Download beta-blockers

DRUGS AFFECTING THE
CARDIOVASCULAR and RENAL
SYSTEMS
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CARDIAC PROBLEM AREAS
 PUMP
 CIRCULATION TO MUSCLE
 ELECTRICAL SYSTEM
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Winter 2013
CARDIAC A&P REVIEW
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CARDIAC A&P REVIEW
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CARDIAC A&P REVIEW
Winter
5 2013
HEART FAILURE
Chapter 22
 LEFT SIDED HEART FAILURE (CHRONIC
HEART FAILURE)
 RESTLESS
 ORTHOPNEA
 SOB (SHORTNESS OF BREATH)
 DOE (DYSPNEA ON EXERTION)
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Common Causes for Heart Failure
 Inadequate Contractility
 Myocardial Infarction
 Inadequate Filling
 Atrial fibrillation
 Pressure Overload
 Hypertension
 Volume Overload
 Hypervolemia
 Complete list on pg. 336
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DRUG CLASSES FOR HEART FAILURE
 ANGIOTENSIN – CONVERTING ENZYME





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INHIBITORS
ANGIOTENSIN II RECEPTOR BLOCKERS
BETA-BLOCKERS
B-TYPE NATRIURETIC PEPTIDE
PHOSPHODIESTERASE INHIBITORS
CARDIAC GLYCOSIDES
Winter 2013
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ANGIOTENSIN –CONVERTING ENZYME
INHIBITORS
 ACE Inhibitors
 Prevents vasoconstriction, sodium and water
resorption
 Lisinopril
 Indicated for heart failure, hypertension, acute
Myocardial Infarction
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ANGIOTENSIN II RECEPTOR BLOCKERS
 ARBs
 valsartan (Diovan)
 Potent vasodilating effects
 Decreases systemic vascular resistance
 Used in combination with diuretics to treat Heart
Failure and Hypertension
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BETA-BLOCKERS
 Block sympathetic nervous system stimulation of
the heart
 Reduce heart rate, delayed AV node conduction,
reduced myocardial contractility and decreased
myocardial automaticity.
 metoprolol
 Decreased workload of the heart
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Synthetic human B-type natriuretic peptide
 Nesiritide (Natrecor)
 Vasodilating effect on both arteries and veins
 Treatment of patients with acutely decompensated
CHF who have dyspnea at rest or with minimal
activity.
 Treatment for severe life-threatening heart failure
 Causes diuresis, urine sodium loss and vasodilation
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PHOSPHODIESTERASE INHIBITORS
 inamrinone and milrinone
 Positive inotropic and vasodilating effects
 Decrease cardiac work load
 Parenteral only
 Short-term management of CHF
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CARDIAC GLYCOSIDES
(aka: digitalis glycosides)
 INCREASE THE EFFICIENCY OF THE HEART BY
IMPROVING THE CONTRACTION OF THE
HEART MUSCLE
 POSITIVE INOTROPIC ACTION
INCREASING THE FORCE OF MYOCARDIAL
CONTRACTION
 Negative chronotropic effect – reduced heart rate
 Negative dromotropic effect – decreased automaticity at the
SA note, AV node and bundle of HIS

 digoxin (Lanoxin)

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Not first line drug in Heart Failure
Winter 2013
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WHY DO WE WANT TO INCREASE THE
MYOCARDIAL CONTRACTILITY??
 INADEQUATE CONTRACTILITY
 MI (MYOCARDIAL INFARCTION)
 CORONARY ARTERY DISEASE
 CARDIOMYOPATHY
 INADEQUATE FILLING
 ATRIAL FIBRILLATION
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Atrial Fibrillation
 NORMAL SINUS
RHYTHM (NSR)
 A FIB
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WHY DO WE WANT TO INCREASE THE
MYOCARDIAL CONTRACTILITY??
 PRESSURE OVERLOAD
 HYPERTENSION
 VOLUME OVERLOAD
 HYPERVOLEMIA
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DIGOXIN (LANOXIN)
 DIGITALIZATION
 The administration of digitalis or one of its glycosides in a
dosage schedule designed to produce and then maintain
optimal therapeutic concentration
 CARDIAC GLYCOSIDES HAVE BEEN USED TO
TREAT HEART FAILURE FOR OVER 200 YEARS
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DIGOXIN (LANOXIN)
 WHAT DOES IT DO???
 INCREASES CARDIAC CONTRACTILITY BY INHIBITING
THE K+/Na+ PUMP AND INFLUENCING CALCIUM
MOVEMENT
 STIMULATES THE VAGUS NERVE = SLOWING THE HEART
RATE NEGATIVE CHRONOTROPIC EFFECT
 POSITIVE INOTROPIC EFFECT – Increases the squeeze!
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ADVERSE EFFECTS OF CARDIAC
GLYCOSIDES MEDICATIONS
 DYSRYTHMIAS
 HEADACHE
 FATIGUE
 ANOREXIA
 N, V, D
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NURSING CONSIDERATIONS
 APICAL PULSE FOR ONE MINUTE PRIOR TO GIVING
DIGOXIN
“HOLD” IF <60
 ANTACIDS INTERFERE WITH ABSORPTION
 AVOID GIVING DIGOXIN WITH HIGH-FIBER FOODS
(FIBER BINDS WITH DIGITALIS)
 TEACH S&S OF TOXICITY
 TRACK BLOOD LEVELS FOR DIG AND
ELECTROLYTES
 DIGOXIN LEVELS MUST BE MONITORED
 0.5 TO 2 ng/ml
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DIGITALIS TOXICITY
 SIGNS AND SYMPTOMS
 N, V
 ANOREXIA
 VISUAL DISTURBANCES
 MAY SEE YELLOW, GREEN, BLUE HALOS
 CONFUSION
 BRADYCARDIA
 EKG CHANGES
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TREATMENT FOR DIG TOXICITY
 STOP TAKING THE DRUG
 DIGOXIN IMMUNE FAB (DIGIBIND)
 WHAT CAUSED THE PROBLEM?
 HYPOKALEMIA R/T DIURETIC DRUGS
 LIVER FAILURE
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ANTIDYSRHYTHMIC DRUGS
Chapter 23
DYSRHYTHMIA (ARRHYTHMIA)
ANY DEVIATION FROM THE “NORMAL”
RHYTHM
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“NORMAL” ELECTRICAL PATTERN OF THE
HEART
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Vaughan Williams Classification
 System commonly used to classify antidysrhythmic
drugs
 Based on the electrophysiologic effect of particular
drugs on the action potential
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Vaughan Williams
Classification (cont’d)
 Class I
 Class Ia
 Class Ib
 Class Ic
 Class II
 Class III
 Class IV
 Other
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Vaughan Williams Classification:
Mechanism of Action
 Class I
 Membrane-stabilizing drugs
 Fast sodium channel blockers
 Divided into Ia, Ib, and Ic drugs,
according
to effects
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Vaughan Williams Classification:
Mechanism of Action and Indications
 Class I: moricizine
 General class I drug
 Has characteristics of all three subclasses
 Used for symptomatic ventricular and
life-threatening dysrhythmias
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Vaughan Williams Classification:
Mechanism of Action and Indications (cont’d)
 Class Ia: quinidine, procainamide, disopyramide




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Block sodium (fast) channels
Delay repolarization
Increase APD (action potential duration)
Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions,
ventricular tachycardia, Wolff-Parkinson-White
syndrome
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
 Class Ib: phenytoin, lidocaine
 Block sodium channels
 Accelerate repolarization
 Increase or decrease APD
 Used for ventricular dysrhythmias only
 Premature ventricular contractions,
ventricular tachycardia, ventricular
fibrillation
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
• Class Ic: flecainide, propafenone
▫ Block sodium channels (more pronounced
effect)
▫ Little effect on APD or repolarization
▫ Used for severe ventricular dysrhythmias
▫ May be used in atrial fibrillation/flutter, WolffParkinson-White syndrome, supraventricular
tachycardia dysrhythmias
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Vaughan Williams Classification:
Mechanism of Action and Indications (cont’d)
 Class II: beta-blockers: atenolol, esmolol,
metaprolol, propranolol
 Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in
the heart’s conduction system
 Depress phase 4 depolarization
 General myocardial depressants for both
supraventricular and ventricular dysrhythmias
 Also used as antianginal and antihypertensive drugs
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Vaughan Williams Classification:
Mechanism of Action and Indications (cont’d)
 Class III: amiodarone, sotalol*, ibutilide, others
 Increase APD
 Prolong repolarization in phase 3
 Used for dysrhythmias that are difficult to treat
 Life-threatening ventricular tachycardia or fibrillation, atrial
fibrillation or flutter—resistant to other drugs
 Sustained ventricular tachycardia
*Sotalol also exhibits Class II properties
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Vaughan Williams Classification:
Mechanism of Action and Indications (cont’d)
 Class IV: verapamil, diltiazem
 Calcium channel blockers
 Inhibit slow-channel (calcium-dependent) pathways
 Depress phase 4 depolarization
 Reduce AV node conduction
 Used for paroxysmal supraventricular
tachycardia (PSVT); rate control for atrial
fibrillation and flutter
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Vaughan Williams Classification:
Other Antidysrhythmics
 Digoxin, adenosine
 Have properties of several classes and are
not placed into one particular class
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Unclassified Antidysrhythmic
 adenosine (Adenocard)
 Slows conduction through the AV node
 Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
 Very short half-life—less than 10 seconds
 Only administered as fast IV push
 May cause asystole for a few seconds
 Other adverse effects minimal
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ADVERSE REACTION TO
ANTIDYSRHYTHMICS
 N, V, D
 DIZZINESS
 HEADACHE
 BLURRED VISION
 CAN CAUSE DYSRHYTHMIAS !!
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NURSING CONSIDERATIONS
 MONITOR PULSE RATE
 IF SENDING PT HOME – TEACH THEM HOW TO
MONITOR THEIR PULSE
 ALWAYS CHECK ALL VS BEFORE
ADMINISTERING THE MEDICATION
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NURSING CONSIDERATIONS
 MONITOR FOR FLUID RETENTION
 DO NOT STOP DRUGS ABRUPTLY
 AVOID ALCOHOL
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CHAPTER 24
Antianginal Drugs
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Angina Pectoris (Chest Pain)
 When the supply of oxygen and nutrients in the
blood is insufficient to meet the demands of the
heart, the heart muscle “aches”
 The heart requires a large supply of oxygen to
meet the demands placed on it
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Ischemia
 Ischemia
 Poor blood supply to an organ
 Ischemic heart disease
 Poor blood supply to the heart muscle
 Atherosclerosis
 Coronary artery disease
 Myocardial infarction (MI)
 Necrosis, or death, of cardiac tissue
 Disabling or fatal
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Types of Angina
 Chronic stable angina
(also called classic or effort angina)
 Unstable angina
(also called preinfarction or
crescendo angina)
 Vasospastic angina
(also called Prinzmetal’s or variant
angina)
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Drug Classifications for Angina
 Nitrates/nitrites
 Beta-blockers
 Calcium channel blockers
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Therapeutic Objectives
 Increase blood flow to ischemic heart
muscle
and/or
 Decrease myocardial oxygen demand
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Therapeutic Objectives (cont’d)
 Minimize the frequency of attacks and decrease
the duration and intensity of anginal pain
 Improve the patient’s functional capacity with as
few adverse effects as possible
 Prevent or delay the worst possible outcome: MI
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Nitrates/Nitrites
Available forms
 Sublingual*
 Buccal*
 Chewable tablets
 Oral capsules/tablets



Transdermal patches*
Ointments*
Translingual sprays*
 Intravenous solutions*
*Bypass the liver and the first-pass effect
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Nitrates/Nitrites (cont’d)
 Cause vasodilation because of relaxation of
smooth muscles
 Potent dilating effect on coronary arteries
 Used for prevention and treatment
of angina
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Nitrates/Nitrites (cont’d)
 Vasodilation results in reduced myocardial
oxygen demand
 Nitrates cause dilation of both large and small
coronary vessels
 Result: oxygen to ischemic myocardial tissue
 Nitrates alleviate coronary artery spasms
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Nitrates/Nitrites (cont’d)
 Rapid-acting forms
 Used to treat acute anginal attacks
 Sublingual tablets
 Intravenous infusion
 Long-acting forms
 Used to PREVENT anginal episodes
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Nitrates/Nitrites (cont’d)
 Nitroglycerin
 Prototypical nitrate
 Large first-pass effect with oral forms
 Used for symptomatic treatment of ischemic heart
conditions (angina)
 IV form used for BP control in perioperative
hypertension, treatment of HF, ischemic pain,
pulmonary edema associated with acute MI, and
hypertensive emergencies
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Nitrates
 Isosorbide dinitrate
(Isordil, Sorbitrate, Dilatrate SR)
 Isosorbide mononitrate
(Imdur, Monoket, ISMO)
 Used for:
 Acute relief of angina
 Prophylaxis in situations that may provoke angina
 Long-term prophylaxis of angina
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Nitrates (cont’d)
Adverse effects
 Headaches
 Usually diminish in intensity and frequency
with continued use
 Tachycardia, postural hypotension
 Tolerance may develop
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Tolerance
 Occurs in patients taking nitrates around the
clock or with long-acting forms
 Prevented by allowing a regular nitrate-free
period to allow enzyme pathways to replenish
 Transdermal forms: remove patch at bedtime for 8
hours, then apply a new patch in the morning
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Beta-Blockers
 atenolol (Tenormin)
 metoprolol (Lopressor)
 propranolol (Inderal)
 nadolol (Corgard)
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Beta Adrenergic Blockers: Mechanism
of Action
 Block beta1 Adrenergic -receptors on the heart
 Decrease HR, resulting in decreased myocardial
oxygen demand and increased oxygen delivery to
the heart
 Decrease myocardial contractility, helping to
conserve energy or decrease demand
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Beta Adrenergic Blockers: Mechanism
of Action (cont’d)
 After an MI, a high level of circulating
catecholamines irritate the heart, causing an
imbalance in supply and demand ratio and even
leading to life-threatening dysrhythmias
 Beta Adrenergic Blockers block the harmful
effects of catecholamines, thus improving survival
after an MI
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Beta Adrenergic Blockers (cont’d)
 Indications
 Angina
 Antihypertensive
 Cardiac dysrhythmias
 Cardioprotective effects, especially after MI
 Some used for migraine headaches, essential
tremors, and stage fright
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Beta Adrenergic Blockers (cont’d)
Adverse effects
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Body System
Adverse Effects
Cardiovascular
Bradycardia, hypotension,
second- or third-degree heart
block; heart failure
Metabolic
Altered glucose and lipid
metabolism
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Beta Adrenergic Blockers (cont’d)
Adverse effects (cont’d)
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Body System
Adverse Effects
CNS
Dizziness, fatigue,
mental depression, lethargy,
drowsiness, unusual dreams
Other
Impotence, wheezing,
dyspnea, constipation
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Calcium Channel Blockers
 verapamil (Calan, Isoptin)
 diltiazem (Cardizem)
 nifedipine (Procardia)
 amlodipine (Norvasc)
 Others
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Calcium Channel Blockers (cont’d)
 Mechanism of action
 Cause coronary artery vasodilation
 Cause peripheral arterial vasodilation,
thus decreasing systemic vascular
resistance
 Reduce the workload of the heart
 Result: decreased myocardial oxygen
demand
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Calcium Channel Blockers (cont’d)
Indications
 First-line drugs for treatment of angina, hypertension,
and supraventricular tachycardia
 Coronary artery spasms (Prinzmetal’s angina)
 Short-term management of atrial fibrillation and flutter
 Several other uses
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Calcium Channel Blockers (cont’d)
Adverse effects
 Very acceptable adverse effect and safety
profile
 May cause hypotension, palpitations,
tachycardia or bradycardia, constipation,
nausea, dyspnea, other adverse effects
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Nursing Implications – All Antidysrhythmic
Drugs
 Before administering, perform a complete
health history to determine presence of
conditions that may be contraindications for
use or those that may call for cautious use
 Obtain baseline VS, including respiratory
patterns and rate
 Assess for drug interactions
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Nursing Implications – All Antidysrhythmic
Drugs
 Patients should not take any medications,
including over-the-counter medications,
without checking with their physician
 Patients should be encouraged to limit
caffeine intake
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Nursing Implications – All Antidysrhythmic
Drugs
 Patients should report blurred vision,
persistent headache, dry mouth,
dizziness, edema, fainting episodes,
weight gain of 2 pounds in 1 day or 5
pounds in 1 week, pulse rates less than
60, and dyspnea
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Nursing Implications – All Antidysrhythmic
Drugs
 Alcohol consumption and spending time in hot
baths or whirlpools, hot tubs, or saunas will result
in vasodilation, hypotension, and the possibility of
fainting
 Teach patients to change positions slowly to
avoid postural BP changes
 Encourage patients to keep a record of their
anginal attacks, including precipitating factors,
number of pills taken, and therapeutic effects
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Nursing Implications
Nitroglycerin
 Instruct patients in proper technique and
guidelines for taking sublingual nitroglycerin for
anginal pain
 Instruct patients never to chew or swallow the
sublingual form
 Instruct patients that a burning sensation felt with
sublingual forms indicates that the drug is still
potent
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Nursing Implications
Nitroglycerin (cont’d)
 Instruct patients to keep a fresh supply of
sublingual medication on hand; potency is lost in
about 3 months after the bottle has been opened
 To preserve potency, medications should be
stored in an airtight, dark glass bottle with a metal
cap and no cotton filler
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Nursing Implications
Nitroglycerin (cont’d)
 Instruct patients in the proper application of
nitrate topical ointments and transdermal forms,
including site rotation and removal of old
medication
 To reduce tolerance, the patient may be
instructed to remove topical forms at bedtime and
apply new doses in the morning, allowing for a
nitrate-free period
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Nursing Implications
Nitroglycerin (cont’d)
 Instruct patients to take prn nitrates at the first
hint of anginal pain
 Monitor vital signs frequently during acute
exacerbations of angina and during IV
administration
 If experiencing chest pain, the patient taking
sublingual nitroglycerin should lie down to prevent
or decrease dizziness and fainting that may occur
because of hypotension
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Nursing Implications
Nitroglycerin (cont’d)
 If anginal pain occurs:
 Stop activity and sit or lie down
 Take a sublingual tablet, if no relief, call
911/Emergency Services immediately!
 If no relief in 5 minutes, take a second sublingual
tablet
 If no relief in 5 minutes, take a third sublingual tablet
 Do not try to drive to the hospital
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Nursing Implications
Nitroglycerin (cont’d)
 IV forms of nitroglycerin must be given with
special non-PVC tubing and bags
 Discard parenteral solution that is blue, green, or
dark red
 Follow specific manufacturer’s instructions for IV
administration
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Nursing Implications
Calcium channel blockers
 Constipation is a common problem; instruct
patients to take in adequate fluids and eat highfiber foods
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Nursing Implications
Beta-blockers
 Patients taking beta-blockers should monitor
pulse rate daily and report any rate lower than 60
beats per minute
 Instruct patients to report dizziness or fainting
 Constipation is a common problem; instruct
patients to take in adequate fluids and eat highfiber foods
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Nursing Implications
Beta-blockers (cont’d)
 Inform patients that these medications should
never be abruptly discontinued because of risk of
rebound hypertensive crisis
 Inform patients that these medications are for
long-term prevention of angina, not for
immediate relief
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Nursing Implications
Antianginal drugs
 Monitor for adverse reactions
 Allergic reactions, headache, lightheadedness,
hypotension, dizziness
 Monitor for therapeutic effects
 Relief of angina, decreased BP, or both
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CHAPTER 25
Antihypertensive Drugs
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ATHEROSCLEROSIS
 DEPOSITS OF
 CALCIUM
 LIPIDS
 CHOLESTROL
 ON THE WALLS OF THE ARTERIES
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The plaque deposited in your arteries is hard
on the outside and soft and mushy on the
inside. Sometimes the hard outer shell cracks.
When this happens, a blood clot forms around
the plaque. If the clot completely blocks the
artery, it cuts off the blood supply to a portion
of the heart. Without immediate treatment,
that part of the heart muscle could be
damaged or destroyed.
5/4/2017
Blood Pressure
 Blood pressure = CO × SVR
 CO = cardiac output
 SVR = systemic vascular resistance
 Hypertension = high blood pressure
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Seventh Report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure (JNC-7)*
Four stages, based on BP measurements
 Normal
 Pre-hypertension
 Stage 1 hypertension
 Stage 2 hypertension
*New guidelines pending
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Compelling Indications
 Post-MI
 High cardiovascular risk
 Heart failure
 Diabetes mellitus
 Chronic kidney disease
 Previous stroke
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JNC-7: Significant Changes
 High diastolic BP (DBP) is no longer
considered to be more dangerous than high
systolic BP (SBP)
 Studies have shown that elevated SBP is
strongly associated with heart failure, stroke,
and renal failure
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JNC-7: Significant Changes (cont’d)
 For those older than age 50, SBP is a more
important risk factor for cardiovascular
disease (CVD) than DBP
 “Prehypertensive” BPs are no longer
considered “high normal” and require lifestyle
modifications to prevent CVD
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Winter 2013
5/4/2017
JNC-7: Significant Changes (cont’d)
 Thiazide-type diuretics should be the initial
drug therapy for most patients with
hypertension (alone or with other drug
classes)
 The previous labels of “mild,” “moderate,”
and “severe” have been dropped
101
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Cultural Considerations
 Beta-blockers and ACE inhibitors have been
found to be more effective in white patients
than in African American patients
 CCBs and diuretics have been shown to be
more effective in African American patients
than in white patients
102
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Primary Hypertension
Hypertension can also be defined by its cause
Unknown cause
Essential, idiopathic, or primary hypertension
 90% of cases
Genetic (hereditary) – 30%

African-American
Obesity
Renal failure
Advanced age
Any of the above factors complicated by lifestyle
103
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Secondary Hypertension
 Known cause
 Secondary hypertension
 10% of cases
 Causes such as Pheochromocytoma, pre-
eclampsia, renal artery disease
104
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Take the Salt quiz
http://www.medicinenet.com/salt_quiz/quiz.
htm
105
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Antihypertensive Drugs
 Medications used to treat hypertension
 Categories






106
Adrenergic drugs
Angiotensin converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers (ARBs)
Calcium channel blockers (CCBs)
Diuretics
Vasodilators
Winter 2013
5/4/2017
Adrenergic Drugs: Centrally Acting Alpha2Receptor Agonists
 clonidine (Catapres)
 methyldopa (Aldomet)
 Can be used for hypertension in pregnancy
107
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Adrenergic Drugs: Peripherally Acting
Mechanism of Action
 Peripheral alpha1-blockers/antagonists
 Block alpha1-adrenergic receptors
 doxazosin (Cardura)
 terazosin (Hytrin)
 Results in decreased blood pressure
108
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Adrenergic Drugs:
Mechanism of Action (cont’d)
 Beta-blockers
 Reduce BP by reducing heart rate through
beta1-blockade
 Cause reduced secretion of renin
 Long-term use causes reduced peripheral vascular
resistance
 Propranolol, atenolol, others
 Newest: nebivolol (Bystolic)—beta1-selective
 Result: decreased blood pressure
109
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5/4/2017
Adrenergic Drugs:
Mechanism of Action (cont’d)
 Dual-action alpha1- and beta1-receptor blockers
 Block alpha1-adrenergic receptors
 Reduction of heart rate (beta1-receptor blockade)
 Vasodilation (alpha1-receptor blockade)
 carvedilol (Coreg) and labetalol
 Result in decreased blood pressure
110
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5/4/2017
Adrenergic Drugs:
Adverse Effects
 High incidence of orthostatic hypotension
 Most common
 Dry mouth
 Drowsiness, sedation
 Constipation
 Other





111
Headaches
Sleep disturbances
Nausea
Rash
Cardiac disturbances (palpitations), others
Winter 2013
5/4/2017
112
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5/4/2017
Adrenergic Drugs (cont’d)
 Beta1 Adrenergic blockers
 Act in the periphery
 Reduce heart rate owing to b1-blockade
 Examples: nebivolol (bystolic), propranolol (Inderal),
atenolol (Tenormin), others
113
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5/4/2017
Angiotensin Converting
Enzyme (ACE) Inhibitors
 Large group of safe and effective drugs
 Often used as first-line drugs for HF
and hypertension
 May be combined with a thiazide diuretic or
calcium channel blocker
114
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ACE Inhibitors:
Mechanism of Action
Renin-Angiotensin-Aldosterone System
 Inhibit angiotensin-converting enzyme, which is
responsible for converting angiotensin I (through
the action of renin) to angiotensin II
 Angiotensin II is a potent vasoconstrictor and
causes aldosterone secretion from the adrenal
glands
115
Winter 2013
5/4/2017
ACE Inhibitors:
Mechanism of Action (cont’d)
 Aldosterone stimulates water and sodium
resorption
 Result: increased blood volume, increased
preload, and increased BP
116
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ACE Inhibitors:
Mechanism of Action (cont’d)
 Block angiotensin-converting enzyme, thus
preventing the formation of angiotensin II
 Prevent the breakdown of the vasodilating
substance, bradykinin
 Result in decreased systemic vascular resistance
(afterload), vasodilation, and therefore decreased
blood pressure
117
Winter 2013
5/4/2017
ACE Inhibitors:
Indications
 Hypertension
 HF (either alone or in combination with diuretics or
other drugs)
 Slow progression of left ventricular hypertrophy after
MI (cardioprotective)
 Renal protective effects in patients with diabetes
118
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119
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5/4/2017
ACE Inhibitors: Indications (cont’d)
 Drugs of choice in hypertensive patients with HF
 Drugs of choice for diabetic patients
120
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5/4/2017
ACE Inhibitors (cont’d)
 captopril (Capoten)
 Very short half-life
 enalapril (Vasotec)
 Available in oral and parenteral forms
 lisinopril (Prinivil and Zestril) and quinapril (Accupril),
others
 Newer drugs, long half-lives, once-a-day dosing
 Several other drugs available
121
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5/4/2017
ACE Inhibitors (cont’d)
 Captopril and lisinopril are NOT prodrugs
 Prodrugs are inactive in their administered form and
must be metabolized in the liver to an active form so
as to be effective
 Captopril and lisinopril can be used if a patient has
liver dysfunction, unlike other ACE inhibitors that are
prodrugs
122
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ACE Inhibitors: Adverse Effects
Fatigue
Dizziness
Headache
Mood changes
Impaired taste
Possible hyperkalemia
Dry, nonproductive cough, which reverses when
therapy is stopped
 Angioedema: rare but potentially fatal







NOTE: First-dose hypotensive effect may occur!
123
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124
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5/4/2017
Angiotensin II Receptor Blockers
 (A-II blockers, or ARBs)
 Newer class
 Well tolerated
 Do not cause a dry cough
125
Winter 2013
5/4/2017
Angiotensin II Receptor Blockers: Mechanism of
Action
 Allow angiotensin I to be converted to angiotensin
II, but block the receptors that receive angiotensin
II
 Block vasoconstriction and release of aldosterone
126
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Angiotensin II Receptor Blockers
 losartan (Cozaar, Hyzaar)
 valsartan (Diovan)
 eprosartan (Teveten)
 irbesartan (Avapro)
 Others
127
Winter 2013
5/4/2017
Angiotensin II Receptor Blockers: Indications
 Hypertension
 Adjunctive drugs for the treatment of HF
 May be used alone or with other drugs such as
diuretics
 Used primarily in patients who cannot tolerate
ACE inhibitors
128
Winter 2013
5/4/2017
Angiotensin II Receptor Blockers: Adverse
Effects
 Upper respiratory infections
 Headache
 May cause occasional dizziness, inability to
sleep, diarrhea, dyspnea, heartburn, nasal
congestion, back pain, fatigue
 Hyperkalemia much less likely to occur
129
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5/4/2017
Calcium Channel Blockers:
Mechanism of Action
 Cause smooth muscle relaxation by blocking the
binding of calcium to its receptors, preventing
muscle contraction
 Results in
 Decreased peripheral smooth muscle tone
 Decreased systemic vascular resistance
 Decreased blood pressure
130
Winter 2013
5/4/2017
Calcium Channel Blockers
 Benzothiazepines
 diltiazem (Cardizem, Dilacor)
 Phenylalkamines
 verapamil (Calan, Isoptin)
 Dihydropyridines
 amlodipine (Norvasc), bepridil (Vascor),
nicardipine (Cardene)
 nifedipine (Procardia), nimodipine (Nimotop)
131
Winter 2013
5/4/2017
Calcium Channel Blockers: Indications
 Angina
 Hypertension
 Dysrhythmias
 Migraine headaches
 Raynaud’s disease
132
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5/4/2017
Calcium Channel Blockers:
Adverse Effects
 Cardiovascular
 Hypotension, palpitations, tachycardia
 Gastrointestinal
 Constipation, nausea
 Other
 Rash, flushing, peripheral edema, dermatitis
133
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DIURETICS AND DRUGS THAT
EFFECT THE RENAL SYSTEM
134
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Diuretics
 Decrease plasma and extracellular fluid volumes
 Results
 Decreased preload
 Decreased cardiac output
 Decreased total peripheral resistance
 Overall effect
 Decreased workload of the heart, and decreased
blood pressure
135
Winter 2013
5/4/2017
CARBONIC ANHYDRASE
INHIBITORS (CAIs)
 INHIBIT THE ENZYME ACTIVITY OF CARBONIC
ANHYDRASE
 CA RECEPTORS ARE LOCATED IN THE PROXIMAL
RENAL TUBULE
 CAIs PREVENT THE RESORPTION OF SODIUM =
ELIMINATION OF WATER AND SODIUM
136
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137
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WHEN TO USE CAIs?
 ACETOZOLAMIDE
(DIAMOX)
 USED IN THE TREATMENT OF:
 GLAUCOMA
 EDEMA
 EPILEPSY
 HIGH ALTITUDE SICKNESS (PULMONARY EDEMA)
138
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LOOP DIURETICS
 Have renal, cardiovascular, and metabolic
effects
 Act along the ascending limb of the loop of
Henle.
 Blocks chloride and sodium resorption
 Chemically related to sulfonamides antibiotics
139
Winter 2013
5/4/2017
WHEN DO WE USE LOOP
DIURETICS?
 Heart Failure
 Liver failure
 Hypertension
 Renal failure
 Increase renal excretion of calcium
140
Winter 2013
5/4/2017
FUROSEMIDE (LASIX)
 BLOCK SODIUM AND CHLORIDE RESORPTION
 USEFUL FOR RAPID DIURESIS
 HYPOKALEMIA IS OFTEN A SIDE EFFECT
141
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OSMOTIC DIURETICS
 PRODUCES OSMOTIC PRESSURE IN THE
GLOMERULUS
 PULLS WATER INTO THE RENAL TUBULES
FROM THE SURROUNDING TISSUE 
DECREASING CELLULAR
EDEMA!
142
Winter 2013
5/4/2017
WHEN TO USE AN OSMOTIC DIURETIC?
 CEREBRAL EDEMA
 INCREASED INTRAOCULAR PRESSURE
NOT USED FOR PERIPHERAL EDEMA – NOT ENOUGH
SODIUM LOSS
143
Winter 2013
5/4/2017
MANNITOL (OSMITROL)
 PRODUCES OSMOTIC PRESSURE IN THE
GLOMULAR FILTRATE
 PULLS WATER FROM THE RENAL TUBULES AND
SURRONDING TISSUE
 USED IN ACUTE RENAL FAILURE AND CEREBRAL
EDEMA
144
Winter 2013
5/4/2017
POTASSIUM SPARING
DIURETICS
 WORK IN COLLECTING DUCTS AND DISTAL
CONVOLUTED TUBLES
 INTERFERE WITH SODIUM + POTASSIUM
EXCHANGE
 RELEASE Na+ AND H2O –> RETAIN K+
145
Winter 2013
5/4/2017
WHEN TO USE POTASSIUM SPARING
DIURETICS?
 HYPERTENSION
 CHF (CHRONIC HEART FAILURE)
146
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SPIRONOLACTONE
(ALDACTONE)
 INTERFERES WITH SODIUM AND POTASSIUM
EXCHANGE
 NURSE MUST BE AWARE OF THE DANGER OF
HYPERKALEMIA
147
Winter 2013
5/4/2017
THIAZIDE AND RELATED
DIURETICS
 RELATED TO SULFONAMIDE ANTIBIOTICS (ALSO
CAIs)
 PREVENT RESORPTION OF SODIUM (Na)
POTASSIUM (K) AND CHLORIDE (Cl) IN THE
DISTAL CONVOLUTED TUBULE
148
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5/4/2017
WHEN TO USE THIAZIDE DIURETICS?
 CAN BE USED ALONE OR IN COMBINATION
WITH OTHER DIURETICS TO TREAT:
 EDEMA
 HYPERTENSION
 CRONIC HEART FAILURE
 RENAL FAILURE
149
Winter 2013
5/4/2017
HYDROCHLORTHIAZIDE (HCTZ) (ESIDRIX)
 INHIBIT RESORPTION OF SODIUM, POTASSIUM
AND CHLORIDE
 COMMONLY USED WITH OTHER
ANTIHYPERTENSIVES
 MAJOR SIDE EFFECTS ARE RELATED TO
ELECTROLYTE BALANCE
150
Winter 2013
5/4/2017
Diuretics (cont’d)
 Thiazide diuretics are the most commonly used
diuretics for hypertension
 Listed as first-line antihypertensives in the JNC-
7 guidelines
151
Winter 2013
5/4/2017
Vasodilators:
Mechanism of Action
 Directly relax arteriolar and/or venous smooth
muscle
 Results in:
 Decreased systemic vascular response
 Decreased afterload (PVR)
 Peripheral vasodilation
152
Winter 2013
5/4/2017
Vasodilators
 diazoxide (Hyperstat)
 hydralazine HCl (Apresoline)
 minoxidil (Loniten)
 sodium nitroprusside (Nipride, Nitropress)
153
Winter 2013
5/4/2017
Vasodilators: Indications
 Treatment of hypertension
 May be used in combination with other drugs
 Sodium nitroprusside and intravenous diazoxide
are reserved for the management of hypertensive
emergencies
154
Winter 2013
5/4/2017
Vasodilators: Adverse Effects
 hydralazine
 Dizziness, headache, anxiety, tachycardia, nausea and
vomiting, diarrhea, anemia, dyspnea, edema, nasal
congestion, others
 sodium nitroprusside
 Bradycardia, hypotension, possible cyanide toxicity
(rare)
155
Winter 2013
5/4/2017
Vasodilators: Adverse Effects (cont’d)
 diazoxide
 Dizziness, headache, anxiety, orthostatic hypotension,
dysrhythmias, sodium and water retention, nausea,
vomiting, hyperglycemia in diabetic patients, others
156
Winter 2013
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Nursing Implications
 Remind patients that medication is only part of therapy.
Encourage patients to watch their diet, stress level,
weight, and alcohol intake
 Instruct patients to avoid smoking and eating foods high
in sodium
 Encourage supervised exercise
157
Winter 2013
5/4/2017
Nursing Implications (cont’d)
 Teach patients to change positions slowly to avoid
syncope from postural hypotension
 Instruct patients to report unusual shortness of breath;
difficulty breathing; swelling of the feet, ankles, face, or
around the eyes; weight gain or loss; chest pain;
palpitations; or excessive fatigue
158
Winter 2013
5/4/2017
Nursing Implications (cont’d)
 Male patients who take these drugs may not be aware
that impotence is an expected effect, and this may
influence compliance with drug therapy
 If patients are experiencing serious adverse effects, or if
they believe the dose or medication needs to be
changed, they should contact their physician
immediately
159
Winter 2013
5/4/2017
Nursing Implications (cont’d)
 Hot tubs, showers, or baths; hot weather; prolonged
sitting or standing; physical exercise; and alcohol
ingestion may aggravate low blood pressure, leading to
fainting and injury; patients should sit or lie down until
symptoms subside
160
Winter 2013
5/4/2017
CHAPTER 28
Coagulation Modifier Drugs
161
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Hemostasis
 The process that halts bleeding after injury to a blood
vessel
 Complex relationship between substances that promote
clot formation and either inhibit coagulation or dissolve a
formed clot
162
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Coagulation System
 “Cascade”
 Each activated factor serves as a catalyst that
amplifies the next reaction
 Result is fibrin, a clot-forming substance
 Intrinsic pathway and extrinsic pathway
163
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164
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165
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Coagulation Modifier Drugs
 Anticoagulants
 Inhibit the action or formation of clotting factors
 Prevent clot formation
 Antiplatelet drugs
 Inhibit platelet aggregation
 Prevent platelet plugs
166
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Coagulation Modifier Drugs (cont’d)
 Hemorheologic drugs
 Pentoxifylline(Trental) changes the shape of red blood
cells in your blood. This makes it easier for these blood cells to
fit into small arteries (blood vessels). Pentoxifylline is used to
improve blood flow. Improved blood flow helps to reduce leg
cramps and other symptoms of vascular disease
 Thrombolytic drugs
 Lyse (break down) existing clots
 Hemostatic or antifibrinolytic drugs
 Promote blood coagulation
167
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Anticoagulants
 Also known as antithrombotic drugs
 Have no direct effect on a blood clot that is
already formed
 Used prophylactically to prevent
 Clot formation (thrombus)
 An embolus (dislodged clot)
168
Winter 2013
5/4/2017
Anticoagulants:
Mechanism of Action
 Vary depending on drug
 Work on different points of the clotting cascade
 Do not lyse existing clots
 Heparin and low–molecular-weight heparins
 Turn off coagulation pathway and prevent clot
formation
169
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Anticoagulants:
Mechanism of Action (cont’d)
All ultimately prevent clot formation
 Heparin
 Low–molecular-weight heparins
 warfarin
 (Coumadin)
 Anti-Thrombin (Inhibit thrombin molecule)
 fondaparinux (Arixtra)
 dabigatran (Pradaxa)
170
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5/4/2017
Pradaxa channel 7 and FDA
http://www.thedenverchannel.com/news/call7-investigators/pradaxamaker-sued-over-claims-company-didnt-inform-doctors-aboutdangers-of-blood-thinning-drug
171
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5/4/2017
Anticoagulants (cont’d)
 Prevention of clot formation also prevents:
 Stroke
 Myocardial infarction (MI)
 Deep vein thrombosis (DVT)
 Pulmonary embolism (PE)
172
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Anticoagulants: Indications
 Used to prevent clot formation in certain settings
where clot formation is likely
 Myocardial infarction
 Unstable angina
 Atrial fibrillation
 Indwelling devices, such as mechanical heart valves
 Major orthopedic surgery
173
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Anticoagulants:
Adverse Effects
 Bleeding
 Risk increases with increased dosages
 May be localized or systemic
 Heparin-induced thrombocytopenia (HIT)
 May also cause:
 Nausea, vomiting, abdominal cramps,
thrombocytopenia, others
174
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Anticoagulants (cont’d)
 Heparin
 Monitored by activated partial thromboplastin times
(aPTTs)
 Parenteral (IV or SC)
 Short half-life (1 to 2 hours)
 Effects reversed by protamine sulfate
175
Winter 2013
5/4/2017
Anticoagulants (cont’d)
 Low–molecular-weight heparins
 enoxaparin (Lovenox) and dalteparin (Fragmin)
 More predictable anticoagulant response
o Do not require laboratory monitoring
 Given subcutaneously
176
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5/4/2017
Anticoagulants (cont’d)
 warfarin sodium (Coumadin)
 Given orally only
 Monitored by prothrombin time (PT) and International
Normalized Ratio (INR) (PT-INR)
 Vitamin K can be given if toxicity occurs
177
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Antiplatelet Drugs
 Prevent platelet adhesion
 aspirin
 dipyridamole (Persantine)
 clopidogrel (Plavix) and ticlopidine (Ticlid)
 ADP inhibitors
 tirofiban (Aggrastat), eptifibatide (Integrilin), abciximab
(ReoPro)
 New class, GP IIb/IIIa inhibitors
178
Winter 2013
5/4/2017
Antiplatelet Drugs: Indications
 Antithrombotic effects
 Reduce risk of fatal and nonfatal strokes
 Acute unstable angina and MI
 Adverse effects
 Vary according to drug
179
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Antifibrinolytic Drugs
 Prevent the lysis of fibrin
 Result in promoting clot formation
180
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Antifibrinolytic Drugs (cont’d)
 Enhance blood clotting
 aminocaproic acid (Amicar)
 desmopressin (DDAVP)
 Similar to ADH
 Also used in the treatment of diabetes insipidus
181
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Antifibrinolytic Drugs:
Indications
 Prevention and treatment of excessive bleeding
 Hyperfibrinolysis
 Surgical complications
 Excessive oozing from surgical sites such as chest
tubes
 Reducing total blood loss and duration of bleeding
in the postoperative period
 Treatment of hemophilia or von Willebrand’s
disease
182
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Antifibrinolytic Drugs:
Adverse Effects
 Uncommon and mild
 Rare reports of thrombotic events
 Others include:
 Dysrhythmia, orthostatic hypotension, bradycardia,
headache, dizziness, fatigue, nausea, vomiting,
abdominal cramps, diarrhea, others
183
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Thrombolytic Drugs
 Drugs that break down, or lyse, preformed clots
 Older drugs
 streptokinase and urokinase
 Newer drugs
 Tissue plasminogen activator (t-PA)
 Anisoylated plasminogen-streptokinase activator
complex (APSAC)
184
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Thrombolytic Drugs (cont’d)
 anistreplase (Eminase)
 alteplase (t-PA, Activase)
 reteplase (Retavase)
 tenecteplase (TNKase)
185
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Thrombolytic Drugs:
Mechanism of Action
 Activate the fibrinolytic system to break down the clot
in the blood vessel quickly
 Activate plasminogen and convert it to plasmin,
which can digest fibrin
 Reestablish blood flow to the heart muscle via
coronary arteries, preventing tissue destruction
186
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Thrombolytic Drugs:
Indications
 Acute MI
 Arterial thrombolysis
 DVT
 Occlusion of shunts or catheters
 Pulmonary embolus
 Acute ischemic stroke
187
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Thrombolytic Drugs:
Adverse Effects
 Bleeding
 Internal
 Intracranial
 Superficial
 Other effects
 Nausea, vomiting, hypotension, anaphylactic
reactions
 Cardiac dysrhythmias; can be dangerous
188
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Nursing Implications
Assess:
 Patient history, medication history, allergies
 Contraindications
 Baseline vital signs, laboratory values
 Potential drug interactions—there are MANY!
 History of abnormal bleeding conditions
189
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Heparin: Nursing Implications
 Intravenous doses are usually double-checked with
another nurse
 Ensure that SC doses are given SC, not IM
 SC doses should be given in areas of deep
subcutaneous fat, and sites rotated
190
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Heparin: Nursing Implications (cont’d)
 Do not give SC doses within 2 inches of:
 The umbilicus, abdominal incisions, or open wounds,
scars, drainage tubes, stomas
 Do not aspirate SC injections or massage
injection site
 May cause hematoma formation
191
Winter 2013
5/4/2017
Heparin: Nursing Implications (cont’d)
 IV doses may be given by bolus or IV infusions
 Anticoagulant effects seen immediately
 Laboratory values done daily to monitor coagulation
effects (aPTT)
 Protamine sulfate can be given as an antidote in
case of excessive anticoagulation
192
Winter 2013
5/4/2017
LWMHs: Nursing Implications
 Given subcutaneously in the abdomen
 Rotate injection sites
 Protamine sulfate can be given as an antidote in
case of excessive anticoagulation
193
Winter 2013
5/4/2017
Warfarin Sodium:
Nursing Implications
 May be started while the patient is still on heparin until
PT-INR levels indicate adequate anticoagulation
 Full therapeutic effect takes several days
 Monitor PT-INR regularly—keep follow-up
appointments
 Antidote is vitamin K
194
Winter 2013
5/4/2017
Warfarin:
Nursing Implications
 Many herbal products have potential interactions—
increased bleeding may occur
 Capsicum pepper
 Garlic
 Ginger
 Gingko
 Ginseng
 Feverfew
195
Winter 2013
5/4/2017
Anticoagulants:
Patient Education
Education should include:
 Importance of regular lab testing
 Signs of abnormal bleeding
 Measures to prevent bruising, bleeding, or tissue
injury
196
Winter 2013
5/4/2017
Anticoagulants:
Patient Education (cont’d)
Education should include (cont’d):
 Wearing a medical alert bracelet
 Avoiding foods high in vitamin K (tomatoes, dark leafy
green vegetables)
 Consulting physician before taking other meds or
over-the-counter products, including herbals
197
Winter 2013
5/4/2017
Antiplatelet Drugs:
Nursing Implications
Concerns and teaching tips same as for
Anticoagulants
 Dipyridamole should be taken on an empty stomach
 Drug-drug interactions
 Adverse reactions to report
 Monitoring for abnormal bleeding
198
Winter 2013
5/4/2017
Thrombolytic Drugs:
Nursing Implications
 Follow strict manufacturer’s guidelines for preparation
and administration
 Monitor IV sites for bleeding, redness, pain
 Monitor for bleeding from gums, mucous membranes,
nose, injection sites
 Observe for signs of internal bleeding (decreased BP,
restlessness, increased pulse)
199
Winter 2013
5/4/2017
Coagulation Modifier Drugs:
Nursing Implications
 Monitor for therapeutic effects
 Monitor for signs of excessive bleeding
 Bleeding of gums while brushing teeth, unexplained
nosebleeds, heavier menstrual bleeding, bloody or
tarry stools, bloody urine or sputum, abdominal
pain, vomiting blood
200
Winter 2013
5/4/2017
Coagulation Modifier Drugs:
Nursing Implications (cont’d)
 Monitor for adverse effects
 Increased BP, headache, hematoma formation,
hemorrhage, shortness of breath, chills, fever
201
Winter 2013
5/4/2017