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Master Nursing Pharmacology: Cardiac Agents Quiz

Test Your Competence in Cardiac Drug Therapy

Difficulty: Moderate
Questions: 20
Learning OutcomesStudy Material
Colorful paper art depicting elements related to Nursing Pharmacology Cardiac Agents Quiz.

Looking to strengthen your nursing pharmacology expertise? The Nursing Pharmacology: Cardiac Agents Quiz presents 15 MCQs on cardiac agents, dosing, and monitoring. Ideal for students who want to master heart medication management, the quiz is fully customizable in our editor. For more practice, check out the Pharmacology Review Quiz or the Nursing Pharmacology Knowledge Quiz. Explore additional quizzes to continue honing your skills.

Which of the following best describes the primary mechanism of action of propranolol?
Inhibits calcium influx in vascular smooth muscle.
Blocks both beta-1 and beta-2 adrenergic receptors.
Acts as a positive inotrope by increasing intracellular calcium.
Inhibits ACE, reducing angiotensin II formation.
Propranolol is a nonselective beta-blocker that antagonizes both beta-1 and beta-2 receptors, reducing heart rate and contractility. It does not inhibit calcium channels, ACE, or increase intracellular calcium.
What is the recommended route of administration for nitroglycerin in acute angina attacks?
Sublingual spray or tablet.
Transdermal patch.
Oral tablet swallowed with water.
Intravenous infusion.
Sublingual nitroglycerin provides rapid absorption and onset to relieve acute angina. Oral tablets have slower onset, and patches or IV infusions are used for different indications.
A key adverse effect of ACE inhibitors such as lisinopril is:
Bradycardia.
Hyperglycemia.
Hypokalemia.
Dry, persistent cough.
ACE inhibitors increase bradykinin levels, which commonly causes a dry, persistent cough. They do not typically cause bradycardia or hyperglycemia, and they may cause hyperkalemia rather than hypokalemia.
The primary therapeutic use of digoxin includes:
Acute management of hypertensive crisis.
Rate control in atrial fibrillation and heart failure.
Treatment of ventricular tachycardia storm.
Prophylaxis of myocardial infarction.
Digoxin is used to improve contractility in heart failure and to control ventricular rate in atrial fibrillation. It is not indicated for MI prophylaxis, hypertensive emergencies, or treating ventricular tachycardia storm.
The elimination half-life of a cardiac drug primarily determines:
Volume of distribution.
Route of administration.
Therapeutic index.
Dosing frequency.
A drug's half-life informs how long it stays in the body, guiding how often doses should be given. It does not directly determine therapeutic index, route of administration, or volume of distribution.
Which patient condition is a contraindication for nonselective beta-blocker therapy?
Type 2 diabetes.
Chronic kidney disease.
Hyperlipidemia.
Asthma.
Nonselective beta-blockers block beta-2 receptors in the lungs, which can precipitate bronchoconstriction in asthmatic patients. Diabetes, hyperlipidemia, and CKD are not absolute contraindications.
Which electrolyte imbalance predisposes a patient to digoxin toxicity?
Hypermagnesemia.
Hypoglycemia.
Hypokalemia.
Hypercalcemia.
Low serum potassium enhances digoxin binding at the Na+/K+ ATPase, increasing toxicity risk. Calcium and magnesium levels have different effects, and glucose is unrelated.
What is the primary hemodynamic effect of nitrates in the management of angina?
Increase in myocardial contractility.
Direct blockade of calcium channels.
Increase in afterload by arterial constriction.
Reduction of preload by venous dilation.
Nitrates primarily dilate venous vessels, reducing venous return (preload) and myocardial oxygen demand. They do not block calcium channels or increase contractility or afterload.
What is the initial IV dose of atropine for symptomatic bradycardia?
0.5 mg.
2 mg.
1 mg.
0.1 mg.
The recommended initial IV dose for atropine in symptomatic bradycardia is 0.5 mg. Lower or higher doses are not standard initial therapy.
Which endocrine-related adverse effect is most commonly associated with spironolactone?
Hyperprolactinemia.
Gynecomastia.
Adrenal insufficiency.
Hypothyroidism.
Spironolactone antagonizes androgen receptors, which can lead to gynecomastia in males. It does not cause hypothyroidism, hyperprolactinemia, or adrenal insufficiency.
Which of the following is an absolute contraindication to ACE inhibitor therapy?
Bilateral renal artery stenosis.
Asthma.
Pregnancy.
Hyperlipidemia.
ACE inhibitors are teratogenic and contraindicated in pregnancy. Bilateral renal artery stenosis is a relative contraindication, while asthma and hyperlipidemia are not contraindications.
Which laboratory tests should be monitored when initiating lisinopril?
Blood glucose.
BUN and serum creatinine.
INR and PT.
Liver enzymes (ALT/AST).
ACE inhibitors can affect renal function, so BUN and creatinine should be monitored. They do not directly affect coagulation, liver enzymes, or blood glucose.
Which beta-blocker is cardioselective at low to moderate doses?
Timolol.
Metoprolol.
Nadolol.
Propranolol.
Metoprolol has higher affinity for beta-1 receptors in the heart, making it cardioselective at lower doses. The others are nonselective beta-blockers.
A drug with a high first-pass metabolism will most likely have a low:
Clearance.
Bioavailability.
Volume of distribution.
Half-life.
High first-pass metabolism in the liver reduces the amount of drug reaching systemic circulation, decreasing bioavailability. Clearance, volume of distribution, and half-life are independent properties.
Through which organ is digoxin primarily eliminated?
Kidneys.
Liver.
Lungs.
Gastrointestinal tract.
Digoxin is primarily excreted unchanged by the kidneys. Hepatic, pulmonary, and GI elimination pathways are minimal for this drug.
What pharmacokinetic property of amiodarone accounts for its prolonged half-life?
High water solubility.
Rapid hepatic metabolism.
High lipid solubility.
Low protein binding.
Amiodarone's lipophilicity leads to extensive tissue and fat binding, prolonging its elimination half-life. It is also highly protein bound and metabolized slowly.
Which pharmacogenetic phenotype increases the risk of hydralazine-induced lupus?
Slow acetylator phenotype.
P-glycoprotein overexpressor.
CYP3A4 ultra-rapid metabolizer.
Thiopurine methyltransferase deficiency.
Slow acetylators metabolize hydralazine more slowly, leading to higher drug levels and increased risk of drug-induced lupus. The other traits are unrelated to hydralazine metabolism.
The acute toxicity of sodium nitroprusside is primarily due to accumulation of:
Thiocyanate ions.
Sulfate ions.
Cyanide ions.
Nitrite ions.
Sodium nitroprusside releases cyanide ions, which can cause acute cyanide toxicity. Thiocyanate is a less toxic metabolite formed later.
What is the specific antidote for severe digoxin toxicity?
Digoxin immune Fab.
Calcium gluconate.
Activated charcoal.
Atropine.
Digoxin immune Fab binds free digoxin, neutralizing its effects and is the treatment of choice for severe toxicity. Atropine may address bradycardia but does not reverse toxicity.
To prevent tolerance to transdermal nitroglycerin, which nursing schedule is appropriate?
Double the dose every other day.
Remove the patch for 10 - 12 hours overnight.
Apply continuously without interruption.
Rotate application site weekly.
A daily nitrate-free interval of 10 - 12 hours, often overnight, prevents tolerance. Continuous application or improper rotation does not effectively prevent tolerance.
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Learning Outcomes

  1. Analyse pharmacokinetic and pharmacodynamic properties of cardiac agents
  2. Identify indications and contraindications of major heart medications
  3. Evaluate correct dosages and administration routes for cardiac drugs
  4. Apply monitoring protocols and patient assessment for cardiac therapy
  5. Demonstrate knowledge of adverse effects and nursing interventions

Cheat Sheet

  1. Understand Pharmacokinetics and Pharmacodynamics of Cardiac Agents - Learn how cardiac drugs are absorbed, distributed, metabolized, and excreted, and discover how they exert their magic on the heart. Imagine digoxin as a tightrope walker with a narrow safety net - it's powerful but needs careful monitoring to prevent a tumble! This foundation gives you backstage access to how drugs really work.Nurseslabs: Cardiotonic & Inotropic Drugs
  2. Recognize Indications and Contraindications - Dive into the "when and why" of prescribing so you know which drugs are heroes and which can turn into villains. Nitrates, for example, are angina's best friend but can crash the party if intracranial pressure is sky-high. Spotting these scenarios helps you steer clear of dangerous mix-ups.OpenStax: Cardiac Emergency Drugs
  3. Master Dosages and Administration Routes - Whether it's a tiny tablet or a quick-fix sublingual spray, hitting the right dose at the right site is your superpower. Nitroglycerin under the tongue? That's like summoning an ambulance for instant chest pain relief! Precision here keeps patients safe and symptoms in check.OpenStax: Cardiac Emergency Drugs
  4. Implement Monitoring Protocols - Keep your eyes glued to vital signs and ECG tracings when administering cardiac meds, especially antiarrhythmics. It's like being the DJ at the heart's party - you need to keep the rhythm steady and be ready to change the tune if things go offbeat. Regular checks ensure you catch issues before they escalate.RNPedia: Antiarrhythmic Drug Notes
  5. Identify Adverse Effects and Nursing Interventions - Side effects can gatecrash your care plan, so watch for hypotension, bradycardia, or pulmonary toxicity with drugs like amiodarone. Put on your detective hat and monitor lung sounds and blood pressure like a pro. Quick interventions keep the party going safely.OpenStax: Cardiac Emergency Drugs
  6. Understand Drug Interactions - Some meds love to mingle and others clash - combining digoxin with certain diuretics can spike toxicity levels. Think of your patient's regimen as a royal court; mapping alliances and rivalries helps you keep the peace and avoid dangerous power struggles.Nurseslabs: Cardiotonic & Inotropic Drugs
  7. Educate Patients on Medication Adherence - Medications are VIP guests that must show up on time or the whole event falls apart! Teach your patients why skipping doses can lead to worsening conditions and share fun tips like setting alarms or using colorful pill organizers to keep them on track.CliffsNotes: Cardiac Pharmacology Review
  8. Apply Mnemonics for Drug Classes - Memory hacks to the rescue! Turn "ABCD" into your sidekick - Antiarrhythmics, Beta-blockers, Calcium channel blockers, and Diuretics. Mnemonics add a splash of fun to rote learning and help you ace recall when it matters most.Nurseslabs: Antiarrhythmic Drugs
  9. Stay Updated on Guidelines - Medicine evolves faster than viral trends, so bookmark key guidelines and clinical updates. Regular refreshers keep you ahead of the curve and ensure you deliver top-notch, evidence-based cardiac care every time.OpenStax: Cardiac Emergency Drugs
  10. Practice Dosage Calculations - Strong math skills are as essential as a stethoscope - getting a dose wrong is off the table! Work through practice problems, simulate real-world scenarios, and build confidence so your calculations are always spot on.Wikipedia: Pharmacokinetics
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