NURS 1950: Pharmacology I
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Objective 1: describe the relationship of
calcium to electrical activity of the heart
Resting:
Preload:
Afterload:
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Heart dependent upon influx of calcium
Ca+ enters channels in the cardiac cell
membrane and go into the cell along with Na
K+ comes out
Cardiac cells contract
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Objective 2: describe how the ANS affects the
heart rate
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The ANS is the primary controller of heart
rate
Cholinergic (parasympathetic) vagal fibers are
close to the SA node
Stimulation with acetylcholine slows the heart
rate
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Sympathetic (adrenergic) nerves also
innervate the heart
Stimulation causes norepinephrine to be
released.
Increases heart rate, slows refractory period
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Objective 3: describe how cardiac drugs
affect cardiac action
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1. Increase or decrease the force of
myocardial action
Positive inotropics
Negative inotropics
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2. Increase or decrease heart rate by altering
SA node impulse conduction
Positive chronotropics
Negative chronotropics
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3. Increase or decrease conduction of AV
impulses
Positive dromotropics
Negative dromotropics
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Diuretics to decrease blood volume
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Figure 24.1 Pathophysiology of heart failure
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Objective 4: identify the action of cardiac
glycosides
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Digoxin & relatives
Come from Natural sources
Helpful in CHF
Have a positive inotropic effect
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Increases mechanical efficiency of heart
This pumps more blood
With increased blood to kidneys, diuresis
occurs, edema reduced
Cardiac glycosides also have negative
chronotropic effect,
Negative dromotropic effect
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Action
◦ Thought that they cause release of free calcium
within the cardiac muscle cell
◦ Also change the electrical activity of myocardium
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Decrease velocity of electrical conduction,
prolong refractory period in AV conduction
system
Increase vagal tone
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Objective 5: relate how the effects of digitalis
are beneficial to the client with CHF
Recall the signs/symptoms of CHF
How do you think cardiac glycosides improve
this condition?
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Objective 6: describe the usefulness of
digitalis in the treatment of atrial fibrillation
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What is atrial fibrillation?
What activity of the cardiac glycosides
improve this condition?
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Chronotropic/dromotropic effects
◦ Suppress impulse conduction through the AV node
◦ This prevents excessive atrial activity from reaching
ventricles
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Objective 7: list the generic and brand names
of the digitalis preparations
Digitalis preparations similar in
pharmacological properties, toxic
effects
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Digoxin (Lanoxin, Lanoxicaps): oral or IV
Onset 30-120 minutes oral
Peaks 2-6 hrs
Duration 2-4 days
Eliminated by kidney
◦ Used most often as rapid onset, short duration
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Must take apical pulse 1 minute before
administration
Hold if under 60, contact MD
Blood levels needed
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Objective 8: define digitalization
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Digitalization is the administration of digitalis
that is more than the maintenance dose
This raises the blood level quickly to
therapeutic range
◦ May also be called a loading dose
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Example
◦ Oral dose of digoxin 0.5-0.75 mg
◦ 0.25-0.5 mg then given every 6-8 hours until
desired blood level reached
◦ Then maintenance dose: 0.125-0.5 mg daily
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Objective 9: list symptoms of digitalis toxicity
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Digitalis toxicity:
◦ GI distress: N/V, anorexia, and/or
diarrhea (flu like symptoms)
◦ May have excessive salivation and
abdominal pain
◦ Neurological: restless, irritable, lethargy,
drowsiness, and/or confusion
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May have vision changes, changes in color
◦ May have halos, amblyopia and diplopia
◦ Cardiac effects: development of
arrhythmias (bradycardia, primary AV
block)
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Objective 10: identify factors which
predispose digitalis toxicity
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Toxicity predisposition: hypokalemia as
cardiac muscles more sensitive to the
glycosides
Renal impairment as 60-90% excreted by
kidney
IV administration: rapid accumulation can
occur
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Treatment
◦ Hold the drug
◦ Use digoxin immune fab (Digibind)
 Antigen-binding fragments combine
with digoxin to neutralize its action
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Prototype drug: furosemide (Lasix)
Mechanism of action: to increase urine flow,
reducing blood volume and cardiac
workload
Primary use: to reduce edema and
pulmonary congestion
Adverse effects: dehydration, electrolyte
imbalance, hypotension, ototoxicity
Click here to view an animation on the topic of furosemide.
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Prototype drug: digoxin (Lanoxin)
Mechanism of action: to cause more forceful
heartbeat, slower heart rate
Primary use: to increase contractility or
strength of myocardial contraction
Adverse effects: neutropenia, dysrhythmias,
digitalis toxicity
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Prototype drug: Metoprolol (Lopressor,
Troprol XL)
Mechanism of action: block cardiac action of
sympathetic nervous system to slow heart
rate and B/P, reducing workload of heart
Primary use: to reduce symptoms of heart
failure and slow progression of disease
Adverse effects: fluid retention, worsening
of heart failure, fatigue, hypotension,
bradycardia, heart block
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Drugs: hydralazine (Apresoline); (isosorbide
dinitrate (Isordil)
Mechanism of action: to relax blood vessels
Primary use: to lower blood pressure
Used for clients who cannot take ACE
inhibitors
Adverse reactions: reflex tachycardia,
orthostatic hypotension
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Prototype drug: milrinone (Primacor)
Mechanism of action: to block enzyme
phosphodiesterase in cardiac and smooth
muscle
Primary use: as short-term therapy for heart
failure
Adverse effects: hypokalemia, hypotension,
ventricular dysrhythmias
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Objective 11: describe the nursing
responsibilities associated with administering
cardiac glycosides preparations
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Take apical pulse 1 full minute
Hold if under 60, over 100 in adults
Report any evidence of irregular rhythm
Observe for toxicity S/S
Monitor K+ if on diuretics
Encourage K+ rich foods
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Teach client to take pulse
Teach S/S of toxicity
If hypothyroid, sensitive to digitalis
Draw blood levels periodically
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Atherosclerosis narrows heart’s vessels
Blood flow impeded
Demand exceeds supply = anginal pain
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Objective 12: describe the actions of the
antianginal drugs
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Drugs are used to dilate coronary arteries
This brings in oxygen and nutrients
Supply = demand so no pain
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Objective 13: identify the drugs used to treat
angina pectoris
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Nitroglycerin
Calcium channel blockers
Beta blockers
ACE inhibitors
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Nitroglycerin drugs
Works by relaxing arterial and venous smooth
muscle
Dilate coronary arteries
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Liquid nitroglycerin unstable, highly volatile
Oral tablets stable, non-explosive
Can be given sublingual for rapid, predictable
action
Can be transmucosal, aerosol translingual
spray, IV, transdermal
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Ointment: placed on paper with inches
marked off
Amount prescribed placed on the paper,
taped into place
4-8 hours of action
(Nitro-bid, Nitrol)
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Nitroglycerin patches: worn 12-14 hours
“Patch-off” period of 6-12 hours
Prevents tolerance
(Transderm-Nitro, Nitro-Dur)
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IV nitroglycerin in early treatment, then
another form
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Long acting forms for prophylaxis
◦ Erythrityl tetranitrate (Cardilate)
◦ Pentaerythritol tetranitrate (PETN)
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Objective 14: list the side effects of
nitroglycerin
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Tolerance
Headache
Postural hypotension
Dizziness
Weakness
Syncope
◦ Don’t use alcohol with nitros
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Nitrates can increase intraocular and/or
intracranial pressure
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Objective 15: identify the nursing
responsibilities associated with administering
the nitroglycerin preparations
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Teach: when angina occurs, take 3 tabs in 15
min; if no pain relief, call 911
Keep nitro in original container, cap tightly
closed
Store in cool, dry place
Rotate sites of topical applications
Monitor BP during therapy
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Shelf-life is 6 months. If burning/stinging
sensation under tongue, drug still potent
Replace 3 months after opening bottle
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Objective 16: identify the beta-adrenergic
blocker used to treat angina
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Examples: propranolol, Atenolol
Decrease heart rate, contractility
◦ Results in reduction of myocardial oxygen
consumption
◦ Better if used with nitrates
 Can not use in COPD, CHF, heart block,
bradycardia, DM
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When used with nitrates, hypotensive
episodes more likely to occur
Drugs used
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Atenolol (Tenormin)--prototype
Metoprolol (Lopressor)
Nadolol (Corgard)
Propranolol (Inderal)
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Objective 17: identify the calcium channel
blockers used to treat angina
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Nifedipine (Adalat, Procardia)
Diltiazem HCl (Cardizem, Dilacor SR)-prototype
Verapamil (Calan, Isoptin)
Bepridil (Vascor)
Nicardipine HCl (Cardene)
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These drugs create coronary vasodilation,
increased coronary blood flow, lowered blood
pressure, increased cardiac output, and relax
coronary artery spasms
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Prototype drug: nitroglycerin (Nitrostat)
Mechanism of action: relax both arterial and
venous smooth muscle; dilate coronary
arteries
◦ Short acting-terminate acute angina episode
◦ Long-acting-decrease severity and frequency of
episodes
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Primary use: for lowering myocardial oxygen
demand
Adverse effects: hypotension, dizziness,
headache, flushing of face, rash
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Prototype drug: atenolol (Tenormin)
Mechanism of action: to reduce the cardiac
workload by slowing heart rate and
reducing contractility
Primary use: for prophylaxis of stable angina
Adverse effects: fatigue, insomnia,
drowsiness, impotence, bradycardia,
confusion
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Prototype drug: diltiazem (Cardizem)
Mechanism of action: to reduce cardiac
workload by relaxing arteriolar smooth
muscle; dilate coronary arteries
Primary use: for lowering blood pressure;
bring more oxygen into myocardium
Adverse effects: hypotension, bradycardia,
heart failure, constipation, headaches,
dizziness, edema
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Objective 18: identify the ACE inhibitors used
to treat angina
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The angiotensin-converting enzyme
inhibitors decrease myocardial oxygen
demands
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Captopril (Capoten)
Lisinopril (Prinivil)--prototype
Ramipril (Altace)
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Prototype drug: lisinopril (Prinivil, Zestril)
Mechanism of action: to enhance excretion
of sodium and water
Primary use: to decrease blood pressure and
reduce blood volume; dilate veins
Adverse effects: first-dose hypotension,
cough, hyperkalemia, renal failure
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Objective 19: nursing care
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Frequency, nature, precipitants of angina
attack
Lifestyle changes made
Effectiveness of coronary vasodilators in relief
of pain
Monitor VS, esp. BP
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Ineffective tissue perfusion, cardiac function
RT angina
Risk for injury RT side effects of coronary
vasodilators
Deficient knowledge RT health alteration and
medication regimen
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Client will
◦ Verbalize decrease in attacks
◦ Not experience injury due to coronary vasodilitation
◦ Verbalize s/s of drug toxicity and report to MD
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What teaching is done for clients taking
nitroglycerin?
What teaching is done for clients taking
calcium channel blockers, ACE inhibitors,
beta blockers?
What will the nurse monitor when clients are
on these medications?
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