Cardiac Stimulants and Depressants
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Transcript Cardiac Stimulants and Depressants
Antiarrhythmic Agents:
Cardiac Stimulants
and Depressants
The Heart
Four-chambered organ located in the upper left
thoracic cavity
Purpose
Pumps the blood around the body so that oxygen
and nutrients can be distributed to all areas of the
body
Maintains the blood pressure at an acceptable level
Generates and conducts electrical impulses
Heart rate is controlled by the autonomic nervous
system
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The Heart
Main pacemakers of heart:
Sinoatrial node: 60-100 bpm; primary
pacemaker
Atrioventricular node: Connects atria
and ventricles; 40-60 bpm
Bundle of His and Purkinje fibers:
carry electrical impulses from AV node
to complete ventricle rate pacing; 1540 bpm
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Cardiac medications
Increase /decrease the force of the
myocardial contraction
Increase / decrease the heart rate
Increase / decrease the conduction of
electrical impulses through the
myocardium
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Congestive Heart Failure (CHF)
Cardiac glycosides
-Digoxin
-Treat arrhythmias
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Cardiac Glycosides
Derived from natural sources; treatment for
heart failure:
cardiac distention-inability to pump the
full blood volume
cardiac hypertrophy-prolonged stretching
sodium and water retention-decreased
renal blood flow
Results in weight gain, edema, shortness of
breath, and pulmonary congestion
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Digoxin
Decreases electrical conduction
Negative Dromatotropic Effect
Increases time spent in diastole
Increases the force of the myocardial
contraction
Positive inotropic action
End result: slows and strengthens
contractions
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Digoxin: Dose Considerations
Duration of action
Method of administration
Other
Physical size of the client
Other medications
Renal or hepatic function
Advanced age
Presence of other illnesses
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Digoxin
Low therapeutic index
Toxicity can be life-threatening; occurs
in 10-20% of patients
Many drug-drug, drug herbal
interactions
Routine monitoring of serum
potassium and digoxin levels
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Digoxin: Adverse Effects
Gastrointestinal effects
Nausea and vomiting
Anorexia
Diarrhea
Cardiac effects
Cardiac arrhythmias
Neurological effects
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Cardiac Glycoside Toxicity
Predispose to cardiac glycoside toxicity
Hypokalemia
Renal impairment
Rapid IV administration
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Cardiac Glycoside Toxicity
Treatment
Stop the drug
Physical assessment
Check potassium level
Administer if needed
Monitor heart rate
Administer antiarrhythmics
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Nursing Considerations
Apical pulse for 1 minute. Hold if HR < 60
bpm
Report changes in heart rhythm
Assess for symptoms of toxicity
Monitor digoxin blood levels
Monitor for drug-drug and drug-herbal
interactions
Educate : signs of toxicity and how to
monitor pulse rate
.
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Antiarrhythmic and Antidysrhythmic Drugs
Grouped together according to their similar
actions
Work three ways:
Decrease automaticity of cardiac tissues
in the ectopic sites
Alter rate of conduction
Alter refractory period of cardiac muscle
between consecutive contractions
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Antiarrythmic Agents
Dependent on:
type of dysrhythmia
presence of other conditions
safety of the drug
onset and/or duration of drug action
Administered IV until patient
stabilized, then oral agents given
Arranged into classes
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Antidysrhythmic Medications
Class 1 (1A, 1B, 1C): decrease the influx of
sodium ions, stabilizing membranes
Class 2: decrease contractility, B/P, AV
node conduction
Class 3: Prolong action potential,
refractory period
Class 4: Decrease myocardial
contractility, 02 demand
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Antidysrhythmics
Quinidine gluconate – Class 1
Lidocaine – Class 1B
Dilantin – Class 1B
Propranolol – Class 2
Verapamil HCL – Class 4
Digoxin – Class 4
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Adverse Effects
GI upset
Cardiovascular disorders
Hypersensitivity
Hypotension
Bradycardia
Lightheadedness
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Nursing Considerations
Take patients apical pulse for one
minute
Record rate and rhythm of the
heartbeat
Assess allergies
Monitor blood pressure
Patient should be supine when
administering IV agents
.
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Beta-adrenergic Blocking Agents
Block the hormone epinephrine
Inhibit beta and beta2
sympathetic receptors
Reduce heart rate
Reduces contractility
Slow electrical conduction
Decrease the blood pressure
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Beta-Adrenergic Blocking Agents
Adverse effects
Cause bronchoconstriction
Can cause heart failure
Examples: propranolol
(Inderal), esmolol, bretylium
tosylate (Bretylol)
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Calcium Channel Antagonists
Reduce the influx of calcium into the
cell:
Prevention of reversal of spasms of the
coronary blood vessels
Coronary artery dilation
Reduction of myocardial oxygen
consumption
Example: Verapamil
.
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Adverse Effects
Vasodilation may cause:
Hypotension
Edema
Dizziness
Headache
Slower myocardial conduction may cause:
Bradycardia
Heart failure
Other effects:
Constipation, diarrhea, nausea, fatigue
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Patient Education
Ensure understanding of drug regime
Review signs to report to their health
care provider
Instruct patient how to take their pulse
Remind them of the importance for
proper follow-up
Encourage questions
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