or vomiting
E: emesis (vomiting)
Three killer B’s
o Bradycardia
o Bronchospasm
o Bronchorrhea (respiratory depression)
To reverse a cholinergic crisis  ATROPINE
Reversible vs. Irreversible


Reversible
o Pupil constriction in glaucoma, increases muscle strength in myasthenia gravis
o Muscle cramps, twitching, bradycardia, GI cramps
Irreversible (Echothiophate)
o Produces pupillary constriction in glaucoma, potent due to long lasting effects
 Takes days to weeks for the medication to leave the system
o Increased secretions, bradycardia, GI effects
Anticholinergics




Action
o Inhibit the action of Ach by occupying Ach receptors
o By blocking the parasympathetic nerves, the sympathetic system will dominate
AKA
o Cholinergic blocking agonists, cholinergic or muscarinic antagonists, antiparasympathetic
agents, antimuscarinic agents, and antispasmodics, parasympatholytic
Effects
o Heart
 Large doses will increase heart rate
o Lungs
 Bronchodilation
o GI
 Slows motility
o GU
 Increases sphincter constriction
o Eye
 Dilates pupils, decreases accommodation
o Glands
 Decreases secretions
o CNS
 Decreases tremors and rigidity
 Why we use in Parkinson patients
Too many anticholinergics:
o Hot as Hare
 High temperatures, no sweating
o Mad as a Hatter


 Confusion, delirium
o Red as a Beet
 Flushed face, tachycardia
o Dry as a Bone
 Decreased secretions, thirsty, dry mouth
REMEMBER: anticholinergic toxicity can mimic a psychotic break or psychotic episode
o Psychotic breaks DO NOT have dry mouth, hyperthermia, or dry skin
Treatment for anticholinergic crisis: physostigmine
Atropine




Most common use: when patients are bradycardic for no reason & are not tolerating the decreased heart
rate
Action
o Increases pulse, decreases motility and peristalsis, as well as salivary secretions
Side effects/adverse effects
o Dry mouth and skin, blurred vision, photophobia, tachycardia, congestion, flushing, and urinary
retention
o DO NOT WANT TO USE IN GLAUCOMA  PUPIL CONSTRICTION
o Used as a pre-op intervention to decrease salivary secretions  want to prevent aspiration
Nursing interventions
o Monitor vital signs, urinary output, and bowel sounds
 Watch blood pressure and heart rate
o Monitor safety
 Dizziness, tachycardia, low blood pressure
o Provide mouth care and eyedrops
 Drying of secretions
o Avoid hot environments
 When we dry up secretions, they do not have the ability to sweat
o Avoid ETOH, cigarettes, caffeine, and ASA at bedtime
 Can counteract the normal side effects
o Wear sunglasses in bright light  photophobia
o Teach to avoid motor vehicles or participating in activities which require alertness
o Encourage intake of foods high in fiber
 Because atropine decreases GI motility, which leads to constipation
o These medications can cause confusions  bed alarm to improve safety
Motion Sickness


Treated using anticholinergics (classified as antihistamines)
o Scopolamine
o Dimenhydrinate (Dramamine)
o Meclizine HCl (Antivert)
Side Effects
o Dries secretions, facial flushing, muscle weakness, drowsiness, hypotension, and tachycardia
Chapter 37: Cardiac Glycosides, Antianginals, and Antidysrhythmics
Heart Failure 101




Patho
o In acute heart failure, the heart muscle weakens and enlarges (cardiomegaly)
o It then loses its ability to pump blood adequately
o Compensatory mechanisms then fail
 Decrease in cardiac output  will enter into acute heart failure
o Results in congestion of blood in the lungs (left sided) or periphery (right sided)
Right sided
o Blood backs up in the periphery
o Right ventricle cannot pump sufficiently to pump blood into the lungs for oxygenation
Left Sided
o Blood backs up in the lungs
o Left ventricle cannot work efficiently to pump blood into systemic circulation
BNP
o How we judge heart failure
o Brain natriuretic peptide
o Secreted from atrial cardiac cells and aids in the diagnosis of HF
o Normal Range: < 100 pg/mL
 Can slightly elevate in patients that are obese or elderly
Cardiac Glycosides






Digitalis preparations (Digoxin)
Actions
o Positive inotropic: increases myocardial contractility
o Negative chronotropic: decreases heart rate
o Negative dromotropic: decreases conduction
o Increase in stroke volume=increase in cardiac output
Uses
o Heart failure
o Atrial fibrillation (A-fib)
o Atrial flutter (A-flutter)
Contraindications
o Certain dysrhythmias
 Bradycardia
o Hypothyroidism
o Renal disease
 Will mess with the kidney issues  lowers heart rate, therefore lowering kidney
perfusion
Drug interactions  DOES NOT PLAY WELL WITH OTHERS
o Diuretics: hypokalemia  can send patients into a worsening dysrhythmia
o Glucocorticoids: Na retention  hypernatremia
o Antacids: decreased absorptions  patient is not receiving all of the effects they should
o Use caution with herbal supplements  because digoxin is derived from a plant
Side Effects
o Anorexia, HA, fatigue
o Visual disturbances
o Drowsiness


o Bradycardia
Interventions
o Apical pulse FOR A FULL MINUTE
 Atrium could be contracting faster than the ventricles
o Teach signs of toxicity
o Hold if heart rate is <60
o Monitor Dig levels and K+ (whether they are in the hospital or at home)
o Monitor for edema
 If we are holding on to sodium, we are also holding onto water
Dig Toxicity
o Severe bradycardia
o Intense headaches that lead to visual disturbances: white/green/yellow halos
Angina





Acute cardiac pain caused by a temporary inadequate blood flow to the myocardium either due to plaque
occlusions, or spasms of the coronary arteries
o Should alert the person that their heart isn’t as well as it should be; Precursor to a heart attack
Classic
o Occurs with predictable stress or exertion; resolves with rest
 Ex: running on a treadmill
Unstable
o Occurs frequently with progressive severity unrelated to activity; not resolved with rest
o Not influenced by stress/exertion; unpredictable in intensity
 “What were you doing when it started?”
CLASSIC AND UNSTABLE ANGINA ARE BIG PRECURSORS OF A POTENTIAL MI
Variant
o Occurs during rest
o Due to the coronary vasospasms
o AKA Printzmetal or vasospastic
Antianginal Drugs




Nitrates
o Reduction of venous tone
o Decreases workload of heart
o Vasodilation
Beta Blockers
o Decreases workload of the heart and oxygen demands
CCB
o Decreases workload of the heart and oxygen demands
Nonpharmacological treatments:
o Avoid heavy meals
o Quit smoking
o Avoid extreme weather changes (variant)
o Avoid/decrease strenuous exercise
o Emotional upset/stress
Nitrates





Nitroglycerin
o Action
 Vascular and coronary vasodilation
 Decreases preload and afterload
 Heart will not stretch as much and will not have to work as much
o Contraindications
 Hypotension, increased ICP, severe anemia, on erectile dysfunction (ED) medications
 Never give to a patient with a systolic BP of 100
o Side effects/adverse reactions
 Headache!!!  can give OTC non-opioid medications (Tylenol)
 Decreased BP, vasodilation, reflexive tachycardia
 Fatigue and mental status changes
o Transdermal patch
 Apply to hairless area
 Use new patch-new site- every day  educate patient to rotate sites
o Patch free hours (10-12 hour gap between each patch)
o Wear gloves!!!
o Do not apply in areas where defibrillation may be needed  patches usually go on arms
Oral extended-release capsule and tablet
o Do not chew or crush
o Given sublingually!!!!
Aerosol spray (inhalation, translingual)
o As the nurse, do not inhale  wear a mask upon administration!
Take one on the onset of angina; if no relief in 5 minutes, call 911. Can take one every 5 minutes for up
to 3 doses total
Assess vitals (BP and HR) and pain scale every 5 minutes (before each dose) if in the hospital
Beta Blockers



Decrease heart rate and blood pressure
Decreased workload/O2 demand
Atenolol and Metoprolol
Calcium Channel Blockers



Relax coronary artery spasms  good for vasospastic angina patients (variant)
Decreased peripheral resistance  allows stuff to pass through without the spasms
Amlodipine and diltiazem
Anti-Dysrhythmic Drugs


Arrhythmia vs. dysrhythmia
o Arrhythmia: absence of rhythm (flatline)
o Dysrhythmia: deviation of the normal rate or heart rhythm
Types
o Atrial
 Prevent proper filling of the ventricles and decrease cardiac output
 Can live with these and not even know

o Ventricular
 Life-threatening; causes ineffective filling of the ventricles, leading to decreased or
absent cardiac output  cannot live with these rhythms
Antidysrhythmic drugs
o Goal: restore the cardiac rhythm to normal
o Keeps the dysrhythmias from getting to severe
o Can be prodysrhythmic
o DO NOT WANT THE PATIENT TO GET TO RAPID A-FIB
o Classes (TABLE 37.5)
 Fast (sodium) channel blockers, beta blockers, drug that prolong repolarization, and slow
(Ca+) channel blockers
Class 1




Sodium Channel Blockers (-amide)
o Decreases Na influx into cardiac cells
o Decreased conduction velocity in the cardiac tissues, suppresses automaticity, and increases
recovery time
o Slows down conduction pathway so the conduction has time to get through
Sub classes
o 1A: slows conduction, prolongs repolarization (procainamide, quinidine)
o 1B: slows conduction, shortens repolarization (lidocaine)
 Key medication to treat ventricular dysrhythmias
 Deadly dysrhythmias=LIDOCAINE
o 1C: prolonged conduction with little/no effect on repolarization (flecainide)
Side effects
o Hypotension, heart failure, new or worsening dysrhythmias, N/V/D
Nursing Interventions
o Obtain thorough health and drug history  certain drugs can induce dysrhythmias
o Labs (CBC, CMP, and CEs(cardiac enzymes))  troponin
o Vital signs and continuous cardiac monitoring  will be hooked up to a telemetry machine
o Monitor for signs of edema
o Monitor thyroid, respiratory, and neurological function
o Teach patient to avoid caffeine, ETOH, and tobacco, low sodium diet
 Caffeine and tobacco are stimulants and ETOH has diuretic properties
Chapter 38: Diuretics
Diuretics



Induce voiding  produces fluid removal from the body
Uses
o Decrease hypertension
o Decrease edema in HF and renal/liver disorders
o Main action: diuresis
Action
o Produce diuresis by stopping sodium (Na) and water reabsorption in the kidney tubules


Types
o Thiazide and thiazide-like
o Loop or high-ceiling
o Osmotic
o Carbonic anhydrase inhibitor
o Potassium-sparing
Patho background:
o 50-55% of sodium reabsorption occurs in the proximal tubules
o 35-40% of sodium reabsorption occurs in the Loop of Henle
o 5-10% of sodium reabsorption occurs in the distal tubules
o 2-3% in the collecting ducts
o Diuretics that act of tubules closer to the glomeruli are going to have the greatest effect on
diuresis
Thiazide Diuretics






Action
o Acts on distal convolluted renal tubules
o Promotes Na+, Cl-, and H2O excretion  all follow each other
Use
o Hypertension and peripheral edema
Medications
o Hydrochlorothiazide (HCTZ), Metolazone
Chemistry Abnormalities
o Hypokalemia, hypomagnesemia
o Hypercalcemia, hypochloremia
o Hyperuricemia, hyperglycemia, and hyperlipidemia
Side Effects
o Dizziness, headache, GI distress, electrolyte imbalances
Nursing Interventions
o TEACH TO TAKE IN THE MORNING
o VS, I&Os, daily weight (at home or in the hospital)
o Monitor labs
o Avoid salt and calcium rich foods
o Sun precautions necessary
o Monitor and educate regarding orthostatic hypotension  rise slowly, change position slowly
o Contraindicated in renal patients and patients taking lithium
Loop Diuretics




Action
o Acts on the ascending Loop of Henle
o Excretes Na, H2O, K, Ca, and Mg
Uses
o HTN, pulmonary edema, peripheral edema r/t heart failure, hypercalcemia, and renal disease
Medications
o Furosemide, bumetanide
Caution


o More potent diuretic; can cause more rapid diuresis with decreases in vascular fluid volume,
cardiac output, and BP
Lab changes  sodium, water, potassium, calcium, magnesium
Nursing Considerations
o Same as thiazide diuretics
o Because loop diuretics are more potent, there is an increased risk of hypotension  teach how to
take BP; need to take daily
o Always taken with food to help with absorption
Osmotic Diuretics

Mannitol
o Action
 Increases Na reabsorption in the proximal tubules and Loop of Henle
 Excretes, Na, Cl, K, and H2O
o Uses
 Prevent kidney failure  if creeping towards stage 1, we can use to prolong kidney life
 Decrease ICP and IOP
o Side Effects
 Electrolyte imbalances, pulmonary edema, GI distress, tachycardia, and headache
 Contraindicated in heart and true renal failure
o Need to remember: solution; cannot give if the medication has any crystals present
K+ Sparing Diuretics






Action
o Blocks action of aldosterone
o Promotes Na/H2O excretion and K+ retention
o Mild diuretic; can be used in combo with others; would still need to keep an eye on
Uses
o Edema, HTN, increase urine output (because more mild diuretic), ascites, hypokalemia
Medications
o Spironolactone, amiloride, and triamterene
Side Effects
o Hyperkalemia, GI distress
o Weakness
o Photosensitivity
Contraindications
o Severe renal/hepatic disease and in hyperkalemia  need to look at K+ levels before admin
o Use caution with DM, other HTN meds, and ACE inhibitors (increased K+ levels)
Nursing considerations
o Avoid foods high in potassium