10/22/2015 Winter 2013 1 DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS.
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Transcript of 10/22/2015 Winter 2013 1 DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS.
04/21/23Winter 20131
DRUGS AFFECTING THE CARDIOVASCULAR and RENAL
SYSTEMS
CARDIAC PROBLEM AREAS
Winter 20132
PUMP
CIRCULATION TO MUSCLE
ELECTRICAL SYSTEM
CARDIAC A&P REVIEW
04/21/23Winter 20133
CARDIAC A&P REVIEW
04/21/23Winter 20134
CARDIAC A&P REVIEW
Winter 20135
HEART FAILUREChapter 22
04/21/23Winter 20136
LEFT SIDED HEART FAILURE (CHRONIC HEART FAILURE)
RESTLESSORTHOPNEASOB (SHORTNESS OF BREATH)DOE (DYSPNEA ON EXERTION)
Common Causes for Heart Failure
Inadequate ContractilityMyocardial Infarction
Inadequate FillingAtrial fibrillation
Pressure OverloadHypertension
Volume OverloadHypervolemia
Complete list on pg. 336
04/21/23Winter 20137
DRUG CLASSES FOR HEART FAILURE
04/21/23Winter 20138
ANGIOTENSIN – CONVERTING ENZYME INHIBITORS
ANGIOTENSIN II RECEPTOR BLOCKERSBETA-BLOCKERSB-TYPE NATRIURETIC PEPTIDEPHOSPHODIESTERASE INHIBITORSCARDIAC GLYCOSIDES
ANGIOTENSIN –CONVERTING ENZYME INHIBITORS
ACE InhibitorsPrevents vasoconstriction, sodium and water
resorptionLisinopril
Indicated for heart failure, hypertension, acute Myocardial Infarction
04/21/23Winter 20139
ANGIOTENSIN II RECEPTOR BLOCKERS
ARBsvalsartan (Diovan)
Potent vasodilating effectsDecreases systemic vascular resistanceUsed in combination with diuretics to treat Heart
Failure and Hypertension
04/21/23Winter 201310
BETA-BLOCKERS
Block sympathetic nervous system stimulation of the heartReduce heart rate, delayed AV node conduction,
reduced myocardial contractility and decreased myocardial automaticity.
metoprololDecreased workload of the heart
04/21/23Winter 201311
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 failureCauses diuresis, urine sodium loss and vasodilation
04/21/23Winter 201312
PHOSPHODIESTERASE INHIBITORS
inamrinone and milrinonePositive inotropic and vasodilating effectsDecrease cardiac work load Parenteral onlyShort-term management of CHF
04/21/23Winter 201313
CARDIAC GLYCOSIDES(aka: digitalis glycosides)
04/21/23Winter 201314
INCREASE THE EFFICIENCY OF THE HEART BY IMPROVING THE CONTRACTION OF THE HEART MUSCLEPOSITIVE INOTROPIC ACTION
INCREASING THE FORCE OF MYOCARDIAL CONTRACTION
Negative chronotropic effect – reduced heart rateNegative dromotropic effect – decreased automaticity at the
SA note, AV node and bundle of HIS
digoxin (Lanoxin)Not first line drug in Heart Failure
WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY??
04/21/23Winter 201315
INADEQUATE CONTRACTILITYMI (MYOCARDIAL INFARCTION)CORONARY ARTERY DISEASECARDIOMYOPATHY
INADEQUATE FILLINGATRIAL FIBRILLATION
Atrial Fibrillation
04/21/23Winter 201316
NORMAL SINUS RHYTHM (NSR)
A FIB
WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY??
04/21/23Winter 201317
PRESSURE OVERLOADHYPERTENSION
VOLUME OVERLOADHYPERVOLEMIA
DIGOXIN (LANOXIN)
04/21/23Winter 201318
DIGITALIZATIONThe 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
DIGOXIN (LANOXIN)
04/21/23Winter 201319
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!
ADVERSE EFFECTS OF CARDIAC GLYCOSIDES MEDICATIONS
04/21/23Winter 201320
DYSRYTHMIASHEADACHEFATIGUE
ANOREXIAN, V, D
NURSING CONSIDERATIONS
04/21/23Winter 201321
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
DIGITALIS TOXICITY
04/21/23Winter 201322
SIGNS AND SYMPTOMSN, VANOREXIAVISUAL DISTURBANCES
MAY SEE YELLOW, GREEN, BLUE HALOSCONFUSIONBRADYCARDIAEKG CHANGES
TREATMENT FOR DIG TOXICITY
04/21/23Winter 201323
STOP TAKING THE DRUGDIGOXIN IMMUNE FAB (DIGIBIND)
WHAT CAUSED THE PROBLEM?HYPOKALEMIA R/T DIURETIC DRUGSLIVER FAILURE
ANTIDYSRHYTHMIC DRUGSChapter 23
04/21/23Winter 201324
DYSRHYTHMIA (ARRHYTHMIA)
ANY DEVIATION FROM THE “NORMAL” RHYTHM
“NORMAL” ELECTRICAL PATTERN OF THE HEART
04/21/23Winter 201325
04/21/23Winter 201326
Vaughan Williams Classification
System commonly used to classify antidysrhythmic drugs
Based on the electrophysiologic effect of particular drugs on the action potential
04/21/23Winter 201327
Vaughan Williams Classification (cont’d)
Class IClass IaClass IbClass Ic
Class IIClass IIIClass IVOther
04/21/23Winter 201328
Vaughan Williams Classification:Mechanism of Action
Class IMembrane-stabilizing drugsFast sodium channel blockersDivided into Ia, Ib, and Ic drugs,
according to effects
04/21/23Winter 201329
Vaughan Williams Classification:Mechanism of Action and Indications
Class I: moricizineGeneral class I drugHas characteristics of all three subclassesUsed for symptomatic ventricular and
life-threatening dysrhythmias
04/21/23Winter 201330
Vaughan Williams Classification:Mechanism of Action and Indications (cont’d)
Class Ia: quinidine, procainamide, disopyramide
Block sodium (fast) channelsDelay repolarizationIncrease APD (action potential duration)
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome
04/21/2331 Winter 2013
04/21/2332 Winter 2013
04/21/23Winter 201333
Vaughan Williams Classification:Mechanism of Action and Indications
(cont’d)
Class Ib: phenytoin, lidocaine
Block sodium channelsAccelerate repolarizationIncrease or decrease APDUsed for ventricular dysrhythmias only
Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation
04/21/23Winter 201334
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, Wolff-
Parkinson-White syndrome, supraventricular tachycardia dysrhythmias
04/21/2335 Winter 2013
04/21/2336 Winter 2013
04/21/2337 Winter 2013
04/21/23Winter 201338
Vaughan Williams Classification:Mechanism of Action and Indications (cont’d)
Class II: beta-blockers: atenolol, esmolol, metaprolol, propranololReduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
Depress phase 4 depolarizationGeneral myocardial depressants for both
supraventricular and ventricular dysrhythmiasAlso used as antianginal and antihypertensive drugs
04/21/23Winter 201339
Vaughan Williams Classification:Mechanism of Action and Indications (cont’d)
Class III: amiodarone, sotalol*, ibutilide, others Increase APDProlong repolarization in phase 3Used 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
04/21/23Winter 201340
Vaughan Williams Classification:Mechanism of Action and Indications (cont’d)
Class IV: verapamil, diltiazem
Calcium channel blockersInhibit slow-channel (calcium-dependent) pathways
Depress phase 4 depolarizationReduce AV node conductionUsed for paroxysmal supraventricular
tachycardia (PSVT); rate control for atrial fibrillation and flutter
04/21/2341 Winter 2013
04/21/23Winter 201342
Vaughan Williams Classification: Other Antidysrhythmics
Digoxin, adenosine Have properties of several classes and are
not placed into one particular class
04/21/23Winter 201343
Unclassified Antidysrhythmic
adenosine (Adenocard)Slows conduction through the AV nodeUsed to convert paroxysmal supraventricular
tachycardia to sinus rhythmVery short half-life—less than 10 secondsOnly administered as fast IV pushMay cause asystole for a few secondsOther adverse effects minimal
ADVERSE REACTION TO ANTIDYSRHYTHMICS
04/21/23Winter 201344
N, V, DDIZZINESSHEADACHEBLURRED VISIONCAN CAUSE DYSRHYTHMIAS !!
NURSING CONSIDERATIONS
04/21/23Winter 201345
MONITOR PULSE RATEIF SENDING PT HOME – TEACH THEM HOW TO
MONITOR THEIR PULSE
ALWAYS CHECK ALL VS BEFORE ADMINISTERING THE MEDICATION
NURSING CONSIDERATIONS
04/21/23Winter 201346
MONITOR FOR FLUID RETENTION
DO NOT STOP DRUGS ABRUPTLY
AVOID ALCOHOL
CHAPTER 24CHAPTER 24
Antianginal DrugsAntianginal Drugs
04/21/2347 Winter 2013
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
04/21/2348 Winter 2013
IschemiaIschemia
Poor blood supply to an organIschemic heart disease
Poor blood supply to the heart muscleAtherosclerosisCoronary artery disease
Myocardial infarction (MI)Necrosis, or death, of cardiac tissueDisabling or fatal
04/21/2349 Winter 2013
04/21/23Winter 201350
04/21/23Winter 201351
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)
04/21/2352 Winter 2013
Drug Classifications for Angina
Nitrates/nitritesBeta-blockersCalcium channel blockers
04/21/2353 Winter 2013
Therapeutic Objectives
Increase blood flow to ischemic heart muscle
and/or
Decrease myocardial oxygen demand
04/21/2354 Winter 2013
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
04/21/2355 Winter 2013
Nitrates/Nitrites
Available formsSublingual*Buccal*Chewable tabletsOral capsules/tabletsIntravenous solutions*
*Bypass the liver and the first-pass effect
Transdermal patches* Ointments* Translingual sprays*
04/21/2356 Winter 2013
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
04/21/2357 Winter 2013
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
04/21/2358 Winter 2013
Nitrates/Nitrites (cont’d)
Rapid-acting formsUsed to treat acute anginal attacks
Sublingual tabletsIntravenous infusion
Long-acting formsUsed to PREVENT anginal episodes
04/21/2359 Winter 2013
Nitrates/Nitrites (cont’d)
NitroglycerinPrototypical nitrateLarge 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
04/21/2360 Winter 2013
Nitrates
Isosorbide dinitrate (Isordil, Sorbitrate, Dilatrate SR)
Isosorbide mononitrate (Imdur, Monoket, ISMO)Used for:
Acute relief of anginaProphylaxis in situations that may provoke anginaLong-term prophylaxis of angina
04/21/2361 Winter 2013
Nitrates (cont’d)
Adverse effectsHeadaches
Usually diminish in intensity and frequency with continued use
Tachycardia, postural hypotensionTolerance may develop
04/21/2362 Winter 2013
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 replenishTransdermal forms: remove patch at bedtime for 8
hours, then apply a new patch in the morning
04/21/2363 Winter 2013
Beta-Blockers
atenolol (Tenormin)metoprolol (Lopressor)propranolol (Inderal)nadolol (Corgard)
04/21/2364 Winter 2013
04/21/23Winter 201365
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
04/21/2366 Winter 2013
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
04/21/2367 Winter 2013
Beta Adrenergic Blockers (cont’d)
IndicationsAnginaAntihypertensiveCardiac dysrhythmiasCardioprotective effects, especially after MISome used for migraine headaches,
essential tremors, and stage fright
04/21/2368 Winter 2013
Beta Adrenergic Blockers (cont’d)
Adverse effectsBody System Adverse EffectsCardiovascular Bradycardia, hypotension,
second- or third-degree heart block; heart failure
Metabolic Altered glucose and lipidmetabolism
04/21/2369 Winter 2013
Beta Adrenergic Blockers (cont’d)
Adverse effects (cont’d)Body System Adverse Effects
CNS Dizziness, fatigue, mental depression, lethargy,
drowsiness, unusual dreams
Other Impotence, wheezing, dyspnea, constipation
04/21/2370 Winter 2013
04/21/23Winter 201371
Calcium Channel Blockers
verapamil (Calan, Isoptin)diltiazem (Cardizem)nifedipine (Procardia)amlodipine (Norvasc)Others
04/21/2372 Winter 2013
04/21/23Winter 201373
Calcium Channel Blockers (cont’d)
Mechanism of actionCause coronary artery vasodilationCause peripheral arterial vasodilation,
thus decreasing systemic vascular resistance
Reduce the workload of the heartResult: decreased myocardial oxygen
demand
04/21/2374 Winter 2013
Calcium Channel Blockers (cont’d)
IndicationsFirst-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
04/21/2375 Winter 2013
Calcium Channel Blockers (cont’d)
Adverse effectsVery acceptable adverse effect and safety
profile
May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea, other adverse effects
04/21/2376 Winter 2013
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
04/21/2377 Winter 2013
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
04/21/2378 Winter 2013
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
04/21/2379 Winter 2013
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
04/21/2380 Winter 2013
Nursing Implications
NitroglycerinInstruct 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
04/21/2381 Winter 2013
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
04/21/2382 Winter 2013
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
04/21/2383 Winter 2013
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
04/21/2384 Winter 2013
Nursing Implications
Nitroglycerin (cont’d)If anginal pain occurs:
Stop activity and sit or lie downTake a sublingual tablet, if no relief, call
911/Emergency Services immediately!If no relief in 5 minutes, take a second sublingual
tabletIf no relief in 5 minutes, take a third sublingual
tabletDo not try to drive to the hospital
04/21/2385 Winter 2013
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
04/21/2386 Winter 2013
Nursing Implications
Calcium channel blockersConstipation is a common problem; instruct
patients to take in adequate fluids and eat high-fiber foods
04/21/2387 Winter 2013
Nursing Implications
Beta-blockersPatients 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 high-fiber foods
04/21/2388 Winter 2013
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
04/21/2389 Winter 2013
Nursing Implications
Antianginal drugsMonitor for adverse reactions
Allergic reactions, headache, lightheadedness, hypotension, dizziness
Monitor for therapeutic effectsRelief of angina, decreased BP, or both
04/21/2390 Winter 2013
CHAPTER 25CHAPTER 25
Antihypertensive DrugsAntihypertensive Drugs
04/21/2391 Winter 2013
ATHEROSCLEROSIS
04/21/23Winter 201392
DEPOSITS OF CALCIUMLIPIDSCHOLESTROL
ON THE WALLS OF THE ARTERIES
04/21/23Winter 201393
04/21/23Winter 201394
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.
Blood Pressure
Blood pressure = CO × SVR CO = cardiac outputSVR = systemic vascular resistance
Hypertension = high blood pressure
04/21/2395 Winter 2013
04/21/23Winter 201396
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
04/21/2397 Winter 2013
Compelling Indications
Post-MI
High cardiovascular risk
Heart failure
Diabetes mellitus
Chronic kidney disease
Previous stroke
04/21/2398 Winter 2013
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
04/21/2399 Winter 2013
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
04/21/23100 Winter 2013
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
04/21/23101 Winter 2013
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
04/21/23102 Winter 2013
Primary Hypertension
Hypertension can also be defined by its cause
Unknown cause Essential, idiopathic, or primary hypertension 90% of casesGenetic (hereditary) – 30%
African-AmericanObesityRenal failureAdvanced ageAny of the above factors complicated by lifestyle
04/21/23103 Winter 2013
Secondary Hypertension
Known cause Secondary hypertension 10% of cases
Causes such as Pheochromocytoma, pre-eclampsia, renal artery disease
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Take the Salt quiz
04/21/23Winter 2013105
http://www.medicinenet.com/salt_quiz/quiz.htm
Antihypertensive Drugs
Medications used to treat hypertension
CategoriesAdrenergic drugsAngiotensin converting enzyme (ACE) inhibitorsAngiotensin II receptor blockers (ARBs)Calcium channel blockers (CCBs)DiureticsVasodilators
04/21/23106 Winter 2013
Adrenergic Drugs: Centrally Acting Alpha2-Receptor Agonists
clonidine (Catapres)methyldopa (Aldomet)
Can be used for hypertension in pregnancy
04/21/23107 Winter 2013
Adrenergic Drugs: Peripherally ActingMechanism of Action
Peripheral alpha1-blockers/antagonistsBlock alpha1-adrenergic receptors
doxazosin (Cardura)terazosin (Hytrin)
Results in decreased blood pressure
04/21/23108 Winter 2013
Adrenergic Drugs:Mechanism of Action (cont’d)
Beta-blockersReduce BP by reducing heart rate through
beta1-blockadeCause reduced secretion of reninLong-term use causes reduced peripheral vascular
resistancePropranolol, atenolol, othersNewest: nebivolol (Bystolic)—beta1-selectiveResult: decreased blood pressure
04/21/23109 Winter 2013
Adrenergic Drugs:Mechanism of Action (cont’d)
Dual-action alpha1- and beta1-receptor blockersBlock alpha1-adrenergic receptors
Reduction of heart rate (beta1-receptor blockade)Vasodilation (alpha1-receptor blockade)
carvedilol (Coreg) and labetalolResult in decreased blood pressure
04/21/23110 Winter 2013
Adrenergic Drugs: Adverse Effects
High incidence of orthostatic hypotension Most common
Dry mouth Drowsiness, sedation Constipation
Other Headaches Sleep disturbances Nausea Rash Cardiac disturbances (palpitations), others
04/21/23111 Winter 2013
04/21/23Winter 2013112
Adrenergic Drugs (cont’d)
Beta1 Adrenergic blockers
Act in the peripheryReduce heart rate owing to 1-blockadeExamples: nebivolol (bystolic), propranolol (Inderal),
atenolol (Tenormin), others
04/21/23113 Winter 2013
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
04/21/23114 Winter 2013
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
04/21/23115 Winter 2013
ACE Inhibitors:Mechanism of Action (cont’d)
Aldosterone stimulates water and sodium resorption
Result: increased blood volume, increased preload, and increased BP
04/21/23116 Winter 2013
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
04/21/23117 Winter 2013
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
04/21/23118 Winter 2013
04/21/23Winter 2013119
ACE Inhibitors: Indications (cont’d)
Drugs of choice in hypertensive patients with HF
Drugs of choice for diabetic patients
04/21/23120 Winter 2013
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), othersNewer drugs, long half-lives, once-a-day dosing
Several other drugs available
04/21/23121 Winter 2013
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
04/21/23122 Winter 2013
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!
04/21/23123 Winter 2013
04/21/23Winter 2013124
Angiotensin II Receptor Blockers
(A-II blockers, or ARBs)
Newer class
Well tolerated
Do not cause a dry cough
04/21/23125 Winter 2013
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
04/21/23126 Winter 2013
Angiotensin II Receptor Blockers
losartan (Cozaar, Hyzaar)
valsartan (Diovan)
eprosartan (Teveten)
irbesartan (Avapro)
Others
04/21/23127 Winter 2013
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
04/21/23128 Winter 2013
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
04/21/23129 Winter 2013
Calcium Channel Blockers:Mechanism of Action
Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction
Results inDecreased peripheral smooth muscle toneDecreased systemic vascular resistanceDecreased blood pressure
04/21/23130 Winter 2013
Calcium Channel Blockers
Benzothiazepinesdiltiazem (Cardizem, Dilacor)
Phenylalkaminesverapamil (Calan, Isoptin)
Dihydropyridinesamlodipine (Norvasc), bepridil (Vascor),
nicardipine (Cardene)nifedipine (Procardia), nimodipine (Nimotop)
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Calcium Channel Blockers: Indications
Angina
Hypertension
Dysrhythmias
Migraine headaches
Raynaud’s disease
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Calcium Channel Blockers:Adverse Effects
CardiovascularHypotension, palpitations, tachycardia
GastrointestinalConstipation, nausea
OtherRash, flushing, peripheral edema, dermatitis
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DIURETICS AND DRUGS THAT EFFECT THE RENAL SYSTEM
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Diuretics
Decrease plasma and extracellular fluid volumes
ResultsDecreased preloadDecreased cardiac output Decreased total peripheral resistance
Overall effectDecreased workload of the heart, and decreased
blood pressure
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CARBONIC ANHYDRASE INHIBITORS (CAIs)
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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
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WHEN TO USE CAIs?
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ACETOZOLAMIDE (DIAMOX)
USED IN THE TREATMENT OF:
GLAUCOMAEDEMAEPILEPSY
HIGH ALTITUDE SICKNESS (PULMONARY EDEMA)
LOOP DIURETICS
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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
WHEN DO WE USE LOOP DIURETICS?
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Heart Failure
Liver failure
Hypertension
Renal failure
Increase renal excretion of calcium
FUROSEMIDE (LASIX)
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BLOCK SODIUM AND CHLORIDE RESORPTION
USEFUL FOR RAPID DIURESIS
HYPOKALEMIA IS OFTEN A SIDE EFFECT
OSMOTIC DIURETICS
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PRODUCES OSMOTIC PRESSURE IN THE GLOMERULUS
PULLS WATER INTO THE RENAL TUBULES FROM THE SURROUNDING TISSUE
DECREASING CELLULAR EDEMA!
WHEN TO USE AN OSMOTIC DIURETIC?
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CEREBRAL EDEMA
INCREASED INTRAOCULAR PRESSURE
NOT USED FOR PERIPHERAL EDEMA – NOT ENOUGH SODIUM LOSS
MANNITOL (OSMITROL)
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PRODUCES OSMOTIC PRESSURE IN THE GLOMULAR FILTRATE
PULLS WATER FROM THE RENAL TUBULES AND SURRONDING TISSUE
USED IN ACUTE RENAL FAILURE AND CEREBRAL EDEMA
POTASSIUM SPARING DIURETICS
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WORK IN COLLECTING DUCTS AND DISTAL CONVOLUTED TUBLES
INTERFERE WITH SODIUM + POTASSIUM EXCHANGE
RELEASE Na+ AND H2O –> RETAIN K+
WHEN TO USE POTASSIUM SPARING DIURETICS?
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HYPERTENSIONCHF (CHRONIC HEART FAILURE)
SPIRONOLACTONE (ALDACTONE)
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INTERFERES WITH SODIUM AND POTASSIUM EXCHANGE
NURSE MUST BE AWARE OF THE DANGER OF HYPERKALEMIA
THIAZIDE AND RELATED DIURETICS
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RELATED TO SULFONAMIDE ANTIBIOTICS (ALSO
CAIs)
PREVENT RESORPTION OF SODIUM (Na) POTASSIUM (K) AND CHLORIDE (Cl) IN THE DISTAL CONVOLUTED TUBULE
WHEN TO USE THIAZIDE DIURETICS?
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CAN BE USED ALONE OR IN COMBINATION WITH OTHER DIURETICS TO TREAT:
EDEMAHYPERTENSION
CRONIC HEART FAILURERENAL FAILURE
HYDROCHLORTHIAZIDE (HCTZ) (ESIDRIX)
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INHIBIT RESORPTION OF SODIUM, POTASSIUM AND CHLORIDE
COMMONLY USED WITH OTHER ANTIHYPERTENSIVES
MAJOR SIDE EFFECTS ARE RELATED TO ELECTROLYTE BALANCE
Diuretics (cont’d)
Thiazide diuretics are the most commonly used diuretics for hypertension
Listed as first-line antihypertensives in the JNC-7 guidelines
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Vasodilators:Mechanism of Action
Directly relax arteriolar and/or venous smooth muscle
Results in:Decreased systemic vascular responseDecreased afterload (PVR)Peripheral vasodilation
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Vasodilators
diazoxide (Hyperstat)
hydralazine HCl (Apresoline)
minoxidil (Loniten)
sodium nitroprusside (Nipride, Nitropress)
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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
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Vasodilators: Adverse Effects
hydralazineDizziness, headache, anxiety, tachycardia, nausea
and vomiting, diarrhea, anemia, dyspnea, edema, nasal congestion, others
sodium nitroprussideBradycardia, hypotension, possible cyanide toxicity
(rare)
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Vasodilators: Adverse Effects (cont’d)
diazoxideDizziness, headache, anxiety, orthostatic hypotension,
dysrhythmias, sodium and water retention, nausea, vomiting, hyperglycemia in diabetic patients, others
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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
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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
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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
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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
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CHAPTER 28CHAPTER 28
Coagulation Modifier DrugsCoagulation Modifier Drugs
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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
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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
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Coagulation Modifier Drugs
AnticoagulantsInhibit the action or formation of clotting factorsPrevent clot formation
Antiplatelet drugsInhibit platelet aggregationPrevent platelet plugs
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Coagulation Modifier Drugs (cont’d)
Hemorheologic drugsPentoxifylline(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 drugsLyse (break down) existing clots
Hemostatic or antifibrinolytic drugsPromote blood coagulation
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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 preventClot formation (thrombus)An embolus (dislodged clot)
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Anticoagulants:Mechanism of Action
Vary depending on drug
Work on different points of the clotting cascadeDo not lyse existing clots
Heparin and low–molecular-weight heparinsTurn off coagulation pathway and prevent clot
formation
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Anticoagulants:Mechanism of Action (cont’d)
All ultimately prevent clot formationHeparinLow–molecular-weight heparinswarfarin
(Coumadin)Anti-Thrombin (Inhibit thrombin molecule)
fondaparinux (Arixtra) dabigatran (Pradaxa)
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Pradaxa channel 7 and FDA
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http://www.thedenverchannel.com/news/call7-investigators/pradaxa-maker-sued-over-claims-company-didnt-inform-doctors-about-dangers-of-blood-thinning-drug
Anticoagulants (cont’d)
Prevention of clot formation also prevents:StrokeMyocardial infarction (MI)Deep vein thrombosis (DVT)Pulmonary embolism (PE)
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Anticoagulants: Indications
Used to prevent clot formation in certain settings where clot formation is likely
Myocardial infarctionUnstable anginaAtrial fibrillationIndwelling devices, such as mechanical heart valvesMajor orthopedic surgery
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Anticoagulants:Adverse Effects
BleedingRisk increases with increased dosagesMay be localized or systemicHeparin-induced thrombocytopenia (HIT)
May also cause:Nausea, vomiting, abdominal cramps,
thrombocytopenia, others
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Anticoagulants (cont’d)
HeparinMonitored by activated partial thromboplastin times
(aPTTs)Parenteral (IV or SC)Short half-life (1 to 2 hours)Effects reversed by protamine sulfate
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Anticoagulants (cont’d)
Low–molecular-weight heparinsenoxaparin (Lovenox) and dalteparin (Fragmin)More predictable anticoagulant response
o Do not require laboratory monitoringGiven subcutaneously
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Anticoagulants (cont’d)
warfarin sodium (Coumadin)Given orally onlyMonitored by prothrombin time (PT) and International
Normalized Ratio (INR) (PT-INR)Vitamin K can be given if toxicity occurs
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Antiplatelet Drugs
Prevent platelet adhesionaspirindipyridamole (Persantine)clopidogrel (Plavix) and ticlopidine (Ticlid)
ADP inhibitorstirofiban (Aggrastat), eptifibatide (Integrilin), abciximab
(ReoPro)New class, GP IIb/IIIa inhibitors
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Antiplatelet Drugs: Indications
Antithrombotic effects Reduce risk of fatal and nonfatal strokesAcute unstable angina and MI
Adverse effectsVary according to drug
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Antifibrinolytic Drugs
Prevent the lysis of fibrinResult in promoting clot formation
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Antifibrinolytic Drugs (cont’d)
Enhance blood clottingaminocaproic acid (Amicar)desmopressin (DDAVP)
Similar to ADHAlso used in the treatment of diabetes insipidus
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Antifibrinolytic Drugs:Indications
Prevention and treatment of excessive bleedingHyperfibrinolysisSurgical complicationsExcessive oozing from surgical sites such as chest
tubesReducing total blood loss and duration of bleeding
in the postoperative periodTreatment of hemophilia or von Willebrand’s
disease
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Antifibrinolytic Drugs:Adverse Effects
Uncommon and mildRare reports of thrombotic eventsOthers include:
Dysrhythmia, orthostatic hypotension, bradycardia, headache, dizziness, fatigue, nausea, vomiting, abdominal cramps, diarrhea, others
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Thrombolytic Drugs
Drugs that break down, or lyse, preformed clots
Older drugsstreptokinase and urokinase
Newer drugsTissue plasminogen activator (t-PA)Anisoylated plasminogen-streptokinase activator
complex (APSAC)
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Thrombolytic Drugs (cont’d)
anistreplase (Eminase)alteplase (t-PA, Activase)reteplase (Retavase)tenecteplase (TNKase)
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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
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Thrombolytic Drugs: Indications
Acute MIArterial thrombolysisDVTOcclusion of shunts or cathetersPulmonary embolusAcute ischemic stroke
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Thrombolytic Drugs: Adverse Effects
BleedingInternalIntracranialSuperficial
Other effectsNausea, vomiting, hypotension, anaphylactic
reactionsCardiac dysrhythmias; can be dangerous
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Nursing Implications
Assess: Patient history, medication history, allergiesContraindicationsBaseline vital signs, laboratory valuesPotential drug interactions—there are MANY! History of abnormal bleeding conditions
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Heparin: Nursing ImplicationsIntravenous 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
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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 siteMay cause hematoma formation
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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
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LWMHs: Nursing Implications
Given subcutaneously in the abdomen
Rotate injection sites
Protamine sulfate can be given as an antidote in
case of excessive anticoagulation
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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
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Warfarin:Nursing Implications
Many herbal products have potential interactions—increased bleeding may occur
Capsicum pepperGarlicGingerGingkoGinsengFeverfew
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Anticoagulants:Patient Education
Education should include:Importance of regular lab testing
Signs of abnormal bleeding
Measures to prevent bruising, bleeding, or tissue injury
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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
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Antiplatelet Drugs:Nursing Implications
Concerns and teaching tips same as for
Anticoagulants
Dipyridamole should be taken on an empty stomachDrug-drug interactionsAdverse reactions to reportMonitoring for abnormal bleeding
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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)
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Coagulation Modifier Drugs:Nursing Implications
Monitor for therapeutic effects
Monitor for signs of excessive bleedingBleeding of gums while brushing teeth, unexplained
nosebleeds, heavier menstrual bleeding, bloody or tarry stools, bloody urine or sputum, abdominal pain, vomiting blood
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Coagulation Modifier Drugs:Nursing Implications (cont’d)
Monitor for adverse effectsIncreased BP, headache, hematoma formation,
hemorrhage, shortness of breath, chills, fever
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