DRUGS AFFECTING the
CARDIOVASCULAR SYSTEM
Prepared and Presented by:
Ivy Monteclaro-Cornelia, RN
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THE HIGH RISK GROUPS
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Overview on Cardiovascular Drugs
Anti – Hypertensive Drugs
DiureticsAnti – Arrhythmic
AgentsAnti – Anginal AgentsCardiotonic AgentsDrugs Used to Treat
Anemia
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Anatomy and Physiology
HeartArteries Veins
Capillaries
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The Cardiovascular System:HEART
• located in the MEDIASTINUM• Enclosed by PERICARDIAL MEMBRANES parietal & visceral layer pericardial fluid : 50 ml • 3 layers:1. Epicardium2. Myocardium3. Endocardium
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Heart
• 4 chambers: 2 atria 2 ventricles
right atrium : receives deoxygenated blood
left atrium: receives oxygenated blood
right ventricle: pumps blood for pulmonary circulation
left ventricle: pumps blood for systemic circulation
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Heart
4 valves: 2 atrioventricular valves: tricuspid and
mitral 2 semilunar valves: pulmonic and aortic
prevent backflow or regurgitation
closing of the valves produces heart sounds
thus: S1 : closing of AV valves S2: closing of semilunar valves
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Heart
STARLING’s LAW OF THE HEART
- the farther the cardiac muscle is stretched, the stronger it springs back to its normal size
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THE HEART
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The Cardiac Cycle
• Diastole – period of cardiac muscle relaxation
• Systole - period of cardiac muscle contraction
• Cardiac Cycle – each period of systole followed by diastole
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The Cardiac Cycle
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The Cardiac Cycle
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The Cardiac Cycle
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The Cardiac Cycle
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Arteries, Capillaries and Veins
• resistance system : constrict and dilate
(arterial system)
• capillary system: connects the arterial and venous systems
• capacitance system: veins have the
capacity to hold large quantities of fluids as they distend with fluid volume
(venous system)
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Structure of arteries and Veins
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Structure of arteries and Veins
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ANTI – HYPERTENSIVE DRUGS
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Hypertension vs Hypotension
• Hypertension= pressure is above the normal limits for a sustained period= types:1. Primary/idiopathic/essential2. Secondary= Risk Factorssmoking, DM, high cholesterol level, >60 yrs old, genetic predisposition, gender ,alcohol
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HypertensionCategories Rating the Severity of
Hypertension
target organ damage:stroke or TIA, kidney disease, retinopathy, CHF,CAD
Classification Systolic (mmHg) Diastolic (mmHg)
Normal <120 and < 80
Pre-hypertension 120 – 139 Or 80 – 89
Stage 1 140 – 159 Or 90 – 99
Stage 2 >/= 160 Or >/= 100
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Hypotension• becomes too low, the vital centers in the brain as
well as the rest of the tissues of the body may not receive enough oxygenated blood to continue functioning
• Possible cause:1. When the heart muscle is damaged and unable
to pump effectively2. With severe blood loss, when volume drops
dramatically3. When there is extreme stress and the body’s
level of norepinephrine are depleted, leaving the body unable to respond to stimuli to raise the blood pressure
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Blood Pressure Control
The pressure in the cardiovascular system is determined by three elements:
• Heart Rate• Stroke Volume• Total Peripheral Resistance
Blood Pressure = cardiac output x peripheral resistance
Cardiac output = stroke volume x heart rate
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Renin-Angiotensin System
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Factors affecting BP
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Venous ReturnHeart Rate
Peripheral ResistanceElasticity of large arteries
Viscosity of the bloodLoss of Blood
Hormones
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Drug Therapy
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Lifestyle Modification
Blood Pressure Still Elevated
Start Drug Therapy
Uncomplicated Hypertension- Diuretics
- Beta Blocking Agents
If Complications are Present Recommended Tx- DM w/ proteinuria -ACE inhibitors
- CHF -ACE inhibitors
Diuretics
- Isolated Systolic HPN in older adults - Diuretics (preferred)
- Calcium antagonist
- MI - Beta antagonist
ACE inhibitors
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Procedure: 1) Start with low dose of long acting drug and titrate.
2) May consider use of low dose drug combinations.
Inadequate Patient Response
If no response or with S/E or A/E Drug tolerated but inadequateresponse
Substitute drug from other classificationAdd second drug from otherclassification
Response still inadequate
- Add another antihypertensive agents from other classification- May need to refer to a cardiologist or hypertensive specialist
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DIURETICS
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ACE INHIBITORS
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1. Therapeutic Actions and Indications
prevent ACE from converting angiotensin I to angiotensin II
leads to a decrease in blood pressure and in aldosterone secretion
to decrease the inactivation of bradykinin
increase synthesis of prostaglandin E
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2. Phamacokinetics
metabolized in the liver and excreted in the urine and feces cross the placenta
detected in the breast milk
3. Contraindications and Cautionsallergy impaired renal function pregnancy.caution CHF
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4. Adverse Effects • reflex tachycardia, chest pain, angina, CHF and
cardiac arrhythmias; GI irritations, ulcers, constipation and liver injury; renal insufficiency, renal failure and proteinuria and rash, alopecia, dermatitis and photosensitivity
• unrelenting cough• fatal pancytopenia and MI.
5. Clinically Important Drug – Drug Interaction• allopurinol• taken on an empty stomach, 1 hour before or 2
hours after meals
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Patient Teaching
1. Not to abruptly discontinue the drug.2. Teach how to take blood pressure.3. Explain that dizziness and lightheadedness
are expected during the first week of treatment (CAPOTEN).
4. If drug is taken SL, not to take anything PO for 30 minutes.
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Example of Drugs:
• Captopril (Capoten)• Enalapril (Vasotec)• Lisinopril (Prinivil, Zestril)• Quinalapril (Accupril)
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ANGIOTENSIN II RECEPTOR INHIBITORS
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1. Therapeutic Actions and Indications
binds with angiotensin II receptors sites in the vascular smooth muscle and in the adrenal gland
indicated to be used alone or in combination therapy for the treatment of hypertension and for treatment of CHF in patients who are intolerant to ACE inhibitors
2. Pharmacokineticsmetabolized in the liver by cytochrome P450 system
excreted in feces and urinecross the placenta
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3. Contraindications and Cautions• Allergy • Pregnancy and lactation• Caution : hepatic and renal dysfunction
4. Adverse Effects• associated with decrease in blood pressure • Cough
5. Clinically Important Drug to Drug interactions• decreased serum levels and loss of effectiveness
increases taken in combination with Phenobarbital
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Example of Drugs:
• Candesartan (Atacand)• Eprosartan (Teveten)• Irbesartan (Avapro)• Losartan (Cozaar)• Olmesartan (Olmetec)• Temisartan (Micardis)• Valsartan (Diovan)
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CALCIUM CHANNEL BLOCKERS
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1. Actions and Indicationsinhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells
a. depresses the myocardial contractilityb. slows cardiac impulse formation in the
conductive tissuesc. relaxes and dilates arteries
2. Pharmacokinetics
metabolized in the liver excreted in the urinecross the placenta and enter breast milk
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3. Contraindications and Cautions• Allergy • with heart block or sick sinus syndrome• with renal and hepatic dysfunction • pregnancy and lactation.
4. Adverse Effects• associated with effects on cardiac output and
smooth muscle• CNS effects include: dizziness, light headedness,
headache and fatigue• Cardiovascular effects include: hypotension,
bradycardia and heart block
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5. Clinically Important Drug to Drug Interactions
Drug to drug interactions vary with each of the calcium channel blockers used to treat hypertension
Note!!!!
interact with GRAPEJUICE
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Example of Drugs
• Amlodipine (Norvasc)• Diltiazem (Cardiazem)• Felodipine (Plendil)• Nicardipine (Cardene)• Nifedipine (Adalat) (strongest
peripheral smooth muscle dilator effect)
• Verapamil (Calan SR)
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SYMPATHOLYTICS
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Sympatholytics
5 groups:
1. Beta – adrenergic blockers2. Centrally acting alpha 2
agonists3. Alpha – adrenergic blockers4. Adrenergic neuron blockers
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Beta – Adrenergic BlockersSubclasses :
Beta1 and Beta 2 blockers
Location of Beta Receptors:
Beta 1 Beta 2
Compete with beta adrenergic agonists for available receptor site located on membrane of cardiac muscle, smooth muscle of bronchi and smooth muscles of blood vessels
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Beta – Adrenergic Blockers
Classification according to site of action:
1.Selective
Beta1 Selective, also known as CARDIOSELECTIVE
decrease BP and PR
2.Non – Selective
inhibit both Beta1 and Beta2 cause bronchospasm and impotence (inderal)
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Beta – Adrenergic Blockers
Beta1 antagonists Effects:
a.Atenolol (Tenormin)b.Esmolol (Brevibloc)c.Metoprolol (Lopressors, Betaloc)d.Acebutolol (Sectral)
Beta1 and Beta2 antagonits effects:e.Labetolol (Normodyne)f. Propanolol (Inderal)g.Timolol (Blocadren)h.Cardeviol (Coreg)
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1.Action
decrease COreduce release of renin, impede outflow of sympathetic impulses from
brain stem control center to peripheral , retard release of norepinephrine
2 Pharmacodynamics
metabolized in the liver, excreted in urine
cross placenta and breast milk
Beta – Adrenergic Blockers
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Beta – Adrenergic Blockers Contraindications and Cautions
• Sinus bradycardia• 3rd degree heart block• CAUTION: asthma, hepatic & renal problem,
type 1 diabetes
Adverse EffectsDizziness, drowsiness, hypotension
ALERT!!!!HypoglycemiaBronchospasmBradycardia
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Beta – Adrenergic Blockers
NURSING IMPLICATIONS!
Take apical pulse 1 full minuteMonitor for side/adverse effects
PATIENT TEACHING!!!!
Take radial pulse before administering the drug
Avoid alcoholic beveragesChange position slowly
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Centrally Acting Alpha Agonist
decrease sympathetic response from brainstem to peripheral vessels
decrease sympathetic activityincrease vagus activity
decrease C.O.decrease epinephrine and norepinephrine and
renin release
reduced peripheral resistance
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Centrally Acting Alpha Agonist
for mild to moderate HPN
CAUTION:
CVD, hx of depression, pregnant, CRF, peripheral vascular disease (REYNAUD’S PHENOMENON), blood disorders
Common:
CLONIDINE (catapress)METHYLDOPA (aldoment)
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Centrally Acting Alpha Agonist
CLONIDINE (catapress)
available in TRANSDERMAL PREPARATION : 7 day duration of action
may be left with bathing
Note! ASSESS SKIN IRRITATION
PO: administer 1 hour before or 2 hours after meals
NO ABSOLUTE CONTRAINDICATIONS
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CLONIDINE (catapress)Patient Teaching!
• Advice the importance of periodic examination.
• NO ABRUPT WITHDRAWAL!• Take the last dose before bedtime to reduce daytime drowsiness.
• Move slowly• For long term tx: periodic eye exam (RETINAL DEGENERATION)
Centrally Acting Alpha Agonist
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Centrally Acting Alpha Agonist
METHYLDOPA (aldomet)
not to be used with impaired LIVER FUNCTIONmay cause BLOOD DYSCRASIAS
NOTE!!!
both can retain sodium and water
thus: given with DIURETICS
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Alpha Adrenergic Blockers
prevent norepinephrine from activating alpha1 receptors on vascular smooth muscle to produce
vasoconstriction
VASODILATATION AND DECREASED BP
useful in treating those with lipid abnormalitiesSafe for patients with DM
Common: PRAZOSIN (minipress)
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Alpha Adrenergic Blockers
PRAZOSIN (minipress) can slightly increase HR
Common S/E:Drowsiness, headache,
malaise
NO ABSOLUTE CONTRAINDICATIONS
CAUTION: in people who drive and operate heavy machinery
ALERT!!!Can cause SYNCOPE if taken with nitroglycerin
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Adrenergic Neuron Blockers
block norepinephrine release from sympathetic nerve endings
= decrease BP
can retain SODIUM and WATER
common: RESERPINE and GUANETHIDINE
NOTE!!
Use of RESERPINE can cause vivid dreams, nightmares and suicidal ideation
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Direct Acting Arteriolar Vasodilators
Relax the smooth muscles of blood vessels
Promote blood flow to brain and kidneys
Decreased BPSodium and Water are retained
S/E: REFLEX TACHYCARDIA (treated with Beta Blockers)
Common: HYDRALAZINE MINOXIDIL NITROPUSSIDE DIAZOXIDE
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Direct Acting Arteriolar Vasodilators
HYDRALAZINE (Apresoline)
given in HYPERTENSIVE EMERGENCIES
Given IVTT: onset of action : 10 – 20 minutes peak : 15 – 30 minutes
A/E: headache, dizziness, depression, tachycardia,
SLE symptoms
NOTE!!!If with S/S of infection, DISCONTINUE: blood dyscrasias
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Direct Acting Arteriolar Vasodilators
NITROPRUSSIDE (nipride)given in HYPERTENSIVE EMERGENCIES
Given IVTT: onset of action: 30 – 60 seconds peak : 1 - 2min
administered through an INFUSION PUMP with container WRAPPED in aluminum foil
S/E is due to rapid infusion: GI and CNS
Note!!! Metabolized first to CYANIDE then to THIOCYANATE
DISCONTINUE if with cyanide toxicity:Coma, dilated pupils, pink color, shallow respirations, imperceptible PR, distant heart sounds, hypotension, absent reflexes
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Discharge Instructions for all anti-hypertensive Agents
1.Advice all possible adverse effects of the drug.
2.Do not abruptly discontinue or skip doses of medications.
3.Change position gradually.4.Avoid alcohol and hot bath/showers.5.Do not take OTC without consulting
physician.6.Monitor weight and eat low-sodium food.7.Take BP and have a diary.8.Do no drive or operate heavy machinery
until drug effects are established.
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ANTI – ARRHYTHMIC AGENTS
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Conduction System of the Heart
1.Automaticity= refers to the cell’s ability to spontaneously initiate an impulse
2. Excitability= results from ion shifts across cell membrane and indicates how well a cell responds to an electrical stimulus
3. Conductivity= ability of a cell to transmit an electrical impulse to another cardiac cell
4. Contractility= refers to how well the cell contracts after receiving a stimulus
4 characteristics of CARDIAC CELLS
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ACTION POTENTIAL Phase O
DepolarizationSodium gates open and sodium ion rushes in
Phase 1When sodium ion concentration are equal inside and outside the cell
Phase 2Cell membrane becomes less permeable to sodiumCalcium goes in and potassium begins to leave
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ACTION POTENTIAL
Phase 3
Rapid repolarization as the gates close and potassium rapidly moves out of the cell
Phase 4
Cell comes to rest
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AUTONOMIC INFLUENCES
influence the heart rate, rhythm and strength of contraction
PARASYMPATHETIC SA node, atrial muscles, AV junction
slows the heart rate and decrease the speed of conduction at the AV node
SYMPATHETIC
stimulates the heart to beat speeds up conduction at AV node
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CARDIAC ARRHYTHMIAS
disruption in the cardiac rate or rhythm
DYSRHYTHMIA
interfere work of the heart affecting C.O.arise due to changes in the automaticity/conductivity
influencing factors:
Drugs, acidosis, hypoxia, electrolyte imbalances
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DRUG THERAPY
Class I : SODIUM CHANNEL BLOCKERS
Class II : BETA – ADRENERGIC BLOCKERS
Class III: POTASSIUM CHANNEL BLOCKERS
Class IV: CALCIUM CHANNEL BLOCKERS
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
Blocks the influx of SODIUM into the cell during rapid depolarization (phase O)
For life-threatening VENTRICULAR ARRHYTHMIASHas pro-ARRHYTHMIC EFFECT
CATEGORIES:
1.Class Ia2.Class Ib3.Class Ic
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
PHARMACOKENITECSAbsorbed at GITMetabolized in LIVER and excreted in URINECross placenta, breast milk
CONTRAINDICATIONS and CAUTIONS
AllergyBradycardia or heart blockCHF/shock
CAUTION! Pregnant , liver and kidney dysfunction
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
Class Ia : Bind to sodium channels ad interfere with sodium influx Depression of CONDUCTION VELOCITY
Class Ib: either INCREASE or NO EFFECT on conduction velocity
Class Ic: can cause SINUS ARREST, AV block and LIFE –THREATENING VENTRICULAR ARRHYTHMIAS
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
ADVERSE EFFECTS:Associated with membrane stabilizing effects on action potentialCNS: dizziness, drowsiness, slurred speech, tremors – convulsionGIT : metallic taste, n/vCARDIO: PROARRHYTHMIA, hypotensionRESPI: respiratory depressionOTHERS: bone marrow depression
INTERACT w/!!!Digoxin, beta blockers, oral anticoagulants(quinidine) avoid food that alkalinize urine (citrus juice)
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
QUINIDINEfor atrial fibrillation/flutter, PVC, paroxysmal supraventricular tachycardia
stabilizes cell membrane by preventing ready movement of Na and K
A/E:With indirect ANTICHOLINERGIC EFFECTPeripheral VASODILATION
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
NURSING IMPLICATION• Monitor ECG, VS, eletrolytes, CBC, kidney & liver
function.• Monitor quinidine serum: 3 – 6 mcg/ml• Take apical pulse.• Taken with food if with GI upset.• Clients taking DIGOXIN with quinidine is at risk for
DIGOXIN TOXICITY.PATIENT TEACHING
• Regular dental check-up.• Adverse effects (ex. bleeding gums, s/s of
hypotension)• Not to discontinue without DR’s advice.
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DRUG THERAPY
CLASS I: SODIUM CHANNEL BLOCKERS
PROCAINAMINDE (Pronestyl)Action is similar with quinidine, EXCEPT:
• Less effective in controlling abnormal ectopic pacemaker activity
• Few anticholinergic effects• More potent positive INOTROPIC effects
NURSING IMPLICATIONS:• Given through infusion pump.• ECG monitoring.• VS• Serum level 4 – 8 mcg/ml
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DRUG THERAPY
CLASS Ib: SODIUM CHANNEL BLOCKERS
LIDOCAINE HYDOCHLORIDEDOC for suppressing ventricular arrhythmias (before)Given with loading dose then an infusion thereafter
A/E:CNS stimulation: SEIZURE!!!
NURSING IMPLICATIONS:1.Monitor VS, ECG, neurologic status.2.Monitor serum level : 1.5 – 5mcg/ml.
Other Drug:Tocainide Hcl (Tonocard)
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DRUG THERAPY
CLASS Ic: SODIUM CHANNEL BLOCKERS
FLECAINIDE (Tambocor)NO anticholinergic effects
A/E:Bradycardia, chest pains, heart failure, constipation, headaches
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DRUG THERAPY
CLASS II: BETA ANDRENEGICS
ANTAGONISTS
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DRUG THERAPY
CLASS III: POTASSIUM CHANNEL BLOCKERS
Blocks K+ channels prolonging phase 3, which prolongs repolarization and slows rate and conduction of heart
PHARMACOKINETICSMetabolized in liver and excreted in urine. With little information regarding pregnancy and lactation.
CONTRAINDICATIONS and CAUTIONSNo absolute contraindications!CAUTIONS: shock, hypotension, respiratory depression
Note! Can increase digoxin, & oral anticoagulants
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DRUG THERAPY
CLASS III: POTASSIUM CHANNEL BLOCKERS
ADVERSE EFFECTS:n/v and GI distress, weakness & dizziness, hypotension, CHF and arrhythmia
Common Drugs:
Bretylium tosylate (Bretylate)Amniodarone (Cordarone)Ibutilide fumarateDofetilide (Tikosyn)Sotalol (Betapace, Betapace AF)
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DRUG THERAPY
CLASS III: POTASSIUM CHANNEL BLOCKERS
AMNIODARONE (cordarone)Decrease automaticity, prolongs AV conductionBlocks Ca2+, K+, Na+ and beta receptors (complex effects on heart, therefore limited use)
DOC for VENTRICULAR FIBRILLATION or pulse less VENTRICULAR TACHYCARDIA
NOTE!it can cause PHOTOSENSITIVITYIncrease level of phenytoin, theophylline, digoxin
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DRUG THERAPY
CLASS III: CALCIUM CHANNEL BLOCKERS
blocks calcium channel in the cell membrane leading to depression of depolarization and a
prolongation of phases 1 and 2 slowing automaticity and conduction
with effect on heart muscle;
DILTIAZEM (cardizem)VERAPAMIL (calan)
indicated for: SUPRAVENTRICULAR TACHYCARDIA
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DRUG THERAPY
CLASS III: CALCIUM CHANNEL BLOCKERS
PharmacokineticsMetabolized in the liver and excreted in the urineCan cross the placenta
CONTRAINDICATIONS & CAUTIONSAllergyPregnancy and lactation
Caution!!! CHF and hypotension, liver/kidney disease
Adverse Effects are related to changes in the ACTION POTENTIAL
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
NURSING PROCESS1.Assessment - Baseline Data (present sickness,
laboratory and diagnostics exams2. Nursing Diagnoses - Decreased cardiac output - Risk for activity intolerance - Poor tissue perfusion3. Planning - Client will no longer experience
abnormal sinus rhthym - client will comply
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
ANTI – ANGINAL DRUGS
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
BLOOD SUPPLY TO THE MYOCARDIUM
provided by RIGHT and LEFT CORONARY ARTERIES arising from the BASE of AORTA
Right Atrium and Ventricle = right coronary artery
Left Atrium and Ventricle = left coronary artery (anterior branch and circumflex branch
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
BLOOD SUPPLY TO THE MYOCARDIUM
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
CORONARY ARTERY DISEASE
Coronary Atherosclerotic Heart Disease
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
CORONARY ARTERY DISEASE
Coronary Atherosclerotic Heart Disease
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
CORONARY ARTERY DISEASE
PathophysiologyRISK FACTORS
Non- Modifiable age
Genderrace
heredity
ModifiableStress, diet, sedentary
livingSmoking, alcohol, HPN,
Obesity, DM, OCP
Endothelial Injury
Desquamation of Endothelial Lining
Increased Permeability / Adhesion Molecules
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
CORONARY ARTERY DISEASE
Lipids and Platelets Assimilate into the Area
Oxidized Lipids attracts Monocytes & Macrophages to the site
Plaques begin to form and imbed into the endothelium
Lipids are engulfed by the cells and smooth muscle cells develop
Coronary Atherosclerotic Heart Disease
Decreased Coronary Tissue Perfusion
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
CORONARY ARTERY DISEASE
Coronary Ischemia
Decreased Myocardial Oxygenation
Angina PectorisMyocardial Infarction
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
What is ANGINA/ANGINA PECTORIS?
• acute cardiac pain caused by inadequate blood flow to the myocardium
• Paintransient, paroxysmal substernal or precordial
described as HEAVINESS or TIGHTNESS , INDIGESTION
radiates in one or both arms, left shoulder, jaw, neck, back
precipitated by activity / exertion
relieved by REST and NITROGLYCERIN
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
PAIN PATTERN IN ANGINA
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
PAIN PATTERN IN ANGINA
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
PAIN PATTERN IN ANGINA
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
ANGINA PECTORIS
Pathophysiology
Reduced Coronary Tissue Perfusion
Diminished Myocardial Oxygenation
Anaerobic Metabolism
Increased Lactic Acid Production (Lactic Acidosis)
PAIN
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DRUG THERAPYANTI – ARRHYTHMIC AGENTS
4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
ANGINA PECTORIS
Associated S/S:Pallor
Diaphoresis
Dyspnea
Faintness
Palpitations
Dizziness
Digestive Disturbance
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
The IDEAL Anti – Anginal Drugs:
1.Establish a balance between coronary blood flow and metabolic demands of the heart.
2.Have a local effect rather than systemic.
3.Promote oxygen extraction by the heart from the arterial flow.
4.Be effective when taken orally and have sustained action.
5.Have an absence of tolerance.
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
NITRATES
caused generalized vascular and coronary vasodilation thus increasing blood flow
Directly acts on the smooth muscle
Common Drugs:
Nitroglycerin (Transderm Patch, Nitro – Bid)Isosorbide dinitrate (Isordil)Isosorbide mononitrate (Imdur)
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPYNitroglycerin
Vascular Smooth Muscle Interacts w/ sulfhydryl groups
Nitric Oxide (active form)Activates guanylate cyclase
GTP to GMP
Decrease Intracellular Calcium
VASODILATATION
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
NITROGLYCERIN
SL: rapidly absorbed in JUGULAR VEIN & RIGHT ATRIUM
Common S/E: HEADACHE
Note!!!!should be tapered if discontinuedshould be given slowly if through IV push to
prevent REFLEX TACHYCARDIA
Other S/E: hypotension, dizziness, rashes (using ointment/patch)
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPYNITROGLYCERIN
Route Onset Duration
IV 1 – 2 min 3 – 5 min
SL 1 – 3 min 30 – 60 min
Translingual Spray
2 min 30 – 60 min
Transmucosal Tablet
1 – 2 min 3- 5 min
Oral, SR Tablet 20 – 45 min 8 – 12 min
Topical Ointment
30 – 60 min 4- 8 H
Transdermal 30 – 60 min 24 H
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
NURSING DIANOSIS!!!
• Decreased cardiac output related to hypotensive effects.
• Risk for injury related to CNS or cardiovascular effects.
• Ineffective tissue perfusion (total body) related to hypotension or change in cardiac output.
* Deficient knowledge regarding therapy.
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
NURSING IMPLICATIONS!!!
Check V/S especially blood pressure.
For SL and transbuccal, check the oral mucosa.
Let the patient assume sitting/supine position.
No more than 3 tablets should be taken in 15 – minute period.
Ointment / Patch should be applied in hairless areas.Nitro – Patch usually applied in the morning, rotate site.
Offer sips of water before giving SL nitrates.
Observe for side effects.
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPYDISCHARGE TEACHING!!!!!
Take maximum of 3 doses only at five minute interval.
Change position slowly.
Avoid alcohol.
Carry 3 tablets always in the pocket.
Store in cool, dry, dark colored, airtight container.
“Fizzles” or burns under the tongue indicates potency.
Stored tablets should be discarded after 3 months.
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
Beta Adrenergic Blockers
block the stimulatory effect of sympathetic nervous system
block the beta adrenergic receptors (in the heart and juxtaglomerular apparatus) and vasoconstriction and prevent increase in heart rate and increased intensity of myocardial contraction
Common Drugs:
Metoprolol (Betaloc)Propanolol (Inderal)Nadolol (Corgard)
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
CONTRAINDICATIONS
bradycardia, asthma, COPD
CAUTION
DM and Thyrotoxicosis
ADVERSE EFFECTS
related to blockage of SNSRespiratory System: bronchospasm
and cough
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPYADVERSE EFFECTS
CNS : Headache, dizziness, weaknessGI : N/VCardio : Hypotension and Reflex tachycardia
COMMON DRUGS
Atenolol (Tenormin)Metoprolol tartrate (Lopressor)Nadolol (Corgard)Propanolol (Inderal)
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
Calcium Channel Blockers
Calcium
activates myocardial contraction, increasing workload and the need for more oxygen
Indications:
Angina (Prinzmetal’s angina)Hypertention
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
Therapeutic ActionsCalcium movement(inhibited)
action potential altered & muscle cell contraction blockage
Myocardial contractility depresses
Decrease cardiac workload and O2 consumption
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4. Nursing Interventions - Monitor vital signs. - Administer drug by IV push over 2 – 3 minute period. - Monitor ECG tracing.
5. Evaluation6. Patient Teaching - report S/E - Avoid alcohol, caffeine and tobacco
DRUG THERAPY
Common Drugs:
Amlodipine (Norvasc)Diltiazem (Cardizem)Verapamil (Calan)Nifedipine (Adalat)
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CARDIOTONIC AGENTS
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BASIC ACTION OF CARDIOTONIC AGENTS
affect INTRACELLULAR CALCIUM
increased contractility
increased cardiac output
increased renal blood flow
increased urine output
decreased blood volume
DECREASED CARDIAC WORKLOAD
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CARDIAC MUSCLE
sarcomere
action and myosin
Contraction process requires:
1.Oxygen2.Energy3.Calcium
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CONGESTIVE HEART FAILURE
LEFT SIDED HEART FAILURE
causes:MI, HPN, Aortic/ Mitral
StenosisReduced myocardial
contractilityIncreased cardiac workloadDecreased diastolic filingObstruction of left atrial
emptyingIncreased left atrial pressure
Left Sided CHF
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Blood goes back to Pulmonary beds
Increased pressure in
Pulmonary beds
Fluid shift into intraalveolar
and interarveolar
spaces
Pulmonary edema
Decreased stroke volume
Decreased tissue perfusion
Increased cellular hypoxia
S/S of PULMONARY PROBLEMS
Decreased blood
Flow to the kidneysRAAS
activation
Vasoconstriction & Na &
water reabsorption
Increased ECF volume
Increased total volume
Increased systemic BP
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RIGHT SIDED HEART FAILURE
causes:LSCHF
Pulmonary EmbolismRight Ventricular InfarctionCongenital Septal Defect
Reduced Myocardial Contractility
Increased Cardiac WorkloadDecreased Diastolic FillingObstruction of Right Atrial
EmptyingIncreased Right Atrial Pressure
Blood goes back from RV to RA
S/S of RSCHF
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DRUG THERAPY
VASODILATORS
decrease the workload of the heart
relaxes the vascular smooth muscle decreasing the
afterload
decreases venous return thus decreasing preload
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DRUG THERAPY
VASODILATORS
Nitroprusside (Nipride)Hydralazine (Apresoline)
Nifedipine (a calcium channel blocker)
Captopril (Capoten)
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DRUG THERAPY
DIURETICS
to decrease the circulating blood volume thereby
decreasing the preload
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DRUG THERAPY
BETA ADRENEGIC AGONISTS
stimulate the beta receptors in the SNS increasing calcium
flow thereby increasing contraction
INOTROPIC EFFECT
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DRUG THERAPY
BETA ADRENERGIC AGONISTS
Dobutamine
with direct activation of BETA 1 increasing contraction but
induce less heart rate and less decrease in peripheral vascular
resistance
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DRUG THERAPY
CARDIAC GLYSCOSIDES (digitalis glycosides)
DIGOXIN (LANOXIN)
Action:
increase intracellular calcium during depolarization
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DRUG THERAPY
CARDIAC GLYCOSIDES
1. Positive inotropic effect2. Negative Chronotropic
effect3. Diuretic Effect
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DRUG THERAPY
CARDIAC GLYCOSIDE
with narrow therapeutic margin:
0.5 – 2ng/mlAdverse Effects:
ArrhythmiasBradycardia
Visual disturbance
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DRUG THERAPY
CARDIAC GLYCOSIDES
NURSING IMPLICATIONS:
1. Half life is longer in elderly.2. Monitor CBC, electrolytes,
liver & kidney functions.3. Hold if apical heart rate is:
<60 or > 120 adults<90 or infants<70 children and adolescents
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DRUG THERAPY
CARDIAC GLYCOSIDES
4. Encourage food high in POTASSIUM.5. Give after meals.6. Avoid IM injections.7. S/S of TOXICITY:
bradycardia GI manifestations
halo vision8. ANTIDOTE:
Digoxin Immune Fab (Digi-bind)
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DRUG THERAPY
CARDIAC GLYCOSIDES
ALERT!!!!
increase toxicity with HYPOKALEMIA
serum level increases with QUINIDINE
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DRUG THERAPY
PHOSPHODIESTERASE INHIBITORS
Inotropic agents
blocks phosphodiesterase
increase cAMP
Increase intracellular calcium
Increase contraction
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DRUG THERAPY
PHOSPHODIESTERASE INHIBITORS
Inamrinone (Inocor)Milrinone (Primacor)
Adverse Effects:
HypotensionVentricular arrhythmias
Thrombocytopenia (Inamrinon)
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DRUG THERAPY
PHOSPHODIESTERASE INHIBITORS
ALERT!!!!!
give solution separatelyit PRECIPITATES…….
Drug Used to Treat Anemia
Blood
Slide 10.1b
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 10.1
Anemia
Deficiency in the number of ERYTHROCYTES, quantity of Hgb, & volume of Hct
Not a specific disease, manifestation of pathologic process
Grouped according to:
MORPHOLOGIC
ETIOLOGIC
Anemia
Anemia
ETIOLOGIC CLASSIFICATION1. Decreased Erythrocyte Production
=IDA=Thalassemia
2. Defective DNA Synthesis= Cobalamin (Vitamin B12) Deficiency= Folic Acid Deficiency
3. Decreased Number of Erythrocyte Precursors= Aplastic Anemia= Anemia of Myeloproliferative Disease= Chronic Disease or Disorders
Anemia
ETIOLOGIC CLASSIFICATION
4. Chemotherapy
5. Blood Loss (Acute or Chronic)
6. Increased Erythrocyte Destruction= Intrinsic= Extrinsic
MORPHOLOGIC CLASSIFICATION
Normocytic, Normochromic(normal size & color)
Macrocytic, normochromic(large size, normal color)
Microcytic, hypochromic(small size, pale color)
Anemia
Iron Supplement
Mechanism of Action:
Replaces iron stores needed for RBC development, energy, and O2 transport, utilization
Therapeutic Indications:
Prevention & Correction of IDA
Contraindications:
hypersensitivity
Adverse Effects:
Nausea, epigastric pain, constipation, black stools
ALERT for Oral Iron Therapy!!!
• Enteric Coated or sustained release (SR) should not be used
• Iron should be taken about 1 hour after meals• Vitamin c enhances Iron absorption• Increase fluid and fiber intake• Avoid consumption of milk, tea, coffee with Oral Iron
• Liquid preparation to be administered using straw
• Warn client that it can change color and consistency of stool
Iron Supplement
THANK YOU!!!
questions???clarifications???