Ppt chapter 31

Chapter 31
Drugs Affecting Cardiac Rhythm
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins

Physiology
• Contractions of the heart are dependent on the unique
electrical conduction system of the cardiac muscle.
• The conduction system connects to highly specialized
cardiac cells that allow the heart to beat predictably and
rhythmically.
• The system is composed of the sinoatrial (SA) node, the
atrioventricular (AV) node, the bundle of His, the bundle
branches, and the Purkinje fibers.

Physiology (cont.)
• The SA node, influenced by both the sympathetic and the
parasympathetic nervous systems, is known as the
pacemaker of the heart.
• It is important to understand how potassium, sodium,
and calcium ions bring about electrical changes in the
cardiac cells that stimulate contraction of the cardiac
cells.

Travel of Electrical Current

Electrocardiogram

Movement of Electrolytes

Pathophysiology
• Arrhythmias, also called dysrhythmias, are a disturbance in
the electrical activity of the heart.
• Some arrhythmias are insignificant and do not create any
problems for the patient.
• Others disrupt the function of the heart, increase the
oxygen demand of the heart, and interfere with cardiac
output.
• Changes in the ionic currents through ion channels of the
myocardial cell membrane are the main cause of cardiac
arrhythmia.
• Ionic changes allow arrhythmias to develop in one of the
three ways: through a disorder with impulse formation,
through a disorder of the impulse conduction system, or
through a combination of both.

Drugs and Other Therapies to Treat
Arrhythmias
• Drug therapy previously was the mainstay for treating
arrhythmias; now ICDs are added to that treatment.
• ICDs have an established and definitive role in preventing
sudden cardiac death.
• Arrhythmias can be treated by catheter ablation.
• Antiarrhythmics are agents used to prevent, suppress, or
treat a disturbance in cardiac rhythm.
• The primary outcomes are to decrease automaticity,
decrease speed of conduction, and decrease reentry.
• When antiarrhythmic drugs were developed, a system of
classification was sought in an attempt to organize the
complex information into a conceptually meaningful fashion.

Class I Antiarrhythmic Drugs
• Class I antiarrhythmics are local anesthetics or
membrane-stabilizing agents that depress phase 0 in
depolarization.
• The drugs in subgroups of A, B, and C are not
interchangeable because they have different
pharmacotherapeutics.
• Class IB antiarrhythmics prototype drug: lidocaine
(Xylocaine)

Lidocaine: Core Drug Knowledge
• Pharmacotherapeutics
– Treat all acute ventricular arrhythmias.
• Pharmacokinetics
– Administered: IV. Metabolism: liver. Excreted:
kidneys. T1/2: 1.5 to 2 hours
• Pharmacodynamics
– Decreases automaticity, excitability and membrane
responsiveness. Decreases action potential duration
and effective refractory period of Purkinje fibers and
ventricular muscle

Lidocaine: Core Drug Knowledge (cont.)
• Contraindications and precautions
– Hypersensitivity, several cardiac conditions, digitalis
toxicity, hypovolemia, shock
• Adverse effects
– Cardiac arrhythmias, hypotension, dizziness,
lightheadedness, fatigue, drowsiness
• Drug interactions
– Many classes of drugs

Lidocaine: Core Patient Variables
• Health status
– Determine whether the patient has a type of
ventricular arrhythmia that is an indication for
therapy.
• Life span and gender
– Pregnancy category B
• Environment
– Should be given in hospital or emergency setting
with continuous ECG monitoring

Lidocaine: Nursing Diagnoses and
Outcomes
• Decreased Cardiac Output related to cardiac changes
secondary to adverse effects of drug therapy
– Desired outcome: The patient will not develop
deleterious cardiac changes that alter cardiac output.
• Risk for Injury, such as hepatic toxicity, related to
adverse effects of drug therapy
– Desired outcome: The patient will not incur hepatic
toxicity while on drug therapy.
• Change in level of consciousness related to CNS changes
secondary to adverse effects of drug therapy
– Desired outcome: The patient will not experience
dangerous CNS changes while on therapy.

Lidocaine: Planning and Interventions
• Maximizing therapeutic effects
– After initial (or several) IV push dose of 50 to 100
mg, continuous drip of 1 to 4 mg/minute may be
started.
• Minimizing adverse effects
– Monitor rhythm continuously with ECG.
– Notify prescriber immediately of arrhythmias, CNS
depression or irritability.
– Monitor liver and kidney function tests.

Lidocaine: Teaching, Assessment, and
Evaluations
• Patient and family education
– Explain the purpose of the drug and the potential
adverse effects.
– Explain the rationale for ECG monitoring and
frequent blood testing.
• Ongoing assessment and evaluation
– Monitor the patient’s ECG and pulse throughout
therapy.
– Check lidocaine blood levels, liver enzymes, renal
function, and complete blood counts.

Question
• Serum levels of lidocaine above ______ are considered
toxic.
– A. 2 mcg/mL
– B. 4 mcg/mL
– C. 6 mcg/mL
– D. 8 mcg/mL

Answer
• C. 6 mcg/mL
• Rationale: When serum levels of lidocaine are greater
than 6 mcg/mL, toxicity is present and the patient is
at risk for developing seizures and loss of
consciousness.

Class IA Antiarrhythmics
• The class IA drugs are similar to lidocaine (class IB) and
class IC drugs because they depress phase 0 (although
not as much).
• These drugs also may cause arrhythmias in addition to
treating them.
• Unlike lidocaine, their use in treating life-threatening
ventricular arrhythmias has not been shown to improve
survival.

Class IC Antiarrhythmics
• Class IC drugs are flecainide (Tambocor), propafenone
(Rythmol), and moricizine.
• These drugs depress phase 0 considerably.
• They have a slight effect on repolarization and decrease
conduction substantially.
• Flecainide and propafenone have proarrhythmic effects.
• Both of these class IC drugs can be given orally.
• Their use has been limited to patients with life-threatening
arrhythmias.

Class II Antiarrhythmic Drugs
• Antiarrhythmic class II drugs (beta blockers) depress
phase 4 depolarization. Beta blockers slow heart rate by
suppressing the SA node, slow the speed of conduction
through the AV node, and decrease the force of
contraction.
• They effectively reduce mortality in patients who have
had a recent MI, those with symptomatic heart failure,
and those with congenital long QT syndrome.
• Researchers have found that beta blockers are the most
effective drugs for controlling the ventricular rate in AFib.
• It is important to keep in mind that only some of the beta
blockers are approved for use as antiarrhythmics.

Class III Antiarrhythmic Drugs
• Class III antiarrhythmics produce a prolongation of phase
3 (repolarization).
• Action potential duration and refractory periods are
prolonged, leading to reduction in membrane excitability
of all myocardial tissue.
• Prototype drug: amiodarone (Cordarone, Pacerone)

Amiodarone: Core Drug Knowledge
– Approved for use only in life-threatening arrhythmias
– Absorbed slowly; bioavailability of a single dose of
the drug is about 50%. Highly lipid soluble.
– Prolongation of the refractory period, and
noncompetitive alpha- and beta-adrenergic inhibition

Amiodarone: Core Drug Knowledge (cont.)
– Severe sinus-node dysfunction, 2nd and 3rd degree
AV block
• Adverse effects
– Pulmonary toxicity, exacerbation of the arrhythmia,
and liver disease
– Digoxin, flecainide, and warfarin

Amiodarone: Core Patient Variables
• Health status
– Determine cardiac status.
– Safety has not been established in children.
• Environment
– Assess environment where drug will be given.
• Culture and inherited traits
– May be genetically related, however, little is known
yet about this variation

Amiodarone: Nursing Diagnoses and
Outcomes
• Decreased Cardiac Output related to cardiac arrhythmia.
– Desired outcome: cardiac rhythm will return to
normal, allowing for normal cardiac output.
• Risk for Injury related to adverse effects of drug therapy
– Desired outcome: The patient will not suffer
permanent injury or death as a result of drug
therapy.

Amiodarone: Planning and Interventions
– Administer the prescribed loading doses.
– Mix the drug in glass bottles or polyolefin bags.
– Use a volumetric infusion pump to prevent
underdosage.
– It is important to correct electrolyte disturbances
before beginning therapy.
– Use pulse oximetry or arterial blood gases to assess
for changes in respiratory function.
– Assess for symptoms of visual impairment.

Amiodarone: Teaching, Assessment, and
Evaluations
– Explain the purpose of the drug and possible adverse
effects of the drug.
– Emphasize the importance of returning for follow-up
blood work and ECGs.
– Teach patients to use appropriate protection when
out in the sun and to limit sun exposure.
– The patient’s ECG should be monitored intermittently
throughout therapy.

Question
• The most serious side effect of amiodarone is
– A. Pulmonary toxicity
– B. Other arrhythmias
– C. Liver disease
– D. Seizures

Answer
• A. Pulmonary toxicity
• Rationale: Amiodarone can cause pulmonary toxicity.
It is important to monitor lung function during
therapy.

Class IV Antiarrhythmic Drugs
• Class IV antiarrhythmics depress phase 4 depolarization
and lengthen phases 1 and 2 of repolarization.
• Prototype drug: verapamil (Calan)

Verapamil: Core Drug Knowledge
– Antiarrhythmic for chronic atrial flutter or fibrillation
– Well absorbed after oral administration. Metabolized:
liver. Excreted: kidneys
– Inhibits the movement of calcium ions across the
cardiac and arterial muscle cell membrane

Verapamil: Core Drug Knowledge (cont.)
– Sick sinus syndrome, 2nd or 3rd degree heart block,
and hypotension
• Adverse effects
– Constipation, dizziness, headache, nausea,
hypotension, and peripheral edema
– Several drugs interact with verapamil

Verapamil: Core Patient Variables
• Health status
– Determine type of arrhythmia the patient has.
– Pregnancy category C
• Lifestyle, diet, and habits
– Assess alcohol use.
• Environment
– Assess environment where drug will be given.

Verapamil: Nursing Diagnoses and
Outcomes
• Risk for Constipation related to adverse effects of the
drug
– Desired outcome: The patient will prevent or
minimize constipation by increasing fluid intake and
adding fruit and fiber to the diet.
• Decreased Cardiac Output related to decreased rate and
force of contraction and return to normal rhythm related
to therapeutic effects of drug
– Desired outcome: The patient’s decreased cardiac
output will reduce symptoms of cardiac alterations
without developing adverse cardiac effects from drug
therapy.

Verapamil: Planning and Interventions
– Verify that the IV line is patent before IV
administration.
– Digoxin may be given with verapamil to achieve the
additive effect of slowing at the AV node.
– IV route; do not dilute it with a sodium lactate.
– Do not administer IV verapamil simultaneously with
(or within a few hours of) IV beta blockers.

Verapamil: Teaching, Assessment, and
Evaluations
– Explain the purpose of the drug and its adverse
effects.
– Stress the importance of adequate fluid intake and
dietary fruit and fiber to help prevent constipation.
– Monitor the patient’s ECG and blood pressure
throughout therapy with verapamil.
– It is important to monitor liver function periodically
to detect elevated serum drug levels.

Question
• Verapamil is a pregnancy category ____ drug.
– A. A
– B. B
– C. C
– D. D
– E. X

Answer
• C. C
• Rationale: Verapamil is a pregnancy category C.

Potassium-Removing Resins
• Because hyperkalemia may lead to cardiac arrhythmias,
potassium-removing resins are drugs used to prevent
arrhythmias from occurring.
• These resins bind with potassium and allow it to be
excreted.
• Prototype drug: sodium polystyrene sulfonate
(Kayexalate)

Sodium Polystyrene Sulfonate: Core Drug
Knowledge
– Potassium-removing resin used in treating
hyperkalemia.
– The drug is not absorbed systemically and is excreted
through the GI tract.
– Releases sodium ions that are replaced with
potassium ions.

Sodium Polystyrene Sulfonate: Core Drug
Knowledge (cont.)
– Use caution when giving this drug to anyone who
cannot tolerate a small increase in sodium intake.
• Adverse effects
– Hypokalemia, other electrolyte imbalances, gastric
irritation, anorexia, nausea, vomiting, and
constipation
– When administered with nonabsorbable cation-donating
antacids and laxatives, such as magnesium
hydroxide and aluminum carbonate, systemic
alkalosis can occur.

Sodium Polystyrene Sulfonate: Core
Patient Variables
• Health status
– Monitor the patient’s serum potassium level.
– Note the patient’s age.
• Lifestyle, diet, and habits
– Assess dietary history.
• Environment
– Be aware that sodium polystyrene sulfonate is
administered in the hospital.

Sodium Polystyrene Sulfonate: Nursing
Diagnoses and Outcomes
• Risk for Constipation related to adverse effects of drug
therapy
– Desired outcome: constipation will be prevented by
administering sorbitol, orally or rectally, if warranted.
• Potential complication: hypokalemia.
– Desired outcome: The patient’s potassium level will
be lowered only to the normal range.

Sodium Polystyrene Sulfonate: Planning
and Interventions
– Clear the GI tract with a cleansing enema before
administering the drug by enema.
– When the drug is administered orally, create a
suspension of the powdered formula with water or
syrup for greater palatability.
– If the potassium serum level is severely elevated,
use other methods to reduce potassium.

Sodium Polystyrene Sulfonate: Teaching,
Assessment, and Evaluations
– Explain the therapeutic and possible adverse effects
of the drug.
– Emphasize the importance of repeated blood work to
monitor blood electrolyte concentrations.
– Monitor serum electrolytes throughout therapy.

Question
• Sodium polystyrene sulfonate may be administered
– A. Enema
– B. PO
– C. SC
– D. IV
– E. Both A and B
– F. All of the above

Answer
• E. Both A and B
• Rationale: Sodium polystyrene sulfonate may be given
either orally or as an enema.

Ppt chapter 31

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