Principles of Administration of Cardiac Medications
CARDIAC MEDICATIONS, IF NOT PROPERLY ADMINISTERED, HAVE A HIGH POTENTIAL FOR FATALITY (DEATH!)
! While there are several general principles for initiating, monitoring, and responding to cardiac medications, foremost to remember is that the nurse is a professional and must act professionally by assessing and intervening to each situation with intelligence instead of following regimented rules.
Myocardial Properties | Description | Drugs that Decrease… | Drugs that Increase… |
Contractility | Strength of myocardial muscle contraction (Inotropic) | (negative inotropic) Calcium channel blocking agents or beta blockers | (positive inotropic) beta-adrenergic agonists or cardiac glycosides (e.g., digoxin) |
Excitability/Irritability | Electrical agitation of the myocardium making it more prone to ectopy | lidocaine, procainamide, quinidine, amiodarone | Beta-adrenergic agonists (e.g., epinephrine, isoproterenol) |
Automaticity | Initiation of electrical impulse; heart rate (Chronotropic) | (negative chronotropic) beta blockers, most antidysrhythmics, calcium channel blockers, adenosine, digoxin | (positive chronotropic) atropine, anticholinergic drugs, beta-adrenergic agonists |
Refractoriness | Duration of time until repolarization occurs | (delayed repolarization) amiodarone, quinidine, procainamide |
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Drugs that are being given for an emergency situation, such as a lethal dysrhythmia or shock state, will be generally administered intravenously for rapid distribution.
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Intravenous boluses (IV pushes) are given slowly while patient is closely monitored according to desired parameter, vital signs, and physical assessment.
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Loading doses for many antidysrhythmic medications are required because they bind to plasma proteins (especially albumin). Plasma protein receptor sites must be filled with molecules of a drug prior to molecules being free in the plasma for therapeutic purposes. Serum levels of a drug represent the concentration of molecules that are not bound to plasma proteins. If a patient has low levels of plasma proteins (like hypoalbuminemia), then serum levels of medications can be higher than normal for the same doses. Also, drug interactions are often influenced by displacement of one drug by another drug off plasma proteins. Drug interactions on plasma proteins can cause serum levels to become elevated or subtherapeutic.
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Many antidysrhythmic drugs have narrow therapeutic ranges (index), thus serum levels are monitored periodically and nurses must recognize signs of toxicity.
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Maintenance doses of cardiac drugs are generally administered at even time intervals in order to maintain therapeutic serum levels.
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Intravenous infusions of medications should NEVER be interrupted or stopped for IVPB medications, IV pushes, or other intravenous interventions. Use a second IV line for other IV therapies so that serum levels of medication infusions do not become altered.
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Be alert for changes in electrolyte balances, especially potassium (K+).
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For administration of single maintenance doses of antidysrhythmia medications, CHECK APICAL HEART RATE (HR) FOR 1 FULL MINUTE. Hold the medication if HR < 60/min or > 120/min. If this situation exists during a maintenance dose, then ask yourself whether your patient is stable. DO NOT SIMPLY CHART THE HEART RATE AND LEAVE YOUR PATIENT! Ask the patient how s/he is feeling (e.g., lightheadedness, dizziness, chest pain, dyspnea). Assess other vital signs like blood pressure and respirations. Check cardiac monitor for presence of dysrhythmias. Assess the history of vital signs in the chart. Assess laboratory results for electrolytes. Return and reassess apical heart rate again in 15-30 minutes. If the patient is unstable, notify the physician STAT. If the patient is stable, then inform the physician of the variance (medication was held) and the reason during the physician's visit to the patient.
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The patient needs to learn how to measure one' own pulse. Show the patient how to find one's own radial pulse. Instruct the patient to count the pulse out loud while you monitor the pulse at another site. Instruct the patient to assess one's pulse daily at the same time of day, preferably when one first wakes up or when the medication is scheduled. Advise the patient under what conditions to notify the physician.
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CHECK THE PATIENT'S BLOOD PRESSURE PRIOR TO ADMINISTERING AN ANTIDYSRHYTHMIC MEDICATION OR HEMODYNAMIC MEDICATION (like vasodilators). If systolic blood pressure is < 100 mm Hg or 30 mm Hg below baseline, then hold medication. If one of these situations exist, then ask yourself whether your patient is stable. DO NOT SIMPLY CHART THE BLOOD PRESSURE AND LEAVE YOUR PATIENT! Ask the patient how s/he is feeling (e.g., lightheadedness, dizziness, chest pain, dyspnea). Look for postural hypotension. Assess other vital signs like pulse and respirations. Check cardiac monitor for presence of dysrhythmias. Assess the history of vital signs in the chart. Assess laboratory results for electrolytes. Return and reassess blood pressure again in 15-30 minutes. If the patient is unstable, notify the physician STAT. If the patient is stable, then inform the physician of the variance (medication was held) and the reason during the physician's visit to the patient.
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Keep in mind that if you are treating a patient for a life-threatening situation, the vital signs will already be outside of normal parameters. The medication is the intervention to stabilize the patient. So know what your medications do, and use your intelligence when administering cardiac medications.
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Observe for gastrointestinal alterations such as nausea, vomiting, and diarrhea. When an alteration exists, assess for electrolyte imbalances or toxicity of a cardiac medication.
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Assess for fluid retention through daily weights while the patient is in the hospital. (Weight can be assessed biweekly by the patient at home.)
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Assess the cardiac monitor every shift. Measure the PR interval, the QRS duration, QT interval, and atrial & ventricular rates.
COMMON DRUG INTERACTIONS AMONG ANTIDYSRHYTHMIC MEDICATIONS | ||
DRUG | MECHANISM | RESULT |
Anti-dysrhythmic drugs | Additive Effect | May enhance dysrhythmias or produce hypotension |
Anti-coagulants (e.g. warfarin) | Anti-dysrhythmic drug may displace anti-coagulant from plasma protein binding sites. | More pronounced anticoagulant effects like prolonged INR or PT |
Phenytoin | Anti-dysrhythmic drug may displace phenytoin from plasma protein binding sites. | Potential for toxic levels of phenytoin |
Sulfonylurea compounds | Anti-dysrhythmic drug may displace sulfonylurea from plasma protein binding sites. | Higher risk for hypoglycemia. |