(Test Bank) Cardiovascular Drugs and Medications: Nursing Pharmacology

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Cardiovascular Drugs and Medications: Nursing Pharmacology Test Bank | 80 Questions Question 1 of 80 1. Question Which of the following clients is at greatest risk for digital toxicity? • A. A 25-year-old client with congenital heart disease. • B. A 50-year-old client with CHF. • C. A 60-year-old client after myocardial infarction. • D. An 80-year-old client with CHF. Correct Answer: D. An 80-year-old client with CHF. Extremely old clients are at greater risk for digitalis toxicity. Remember when it comes to adversity, the very old and very young are always at the highest risk. There are no evidence-based guidelines for the management of mild to moderate toxicity so there is a wide variation in treatment. Severe toxicity requires hospital admission and consideration of the need for digoxin-specific antibody fragments. Although digoxin-specific antibody fragments are safe and effective, randomized trials have not been performed. Option A: Digoxin toxicity can emerge during long-term therapy as well as after an overdose. It can occur even when the serum digoxin concentration is within the therapeutic range. Option B: The clinical features of toxicity are often non-specific. They commonly include lethargy, confusion, and gastrointestinal symptoms (anorexia, nausea, vomiting, diarrhea, and abdominal pain). Visual effects (blurred vision, color disturbances, halos, and scotomas) are rarer in contemporary practice. Cardiac arrhythmias account for most deaths. Option C: Digoxin increases intracellular calcium in myocardial cells indirectly, by inhibiting the sodium-potassium pump in the cell membrane. Increased intracellular calcium increases cardiac contractility, but also the risk of tachyarrhythmias. Inhibition of this pump causes hyperkalemia commonly seen in toxicity. Digoxin also causes an increase in vagal activity, reducing activity in the sinus node and prolonging conduction in the atrioventricular node. Question 2 of 80 2. Question Which of the following is a contraindication for digoxin administration? • A. Blood pressure of 140/90.• B. Heart rate above 80. • C. Heart rate below 60. • D. Respiratory rate above 20. Correct Answer: C. Heart rate below 60. The apical heart rate must be monitored during therapy with digoxin, and the drug held for a pulse below 60 and above 120. Remember that digoxin lowers the heart rate; therefore, the choice that reflects a low heart rate is the best selection. Digoxin toxicity is clinically relevant as it can lead to fatal cardiac arrhythmias. The estimated frequency is at about 0.8 to 4% of patients on steady digoxin therapy. The rate of toxicity increases as serum digoxin concentration reaches over 2.0 ng/ml.Option A: However, toxicity can also occur at lower levels, especially in the setting of other risk factors such as low body weight, advanced age, decreased renal function, and hypokalemia. Option B: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart. Digoxin induces an increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility. Cardiac output increases with a subsequent decrease in ventricular filling pressures.Option D: Digoxin has vagomimetic effects on the AV node. By stimulating the parasympathetic nervous system, it slows electrical conduction in the atrioventricular node, therefore, decreases the heart rate. The rise in calcium levels leads to prolongation of phase 4, and phase 0 of the cardiac action potential thus increases the refractory period of the AV node. Slower conduction through the AV node carries a decreased ventricular response. Question 3 of 80 3. Question The action of medication is inotropic when it: • A. Decreased afterload. • B. Increases heart rate. • C. Increases the force of contraction. • D. Is used to treat CHF. Correct Answer: C. Increases the force of contraction.Inotropic drugs increase the force of contraction. Preload, not afterload, is decreased. Chronotropic drugs increase heart rate. Treatment of CHF is an indication for use not an action of the inotropic drug. Inotropes increase cardiac contractility which improves cardiac output (CO), aiding in maintaining MAP and perfusion to the body. Option A: Vasodilation can also be achieved with ACE inhibitors or angiotensin II receptor blockers (ARBs). Medications from these categories achieve a reduction in afterload–and consequently less myocardial workload–by promoting vasodilation.Option B: Atropine is used to increase heart rate through vagolytic effects, causing an increase in cardiac output. Option D: Doctors usually treat heart failure with a combination of medications. Depending on the symptoms, the client might take one or more medications, including Angiotensin-converting enzyme (ACE) inhibitors. These drugs help people with systolic heart failure live longer and feel better. 1.Question 4 of 80 4. Question Which is the most appropriate action for the nurse to take before administering digoxin? • A. Monitor potassium level. • B. Assess blood pressure. • C. Evaluate urinary output. • D. Avoid giving with thiazide diuretic.Correct Answer: A. Monitor potassium level. Monitoring potassium is especially important because hypokalemia potentiates digoxin toxicity. Digoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium, cation exchanger. Blood pressure and urinary output are because these data reflect overall CV status but are not specific for digoxin. •Option B: Higher intracellular calcium increases inotropy which can be of symptomatic benefit in CHF. At toxic levels, automaticity can be increased as well. Digoxin also increases vagal tone by decreasing dromotropy at the AV node. This can be used to control atrial tachydysrhythmias. •Option C: Gastrointestinal upset is the most common symptom of digoxin toxicity. Patients also may report visual symptoms, which classically present as a yellow-green discoloration, and cardiovascular symptoms, such as palpitations, dyspnea, and syncope. Elderly patients frequently will present with vague symptoms, such as dizziness and fatigue. The most important historical detail in evaluating a random digoxin level is the time of the last dose.•Option D: Thiazide diuretics are usually administered with digoxin. Among patients taking digoxin (Lanoxin), low levels of potassium caused by concurrent digoxin and diuretics (thiazide & loop diuretics) may cause weakness, cramps, and irregular heartbeats. 1.Question 5 of 80 5. Question The therapeutic drug level for digoxin is: • A. 0.1-2.0 ng/mg • B. 1.0-2.0 ng/mg • C. 0.1-0.5 ng/mg • D. 0.5-2.0 ng/mg Correct Answer: D. 0.5-2.0 ng/mgThis is the correct therapeutic range for digoxin. Every nurse should know this information. The rate of toxicity increases as serum digoxin concentration reaches over 2.0 ng/ml. However, toxicity can also occur at lower levels, especially in the setting of other risk factors such as low body weight, advanced age, decreased renal function, and hypokalemia. •Option A: Digoxin toxicity is clinically relevant as it can lead to fatal cardiac arrhythmias. The estimated frequency is at about 0.8 to 4% of patients on steady digoxin therapy. •Option B: Symptoms may be mild and include nausea, vomiting, and anorexia. Visual side effects might include color changes, also known as xanthopsia. But yellow or green-tinted vision is usually associated with digoxin toxicity. Patients may also highlight blurry vision or photopsia. •Option C: At toxic levels, digoxin is proarrhythmic. An impaired ventricle is more prone to ventricular tachyarrhythmias and ectopy. Abnormally high levels of digoxin stimulate atrial activation, thus atrial tachycardias, which, in a patient on digoxin, is highly suggestive of toxicity. These atrial tachycardias are persistent and resolve with a decrease in serum digoxin levels. 1.Question 6 of 80 6. Question Blurred vision or halos are signs of: • A. Subtherapeutic digoxin levels. • B. Digoxin toxicity. • C. Nothing related to digoxin. • D. Corneal side effects of digoxin.Correct Answer: B. Digoxin toxicity. Halos is a hallmark sign of digoxin toxicity. Digoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium, cation exchanger. A, C and D are because subtherapeutic digoxin levels have no such effects. •Option A: Digoxin’s therapeutic half-life is between 30 to 40 hours, but this may change in overdose. Digoxin excretion is primarily renal, and for this reason, patients with poor or worsening renal function, such as patients who are elderly or have CKD, are more likely to develop toxicity. •Option C: Digoxin levels start to plateau at 6 hours, which is after tissue redistribution has occurred; earlier levels may thus be misleadingly high. Cardiovascular toxicity may have delayed manifestation of up to 8 to 12 hours post-ingestion. •Option D: Visual side effects might include color changes, also known as xanthopsia. But yellow or green-tinted vision is usually associated with digoxin toxicity. Patients may also highlight blurry vision or photopsia. 1.Question 7 of 807. Question Amrinone (Inocor) is used for short term therapy for CHF and acts by which of the following mechanisms? • A. Increasing stroke volume and heart rate. • B. Slowing ventricular rate and increasing cardiac output. • C. Vasodilating and increasing peripheral vascular resistance. • D. Increasing cardiac output and enhancing renal perfusion. Correct Answer: A. Increasing stroke volume and heart rate. The action of amrinone (Inocor) is to increase stroke volume, ejection fraction, and heart rate. Inamrinone, also known as amrinone, is a drug that increases cardiac output through its positive inotropic and vasodilatory effects. It is prescribed for the short-term management of congestive heart failure, relieving symptoms of the condition such as fatigue, weakness, edema, dyspnea orthopnea, and paroxysmal nocturnal dyspnea.•Option B: Lanoxin, not amrinone, slows ventricular rate, and increases cardiac output. It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart. Digoxin induces an increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility. Cardiac output increases with a subsequent decrease in ventricular filling pressures. •Option C: The vasodilator effect of amrinone decreases peripheral vascular resistance. Indeed, an increase in cyclic adenosine phosphate within the vascular smooth muscle causes a reduction in the intracellular calcium concentration; subsequently, relaxing the vascular smooth muscle. This systemic vasodilation results in a decrease in total peripheral and pulmonary vascular resistance, reducing both preload and afterload. •Option D: Any increase in cardiac output will enhance renal perfusion; this is not just specific to amrinone. The subsequent relative ease in which blood can flow around the vascular network in combination with a stronger heartbeat increases stroke volume and, potentially, cardiac output. It is these vasodilatory and positive inotropic effects that are central in reversing the potentially deadly symptoms of heart failure. 1.Question 8 of 808. Question Before giving milrinone (Primacor) by an IV infusion to a client with symptoms of CHF, which of the following nursing actions is necessary? • A. Record sodium level. • B. Administer loading dose over 15 minutes. • C. Assess CV status. • D. Review medication regimen to identify if client is on IV furosemide (Lasix). Correct Answer: D. Review medication regimen to identify if client is on IV furosemide (Lasix). Milrinone (Primacor) is incompatible with IV furosemide (Lasix), and many clients with CHF are taking furosemide. Use of milrinone is generally contraindicated in patients with acute renal failure and end-stage renal disease, as it primarily undergoes renal excretion, although studies demonstrate that the dose-dependent relationship of adverse events is scarce and there is no clear guidance for milrinone use or dosing in chronic renal disease. •Option A: Assessing potassium, not sodium, is essential. Cardiovascular toxicity is primarily seen in patients receiving milrinone chronically and manifests as tachyarrhythmias and sudden cardiac death. At high dosing, patients may also experience hypotension and syncope. •Option B: Administering a loading dose over 15 min is not done before administration but during administration. Milrinone is primarily for use in the ICU and perioperative setting. Before initiation of this medication, a right heart catheterization may be a consideration for obtaining hemodynamic measurements to establish the patient’s baseline parameters and to gauge the patient response to continuous infusion. •Option C: Assessment of CV status is not specific for milrinone and is indicated for any drug that affects the circulatory system. Repeat or dosing monitoring is not routine due to the risks associated with repeat vascular access or risks related to continuous indwelling catheters. Pulmonary artery catheterization for monitoring of pulmonary pressures should be done with discretion and only after considering a risk-benefit analysis on a case-by- case basis. 1.Question 9 of 809. Question Johanna has ventricular ectopy, which of the following drugs is the first line used to treat her condition? • A. quinidine (Cardioquin). • B. digoxin (Lanoxin). • C. procainamide ( Pronestyl). • D. lidocaine (Xylocaine). Correct Answer: D. lidocaine (Xylocaine). Lidocaine is the only choice used to treat ventricular ectopy. A and C are class IA antiarrhythmics. •Option A: Quinine is a derivative of the bark of the South American cinchona tree. Quinidine is a stereoisomer of quinine; it is a “class 1a antiarrhythmic drug” and also an antimalarial agent. Class 1a antiarrhythmic agents (for example – quinidine, procainamide, disopyramide, ajmaline) work by inhibiting the fast inward sodium current, depressing the phase 0 of the action potential hence dampening the excitability of cardiac muscles which in turn prolongs the action potential and decreases automaticity. •Option B: Digoxin comes from the foxgloves plant known as Digitalis purpurea. It is a cardiotonic glycoside and belongs to the digitalis class. It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart. Digoxin has vagomimetic effects on the AV node.•Option C: Procainamide is a medication used in the management and treatment of ventricular arrhythmias, supraventricular arrhythmias, atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, and Wolf-Parkinson- White syndrome. It is a Class 1A antiarrhythmic agent. Procainamide is a class 1A antiarrhythmic that binds to fast sodium channels inhibiting recovery after repolarization. It also prolongs the action potential and reduces the speed of impulse conduction. This action results in decreased myocardial excitability, slowed conduction velocity, and reduced myocardial contractility. 1.Question 10 of 80 10. Question Class IA antiarrhythmic agents have little effect on: • A. AV node.• B. SA node. • C. Purkinje fibers. • D. Bundle of His. Correct Answer: B. SA node. Class IA antiarrhythmics have little effect on the SA node. It causes moderate degree blockage of fast sodium channels. Drugs include quinidine, procainamide, and disopyramide. These are the most pro-arrhythmic of the sodium channel blockers due to prolonged QTc interval; use is limited due to proarrhythmic potential. •Option A: Quinidine is used in selected patients with Brugada syndrome as an alternative to the implantable cardioverter-defibrillator placement (ICD).