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Cardiovascular
Drugs
NUR104
Fall 2011
Learning Objectives
• Students will be able to:
– Discuss the major categories of drugs as
they relate to the treatment of Cardiac
Disease.
– Describe the major effects of various
medications on cardiac function.
– Discuss major nursing implications when
administering above medications.
Hypertension
• Defined as a consistent elevation of the
systolic or diastolic blood pressure above
140/90mm Hg
• On two elevated readings (sitting and
supine) on separate office visits
• Two types hypertension
– Primary: no known cause
– Secondary: consequence of underlying
disease or condition
CLASSIFICATION OF
HYPERTENSION
Hypertension is classified as follows:
• Prehypertension: BP 120 to 139 / 80 to
89 mm Hg
• Hypertension, Stage 1: BP 140 to 159 /
90 to 99 mm Hg
• Hypertension, Stage 2: systolic BP
greater than or equal to 160 or diastolic BP
greater than or equal to 100 mm Hg.
Goal with hypertension:
• Two primary regulatory factors:
– Blood flow (volume)
– Peripheral Vascular Resistance (PVR)
• Goal is to optimise these two in
order to get pressure below 140/90
mm Hg
o
Pharmacotherapy
•Primary:
•Diuretics
•ACE Inhibitors
•ARBs
•Beta-blockers
•Calcium channel
blockers
•Alternate:
•Alpha1-blockers
•Alpha2-blockers
•Direct-acting vasodilators
•Peripheral adrenergic
antagonist
Diuretics
Therapeutic Effects (overall)
• General site of action is the nephron
structure in the kidney (exact area
depends on drug)
• Increases urine formation and output
resulting in a net loss of H2O from the
body and decreased BP
Loop Diuretics
Mechanism of action:
• Inhibits Na+ and Clresorption in the
loop of Henle and
so H2O (water
follows sodium)
• Dilates blood
vessels
Loop Diuretics
Therapeutic effects:
• Potent diuresis resulting in substantial fluid loss
• Treats edema associated with CHF and hepatic
or renal disease
Adverse effects:
• hypokalemia
• metabolic alkalosis
• dehydration (hypovolemia), leading to
hypotension
• dose-related hearing loss (ototoxicity)
Loop Diuretics
Specific Drugs
• furosemide
• Torsemide
• bumetanide
Nursing actions:
•
•
•
•
Monitor I/O and BP
Monitor effects of Lanoxin (digoxin)
Baseline and close monitoring of K+
Assess for:
• Dehydration
• Hypotension
• Hearing loss
Thiazide
Mechanism of action:
– inhibit the sodium-chloride
transporter in the distal
tubule. Because this
transporter normally only
reabsorbs about 5% of
filtered sodium, these
diuretics are less
efficacious than loop
diuretics in producing
diuresis and natriuresis.
Thiazide
Therapeutic effects:
– Excretion of Na+, Cl-, K+ and H2O
without altering pH
– Treatment of edema
Side effects
– Hypokalemia
– Headache, dizziness
Thiazide
Specific Drug
• Hydrodiuril (hydrochlorthiazide)
• Zaroxolyn (Metolazone)
NCs: Thiazide
Nursing actions:
•
•
•
•
•
•
Monitor I/O, BP and K+
Monitor effects of Lanoxin (digoxin)
Monitor electroytes
Adequate dietary K+
Monitor uric acid
Crosses placenta and into breastmilk
Potassium Sparing Diuretics
Mechanism of action:
• antagonize the actions of aldosterone
(aldosterone receptor antagonists) at
the distal segment of the distal tubule. This
causes more sodium (and water) to pass
into the collecting duct and be excreted in
the urine.
Therapeutics effects:
• Diuresis
• Decreased K+ excretion
Potassium Sparing Diuretics
cont
Adverse effects:
• Electrolyte imbalance with potential
elevation in K+
• Headache, dizziness
Prototype:
• Aldactone (spironolactone)
NCs: Potassium Sparing
Diuretics
Nursing actions:
–
–
–
–
•
•
•
•
Monitor I/O, BP and K+
Monitor effects of Lanoxin (digoxin)
No salt substitutes or K+ rich foods
Contraindicated:
• Pregnancy, lactation
Initial and follow-up uric acid levels
Monitor CBC
Watch for s/s of infection
Spironalactone
• Gynecomastia
• Testicular atrophy
• Hirsutism
Calcium Channel Blockers
Mechanism of action:
• Inhibits transport of calcium into
myocardial and smooth muscle cells
• Dilates peripheral arterioles, decreasing
afterload
• Decreases heart contractility (negative
ionotrope)
• Decreases SA node firing rate and
conductivity of AV node (negative
chronotrope)
Calcium Channel Blockers cont.
Therapeutic Effects:
• Lowers HR and BP- Depending on drug in
class
• Decreases myocardial O2 demand
• Decreases coronary artery spasm
• Decreases angina and rhythm
disturbances
Calcium Channel Blockers cont.
Side effects:
• Bradycardia, reflex tachycardia
• Peripheral edema
Interactions:
• Other antihypertensives and diuretics
(increased hypotensive effects)
Calcium Channel Blockers cont.
Prototypes:
• Calan (verapamil), Cardiazem (diltiazem)
and Norvasc (amlodipine)
Nursing considerations:
• Monitor BP, HR, I/O, daily weight, side
effects
• Focus assessment-cardiac and pulmonary
NCs: Calcium Channel Blockers
• Baseline ECG, HR, BP
• Frequent assessment of VS
• Contraindicated:
• complete heart block
•
•
•
•
Pregnancy Category C
No grapefruit juice
May worsen Heart Failure
Evaluate any c/o chest pain
e
RENIN-ANGIOTENSIN-ALDOSTERONE
SYSTEM (RAAS)
↓Serum Sodium
↓Blood volume
Juxtaglomerular
cells-kidney
RENIN
Angiotensinogen
in plasma
Angiotensin
I Angiotensin-
↑Sodium
resorption
(H2O
resorbed with
sodium); ↑
Blood volume
Via vasoconstriction of arterial smooth muscle
converting
enzyme
Angiotensin II
Kidney
tubules
Intestine,
sweat glands,
Salivary
glands
ALDOSTERONE
Adrenal
Cortex
Angiotensin Converting Enzyme
Inhibitors (ACE-I)- “prils”
• Mechanism: Blocks interaction between
Angiotensin I and Renin, preventing production
of Angiotensin II
• Angiotensin II not produce resulting in
decreased vasoconstriction and decreased
afterload
• Decreased aldosterone production results in
decreased Na and H2O reabsorption so
decreased BP
Angiotensin Converting Enzyme
Inhibitors (ACE-I)- “prils” cont.
• Adverse Effects
– Most common: dry, nonproductive cough
– Dizziness, increased potassium levels
• Interactions: Other antihypertensives and
diuretics (increased hypotensive effects)
• Prototypes:
• Vasotec (enalapril) and Zestril (lisinopril)
te
NCs: ACE Inhibitors
•
•
•
•
•
•
•
•
•
Baseline VS
Captopril- oral dose 1 hour pc
First dose phenomenon
IV: monitor BP carefully
Monitor for Angioedema
Monitor K+, CBC
Assess for S/S infection
Pregnancy Category D
Assess for minor side effects
Angiotensin II Receptor Blockers
(ARB’s)- “sartans”
• Mechanism of action: Blocks binding of
Angiotensin II to its receptor sites
• Therapeutic effects
– Decreased BP: Decreased vasoconstriction,
decreased vascular resistance, decreased afterload
– Major use is afterload reduction in CHF and MI
– Frequently a second line treatment for patients who
do not tolerate ACE-I
Angiotensin II Receptor Blockers
(ARB’s)- “sartans” cont.
• Adverse effects
– Most common is headache
• Interactions: Other antihypertensives and
diuretics (increased hypotensive effects)
• Prototype:
• Cozaar (losartan) and Diovan (valsartan)
Angiotensin II Receptor Blockers
(ARB’s)- “sartans” cont
Nursing considerations
• Monitor BP, I/O, daily weight, side effects
• Monitor Potassium levels and renal function
• Reinforce patient education
• Contraindicated to pregnant women
• Can be taken without regard to food
• First Dose Phenomenon
• Orthostatic BP checks
• Monitor renal, hepatic, and electrolyte level
Beta Blockers- “olols
Mechanism of action:
• Cardioselective: Bind to and block B1 receptors
on the hearts conduction system and throughout
the myocardium
• Nonselective: bind to, and block, B1 and B2
receptors (heart and lungs)
• Decreases heart contractility (Negative
ionotrope) reducing O2 requirements of
myocardial cells
• Decrease SA node firing rate (negative
chronotrope)
Beta Blockers- “olols cont.
Therapeutic Effects
– Decreased heart rate and decreased
myocardial oxygen demand
– Decreased angina
– Fewer rhythm disturbances
– Decreased renin release
Beta Blockers- “olols cont.
Adverse effects:
– Dysrhythmias (bradycardia), heart
failure
– Bronchospasm / bronchoconstriction
– Fatigue, depression, impotence
Interactions:
– Other antihypertensives and diuretics
(increased hypotensive effects)
Beta Blockers- “olols cont.
Prototypes:
– Inderal (propranolol), Lopressor (metoprolol)
and Tenormin (atenolol)
Nursing Actions:
– Monitor BP, HR, I/O, daily weight, side effects
– Focus assessment-cardiac and pulmonary
– Contrindicated with some dysrhythmias, CHF
and some lung diseases
NCs: Beta-adrenergic Blockers
• May take two weeks for optimal therapeutic
response
• Check BP and pulse prior to dose
• Monitor cardiac function
• Assess for:
• Respiratory distress
• Bradycardia, heart block, fatigue, activity
intolerance
• DO NOT STOP SUDDENLY
y
Alpha1-adrenergic Antagonists
Mechanism of action
-selectively inhibits alpha-1 adrenergic
receptors. Blockages of the alpha-1
adrenergic action on the vascular smooth
muscles lead to a decrease in vascular
resistance and antihypertensive activity.
NCs: Alpha1-adrenergic
Blockers
•
•
•
•
First dose phenomenon
Assess BP prior to and during RX
Persistent orthostatic hypotension
Assess for:
• Weakness, dizziness, headache, GI
complaints
• Closely monitor elderly
Direct Vasodilators
• Relaxes smooth muscle in arterioles  <
PVR
• Highly effective but many side effects
(some serious)
• Reflex tachycardia
• Sodium/water retention
• Not a first choice drug
• Primary use: emergency situations where
immediate ↓ in BP is needed
NCs: Direct Vasodilators
•
•
•
•
Monitor: VS, ECG, SpO2 during RX
Assess for increased HR
BP q 5 min if not continuous monitor
Contraindicated: hypersensitivity, CAD,
rheumatic mitral valve disease, CVA, renal
insufficiency, SLE
• Priapism- medical emergency
Direct Vasodilators
• IV Nitroprusside (Nitropress):
• Continuously monitored
• Only dilute in D5W
• Brown color; protect from light
• Minoxidil (Loniten):
• BP & pulse both arms, three positions
• Assess for orthostatic hypotension
• Diazoxide (Hyperstat):
• For hypetensive crisis in L&D
Cardiac Glycosides
• AKA digitalis glycosides
• Group of drugs that inhibit the sodiumpotassium pump, thus increasing
intracellular calcium which causes cardiac
muscle fibers to contract more efficiently
Action Potential
Cardiac Glycosides
Therapeutic Effects
1. Positive Inotropic action
2. Negative Chronotropic action
3. Negative Dromotropic effect
Inotropes
Inotropes
• Agents that affect myocardial contraction
• Positive Inotropes
– Cardiac glycosides
– Catecholamines
• Negative Inotropes
– BB
– CCB
– Class IA & IC anti-arrhythmics
Class Participation
Which of the following is an
example of a positive inotrope?
a) Docusate
b) Digoxin
c) HCTZ
d) Propranolol
e) Nitroglycerin
Class Participation
Which of the following is an
example of a positive inotrope?
a) Docusate
b) Digoxin
c) HCTZ
d) Propranolol
e) Nitroglycerin
Cardiac Glycosides
• Prototype: Digoxin (Lanoxin®, Digitek®,
Lanoxicaps®)
Digoxin MOA
Digoxin (cont’d)
 Nursing Responsibilities
– Assess heart rate before administration; if
below 60 bpm withhold the drug.
– Monitor serum potassium
– Assess for signs of Digitalis toxicity
• Bradycardia
• GI manifestations (anorexia, nausea, vomiting and
diarrhea)
• Dysrhythmias
• Altered visual perceptions
• In males: gynecomastia, decreased libido and
impotence
Chronotropes
Chronotropes
• Agents that change heart rate
– affects the nerves controlling the heart
– changes the rhythm produced by the SA node
Chronotropes (cont’d)
• Positive Chronotropes • Negative Chronotropes
–
–
–
–
–
–
Atropine
Quinidine
Dopamine
Dobutamine
Epinephrine
Isuprel
–
–
–
–
–
–
–
Beta-blockers
Acetylcholine
Digoxin
Diltiazem
Verapamil
Ivabradine
Metoprolol
Positive Chronotrope
Prototype: Atropine
• belladonna alkaloid
• d,l-hyoscyamine
• Anticholinergic
• Uses
– Symptomatic bradycardia
– Aspiration prophylaxis
– Produces mydriasis
– Organophosphate toxicity
– Adjunct nerve agent &
insecticide poisoning
Atropine (cont’d)
• MOA
– competitive inhibitor at autonomic postganglionic
cholinergic receptors
• Clinical effects
– “anti-SLUD” Salivation, Lacrimation, Urination,
Digestion, Defecation
– ↓ in salivary bronchial, & sweat gland secretions;
mydriasis; changes in heart rate; contraction of the
bladder detrusor muscle and of the GI smooth
muscle; ↓ gastric secretion; and ↓ GI motility
Nursing Responsibilities
• Monitor HR---note rhythm, quality, and
rate
• Monitor I&O
• Assess for dryness or mucus membranes
• Monitor GI function
Anti-anginal
Drugs
Antianginal Drugs
• Prototype: Nitrites &
Nitrates
• BB
• Calcium Channel
Blockers (CCBs)
Angina Pectoris
Definition:
Angina:
Choking or suffocation.
Pectoris:
Chest.
Angina pectoris, is the medical term used to describe
acute chest pain or discomfort.
Angina occurs when the heart’s need for oxygen
increases beyond the level of oxygen available from
the blood nourishing the heart.
It has 3 types
• Stable Angina
• Un stable angina &
• Variant Angina (Prinzmetal’s or resting angina) :
Types of Angina
• Stable angina:
– People with stable angina have episodes of
chest discomfort that are usually
predictable. That occur on exertion or under
mental or emotional stress.
Normally the chest discomfort is relieved
with rest,
nitroglycerin (GTN) or both.
– It has a stable pattern of onset, duration
and intensity of symptoms.
• Unstable angina:
– It is triggered by an un predictable
degree of exertion or emotion.
– (progressive), more severe than
stable. Characterized by increasing
frequency & severity. Provoked by
less than usual effort, occurring at
rest &
– interferes with pt lifestyle.
• Variant Angina (Prinzmetal’s or resting
angina) :
occur spontaneously with no
relationship to activity. Occurs at rest
due to spasm. Pt discomfort that
occurs rest usually of longer duration.
Appears to by cyclic & often occurs at
about the same time each day (usually
at night). Thought to be caused by
coronary artery spasm
Symptoms of Angina
Nitrites/Nitrates
• Previously known as “coronary dilators”
• Main effect: to produce general
vasodilation of systemic vein & arteries
– ↓preload & ↓afterload
– ↓ cardiac work & oxygen consumption
• 2 main uses
– Angina attacks
– Angina prophylaxis
Class Participation
Which is the PREFERRED route for
nitroglycerin during angina attacks?
a)
b)
c)
d)
e)
Topical (ointment 2%)
IV infusion
Transdermal
SL
Extended release tablets/capsules
Class Participation
Which is the PREFFERED route for
nitroglycerin during angina attacks?
a)
b)
c)
d)
e)
Topical (ointment 2%)
IV infusion
Transdermal
SL
Extended release tablets/capsules
Drug
(Trade Name)
Common
Dosage
Onset
Duration
Amyl nitrate
0.3 ml
inhalation
30-60 sec
10 min
(Vaporole®)
ISDN
2.5 - 10 mg SL 2-5 min
5 - 30 mg po qid
2 - 4 hr
(Nitro-bid®)
2% ointment
15 min
4 - 8 hr
(Nitrostat®)
0.3 - 0.6 mg SL
1-3 min
10 - 45 min
(Nitrogard®)
1,2,3 mg XR tab 30 min
8 - 12 hr
(TransdermNitro®)
2.5 - 15 mg/day 30-60 min
Transdermal
patch
24 hr
(Isordil®)
Nitroglycerin
MOA
Direct relaxation of arterial and venous smooth
muscle
– Venodilation predominates at therapeutic doses
which reduces preload
– Arteriodilation at high doses (high therapeutic/toxic)
which produces hypotension compensated by
sympathetics (heart/vascular)to produce tachycardia
Nitroglycerin (NG)
• Indications
– Angina
– Acute MI
– HF
– HTN
– Hypertensive emergency
– Hypotension induction
– Peri/postoperative HTN
– Pulmonary edema
– Pulmonary HTN
NG (cont’d)
• Dosing
– 1 tablet (0.3 mg, 0.4 mg, or
0.6 mg strength) SL,
dissolved under the tongue
or in buccal pouch
immediately following
indication of anginal attack
– During drug administration,
the patient should rest,
preferably in the sitting
position
– Symptoms typically improve
within 5 minutes. If needed
for immediate relief of stable
angina symptoms, SL
nitroglycerin may be
repeated every 5 minutes as
needed, up to 3 doses
NG (cont’d)
• Adverse Effects
– dizziness or fainting
– flushing of the face or
neck
– headache, this is
common after a dose,
but usually only lasts
for a short time
– irregular heartbeat,
palpitations
– nausea, vomiting
• Contraindication:
– sildenafil (Viagra®)
– tadalafil (Cialis®)
– vardenafil (Levitra®)
• Lab monitoring not
necessary
Antidysrhythmics
Antiarrhythmics
What are Arrhythmias?
• Cardiac disorder of
– Rate
– Rhythm
– Impulse generation
– Conduction of electrical
impulses in the heart
• Causes
– May develop from a
diseased heart
– Consequence of chronic
drug therapy
• Symptoms
– Mild palpitations 
cardiac arrest
• Treatment goal
– Covert arrhythmia to a
normal rhythm
Antidysrhythmics/Antiarrhythmics
• Uses
– restore normal cardiac
rhythm
– Successful conversion
of an arrhythmia
depends on the type of
arrhythmia present
Antidysrhythmics/Antiarrhythmics
• 4 major classes
– Class I
• Class IA
• Class IB
• Class IC
– Class II
– Class III
– Class IV
Cardiac Action Potential
4: resting membrane
potential; steady K+
flux
0: Na+ influx into cell
1: K+ efflux
2: K+ efflux & Ca+
influx
3: K+ efflux
Antiarrthymics: Class I
• Na channel blockers
• Common features
– Local anesthetic activity
– Interferes with movement of Na ions
– Slow conduction velocity
– Prolong refractory period
– Decreases automaticity of the heart
Class IA
• Quinidine (Quinidine sulfate®,
Quinaglute®, Quinidex®, Cardioquin®)
• Disopyramide (Norpace®)
• Procainimide (Procainimide HCI®,
Procan®, Procanabid®, Pronestyl®)
Class 1A – Quinidine
• Derived from cinchona tree
• Depresses both the myocardium & conduction
system
• Overall effect: slows heart rate
• Pharmacokinetics
–
–
–
–
Well absorbed in GI tract after po administration
Metabolized to several active metabolites
Primarily excreted by urinary tract
Cardiac poison when large amounts are present in
blood
Class 1A – Quinidine (cont’d)
• Adverse Effects
– N/V, diarrhea, weakness, fatigue, cinchonism
• Drug Interactions
– Hyperkalemia
– Digitalis
– propranolol
• Monitoring
– CBC
– ECG
– serum quinidine concentrations (target range
2-6 µg/ml or higher)
• CI: AV block
Class IB
•
•
•
•
prototype: Lidocaine (Xylocaine®)
Tocainide (Tonocard®)
Mexiletene (Mexitel®)
Phenytoin (Dilantin®)
Lidocaine – Class IB
• MOA: blocks influx of Na fast channel
• Indication: ventricular arrhythmias
Lidocaine – Class IB (cont’d)
• Common Adverse Effects
– anxiety, nervousness
– dizziness, drowsiness
– feelings of coldness, heat, or numbness; or
pain at the site of the injection
– N/V
• Monitoring
– serum lidocaine concentrations (target range
2-6 µg/ml): parenteral use
Class IC
• prototype: Flecainide (Tambocor®)
• Propafenone (Rhythmol®)
Flecainide – Class IC
• MOA
– Blocks fast Na channels depresses the upstroke of the
action potential, which is manifested as a decrease in the
maximal rate of phase 0 depolarization.
– significantly slow His-Purkinje conduction and cause QRS
widening
– shorten the action potential of Purkinje fibers without
affecting the surrounding myocardial tissue.
• Indications
– Afib
– Atrial flutter
– Ventricular tachycardia prophylaxis
Flecainide – Class IC
• Adverse Reactions
– visual impairment, dizziness, asthenia, edema, abdominal
pain, constipation, headache, fatigue, and tremor, N/V,
arrhea, dyspepsia, anorexia, rash, diplopia, hypoesthesia,
paresthesia, paresis, ataxia, flushing, increased sweating,
vertigo, syncope, somnolence, tinnitus, anxiety, insomnia,
and depression.
• Avoid in
– CHF
– Acute MI
– Hx of MI (LVEF < 30%)
• Monitoring
– ECG
– serum creatinine/BUN: baseline
Class II – Beta Blockers
•
•
•
•
•
•
•
•
•
•
Propranolol (Inderal®)
Acebutolol (Sectral®)
Atenolol (Tenormin®)
Betaxolol (Kerlone®)
Bisoprolol (Zebeta®)
Carvedilol (Coreg®)
Esmolol (Brevibloc®)
Metoprolol(Toprol®, Lopressor®)
Nadolol (Corgard®)
Timolol (Blocadron®)
Propranolol Warning
• 2 situations in which propranolol requires
extreme caution
– AV block
– CHF
– Asthma or emphysema
Class III
• K+ channel blockers
• Drugs:
– Prototype: Amiodarone (Cordarone)
– Bretylium (Bretylol)
– Sotalol (Betapace)
Amiodarone – Class III
MOA
– noncompetitively inhibits alpha- and beta-receptors,
– possesses both vagolytic and calcium-channel
blocking properties
– relaxes both smooth and cardiac muscle
• Indications
– Vfib
– Vtach
Amiodarone – Class III (cont’d)
• Monitoring
– CBC
– chest x-ray
– ECG
– ophthalmologic exam
– thyroid function tests (TFTs)
Class IV
• Ca channel blockers
• Drugs
– Adenosine (Adenocard ®)
– Diltiazim (Cardizem®, Tiazac®)
– Verapamil (Dovera®, Isoptin®, Calan®)
• Clinical Effects
– widen the blood vessels
– may decrease the heart’s pumping strength
Sympathomimetics
Sympathomimetics
• 2 classes:
– α- agonist
• Phenylephrine
• Clonidine
• Oxymetazoline
• Tetrahydralazine
• Xylometazoline
– β-agonist
• Prototype: Epinephrine
• Norepinephrine
• Dopamine
• Dobutamine
• Isoproterenol
• SE:
– hypertension,
– excessive cardiac
stimulation
– cardiac arrhythmias
– Long-term use increases
mortality in heart failure
patients.
• CI
– CAD
Epinephrine
• “fight or flight “hormone
• Aka “adrenaline”
• increases heart rate
and stroke volume
• dilates the pupils
• constricts arterioles in
the skin and
gastrointestinal tract
while dilating arterioles
in skeletal muscles
Epinephrine MOA
Epinephrine (cont’d)
• Indications
–
–
–
–
Vfib
Ventricular asystole
Cardiac arrest
Pulseless electrical
activity
• IV Dosage
– IV: 1 mg (10 ml of a
1:10,000 solution) IV;
may repeat every 3-5
minutes
– Each dose may be
given by peripheral
injection followed by a
20 ml flush of IV fluid.
Epinephrine
• Common Adverse Effects
–
–
–
–
–
–
–
anxiety or nervousness
dry mouth
drowsiness or dizziness
headache
increased sweating
nausea
weakness or tiredness
• Monitoring
– ECG: in patients receiving IV therapy
Vasopressors
Vasopressors
• Vasoconstrictors vs. Vasodilators
• 2 Vasoconstrictor Classes
– Sympathomimetics
– Vasopressin Analogs
• Vasodilators
• Alpha-adrenoceptor antagonists (alpha-blockers)
• Angiotensin converting enzyme (ACE) inhibitors
• Angiotensin receptor blockers (ARBs)
• Beta2-adrenoceptor agonists (b2-agonists)
• Calcium-channel blockers (CCBs)
• Centrally acting sympatholytics
• Direct acting vasodilators
• Endothelin receptor antagonists
• Ganglionic blockers
• Nitrodilators
• Phosphodiesterase inhibitors
• Potassium-channel openers
• Renin inhibitors
Vasoconstrictor
• any agent that produces vasoconstriction
and a rise in blood pressure (usually
understood as increased arterial pressure)
• Drugs
– Prototype: Vasopressin
– Epinephrine
– Dobutamine
– Dopamine
– Norepinephrine
Vasopressin
• aka : “ADH”
• MOA
– ↑ the resorption of
water at the renal
collecting ducts
– Vasoconstrictive
property: stimulates
the contraction of
vascular smooth
muscle in coronary,
splanchnic, GI,
pancreatic, skin, and
muscular vascular
beds
Vasopressin (cont’d)
Indications:
– Cardiac arrest
– Cardiogenic shock
– Cardiopulmonary resuscitation
– Hypotension
– Septic shock
– Diabetes Insipidus
Vasopressin (cont’d)
• Dosage for cardiac arrest including
ventricular asystole and pulseless electrical
activity (PEA) during cardiopulmonary
resuscitation (CPR)
– IV or intraosseous dosage:
• Adults: A single dose of 40 units IV (or intraosseous)
may be given one time to replace the first or second
dose of epinephrine during cardiac arrest
• Do not interrupt cardiopulmonary resuscitation to
administer drug therapy.
Vasopressin (cont’d)
• Adverse Effects
– Cardiovascular: Cardiac arrest; circumoral pallor;
arrhythmias; decreased cardiac output; angina;
myocardial ischemia; peripheral vasoconstriction; and
gangrene
– CNS: Tremor; vertigo; “pounding” in head
– Dermatologic: Sweating; urticaria; cutaneous gangrene
– GI: Abdominal cramps; nausea; vomiting; passage of gas
– Hypersensitivity: Anaphylaxis (cardiac arrest and/or
shock) has been observed shortly after injection
– Respiratory: Bronchial constriction.
• Monitoring
– serum osmolality
– serum Na
Anticoagulants
Antiplatelets/Anticoagulants
• Prevents/interferes with coagulation
• Uses
– deep vein thrombosis (DVTs), pulmonary
embolism, myocardial infarctions & strokes in
those who are predisposed
Types of
Antiplatelets/Anticoagulants
• Antiplatelets
– Aspirin
– Dipyridamole
– Thienopyridines
• Clopidogrel (Plavix)
• Ticlopidine (Ticlid)
– Glycoprotein IIb/IIIa antagonists
• Abciximab (ReoPro)
• Eptifibatide (Integrelin)
• Tirofiban (Aggrastat)
Antiplatelets/Anticoagulants
• Anticoagulants
– Heparin
– LMWH
• Enoxaparin (Lovenox®)
• Dalteparin (Fragmin®)
• Tinzaarin (Innohep®)
– Factor Xa inhibitors
• Fondaparinux (Arixtra®)
– Direct Thrombin Inhibitors
• Argatroban
• Lepirudin (Refludan®)
– Oral Anticoagulants
• Prototype: Warfarin
Coagulation Cascade
Warfarin – Oral Anticoagulant
• MOA: Warfarin inhibits the synthesis of vitamin K-dependent
coagulation factors II, VII, IX, and X and anticoagulant
proteins C and S
Warfarin (cont’d)
• Indications
–
–
–
–
–
Stroke
DVT
Post MI
Afib
Cardiomyopathy
Warfarin Warnings
Bleeding Risk!
• Warfarin can cause major or fatal bleeding
• Risk factors for bleeding
–
–
–
–
–
–
–
–
65 years of age and older
history of GI bleeding
Hypertension
cerebrovascular disease
anemia, malignancy
Trauma
renal function impairment
long duration of warfarin therapy.
• Pregnancy Category X
Warfarin (cont’d)
•
SE
– Hemorrhage: Signs of severe bleeding resulting in the loss of large amounts of
blood depend upon the location and extent of bleeding. Symptoms include:
chest, abdomen, joint, muscle, or other pain; difficult breathing or swallowing;
dizziness; headache; low blood pressure; numbness and tingling; paralysis;
shortness of breath; unexplained shock; unexplained swelling; weakness
Nursing responsibilities
Patients should be instructed about prevention measures to minimize risk of bleeding and to
report immediately to health care provider signs and symptoms of bleeding
–
–
–
–
prothrombin time (PT)
stool guaiac
bleeding
DDIs
• NSAIDs
• 3 G’s
– Garlic
– Ginger
– Ginsing
– Vitamin K intake
Class Participation Question #5:
Which foods are high in vitamin K?
Class Participation Question #5:
Which foods are high in vitamin K?
Fibrinolytic Enzymes
Fibrinolytic Enzymes
• “clotbusters”
• MOA: stimulate the synthesis of
fibrinolysin which breaks the clot into
soluble products
• Drugs
– Urokinase (Abbokinase®)
– Anistreplase (Eminase®)
– Alteplase (Activase®)
– Reteplase (Retevase®)
– Prototype: Streptokinase (Strepase®)
Streptokinase (cont’d)
• Indications
– Acute MI
– Acute ischemic stroke
– Pulmonary embolism
– Lysis of DVT
• Dose Administration
– Parental infusion (usually IV)
– Deep vein or arterial thrombosis
• IV: 250,000 IU over 30 min followed by 100,000 IU
per hour up to 72 hours
Streptokinase (cont’d)
• Adverse Effects
– Hemorrhage
– Concomitant use of heparin, oral
anticoagulants, NSAIDs is NOT
recommended because of the increased risk
of bleeding
– Allergic reactions
Streptokinase (cont’d)
Antilipidemics
Antilipidemics
• Drugs that lower down abnormal blood
lipid levels.
Types of antilipidemics
– Statin drugs work by inhibiting the synthesis of cholesterol
in the liver. Liver enzymes must be regularly monitored.
(ex. Simvastatin)
– Niacin, a water-soluble B vitamin, is highly effective in
lowering LDL and triglyceride levels by interfering with their
synthesis. Niacin also increases HDL levels better than
many other lipid-lowering drugs.(Ex. Niacin SR)
– Fibric acid derivatives work by accelerating the
elimination of VLDLs and increasing the production of
apoproteins A-I and A-II. (ex. Lipofen, Tricor)
– Bile-acid sequestrants increase conversion of cholesterol
to bile acids and decrease hepatic cholesterol content. The
primary effect is a decrease in total cholesterol and LDLs.
(ex. Questran)
Side effects
•
•
•
•
Constipation
Peptic ulcer
Flushing
Headache
Nursing responsibilities
• Monitor client’s lipid levels
• Observe for signs of GI upset
• Instruct to take with sufficient fluids or
meals
• Low fat diet
• Instruct not to abruptly stop intake
Questions?