Cardiac Pharmacology

What class of lipid lowering drugs may actually increase triglyceride levels and therefore should not be used in patients with triglyceride levels elevated ? A. Bile acid sequestrants. B. Niacin (nicotinic acid). C. HMG-CoA reductase inhibitors. D. Fibrates.

A. Because bile acid sequestrants can increase triglyceride levels, they are contraindicated in patients with elevated triglycerides > 500 mg/dL or in patients with a history of pancreatitis secondary to elevated triglycerides. These medications should be used with caution in patients with triglycerides > 200 to 300 mg/dL.

Drugs whose generic name ends in 'olol' are: A. Beta blockers. B. Inotropes. C. ARBs (angiotensin receptor blockers). D. ACE inhibitors.

A. Most beta blockers have generic names that end in 'olol'. Examples include atenolol, metoprolol, propranolol, bisoprolol.

When administering a Class III antiarrhythmic such as ibutilide (Corvert) or dofetilide (Tikosyn) the nurse knows that it is very important to assure the patient does not have a deficit in which electrolyte: A. Calcium. B. Potassium. C. Phosphorous. D. Sodium.

B. Class III agents work on phase 3 of the cardiac action potential by blocking potassium channels. Phase 3 of the action potential is cellular repolarization and is associated with the T wave on the surface ECG. Class III agents prolong repolarization and thus prolong the QT interval. Torsades de pointes is a complication / risk associated with the administration of Class III agents such as ibutilide. Since class III agents are potassium channel blockers, hypokalemia will increase the risk of QT prolongation.

Which of these drugs are aldosterone blockers used in treating heart failure: A. Digoxin, dobutamine. B. Spironolactone, eplerenone. C. Furosemide, hydrochlorothiazide. D. Losartan, enalapril.

B. Spironolactone (Aldactone) is a non-selective aldosterone blocker and a K+ sparing diuretic. Eplerenone (Inspra) is a more selective aldosterone blocker without some of the side effects of spironolactone. Digoxin and dobutamine are positive inotropes used to increase contractility. Furosemide and hydrochlorothiazide are diuretics. Losartan (Cozaar) is an angiotensin receptor blocker (ARB) and enalapril (Vasotec) is an ACE inhibitor, both used to block the RAAS in heart failure.

Drugs used to increase contractility in systolic heart failure include: A. Amlodipine, diltiazem. B. Enalapril, captopril. C. Digoxin, dobutamine, milrinone. D. Furosemide, spironolactone.

C. Digoxin, dobutamine, and milrinone are positive inotropic agents that increase cardiac contractility. Digoxin is the only oral inotrope available and is used in chronic heart failure. Dobutamine and milrinone can be used in acute heart failure but are only available in IV form. Lasix and spironolactone are diuretics used for fluid management. Spironolactone (Aldactone) is a K+ sparing diuretic and aldosterone blocker. Enalapril and captopril are ACE inhibitors with preload and afterload reducing effects. Amlodipine and diltiazem are calcium channel blockers and are not indicated for treatment of systolic heart failure because they can decrease contractility.

Your patient returns from the cath lab after receiving a stent to the circumflex artery. He is in atrial fibrillation with ventricular rate in the 80s, BP is 126/68, skin is warm and dry, groin site is stable with the sheath still in place. He is on an eptifibatide (Integrilin) IV drip. His post procedure orders include: ASA daily, clopidogrel (Plavix) daily, metoprolol daily, enalapril daily, and diltiazem twice a day. You know that the combination of metoprolol and diltiazem can contribute to which of the following side effects: A. Bleeding. B. Acute kidney injury. C. Bradycardia or heart block. D. Gastroesophageal reflux.

C. Metoprolol is a beta blocker and diltiazem is a calcium channel blocker. Both types of drugs have the same effect on slowing heart rate and decreasing conduction velocity through the AV node, therefore the combination of the two can result in bradycardia or heart block.

When assessing for train of four for the appropriate response in a patient receiving neuromuscular blockade what is the goal: A. Dose that results in 4 twitches (out of a possible 4) in response to peripheral nerve stimulation. B. Dose that results in 0 twitches (out of a possible 4) in response to peripheral nerve stimulation. C.Dose that results in 1 to 2 twitches (out of a possible 4) in response to peripheral nerve stimulation. D. Dose that results in 2 to 3 twitches (out of a possible 4) in response to peripheral nerve stimulation.

C. When monitoring train of four for appropriate amount of blockade, an adjustment of neuromuscular blockade should occur to achieve 1 to 2 twitches (out of a possible 4) in response to peripheral nerve stimulation. A commonly used muscle nerve combination is the ulnar nerve and adductor pollicus.

The mechanism of action for ezetimibe is: A. Unknown. B. Inhibit cholesterol synthesis. C. Inhibit hepatic secretion of VLDL-C. D. Intestinal absorption inhibitor.

D. Ezetimibe is an intestinal absorption inhibitor. HMG-CoA reductase inhibitors inhibit cholesterol synthesis. Fibrates inhibit hepatic secretion of VLDL-C.

Nursing considerations related to the administration of digoxin include the following: A. Holding digoxin if the patient develops atrial fibrillation. B. Administering calcium chloride to treat digoxin toxicity. C. Administering digoxin at bedtime to assure absorption. D. Assuring potassium level is normal prior to initiation.

D. Hypokalemia enhances the effect of digoxin and increases the risk for digoxin toxicity. It is not necessary to administer digoxin at bedtime for adequate absorption. 75% - 80% of an oral dose is rapidly absorbed and is not affected by meals. Calcium should not be given in the presence of digoxin toxicity. Digitalis inhibits the Na/K pump on the cell membrane and results in an increased intracellular calcium level (the mechanism of its positive inotropic effect). Administering calcium can potentiate digitalis toxicity. Digoxin administration is not contraindicated if a patient develops atrial fibrilation. Digoxin slows AV conduction and helps control the ventricular rate in atrial fib.

Drugs with a positive mortality benefit in heart failure include: A. Dobutamine, milrinone. Diuretics, calcium channel blockers. B. Digoxin, diuretics, beta blockers, calcium channel blockers. C. Calcium channel blockers, digoxin, beta blockers, ACE inhibitors. D. Beta blockers, ACE inhibitors, ARBs, aldosterone blockers.

D. Only 4 groups of drugs have been shown to have a positive mortality benefit in heart failure: beta blockers, ACEI, ARBs, and aldosterone blockers. Diuretics and digoxin have symptom benefit but no mortality benefit. Inotropes (dobutamine, milrinone, etc.) are associated with increased mortality in heart failure. Calcium channel blockers are generally contraindicated in heart failure but can be used with caution if needed for angina or hypertension control.

All of the following are reported side effects from loop diuretics EXCEPT: A. Gout. B. Hypokalemia. C. Dizziness. D. Visual disturbances described as halos.

D. This describes the visual disturbances seen with digoxin toxicity. Common adverse drug reactions with loop diuretics include the following: hyponatremia, hypokalemia, hypomagnesaemia, dehydration, hyperuricemia, gout, dizziness, postural hypotension, syncope

You are caring for a 83 year old male patient admitted for observation for chest pain. The patient has a history of hypertension and atrial fibrillation. He is on lisinopril, metoprolol succinate and warfarin. His rhythm is atrial fibrillation with a heart rate of 76. His blood pressure is 158/88. He has completed the chest pain protocol with no abnormal findings. He is currently pain free. Discharge is pending. What actions do you take: A. Discharge the patient and reinforce that he should begin taking a baby aspirin each day to prevent further chest pain. B. Discuss options for improved blood pressure control with the provider and provide patient counseling on the importance of maintaining blood pressure control when on warfarin to reduce the risk of hemorrhagic stroke in addition to reducing the risk of myocardial infarction, ischemic stroke, and heart failure. C. Instruct the patient to follow up with his primary care physician regarding his metoprolol succinate since that medication will probably need to be discontinued since he had an episode of chest pain. D. Notify the provider that you are concerned that the patient is prescribed warfarin since he is older than age 80 years and you know that warfarin is not to be used in this age group.

D. When caring for an elderly patient on warfarin therapy the nurse should be diligent in advocating for patient safety by providing patient education on the importance of strict blood pressure control and in reporting of elevated blood pressures to the patient's provider. Blood pressure control in elderly patients on oral anticoagulation is very important to reduce the risk of intracranial hemorrhage. Systolic blood pressure should be maintained at < 140 mmHg. Hypertension is also a risk factor for myocardial infarction, ischemic stroke, and heart failure. The use of aspirin in addition to warfarin is known to increase the risk of intracranial and other hemorrhage. In patients with stable coronary artery disease warfarin is effective in reducing the risk of recurrent myocardial infarction and therefore warfarin alone is used rather than warfarin plus aspirin. In patients with atrial fibrillation who experience an acute coronary syndrome (ACS) or have a percutaneous coronary intervention (PCI), antiplatelet therapy will need to be added to warfarin for a period of time. This patient has no evidence of having an acute coronary syndrome.

Potential complications of the use of sodium bicarbonate in critically ill patients are: A. Decrease in ionized calcium. B. Increase in lactate. C. Increase in PaCO2. D. Sodium and fluid overload. E. All of the above.

E. Bicarbonate administration has the following potential negative effects: sodium and fluid overload, increase in lactate and PaCO2, and decrease in ionized calcium.

Combing bronchodilators with different mechanisms of action and different durations is contraindicated: True. False.

False. Combing bronchodilators with different mechanisms of action and different durations increases the effectiveness of bronchodilation.

Routine monitoring of liver enzymes is not required in patients taking statin medication: True. False.

True. Liver enzymes should be assessed at baseline and as clinically indicated. Routine monitoring of liver enzymes is not necessary. If liver enzymes become elevated, repeat assessments should be made until results return to baseline. Statin therapy can result in an elevation of liver enzymes not associated with liver toxicity. An elevation of liver enzymes should be correlated with other clinical factors including jaundice, elevated bilirubin, and symptoms of liver toxicity. Elevations in liver enzymes are more associated with higher dose statin therapy.

Drugs used to block the renin-angiotensin-aldosterone system (RAAS) in heart failure and hypertension include: A. ACE inhibitors, angiotensin receptor blockers (ARB), aldosterone blockers. B. Calcium blockers and beta blockers. C. Inotropes, diuretics, aldosterone blockers. D. Inotropes and arterial dilators.

A. ACE inhibitors, angiotensin receptor blockers (ARB), aldosterone blockers are used to block the RAAS in heart failure. ACEI and ARBs cause venous and arterial dilation which results in preload and afterload reduction. Aldosterone blockers prevent aldosterone-mediated Na+ and H2O retention in renal tubules and therefore contribute to preload reduction. Inotropes increase contractility in heart failure but have no direct effect on the RAAS. Diuretics are used for fluid management and preload reduction but do not work through the RAAS. Beta blockers are useful in heart failure to attenuate the effects of chronic sympathetic nervous system stimulation. They also have an affect on the RAAS by blocking renin release by juxtaglomerular cells in the kidney. Calcium blockers are not indicated in treating heart failure because they decrease contractility and have no beneficial effects on the neurohormonal compensatory mechanisms in heart failure. Arterial dilators are used for afterload reduction but do not work directly through the RAAS.

Which antiarrhythmics are appropriate for treating stable ventricular tachycardia: A. Amiodarone, lidocaine. B. Adenosine, magnesium. C. Diltiazem, verapamil. D. Epinephrine, atropine

A. Amiodarone and lidocaine are the antiarrhythmics recommended in the ACLS guidelines for managing ventricular tachycardia. Epinephrine is used during CPR as a vasopressor to help shunt cardiac output into heart and brain. Atropine is used to treat symptomatic bradycardia. Diltiazem and verapamil are used to treat SVT and for ventricular rate control in atrial fib or flutter. Adenosine is used to terminate AV nodal active SVTs (AVNRT and AVRT). Magnesium is used to treat Torsades de Pointes.

Which of these drugs are used for pharmacological conversion of atrial fibrillation: A. Dofetilide, ibutilide, flecainide, propafenone. B. Amiodarone, digoxin, beta blockers, dofetilide. C. Amiodarone, ibutilide, adenosine, beta blockers. D. Diltiazem, verapamil, adenosine, procainamide.

A. Amiodarone is an option for conversion of atrial fib and is effective in maintaining sinus rhythm after conversion. Procainamide can also be effective in converting atrial fibrillation but is not commonly used. Adenosine is not indicated for treatment of atrial fibrillation because it does not convert it and its half-life is too short to be of use in rate control. Diltiazem and verapamil are calcium channel blockers often used for ventricular rate control in atrial fibrillation but not for conversion. Beta blockers are also used for rate control but not for conversion. Digoxin can be used for rate control in patients with hypotension or impaired left ventricular function who cannot tolerate calcium channel blockers or beta blockers.

When providing patient education to a patient newly prescribed an anticholinergic bronchodilator, the nurse should inform the patient that the most commonly experienced side effect is: A. Dry mouth. B. Headache. C. Nausea. D. Tremors.

A. Anticholinergic medications block acetylcholine's effect on the muscarinic receptors. Short acting agents can have effects up to 8 hours. The effects of long acting agents range from > 12 hours to > 24 hours. The main side effect of these medications is dry mouth.

You are caring for a patient with a previous ankle brachial index of .88. He has not previously had any lower extremity symptoms. He has a history of diabetes mellitus type 2. He is taking a statin and an oral antidiabetic agent. Today he presents to the office and he is complaining of intermittent lower extremity claudication. His blood pressure is 112/72 mmHg. What medication do you anticipate will be added to his regime: A. Aspirin. B. Gabapentin. C. ACE inhibitor. D. Beta blocker.

A. Antiplatelet therapy should be used in all patients with symptomatic lower extremity PAD to reduce the risk of MI, stroke and vascular death. Aspirin 75 mg to 325 mg daily is used. An ACE-inhibitor would be the agent of choice to treat hypertension if present since the patient has type 2 diabetes mellitus.

Atropine 0.5 mg IV would be appropriate for which of these situations: A. Sinus bradycardia at a rate of 36 with hypotension and dizziness, or symptomatic Type I second degree AV block. B. Symptomatic third degree AV block or Type II AV block. C. Asystole and symptomatic bradycardia. D. Unstable VT and PEA.

A. Atropine is the drug of choice for treating symptomatic bradycardia. Symptoms resulting from bradycardia can include hypotension, chest pain, SOB, dizziness, syncope or near syncope. Causes of symptomatic bradycardia include sinus bradycardia, second degree AV block, third degree AV block, slow junctional rhythm, idioventricular rhythm. Atropine works best on bradycardia that is sinus or junctional in origin and for AV block that occurs at the level of the AV node (Type I second degree AV block or Wenckebach). Atropine is not recommended for asystole and it is not appropriate for treating ventricular arrhythmias or SVT. Atropine does not work for Type II AV block (block that occurs below the AV node) or in 3rd degree AV block with a ventricular escape pacemaker. If 3rd degree AV block has a junctional escape pacemaker, atropine may increase the rate of the junctional pacemaker but it does not reestablish AV conduction. Pacing is the preferred treatment for bradycardia that is unresponsive to atropine.

A 58 you woman is admitted to the telemetry unit with 'rapid heart rate' and mild SOB. She has a history of mitral valve disease and intermittent palpitations. She woke up today with palpitations and her heart rate did not slow down so she is admitted for diagnosis and treatment. You record this rhythm strip (AFIB). What drug therapy do you anticipate: A. Diltiazem or metoprolol. B. Adenosine. C. Amiodarone. D. Atropine.

A. Calcium channel blockers (diltiazem or verapamil) or beta blockers (i.e. metoprolol) are recommended for rate control in atrial fib or flutter. Amiodarone is a potent antiarrhythmic and can be used to convert atrial fibrillation. It can be effective in rate control but it has many side effects and using it for rate control is not the best option. Adenosine is not indicated for treating atrial fib or flutter. Its main indication is for terminating SVTs in which the AV node is part of the circuit that maintains the tachycardia: AV nodal reentry tachycardia (AVNRT) and AV reentry tachycardia (AVRT) in patients with WPW syndrome. Atropine is used to speed up a slow heart rate and is contraindicated here.

Which of the following drugs can be used to manage angina due to coronary artery vasospasm: A. Calcium channel blockers, nitrates. B. Diuretics, vasopressors. C. ACE inhibitors, beta blockers. D. Beta blockers, calcium channel blockers.

A. Calcium channel blockers and nitrates cause coronary artery vasodilation and can be used to prevent vasospastic angina. Diuretics, beta blockers, and ACE inhibitors have no direct effect on the muscle layer of the coronary blood vessel so do not prevent vasospasm. Vasopressors could contribute to coronary vasospasm by constricting coronary vessels.

Drugs used to block the renin-angiotensin-aldosterone system (RAAS) either directly or indirectly in heart failure include all of the following EXCEPT: A. Calcium channel blockers. B. Angiotensin receptor blockers (ARBs). C. Beta blockers. D. ACE inhibitors.

A. Calcium channel blockers do not block any portion of the RAAS. Beta blockers inhibit renin release. ACE inhibitors prevent conversion of angiotensin I to angiotensin II. ARBs block the effect of angiotensin II at its receptor site.

Which of the following drugs is an oral direct thrombin inhibitor used for prevention of stroke in patients with nonvalvular atrial fibrillation: A. Dabigatran (Pradaxa). B. Apixaban (Eliquis). C. Ticagrelor (Brilinta). D. Rivaroxaban (Xarelto). E. Warfarin.

A. Dabigatran is a relatively new oral direct thrombin inhibitor approved for prevention of stroke and systemic embolization in patients with nonvalvular atrial fibrillation. Rivaroxaban and apixaban are new oral factor Xa inhibitors approved for prevention of stroke and systemic embolization in patients with nonvalvular atrial fibrillation. Warfarin is a Vitamin K antagonist used for prevention of stroke in atrial fibrillation. Ticagrelor is an antiplatelet agent that blocks the P2Y12 receptor on the ADP pathway of platelet activation.

Which of the following is NOT a treatment option for AV nodal reentry tachycardia: A. A dihydropyridine calcium channel blocker. B. Ablation. C. Carotid massage. D. Adenosine.

A. Dihydropyridine calcium channel blockers (those that end in 'pine' like amlodipine, etc.) have little impact on heart rate or conduction through the AV node. Verapamil and diltiazem are considered the 'heart rate lowering' calcium channel blockers and would be appropriate for treating AVNRT. They are not Dihydropyridines. Adenosine is the drug of choice for terminating AVNRT because it is fast acting, slows conduction through the AV node, and has a half-life of about 9 seconds so it doesn't cause long lasting side effects. Ablation can be used to permanently treat AVNRT by ablating the slow conducting fibers of the reentry circuit. Carotid massage and other vagal maneuvers can be used to slow conduction through the AV node and break the reentry cycle of AVNRT.

Your patient returns from the cath lab after receiving a stent to the circumflex artery. He is in atrial fibrillation with ventricular rate in the 80s, BP is 126/68, skin is warm and dry, groin site is stable with the sheath still in place. He is on an eptifibatide (Integrilin) IV drip. His post procedure orders include: ASA daily, clopidogrel (Plavix) daily, metoprolol daily, enalapril daily, and diltiazem bid. You know that the following drugs are being given for their antiplatelet effects following stent placement: A. Eptifibatide, ASA, clopidogrel. B. Eptifibatide, metoprolol, diltiazem. C. Diltiazem, enalapril, clopidogrel. D. ASA, metoprolol, diltiazem.

A. Eptifibatide (Integrilin) is a GP IIb/IIIa platelet inhibitor indicated as adjunctive therapy in PCI procedures to prevent platelet aggregation. ASA and clopidogrel inhibit platelet activation and are indicated following PCI procedures and in the patient with ACS. Clopidogrel blocks the adenosine diphosphate (ADP) pathway of platelet activation. ASA blocks the formation of thromboxane A inside the platelet which is one pathway of platelet activation. Metoprolol is a beta blocker and has no antiplatelet effects. Diltiazem is a calcium channel blocker with no antiplatelet effects. Enalapril is an ACE inhibitor and has no antiplatelet effects.

The class of medications most effective in lowering LDL-C is: A. HMG-CoA reductase inhibitors (statins). B. Nicotinic acid. C. Fibrates. D. Bile acid sequestrants.

A. HMG-CoA reductase inhibitors (statins) are the most effective medications for lowering LDL-C. In addition, they also have been shown to have mortality benefit in both primary and secondary prevention. Statins are usually the first line agent used in dyslipidemia because of their proven results, their overall safety profile, and their ability to be well tolerated by most patients. Bile acid sequestrants lower LDL-C but not as much as statins. Nicotinic acid and fibrates are especially effective at lowering triglycerides, and they lower LDL-C mildly.

The ability of heparin to bind to platelet factor 4 (PF4) can cause which of these potentially dangerous side effects: A. HIT (heparin induced thrombocytopenia). B. Osteoporosis. C. Uncontrolled bleeding. D. Heparin rebound.

A. Heparin binds with platelet factor 4, forming a heparin-PF4 complex that stimulates an immune reaction involving formation of antibodies against the complex. The heparin-PF4-antibody complex binds to platelets, causing platelet activation and thrombin generation that results in intravascular thrombosis. Activated platelets are removed from circulation, leading to thrombocytopenia. Bleeding and osteoporosis can be side effects of heparin but are not due to binding of heparin with PF4. Heparin rebound is the reappearance of anticoagulant activity after adequate neutralization of heparin with protamine at the end of cardiac surgery. A significant amount of heparin is bound to plasma proteins and tissues, and its slow release following surgery results in anticoagulation after protamine has worn off. Heparin rebound is not due to heparin binding with PF4.

Which of the following can be used to decrease afterload in cardiogenic shock: A. IABP. B. Low dose dopamine. C. Dobutamine. D. High dose dopamine.

A. IABP therapy is a mechanical form of afterload reduction. When the balloon deflates at the onset of systole, it creates and 'empty' space in the aorta that reduces afterload and makes it easier for the LV to eject. Dopamine in low doses stimulates dopaminergic receptors in renal and other blood vessels and may improve renal blood flow. It does not cause significant peripheral arterial dilation to reduce LV afterload. High dose dopamine stimulates alpha receptors in peripheral blood vessels and increases afterload by causing vasoconstriction. Dobutamine is a positive inotropic drug that increases contractility but has no net effect of peripheral blood vessels.

You have performed a daily awakening trial on a patient who had been appropriately sedated on a propofol drip at 30 mcg/kg/min. The patient awakened and followed simple commands. Thirty minutes after awakening the patient becomes restless and is no longer able to focus on verbal instruction. What is the appropriate action: A. Resume the propofol drip at 15 mcg/kg/min and titrate up if needed at 5 minute intervals. B. Call for new sedation orders because the daily awakening trial nullifies the sedation protocol. C. Resume the propofol drip at 30 mcg/kg/min and titrate up to 50 mcg/kg/min to achieve adequate sedation within 5 minutes. D. Resume the propofol drip at 30 mcg/kg/min.

A. If sedation needs to be resumed after a daily awakening, it should be resumed at ½ the dose prior to awakening and then titrated based on the patient's sedation scale. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect.

Which bronchodilator is the least preferred in the treatment of chronic obstructive pulmonary disease (COPD): A. Slow released theophylline. B. Ipratropium bromide. C. Tiotropium. D. Salmeterol. E. Levalbuterol.

A. Methylxanthines: The exact mechanism of these medications is not known. They may act as non-selective phosphodiesterase inhibitors. Slow released theophylline is the most commonly used drug in this class although it is less effective and less well tolerated than the inhaled long acting bronchodilators. It is not recommended if long acting inhaled bronchodilators are affordable. A major problem with drugs in this class is that the therapeutic effect occurs at a near toxic dose. Serious side effects occur including cardiac arrhythmias and grand mal seizures Beta2-agonsits and anticholinergics are the preferred bronchodilators in the treatment of chronic obstructive pulmonary disease. Salmeterol: Long acting beta2- agonist Levalbuterol: Short acting beta2- agonist Ipratropium bromide: Short acting anticholinergic. Tiotropium: Long acting anticholinergic.

An early sign of HIT (heparin induced thrombocytopenia) is: A. Drop in platelet count by about 50%. B. Excessive bleeding from gums, puncture sites, GI system. C. Stroke, MI, or DVT. D. Massive organ failure.

A. Platelet count usually falls by 50% or more from baseline, usually within 4-10 days after heparin is started. Excessive bleeding can occur with any anticoagulant therapy but is not associated with HIT. HIT results in arterial and venous thrombosis that can cause DVT, pulmonary embolism, limb gangrene, stroke, MI and other organ failure - but these events occur after the initial drop in platelet count.

When administering the medications spironolactone or eplerenone to a patient, the nurse knows the following is true: A. The patient is at risk for hyperkalemia. B. The patient is at risk for hypervolemia. C. The patient is at risk for increased bleeding. D. The patient is at risk for thrombocytopenia.

A. Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone blockers. Aldosterone promotes Na+ retention which results in the loss of K+, so blocking aldosterone promotes loss of Na+ and K+ retention and can lead to hyperkalemia, especially when the patient is also taking ACE inhibitors or angiotensin receptor blockers (ARB). Aldosterone causes Na+ and H2O retention which can lead to hypervolemia. Aldosterone blockers cause loss of Na+ and H2O and result in intravascular volume reduction. Aldosterone blockers do not have a direct effect on platelet function and do not increase the risk of bleeding.

What class of medications are used in acute exacerbations of chronic obstructive pulmonary disease (COPD) to improve lung function and hypoxemia, shorten recovery time and length of stay, and reduce the risk for early repeat exacerbation: A. Systemic corticosteroids. B. Antibiotics. C. Intravenous beta2-agonsits. D. Anti virals.

A. Systemic corticosteroids (oral or intravenous) are used in acute exacerbations to improve lung function and hypoxemia, shorten recovery time and length of stay, and reduce the risk for early repeat exacerbation. A dose of 40mg of prednisone or prednisolone for 5 days is often used although the optimal duration of therapy is not certain. Prednisone is activated by the liver into prednisolone. Oral prednisolone is preferred and should always be used in the presence of liver dysfunction.

Your patient develops atrial fibrillation with a ventricular rate in the 130s. She is slightly SOB and feels palpitations but BP is 124/70, RR 18, skin warm and dry. Which of the following treatments would you anticipate first: A. Administration of diltiazem for rate control. B. Immediate synchronized cardioversion. C. Administration of adenosine for rate control. D. Administration of warfarin for thromboembolism prevention.

A. The first goal of management in atrial fibrillation is ventricular rate control. A secondary goal might be conversion to sinus rhythm, but rate control is more important acutely unless the patient is hemodynamically unstable. Drugs appropriate for rate control in atrial fibrillation include calcium channel blockers and beta blockers. Diltiazem is a calcium channel blocker that has less negative inotropic effect than beta blockers and is a first-line drug for rate control. Adenosine is not appropriate for treatment of atrial fibrillation due to its very short half- life. Immediate cardioversion would be indicated in hemodynamically unstable atrial fibrillation but this patient is not unstable. Warfarin is indicated for thromboembolism prevention in paroxysmal or permanent atrial fibrillation and might eventually be prescribed, but it is not the first treatment.

Your patient is having an anaphylactic reaction to the new antibiotic that is being administered IV. You know that the most important immediate therapy for anaphylaxis in order to prevent shock and death is administration of: A. Epinephrine to reverse bronchospasm and cause peripheral vasoconstriction. B. Methylprednisolone to decrease inflammatory response. C. Albuterol inhaler for bronchospasm. D. Diphenhydramine (Benadryl) for antihistamine effects.

A. The most important immediate therapy in anaphylaxis is epinephrine. There are no absolute contraindications to epinephrine in the setting of anaphylaxis. Epinephrine is the only drug that prevents or reverses obstruction to airflow due to bronchoconstriction, and prevents or reverses cardiovascular collapse by causing vasoconstriction in peripheral vessels to counteract the massive vasodilation in anaphylaxis. Epinephrine also decreases inflammatory mediator release from mast cells and basophils. The recommended adult dose of epinephrine for anaphylaxis is 0.3 to 0.5 mg IM of the 1:1000 dilution of epinephrine which contains 1 mg per mL. The IM route is preferred over subcutaneous route because of more rapid absorption. This treatment may be repeated at 5 to 15 minute intervals as necessary to reverse shock and bronchospasm. Care must be taken with epinephrine to make sure that the IM strength of 1:1000 is not mistaken for the IV strength of 1:10,000 used in cardiac arrest. Patients on beta-blockers may not respond to epinephrine and can be given glucagon 1 to 2 mg IV over 5 minutes, followed by infusion of 5 to 15 micrograms per minute. In addition to epinephrine administration, rapid administration of normal saline is usually needed to fill up the dilated vascular space and support BP until epinephrine can counteract the vasodilation. Albuterol via nebulizer or inhaler can be used as an adjunctive therapy in anaphylaxis to treat bronchospasm but should not be used in place of epinephrine. Albuterol does not treat the vasodilation or mediator release that occurs in anaphylaxis. Methylprednisolone is a glucocorticoid that can be used as adjunctive therapy to decrease the inflammatory response that causes anaphylaxis, but it does nothing to manage the acute airway constriction or massive vasodilation that can be fatal in anaphylaxis. Diphenhydramine (Benadryl) is an H1 antihistamine used to relieve itching and hives. It can be used as an adjunctive therapy in allergic reactions, but should not replace or delay epinephrine administration in anaphylaxis. Antihistamines do not relieve airway obstruction, gastrointestinal symptoms, or shock, and do not inhibit mediator release from mast cells and basophils.

When initiating warfarin in a patient receiving unfractionated heparin for a known pulmonary embolus (PE) what does the nurse know to be true: A. A paradoxical hypercoagulable state can occur if the unfractionated heparin is discontinued prematurely (before INR is therapeutic for 24 hours). B. Unfractionated heparin must be changed to another anticoagulant because it cannot be given simultaneous with heparin. C. Unfractionated heparin should be stopped after the first dose of warfarin to reduce bleeding risks. D. Unfractionated heparin should be stopped prior to the first dose of warfarin to avoid medication interactions.

A. The parenteral anticoagulation should not be discontinued until the INR is at least 2.0 for 24 hours or no sooner than 5 days. A paradoxical hypercoagulable state can occur if the initial anticoagulation is discontinued prematurely. The reason for this initial paradoxical state is related to action of warfarin prior a therapeutic INR being established. When warfarin is first started, it inhibits protein C and factor VII more than factors II, IX, and X because protein C and factor VII have shorter half-lives than the other factors. The coagulation factor imbalance in the initial stages of warfarin initiation leads to a paradoxical activation of coagulation. This can result in unintended thrombus formation.

When administering a propofol infusion to a patient receiving mechanical ventilation the nurse recognizes the following nursing implications: A. Propofol has a high lipid content and increases the patient's risk for infection. B. Propofol-related infusion syndrome is a common complication that results in the patient having amnesia. C. Propofol provides light enough sedation that it can be continued into the post extubation period. D. Hypertension is a common side effect and can usually be treated by adding a beta blocker to the patient's medication regime.

A. The tubing and any unused portions of propofol emulsion should be discarded after 12 hours because propofol emulsion contains no preservatives and is capable of supporting growth of microorganisms. Strict aseptic technique should be used when handling propofol. Hypotension is a common complication. Hypotension is most commonly associated with bolus dosing and in hypovolemic patients. Hypotension is a result of venous vasodilatation and mild cardiac depressive effects. Propofol-related infusion syndrome is a potentially life threatening complication characterized by the onset of metabolic acidosis, dysrhythmias, hyperkalemia, rhabdomyolysis (or elevated CPK levels), and cardiac failure. Short term administration of large doses or long term administration (>48 hours) at high doses (>80 mcg/kg/min) may increase the risk of propofol infusion syndrome. Propofol decreases awareness and respiratory drive (apnea can occur during therapeutic sedation). Nurses should only use propofol for sedation in patients receiving mechanical ventilation.

You are caring for a patient who has been prescribed atorvastatin 40 mg after experiencing an acute coronary syndrome event. At a follow up visit he complains of lower extremity muscle aching that he says is new since his recent hospitalization. You have lab results from a complete metabolic profile and a total CPK drawn 3 days ago and all parameters are within normal limits. What is the best option for this patient: A. Discontinue the atorvastatin and try a water soluble statin such as rosuvastatin to see if this results in an improvement in the patient's symptoms. B. Explain to the patient that he will need to learn to live with these symptoms because secondary prevention with atorvastatin is the highest priority. C. Stop the atorvastatin and mark his medical record as being allergic to all statins. D. Increase his atorvastatin to 80 mg daily to assure he is receiving a high intensity statin.

A. This patient is experiencing myalgia. There is no evidence of myopathy because the total CPK is normal. A patient who develops myalgia or myopathy while taking a lipid soluble statin such as atorvastatin or simvastatin may be able to tolerate a water soluble statin such as pravastatin or rosuvastatin. The dosage should not be increased when the patient is experiencing side effects at the current dose. Secondary prevention with a statin is important in this patient. However, long term adherence will not be achieved in a patient who is experiencing ongoing side effects. The patient's provider needs to work with him to try other statins before determining that he is intolerant of statin therapy. Myalgia is a side effect but it does not represent an allergic reaction to all statins.

Drugs whose generic name ends in 'sartan' are: A. Calcium channel blockers. B. Angiotensin receptor blockers (ARB). C. ACE inhibitors. D. Beta blockers.

B. ARBs have generic names ending in 'sartan'. Examples include losartan, candesartan, irbesartan, aprosartan.

Side effects of non-cardioselective beta blockers can include: A. Angina, hypertension, sexual dysfunction, depression. B. Bradycardia, heart block, hypotension, bronchoconstriction. C. Tachycardia, hypertension, depression, fluid retention. D. Ventricular tachycardia, hypotension, fatigue, heart failure.

B. All beta blockers block beta-1 receptors and decrease heart rate, AV conduction velocity, and contractility; therefore side effects can include bradycardia, heart block, and hypotension. Non-cardioselective beta blockers can cause bronchial constriction in patients with reactive airway disease by blocking the bronchodilating beta-2 receptors in the lung.

What is true concerning the use of benzodiazepines for sedation in the patient receiving mechanical ventilation: A. A continuous infusion is preferred over intermittent dosing. B. Their use is associated with increased risk of delirium. C. Lorazepam has a quicker onset of action compared to midazolam. D. When possible benzodiazepines are the sedative of choice in patients receiving mechanical ventilation.

B. Continuous sedation offers the advantage of a more consistent level of sedation but also carries the risk of a deeper than needed level of sedation. Continuous sedation infusions result in longer mechanical ventilation times and longer ICU length of stay, as well as increased risk for delirium. For this reason bolus dosing of benzodiazepines over continuous infusion of benzodiazepines is preferred. However, when possible non benzodiazepines are preferred for sedation due to possible decreased risk of delirium. The onset of action for midazolam is 30 seconds to 5 minutes. Lorazepam has a slower onset of action.

Which of these drugs are used for pharmacological conversion of atrial fibrillation: A. Diltiazem, verapamil, adenosine, procainamide. B. Dofetilide, ibutilide, flecainide, propafenone. C. Amiodarone, digoxin, beta blockers, dofetilide. D. Amiodarone, ibutilide, adenosine, beta blockers.

B. Dofetilide (Tikosyn), ibutilide (Corvert), flecainide (Tambocor) and propafenone (Rhythmol) are recommended for pharmacological conversion of atrial fibrillation to sinus rhythm. Amiodarone is an option for conversion of atrial fib and is effective in maintaining sinus rhythm after conversion but it is recommended as a second line drug. Procainamide can also be effective in converting atrial fibrillation but is not commonly used. Adenosine is not indicated for treatment of atrial fibrillation because it does not convert it and its half-life is too short to be of use in rate control. Diltiazem and verapamil are calcium channel blockers often used for ventricular rate control in atrial fibrillation but not for conversion. Beta blockers are also used for rate control but not for conversion. Digoxin can be used for rate control in patients with heart failure who cannot tolerate calcium channel blockers or beta blockers.

What is true regarding the use of bronchodilator therapy in the treatment of chronic obstructive pulmonary disease: A. Bronchodilators are given to reduce mortality from COPD. B. Anticholinergics and beta 2-agonists are the primary bronchodilators used in the treatment of COPD. C. Short acting agents are preferred over long acting agents. D. The preferred method for delivery is oral.

B. Inhaled therapy is the preferred mode of delivery and long acting agents are preferred over short acting agents. Anticholinergics and beta 2-agonists are the primary bronchodilators used in the treatment of COPD. To date there is no definitive evidence that existing medications are able to alter the long term decline in lung function.

You are caring for a patient with an acute Type A thoracic aortic dissection. The patient is scheduled for life flight to a tertiary care center. The patient is currently being treated with labetalol. Which of the following is true: A. Labetalol is an intravenous form of metoprolol tartrate. B. Labetalol is a beta blocker and an alpha1 blocker. This allows both heart rate and blood pressure to potentially be controlled with one medication. C. Labetalol is non selective beta blocker and is preferred over oral carvedilol because it does not have alpha1 blocking properties. D. Labetalol should always be used with diltiazem or verapamil because it is the only beta blocker that is a pure vasodilator.

B. Labetalol is a beta blocker and an alpha1 blocker. Alpha1 receptors cause vasoconstriction when stimulated and thus alpha blockers prevent vasoconstriction. All beta blockers block beta1 and therefore reduce heart rate. Labetalol and metoprolol tartrate are not the same medications.

In the patient with hypertrophic obstructive cardiomyopathy, medications that can potentially worsen the obstruction include: A. Nitroglycerine and beta blocker. B. Dobutamine and furosemide. C. Beta blocker and ACE inhibitor. D. Calcium channel blocker and beta blocker.

B. Left ventricular outflow tract obstruction worsens with anything that increases contractility or decreases left ventricular filling (preload). Furosemide, nitroglycerine, and ACE inhibitors decrease left ventricular preload and can worsen outflow track obstruction. Dobutamine and other positive inotropes increase myocardial contractility, which can also contribute to narrowing of the outflow tract. Beta blockers and calcium channel blockers decrease heart rate and decrease contractility. A slower heart rate allows for increased ventricular filling time which can increase volume in the LV and help keep the outflow tract open.

What is true regarding pharmacological treatment of diabetes mellitus type 2: A. Incretin mimetics are a second generation to metformin. They have the same mechanism of action as metformin with less side effects. B. Metformin is the preferred agent unless contraindicated. C. Insulin should be the first line agent in any patient with an A1C > 7.0%. D. Thiazolidinedione oral agents are the preferred agents in patients with active heart failure.

B. Metformin (unless contraindicated) is the preferred pharmacological agent in type 2 diabetes. Metformin has evidence for both efficacy and safety. It may also reduce the risk of cardiovascular disease. Metformin may be used in patients with stable heart failure and normal renal function. If metformin alone does not achieve the desired A1C goal within three to six months, another oral agent, a glucagon-like peptide-1(incretin mimetics), or insulin can be added to the regime. In newly diagnosed patients with markedly elevated glucose levels, insulin may be added to the initial regime. The actions of metformin include: • Decrease in hepatic glucose production • Decrease in intestinal absorption of glucose • Improved insulin sensitivity through increased peripheral glucose uptake and utilization. The actions of glucagon-like peptide-1 medications (incretin mimetics) include: • Increase in glucose dependent insulin secretion • Decrease in inappropriate glucagon secretion • Increase in beta cell growth and replication • Slowing of gastric emptying and resultant decrease in food intake. Thiazolidinedione oral agents (also known as glitazones) should not be used in patients with symptomatic heart failure or in patients with stable ischemic coronary disease.

Treatment for nicotine withdrawal is best accomplished with: A. Varenicline (Chantix). B. Nicotine replacement therapy. C. Benzodiazepines D. Bupropion (Wellbutrin SR).

B. Nicotine replacement therapy is effective in treating withdrawal syndrome because it provides controlled amounts of nicotine which limits withdrawal symptoms. All other therapies, while helpful in smoking cessation, do not provide the same level relief from nicotine withdrawal symptoms.

Which of the following drugs is indicated for treatment of acute myocardial ischemia: A. Atropine. B. Nitroglycerin. C. Captopril. D. Sublingual nifedipine.

B. Nitroglycerin dilates coronary arteries and can relieve myocardial ischemia by improving blood flow through collateral vessels. Its major hemodynamic effect is venous dilation, which reduces preload and helps decrease myocardial O2 demand. Sublingual Nifedipine causes potent peripheral vasodilation which causes hypotension that can increase myocardial ischemia. Nifedipine should never be used sublingually to treat chest pain. Captopril is an ACE inhibitor but has no direct effect of coronary blood flow. Atropine is used to treat symptomatic bradycardia.

The main cardiovascular effects of beta blockers include: A. Decreased heart rate, positive inotropic activity, vasoconstriction. B. Decreased heart rate, decreased contractility, decreased AV conduction velocity. C. Peripheral vasodilation and increased contractility. D. Peripheral vasoconstriction and increased heart rate.

B. Noncardioselective beta blockers can block peripheral beta-2 receptors (which cause vasodilation,) thus leaving the vasoconstricting alpha receptors unopposed. Labetalol and carvedilol are beta blockers that have alpha blocking effects which cause peripheral vasodilation. Nebivolol is a newer beta blocker that causes vasodilation by increasing nitric oxide production in vascular tissue.

Pharmacological treatment of bleeding gastric ulcers or gastritis can include all of the following EXCEPT: A. Antacids or sucralfate to protect stomach mucosa. B. Nonsteroidal anti-inflammatory drugs (NSAIDS) to decrease gastric inflammation. C. Antibiotics to treat H. pylori infections. D. Histamine H2 blockers or proton pump inhibitors (PPI) to decrease acid production.

B. Patients with gastric ulcers should avoid NSAIDs because they can contribute to development of ulcers by inhibiting prostaglandins. Stomach or duodenal ulcers are common side effects of long-term NSAID use. Histamine H2 blockers decrease stimulation of H2 receptors in gastric cells that are responsible for secretion of hydrochloric acid, resulting in a decrease in gastric acid secretion. PPIs totally block stomach acid secretion and are the most powerful drugs for treating peptic ulcer disease. Antacids neutralize stomach acid to decrease irritation and inflammation of gastric mucosa. Sucralfate coats the gastric mucosa to reduce its exposure to stomach acids. 80% to 90% of gastric ulcers are caused by infection with Heliobacter pylori (H. pylori) bacteria. Antibiotics used to treat H. pylori infections include tetracycline, amoxicillin, clarithromycin (Biaxin), and metronidazole (Flagyl).

The following sympathomimetic medications exhibit inotropic properties at therapeutic doses EXCEPT for: A. Dopamine. B. Phenylephrine (Neosynephrine). C. Epinephrine. D. Dobutamine.

B. Phenylephrine is a pure alpha drug with no beta effects, so its major effect is peripheral vasoconstriction. Dobutamine, dopamine, and epinephrine all stimulate beta-1 receptors and therefore can all increase contractility (positive inotropic effect).

The following drugs are oral factor Xa inhibitors used for treatment of nonvalvular atrial fibrillation and DVT prophylaxis/treatment: A. Warfarin and clopidogrel (Plavix). B. Dabigatran (Pradaxa) and rivaroxaban (Eliquis). C. Rivaroxaban (Xarelto) and apixaban (Eliquis). D. Prasugrel (Effient) and ticagrelor (Brilinta).

B. Rivaroxaban and apixaban are new oral factor Xa inhibitors approved for prevention of stroke and systemic embolization in patients with nonvalvular atrial fibrillation, and for prophylaxis and treatment of DVT. Dabigatran (Pradaxa) is an oral direct thrombin inhibitor. Prasugrel (Effient) and ticagrelor (Brilinta) are antiplatelet agents that inhibit platelet activation.

Which of the following drugs are Factor Xa inhibitors used for prevention of stroke in patients with nonvalvular atrial fibrillation: A. Dabigatran (Pradaxa) and Ticagrelor (Brilinta). B. Rivaroxaban (Xarelto) and Apixaban (Eliquis). C. Prasugrel (Effient) and Apixaban (Eliquis). D. Ticagrelor (Brilinta) and Prasugrel (Effient).

B. Rivaroxaban and apixaban are oral factor Xa inhibitors approved for prevention of stroke and systemic embolization in patients with nonvalvular atrial fibrillation. Dabigatran is an oral direct thrombin inhibitor approved for prevention of stroke and systemic embolization in patients with nonvalvular atrial fibrillation. Ticagrelor and prasugrel are antiplatelet agents that block the P2Y12 receptor on the ADP pathway of platelet activation.

A patient with a low density lipoprotein cholesterol (LDL-C) of 198 mg/dL is statin intolerant and is placed on a bile acid sequestrant to lower his LDL-C. What information do you provide to the patient when giving instructions: A. This medication causes diarrhea as a primary side effect but it will only last for the first two days until your body adjusts. B. It will be very important for you to drink plenty of water while taking this medication because constipation is a common side effect. C. This medication may cause some skin discoloration because it also increases your bilirubin. D. This medication causes a 'flush' that is usually prevented if you take your aspirin 30 minutes before you cholesterol medicine.

B. Side effects of bile acid sequestrants include gastrointestinal (GI) distress and constipation. Constipation is the most common and troublesome side effect. Niacin (Nicotinic Acid) causes prostacyclin mediated vasodilation that is responsible for the classic "flush" associated with niacin use. This vasodilation can also produce pruritus, headaches, or other pain. This is the most common side effect that has interfered with tolerance. Flushing is diminished by gradual increase in dosing until a therapeutic dose is achieved. Aspirin given 30 minutes before niacin can diminish the flushing response.

When using statin therapy to reduce risk of cardiovascular disease, high intensity statin therapy is defined as: A. A daily dose that lowers LDL-C by 30% - <50%. B. A daily dose that lowers LDL-C by > 50%. C. The highest dose the patient can tolerate without side effects. D. The dose required to get LDL-C below 100mg/dl.

B. The 2013 ACC/AHA Blood Cholesterol Guidelines define high intensity statin therapy as a daily dose that lowers LDL-C by approximately 50% or more. Moderate intensity statin therapy is defined as a daily dose that lowers LDL-C by 30% to <50%. The guidelines no longer recommend targeting a specific LDL-C level of <70 mg/dl or <100 mg/dl as they did in the past because there is no evidence to support the use of specific LDL-C and/or non-HDL-C treatment targets. The new guidelines recommend using the highest tolerated statin dose to reduce atherosclerotic cardiovascular disease (ASCVD) events in patients most likely to benefit from therapy.

Side effects of ACE inhibitors can include which of the following: A. Cough, hypotension, hypokalemia, hypernatremia. B. Cough, hypotension, hyperkalemia, angioedema. C. Bradycardia, blue skin tone, hypokalemia. D. Hypertension, rash, bradycardia.

B. The cough is probably due to increased levels of bradykinin caused by ACE inhibitors. ARBs do not increase bradykinin levels and do not cause cough as often as ACEI. Hypotension can occur because of arterial and venous dilation caused by ACE inhibitors. Hyperkalemia can occur because ACE inhibitors block aldosterone release from the adrenal cortex. Aldosterone causes the renal tubules to retain Na+, and whenever Na+ is retained K+ is lost. Blocking this aldosterone effect causes loss of Na+ and retention of K+ (hyperkalemia). Angioedema is an allergic reaction involving swelling, numbness, tingling of oral mucosa, tongue, airways and can lead to respiratory problems. Prior angioedema is an absolute contraindication for the administration of ACE inhibitors.

Your patient is having an anaphylactic reaction to the new antibiotic that is being administered IV. You know that the most important immediate therapy for anaphylaxis in order to prevent shock and death is administration of: A. Diphenhydramine (Benadryl) for antihistamine effects. B. Epinephrine to reverse bronchospasm and cause peripheral vasoconstriction. C. Albuterol inhaler for bronchospasm. D.D. Methylprednisolone to decrease inflammatory response.

B. The most important immediate therapy in anaphylaxis is epinephrine. There are no absolute contraindications to epinephrine in the setting of anaphylaxis. Epinephrine is the only drug that prevents or reverses obstruction to airflow due to bronchoconstriction, and prevents or reverses cardiovascular collapse by causing vasoconstriction in peripheral vessels to counteract the massive vasodilation in anaphylaxis. Epinephrine also decreases inflammatory mediator release from mast cells and basophils. The recommended adult dose of epinephrine for anaphylaxis is 0.3 to 0.5 mg IM of the 1:1000 dilution of epinephrine which contains 1 mg per mL. The IM route is preferred over subcutaneous route because of more rapid absorption. This treatment may be repeated at 5 to 15 minute intervals as necessary to reverse shock and bronchospasm. Care must be taken with epinephrine to make sure that the IM strength of 1:1000 is not mistaken for the IV strength of 1:10,000 used in cardiac arrest. Patients on beta-blockers may not respond to epinephrine and can be given glucagon 1 to 2 mg IV over 5 minutes, followed by infusion of 5 to 15 micrograms per minute. In addition to epinephrine administration, rapid administration of normal saline is usually needed to fill up the dilated vascular space and support BP until epinephrine can counteract the vasodilation. Albuterol via nebulizer or inhaler can be used as an adjunctive therapy in anaphylaxis to treat bronchospasm but should not be used in place of epinephrine. Albuterol does not treat the vasodilation or mediator release that occurs in anaphylaxis. Methylprednisolone is a glucocorticoid that can be used as adjunctive therapy to decrease the inflammatory response that causes anaphylaxis, but it does nothing to manage the acute airway constriction or massive vasodilation that can be fatal in anaphylaxis. Diphenhydramine (Benadryl) is an H1 antihistamine used to relieve itching and hives. It can be used as an adjunctive therapy in allergic reactions, but should not replace or delay epinephrine administration in anaphylaxis. Antihistamines do not relieve airway obstruction, gastrointestinal symptoms, or shock, and do not inhibit mediator release from mast cells and basophils.

A 67 year old female is admitted to your unit following a stent to the RCA for an inferior wall MI. Her BP has dropped from 110/58 to 88/66 and she is c/o nausea and dizziness. The monitor shows this rhythm Wenckebach. What would be an appropriate drug for treatment: A. Metoprolol 5 mg IV. B. Atropine 0.5 mg IV. C. Epinephrine 1 mg IV. D. Lidocaine 100 mg IV.

B. The rhythm is Type I second degree AV block (Wenckebach) and the presence of hypotension, nausea and dizziness indicate the need for treatment. Epinephrine is a vasopressor used to support blood pressure during CPR in pulseless rhythms. It also has positive inotropic effects that can support contractility once a perfusing rhythm is restored. An epinephrine drip at 2 to 10 mcg/min can be used to support heart rate and blood pressure if symptomatic bradycardia is unresponsive to atropine. Lidocaine is an antiarrhythmic used to treat ventricular arrhythmias. Metoprolol is a beta blocker and can be used for rate control in atrial fib/flutter or for other SVTs.

Class III antiarrhythmic drugs that block potassium channels and prolong myocardial repolarization time include: A. Diltiazem, verapamil. B. Amiodarone, sotalol (Betapace), dofetilide (Tikosyn), ibutilide (Corvert). C. Disopyramide (Norpace), procainamide (Pronestyl). D. Atenolol, metoprolol.

B. These drugs are class III antiarrhythmics that inhibit potassium channels and prolong repolarization time in myocardial tissue. Disopyramide and procainamide are class I antiarrhythmics that block sodium channels. Diltiazem and verapamil are calcium channel blockers and are considered class IV antiarrhythmics. Atenolol and metoprolol are beta blockers and are class II antiarrhythmics.

A 68 year old woman is admitted to the telemetry unit for chemical conversion of atrial fibrillation. She is started on dofetilide (Tikosyn) and an hour later the monitor technician brings the attached rhythm strip to your attention (torsades). What is appropriate treatment: A. No treatment is necessary since the arrhythmia is not sustained. B. Discontinue dofetilide and give magnesium. C. Immediate defibrillation. D. Diltiazem to decrease ventricular rate. E. Start CPR and give epinephrine 1 mg IV.

B. This rhythm is torsades de pointes due to QT interval prolongation from dofetilide. Dofetilide is a class III antiarrhythmic agent that blocks potassium channels and prolongs ventricular repolarization, increasing the risk of torsades. Management of torsades includes discontinuing the causative drug and using magnesium or overdrive ventricular pacing to control episodes of torsades until the causative drug is eliminated. Defibrillation is only indicated if torsades becomes sustained and results in loss of consciousness. Torsades often occurs in short bursts that self-terminate every few seconds so defibrillation is not effective. If the rhythm does become sustained and pulseless then CPR and defibrillation would be appropriate. Diltiazem is useful for decreasing ventricular rate in atrial fibrillation but not for treating torsades.

Drug therapy for heart failure includes which of the following types of drugs: A. Beta blockers, calcium channel blockers, inotropes. B. Diuretics, beta blockers, ACE inhibitors, aldosterone blockers. C. Platelet inhibitors, nitrates, calcium channel blockers. D. Diuretics, calcium channel blockers, vasopressin.

B. Treatment of heart failure includes preload reduction with diuretics and venous dilators, afterload reduction with arterial vasodilators, blocking chronic sympathetic nervous system activity with beta blockers, and blocking the renin-angiotensin-aldosterone system with ACE inhibitors, angiotensin receptor blockers, and aldosterone blockers. Inotropes can be used in decompensated heart failure to increase contractility, but they have a negative effect on mortality and are only indicated for short-term use in decompensated failure or for palliation of symptoms in end-stage patients.

A patient is admitted to the telemetry unit following a syncopal episode at home. Her rhythm is sinus bradycardia at a rate of 32 beats per minute. She is on multiple medications for treatment of angina and hypertension. Which of the following medications might be contributing to her bradycardia and syncope: A. Atenolol and atorvastatin. B. Atorvastatin and ASA. C. Atenolol and diltiazem. D. Lisinopril and diltiazem.

C. Atenolol is a beta blocker and diltiazem is a calcium channel blocker. Both groups of drugs decrease heart rate and slow AV conduction, which can lead to bradycardia and syncope. Lipitor is a statin used to decrease LDL-C and has no effect on heart rate. Lisinopril is an ACE inhibitor used to treat heart failure and hypertension and has no effect on heart rate. ASA is used for its cardiovascular protective effects and has no effect on heart rate.

Vasodilators should be used very cautiously in patients with the following conditions: A. Right ventricular infarct and acute mitral regurgitation. B. Heart failure. C. Aortic stenosis and hypertrophic cardiomyopathy. D. Aortic stenosis and aortic dissection.

C. Because there is a fixed valve area in aortic stenosis, patients have limited ability to increase their cardiac output in response to hypotension that could result from vasodilation. The same is true when hypertrophic cardiomyopathy results in LV outflow tract obstruction. Vasodilators (particularly venous vasodilators) are also used cautiously in patients with hypertrophic cardiomyopathy because there is reduced ventricular filling space is a stiff noncompliant ventricle. The ventricle needs to be kept as full as possible to assure adequate cardiac output. Vasodilators should also be used with caution in patients with right ventricular infarcts. It is important to keep the right ventricle full (fluids are indicated) in order to get an adequate amount of blood to the left ventricle. Vasodilators are a vital part of the treatment of aortic dissection where blood pressure needs to be kept as low as possible while still maintaining end organ perfusion. Vasodilators are also a primary treatment for patients with mitral regurgitation and heart failure. In acute mitral regurgitation, afterload reduction is used to improve forward flow through the aortic valve which will reduce the amount of backflow through the incompetent mitral valve. Both arterial and venous dilators are important for preload and afterload reduction in heart failure.

The following is true regarding bupropion (Wellbutrin SR) when it is used for smoking cessation: A. It is not safe to initiate bupropion in the first 2 weeks after a myocardial infarction. B. Bupropion may not be used with nicotine replacement therapy. C. Bupropion should be initiated one week prior to cessation date with instructs to the patient to pick a quit date the second week of therapy. D. Bupropion therapy can continue for up to 6 months allowing the patient ample time to be successful.

C. Bupropion therapy is usually continued for 7 to 12 weeks. It is recommended to discontinue therapy if cessation has not occurred by week 12. Bupropion may be used with nicotine replacement therapy. Bupropion appears to be safe in the post myocardial infarction patient, however, may not be effective as a cessation aide in this population.

You are caring for a patient with symptomatic lower extremity peripheral arterial disease (PAD). His past medical history includes diabetes mellitus type 2 and systolic heart failure with an ejection fraction of 25%. He states he has a neighbor who is taking Cilostazol (Pletal) for claudication symptoms. The patient asks you why his physician has not prescribed this medication for him. What is your best response: A. This medication interacts with diabetes medications and causes low blood sugar. B. Cilostazol (Pletal) is a medication used in PAD for patients who cannot take aspirin. It is not used to treat symptoms. C. Unfortunately that medication cannot be used in patients who have the type of heart failure you have. D. That medication is an old medication and it is no longer used in the treatment of PAD.

C. Cilostazol (Pletal) is a platelet aggregation inhibitor that has vasodilator properties. It is dosed at 100 mg PO BID. Cilostazol is recommended in all patients with lifestyle limitations who do not have systolic heart failure. An improvement in walking distance of approximately 40-60% is seen after 12 to 24 weeks of therapy. Cilostazol is a phosphodiesterase (PDE) III inhibitor. Other drugs in this class, such as milrinone, have been studied for their long term effectiveness as inotropic agents in severe heart failure, and have shown increased mortality in the presence of systolic dysfunction. For this reason, cilostazol should not be used in patients with systolic heart failure.

Diltiazem and verapamil are examples of drugs in which classification: A. ACE inhibitors. B. Platelet inhibitors. C. Calcium channel blockers. D. Beta blockers.

C. Diltiazem and verapamil are the two calcium channel blockers referred to as the 'heart rate lowering' calcium blockers because they have the most effect on decreasing heart rate and slowing AV conduction velocity. They can be used as antiarrhythmics for rate control in atrial fibrillation and for treating other supraventricular tachyarrhythmias. Dihydropyridine calcium channel blockers, those whose generic name ends in 'pine' (like amlodipine, felodipine, etc.), have peripheral vasodilating effects and less effect on heart rate and contractility.

Which of the following drugs are fibrinolytic agents that dissolve thrombus in blood vessels: A. Clopidogrel, prasugrel. B. Rivaroxaban, apixaban. C. tPA (Alteplase), rPA (Reteplase), TNK-tPA (Tenecteplase). D. Heparin, enoxaparin.

C. Fibrinolytic agents accelerate the conversion of plasminogen to plasmin which then breaks up fibrin strands and dissolves clot. Alteplase, Reteplase, and Tenecteplase are fibrinolytic agents most commonly used in STEMI. Heparin and enoxaparin (a LMWH) are anticoagulants that inactivate thrombin and also have antiplatelet effects (inhibit the thrombin pathway of platelet activation). Clopidogrel and prasugrel are antiplatelet agents that inhibit theP2Y12 receptor on the ADP pathway of platelet activation. Rivaroxaban and apixaban are oral direct thrombin inhibitors and are used as anticoagulants, not antifibrinolytics.

Drugs used to prevent GI bleeding in critically ill patients include which of the following: A. ACE inhibitors and angiotensin receptor blockers (ARBs). B. Aldosterone blockers and beta blockers. C. Proton pump inhibitors (PPI) and histamine-2 receptor blockers (H2 blockers). D. Beta blockers and calcium channel blockers.

C. H2 blockers and PPI reduce gastric acid secretion. Examples of H2 blockers include cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepsid), and nizatidine (Axid). Examples of PPI include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), and pantoprazole (Protonix). Other drugs that can be used include sucralfate (Carafate) which coats and protects the gastric mucosa without altering gastric acid secretion, and antacids which neutralize gastric acid to protect the gastric mucosa. ACE inhibitors prevent conversion of angiotensin I to angiotensin II and ARBs block angiotensin II at its receptor site. Both are used to treat heart failure and hypertension. Aldosterone blockers are used in heart failure to block aldosterone's effect on Na+ and water reabsorption by the kidney. Beta blockers and calcium channel blockers can be used to treat hypertension and angina. Beta blockers are indicated in heart failure as well.

Complications of long term inhaled corticosteroid therapy in patients with chronic obstructive pulmonary disease include: A. Peripheral arterial disease. B. Monocular blindness. C. Increased risk for pneumonia. D. Nephropathy.

C. Inhaled corticosteroids in the treatment of COPD remain controversial and they are used as part of chronic treatment in stable patients only in specific situations. Regular treatment can reduce symptoms and improve quality of life in patients with a FEV1 < 60%. Long term therapy, however, does not modify the long term course of the disease nor does it reduce mortality. Long term treatment with inhaled corticosteroids increases the risk for pneumonia. Inhaled corticosteroids can be used in combination with long acting beta 2-agonists. Long term use of oral steroid therapy in COPD patients can result in steroid myopathy resulting in muscle weakness, decreased functional status, and potential respiratory failure.

Which type of diuretic is the first line choice for managing heart failure: A. Combination of loop and thiazide. B. Potassium sparing diuretics. C. Loop diuretics. D. Thiazides.

C. Loop diuretics are the preferred diuretic in heart failure because they have a rapid onset of action, have increasing effects at increasing doses (high ceiling diuretics), are more potent than thiazides, and may be effective even in the presence of renal failure, which often accompanies heart failure. Other types of diuretics can be added to a loop diuretic if necessary in treating heart failure.

When caring for a patient receiving propofol for sedation while on a mechanical ventilation what does the nurse know to be true regarding dosing: A. The infusion should be initiated at a rate of 50 mcg/kg/min. B. Propofol is recommended to be given in bolus doses for breakthrough agitation. C. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect. D. Propofol is never to be titrated.

C. Mechanically ventilated patients should have infusion initiated slowly at a rate of 5 mcg/kg/min. The infusion rate should be increased by increments of 5 to 10 mcg/kg/min. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect. Most adult patients require a maintenance dose of 5 to 50 mcg/kg/min, although sometimes a higher dose may be required. Nurses should never administer a bolus of propofol.

Your patient returns from the cath lab after receiving a stent to the circumflex artery. He is in atrial fibrillation with ventricular rate in the 80s, BP is 126/68, skin is warm and dry, groin site is stable with the sheath still in place. He is on an eptifibatide (Integrilin) IV drip. His post procedure orders include: ASA daily, clopidogrel (Plavix) daily, metoprolol daily, enalapril daily, and diltiazem bid. You know that the combination of metoprolol and diltiazem can contribute to which of the following side effects: A. Acute renal failure. B. Bleeding. C. Bradycardia or heart block. D. Gastroesophageal reflux.

C. Metoprolol is a beta blocker and diltiazem is a calcium channel blocker. Both types of drugs have the same effect on slowing heart rate and decreasing conduction velocity through the AV node, therefore the combination of the two can result in bradycardia or heart block.

Which of the following drugs are venous or arterial vasodilators: A. Dobutamine, dopamine, nitroprusside. B. Milrinone, epinephrine, nesiritide. C. Nitroprusside, nesiritide, hydralazine. D. Vasopressin, digoxin, nitrates

C. Other drugs that also cause vasodilation include ACE inhibitors, angiotensin receptor blockers, and calcium channel blockers. Vasodilators can dilate veins, arteries or both. The actions of some vasodilators are dose dependent. Vasopressin, high-dose epinephrine, and high-dose dopamine are vasoconstrictors. Digoxin, dopamine, dobutamine, epinephrine and milrinone have positive inotropic effects and increase contractility. Milrinone does have vasodilator effects as well, while dopamine and epinephrine have vasoconstrictor effects at high doses.

When administering an IV vasoactive agent with a half-life of 2 minutes the nurse knows: A. The half-life of a drug does not affect how quickly it is safe to discontinue an IV drip. B. It is OK to just turn off the drip when it is time to discontinue the medication. C. A 2 minute half life is short and requires that the drug be titrated down and the patient's response evaluated prior to discontinuing the drip. D. The longer the half life of a drug the more gradually it needs to be weaned off.

C. The half-life of a drug is the amount of time it takes for the plasma concentration to fall to half its original level. Drugs with a short half-life need to be weaned gradually and the patient's response to decreasing doses needs to be evaluated. Drugs with a long half life (like lidocaine or milrinone) can be discontinued and the body will continue to metabolize the drug over a period of time.

The following is true regarding Varenicline (Chantix) when it is used for smoking cessation: A. Smoking cessation should occur prior to initiation. B. Must be stopped after 12 weeks to minimize the incidence of serious side effects. C. The most common side effect is nausea. D. Can be used with nicotine replacement therapy

C. The most common side effect is nausea. Starting at a low dose and titrating up, taking after eating, and taking with a full glass of water can decrease nausea. Dose adjustments are required for patients with advanced renal dysfunction. Prescribed for a minimum of 12 weeks. For patients who have successfully stopped smoking after 12 weeks, an additional 12 weeks is considered to improve the chance of continued cessation. Not to be used with NRT. Started one week prior to an established quit date.

You are caring for a patient who recently had an anterior wall ST segment elevation MI (STEMI). The patient was started on atorvastatin 80 mg at discharge and is tolerating therapy. On statin therapy his low density lipoprotein cholesterol (LDL-C) was reduced from 120 mg/dL to 60 mg/dL and his high density lipoprotein cholesterol (HDL-C) is 32 mg/dL. What do you know is true regarding adding nicotinic acid or a fibrate to increase the HDL-C: A. Nicotinic acid and fibrates do not raise HDL-C and for this reason are not the lipid lowering drugs of choice. B. Raising the HDL-C to goal is an important part of treatment post myocardial infarction and nicotinic acid is the only recommended drug to be used. C. There is no evidence that using these medications to raise HDL-C will reduce mortality. D. These agents should be added whenever the HDL-C remains below goal on a statin medication.

C. The purpose of the AIM-HIGH trial was to test whether adding Niaspan to patients at LDL-C goal but with continued low HDL-C levels, would improve cardiovascular outcomes. The patients who received Niaspan had a statistically significant improvement in HDL-C and a reduction in triglycerides and LDL-C. However, despite an improvement in lipid levels the study was stopped early due to lack of effectiveness in achieving the primary endpoint which was a composite of cardiovascular death, non-fatal myocardial infarction, acute coronary syndrome, ischemic stroke, or symptom driven cardiac or cerebral revascularization. The HPS2-Thrive study tested the effectiveness of extended release niacin combined with laropiprant when added to statin therapy. The study found no significant benefit of the extended release niacin plus laropiprant on major vascular events. The results of these two studies show no incremental benefit when adding extended release niacin to patients with a low LDL-C.

Drugs used to decrease preload in patients with heart failure include which of the following: A. Epinephrine, digoxin, dobutamine. B. Dopamine, dobutamine, milrinone. C. Furosemide, nitrates, ACE inhibitors. D. Digoxin, diltiazem, amiodarone.

C. The two main ways to reduce preload are diuretics to remove volume from the circulation and venous dilators to hold blood in the dilated venous space and prevent it from returning to the heart. Furosemide (Lasix) is a diuretic; nitrates and ACE inhibitors dilate veins. Dopamine, dobutamine, milrinone, and digoxin are positive inotropes used to increase contractility. They are useful in heart failure to support contractility but not as direct preload reducers. Epinephrine has inotropic and vasopressor effects and is contraindicated in heart failure because it increases afterload and makes the heart work harder.

Which of the following drugs are sympathomimetic agents: A. Milrinone, nitroglycerine, vasopressin, norepinephrine. B. Vasopressin, norepinephrine, isoproterenol, epinephrine. C. Dobutamine, dopamine, epinephrine, norepinephrine. D. Digoxin, nitroglycerine, dobutamine, dopamine.

C. There are 6 drugs used clinically that mimic the sympathetic nervous system by stimulating alpha receptors, beta receptors, or both: phenylephrine (pure alpha), isoproterenol (both beta-1 and beta-2 stimulation), dobutamine (primarily beta-1); dopamine, epinephrine, and norepinephrine all stimulate both beta-1 and alpha receptors. Other drugs have some of the same effects on cardiac contractility and peripheral blood vessels but they have different mechanisms of action and do not work by mimicking sympathetic activity. These drugs include milrinone, digoxin, and vasopressin.

A 60 year old male presents with severe chest pain, SOB, BP 90/60 mmHg. He is alert and talking to you when you notice the attached rhythm (VTACH POLYMORPHIC). What drugs would be appropriate treatment for this rhythm: A. Diltiazem or verapamil. B. Epinephrine or vasopressin. C. Lidocaine or amiodarone. D. No treatment is necessary because this is monitor artifact.

C. This rhythm is polymorphic VT but the QT interval is not prolonged, so it is not torsades de pointes. Polymorphic VT with a normal QT interval can be treated with lidocaine or amiodarone the same as monomorphic VT. Beta blockers may also be useful for polymorphic VT with a normal QT interval because ischemia is a common cause in patients having acute MI. This patient is having an anterior wall MI - note ST elevation in lead V1 and reciprocal ST depression in lead III. He really needs a trip to the cath lab and a stent in his LAD! Revascularization is indicated as a treatment for polymorphic VT when ischemia is the cause. Diltiazem and verapamil are used for ventricular rate control in atrial fib or flutter and for managing other types of SVTs. Epinephrine and vasopressin are not antiarrhythmics - they are vasopressors used to support BP. Epinephrine has positive inotropic effects which can support contractility after a perfusing rhythm is restored.

Drugs whose generic name ends in 'pril' are: A. Angiotensin receptor blockers (ARBs). B. Beta blockers. C. Calcium channel blockers. D. ACE inhibitors.

D. ACE inhibitors have generic names ending in 'pril'. Examples include captopril, enalapril, fosinopril, lisinopril.

You are caring for a patient with a long standing history of resistant hypertension who is on clonidine as one of her four antihypertensive medications. She has been taking this medication for approximately two years. She tells you she is refusing this because her friend told her there are too many side effects. What information do you provide to the patient: A. It is your right to take or refuse any medication. I will make a note of the reason on your chart. B. If you refuse your clonidine you will never be eligible for any other type of blood pressure medication. I want to make sure you are informed when you make your decision. C. For your safety I am obligated to inform you that there is a very high chance that you will develop a delayed allergic reaction by stopping this medication. I will have to get an order for steroids for you. D. The abrupt stopping of your clonidine can potentially be dangerous due to high blood pressure and high heart rate. I would like you to discuss this with your physician before you refuse. If you still decide to stop taking it, she can help us develop a safe plan for discontinuation.

D. Abrupt discontinuation of clonidine has been associated with adverse events including hypertension, tachycardia, agitation, tremors, and headache. There have even been rare cases of hypertensive encephalopathy and stroke. If being discontinued the dose should be reduced over two to four days.

Treatment of HIT involves discontinuing all heparin products (including heparin coated catheters) and using which of these drugs to manage intravascular clotting: A. Clopidogrel (Plavix) and ASA. B. Warfarin. C. LMWH: Enoxaparin (Lovenox) or dalteparin (Fragmin). D. Argatroban (Novastan), bivalirudin (Angiomax), or fondaparinux (Arixtra).

D. Argatroban and bivalirudin are direct thrombin inhibitors that bind directly to soluble and clot-bound thrombin and do not bind to platelet factor 4 as heparin does, therefore they do not cause HIT. Fondaparinux is an indirect factor Xa inhibitor that does not cause HIT. Newer oral factor Xa inhibitors (rivaroxaban and apixaban) and the oral thrombin inhibitor dabigatran should theoretically be effective as anticoagulants in patients with HIT, but at this time data is lacking on their use in treating patients with HIT. LMWH (low molecular weight heparin) can cause HIT but not as often as unfractionated heparin. However, all forms of heparin must be discontinued in the treatment of HIT. Warfarin is not indicated for managing intravascular clotting in HIT because its onset of action is delayed for 2-7 days until normal clotting factors are cleared from the circulation. Clopidogrel and ASA inhibit platelet activation but have no effect on thrombin so are not effective in managing intravascular clotting in HIT.

The following is true concerning arterial vasodilators: A. They are contraindicated in patients with heart failure. B. They increase myocardial contractility and oxygen demand. C. They have a direct impact on reducing right ventricular preload. D. They reduce left ventricular afterload by decreasing systemic vascular resistance.

D. Arterial vasodilators reduce left ventricular afterload by decreasing systemic vascular resistance (SVR). SVR is determined primarily by the diameter of the systemic arterioles. Venous dilators reduce right ventricular preload by causing blood to pool in dilated veins. Arterial vasodilators can cause a reflex tachycardia in response to a drop in blood pressure. They are used in heart failure to reduce systemic vascular resistance and decrease the workload of the left ventricle.

Digitalis toxicity can be associated with which of the following arrhythmias: A. Atrial tachycardia with block and Torsades de Pointes. B. Atrial fibrillation with aberrant conduction and sinus tachycardia. C. Torsades de Pointes and atrial fibrillation. D. Atrial fibrillation with complete AV block, bidirectional VT, atrial tachycardia with block.

D. Atrial fibrillation with complete AV block, bidirectional VT, atrial tachycardia with block. Digitalis toxicity can cause both heart block and tachycardias. Aberrant conduction is not directly related to digitalis toxicity. Torsades de pointes is due to abnormal ventricular repolarization, not digitalis toxicity. Digitalis slows the sinus node and slows conduction through the AV node, so sinus bradycardia (not tachycardia) would occur with digitalis toxicity.

Which drugs are used for ventricular rate control in atrial fibrillation and flutter: A. Amiodarone, lidocaine. B. Adenosine. C. Dopamine, vasopressin. D. Calcium channel blockers, beta blockers.

D. Calcium channel blockers and beta blockers slow conduction through the AV node and are effective in providing long lasting rate control in atrial fib or flutter. They can also be used to treat AV nodal active SVTs (AVNRT and AVRT). Amiodarone and lidocaine are used to treat ventricular arrhythmias. Amiodarone can also be used to convert atrial fib or flutter to sinus rhythm and to slow or block the accessory pathway in patients with WPW syndrome. Adenosine is used to terminate AV nodal active SVTs - AVNRT and AVRT. Dopamine and vasopressin are vasopressors used to support blood pressure.

Calcium channel blockers can be used to manage which of the following: A. Ventricular tachyarrhythmias, angina, acute ST elevation MI, heart failure. B. Angina, heart block, heart failure, ventricular tachyarrhythmias. C. Hypertension, type II diabetes, acute renal failure, supraventricular arrhythmias. D. Hypertension, angina, supraventricular arrhythmias, hypertrophic obstructive cardiomyopathy.

D. Calcium channel blockers cause vasodilation in both coronary and peripheral arteries; therefore, they can be used to treat hypertension and vasospastic angina. They can also decrease contractility and heart rate so they are useful in managing angina. Diltiazem and verapamil are the calcium blockers with the most effect on lowering heart rate and slowing conduction through the AV node. Calcium blockers whose generic name ends in 'pine' (like amlodipine, felodipine, isradipine, etc.) have more peripheral vasodilating effect and therefore have less effect on lowering heart rate because peripheral vasodilation can cause a reflex increase in heart rate. Diltiazem and verapamil are useful in controlling ventricular rate in atrial fib/flutter and for treating other types of SVTs. Calcium blockers can cause bradycardia and heart block and can decrease contractility so are not generally indicated for managing heart failure. In addition, calcium blockers do not have the beneficial effect of neurohormonal blockade in heart failure like beta blockers do. There is one type of ventricular tachycardia that is sensitive to verapamil, but in general calcium blockers are not indicated for treating ventricular arrhythmias. Calcium blockers are not indicated for managing STEMI because of their effect on decreasing contractility and causing peripheral vasodilation which can decrease cardiac output and worsen myocardial perfusion.

When administering a Class III antiarrhythmic such as ibutilide (Corvert) or dofetilide (Tikosyn) the nurse knows that it is very important to assure the patient does not have a deficit in which electrolyte: A. Calcium. B. Sodium. C. Phosphorus. D. Potassium.

D. Class III agents work on phase 3 of the cardiac action potential by blocking potassium channels. Phase 3 of the action potential is cellular repolarization and is associated with the T wave on the surface ECG. Class III agents prolong repolarization and thus prolong the QT interval. Torsades de pointes is a complication / risk associated with the administration of Class III agents such as ibutilide. Since class III agents are potassium channel blockers, hypokalemia will increase the risk of QT prolongation and torsades.

Complications of neuromuscular blockade include all the following except: A. Acute quadriplegic myopathy syndrome. B. Prolonged recovery. C. Myopathy. D. Hypertonicity.

D. Complications of neuromuscular blockade: • Prolonged recovery from the agents • Myopathy, especially when used with corticosteroids and when used longer than 1 to 2 days. • Acute quadriplegic myopathy syndrome (triad of symptoms): 1) Acute paresis, 2) Myonecrosis (increased CPK enzymes), and 3) Abnormal EMG.

Which of the following drugs are inotropes used to increase cardiac contractility: A. Hydrochlorothiazide, furosemide, spironolactone. B. ACE inhibitors, angiotensin receptor blockers (ARBs). C. Norepinephrine, epinephrine, vasopressin. D. Digoxin, dobutamine, milrinone.

D. Digoxin is the only oral inotrope used in cardiovascular medicine. Dobutamine and milrinone (Primacor) are used IV to increase contractility in heart failure and shock. ACE inhibitors and ARBs are vasodilators that reduce both preload and afterload. Norepinephrine, epinephrine, and vasopressin are vasoconstrictors used to support BP. Hydrochlorothiazide, furosemide, and spironolactone are diuretics used to reduce preload.

Drugs used as vasopressors to support BP in severely hypotensive patients who do not respond to fluid administration include: A. Amlodipine, atenolol. B. Nitroprusside, nitroglycerin. C. Dobutamine, milrinone. D. Dopamine, norepinephrine.

D. Dopamine in higher doses and norepinephrine (Levophed) are vasoconstrictors that can be used to support BP in hypotensive patients who do not respond to volume. BP = CO X SVR. In order to increase BP one must increase either CO or SVR or both. Vasopressors increase SVR to support BP. Nitroprusside and nitroglycerin are vasodilators that can reduce preload and afterload and decrease BP. Dobutamine and milrinone have positive inotropic effects that can improve cardiac output in patients with left ventricular dysfunction. Dobutamine stimulates beta-1 receptors to increase cardiac contractility. Milrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator effects. Both drugs can support BP by increasing cardiac contractility but not by causing vasoconstriction. Amlodipine is a calcium channel blocker with vasodilator properties and can decrease SVR and BP. Atenolol is a beta blocker and can decrease CO by decreasing contractility and heart rate which can result in a decrease in BP.

Epinephrine is a first line drug for any pulseless condition because it has the following actions: A. It slows the heart rate and improves contractility. B. It coverts VF to sinus rhythm. C. It decreases myocardial O2 demand by slowing the heart rate and causing peripheral vasodilation. D. It has positive inotropic effects and selectively shunts blood to heart and brain.

D. Epinephrine has both alpha and beta stimulating effects. Beta stimulation increases myocardial contractility. Alpha stimulation causes vasoconstriction, but epinephrine is a selective vasoconstrictor - it causes vasoconstriction in all vascular beds except heart, brain and skeletal muscle. Therefore, it can help shunt cardiac output generated by CPR into heart and brain.

You are caring for a patient who is undergoing a transesophageal echocardiogram and the patient has received a topical benzocaine. The patient develops a diffuse cyanosis, dyspnea, headache, chest pain, and palpitations. His oxygen saturation remains consistent with his pre-procedural level. What treatment do you anticipate: A Sublingual nitroglycerin. B. Emergency surgery for tracheostomy. C. BiPAP with 100% FIO2. D. Intravenous (IV) methylene blue as the first-line antidotal agent.

D. Methemoglobinemia is caused by increased levels of methemoglobin (with iron in the ferric state). Iron atoms in the ferric state will not bind with oxygen. Methemoglobinemia is commonly caused by nitrite poisoning or can be caused by a toxic reaction to oxidant drugs. A common cause of acquired methemoglobinemia is exposure to topical benzocaine during a procedure such as a transesophageal echocardiogram. Intravenous methylene blue is the treatment of choice for methemoglobinemia.

Inotropic support is often needed for the first few hours following CABG surgery when there is left ventricular dysfunction present. Which of the following drugs are appropriate for inotropic support: A. Esmolol, metoprolol, or nicardipine. B. Nitroglycerine or nitroprusside. C. Norepinephrine or vasopressin. D. Milrinone, dobutamine, dopamine, or epinephrine.

D. Milrinone, dobutamine, dopamine, and epinephrine all increase contractility. Milrinone is also a vasodilator so would be indicated when inotropic support is needed in the presence of a high SVR. Dobutamine, dopamine, and epinephrine all have beta adrenergic effects to increase contractility. Epinephrine is often the preferred inotropic agent because it causes less tachycardia than dopamine or dobutamine and also has some peripheral vasoconstrictor effects that can help support the blood pressure. Nitroglycerin and nitroprusside are both vasodilators with no inotropic effect. Nitroglycerin is primarily a venous dilator and is used for preload reduction. Nitroprusside has both venous and arterial vasodilating effects with somewhat more arterial effect and is used to manage postoperative hypertension. Esmolol and metoprolol are beta blockers and nicardipine is a calcium channel blocker. Beta blockers and calcium channel blockers are negative inotropic drugs and decrease contractility. Nicardipine is also a peripheral vasodilator and can be used to treat postoperative hypertension.

Treatment of pulmonary arterial hypertension (PAH) is aimed at treating the underlying cause and using drugs that reduce pulmonary vascular resistance, including: A. Nitroglycerine, dobutamine (Dobutrex), eptifibatide (Integrilin). B. Metoprolol (Lopressor), atenolol (Tenormin), diltiazem (Cardizem). C. Lisinopril (Zestril), nitroglycerine, verapamil (Calan). D. Epoprostenol (Flolan), sildenafil (Viagra, Revatio), iloprost (Ventavis).

D. Most drugs used to treat PAH cause pulmonary vasodilation and decrease cell proliferation in pulmonary vascular tissue. Such drugs include: prostanoids (e.g. epoprostenol [Flolan], treprostinil [Remodulin], iloprost [Ventavis]); endothelin receptor antagonists (bosentan [Tracleer]; and phosphodiesterase inhibitors (sildenafil [Revatio, also known as Viagra]). Beta blockers can cause pulmonary bronchoconstriction and are not indicated in PAH. Calcium channel blockers can be effective in some patients with PAH because they can cause pulmonary vasodilation, however they have no antiproliferative effects and work only in a small number of patients. Aldosterone blockers are indicated for treating heart failure but have no effect on pulmonary vascular resistance. ACE inhibitors dilate arteries and veins and are used as afterload and preload reducers to treat heart failure and systemic hypertension.

Patients taking HMG-CoA reductase inhibitors (statins) should receive which of the following instructions: A. Always take the medication with grapefruit juice. B. Flushing is a common side effect when initiating therapy. C. Do not take the medication if you are also taking beta-blockers or angiotensin-converting enzyme (ACE) inhibitors. D. Immediately report any muscle weakness your prescriber.

D. Myopathy and liver dysfunction are two of the uncommon but potentially serious adverse effects of statins. Myopathy can progress to rhabdomyolysis and cause acute renal failure. For this reason it is important for patients to report any muscle weakness to their physician so statin therapy can be discontinued if myopathy exists. Statins are commonly used along with beta blockers and ACE inhibitors in the secondary prevention of coronary artery disease. Grapefruit juice contains an agent that slows the activity of the liver enzyme that metabolizes some of the agents in this class, particularly simvastatin and atorvastatin. Therefore, grapefruit juice consumption can increase the expected drug levels for a given dose and increase the risk of rhabdomyolysis. Patients should be instructed not to consume large quantities of grapefruit juice when taking these drugs. Flushing is a common side effect of niacin when initiating therapy and usually subsides within 2 weeks of therapy at a stable dose.

All of the following are true regarding the use of nicotine replacement therapy EXCEPT: A. Nicotine replacement therapy should be tapered over 9-12 weeks. B. Nicotine replacement therapy can be used in stable patients with a recent MI. C. Nicotine replacement therapy may be used in combination with buproprion. D. Nicotine replacement is indicated in all smokers including those users of smokeless tobacco.

D. NRT includes patches, gum, lozenges, nasal spray, and inhalers. Patches are used for continuous coverage and gum, lozenges, nasal spray or inhalers are used for bolus dosing. Dosing is recommended as 4 mg if first cigarette is within 30 minutes of awakening - or 2 mg if > 30 minutes after awakening. Dosing schedule usually involves dose tapering over 9 to 12 weeks. NRT may be used in combination with bupropion. Safe in patients with stable disease; should be used with caution in patients with very recent MI (within 2 weeks), worsening angina, or serious arrhythmias. Not indicated for those who smoke < 10 cigarettes per day, pregnant women, adolescents, or users of smokeless tobacco. Apply to area of skin with no hair. New patch should be applied in the morning. If the patch is associated with insomnia or vivid dreams it can be taken off for sleep. The patch cannot be cut.

Which drugs are used as vasodilators in managing acute decompensated heart failure: A. Furosemide, spironolactone. B. Dobutamine, milrinone. C. Metoprolol, diltiazem. D. Nitrates, nesiritide.

D. Nitrates such as nitroglycerin are primarily venous dilators, while nesiritide is both a venous and arterial dilator. Both can be used for preload reduction in acute decompensated heart failure to relieve dyspnea, but they have no mortality benefit. Dobutamine and milrinone are positive inotropes used to increase contractility. Lasix and spironolactone are diuretics used for preload reduction. Spironolactone is also an aldosterone blocker. Beta blockers are used to block the effects of chronic sympathetic stimulation in heart failure, but they should not be used in the acutely decompensated patient because they can decrease contractility.

What is true concerning vasopressor therapy in severe sepsis and septic shock: A. Vasopressors are the priority over fluid resuscitation in the treatment of sepsis. B. The mean arterial pressure goal is 50 to 60 mmHg. C. Vasopressin should not be used due to elevated endogenous vasopressin levels in patients with severe sepsis and septic shock. D. Norepinephrine is the vasopressor of choice.

D. Patients requiring vasopressor support should have an arterial line in place to provide an immediate assessment of the effectiveness of therapy. Norepinephrine is the preferred vasopressor in severe sepsis and septic shock. Vasopressors should be used to achieve a MAP of 65 mmHg. Epinephrine is the preferred second line vasopressor. Due to stimulation of the beta 2 receptors in skeletal muscle, epinephrine can increase aerobic lactate production. Therefore, when epinephrine is used as a vasopressor, lactate levels are not a reliable resuscitation endpoint. Endogenous vasopressin levels should be elevated in the presence of hypotension. Patients with septic shock have been found to have a relative vasopressin deficiency within 24 to 48 hours of shock onset. Vasopressin at the dose of 0.03 units / minute can be added to norepinephrine to raise the MAP or to decrease the required dose of norepinephrine. Low dose vasopressin should not be used as the sole vasopressor. Vasopressin may have other beneficial physiological effects in addition to raising the MAP. Doses higher than 0.03 to 0.04 have been associated with ischemia and should not routinely be used except as a salvage strategy. Dopamine is not routinely used as the first line agent due to concern for tachyarrhythmias and risk for adverse outcomes (De Backer et al., 2012; De Backer et al., 2010; Patel et al., 2010). It may be considered in select patients with a low risk for tachyarrhythmias or in patients who are bradycardic. Phenylephrine does not cause tachycardia, but it can result in a reduction in stroke volume, and is not used except in special circumstances or as a salvage therapy (Dellinger et al., 2013).

Pharmacological prophylaxis of deep vein thrombosis (DVT) in the acutely ill patient can be achieved by all of the following except: A. Low-dose unfractionated heparin BID or TID. B. Low-molecular-weight heparin (LMWH). C. Fondaparinux. D. Clopidogrel.

D. The American College of Chest Physicians makes the following recommendations: • For acutely ill hospitalized medical patients at increased risk of thrombosis, the following three pharmacological approaches are an option for prophylaxis: (a) low-molecular-weight heparin (LMWH), (b) low-dose unfractionated heparin BID or TID, or (c) fondaparinux. Fondaparinux is not recommended for prophylaxis in the critically ill patient. • For acutely ill hospitalized medical patients at low risk of thrombosis prophylaxis can be achieved by one of the above three pharmacological options or with mechanical prophylaxis. • For acutely ill hospitalized medical patients who are bleeding or who at high risk for bleeding, anticoagulant prophylaxis should not be used.

The four main classes of drugs recommended for initial blood pressure control in hypertension are: A. Loop diuretic, ACEI, ARB, beta blocker. B. Thiazide diuretic, beta blocker, ACEI, aldosterone blocker. C. Beta blocker, calcium channel blocker, ACEI, ARB. D. Thiazide diuretic, calcium channel blocker, ACEI, ARB.

D. The guidelines state that In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACEI), or angiotensin receptor blocker (ARB). In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide diuretic or calcium channel blocker. If goal BP cannot be reached using only these drugs because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used. They also recommend not using an ACEI and an ARB together.

The two classes of medications most effective in lowering triglycerides are: A. Fibrates and bile acid sequestrants. B. HMG-CoA reductase inhibitors and bile acid sequestrants. C. Nicotinic acid and HMG-CoA reductase inhibitors. D. Nicotinic acid and fibrates.

D. The most effective agents for improving triglyceride and HDL-C levels are nicotinic acid (niacin) and the fibrates. Statins, especially simvastatin and atorvastatin, also lower triglycerides and increase HDL-C but not to the degree that nicotinic acid (niacin) and fibrates do. Bile acid sequestrants may actually cause a transient compensatory increase in triglyceride levels.

You are caring for a patient whose creatinine today is 1.7 mg/dL. Yesterday the creatinine was 1.01 mg/dL. Blood pressure is 126/80 mmHg and HR is 74. What ordered medications should be held and clarified with the provider: A. Amiodarone. B Warfarin. C. Metoprolol succinate. D. Lisinopril.

D. This patient has evidence of acute kidney injury (AKI) and all potentially nephrotoxic medications should be held. Aminoglycoside antibiotics and amphotericin B (antifungal) are examples of nephrotoxic medications. Metformin should be discontinued in patients with GFR < 30 ml/min/1.73 m2. ACE-inhibitors and ARBs are indicated in patients with CKD to slow the progression of the disease. However, these medications can result in worsening renal function if given to a patient with AKI or at high risk for AKI. The reason is that patients with an acute reduction in forward flow through the afferent arterioles depend on a compensatory efferent arteriole vasoconstriction in order to maintain an adequate GFR. ACE-inhibitors and ARBs prevent both afferent and efferent arteriole vasoconstriction. Non-steroidal antiinflammatory medications should also be avoided in both chronic kidney disease and AKI.

The mechanism of anticoagulant action of warfarin is: A. Inhibits factor Xa. B. Inactivates circulating thrombin. C. Interferes with platelet activation and aggregation. D. Interferes with prothrombin formation and formation of other clotting factors in the liver. E. All of the above.

D. Warfarin (Coumadin) inactivates vitamin K in the liver and interferes with the production of prothrombin and several other clotting factors in the liver. Drugs that interfere with platelet activation and aggregation include ASA, clopidogrel, prasugrel, ticagrelor, and the IIb/IIIa inhibitors. Heparin inactivates circulating thrombin and other clotting factors. Rivaroxaban and apixaban are factor Xa inhibitors. Dabigatran is a direct thrombin inhibitor.

Which of the following clinical factors increases the risk of a patient developing myopathy when taking a statin: A. Small body size. B. Undertreated hypothyroidism. C. Age > 80 years. D. All of the above.

D. • There is an increased risk of myopathy in patients with advanced age (> 80 years), frailty, small body size, renal insufficiency, and under treated hypothyroidism. • Patients taking other drugs associated with myopathy such as colchicine are also at higher risk.

When caring for a patient with chronic heart failure the nurse recognizes that the following may predispose the patient to the development of hyperkalemia: A. Angiotensin receptor blockers (ARBs). B. Aldosterone antagonists. C. Salt substitutes. D. ACE inhibitors. E. All of the above.

E. ACE inhibitors block the formation of angiotensin II, and ARBs block the effects of angiotensin II at its receptor sites. Angiotensin II results in a release of aldosterone, which causes the renal tubules to retain sodium and water and excrete potassium. Aldosterone antagonists, such as spironolactone and eplerenone, directly block aldosterone and result in an increased retention of potassium. Salt substitutes can contain potassium chloride and predispose to hyperkalemia.

When administering a beta 2- agonist for the treatment of chronic obstructive pulmonary disease the nurse incorporates the following knowledge into practice: A. The addition of a high dose as needed short acting agent to patients already taking a long acting agent is recommended. B. The effects of short acting agents last for 30 minutes to 1 hour. C. Beta 2- agonists block the beta 2 receptors. D.Short acting agents can only be used PRN with no more than 3 doses a week. E. Body tremors can occur in older patients and limit the dose.

E. Beta 2- agonists stimulate the beta 2 receptors and this results in a functional block of bronchoconstriction. The effects of short acting agents last for 4 to 6 hours. Short acting agents can be scheduled or taken as needed. Long acting agents have a duration of 12 to 24 hours depending on the agent. The addition of a high dose as needed short acting agent to patients already taking a long acting agent is not recommended. A common side effect of beta 2-agonists is resting tachycardia. Body tremors can occur in older patients and limit the dose.

The critical care nurse knows the following is true regarding sedation and neuromuscular blockade in patients receiving mechanical ventilation: A. Neuromuscular blockade should seldom be needed in patients who receive adequate analgesia and sedation. B. Sedation is required before and throughout the administration of neuromuscular blockade. C. Sedation to achieve complete amnesia is required when neuromuscular blockade is utilized. D. Prior to determining if a patient needs neuromuscular blockade, it is imperative to assure the patient has adequate analgesia and sedation. E. All of the above.

E. Neuromuscular blockade is most typically not needed for mechanically ventilated patients. Prior to determining if a patient needs neuromuscular blockade, it is imperative to assure the patient has adequate analgesia and sedation. If neuromuscular blockade is needed, sedation is required before and throughout administration. Sedation to achieve complete amnesia is required when neuromuscular blockade is utilized.

All statin medicines need to be administered at bedtime for maximum effectiveness: True. False.

False. The mechanism of action of statins involves the inhibition of HMG-CoA reductase. HMG-CoA reductase catalyzes an early step in cholesterol synthesis. The most active time for cholesterol biosynthesis is during the very early morning hours. For this reason, those statins with a shorter half-life or unknown half-life are more effective when administered in the evening. Statins with a longer half-life can be administered regardless of time of day. Simvastatin, lovastatin, and fluvastatin need to be administered in the evening.

Examples of arterial vasodilators include the following: A. Beta blockers and morphine sulfate. B. ACE inhibitors and calcium channel blockers. C. ACE inhibitors and digoxin. D. Beta blockers and calcium channel blockers.

B. ACE inhibitors and calcium channel blockers cause arterial dilation. ACE inhibitors block the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor. Calcium is necessary for contraction of the muscle layer in arteries, which causes vasoconstriction. Calcium channel blockers cause vasodilation by blocking the movement of extracellular Ca++ into vascular smooth muscle cells. Beta blockers block beta-1 receptors in the heart and beta-2 receptors in peripheral vessels. Beta-2 receptors cause vasodilation in peripheral vessels, so blocking them with beta blockers allows the alpha-1 receptors to dominate and cause peripheral vasoconstriction. Unless a beta blocker is a combined alpha & beta blocker, like carvedilol, there is no arterial vasodilation effect. Digoxin is a positive inotropic agent and is used to increase contractility. It has no major peripheral effects. Morphine sulfate is an opioid analgesic with venous dilating effects.