A) Heparin induced thrombocytopenia (HIT): Argatroban is an indirect thrombin inhibitor specifically used for anticoagulation in patients with HIT. This condition involves a significant drop in platelet counts due to heparin therapy, and argatroban is an appropriate alternative for preventing thrombosis in these patients.

B) Ventricular Dysfunction: While managing anticoagulation may be important in patients with ventricular dysfunction, this condition does not specifically necessitate the use of argatroban. Other anticoagulants may be used based on the clinical situation.

C) Myocardial infarction: Although anticoagulation may be warranted in the setting of a myocardial infarction, argatroban is not specifically indicated for this condition. Other antithrombotic therapies, such as aspirin or heparin, are more commonly used.

D) Hepatotoxicity: Argatroban is metabolized in the liver, so caution is warranted in patients with liver dysfunction. Hepatotoxicity itself would not be a reason to use argatroban; rather, it may require close monitoring or adjustment of dosage.

A) Atenolol: This is a beta-blocker that can be used for various cardiac conditions, including hypertension and certain arrhythmias, but it is not typically the first-line treatment for acute life-threatening ventricular dysrhythmias in the emergency setting.

B) Lisinopril: This medication is an ACE inhibitor primarily used to manage hypertension and heart failure. It does not address acute ventricular dysrhythmias and would not be appropriate for immediate use in this scenario.

C) Adenosine: While adenosine is effective for certain types of supraventricular tachycardia, it is not indicated for life-threatening ventricular dysrhythmias. It has a very short duration of action and is not the drug of choice in this context.

D) Procainamide: This antiarrhythmic medication is specifically used to treat life-threatening ventricular dysrhythmias. It works by stabilizing the cardiac membrane and is indicated in emergency situations to manage these types of arrhythmias. Therefore, preparing procainamide is the most appropriate action for the nurse in this scenario.

A) "Increase your potassium intake by eating more bananas and apricots.": Doxazosin is not a potassium-sparing medication, and there is no specific indication for increased potassium intake with this drug. This advice may be misleading, especially since excessive

potassium can pose risks, particularly in certain populations.

B) "Weigh yourself daily, and report any weight loss to your prescriber.": Daily weighing can be important for monitoring fluid retention in some conditions, but weight loss is not a common side effect of doxazosin. Instead, clients should be more concerned about weight gain due to fluid retention or potential side effects from the medication.

C) "The impaired taste associated with this medication usually goes away in 2 to 3 weeks.": Impaired taste is not a well-documented side effect of doxazosin. While some medications may cause changes in taste, this statement is not relevant for doxazosin and does not address the most critical aspects of its administration.

D) "Be sure to lie down after taking the first dose, because first-dose hypotension may make you dizzy.": This statement is accurate and important. Doxazosin can cause first-dose hypotension, leading to dizziness or fainting. Advising the client to lie down after the first dose helps mitigate the risk of hypotensive effects, making this the most appropriate emphasis for the nurse.

A) Angioedema: Quinapril, an ACE inhibitor, can cause angioedema, which is a serious allergic reaction characterized by swelling of the deeper layers of the skin. This side effect is critical to monitor, as it can lead to airway obstruction.

B) Dry non-productive cough: A persistent dry cough is a well-known side effect of ACE inhibitors like quinapril. This occurs due to the accumulation of bradykinin and can be bothersome enough to require discontinuation of the medication.

C) Hyperkalemia: Quinapril can lead to increased potassium levels in the blood, a condition known as hyperkalemia. This is due to the drug's mechanism of action, which reduces aldosterone secretion, leading to decreased potassium excretion.

D) First dose phenomenon: This refers to a significant drop in blood pressure following the first dose of an ACE inhibitor, which can lead to dizziness or fainting. Patients are often advised to take the first dose at bedtime to minimize this risk.

E) Hypotension: Quinapril can cause hypotension, particularly after the initial dosing or in patients who are dehydrated or on diuretics. It’s important for patients to be aware of this potential side effect.

F) Hypertension: Quinapril is used to treat hypertension, so it is not a side effect associated with this medication. Instead, the goal of treatment is to lower blood pressure, making this option incorrect.

A) Pancytopenia: While some medications can cause pancytopenia, it is not a common or direct side effect of alteplase. This condition involves a reduction in red blood cells, white blood cells, and platelets, and is not typically associated with thrombolytics.

B) Hypertension: Alteplase is not known to cause hypertension. In fact, the goal of administering alteplase in the context of a pulmonary embolism is to dissolve the clot and restore normal blood flow, which may help stabilize blood pressure.

C) Hypokalemia: This condition, characterized by low potassium levels, is not a common side effect of alteplase. There are other medications that may cause electrolyte imbalances, but alteplase itself is not typically linked to hypokalemia.

D) Internal bleeding: This is a significant risk associated with alteplase, as it is a thrombolytic agent that dissolves clots. The nurse should closely monitor for signs of internal bleeding, such as changes in vital signs, unexplained bruising, or blood in urine or stool. This is the most critical side effect to assess for in a client receiving alteplase

A) Losartan (Cozaar): This medication is an angiotensin II receptor blocker (ARB) and is often used as an alternative for patients who experience a cough due to ACE inhibitors. Unlike ACE inhibitors, ARBs do not typically cause a cough because they do not affect bradykinin levels, making losartan an appropriate choice for managing hypertension without the adverse effect of a persistent cough.

B) Hydralazine HCL (Apresoline): While hydralazine is an antihypertensive, it works through a different mechanism (direct vasodilation) and is not a first-line alternative for patients with a history of ACE inhibitor-induced cough. It's generally used in specific situations, such as severe hypertension or heart failure.

C) Furosemide (Lasix): This is a loop diuretic primarily used for conditions like heart failure or edema, rather than for the management of hypertension alone. It does not address the underlying hypertension in the same manner as ACE inhibitors or ARBs.

D) Metoprolol (Lopressor): This is a beta-blocker that can be used for hypertension, but it does not directly address the issue of cough related to ACE inhibitors. Switching to a beta-blocker may not be the best option if the client is specifically seeking to avoid the cough associated with ACE inhibitors.

A) Platelet counts: Monitoring platelet counts is not necessary with atorvastatin therapy. While certain medications may affect platelet levels, atorvastatin primarily targets lipid levels and does not have a significant impact on platelet function.

B) Lung function test: Lung function tests are not relevant for atorvastatin use. These tests are typically utilized for assessing respiratory conditions and are not part of the routine monitoring for cholesterol-lowering medications.

C) Liver function test: Atorvastatin can affect liver function, so it is essential to monitor liver

enzymes (such as AST and ALT) regularly. Routine liver function tests help identify any potential hepatotoxicity early, allowing for timely intervention if liver function declines.

D) Bun and creatinine levels: While monitoring renal function can be important in some contexts, it is not a routine requirement specifically for atorvastatin. However, it may be necessary in certain patient populations or if there are concerns about kidney function, but liver function tests are the primary focus with this medication.

A) Constipation: While constipation can occur with digoxin use, it is not a classic sign of digoxin toxicity. Therefore, it is less critical for the client to monitor this symptom specifically in relation to toxicity.

B) Dark red urine: Dark red urine is not typically associated with digoxin toxicity. This symptom could indicate other conditions, such as blood in the urine or issues with the kidneys, but it is not a direct manifestation of digoxin toxicity.

C) Bradycardia: Digoxin toxicity can lead to bradycardia, characterized by a slower than normal heart rate. The client should be instructed to monitor their pulse and report any significant changes, especially if the heart rate drops below 60 beats per minute.

D) Nausea: Nausea is a common symptom of digoxin toxicity. Clients should be aware of this and report any persistent or severe nausea, as it may indicate that the digoxin levels in their system are too high.

E) Vomiting: Vomiting is another classic sign of digoxin toxicity. Clients should be instructed to report any episodes of vomiting, as this can further complicate their condition and may require adjustment of their medication.

F) Anorexia: Anorexia, or loss of appetite, can also occur with digoxin toxicity. Clients should be advised to monitor their appetite and report any significant changes, as this can be an early indicator of toxicity.

A) Masking of hypoglycemia: Propranolol can mask the symptoms of hypoglycemia, such as tachycardia, which is important for clients with diabetes to be aware of. This means that while they may have low blood sugar, they might not experience the typical warning signs due to the medication's effects on the autonomic nervous system.

B) Tachycardia: Propranolol is a beta-blocker that is used to reduce heart rate and blood pressure. Therefore, tachycardia is not a side effect associated with this medication; in fact, it generally works to prevent this condition.

C) Bradycardia: Bradycardia, or a slow heart rate, is a common side effect of propranolol due to its action on beta-adrenergic receptors. Clients should be educated about monitoring their heart rate and reporting any significant drops.

D) Orthostatic Hypotension: This is a potential side effect of propranolol, especially when starting the medication or increasing the dose. Clients should be advised to rise slowly from sitting or lying positions to minimize the risk of dizziness or fainting.

E) Hypertension: Propranolol is prescribed to manage hypertension, so it should not be expected as a side effect. In fact, it is intended to lower blood pressure, and clients should be educated that they should not experience increased hypertension while taking this medication.

A) Migraine headache: While migraines can be uncomfortable and distressing, they are not a known serious side effect of atorvastatin. Clients may experience headaches, but this symptom does not typically require immediate reporting unless accompanied by other concerning signs.

B) Bradycardia: Bradycardia, or a slow heart rate, is not a common side effect of atorvastatin. While monitoring heart rate is important, bradycardia alone does not necessitate immediate reporting unless it leads to significant symptoms or complications.

C) Dark-red urine: Dark-red urine is a concerning finding that could indicate serious conditions, such as hematuria or rhabdomyolysis, particularly when associated with statin use. This symptom requires immediate reporting to the healthcare provider, as it may signify potential muscle breakdown or kidney issues, which are serious complications of atorvastatin therapy.

D) Elevated HDL cholesterol: Increased levels of HDL (high-density lipoprotein) cholesterol are generally considered beneficial and a positive outcome of treatment. Therefore, this finding would not necessitate immediate reporting to the healthcare provider.

A) Gallstones: Gemfibrozil is associated with an increased risk of gallstones. This medication can alter the metabolism of lipids and bile, potentially leading to the formation of gallstones. Clients should be monitored for symptoms such as abdominal pain or discomfort that could indicate gallbladder issues.

B) Decreased PT time: Gemfibrozil does not typically affect prothrombin time (PT). Instead, it may interact with anticoagulants and potentially increase PT time, requiring careful monitoring in patients taking both medications.

C) Hyperkalemia: While hyperkalemia can occur with certain lipid-lowering medications, it is not a common side effect associated with gemfibrozil. This drug primarily affects triglycerides and cholesterol levels without significantly impacting potassium levels.

D) Increased creatinine clearance: Gemfibrozil is not known to increase creatinine clearance; in fact, it can sometimes affect renal function. Monitoring kidney function is important, but increased creatinine clearance is not an expected outcome with this medication.

A) Beta Blockers: While beta blockers can be used to manage some side effects of various medications, they are not typically indicated for managing niacin-induced flushing. Their primary use is in cardiovascular conditions rather than specifically addressing flushing.

B) Calcium Channel Blockers: Calcium channel blockers are primarily used to treat hypertension and certain heart conditions. They do not specifically address the flushing associated with niacin and would not be the expected choice for this side effect.

C) NSAIDs: Nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective in managing niacin-induced flushing. Administering an NSAID, such as ibuprofen, prior to taking niacin can help reduce the flushing response by inhibiting the prostaglandins that contribute to this side effect.

D) Fibric Acid Derivatives: These medications, such as gemfibrozil, are used to lower triglycerides and cholesterol levels, but they do not address the flushing side effect caused by niacin. Their mechanism of action is different and not focused on alleviating flushing symptoms.

A) Inhibits platelet aggregation: The primary benefit of aspirin following a myocardial infarction (MI) is its ability to inhibit platelet aggregation. By preventing platelets from clumping together, aspirin reduces the risk of further clot formation, which is critical in preventing additional cardiac events and improving overall cardiovascular outcomes.

B) Anti-inflammatory properties: While aspirin does have anti-inflammatory effects, this is not the primary reason it is prescribed after an MI. The focus in the post-MI setting is on its role in preventing clot formation rather than addressing inflammation.

C) Antiemetic: Aspirin is not an antiemetic and does not alleviate nausea or vomiting. Clients experiencing gastrointestinal issues or nausea would require different medications for those symptoms.

D) Anti-pyretic: Although aspirin can reduce fever, this effect is not the primary concern in the post-MI setting. The immediate goal is to improve heart health and prevent further thrombotic events, making platelet inhibition the most relevant benefit.

A) Dry, non-productive cough: One of the most common side effects associated with ACE inhibitors is a dry, non-productive cough. This occurs due to the accumulation of bradykinin, a peptide that can increase in the body when ACE is inhibited. Nurses should assess for this symptom, as it may require changing the medication if it becomes bothersome to the client.

B) Nausea and vomiting: While nausea and vomiting can occur with various medications, they are not specific or common side effects of ACE inhibitors. If these symptoms do arise, they may be due to other factors and should be investigated further.

C) Hypokalemia and vomiting: ACE inhibitors are more commonly associated with hyperkalemia (elevated potassium levels) rather than hypokalemia. Monitoring potassium levels is important, but vomiting is not a typical side effect of ACE inhibitors.

D) Epistaxis and headache: Although headaches can occur with many medications, epistaxis (nosebleeds) is not a common side effect associated with ACE inhibitors. While headache assessment is appropriate, the dry cough is the more characteristic and important symptom to monitor in clients on these medications.

A) "This medication decreases chest pain by dissolving blood clots that are occluding the arteries.": This statement is incorrect because nitroglycerin does not dissolve blood clots. Instead, it works by relaxing and dilating blood vessels, which helps improve blood flow to the heart muscle and relieve angina.

B) "Place one tablet under your tongue every 15 minutes and repeat up to 5 times for relief of chest pain.": This is not accurate; while nitroglycerin can be taken sublingually, the typical recommendation is to take one tablet every 5 minutes as needed for chest pain, not every 15 minutes, and not to exceed 3 tablets within 15 minutes.

C) "This medication is the first-line treatment for hypertension.": Although nitroglycerin can lower blood pressure, it is not typically considered a first-line treatment for hypertension. It is primarily used for angina relief rather than as a primary antihypertensive agent.

D) "This medication dilates cardiac blood vessels to deliver more oxygen to the heart.": This statement accurately describes the action of nitroglycerin. By dilating the coronary arteries, nitroglycerin increases blood flow and oxygen delivery to the heart muscle, which helps alleviate angina symptoms. This is a key point to emphasize during patient education.

A) "Acts on the beta cells within the heart and lungs to regulate cardiac rhythm.": This statement is incorrect because calcium channel blockers do not primarily act on beta cells. Instead, they block calcium channels in cardiac and smooth muscle, which affects heart contractility and conductivity.

B) "Increases heart rate and increases myocardial contractility.": Calcium channel blockers typically do the opposite; they decrease heart rate and myocardial contractility by inhibiting calcium entry into the heart muscle cells. Therefore, this statement does not accurately describe their mechanism of action.

C) "Reduces the contractility and conductivity of the heart.": This statement accurately reflects the action of calcium channel blockers. By blocking calcium entry, these medications decrease myocardial contractility and slow down electrical conduction through the heart, which can help manage dysrhythmias.

D) "Increase oxygen to the systemic circulation.": While calcium channel blockers can improve blood flow and reduce myocardial oxygen demand by decreasing heart workload, their primary action does not directly focus on increasing oxygen delivery to systemic circulation. Their primary role is in managing heart contractility and rhythm.

A) Carvedilol: While carvedilol is a beta-blocker that can be used to treat hypertension, it is not considered a first-line treatment. Beta-blockers are typically used when other first-line agents are not effective or in specific situations such as heart failure or ischemic heart disease.

B) Lisinopril: Lisinopril is an ACE inhibitor and is considered a first-line treatment for hypertension. It effectively reduces blood pressure by inhibiting the angiotensin-converting enzyme, leading to vasodilation and decreased blood volume. Its well-documented efficacy and favorable side effect profile make it a common choice for initial therapy.

C) Clonidine: Clonidine is an alpha-2 adrenergic agonist that can lower blood pressure but is generally not used as a first-line treatment due to its side effects and potential for rebound hypertension if discontinued abruptly.

D) Doxazosin: Doxazosin is an alpha-1 blocker that can be used to treat hypertension but is not typically a first-line choice. It may be used in specific cases, such as in patients with benign prostatic hyperplasia, but other classes of medications are usually preferred for initial hypertension treatment.

A) Aspirin: While aspirin is an antiplatelet medication that can help prevent further clot formation, it does not have thrombolytic properties and does not directly lyse existing clots. Therefore, it is not appropriate for this purpose.

B) Heparin: Heparin is an anticoagulant used to prevent the extension of existing clots and reduce the risk of new clots forming, but it does not dissolve existing clots. It helps manage deep vein thrombosis but does not have thrombolytic activity.

C) Warfarin (Coumadin): Warfarin is an oral anticoagulant that is used to prevent new clot formation and the growth of existing clots. However, like heparin, it does not actively lyse or dissolve existing clots.

D) Alteplase (Activase): This medication is a thrombolytic agent that actively dissolves blood clots by activating plasminogen to plasmin, leading to clot breakdown. It is appropriate for use in cases of deep vein thrombosis when clot lysis is indicated.

E) Anistreplase (Eminase): Similar to alteplase, anistreplase is another thrombolytic agent used to lyse existing clots. It acts by converting plasminogen to plasmin, effectively breaking down fibrin in clots, making it suitable for the treatment of deep vein thrombosis.

A) Hypokalemia: Hypokalemia, or low potassium levels, significantly increases the risk of digoxin toxicity. Since digoxin competes with potassium for binding at the sodium-potassium ATPase site in the heart, low potassium levels can lead to increased digoxin effects and toxicity. Therefore, it is crucial to monitor potassium levels and correct any deficiencies before administering digoxin.

B) Hyperkalemia: While hyperkalemia is a serious concern and can also affect digoxin therapy, it usually results in decreased effectiveness of digoxin rather than increasing toxicity. Elevated potassium levels can diminish the drug's positive inotropic effect.

C) Hypocalcemia: Although calcium levels can influence cardiac function, hypocalcemia is not directly related to digoxin toxicity. Monitoring calcium is important for overall cardiac health, but it is not the primary focus when assessing the risk for digoxin toxicity.

D) Hypernatremia: Elevated sodium levels do not have a direct impact on the efficacy or toxicity of digoxin. While sodium levels are essential to monitor for overall health, they are not critical in the context of digoxin administration and toxicity risk.

A) Pulse oximetry of 92%: While a pulse oximetry reading of 92% is slightly below normal, it is not a definitive reason to hold verapamil. This reading indicates mild hypoxemia, but it does not directly contraindicate the use of verapamil. Other factors should be considered before making a decision based solely on this value.

B) Pulse of 78: A pulse rate of 78 beats per minute is within the normal range for adults and does not warrant holding verapamil. This finding alone does not indicate any immediate concerns related to the administration of the medication.

C) Respiratory rate of 12: A respiratory rate of 12 breaths per minute is within the normal range for adults. This finding does not provide any indication that verapamil should be withheld. It is important to consider other clinical factors when assessing the appropriateness of medication administration.

D) History of myocardial infarction a week ago: Verapamil, a calcium channel blocker, can have significant effects on cardiac function. Administering it to a client who recently experienced a myocardial infarction (heart attack) could exacerbate cardiac issues and lead to complications. Therefore, it is crucial to hold the medication and consult with the healthcare provider before proceeding.

A. "Depending on the level of your PT/INR, the clot will begin to dissolve.": This response is misleading, as heparin's effect is not primarily monitored by PT/INR; rather, heparin is monitored by activated partial thromboplastin time (aPTT). Moreover, heparin does not directly dissolve clots; it prevents further clot formation.

B. "After the first dose, the clot will begin to dissolve.": This statement inaccurately suggests that heparin has an immediate effect on dissolving existing clots. While heparin acts quickly to inhibit further clotting, it does not lead to the dissolution of clots after the first dose.

C. "It usually takes heparin at least 2 to 3 days to reach a therapeutic blood level.": This is not accurate for heparin, which has an immediate effect on coagulation. While the therapeutic effects can be optimized over several days, heparin begins to work right away to prevent further clotting.

D. "Heparin does not dissolve clots. It stops new clots from forming.": This response accurately describes the mechanism of action of heparin. Heparin prevents the extension of existing clots and the formation of new clots, but it does not actively dissolve clots. This clarification is essential for the client’s understanding of their treatment and expectations regarding DVT management.