Download Normandale-Cardiac-Medication-Handout

Towards a Greater Understanding of Cardiac
Medications
But first a little cardiac patho…
Foundational Cardiac Concepts:
Cardiac Output (CO) …CO=SVxHR
 Stroke volume-amount of blood that returns to right atrium from venous
circulation and left atrium from pulmonary veins
o Larger SV increases workload of the heart
o Faster HR increases cardiac O2 demands and workload
o Goal of medication therapy with any cardiac client is to DECREASE
cardiac workload through influencing SV, HR, Preload, Afterload and
Contractility
I. Preload
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Preload is the filling pressure of the RV-LV and is influenced by venous
return…higher venous return or blood volume in atria-the higher the SV will
be…opposite is also true
Pressure/Stretch in ventricles end diastole just before contraction
In a healthy heart, as you INCR Preload…You will increase stroke volume which
will increase force of contraction
Only up to a certain point-then further stretching may actually decrease
contractility
Drugs that cause venous dilation (nitrates)-DECREASE preload
Diuretics that eliminate excess fluid volume DECREASE preload
Starling’s Law of the Heart:
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The greater the preload- greater quantity of blood that can be
ejected during systole due ti INCR stretch of myocardium
But only up to a maximal point. Greatest force of contraction is
when the muscle fibers are stretched 2 ½ times their normal
length
Overstretch of cardiac muscle is like an overstretched rubber
band-will DECREASE cardiac contractility and efficiency over time
2). Afterload
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Force of resistance that the LV must generate to open aortic valve
Correlates w/SBP…How much pressure is needed to push blood out of the heart
into the aorta and into entire systemic circulation
Influenced by resistance of blood vessels in the body-are the arteries dilated or
constricted
Arterial vasodilators (Ca++ channel blockers (CCB), ACE inhibitors) DECREASE
afterload
©2011 Keith Rischer/www.KeithRN.com
3) Contractility: Inotropic-influencing contractility independent of Starling mechanism
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Ability of heart to change force of inherent contraction strength
Influenced by Ca++ in action potential…therefore CCB will do what to
contractility?
Decrease contractility (inotropic) DECREASE cardiac workload and O2 demands
Negative inotropic meds: CCB, beta blockers
Positive inotropic: Digoxin, Dopamine & Epinephrine gtts.
Ejection Fraction (EF) on echocardiogram
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65-70% normal
reflects that with each contraction 65-70% of the blood in the LV is
ejected into circulation
As this % goes down it is reflecting the loss of cardiac contractility and
degree of CHF
35% EF is half the normal cardiac output with each contraction
10-15% EF end-stage heart failure-near death
I.Angiotensin Converting Enzyme (ACE) Inhibitors…(end in “pril”)
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Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil)
Mechanism of Action: A normal plasma protein-renin is secreted by the kidneys when
BP falls which converts inactive liver protein angiotensinogen to angiotensin I. The
conversion to angiotensin II is enhanced by angiotensin-converting-enzymes (ACE) from
the lungs to one of the most potent vasoconstrictors known. The effects of angiotensin II
are:
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Vasoconstriction of arterioles and veins (incr. afterload)
Stimulation of the sympathetic nervous system (incr. workload of heart)
Retention of water by the kidneys due to aldosterone a hormone secreted by the
adrenal glands (incr. preload)
ACE inhibitors block the conversion of angiotensin I to angiotensin II. This inhibition
decreases angiotensin II concentrations and causes:
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Vasodilation which decreases BP (decr. Afterload) and decrease sodium and
water retention (decr. Preload).
Uses: HTN, CHF, CAD
Side Effects-most common: hypotension, dry cough, dizziness
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Angioedema (life threatening) Laryngeal swelling that can cause asphyxia.
Facial swelling also concerning precursor.
©2011 Keith Rischer/www.KeithRN.com
Nursing Considerations:
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Obtain BP before administering-hold typically if SBP <90
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Change position slowly-especially with elderly to prevent orthostatic changes
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Monitor for decreased WBC count, hyperkalemia as well as liver function, and
GFR, creatinine (metabolized by liver-excreted by kidneys)
II.Beta Blockers…(end in “lol”)
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Metoprolol (Lopressor)
Atenolol (Tenormin)
Propranolol (Inderal)
Mechanism of Action: Selectively inhibit beta (sympathetic/fight or flight) receptors
primarily of the heart (Beta 1). Sympathetic nervous system (SNS) stimulation normally
causes:
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Increased heart rate
Increased BP
Increase myocardium contractility and oxygen demand
ALL THESE EFFECTS INCREASE WORKLOAD OF THE HEART
By blocking the normal effects of SNS it effectively causes the opposite effects and
DECREASES workload of the heart…decreased heart rate, decreased BP, and
decreased contractility. This is why it must be used with caution in those with history of
congestive heart failure (CHF). CHF clients have excessive activation of SNS which will
worsen CHF over time. B-Blockers very effective to manage this complication of CHF.
Uses: HTN, CHF, acute MI, CAD, ventricular dysrhythmias
Side Effects-most common: bradycardia, hypotension, fatigue, weakness
Nursing Considerations:
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Obtain BP and HR before administering-hold typically if SBP <90. HR <60
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Change position slowly-especially with elderly to prevent orthostatic changes
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Contraindicated in worsening CHF, bradycardia of heart block…use with caution
in diabetes, liver disease
III.Calcium Channel Blockers
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Diltiazem (Cardizem)-arterial dilator and cardiac
Verapamil (Calan)- arterial dilator and cardiac
Nifedipine (Procardia)-primary arterial dilator
©2011 Keith Rischer/www.KeithRN.com
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Amlodipine (Norvasc)- primary arterial dilator
Mechanism of Action: Inhibits or “blocks” the influx of extracellular calcium into the
membranes of the heart and vascular smooth muscle cells of heart and body. This
blocking of calcium ions is responsible for causing the following:
 Dilation of coronary and systemic arteries w/resultant decrease in BP (improves
cardiac 02 supply & decr, afterload)
 Decrease of myocardium contractility (decr. Workload)
 Slows AV node conduction (decr. in heart rate)
Uses: HTN, angina, controlling rapid heart rate in SVT or atrial fibrillation
Side Effects-most common: peripheral edema, hypotension, constipation
Nursing Considerations:
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Change position slowly-especially with elderly to prevent orthostatic changes
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Measure I&O closely and fluid status due to potential for edema
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Monitor liver and kidney function (metabolized in liver-excreted by kidneys)
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Obtain BP and HR before administering-hold typically if SBP <90. HR <60
IV. Nitrates
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Nitroglycerine subl. (Nitrostat)-SHORT acting
Isosorbide Mononitrate (Imdur)-LONG acting
Isosorbide Dinitrate (Isordil)-LONG acting
Nitrodur topical patches-LONG acting
Mechanism of Action: Able to relax and dilate both coronary arterial vessels and
systemic venous smooth muscle.
 Dilation of veins reduces amount of blood that returns to heart (preload) so
chambers contain smaller volume. With less blood to pump, cardiac output is
reduced and workload of the heart decreased lowering myocardial oxygen
demand
 Dilation of coronary arteries can help improve blood flow to heart as well as well
as relieve angina caused by coronary artery vasospasm
Uses: Angina
Side Effects-most common: hypotension, tachycardia, dizziness, headache (dilates
cerebral vessels causing mini migraine)
Nursing Considerations:
©2011 Keith Rischer/www.KeithRN.com
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Tolerance common and serious problem with long acting nitrates. Nitrates lose
their effectiveness if transdermal patches remain on continually. Patches must be
taken off at night and then reapplied in the morning
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Contraindicated if client taking any erectile dysfunction meds as these are a
similar nitrate that improves blood circulation to the penis-synergistic effect can
cause dramatic hypotension
V. Diuretics
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Lasix (furosemide)-most potent-Loop of Henle-K+ waster
Bumex (bumetanide)
Hydrochlorathiazide (HCTZ)-mod. Potency-mod. K+ waster
Spirinolactone (Aldactone)-mild potency-K+ sparing
Mechanism of Action:
 Loop diuretics-most potent diuretics that prevent sodium reabsorption in the
loop of henle causing rapid/large diuresis with resultant loss of K+. Because of
their potency are not used for maintenance but when large diuresis is desired
such as in acute CHF exacerbation (decr. Preload).
 Thiazide diuretics-increases excretion of sodium and water by inhibiting sodium
reabsorption in distal tubule. Most common maintenance diuretic
 Potassium sparing diuretics-weakest of all diuretics due to not blocking
reabsorption of sodium. Used when client is at risk for developing hypokalemia
Uses: HTN, CHF, renal insufficiency/acute renal failure
Side Effects-most common: dehydration, orthostatic hypotension, hypokalemia,
hyponatremia, hypomagnesemia with loop and thiazide diuretics, potential for
hyperkalemia w/Aldactone
Nursing Considerations:
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Change position slowly-especially with elderly to prevent orthostatic changes
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Obtain BP before administering-hold typically if SBP <90
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Monitor sodium and K+ levels closely as well as GFR and creatinine
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Aldactone and ACE inhibitors can cause resultant hyperkalemia
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If on Aldactone-make sure does not use potassium based salt substitutes or
foods rich in K+
©2011 Keith Rischer/www.KeithRN.com
©2011 Keith Rischer/www.KeithRN.com