1. Cardiovascul
ar Drugs
Nelia B. Perez RN, MAEd, MSN
PCU – MJCN Class 2014 - Pharmacology

2. 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.

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4. 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

5. 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.

6. 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

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8. Pharmacotherapy
•Primary: •Alternate:
•Diuretics •Alpha1-blockers
•ACE Inhibitors •Alpha2-blockers
•ARBs •Direct-acting vasodilators
•Beta-blockers •Peripheral adrenergic
•Calcium channel antagonist
blockers

10. 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

11. Loop Diuretics
Mechanism of
action:
• Inhibits Na+ and Cl-
resorption in the
loop of Henle and
so H2O (water
follows sodium)
• Dilates blood
vessels

12. 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)

13. 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

14. 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.

15. Thiazide
Therapeutic effects:
– Excretion of Na+, Cl-, K+ and H2O without
altering pH
– Treatment of edema
Side effects
– Hypokalemia
– Headache, dizziness

16. Thiazide
Specific Drug
• Hydrodiuril (hydrochlorthiazide)
• Zaroxolyn (Metolazone)

17. 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

18. 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

19. Potassium Sparing Diuretics
cont
Adverse effects:
• Electrolyte imbalance with potential
elevation in K+
• Headache, dizziness
Prototype:
• Aldactone (spironolactone)

20. 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

21. 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)

22. 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

23. Calcium Channel Blockers cont.
Side effects:
• Bradycardia, reflex tachycardia
• Peripheral edema
Interactions:
• Other antihypertensives and diuretics
(increased hypotensive effects)

24. 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

25. 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

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27. RENIN-ANGIOTENSIN-ALDOSTERONE
SYSTEM (RAAS)
Juxtaglomerular RENIN Angiotensinogen
↓Serum Sodium
↓Blood volume cells-kidney in plasma
Angiotensin
I Angiotensin-
converting
Via vasoconstriction of arterial smooth muscle enzyme
↑Sodium Angiotensin II
resorption
Kidney
(H2O ALDOSTERONE
tubules Adrenal
resorbed with
sodium); ↑ Cortex
Blood volume Intestine,
sweat glands,
Salivary
glands

28. 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

29. 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)

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32. 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

33. 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

34. 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)

35. 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

36. 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)

37. Beta Blockers- “olols cont.
Therapeutic Effects
– Decreased heart rate and decreased
myocardial oxygen demand
– Decreased angina
– Fewer rhythm disturbances
– Decreased renin release

38. Beta Blockers- “olols cont.
Adverse effects:
– Dysrhythmias (bradycardia), heart
failure
– Bronchospasm / bronchoconstriction
– Fatigue, depression, impotence
Interactions:
– Other antihypertensives and diuretics
(increased hypotensive effects)

39. 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

40. 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

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43. 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.

44. 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

46. 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

47. 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

48. 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

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50. Cardiac Glycosides
• AKA digitalis glycosides
• Group of drugs that inhibit the sodium-
potassium pump, thus increasing
intracellular calcium which causes cardiac
muscle fibers to contract more efficiently

51. Action Potential

52. Cardiac Glycosides
Therapeutic Effects
1.Positive Inotropic action
2.Negative Chronotropic action
3.Negative Dromotropic effect

53. Inotropes

54. Inotropes
• Agents that affect myocardial contraction
• Positive Inotropes
– Cardiac glycosides
– Catecholamines
• Negative Inotropes
– BB
– CCB
– Class IA & IC anti-arrhythmics

55. Class Participation
Which of the following is an
example of a positive inotrope?
a) Docusate
b) Digoxin
c) HCTZ
d) Propranolol
e) Nitroglycerin

56. Class Participation
Which of the following is an
example of a positive inotrope?
a) Docusate
b) Digoxin
c) HCTZ
d) Propranolol
e) Nitroglycerin

57. Cardiac Glycosides
• Prototype: Digoxin (Lanoxin®, Digitek®,
Lanoxicaps®)

58. Digoxin MOA

59. 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

60. Chronotropes

61. Chronotropes
• Agents that change heart rate
– affects the nerves controlling the heart
– changes the rhythm produced by the SA node

62. Chronotropes (cont’d)
• Positive Chronotropes • Negative Chronotropes
– Atropine – Beta-blockers
– Quinidine – Acetylcholine
– Dopamine – Digoxin
– Dobutamine – Diltiazem
– Epinephrine – Verapamil
– Isuprel – Ivabradine
– Metoprolol

63. Positive Chronotrope
Prototype: Atropine
• belladonna alkaloid
• d,l-hyoscyamine
• Anticholinergic
• Uses
– Symptomatic bradycardia
– Aspiration prophylaxis
– Produces mydriasis
– Organophosphate toxicity
– Adjunct nerve agent &
insecticide poisoning

64. 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

65. Nursing Responsibilities
• Monitor HR---note rhythm, quality, and
rate
• Monitor I&O
• Assess for dryness or mucus membranes
• Monitor GI function

66. Anti-anginal
Drugs

67. Antianginal Drugs
• Prototype: Nitrites &
Nitrates
• BB
• Calcium Channel
Blockers (CCBs)

68. 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) :

69. 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.

70. • 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.

71. • 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

72. Symptoms of Angina

73. 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

74. Class Participation
Which is the PREFERRED route for
nitroglycerin during angina attacks?
a) Topical (ointment 2%)
b) IV infusion
c) Transdermal
d) SL
e) Extended release tablets/capsules

75. Class Participation
Which is the PREFFERED route for
nitroglycerin during angina attacks?
a) Topical (ointment 2%)
b) IV infusion
c) Transdermal
d) SL
e) Extended release tablets/capsules

76. Drug Common Onset Duration
(Trade Name) Dosage
Amyl nitrate 0.3 ml 30-60 sec 10 min
(Vaporole®) inhalation
ISDN 2.5 - 10 mg SL 2-5 min 2 - 4 hr
(Isordil®) 5 - 30 mg po qid
Nitroglycerin
(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
(Transderm- 2.5 - 15 mg/day 30-60 min 24 hr
Nitro®) Transdermal
patch

77. 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

78. Nitroglycerin (NG)
• Indications
– Angina
– Acute MI
– HF
– HTN
– Hypertensive emergency
– Hypotension induction
– Peri/postoperative HTN
– Pulmonary edema
– Pulmonary HTN

79. 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

80. NG (cont’d)
• Adverse Effects • Contraindication:
– dizziness or fainting – sildenafil (Viagra®)
– flushing of the face or – tadalafil (Cialis®)
neck – vardenafil (Levitra®)
– headache, this is
common after a dose,
but usually only lasts
• Lab monitoring not
for a short time necessary
– irregular heartbeat,
palpitations
– nausea, vomiting

81. Antidysrhythmics
Antiarrhythmics

82. 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

83. Antidysrhythmics/Antiarrhythmics
• Uses
– restore normal cardiac
rhythm
– Successful conversion
of an arrhythmia
depends on the type of
arrhythmia present

84. Antidysrhythmics/Antiarrhythmics
• 4 major classes
– Class I
• Class IA
• Class IB
• Class IC
– Class II
– Class III
– Class IV

85. 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

86. 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

87. Class IA
• Quinidine (Quinidine sulfate®,
Quinaglute®, Quinidex®, Cardioquin®)
• Disopyramide (Norpace®)
• Procainimide (Procainimide HCI®,
Procan®, Procanabid®, Pronestyl®)

88. 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

89. 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

90. Class IB
• prototype: Lidocaine (Xylocaine®)
• Tocainide (Tonocard®)
• Mexiletene (Mexitel®)
• Phenytoin (Dilantin®)

91. Lidocaine – Class IB
• MOA: blocks influx of Na fast channel
• Indication: ventricular arrhythmias

92. 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

93. Class IC
• prototype: Flecainide (Tambocor®)
• Propafenone (Rhythmol®)

94. 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

95. 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

96. 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®)

97. Propranolol Warning
• 2 situations in which propranolol requires
extreme caution
– AV block
– CHF
– Asthma or emphysema

98. Class III
• K+ channel blockers
• Drugs:
– Prototype: Amiodarone (Cordarone)
– Bretylium (Bretylol)
– Sotalol (Betapace)

99. 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

100. Amiodarone – Class III (cont’d)
• Monitoring
– CBC
– chest x-ray
– ECG
– ophthalmologic exam
– thyroid function tests (TFTs)

101. 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

102. Sympathomimetics

103. Sympathomimetics
• 2 classes: • SE:
– α- agonist
– hypertension,
• Phenylephrine
– excessive cardiac
• Clonidine stimulation
• Oxymetazoline
– cardiac arrhythmias
• Tetrahydralazine
– Long-term use increases
• Xylometazoline mortality in heart failure
patients.
– β-agonist • CI
• Prototype: Epinephrine
– CAD
• Norepinephrine
• Dopamine
• Dobutamine
• Isoproterenol

104. 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

105. Epinephrine MOA

106. Epinephrine (cont’d)
• Indications • IV Dosage
– Vfib – IV: 1 mg (10 ml of a
– Ventricular asystole 1:10,000 solution) IV;
– Cardiac arrest may repeat every 3-5
minutes
– Pulseless electrical
– Each dose may be
activity
given by peripheral
injection followed by a
20 ml flush of IV fluid.

107. 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

108. Vasopressors

109. 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

110. 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

111. 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

112. Vasopressin (cont’d)
Indications:
– Cardiac arrest
– Cardiogenic shock
– Cardiopulmonary resuscitation
– Hypotension
– Septic shock
– Diabetes Insipidus

113. 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.

114. 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

115. Anticoagulants

116. Antiplatelets/Anticoagulants
• Prevents/interferes with coagulation
• Uses
– deep vein thrombosis (DVTs), pulmonary
embolism, myocardial infarctions & strokes in
those who are predisposed

117. Types of
Antiplatelets/Anticoagulants
• Antiplatelets
– Aspirin
– Dipyridamole
– Thienopyridines
• Clopidogrel (Plavix)
• Ticlopidine (Ticlid)
– Glycoprotein IIb/IIIa antagonists
• Abciximab (ReoPro)
• Eptifibatide (Integrelin)
• Tirofiban (Aggrastat)

118. 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

119. Coagulation Cascade

120. 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

121. Warfarin (cont’d)
• Indications
– Stroke
– DVT
– Post MI
– Afib
– Cardiomyopathy

122. 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

123. 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

124. Class Participation Question #5:
Which foods are high in vitamin K?

125. Class Participation Question #5:
Which foods are high in vitamin K?

126. Fibrinolytic Enzymes

127. 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®)

128. 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

129. 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

130. Streptokinase (cont’d)

131. Antilipidemics

132. Antilipidemics
• Drugs that lower down abnormal blood
lipid levels.

133. 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)

134. Side effects
• Constipation
• Peptic ulcer
• Flushing
• Headache

135. 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

136. Questions?