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62 Cards in this Set

  • Front
  • Back
Drug Therapy for HF
•General aims are for benefit of
heart or kidneys
drugs Improve cardiac contractility
ACE inhibitors or ARBs
•Cardiac glycosides
drug Reduce preload
diuretics to reduce excess fluid
drug Reduce afterload:
vasodilators
Ventricular restructuring and rate control
•beta-blocker
Digitalis (Cardiac Glucosides)
•Prototype:
digoxin (Lanoxin)
Digitalis (Cardiac Glucosides)
•Prototype: digoxin (Lanoxin)
•Action AND ADME
action
–positive inotrope, negative chronotrope and negative dromotrope
–potent, small doses (0.125 or 0.25 mg/day)
•ADME
–oral, IM, or IV administration
•formulation greatly affects absorption
–t 1/2 is 36 hrs
–narrow therapeutic range: 0.5-0.8 mg/mL
Digoxin
•Pharmacological effects and indication
•Pharmacological effects
–increases cardiac contractility
–decreases electrical conduction rate
–indirectly decreases HR and increases sodium and water excretion
•Indications
–HF
–atrial fibrillation or other supraventricular dysrhythmia when ventricular rate too rapid
What is a pulse deficit?
Difference between
apical and radial
digoxin Drug-drug interactions
Drug-drug interactions
– drugs that reduce absorption or decrease fxn
• antacids, laxatives, cholesterol-lowering agents, ACE/ARB
– drugs that depress cardiac function
• beta blockers, calcium channel blockers
– hypokalemia
• the most common cause of dig overdose
• even therapeutic levels may be too high if K is low
• most common offender is diuretic use
Nursing Considerations of Digoxin
• Cardiac function
– watch HR, dysrhythmias
• Electrolyte imbalances
– hypokalemia and hypomagnesemia increase risk of toxicity
Monitor effect of other drugs containing
sodium or potassium, use of diuretics
• Check heart rate:
– Need to take apical pulse for 1 full minute prior to
administering drug
– Okay to give with food but not if meal has high
fiber content--best if 1 hr ac or 2 hr pc
– hyperkalemia and hypercalcemia may produce
dysrhythmias
• Renal insufficiency patients
– decreases excretion of dig; easier toxic
• Female patients
def Angina Pectoris
•Myocardial ischemia
–inadequate flow of oxygenated blood to the heart muscle
–S/S: constricting pain in the chest which can radiate to the L arm, jaw, face, back, etc.
•Is not the same as Myocardial infarction
–Angina is ischemia of heart tissue, not death
–If remove trigger (i.e. rest) pain subsides
Chronic Angina
•Treatment
Chronic Angina
•Treatment
–first line is drug therapy
–secondly angioplasty(血管重建術)/stent or bypass
Chronic Angina three drug categories
•Three drug categories
–beta adrenergic blockers
–calcium channel blockers
–organic nitrate vasodilators
Chronic Angina
•Goals of treatment
–relieve pain
–bring balance to MvO2supply and demand
–decrease the severity and frequency of anginal episodes
–Prevention of future MI
What is MVO2?
Myocardial oxygen
Organic Nitrate Vasodilators
•Prototype:
nitroglycerin (NTG)
nitroglycerin (NTG) action
Action
–vasodilates vessels in the periphery thereby decreases workload of the heart
–Dilates coronary arteries improving blood flow
–does not dilate plaque covered, damaged vessels
–comes in metered tablets, sprays, ointments
nitroglycerin (NTG)
•Effects
NTG
•Effects
–Dilation of peripheral vessels by relaxing smooth muscle lining of vessels.
•Decreases afterload
–Decreases the amount of blood returning to the heart (preload)
–Reflex tachycardia
•anytime BP falls, sympathetic activity occurs
nitroglycerin (NTG) indication and nursing implication
Indications: angina
–Emergent CP: SL tablet, wait 5 min; if pain continues, can repeat with second and third dose. If CP continues after second dose, call 911 (used to be 3 doses)
–Allow to dissolve slowly, don’t eat, drink, or smoke. Patient should feel tingling sensation under tongue, if not present the drug may have lost its potency.
Nirtoglycerin nursing implication
IV: for emergent use following an MI or severe refractory angina
–IV NTG binds with PVC, need to use special tubing and glass bottle
•glass bottles need vented spike on tubing!!
–Must run through pump
–Close monitoring of BP
–High falls risk
Long term use
–ointment: measured length, apply to hairless surface and cover with plastic
–transdermal patch:
•don’t soak in water
•rotate placement
•12 hr on and 12 hr off
•Nurses wear gloves
Toxicity of Nitroglycerin
NTG
• Toxicity
– dose dependent hypotension and reflex
tachycardia
– nitro has a very short half-life so is gone quickly
– Tx: vasopressors (but not epinephrine) and O2
Name two Beta blockers we use to treat angina
Beta blockers
– those approved for angina include propranolol
and atenolol
• remember that propranolol is non-selective and has
affinity for all beta receptors
• atenolol is cardioselective with affinity for beta1
some things to considered about for betablockers
prophylaxis only, not short term tx
– worsens vasospastic angina
– don’t stop drug abruptly
Ca channel blocker
CCBs
•Action
–decreases myocardial contractile force (negative inotropic effect)
–decreases HR (chronotropic effect)
–decreases automaticity (dromotropic effect)
–decreases vasoconstriction in coronary and systemic circulations
–this explains why CCBs are effective in vasospastic angina
def Dysrhythmias
Defined as a deviation from the normal rhythm of the heartbeat
cause of dysrhythimias
abnormal automaticity
abnormal conduction
block of impulse conduction
re-entry phenomenon
Ectopic Impulse
Increased automaticity from elsewhere
hypoxia, ischemia, drugs
Electricity outside normal pathway
atrial, ventricular, anywhere on pathway
Can discharge on regular or irregular pattern
Can be an escape beat
Def Refractory period
Refractory period
time it takes for the cell to recover and prepare for action again
Def conductivity.
Impulse of the heart to beat originates in the SA node (primary pacemaker) and passes the current from cell to cell in a ripple effect to cause myocardial This is conductivity.
The time where an action potential CANNOT be produced is….
The absolute refractory period
Labeled by their source of origination
name two categories of dysrhythmias
supraventricular
sinus tachycardia, atrial flutter, atrial fibrillation, premature atrial contractions (PACs)
ventricular
Premature ventricular contractions (PVCs), ventricular tachycardia, ventricular fibrillation
the only way to access if the antidysrthythmics drugs work is through
EKG
when taking what drugs we need to monitor their HR for one full minutes before dose
1. all antidysrhythmics
2. glycoside
why antidysrhythmics falling our of favor
All antidysrhythmics have the potential to worsen the dysrhythmia or create a new one
name four different drugs categories for Antidysrhythmic Drugs
fast sodium channel blockers
belta blockers
potassium channel blockers
calcium antagonists
fast sodium channel blockers prototype
Prototype: quinidine
action of quinidine
Action
slow depolarization and repolarization in the atria, ventricles, and His-Purkinje system
stabilizes cell membrane, prevents influx of sodium, result is depression of conduction velocity
effect of quindine
Effects
works by directly depressing the excitability of cardiac tissues, slows conduction through both SA and AV nodes
blocks vagal input into the heart
indication of quindine
Indications
long-term prophylaxis of supraventricular rhythms, often used after cardioversion of atrial flutter or atrial fibrillation
SE for quinidine
SE
CV--depressed cardiac function, heart block
CNS: confusion, tinnitus, vision changes
GI--n/v/d, bitter taste
hypotension
Drug-drug interactions for quinidine
Drug-drug interactions
Decreases digoxin excretion
nursing implication for quinidine
Low Margin of safety (narrow window)
Measure width of QRS
Stop drug if increases by 50%
Increases risk of Digoxin toxicity
Monitor for heart block
Group I-B--Sodium channel blockers prototype
lidocaine (Xylocaine)
Prototype: lidocaine (Xylocaine)
Action and implication
Action
slows depolarization of muscle contraction and has a preferential effect on abnormally functioning tissue, e.g., ectopic foci or infarcted tissues (shortens duration action potential)
Indications
acute ventricular dysrhythmias
what is Lidocaine also used for
local anesthesia
SE and things to watch for Lidocaine
Low margin of safety: Toxicity
max dose 3 mg/kg
tremors, twitching, blurred vision, tinnitus
dyspnea, severe dizziness, fainting, bradycardia, convulsions (esp in elders)
Needs EKG monitoring
Group I-C--Sodium channel blockers prototype
flecainide (Tambocor)
Action, indication and SE for Flecainide
Action
suppresses PVCs (Premature ventricular contractions )
Indications
used in serious ventricular dysrhythmias only
prophylaxis of supraventricular dysrhythmias
SE
blurred vision, dizziness
indications of Beta Blocker
ventricular dysrhythmias
shown to be particularly effective with post-MI dysrhythmias
HTN
Hyperanxiety (stage fright)
Also hyperthyroid (racing heart)
what do Group III—Potassium Channel Blockers do
Delay Repolarization
Prototype: amiodarone (Cordarone) action ?
Prototype: amiodarone (Cordarone)
Action
prolongs action potential, increases the refractory period in all cardiac tissues
decreased automaticity, prolonged AV conduction, blocks sodium, potassium, and calcium channels
what is Prototype for Potassium Channel Blockers
Prototype: amiodarone (Cordarone)
side effect for amiodarone
pulmonary fibrosis, thyrotoxicosis
blue-gray skin color
prototype for Cacium channel blocker (antidysrthymics)
adenosine (Adenocard)
What is different about adenosine delivery compared to other meds?
Must infuse it very fast over 3 seconds
action, indicaiton and SE for adenosine
Action
slows AV node conduction
Indication
PSVT (paraoxsysmal supraventricular tachycardia)
SE
chest pain
what others two drugs also used to treat dysrhymics
Atropine and Digoxin
how Atropine act to help dysrthymia
action is anticholinergic effect, blocks vagal stimulation and increases HR (increases conduction thru the AV node)
indication is bradycardia
how digoxin act to help dysrthymia
action is to slow HR and improve conduction and increase contractility
what test is an indication of the inflammation
When there is inflammation, cholesterol is more likely to be deposited.
C-reactive protein levels indicate if present
what we do to treat hyperlipidemia initialy
1 lifestyle modification for 3-6 mth
2. Reduce lipid elevating drugs, such as Thiazides, and estrogens