Cardiac Glycosides & Heart Failure Practice Flashcards

Epinephrine (Adrenalin): Adrenergic Agonists and Catecholamines

• Classification and Prototype Context

  • Classified as a nonselective alpha-1, beta-1, and beta-2 adrenergic agonist.

  • Identified as the prototype catecholamine.

  • Falls under the category of Adrenergic Agonists / Catecholamines as discussed in ATI Chapters $18-23$.

• Core Physiological Mechanism

  • Alpha-1 Stimulation: Causes vasoconstriction of the blood vessels. This action raises blood pressure and reduces swelling in the airways.

  • Beta-1 Stimulation: Stimulates the cardiac tissue to increase heart rate and myocardial contractility.

  • Beta-2 Stimulation: Triggers bronchodilation in the lungs and reduces the release of mediators from mast cells.

• Therapeutic Indications

  • Serves as the first-line emergency medication for anaphylaxis.

  • Utilized during cardiac arrest and selected severe shock situations.

  • Provides rapid support for airway, breathing, and circulation (the ABCs).

• Expected Pharmacologic Effects and Side Effects

  • Sympathetic stimulation commonly results in tremors, anxiety, headache, palpitations, and restlessness.

  • Tachycardia and elevated blood pressure are expected outcomes of its adrenergic activity.

  • Nausea and sweating may occur during the sudden adrenergic surge.

• Serious Adverse Reactions

  • Cardiovascular complications include ventricular dysrhythmias, severe hypertension, and myocardial ischemia.

  • Respiratory complications include pulmonary edema.

  • Dosing errors, particularly with intravenous (IV) concentrations or administration, can be fatal.

  • Extravasation: Local vasoconstriction at the IV site can be so severe that it results in tissue necrosis.

• Nursing Interventions and Clinical Focus

  • Anaphylaxis Administration: Administer promptly via intramuscular (IM) injection in the mid-outer thigh following emergency protocols.

  • Safety Verification: Carefully verify the concentration, dose, and route, as emergency products vary significantly.

  • Monitoring: Continuously monitor the airway, oxygenation, ECG, blood pressure, and overall perfusion. Repeat doses only as specifically ordered or dictated by protocol.

  • Extravasation Management: Treat promptly according to facility policy; this often involves the local administration of phentolamine.

Dobutamine (Dobutrex): Specific Beta-1 Adrenergic Stimulation

• Classification and Prototype Context

  • Primarily functions as a beta-1 adrenergic agonist and a positive inotrope.

  • Listed alongside epinephrine as a prototype catecholamine under adrenergic agonists.

• Core Physiological Mechanism

  • Selectively stimulates beta-1 receptors in the heart.

  • Increases contractile force and stroke volume, which leads to an increase in total cardiac output.

  • Generally has less of a direct effect on systemic vascular resistance compared to pure vasopressors.

• Therapeutic Indications

  • Indicated for short-term management of severe heart failure, cardiogenic shock, or other low-output states.

  • Improves tissue perfusion when the cardiac muscle is too weak to pump effectively.

  • Used as a pharmacological agent during cardiac stress testing when physical exercise is not an option for the patient.

• Side Effects and Adverse Reactions

  • Common reactions include tachycardia, palpitations, headache, and nausea.

  • Increased cardiac excitability can lead to premature beats (ectopy) or ventricular dysrhythmias, which may reduce cardiac output or become life-threatening.

  • Blood pressure may either rise or fall depending on individual patient response and titration.

  • Increased myocardial oxygen demand can trigger angina or myocardial ischemia.

• Nursing Interventions and Clinical Focus

  • Administration: Must be given via an intravenous (IV) infusion pump.

  • Hemodynamic Monitoring: Requires continuous ECG monitoring and frequent blood pressure checks.

  • Volume Status: Always correct hypovolemia before starting the infusion; the medication is ineffective if there is an "empty tank" to pump.

  • Assessment: Monitor urine output, mental status, skin perfusion, and lung sounds.

  • Titration: Adjust the dose to reach specific clinical goals and immediately report any instances of chest pain or increasing dysrhythmias.

Sacubitril / Valsartan (Entresto): Angiotensin Receptor-Neprilysin Inhibitors (ARNI)

• Classification and Components

  • Belongs to the class of Angiotensin Receptor-Neprilysin Inhibitors (ARNI).

  • A combination prototype consisting of Sacubitril and Valsartan.

• Core Physiological Mechanism

  • Sacubitril: Inhibits the enzyme neprilysin. This inhibition prevents the breakdown of natriuretic peptides, allowing them to remain active longer to promote vasodilation and the excretion of sodium and water.

  • Valsartan: An Angiotensin II Receptor Blocker (ARB) that targets $AT1$ receptors to reduce vasoconstriction and aldosterone secretion.

  • The dual action raises helpful peptides while simultaneously blocking the harmful effects of Angiotensin II.

• Therapeutic Indications

  • Used in the management of chronic heart failure to reduce the risk of hospitalization and cardiovascular-related death.

  • Decreases cardiac workload and facilitates the removal of excess sodium and water.

  • Can replace traditional ACE inhibitors or ARBs in stable patients.

• Side Effects and Adverse Reactions

  • Vasodilation can lead to hypotension and dizziness.

  • Lab changes may include elevations in potassium (hyperkalemia) and creatinine (potential kidney injury).

  • Cough may occur, though it is generally less common than with ACE inhibitors.

  • Serious Risks: Includes angioedema (airway obstruction) and fetal injury or death if taken during pregnancy.

• Nursing Interventions and Clinical Focus

  • ACE Inhibitor Contrast: Never administer concurrently with an ACE inhibitor. A minimum washout period of $36\,\text{hours}$ is required when switching from an ACE inhibitor to Sacubitril/Valsartan.

  • ARB Contraindication: Do not combine with other ARBs because Valsartan is already a component of the drug.

  • Monitoring: Track blood pressure, potassium levels, renal function, weight, edema, and clinical symptoms of heart failure.

  • Patient Education: Instruct patients to report facial or tongue swelling, pregnancy, fainting, or reduced urine output immediately.

Digoxin (Lanoxin): Cardiac Glycosides

• Classification and Overview

  • Classified as a cardiac glycoside and a positive inotrope.

  • Also categorized as a Class VI rhythm medication.

• Core Physiological Mechanism

  • Na-K ATPase Inhibition: Inhibits the sodium-potassium ATPase pump, which subsequently increases intracellular calcium within cardiac muscle cells.

  • Force and Rate: Increased calcium leads to stronger myocardial contractions (positive inotropy). Simultaneously, it increases vagal tone, which slows the sinoatrial (SA) rate and atrioventricular (AV) node conduction (negative chronotropy).

  • The result is a heart that beats slower but stronger, improving cardiac output without increasing sympathetic stimulation.

• Therapeutic Indications

  • Symptom management in patients with heart failure.

  • Rate control for the resting ventricular rate in patients with chronic atrial fibrillation.

• Therapeutic Window and Toxicity

  • Narrow Safety Range: The drug has a very narrow therapeutic index.

  • Therapeutic Levels: The target serum level is $0.6-1.2\,ng/mL$.

  • Toxic Levels: Levels exceeding $1.2\,ng/mL$ are considered high. Specific toxic examples include values such as $2.8$ or $2.9$.

  • Risk Factors for Toxicity: Hypokalemia (low potassium), hypomagnesemia, hypercalcemia, and renal impairment significantly increase the risk of toxicity.

• Symptoms of Toxicity

  • Gastrointestinal: Nausea, vomiting, general GI upset, and anorexia (loss of appetite).

  • Neurologic/Visual: Fatigue, confusion, weakness (especially in older adults), and visual disturbances such as yellow/green vision or seeing halos.

  • Cardiac: Severe bradycardia, heart block, or ventricular dysrhythmias.

• Drug Interactions

  • Loop Diuretics: Medications such as furosemide (Lasix) or bumetanide (Bumex) cause the loss of sodium, water, chloride, and potassium.

  • Interaction Significance: The resulting hypokalemia from diuretic use drastically increases the risk of digoxin toxicity.

• Nursing Interventions and Clinical Focus

  • Pre-administration Assessment: Always count the apical pulse for one full minute prior to administration.

  • Hold Parameters: Withhold the dose and notify the provider if the heart rate is less than $60\,\text{beats/min}$.

  • Lab Monitoring: Regularly check renal function, potassium, magnesium, calcium, and serum digoxin levels. Ensure digoxin levels are drawn at the appropriate post-dose interval.

  • Emergency Response: For life-threatening toxicity, digoxin immune Fab is used as the antidote.

  • Patient Education: Advise taking the medication at the same time every day and never doubling a missed dose.